“What is lamina dura? A detailed question and answers guide”

Lamina dura.

The lamina dura is a key component of dental health that often gets overlooked. It’s the thin layer of dense bone surrounding the tooth root, and it plays a vital role in keeping our teeth stable. As people age, this structure can change, which may affect overall dental health. Understanding the lamina dura can help us recognize its importance in periodontal health and how it relates to age-related changes and systemic conditions. Let’s explore what the lamina dura is, its significance, and how it can be assessed through various methods.

Lamina

• The lamina dura is crucial for tooth stability, connecting the periodontal ligament to the alveolar bone.
• Changes in lamina dura can indicate periodontal disease and other systemic conditions.
• As we age, the lamina dura may deteriorate, affecting dental health and bone remodeling.
• Radiological assessments are essential for evaluating the lamina dura’s health and identifying potential issues.
• Research continues to uncover the lamina dura’s role in dental health and its connection to various systemic diseases.
• Radiographically the alveolar bone proper is seen as a radiopaque white line.
• Periosteum
• Outer circumference lamella
• Osteocyle
• Concentric lamella
• Interstitial lamella
• Haversian canal

“Understanding lamina dura through FAQs: Structure, functions, and uses explained”

Understanding Lamina Dura Structure

Definition and Composition

Okay, so what is the lamina dura? Basically, it’s a layer of dense bone that lines the tooth socket. Think of it as the immediate bony wall surrounding the root of your tooth. It’s made up of compact bone, which is super strong and hard. This compact bone is also sometimes called the cribriform plate because it has tiny holes in it. These holes are important because they allow blood vessels and nerves to pass through, keeping the bone and surrounding tissues alive and well.

Location in the Tooth Socket

Where exactly do you find this lamina dura? Well, it’s pretty straightforward. It’s right there inside the alveolar ridge, forming the inner wall of the tooth socket. It’s snuggled up against the periodontal ligament (PDL), which is the tissue that connects the tooth to the bone. You can’t really see it with your naked eye, but on an X-ray, it shows up as a distinct white line around the tooth root. This is because it’s denser than the surrounding bone. It’s a key landmark for dentists when they’re looking at dental X-rays.

“Importance of studying lamina dura for dental students: Questions explained”

Role in Tooth Stability

So, why is the lamina dura so important? It plays a big role in keeping your teeth stable. It acts as an anchor for the periodontal ligament, which is like a strong, stretchy rope that holds your tooth in place. The lamina dura helps distribute the forces of chewing evenly around the tooth root, preventing it from getting overloaded in one spot. It’s constantly being remodeled by cells called osteoblasts and osteoclasts, which help to maintain its structure and adapt to changes in the forces acting on the tooth. Without a healthy lamina dura, your teeth would be much more likely to become loose or shift out of alignment.

The lamina dura is not a static structure; it’s constantly changing in response to the forces placed on your teeth. This remodeling process is essential for maintaining tooth stability and overall dental health.

Here’s a quick rundown of its functions:

• Anchoring the periodontal ligament
• Distributing chewing forces
• Participating in bone remodeling
• Maintaining tooth position

“Common challenges in mastering lamina dura notes effectively: FAQs provided”

Lamina Dura and Periodontal Health

Indicator of Periodontal Disease

Okay, so the lamina dura? It’s not just some bone hanging out in your jaw. It’s actually a pretty big deal when it comes to figuring out if your gums are healthy. Think of it like this: the lamina dura is like a report card for your periodontal health. If it looks good, things are probably okay. If it looks weird, it might be time to worry. A healthy lamina dura typically appears as a continuous white line around the tooth socket on X-rays.

• Changes in its appearance (like thinning or disappearing) can be early signs of gum disease.
• Dentists use the lamina dura’s appearance to help diagnose periodontal issues.
• It’s not the only thing they look at, but it’s a key piece of the puzzle.

Impact of Bone Resorption

Bone resorption? That’s when your body starts breaking down bone faster than it’s building it. Not good. And guess what? It can really mess with the lamina dura. When bone resorption happens because of periodontal disease, the lamina dura can start to fade away. It’s like the foundation of a house crumbling. If the bone supporting the tooth goes, the lamina dura goes with it. This is why dentists keep a close eye on the lamina dura in patients with gum disease. It’s a direct reflection of how much bone loss is happening. Effective use of conservative techniques is important to maintain dental health.

“Factors influencing success with lamina dura studies: Q&A”

Relationship with Periodontal Ligament

The periodontal ligament (PDL) and the lamina dura? They’re like best friends. The PDL is the tissue that connects the tooth to the bone, and the lamina dura is the bone that lines the tooth socket. They work together to keep your teeth stable. If the PDL gets inflamed (like in periodontitis), it can affect the lamina dura. And if the lamina dura is damaged, it can affect the PDL. It’s a two-way street. Think of it as a team effort – when one player is down, the whole team suffers. The lamina dura provides mechanical stability during mastication, which prevents tooth displacement and maintains proper occlusion.

The lamina dura is a critical component in maintaining tooth stability and reflecting the health of the surrounding periodontal tissues. Its integrity is closely linked to the periodontal ligament and alveolar bone, making it a key indicator of periodontal disease progression.

Age-Related Changes in Lamina Dura

Deterioration Over Time

As we get older, the lamina dura, like other bony structures in the body, can undergo changes. It’s not uncommon to see a gradual thinning or decreased visibility of the lamina dura on dental X-rays as people age. This deterioration is often linked to the natural aging process and shifts in bone metabolism. It’s worth noting that the degree of change can vary significantly from person to person.

“Steps to explain the structure of lamina dura: Compact bone vs alveolar socket: Q&A guide”

Influence of Bone Remodeling

Bone remodeling is a continuous process where old bone tissue is replaced with new bone. This process slows down with age, which can affect the lamina dura. The balance between bone formation and bone resorption shifts, potentially leading to a net loss of bone density in the alveolar bone, including the lamina dura. This can make the lamina dura appear less distinct on radiographs. The thickened lamina dura could be an indicator of other conditions.

Variations in Visibility Across Age Groups

Studies have shown that the visibility and continuity of the lamina dura can differ significantly between age groups. For example, research on impacted third molars has demonstrated noticeable differences in the appearance of the lamina dura in younger versus older individuals. These variations are often attributed to:

• Decreased bone remodeling capacity
• Increased potential for bone resorption
• Changes in mechanical stimuli affecting bone density

It’s important to remember that while age-related changes in the lamina dura are common, they don’t automatically indicate a problem. However, they can be a factor to consider when evaluating overall dental health and diagnosing potential issues.

“Role of compact bone in forming lamina dura: Questions answered”

Radiological Assessment of Lamina Dura

X-ray Appearance

When we look at dental X-rays, the lamina dura usually shows up as a dense, white line surrounding the tooth root. It’s basically the bony socket’s wall. Its uniform appearance is a good sign, but several things can mess with how it looks. Tooth position, the angle of the X-ray, and even just normal anatomical stuff can make it seem irregular or even like it’s not there at all. Getting the X-ray angle right is super important; the rays need to pass through the structure correctly to see it well. If the angle is off, or if there’s some weird anatomy going on, it can hide the lamina dura. It’s not always a straightforward thing to spot!

Advanced Imaging Techniques

Regular X-rays are helpful, but sometimes you need a closer look. That’s where advanced imaging comes in. Cone-beam computed tomography, or CBCT, is a game-changer. It gives us a 3D view, which is way better for seeing small changes in the lamina dura. These advanced techniques have shown that thinning, discontinuity, or complete loss of lamina dura correlates with periodontal inflammation, periodontal ligament damage, and alveolar bone resorption, ultimately affecting periodontal stability. CBCT can show things that you’d totally miss on a regular X-ray. It’s especially useful for figuring out if there’s periodontal disease or other problems affecting the bone around the teeth.

Interpretation Challenges

Okay, so you’ve got an X-ray or a CBCT scan. Now what? Interpreting what you see isn’t always easy. Lots of things can affect how the lamina dura looks. For example:

• Tooth position
• X-ray angles
• Anatomical variations

The lamina dura’s appearance can be influenced by various factors including tooth position, X-ray angulation, and anatomical structures, making it an unreliable sole indicator for systemic conditions like osteoporosis and endocrine disorders.

“How does lamina dura support tooth stability? FAQ explained”

Plus, exposure times and the way the film is processed can also play a role. Because of all these variables, it’s important not to jump to conclusions based on just one X-ray. You have to consider everything else going on with the patient and maybe even get a second opinion. It’s like trying to solve a puzzle – you need all the pieces to get the right picture.

Lamina Dura in Systemic Conditions

The lamina dura, that thin layer of bone hugging the tooth roots, isn’t just about teeth. It can actually reflect what’s going on elsewhere in your body. Systemic conditions, meaning diseases affecting the whole body, can leave their mark on the lamina dura, making it a useful indicator for dentists.

Connection to Osteoporosis

Osteoporosis, a condition characterized by decreased bone density, can significantly impact the lamina dura. The reduced bone density associated with osteoporosis can lead to a thinning of the lamina dura, making it appear less distinct on X-rays. This thinning is a result of the overall bone loss affecting the entire skeleton, including the jaw. It’s not a direct cause-and-effect, but more of a reflection of the body’s overall bone health. Dentists might notice this during routine checkups and use it as a clue, prompting further investigation into a patient’s bone density. This is why understanding bone density is important.

Effects of Diabetes Mellitus

Diabetes, especially if poorly controlled, can wreak havoc on oral health. It’s not just about cavities; it can also affect the lamina dura. Diabetes can impair the body’s ability to heal and fight off infections, which can lead to periodontal disease. This, in turn, can cause bone resorption around the teeth, affecting the lamina dura’s appearance. The lamina dura might appear less defined or even be absent in areas where bone loss is significant.

Impact of Hyperparathyroidism

Hyperparathyroidism, a condition where the parathyroid glands produce too much parathyroid hormone, is probably the most common systemic cause of lamina dura changes. This excess hormone leads to increased calcium levels in the blood, often at the expense of bone. The lamina dura, being a part of the alveolar bone, is susceptible to resorption in hyperparathyroidism. This resorption can cause the lamina dura to appear thin, indistinct, or even completely absent on radiographs. It’s a key indicator for dentists, and if they spot it, they’ll likely refer you for further medical evaluation.

Changes in the lamina dura, while indicative, aren’t definitive proof of a systemic condition. Other factors, like X-ray technique and individual anatomy, can also influence its appearance. It’s just one piece of the puzzle, and dentists use it in conjunction with other clinical findings and patient history to make a proper diagnosis.

“Early warning signs of gaps in understanding structural principles: Common questions”

Clinical Significance of Lamina Dura

Role in Diagnosis

Okay, so the lamina dura? It’s not just some random line on an X-ray. It’s actually a pretty big deal when it comes to figuring out what’s going on in your mouth. Think of it as a first responder, signaling potential problems. If it looks weird, dentists start digging to see what’s up. It’s like a visual cue that something might not be right, prompting further investigation. It’s not foolproof, but it’s a solid starting point.

Indicators of Pathological Conditions

Alright, let’s get into the nitty-gritty. The lamina dura can point to a bunch of different issues. We’re talking about everything from run-of-the-mill periodontal disease to some pretty serious systemic stuff. Here’s a quick rundown:

• Periodontal Problems: Thinning or a fuzzy look often means gum disease is brewing. The lamina dura’s appearance changes as the bone around the teeth gets eaten away.
• Osteosarcoma: This nasty bone cancer can straight-up obliterate the lamina dura. It’s like it was never even there.
• Systemic Diseases: Conditions like hyperparathyroidism can mess with the lamina dura’s appearance, making it look less dense than it should.

Basically, if the lamina dura looks off, it’s a red flag. It doesn’t automatically mean you have a terrible disease, but it does mean your dentist needs to investigate further. It’s all about connecting the dots and figuring out the root cause.

Importance in Treatment Planning

So, you’ve got a wonky-looking lamina dura. Now what? Well, it plays a key role in figuring out the best way to treat whatever’s going on. For example:

1. Implants: If you’re thinking about getting dental implants, the lamina dura’s condition helps determine if your bone is strong enough to support them. If it’s not, you might need bone grafts first.
2. Periodontal Treatment: The state of the lamina dura helps guide treatment for gum disease. If it’s severely damaged, more aggressive treatments might be needed.
3. Orthodontics: Even braces can be affected. The lamina dura gives clues about how your teeth are anchored, which can influence how your teeth move during orthodontic treatment.

“Asymptomatic vs symptomatic effects of ignoring lamina dura basics: Q&A”

Research Developments on Lamina Dura

Recent Studies and Findings

Okay, so research on the lamina dura is actually pretty interesting lately. A lot of studies are focusing on how it changes with age, and what those changes really mean for our teeth. For example, there’s been some work looking at impacted wisdom teeth and how the lamina dura around them looks different in older versus younger people. It seems like as we get older, the lamina dura can become less visible, and that’s probably because our bones just aren’t remodeling as well as they used to. But it’s not just age; things like how close the enamel is and how much stress the bone is under also play a role.

Future Directions in Research

Where is all this lamina dura research headed? Well, one big area is trying to figure out exactly how changes in the lamina dura can help us predict problems before they become major issues. Think of it like this: if we can spot early signs of bone loss or other problems just by looking at the lamina dura, we could start treatment sooner and maybe even prevent some serious dental problems down the road. Also, there’s a lot of interest in using the lamina dura as a way to monitor how well treatments are working. If a treatment is helping to rebuild bone, we should see positive changes in the lamina dura over time. It’s all about getting a better, more detailed picture of what’s going on beneath the surface. Two-dimensional imaging has limitations, but new research is helping to overcome them.

Technological Advances in Imaging

Technology is making a huge difference in how we study the lamina dura. We’re not just stuck with regular X-rays anymore. Now, we have things like cone-beam computed tomography (CBCT), which gives us way more detailed, 3D images. This means we can see the lamina dura much more clearly and spot even small changes that we might have missed before.

The cool thing about these advanced imaging techniques is that they’re not just for looking at the lamina dura. They can also help us see other important structures in the mouth, like the periodontal ligament and the alveolar bone. This gives us a much better overall view of dental health.

Here’s a quick look at how imaging tech is evolving:

• Traditional X-rays: Still useful, but limited detail.
• CBCT: 3D imaging, much higher resolution.
• Digital Subtraction Radiography: Helps detect small changes over time.

And here’s a table showing how different imaging methods compare in terms of resolution:

“Can targeted interventions reduce risks of misinterpretation? FAQs provided”

The Importance Of The Lamina Dura

In conclusion, the lamina dura is more than just a thin line on an X-ray; it plays a key role in dental health. It helps keep our teeth stable and connected to the bone, which is crucial for chewing and overall oral function. As we age, changes in the lamina dura can signal shifts in our bone health, making it important for dentists to pay attention to its condition. While it can be influenced by various factors, understanding its role can help in diagnosing potential issues, from periodontal disease to systemic conditions. So, next time you visit the dentist, remember that the lamina dura is working hard behind the scenes to keep your smile intact.

Frequently Asked Questions

What is the lamina dura?

The lamina dura is a thin layer of dense bone that surrounds the roots of teeth in the jaw. It helps keep the teeth stable and is important for dental health.

How does the lamina dura relate to gum disease?

The lamina dura can show signs of gum disease. If it becomes thinner or disappears, it may indicate that there is a problem with the gums or the bone supporting the teeth.

What changes happen to the lamina dura as we age?

As people get older, the lamina dura can become weaker and less visible on X-rays. This is due to changes in bone health and remodeling.

“Differential applications of traditional vs modern teaching tools: Questions answered”

How can dentists see the lamina dura?

Dentists can see the lamina dura using X-rays. It appears as a white line around the tooth roots, helping them assess dental health.

What systemic conditions affect the lamina dura?

Conditions like osteoporosis, diabetes, and hyperparathyroidism can affect the lamina dura, leading to changes that might be visible on X-rays.

Why is the lamina dura important in dental treatment?

The lamina dura is crucial for diagnosing dental issues and planning treatments. Its condition can indicate the health of the teeth and surrounding structures.

The post Exploring the Lamina Dura: Its Role in Dental Health and Age-related Changes appeared first on BDS Notes.

“What are osteoblasts? A detailed question and answers guide”

Osteoblast

• Cuboidal cell
• Contains
• Rough endoplasmic reticulum
• Large Golgi apparatus
• Secretory vesicles

Functions:

• Synthesizes osteoid and collagen
• Regulates mineralization

Precursor:

• Progenitor cells

Osteoblast

Osteoblasts are essential cells in our body that play a significant role in building and maintaining our bones. These cells are like construction workers, laying down new bone material and helping to repair existing bones. Understanding how osteoblasts function is crucial for maintaining bone health and preventing disorders related to bone density. In this article, we will explore the various aspects of osteoblasts, their differences from osteocytes, factors that affect their activity, and the latest research in this field.

“Understanding osteoblasts through FAQs: Composition, functions, and uses explained”

Osteoblast Significance

• Osteoblasts are responsible for creating new bone tissue and repairing damaged bones.
• They convert bone matrix into hard bone through a process called mineralization.
• Osteoblasts transform into osteocytes once their job is done, playing a role in monitoring bone health.
• Factors like nutrition, hormones, and exercise significantly affect osteoblast activity.
• Imbalances between osteoblasts and osteoclasts can lead to bone disorders such as osteoporosis.

Role Of Osteoblasts In Bone Formation

Osteoblasts are basically the construction workers of your bones. They’re the cells responsible for building new bone tissue, which is a pretty big deal. Think of them as constantly working to keep your skeleton strong and healthy. They don’t just slap bone together randomly, though; it’s a carefully orchestrated process.

Understanding Bone Matrix Synthesis

So, what exactly do osteoblasts build? It’s called the bone matrix, and it’s a mix of collagen and other proteins. Collagen provides a framework, kind of like the rebar in concrete. Osteoblasts secrete these proteins, which then assemble to form the initial structure of the bone. It’s not rock-solid yet, though. This unmineralized matrix is called osteoid. It’s a crucial first step in bone formation.

Role Of Osteoblasts In Bone Formation

The Process Of Bone Mineralization

Okay, so you’ve got this protein framework, but it’s still soft. That’s where mineralization comes in. Osteoblasts release enzymes that trigger the deposition of calcium and phosphate crystals within the bone matrix. These minerals gradually fill in the spaces, hardening the bone and making it strong. It’s like the concrete setting and becoming a solid sidewalk. This process is tightly controlled to ensure the bone is dense and resilient. Think of it like this:

• Osteoblasts lay down the protein framework.
• Enzymes trigger mineral deposition.
• Calcium and phosphate crystals harden the bone.

“Importance of studying osteoblasts for medical students: Questions explained”

Osteoblasts In Bone Repair

But what happens when you break a bone? Osteoblasts jump into action! They migrate to the fracture site and start laying down new bone matrix to repair the damage. It’s a similar process to initial bone formation, but now it’s focused on mending the break. They essentially rebuild the bone, bridging the gap and restoring its strength. Osteocytes, acting like a security system, signal the osteoblasts to repair damaged bone tissue. It’s pretty amazing how your body can fix itself, all thanks to these hard-working cells.

Osteoblasts And Bone Health

Bone remodeling is a continuous process involving both bone formation (by osteoblasts) and bone resorption (by osteoclasts). This ensures that bone tissue is constantly renewed and adapted to meet the body’s needs.

Differences Between Osteoblasts And Osteocytes

“Common challenges in mastering osteoblast notes effectively: FAQs provided”

Functionality Of Osteoblasts

Okay, so osteoblasts are basically the construction workers of your bones. Their main job is to build new bone. They do this by producing something called bone matrix, which is like the concrete of your skeleton. This matrix is made of collagen and other proteins. Once the matrix is laid down, osteoblasts help mineralize it, making it hard and strong. Think of them as the ones who show up on site, pour the foundation, and make sure everything is solid. They’re super active when bones are growing or when there’s a fracture that needs fixing. They’re also cube-shaped, which is kind of neat.

Role Of Osteocytes In Bone Health

Osteocytes, on the other hand, are more like the maintenance crew. They start out as osteoblasts, but once they’re done building, they get trapped inside the bone matrix they created. Now they chill inside these little spaces and act like sensors. They monitor the bone for any stress or damage. If they detect something, they send signals to osteoblasts and osteoclasts (the bone breakers) to come and remodel the area. They’re also connected to each other through tiny channels, forming a network that allows them to communicate throughout the bone. It’s like they’re running a constant diagnostic check to keep everything in good shape. They are the most common type of cell in bones.

“Factors influencing success with osteoblast studies: Q&A”

Transformation From Osteoblasts To Osteocytes

So, how does an osteoblast become an osteocyte? Well, after an osteoblast has done its job of secreting bone matrix, it can either chill out on the bone surface as a bone lining cell, die off (apoptosis), or it can become embedded within the matrix. When it gets trapped, it transforms into an osteocyte. This transformation involves changes in the cell’s shape and function. The osteocyte develops long, branching processes that connect it to other osteocytes and cells on the bone surface. It’s like the construction worker settling into a management role, overseeing the structure they helped build. It’s a pretty cool example of cellular adaptation.

Think of it this way: osteoblasts are the builders, laying down new bone. Osteocytes are the caretakers, maintaining and monitoring the bone’s health from within. They work together to ensure your skeleton stays strong and functional throughout your life.

Factors Influencing Osteoblast Activity

Nutritional Requirements For Osteoblasts

Osteoblasts, like any other cell in the body, need the right fuel to do their job. Calcium is the big one everyone knows about, but it’s not the only thing. Vitamin D is super important because it helps your body absorb calcium in the first place. Without enough Vitamin D, you could be eating all the calcium in the world, and it wouldn’t do much good. Then there’s Vitamin K, which helps direct the calcium to your bones instead of your arteries. It’s like a GPS for calcium! And don’t forget protein! Osteoblasts use protein to build the bone matrix, so a protein deficiency can really slow things down.

• Calcium: Essential for bone mineralization. Aim for adequate daily intake through diet or supplements.
• Vitamin D: Facilitates calcium absorption. Sunlight exposure and fortified foods are good sources.
• Vitamin K: Directs calcium to bones. Found in leafy green vegetables.
• Protein: Building block for bone matrix. Include lean meats, dairy, and plant-based sources in your diet.

“Steps to explain cell types involved in bone formation: Osteoblasts vs osteocytes: Q&A guide”

Impact Of Hormones On Osteoblast Function

Hormones are like the body’s messengers, and they have a huge say in how osteoblasts behave. For example, estrogen is a big player in bone health, especially for women. When estrogen levels drop, like during menopause, bone loss can accelerate. That’s why osteoporosis is more common in older women. Parathyroid hormone (PTH) also plays a role, helping to regulate calcium levels in the blood, which indirectly affects bone formation. Growth hormone is important too, especially during childhood and adolescence when bones are growing rapidly. Even thyroid hormones can influence bone remodeling. It’s a complex hormonal dance that keeps our bones in good shape. If you are concerned about your hormone levels, you should consult with a Primary Care Provider.

Effects Of Physical Activity On Osteoblasts

Physical activity isn’t just good for your muscles; it’s great for your bones too! Weight-bearing exercises, like walking, running, and weightlifting, put stress on your bones, which signals osteoblasts to get to work and build more bone. It’s like telling your bones, “Hey, we need to be stronger!” On the other hand, a sedentary lifestyle can lead to bone loss because there’s no stimulus for osteoblasts to do their thing. Even simple things like standing up more often can make a difference. So, get moving and give your osteoblasts a reason to build strong bones!

Regular physical activity is a cornerstone of bone health. Weight-bearing and resistance exercises are particularly effective in stimulating osteoblast activity and promoting bone density. Aim for at least 30 minutes of moderate-intensity exercise most days of the week to maintain healthy bones. It’s a simple yet powerful way to invest in your long-term skeletal health.

“Role of osteoblasts in synthesizing collagen: Questions answered”

Common Disorders Affecting Osteoblasts

“Early warning signs of undiagnosed cell type-related issues: Common questions”

Understanding Osteoporosis

Osteoporosis is a big deal, especially as we get older. It’s basically when your bones become weak and brittle, making them way more likely to break. Osteoblasts play a central role because they’re the cells responsible for building new bone. In osteoporosis, the osteoblasts aren’t working as well as they should, so the bone isn’t being replaced as quickly as it’s being broken down. This leads to a decrease in bone density. It’s more common in women after menopause, but men can get it too. Things like genetics, diet, and lifestyle all play a part.

The Role Of Osteoblasts In Osteopenia

Think of osteopenia as osteoporosis’s less severe cousin. It’s when your bone density is lower than normal, but not low enough to be considered osteoporosis. It’s often a precursor to osteoporosis, so it’s a sign that you need to take action to protect your bones. Osteoblasts are still involved here. They might be working okay-ish, but not at their peak performance. Boosting osteoblast activity through diet and exercise can help prevent osteopenia from turning into full-blown osteoporosis.

Understanding Osteoblasts

Impact Of Aging On Osteoblast Function

As we age, pretty much everything in our body starts to slow down, and osteoblasts are no exception. Their activity decreases, meaning they’re not building bone as efficiently as they used to. This is one reason why older adults are more prone to bone fractures. It’s not just about the number of osteoblasts, but also how well they function. Factors like hormonal changes and decreased physical activity can also contribute to this decline.

It’s important to remember that while aging is inevitable, there are things you can do to support your osteoblasts as you get older. Eating a balanced diet, staying active, and getting enough vitamin D can all help keep your bones strong.

The Relationship Between Osteoblasts And Osteoclasts

Cooperation In Bone Remodeling

Okay, so picture this: your bones are not just these static things holding you up. They’re actually super dynamic, constantly being remodeled. This remodeling is a team effort, and the stars of the show are osteoblasts and osteoclasts. Osteoblasts are like the construction crew, building new bone. Osteoclasts? They’re the demolition team, breaking down old or damaged bone. This constant cycle of building and breaking down is what keeps your bones strong and healthy.

Balance Between Bone Formation And Resorption

It’s all about balance. If osteoblasts are working overtime and building more bone than osteoclasts are breaking down, your bone density increases. If osteoclasts are too aggressive, you lose bone density. Think of it like a seesaw. You want both sides to be relatively even for optimal bone health. Factors like age, diet, and hormones can all affect this balance. For example, as we age, the activity of osteoblasts tends to slow down, while osteoclasts might keep doing their thing at the same rate, leading to bone loss. Maintaining this bone formation balance is key to preventing conditions like osteoporosis.

“Asymptomatic vs symptomatic effects of delayed interventions: Answered”

Consequences Of Imbalance In Osteoblasts And Osteoclasts

When the balance between osteoblasts and osteoclasts gets thrown off, things can go wrong. Really wrong. If osteoclasts are breaking down bone faster than osteoblasts can build it, you can end up with:

• Osteoporosis: Weak, brittle bones that are prone to fractures.
• Osteopenia: A precursor to osteoporosis, where bone density is lower than normal.
• Paget’s disease: A condition where bone is broken down and rebuilt at an accelerated rate, resulting in deformed and weakened bones.

An imbalance can also occur in the opposite direction, although it’s less common. If osteoblasts are too active, it can lead to abnormally dense bones, which can also cause problems. It’s a delicate dance, and when the music stops, and someone is out of step, your bones suffer.

Osteoblasts And Bone Health

To keep things in check, it’s important to make sure you’re getting enough calcium and vitamin D, and that you’re engaging in regular weight-bearing exercise. These things help to support osteoblast activity and maintain that crucial balance.

Maintaining Healthy Osteoblast Function

Dietary Recommendations For Bone Health

Okay, so you want to keep your bones strong? It all starts with what you eat. Calcium is super important, everyone knows that, but it’s not the only thing. You also need Vitamin D to help your body actually absorb the calcium. Think of Vitamin D as the key that unlocks calcium’s bone-building power. Dairy products are great for calcium, but if you’re not into dairy, leafy greens and fortified foods can also do the trick. Don’t forget about protein either! It’s a key building block for bone matrix.

Importance Of Regular Exercise

Sitting around all day isn’t doing your bones any favors. Weight-bearing exercises, like walking, jogging, or even dancing, are fantastic for stimulating osteoblast activity. When you put stress on your bones, they respond by getting stronger. It’s like they’re saying, “Hey, we need to be able to handle this!” Resistance training, like lifting weights, is also great because it helps build muscle, which in turn supports your bones. Aim for at least 30 minutes of moderate-intensity exercise most days of the week.

“Differential applications of conservative vs experimental analyses: Questions answered”

Preventive Measures Against Bone Disorders

Preventing bone disorders is way easier than trying to fix them later. Besides diet and exercise, there are a few other things you can do. First, avoid smoking. Smoking messes with bone density and makes you more likely to break a bone. Second, limit your alcohol intake. Too much alcohol can also weaken your bones. Finally, talk to your doctor about your risk factors for osteoporosis. They might recommend a bone density test or other screening measures.

Taking care of your bones is a long-term game. It’s not something you can do for a week and then forget about. It’s about making healthy choices every day, so your bones can stay strong and healthy for years to come.

Here’s a quick checklist:

• Eat a balanced diet rich in calcium, vitamin D, and protein.
• Engage in regular weight-bearing and resistance exercises.
• Avoid smoking and excessive alcohol consumption.
• Talk to your doctor about your bone health risk factors.

“Steps to explain clinical relevance of osteoblasts: Diagnosing disorders vs planning treatments: Q&A guide”

Research And Advances In Osteoblast Studies

Current Trends In Osteoblast Research

Osteoblast research is really taking off! Scientists are exploring all sorts of things, from how osteoblasts are affected by different materials to how they respond to various drugs. A big focus is on understanding the signaling pathways that control osteoblast activity. This could lead to new ways to treat bone diseases. For example,recent studies show that NGR1 effectively reduces ROS-induced mitochondrial damage and promotes osteoblast differentiation by inhibiting the MAPK-JNK pathway.

Innovations In Bone Regeneration

Bone regeneration is getting a lot of attention, and osteoblasts are at the center of it all. Researchers are developing new scaffolds and biomaterials that can help osteoblasts grow and form new bone tissue. These innovations could be game-changers for people with bone fractures or bone defects. Some of the exciting areas include:

• 3D-printed scaffolds that mimic the natural structure of bone.
• Growth factors that stimulate osteoblast activity.
• Gene therapy approaches to enhance bone formation.

Future Directions In Osteoblast Therapy

Looking ahead, osteoblast therapy has huge potential. The goal is to find ways to boost osteoblast function to treat bone disorders and improve bone healing. This might involve:

• Developing drugs that specifically target osteoblasts.
• Using stem cells to create new osteoblasts.
• Personalized medicine approaches that tailor treatments to individual patients.

The future of osteoblast therapy is bright. As we learn more about these amazing cells, we’ll be able to develop more effective treatments for a wide range of bone-related conditions. It’s an exciting time for bone research!

Bone Formation By Osteoblasts

The Role of Osteoblasts in Bone Health

In summary, osteoblasts are essential for building and maintaining our bones. They work hard to create new bone tissue and repair any damage. Think of them as the construction workers of our skeletons, always on the job. Without them, our bones wouldn’t be able to grow or heal properly. Keeping these cells healthy is key to having strong bones throughout our lives. So, whether it’s through a balanced diet, regular exercise, or just staying active, taking care of your bones is super important. Remember, healthy bones mean a healthier you!

“Role of imaging techniques like X-rays in assessing osteoblast activity: Questions answered”

Frequently Asked Questions

What are osteoblasts?

Osteoblasts are special cells in your body that help build new bones. They create a substance called bone matrix, which helps bones grow and get stronger.

How do osteoblasts help in bone healing?

When a bone gets hurt or broken, osteoblasts come in to repair it. They lay down new bone material to fill in the gaps and help the bone heal.

What is the difference between osteoblasts and osteocytes?

Osteoblasts build new bones, while osteocytes are older cells that help keep bones healthy by sensing changes and signaling for repairs.

“Early warning signs of undiagnosed clinical manifestations: Common questions”

What factors affect how well osteoblasts work?

Osteoblast activity can be influenced by what you eat, hormones in your body, and how much you exercise.

What happens if osteoblasts are not working properly?

If osteoblasts don’t work well, it can lead to bone problems like osteoporosis, where bones become weak and break easily.

How can I support healthy osteoblast function?

You can keep your osteoblasts healthy by eating a balanced diet rich in calcium and vitamin D, exercising regularly, and avoiding smoking.

The post Understanding Osteoblasts: Bone Formation and Health appeared first on BDS Notes.

“What is the difference between tachycardia and bradycardia? A detailed question and answers guide”

1. Atrial fibrillation:

• In this, the atria shows irregular and rapid beats.
• Rate reaches 300-400 beats/minute.

Cause:

• Due to circus movement of impulses within atrial musculature.

2. Ventricular fibrillation:

• In this, ventricles beat very rapidly and irregularly.
• Rate reaches 400-500 beats/minute.

Cause:

• Circus movement of impulses within ventricular, musculature.

“Understanding tachycardia and bradycardia through FAQs: Causes, symptoms, and treatments explained”

Tachycardia and bradycardia.

When it comes to heart health, understanding how your heart functions is key. Two common conditions that can affect heart rate are tachycardia and bradycardia. While they both relate to heart rate, they represent opposite ends of the spectrum—one being too fast and the other too slow. This article aims to clarify the difference between tachycardia and bradycardia, helping you recognize symptoms, causes, and treatment options for each condition. Knowing these differences can be crucial for maintaining your heart’s well-being.

Atrial Fibrillation Significance

• Tachycardia is a fast heart rate, typically over 100 beats per minute, while bradycardia is a slow heart rate, generally under 60 beats per minute.
• Symptoms of tachycardia include palpitations, dizziness, and chest pain, whereas bradycardia may cause fatigue, weakness, and fainting.
• Causes of tachycardia can range from stress and anxiety to underlying heart conditions, while bradycardia can be linked to medications and health issues like sleep apnea.
• Monitoring your heart rate is essential; knowing what’s normal for you can help catch potential issues early.
• Both conditions can be managed through lifestyle changes, medications, or in some cases, surgery, depending on their severity.

Understanding Heart Rate Variations

Normal Heart Rate Ranges

Okay, so what’s normal when it comes to heart rate? It’s not a one-size-fits-all thing. A typical resting heart rate for adults falls somewhere between 60 and 100 beats per minute (bpm). But, that’s just a general guideline. Age plays a big role. Infants, for example, have much faster heart rates, often between 120 and 160 bpm, because their bodies are growing so rapidly. As we get older, things tend to slow down a bit. Even fitness level matters; athletes often have lower resting heart rates, sometimes as low as 40 bpm, because their hearts are super efficient. It’s all about how well your heart pumps blood. Knowing your normal heart rate is the first step in understanding your heart health.

“How do tachycardia and bradycardia affect heart health? FAQ answered”

When to Seek Medical Attention

It’s important to know when a weird heart rate is just a temporary thing and when it’s a sign of something more serious. If your heart rate is consistently above 100 bpm (tachycardia) or below 60 bpm (bradycardia) at rest, it’s worth getting checked out. Don’t panic, but don’t ignore it either. Other red flags include palpitations (that feeling of your heart racing or fluttering), dizziness, shortness of breath, chest pain, or fainting. These symptoms, especially when they happen together, could indicate a problem that needs medical attention. It’s always better to be safe than sorry when it comes to your heart.

The Importance of Monitoring Heart Rate

Keeping an eye on your heart rate is a simple way to stay informed about your overall health. It’s like checking the engine of your car – it gives you a sense of how things are running. Regular monitoring can help you spot potential problems early on, before they become serious. Plus, it can give you insights into how your body responds to different activities and stressors. For example, you might notice that your heart rate spikes when you’re stressed or after drinking caffeine. This information can help you make lifestyle changes to better manage your heart health. Monitoring your heart rate doesn’t have to be complicated; there are plenty of apps and devices that make it easy to track your pulse throughout the day.

“Importance of studying tachycardia and bradycardia for medical students: Questions explained”

Monitoring your heart rate is a simple yet powerful way to stay on top of your heart health. Recognizing abnormal rates early on can help prevent serious complications, making it essential to consult a cardiologist if you notice any irregularities. The normal rate of heaving is believed to indicate the heart’s efficiency, while variation could be a sign of early complications.

Defining Tachycardia And Bradycardia

“Common challenges in mastering tachycardia and bradycardia notes effectively: FAQs provided”

What Is Tachycardia?

Tachycardia is when your heart beats too fast. Generally, this means a heart rate over 100 beats per minute at rest. It’s not always a bad thing; your heart rate naturally increases when you exercise or feel stressed. But when your heart races for no clear reason, it could signal an issue. Tachycardia can be caused by things like:

• Anxiety or stress
• Too much caffeine or alcohol
• Underlying medical conditions

What Is Bradycardia?

Bradycardia is the opposite of tachycardia; it’s when your heart beats too slowly. For adults, this usually means a heart rate below 60 beats per minute. Now, a slow heart rate isn’t always a problem. Athletes, for example, often have lower resting heart rates because their hearts are very efficient. However, if bradycardia causes symptoms like dizziness or fatigue, it needs to be checked out. Some potential causes of bradycardia include:

• Certain medications, like beta-blockers
• Problems with the heart’s electrical system
• Underlying health conditions, such as hypothyroidism

Key Differences in Definitions

The main difference is simple: speed. Tachycardia is a fast heart rate, while bradycardia is a slow one. But it’s not just about the numbers. It’s about what’s normal for you and whether the change in heart rate is causing any symptoms or arrhythmia. Here’s a quick comparison:

“Why is proper understanding of tachycardia and bradycardia critical for diagnosing arrhythmias? Answered”

It’s important to remember that both tachycardia and bradycardia can be normal in certain situations. However, if either condition is persistent or causing symptoms, it’s crucial to seek medical advice. Ignoring these issues could lead to more serious heart problems down the road.

Tachycardia And Bradycardia – What’S The Difference?

Symptoms of Tachycardia

Common Symptoms to Watch For

So, you think your heart might be beating too fast? Well, let’s talk about what that might feel like. Tachycardia, as you probably know by now, is when your heart rate is consistently over 100 beats per minute at rest. But it’s not just about the numbers; it’s about how you feel.

Here’s a rundown of common symptoms:

• Palpitations: This is probably the most common one. It feels like your heart is racing, fluttering, or pounding in your chest. It can be pretty unnerving.
• Chest discomfort: Some people describe it as tightness or pressure. It’s not always severe pain, but it’s definitely something you’d notice.
• Shortness of breath: Feeling like you can’t catch your breath, even when you’re just sitting still.
• Dizziness or lightheadedness: This happens because your heart isn’t pumping blood as efficiently as it should.
• Fatigue: Just feeling super tired, even after a good night’s sleep.
• Sweating: Excessive sweating, especially when it’s not hot or you haven’t been exercising.

When Symptoms Indicate a Problem

Okay, so you’ve got some of these symptoms. When should you actually be concerned? It’s important to pay attention to how often these symptoms occur and how severe they are. If you experience these symptoms frequently, or if they’re intense, it’s time to get checked out.

If you’re having chest pain, severe shortness of breath, or fainting spells, don’t wait. Get medical help immediately. These could be signs of a serious problem.

Long-Term Effects of Untreated Tachycardia

Ignoring tachycardia isn’t a great idea. Over time, a consistently fast heart rate can lead to some serious problems. Your heart is working harder than it should, and that can take a toll. Here’s what can happen if tachycardia goes untreated:

• Heart failure: Your heart muscle can weaken and become less efficient at pumping blood.
• Stroke: Blood clots can form and travel to your brain, causing a stroke.
• Sudden cardiac arrest: In rare cases, tachycardia can lead to a sudden, life-threatening heart rhythm.
• Increased risk of blood clots: The heart not pumping efficiently can cause blood to pool and clot.

So, yeah, it’s worth getting it checked out. Don’t ignore those weird heart flutters!

Tachycardia And Bradycardia Explained

Symptoms of Bradycardia

“Factors influencing success with heart rhythm studies: Q&A”

Recognizing Bradycardia Symptoms

Bradycardia, characterized by a slow heart rate (typically below 60 bpm), doesn’t always present obvious symptoms. In fact, some people, especially athletes, may naturally have a lower heart rate without experiencing any issues. However, when bradycardia prevents the body from getting enough oxygen-rich blood, symptoms can arise. These symptoms can vary in intensity and may include fatigue, dizziness, and shortness of breath.

Here’s a list of common symptoms:

• Feeling unusually tired or weak, even after rest.
• Experiencing dizziness or lightheadedness, sometimes leading to fainting.
• Having difficulty concentrating or feeling confused.
• Shortness of breath, especially during physical activity.
• Chest pain or discomfort.

Potential Complications

If left untreated, bradycardia can lead to several complications. One of the most concerning is frequent fainting spells, which can result in injuries from falls. In severe cases, persistent bradycardia can contribute to high blood pressure or even heart failure, as the heart struggles to pump enough blood to meet the body’s needs. It’s important to monitor for bradycardia symptoms and seek medical attention if they become frequent or severe.

Bradycardia can sometimes be subtle, with symptoms that are easily dismissed as normal fatigue or aging. However, it’s important to pay attention to these signs, especially if they are new or worsening. Early detection and management can help prevent more serious complications.

Heart Rate Conditions – Tachycardia And Bradycardia

Impact on Daily Life

The impact of bradycardia on daily life can range from mild inconvenience to significant disability. Simple activities like climbing stairs or walking can become challenging due to shortness of breath and fatigue. Dizziness and lightheadedness can make it difficult to concentrate at work or school, and the fear of fainting can limit social activities. The severity of the impact depends on the underlying cause of the bradycardia and the individual’s overall health. For example, the impact of medications can be a contributing factor. In some cases, lifestyle adjustments and medical interventions may be necessary to improve quality of life.

“Steps to explain causes of tachycardia and bradycardia: Electrical disturbances vs structural issues: Q&A guide”

Causes of Tachycardia

So, your heart’s been racing, huh? Faster than it should be? Tachycardia, that’s what they call it. It’s not always a big deal, but sometimes it can point to something more serious. Let’s look at what might be making your heart go into overdrive.

Physical and Emotional Triggers

Okay, first things first: stress and anxiety. We all get stressed, right? But when you’re super anxious, your body dumps adrenaline into your system. Adrenaline is like a shot of espresso for your heart, making it beat faster. Physical stuff can do it too. Think about when you’re working out – your heart rate goes up because your body needs more oxygen. But sometimes, even simple things like standing up too fast can trigger a racing heart.

• Stress
• Anxiety
• Exercise

Medical Conditions Linked to Tachycardia

Sometimes, tachycardia isn’t just about stress; it’s a sign of something else going on in your body. Thyroid problems are a big one. If your thyroid is overactive (hyperthyroidism), it can mess with your heart rate. Heart conditions themselves, like atrial fibrillation or even just plain old heart failure, can also cause tachycardia. And don’t forget anemia – when you don’t have enough red blood cells, your heart has to work harder to get oxygen around, which can lead to a faster heartbeat.

“Role of electrical disturbances in triggering tachycardia: Questions answered”

Medications That May Cause Tachycardia

Believe it or not, some of the meds you’re taking could be speeding up your heart. Asthma medications, for example, can sometimes have that effect. Even some over-the-counter cold medicines can do it because they contain stimulants. And if you’re on anything for your thyroid, that could also be a culprit. Always a good idea to double-check with your doctor or pharmacist about side effects, especially if you’re already prone to a racing heart.

It’s important to remember that everyone is different. What triggers tachycardia in one person might not affect another. If you’re concerned about your heart rate, it’s always best to talk to a doctor. They can help you figure out what’s going on and what you can do about it.

Causes of Bradycardia

Bradycardia, a slower than normal heart rate, can stem from various underlying issues. While a low heart rate is normal for athletes, it can be problematic for others. Let’s explore some common causes.

Underlying Health Conditions

Several health conditions can mess with your heart’s rhythm and lead to bradycardia. One of the most common is sick sinus syndrome, where the heart’s natural pacemaker (the sinus node) doesn’t work correctly. Other conditions include:

• Heart block: Disrupts electrical signals.
• Hypothyroidism: An underactive thyroid can slow down many body functions, including heart rate.
• Sleep apnea: Repeated breathing interruptions during sleep can lead to temporary drops in heart rate.

“How do structural issues contribute to bradycardia? FAQ explained”

Impact of Medications

Certain medications can also contribute to bradycardia as a side effect. It’s always a good idea to review your medications with your doctor, especially if you’re experiencing symptoms of a slow heart rate. Some common culprits include:

• Beta-blockers: Often prescribed for high blood pressure.
• Calcium channel blockers: Used for high blood pressure and other heart conditions.
• Digoxin: Used to treat heart failure and irregular heartbeats.

Lifestyle Factors Contributing to Bradycardia

Believe it or not, lifestyle choices can also play a role in your heart rate. While these factors might not be the sole cause of bradycardia, they can certainly contribute:

• High fitness level: Athletes often have lower resting heart rates.
• Vagal nerve stimulation: This nerve can slow heart rate when stimulated.
• Electrolyte imbalances: Low potassium or calcium levels can affect heart function.

It’s important to remember that bradycardia isn’t always a cause for concern. However, if you’re experiencing symptoms like dizziness, fatigue, or shortness of breath, it’s best to consult with a healthcare professional to determine the underlying cause and appropriate treatment.

“Early warning signs of undiagnosed cause-related issues: Common questions”

Treatment Options for Tachycardia

Lifestyle Changes and Management

Sometimes, managing tachycardia can start with simple changes to your daily routine. It’s not always about medication or surgery; sometimes, it’s about tweaking your habits to support a healthier heart. For example, managing stress is a big one. Things like yoga, meditation, or even just taking a few minutes each day for deep breathing can make a difference. Also, what you eat and drink plays a role. Cutting back on caffeine and alcohol can help regulate your heart rate. Regular physical activity is important too, but it’s best to talk to your doctor about what’s safe for you. Staying hydrated is also key; dehydration can sometimes trigger a faster heartbeat. These lifestyle adjustments can be surprisingly effective in managing stress management and preventing episodes of tachycardia.

Medications for Tachycardia

When lifestyle changes aren’t enough, medications can help control a rapid heart rate. Several types of drugs are used, and the choice depends on the type of tachycardia you have and any other health conditions you might have. Beta-blockers are common; they slow down the heart rate and reduce blood pressure. Antiarrhythmics are another option; these drugs help restore a normal heart rhythm. Calcium channel blockers can also be used to slow the heart rate. It’s important to take these medications exactly as prescribed and to talk to your doctor about any side effects you experience. Finding the right medication and dosage can take some time, but it can make a big difference in managing your symptoms. Adenosine is often the first choice for acute episodes, especially when atrioventricular node involvement is suspected.

“Differential applications of conservative vs experimental analyses: Questions answered”

Surgical Interventions

In some cases, surgery might be necessary to treat tachycardia, especially if medications aren’t effective or if the tachycardia is caused by a specific heart problem. One common procedure is catheter ablation. This involves threading a thin tube through a blood vessel to the heart. Once there, the doctor uses energy to destroy the small area of heart tissue that’s causing the abnormal heart rhythm. Another option is a surgical procedure to implant a pacemaker or an implantable cardioverter-defibrillator (ICD). A pacemaker helps regulate the heart rate, while an ICD can deliver an electrical shock to restore a normal rhythm if the heart beats too fast or irregularly. These surgical options are usually considered when other treatments haven’t worked, and they can significantly improve the quality of life for people with severe tachycardia.

It’s important to remember that everyone’s situation is unique, and the best treatment plan will depend on your specific type of tachycardia, your overall health, and your preferences. Talk to your doctor about all your options and work together to find the best approach for you.

Treatment Options for Bradycardia

Monitoring and Observation

Sometimes, mild bradycardia doesn’t need immediate treatment. If you’re not experiencing significant symptoms, your doctor might just recommend regular check-ups to keep an eye on your heart rate. This is especially true if the slow heart rate is due to something temporary or reversible. Regular monitoring can help determine if the condition is stable or progressing, and whether further intervention is needed. It’s all about keeping a close watch and being proactive.

Medications to Manage Bradycardia

While there aren’t many medications specifically designed to increase heart rate, some drugs can help manage the symptoms or underlying causes of bradycardia. For example, if a medication you’re taking is causing your heart rate to slow down, your doctor might adjust the dosage or switch you to a different drug. In some cases, medications like atropine can be used temporarily to increase heart rate in emergency situations. However, these are usually short-term solutions. It’s important to discuss all your medications with your doctor to identify potential contributors to bradycardia.

“Can preventive measures reduce risks of dysfunction? FAQs provided”

When Surgery Is Necessary

For more severe cases of bradycardia, especially those caused by problems with the heart’s electrical system, surgery might be necessary. The most common surgical intervention is the implantation of a pacemaker. A pacemaker is a small device that’s placed under the skin, usually near the collarbone, and it sends electrical signals to your heart to help it beat at a normal rate.

Pacemakers are generally recommended when bradycardia is causing significant symptoms or when there’s a high risk of complications. The procedure to implant a pacemaker is usually minimally invasive, and most people can return to their normal activities within a few weeks. Regular follow-up appointments are needed to ensure the pacemaker is working correctly and to adjust the settings as needed. For some, a permanent pacemaker is the best solution.

Here are some reasons why surgery might be necessary:

• Significant symptoms like fainting or dizziness
• Underlying heart conditions causing severe bradycardia
• Medications are ineffective or not an option

Keeping an eye on your heart rate is a smart move for your overall health. Spotting any unusual changes early can help you avoid bigger issues down the line. If you notice your heart racing or slowing down too much, it’s a good idea to chat with a doctor. Understanding the signs of tachycardia and bradycardia, along with their causes, can really help you steer clear of serious heart problems. Whether it’s through better eating habits, regular exercise, or medications, managing your heart rate is key to staying healthy.

Frequently Asked Questions

What is tachycardia?

Tachycardia is when your heart beats faster than normal, usually over 100 beats per minute while at rest.

What is bradycardia?

Bradycardia is when your heart beats slower than normal, typically below 60 beats per minute.

What causes tachycardia?

Tachycardia can be caused by stress, anxiety, certain medications, or health issues like heart disease.

“Asymptomatic vs symptomatic effects of delayed interventions: Answered”

What causes bradycardia?

Bradycardia can happen due to health conditions, certain medications, or even being very fit, like in athletes.

How can I tell if I have tachycardia or bradycardia?

You may notice symptoms like a racing heart for tachycardia or feeling dizzy and tired for bradycardia. It’s best to see a doctor for a proper check.

What treatments are available for these conditions?

Tachycardia may be treated with lifestyle changes or medications, while bradycardia might need monitoring or sometimes a pacemaker.

The post Understanding the Difference Between Tachycardia and Bradycardia: Key Insights for Heart Health appeared first on BDS Notes.

“What is apoptosis? A detailed question and answers guide”

Apoptosis, or programmed cell death, is a natural process that our bodies use to remove cells that are no longer needed or are damaged. This mechanism is crucial for maintaining health and preventing diseases.

Understanding apoptosis can shed light on its vital role in various biological processes, from fetal development to immune response and even in the context of diseases like cancer and neurodegenerative disorders.

In this article, we will explore how apoptosis works, its significance in health and disease, and its potential therapeutic implications.

“Understanding apoptosis through FAQs: Composition, functions, and uses explained”

Apoptosis Definition:

• It is defined as the programmed cell death under genetic control.

Apoptosis Significance:

• Responsible for regression of duct system during sex differentiation in the foetus.
• Respondible for degeneration and regeneration of neurons.
• Responsible for removal of inappropriate clones of immune cells.
• Responsible for cyclic sheeding of endometrium at the time of menstruation.
• Responsible for cell shed from the tip of the villi in the small intestine.
• Removes auto-aggressive T cells and prevents autoimmune diseases.
• Plays vital role in cellular hoemostasis.
• Useful for removal of a cell that is damaged by a virus or toxin.

Apoptosis Mechanism

• Apoptosis is a controlled process that helps eliminate damaged or unnecessary cells.
• It plays a vital role in fetal development and tissue maintenance after birth.
• Dysregulation of apoptosis can lead to diseases such as cancer and neurodegenerative disorders.
• Understanding apoptosis can improve approaches to cancer treatment and regenerative medicine.
• Different forms of cell death, like necrosis and pyroptosis, are related but distinct from apoptosis.

The Mechanism of Apoptosis

How Does Apoptosis Work?

So, apoptosis, or programmed cell death, is like the body’s way of cleaning house. It’s a carefully controlled process that eliminates cells that are no longer needed or are a threat to the organism. Think of it as a cellular self-destruct button. Certain proteins, like p53 (a tumor suppressor), can trigger apoptosis if a cell’s DNA is too damaged to repair.

Once apoptosis starts, the cell breaks down into smaller pieces. These pieces are then consumed by other cells, called phagocytes, preventing inflammation. It’s a neat and tidy process, unlike necrosis, which is a much messier form of cell death.

“Importance of studying apoptosis for medical students: Questions explained”

Key Proteins Involved in Apoptosis

Apoptosis isn’t a random event; it’s orchestrated by a bunch of key proteins. These proteins can be broadly classified into two groups: initiators and executioners.

• Initiator caspases start the process.
• Executioner caspases carry out the cell’s dismantling.
• Bcl-2 family proteins regulate the process, either promoting or inhibiting apoptosis.

The balance between pro-apoptotic (cell death promoting) and anti-apoptotic (cell death inhibiting) proteins determines whether a cell lives or dies. It’s a complex interplay, and disruptions in this balance can lead to diseases like cancer.

For example, mitochondrial degradation is a critical step involving proteins like Bax and Bak that poke holes in the mitochondria, releasing factors that activate caspases.

Stages of Apoptosis

Apoptosis unfolds in a series of distinct stages:

1. Initiation: Triggered by internal or external signals.
2. Regulation: Involves a delicate balance of pro- and anti-apoptotic proteins.
3. Execution: Caspases dismantle the cell.
4. Removal: Phagocytes clear away the cellular debris.

Each stage is tightly controlled, and problems at any step can have serious consequences. For instance, if the removal stage fails, cellular debris can accumulate, leading to inflammation and potentially autoimmune diseases. Understanding these stages is key to developing therapies that target apoptosis in various diseases.

The Role of Apoptosis in Development

“Common challenges in mastering apoptosis notes effectively: FAQs provided”

Apoptosis isn’t just about getting rid of bad cells; it’s also super important during development. Think of it like a sculptor carefully chipping away at a block of marble to reveal the statue inside. In our bodies, apoptosis helps shape tissues and organs as we grow, both before and after birth. It’s a pretty neat process, actually.

Apoptosis in Fetal Development

Apoptosis is a key player in shaping a fetus. It’s responsible for things like forming fingers and toes by removing the tissue between them. Without it, we’d all have webbed hands and feet! It also helps in the development of the nervous system, making sure we have the right number of neurons and that they’re connected properly. It’s kind of wild to think about how much cell death is needed to create something as complex as a human being. This process ensures that the fetal tissues turn into different parts.

“Factors influencing success with apoptosis studies: Q&A”

Cellular Remodeling After Birth

Apoptosis doesn’t stop after birth; it continues to play a role in remodeling tissues and organs as we grow and mature. For example, it helps to shape the heart and other organs. It’s also involved in the development of the immune system, making sure we have the right types of immune cells and that they’re working properly. It’s like a constant process of fine-tuning and adjustment, ensuring that everything is working as it should.

Importance in Tissue Homeostasis

Tissue homeostasis, or balance, is crucial for keeping our bodies healthy. Apoptosis helps maintain this balance by removing old, damaged, or unnecessary cells. This makes room for new cells and prevents the buildup of cells that could cause problems. Think of it like a gardener constantly pruning a plant to keep it healthy and productive. Without apoptosis, our tissues would become overgrown and dysfunctional. Here are some key roles:

• Supporting the body’s constant need to replace old cells and tissues.
• Helping the immune system fight infections.
• Ridding the body of damaged cells that can’t be repaired.

Apoptosis is essential for maintaining tissue homeostasis. It ensures that the number of cells in a tissue remains constant and that damaged or unwanted cells are removed efficiently. This process is vital for preventing diseases like cancer and autoimmune disorders.

Apoptosis and Immune Function

Apoptosis, or programmed cell death, plays a really big part in keeping our immune system working right. It’s not just about getting rid of old cells; it’s a key way the body controls immune responses and prevents things like autoimmunity. Think of it as the immune system’s way of cleaning house and making sure everything stays balanced.

“Steps to explain functions of apoptosis: Tissue development vs immune regulation: Q&A guide”

How Apoptosis Affects Immune Response

Apoptosis is super important for keeping the immune system in check. It helps to remove immune cells that are no longer needed after an infection is cleared. If apoptosis doesn’t happen enough, immune cells can stick around too long and cause problems. On the other hand, too much apoptosis can weaken the immune system, making it harder to fight off infections. It’s a delicate balance.

• Controls the number of immune cells
• Prevents excessive inflammation
• Maintains immune tolerance

Role in Eliminating Infected Cells

One of the main jobs of the immune system is to get rid of cells that are infected with viruses or other pathogens. Apoptosis is a key way this happens. When a cell is infected, the immune system can trigger apoptosis to kill the infected cell before it can spread the infection to other cells. This is a really important defense mechanism. The caspase cascade is often activated in these scenarios.

Impact on Autoimmunity

Autoimmunity happens when the immune system mistakenly attacks the body’s own cells. Apoptosis plays a role in preventing this by getting rid of immune cells that are reactive to self-antigens. If this process doesn’t work right, these self-reactive cells can survive and cause autoimmune diseases. Problems with immune balance can lead to conditions like:

• Type 1 diabetes
• Multiple sclerosis
• Lupus

Apoptosis is a critical mechanism for maintaining immune homeostasis. When this process is disrupted, it can lead to a variety of immune-related disorders, highlighting its importance in overall health.

“Role of tissue development in eliminating unnecessary cells: Questions answered”

Apoptosis in Disease

Consequences of Dysregulated Apoptosis

When apoptosis goes wrong, it can have serious effects. Too much or too little programmed cell death can contribute to a range of diseases. If apoptosis happens too much, it can lead to the loss of essential cells, like in neurodegenerative disorders. On the other hand, if it doesn’t happen enough, damaged cells can accumulate, potentially leading to cancer or autoimmune diseases.

“Early warning signs of undiagnosed function-related issues: Common questions”

Apoptosis in Cancer Development

Apoptosis is a crucial mechanism that prevents cancer. When cells have damaged DNA, apoptosis should kick in to eliminate them. However, cancer cells often find ways to evade apoptosis, allowing them to grow uncontrollably. This resistance to apoptosis is a hallmark of cancer. Understanding how cancer cells bypass this process is key to developing effective treatments. For example, certain proteins might prevent apoptosis from happening when it should, resulting in damaged cells sticking around, and tumors can grow. Researchers are looking into drugs that can block the action of these proteins, in turn allowing apoptosis to occur.

Role in Neurodegenerative Diseases

In neurodegenerative diseases like Alzheimer’s and Parkinson’s, excessive apoptosis can lead to the loss of neurons, contributing to cognitive decline and motor dysfunction. The exact mechanisms that trigger this excessive cell death are still being investigated, but factors like oxidative stress, inflammation, and protein misfolding are thought to play a role. Therapies aimed at slowing down or preventing neuronal apoptosis could potentially slow the progression of these devastating diseases. Apoptosis doesn’t happen when it should, or doesn’t happen enough, damaged cells stick around in your body and continue to grow and multiply. Either way, when apoptosis doesn’t happen the way it should, it can harm you and lead to serious problems.

Apoptosis is one of many processes that occur every day inside your body to help keep you alive. You can’t see it happening, but programmed cell death is vital in supporting your health and preventing illness. Your healthcare provider can tell you more about the role apoptosis plays in your specific diagnosis and what this means for you.

“Asymptomatic vs symptomatic effects of delayed treatment: Answered”

Therapeutic Implications of Apoptosis

Targeting Apoptosis in Cancer Treatment

Apoptosis, or programmed cell death, is a big deal when it comes to cancer. Cancer cells often find ways to dodge apoptosis, which lets them grow uncontrollably. So, a major area of research is figuring out how to re-activate apoptosis in these cells. One approach involves developing drugs that target the proteins that prevent apoptosis. For example, some drugs aim to block the action of proteins that normally inhibit apoptosis, essentially removing the brakes and allowing the cancer cells to self-destruct. Another strategy is to boost the activity of proteins that promote apoptosis. It’s a delicate balance, but the goal is to selectively kill cancer cells while sparing healthy ones.

Potential in Regenerative Medicine

While we often think about boosting apoptosis to fight cancer, there are situations where we want to prevent it. In regenerative medicine, the goal is to repair or replace damaged tissues and organs. Sometimes, cells die off due to injury or disease, hindering the healing process. By understanding the mechanisms that trigger apoptosis in these situations, we might be able to develop therapies that keep cells alive longer, giving them a chance to repair the damage. This could be useful in treating conditions like heart disease or neurodegenerative disorders, where cell loss is a major problem. One promising area involves using apoptotic vesicles to promote tissue repair.

Future Research Directions

Research into apoptosis is still going strong, and there are many exciting avenues being explored. Here are a few:

• Developing more selective drugs: The goal is to create drugs that target cancer cells specifically, without harming healthy cells. This could reduce side effects and improve treatment outcomes.
• Understanding the role of apoptosis in different diseases: Apoptosis is involved in a wide range of conditions, from cancer to autoimmune disorders to neurodegenerative diseases. Learning more about its role in each of these diseases could lead to new and more effective treatments.
• Exploring new ways to manipulate apoptosis: Researchers are looking at various approaches, including gene therapy and immunotherapy, to control apoptosis and fight disease.

Understanding how apoptosis works and how to control it has huge potential for treating a wide range of diseases. It’s a complex process, but the more we learn, the better equipped we’ll be to develop new and effective therapies.

“Can early intervention reverse apoptosis risks? FAQs provided”

Comparing Apoptosis and Other Cell Death Mechanisms

Necrosis vs. Apoptosis

Okay, so apoptosis is like the body’s way of neatly cleaning house, but what happens when things get messy? That’s where necrosis comes in. Apoptosis is programmed cell death, while necrosis is often the result of injury or infection. Think of it this way: apoptosis is like a planned demolition, while necrosis is like a building collapsing because of a fire.

• Apoptosis doesn’t cause inflammation; necrosis does.
• Apoptosis is controlled; necrosis is often uncontrolled.
• Apoptosis involves cell shrinkage; necrosis involves cell swelling.

Necrosis used to be seen as just a chaotic, accidental form of cell death. But now, we know there are actually some controlled forms of necrosis too. It’s not always just a random mess; sometimes, the body has a reason for choosing this path.

Programmed Necrosis: Necroptosis

So, you might be thinking, “Wait, controlled necrosis?” Yep, that’s necroptosis. It’s basically a backup plan when apoptosis can’t happen. Necroptosis is a programmed form of necrosis, and it’s triggered by different signals than apoptosis. It’s like having a second option for cell death, just in case the first one is blocked.

Pyroptosis And Its Implications

Now, let’s throw another player into the mix: pyroptosis. This one’s a bit different because it’s usually triggered by infections, especially inside cells. Pyroptosis is a type of programmed cell death that’s often associated with inflammation. It’s like the cell is sacrificing itself to alert the immune system.

Here’s a quick comparison:

Understanding Apoptosis in Clinical Contexts

“Differential applications of pharmacological vs non-pharmacological treatments: Questions answered”

Apoptosis in Chronic Diseases

Apoptosis, or programmed cell death, plays a big role in many chronic diseases. When apoptosis doesn’t work right, it can lead to problems. For example, too little apoptosis can cause cells to build up, potentially leading to cancer. On the other hand, too much apoptosis can destroy healthy cells, which happens in diseases like Alzheimer’s. Understanding how apoptosis is involved can help us find better ways to treat these conditions.

It’s wild to think that something happening at the cellular level can have such a huge impact on our overall health. Apoptosis is like the body’s way of cleaning house, and when that process gets messed up, things can go wrong pretty quickly.

Diagnostic Tools for Apoptosis Assessment

So, how do doctors figure out if apoptosis is happening correctly? Well, there are several diagnostic tools they can use. These tools help them see if cells are dying when they should, or if there’s too much or too little cell death. Here are a few common methods:

• Flow Cytometry: This technique uses fluorescent dyes to label cells undergoing apoptosis, allowing doctors to count and analyze them.
• TUNEL Assay: This test detects DNA fragmentation, a hallmark of apoptosis. It’s often used on tissue samples.
• Caspase Activity Assays: Caspases are key enzymes in the apoptotic pathway. Measuring their activity can indicate whether apoptosis is occurring.

These tools are super important for diagnosing and monitoring diseases where apoptosis is a factor. They help doctors understand what’s going on at a cellular level, which can guide treatment decisions. For example, apoptosis intiation is a key factor in cancer treatment.

“Steps to explain disorders affecting apoptosis: Cancer vs neurodegeneration: Q&A guide”

Patient Management and Apoptosis

Okay, so what does all this mean for patients? Well, understanding apoptosis can help doctors manage diseases more effectively. If a patient has a condition where apoptosis is messed up, doctors can try to fix it with different treatments. This might involve using drugs to either increase or decrease apoptosis, depending on the situation. It’s all about finding the right balance. Here’s a simple breakdown:

• Cancer: Treatments might aim to trigger apoptosis in cancer cells.
• Autoimmune Diseases: Therapies might focus on reducing apoptosis to protect healthy cells.
• Neurodegenerative Diseases: Strategies could involve preventing excessive apoptosis of neurons.

Ultimately, the goal is to use our knowledge of apoptosis to improve patient outcomes and quality of life. It’s a complex process, but the more we learn, the better we can help people.

“Role of apoptosis evasion in causing cancer: Questions answered”

The Importance of Apoptosis

In summary, apoptosis is a natural process that plays a big role in keeping our bodies healthy. It helps get rid of cells that are old or damaged, which is super important for preventing diseases like cancer. But when things go wrong, and apoptosis happens too much or not enough, it can lead to serious health issues. Understanding how apoptosis works can give you insights into your health and help you communicate better with your doctor about any concerns. So, whether it’s for you or someone you care about, knowing about apoptosis can really make a difference.

Frequently Asked Questions

What is apoptosis?

Apoptosis is how your body gets rid of cells that are damaged or no longer needed. It’s a planned process where cells die in a controlled way.

How does apoptosis work?

Apoptosis starts when certain proteins in your body, like p53, tell the cell to stop dividing if it’s damaged. Then, the cell breaks down into small pieces that other cells can clean up.

Why is apoptosis important?

Apoptosis helps keep your body healthy by removing old or damaged cells. This is important for growth and for preventing diseases like cancer.

“Differential applications of surgical vs non-surgical treatments: Questions answered”

Can too much apoptosis be harmful?

Yes, if too many healthy cells die, it can lead to problems like neurodegenerative diseases, where important brain cells are lost.

How does apoptosis relate to cancer?

In cancer, apoptosis doesn’t work properly. Cancer cells often avoid apoptosis, allowing them to grow and multiply uncontrollably.

What role does apoptosis play in the immune system?

Apoptosis helps the immune system by removing infected or harmful cells, which is crucial for fighting off infections.

The post Understanding Apoptosis: The Key to Programmed Cell Death in Health and Disease appeared first on BDS Notes.

Question.1.Write short note on vitamin A defiiency.

Or
Describe the clinical features of vitamin A defiiency.

Answer. Defiiency of vitaminA causes interference with growth,reduced resistance to infections and interference with nutrition of cornea, conjunctiva, trachea, hair follicle and renal pelvis.

• VitaminA defiiency interferes with ability ofeyes to adapt to darkness and impairs visual affity.
• Children with vitamin A deficiency will experience impaired growth and development.

Causes

• Poor intake
• Malabsorption
• Disease of liver and intestine.

“Understanding nutrition and metabolic defects through FAQs: Causes, symptoms, and treatments explained”

Clinical Features

• Earliest sign of defiiency of vitamin is diffilty in reading or sewing at night or fiding anything in darkness.
• Conjunctiva becomes dry and small grayish white raised spots appear. Bitot’s spots form grayish white triangular plaques on conjunctival surface lateral to cornea.
• Microcytic anemia.
• Cornea subsequently becomes dry and lusterless, and if there is lack of treatment changes are irreversible.
• *Keratomalacia involving the cornea leading to the ulceration and blindness may result.
• Children with vitaminA defiiency not only have retarded growth but also increased tendency to chest infection.
• Skin become dry and rough
• Imperfect enamel formation of teeth.
• Hemeralopia: Patient is unable to see bright light.
• Asteatosis, i.e. persistent dry scaling of the skin is the earliest manifestation.
• Phrynoderma, i.e. toad skin. Brown to dark brown,dry, rough, hyperkeratotic follicular papules with central keratotic horny spurs. Bilateral and symmetrical distribution in anterolateral aspects of thighs, posterolateral aspects of arms.

Read And Learn More: General Medicine Question And Answers

“Importance of studying nutrition and metabolic defects for healthcare professionals: Questions explained”

Treatment

• Prevention of vitamin A deficiency by giving good nutrition, intake of fresh leafy green vegetables and addition of vitamin A to food stuff.
• Single dose of oral retinol palmitate 60 mg or 200,000 IU should be given. In cases of diarrhea 50 mg IV may be given. Second dose is repeated next day and the third and last dose is given at the time of follow­up visit.
• Various other associated conditions such as diarrhea, dehydration, electrolytic imbalance, protein energy malnutrition should be treated by appropriate measures.
• For local treatment of eyes patient should be sent to ophthalmologist.
• If primary or secondary infections are present, antibiotics should be given to the patient.

Question.2. Write short notes on beriberi.

Answer. Beriberi is caused due to the defiiency of vitamin B1,i.e. thiamine.
Defiiency of vitamin B1 affcts growth, nutrition and carbohydrate metabolism.

Etiology

Defiiency of vitamin B1 occurs due to:

• Chronic alcohol intake
• Severe malnutrition
• Chronic debilitating diseases

Pathogenesis

Thiamine forms an essential part of two coenzymes which are important in oxidative decarboxylation of alpha­ketoacidosis.

Deficiency of vitamin leads to accumulation of alphaketoacidosis whose toxic effcts results in production ofberiberi.

Types Of Beriberi

• Wet Beriberi or cardiovascular beriberi: Beriberi is wet when there is cardiac involvement.
• Dry beriberi or neuritic type: Beriberi is dry when there is CNS involvement.

Clinical Features

• Beri-beri
• Wet beriberi: Palpitation, dyspnea, Cardiomegaly,warm extremities, anasarca (severe generalized edema), signs of congestive heart failure in late stage.
• Dry beriberi: Cramps, tingling and numbness in the limbs, nystagmus (cyclic movements of eyes), wrist and foot drop, ataxia, loss of equilibrium, parasthesia and confusion.
• Wernick’s encephalopathy: There is involvement of brain which is characterized by ataxia, ophthalmoplegia,confusion and disorientation.
• Korsakoff psychosis: It occurs due to involvement of mammillary bodies and confabulates with amnesia.
• Presence of angular stomatitis.

Diagnosis

• Blood thiamine is low
• Raised pyruvate and lactate levels.
• Low urinary excretion of thiamine and its metabolites
• Measuring of whole blood or erythrocyte transketolase activity before and after addition of thiamine.
  In this there is low transketolase activity which increases by 15% after addition of thiamine confim the diagnosis.
• There is clinical improvement after single dose of thiamine,i.e. 50 mg IM with increase in diastolic blood pressure and decrease in heart rate is another diagnostic criteria.

Treatment

• Vitamin B1 (50–100 mg daily) IM or IV is given.
• As acute crisis is over, patient has given small dose of 5 mg daily along with nourishing diet.
• Diet consists of high B complex and protein content like eggs, milk, nuts and green vegetables.
• Wet beriberi with cardiac involvement require digoxin and diuretics, if congestive heart failure is present.

“Common challenges in diagnosing and managing metabolic defects effectively: FAQs provided”

Question.3.Describe briefly vitamin D defiiency.

Answer.

• Vitamin D defiiency leads to rickets in growing child and osteomalacia in adults.
• Vitamin D is essential in calcium and phosphorus metabolism. It is required for normal development of bones and teeth.
• Deficiency of vitamin D causes imperfect skeletal formation, bone disease, rickets and caries.

Vitamin D Deficiency Rickets

It occurs generally in growing children.

Clinical Features

• Infistsixmonths oflife tetanyand convulsions are common.
  These above manifestations are due to hypocalcaemia.
• Wrist and ankles are swollen
• Changes in bone are found in epiphyseal plates, metaphysis and shaft.
• Localized area of thinning are sometime present in skull so that a figer can produce indentation. This condition is called craniotabes.
• Pigeon breast is present.
• Developmental abnormalities of dentin and delayed eruption.
• Higher caries index.
• Hypoplasia of enamel is present.
• Pulp chamber is large.
• Malocclusion of teeth is present.

Investigations

• Radiological: Radiograph of wrist show widening of distal ends of shaft of both radius and ulna.
  Zone of epiphyseal cartilage get thickened.
  As these changes get completely developed, they cause saucer shaped deformity.
• Biochemical changes:

• Low plasma calcium and phosphate levels
• High serum alkaline phosphatase levels
• Plasma 25 dehydroxy cholecalciferol is low or absent.

Vitamin D Defiiency Osteomalacia

It is also known as adult rickets. Only flt bones and diaphysis of long bones are affcted.

Clinical Features

• Pelvic deformities are seen in females.
• Remodeling of bone occur in absence of adequate calcium resulting in softening and distortion of skeleton.
• Bone pain and muscle weakness is present.
• Severe periodontitis is present.

Management of rickets and osteomalacia

• Dietary enrichment of vitamin D in form of milk.
• If tetany is present give IV calcium gluconate. Daily dose is 1000–2000 IU of vitamin D combined with 500–1000 mg of calcium.
• Curative treatment includes 2000–4000 IU of calcium daily for 6–12 weeks followed by daily maintenance dose of 2000–4000 IU for long period.
• Patients with osteomalacia require large dose of vitamin D and calcium, i.e. 40,000–1,00,000 IU of vitamin D and 15–20 gm of calcium lactate per day.

“Factors influencing success with nutrition and metabolic defect knowledge: Q&A”

Question.4. Write short note on protein calorie malnutrition.

Answer. Protein calorie malnutrition leads to two diseases known as marasmus and kwashiorkor.

Marasmus
It is seen in infants and young children.

In marasmus, there is total defiiency of calories including protein defiiency.

Causes

• Poor intake of breastfeeds and or inadequate supply of milk and other nutrients.
• Lack of digestion
• Impaired absorption of protein.
• Protein is absorbed but cannot be metabolized satisfactorily.
• Protein is metabolized but not properly utilized.

Clinical Features

• It occurs below the age of 1 year
• There is progressive loss of subcutaneous fat.
• Child is irritable and cries excessively.
• Typical appearance of monkey face.
• Sunken and lusterless eyes.
• Delay in sittng, standing and walking.
• Abdomen may be *distended or sunken and it does not has fat in wall Lack of playful movements and persistent crying.
• Gross degree of muscle wasting is present
• Limbs are thin, look like sticks and buttcks do not contain fat.
• Head is large for body and ribs are visible.

Management

• Correction of flid, electrolytes, acidosis, hypoglycemia,hypothermia.
• Look for the infections and treat them from proper antibiotic therapy.
• Diet is given to the child which is rich in proteins, energy and essential nutrients.
  Diet therapy should be continued till the child attins normal weight as well as nutritional status.

Kwashiorkor

It occurs in children between 1 to 4 years.

In Kwashiorkor there is defiiency of proteins and amino acids

cause

• Prolong febrile illness, massive burns and large chronic ulcers.
• Stress, starvation, persisting vomiting and diarrhea.
• Chronic infections, i.e. urinary tract infections, TB and parasitic infections.

Clinical Features (Signs And Symptoms)

• Growth: Failure of growth is present, child appears lean and thin. Presence of generalized edema.
• Hair: Change in the color of hair from black to blond,reddish or grey. Hairs are fie, straight and show sparse pigmentation.
• Skin: Skin become thick, pigmented, desquamated and ulcerated. A severe case with desquamation looks like the child is burnt. Dermatosis with fisuring is also seen in moderate cases.
• Gastrointestinal tract: Anorexia and diarrhea are common.
  Liver is enlarged and palpable due to fatt changes.
• Blood: There is presence of moderate degree of anemia.
• Mucosa changes: There is presence of stomatitis, chelosis,smooth tongue and ulceration is present around anus.
• Mental changes: Child becomes miserable, apathetic and has mewing cry.
• Muscles and fats: Presence of wasting of muscles of chest,upper arm, legs and hips. Fat is seen plentiful at these sites.
• Vitamin defiiencies: Vitamin A defiiency is present,folate defiiency is common, defiiency of vitamin K can cause purpura and bleeding.

Management
Diet

• Diet for mild-to-moderate cases: Diet should be easily digestable.
  It should be rich in proteins, minerals and vitamins with extra calories.
  Milk should be given.
  Egg is a good flp with milk and water as a source of fist class protein Plant protein mixtures such as corn,soya, diet milk can be given.
  Additional fats should be included. If there is lactose intolerance dal, rice and buttr can be given.
• Diet for acute cases: Protein intake should be 3 to 4 g/Kg/day and energy intake of 150 kcal/kg/day. If child is unable to take diet from mouth go for nasogastric intubation.
  Care mustbe takento take suffientamount of plant, animal proteins and fats to maintain the weight.

Vitamins and mineral supplementations

• Vitamin A, D, B complex and C are given at therapeutic dosages.
• In vitamin A defiiency 30 mg of Vitamin A should be given for 3 days.
• 0.5–1 g of potassium chloride dissolve in feeds or water should be given daily in divided dosages.

Maintenance of body temperature

• For maintainence of body temperature at night blankets or room heaters are useful.

Skincare

• In cases of dermatoses skin should be kept clean and protected.

In Hospital treatment

• Correction of dehydration, electrolyte disturbances,hypoglycemia, acidosis and hypothermia.
• Parenteral therapy with half of saline and 2.5% glucose before diet therapy.
• In anemia, packed erythrocyte infusion is given.

“Steps to explain nutrition and metabolic defects: Causes vs symptoms vs management: Q&A guide”

Question.5. Write causes and management of malnutrition in India.

Answer.

Causes of Malnutrition

1. Due to defective intake offood:

• Loss of appetite due to depression, anxiety, anorexia nervosa, etc.
• Due to persistent vomiting
• Alcohol intake
• Unbalanced therapeutic diet
• Administration of prolong IV flids, parenteral flids in hospitalized patients

2. Maldigestion and disordered absorption:

• In hypochlorhydria or achlorhydria
• In steatorrhea
• Intestinal hurry due to surgical resection
• Due to prolong use of antibiotics

3. Defective utilization:

• In cirrhosis of liver
• In malignancy
• In infections
• In renal failure
• Due to inborn error of metabolism, i.e. hartnup’s disease
• Due to drugs such as anti­epileptics

4. Loss ofnutrients from body:

• Proteinuria in nephrotic syndrome leads to hypoproteinemia.
• In diabetes mellitus, glycosuria causes loss of energy and undernutrition
• Due to excessive menstrual blood loss
• Hypokalemia due to severe persistant diarrhea.

5. Due to increased demands:

• In pregnancy, lactation, adolescence, illness and heavy manual work.
• In fever and thyrotoxicosis
• In burn, surgery and trauma, there is increase in catabolism of proteins and vitamin C.
• Malignant cachexia causes loss of weight due to increased demand.

Treatment of Malnutrition

In adults

• For mild starvation, adequate supplementation of nutrients is necessary
• In moderately starved people, extra­feeding is needed
• In severely starved persons, food is given in small amount at frequent intervals. Food should be staple meal, i.e. cereal with some sugar, milk and oils, salt is restricted. Potassium, magnesium and vitamins are adequately given. This is continued till patient feel active.

In children

Diet

• Diet for mild-to-moderate cases: Diet should be easily digestable. It should be rich in proteins, minerals and vitamins with extra calories.
  Milk should be given.
  Egg is a good flp with milk and water as a source of fist class protein.
  Plant protein mixtures such as corn,soya, diet milk can be given.
  Additional fats should be included.
  If there is lactose intolerance dal, rice and buttr can be given.
• Diet for acute cases: Protein intake should be 3 to 4 g/Kg/day and energy intake of 150 Kcal/kg/day.
  If child is unable to take diet from mouth go for nasogastric intubation.
  Care must be taken to take suffieicnt amount of plant, animal proteins and fats to maintain the weight.

Vitamins and mineral supplementations

• Vitamin A, D, B complex and C are given at therapeutic dosages.
• In vitamin A defiiency 30 mg of vitamin A should be given for 3 days.
• 0.5–1 gm of potassium chloride dissolve in feeds or water should be given daily in divided dosages.

Maintenance of body temperature

For maintenance of body temperature at night blankets or room heaters are useful.

Skincare

• In cases of dermatoses skin should be kept clean and protected.

In hospital treatment

• Correction of dehydration, electrolyte disturbances,hypoglycemia, acidosis and hypothermia.
• Parenteral therapy with half of saline and 2.5% glucose before diet therapy.
• In anemia, packed erythrocyte infusion is given.

Question.6. Write short note on osteoporosis.

Answer. Osteoporosis is a group of skeletal disorders characterized by reduction in bone mass per unit bone volume, which results in increased risk of fracture, even in absence of noticeable injury.

Causes

• Dietary calcium deficiency: Especially in case of women both premenopausal and postmenopausal .
  Apart from increased requirements, degree of calcium absorption from intestine decreases with age.
• Excessive alcohol or caffine.
• Genetic inflences.

Other disorders affcting mineral homeostasis:

• Endocrine: Cushing syndrome, hyperthyroidism, type I diabetes mellitus, hypogonadism and acromegaly
• Drugs: Glucocorticoids, thyroxin and diuretics.

Clinical Features

• Bone loss progresses for many years without causing symptoms.
• Shortened heights, bone pain, low back pain, diffilty in gettng up from chair are complaints in women at menopause with osteoporosis.
• Signs of osteoporosis include deformities of skeleton,such as kyphosis (Dowager’s hump) and loss of height especially in vertebral compression fracture.

Diagnosis

• History offracture: Fractures associated with osteoporosis are vertebral fractures, hip fractures and Colle’s fracture of distal radius.
• Radiograph: It shows prominence of vertical trabeculae,generalized loss of contrast between bone and soft tissue.
• Bonedensity measurement: Dual-energy X­ray absorptiometry is the gold standard. It is performed in spine, both hips and both wrists.
  Bone densities are then plottd against normal database to provide standard deviation from normal, i.e.

T score. For post­menopausal women, T score values are:

Management

• Active physical activity helps to maintain strength,flxibility and co-ordination of body improves.
• Calcium 1.5–2 g/day, if calcium malabsorption is there,cholecalciferol 0.25 mg, alfacalcidol 0.5 µg/day.
• Estrogen therapy: 0.635 mg daily estrogen is given in small thin women, early women, etc.
• Biphosphates, i.e. etidronate 400 mg/day for 2 weeks inhibit bone resorption.
• Calcitonin 100 IU SC inhibits bone resorption.
• Sodium floride 40–60 mg/day stimulates osteoblasts and causes bone formation.

“Role of dietary deficiencies in causing metabolic defects: Questions answered”

Question.7. Mention the complications of diabetes mellitus.
Or
Write short note on complications of diabetes mellitus.
Or
Enumerate the complications of diabetes mellitus.
Or
Write notes on ten complications of diabetes mellitus.

Answer. Diabetes mellitus is collection of disorders that have hyperglycemia as hallmark.

Complications

Acute Or Immediate Complications

• Diabetic ketoacidosis or coma
• Hypoglycemia or hypoglycemic coma
• Non­ketotic hyperosmolar diabetic coma
• Lactic acidosis

First two complications occur in Type I diabetes mellitus and other two occur in Type II diabetes mellitus.

Diabetic Ketoacidosis

• It is an exclusive complication of type I diabetes. It can develop in patients with severe insulin defiiency combined with glucagon excess.
  Failure to take insulin and exposure to stress are precipitating causes.
• As the ketogenesis continues the excess ketone bodies produced cannot be degraded by the muscles and other tissues resulting in ketosis, which manifests as anorexia, nausea, vomiting, deep and fast breathing, mental confusion and coma. However, most of the patients recover.

Hypoglycemia

• It is defied as fall in blood glucose concentration below 3.1 mmol/L.
• It is seen in type I diabetes patients due to excessive administration of insulin, missing a meal or due to stress.
• As the hypoglycemia continues, it can lead to comma,cardiac arrhythmias and is fatal.
• This can lead to worsening of control of diabetes and rebound hyperglycemia.

Nonketotic Hyperosmolar Diabetic Coma

• It is common in type II diabetes mellitus.
• The clinical hallmark is hyperglycemia, hyperosmolality and dehydration without ketoacidosis.
• Precipitating features are infection, myocardial infarction,drugs such as thiazides, steroids, diphenylhydantoin.
• Loss of glucose in urine is so intense that the patient is unable to drink suffient water to maintain urinary flid loss.
• Because of high viscosity of blood, thrombotic and bleeding complications are frequent. Mortality rate is high in this complication.

Lactic Acidosis

• It is seen in type II diabetes mellitus.
• It is caused due to excess lactate production and/or inadequate utilization.
• This can be precipitated by metformin or other systemic disorders such as liver or renal failure, pancreatitis or leukemia.
• Cardiovascular collapse leads to mortality.

Chronic or late-onset complications

These complications are due to changes in small blood vessels i.e.microangiopathy or in large blood vessels, i.e. macroangiopathy.

Microvascular are retinopathy, neuropathy, nephropathy and miscellaneous

Macrovascular are atherosclerosis, hypertension, peripheral vascular disease and diabetic foot ulcer

The chronic complications occur more frequently in Type II diabetes mellitus rather than Type I diabetes mellitus.

Diabetic Retinopathy

• This is the very important cause of blindness in diabetic patients.
• Dilatation of retinal capillaries is earliest sign. Besides these there is also presence of microaneurysms, retinal hemorrhage, neovascularization, hard and soft exudates,vitreous hemorrhage and firosis.
• Frequency, onset and severity of retinopathy vary in diabetic patients.
• Background retinopathy is most common and proliferative retinopathy is less common.

Diabetic Neuropathy

• It can involve any part of nervous system except the brain.
• Neuropathy is an early and common complication which leads to morbidity and disability.
• Poor glycemic control and long duration of diabetes is associated with high incidence of neuropathy.
• Sign and symptoms are of peripheral nervous system.
• Main pathological changes in peripheral nerves are axonal degeneration of myelinated and non-myelinated fiers,
  Segmental demyelination, Schwann cell injury.

Diabetic Nephropathy

• This is the most common cause of mortality and morbidity in diabetic patients.
• 40 to 50% of type II diabetes patient develop it and 25% patients with type I diabetes develop end stage renal disease and die of it.
• It is divided into three stages, in fist stage patient is asymptomatic but has high GFR, in next stage there is renal hypertrophy which leads to microalbuminuria.
• In advance stage, patient develop macroproteinuria and passes onto nephrotic syndrome.
• 25% of patients with diabetic nephropathy can go directly at end stage renal disease with hypertension and undergo chronic renal failure.

Miscellaneous

It consists of various infections, gastroparesis, arthropathy.

Atherosclerosis

• In diabetic patient development of athroma is faster as compared to normal individual.
• Hyperlipidemia, decreased HDL levels, increased platelet adhesiveness, obesity and associated hypertension are contributory factors for athrosclerosis.
• Atherosclerosis leads to coronary artery disease, silent myocardial infarction, cerebral stroke and gangrene of toes and feet.

Diabetic Foot Ulcer

• This is the frequent site of complication in diabetes.
• Pathogenic components of diabetic foot are neuropathy,peripheral vascular disease causing ischemia and secondary infection causing ulceration.

Question.8. Outline the management of diabetes mellitus.
Or
Write short note on treatment of diabetes mellitus

Answer. Management

Diet Management

• Restoration of normal blood glucose and optimum levels.
• Maintenance of blood glucose levels as near to physiologic levels to prevent onset or progression of complications.
• Maintenance of normal growth rate in children and adolescents as well as attinment and maintenance of reasonable body weight in adolescents and children.
• Provision of adequate nutrition for pregnant women and fetus during lactation.
• Consistency in timing of meals and snacks to prevent inordinate swings in blood glucose level.
• Motivation to have small frequent meals.
• Determination of meal plan appropriate for individual and based on dietary history to have good compliance.
• Management of weight reduction for obese individuals with NIDDM.
• Improvement in the overall health of patients with diabetes through optimal nutrition.

Total Calories

Requirements are determined by the patients activity:

• Overweight NIDDM should be encouraged to establish their weight within a desirable range. A reduction of approximately 500 kcal/ day can result in loss of 1–2 kg/month.
• Carbohydrates: Carbohydrates should be taken in form of starch and complex sugars. 100–300 g of carbohydrates should be spreaded over 3 meals, i.e. 60g each and 3 snacks,i.e. 30 geachwithhalflitre ofmilk. Unrefied carbohydrates should be substituted by refied carbohydrates to the extent possible.
• Proteins: Recommended dietary allowance of 0.85 g/kg body weight for adult is an appropriate guide.
• Fat: Fat intake should be 50–150 g daily divided between the meals. Replacement of saturated with polyunsaturated fat is desirable to reduce cardiovascular risk. Cholesterol intake should be < 300 mg/day.
• Fiber: Increased consumption of dietary fier especially soluble fier are associated with lower levels of blood glucose and serum lipids. The water insoluble fiers such as cellulose, lignin and most hemicelluloses found in whole grain breads, cereals and wheat bran affct gastrointestinal transit time and fecal bulk with litte impact on plasma glucose. However highly viscous water soluble fiers such
  as pectins, gums and storage polysaccharide found in fruits, legumes, lentils roots, tubers, oat and oat bran, when eaten in purifid form, reduce serum levels of glucose and insulin. Ideal recommended amount of fier in patient’s diet is 35–40 g/day.
• Alternative sweeteners: Both nutritive and non­nutritive sweeteners are acceptable in diabetes management.
• Sodium: It should be restricted to 1000 mg/1000 kcal, not to exceed 3000 mg/day to minimize symptoms of hypertension.
• Alcohol: It should be taken in moderation and may need to be restricted entirely by person with diabetes and insulin—induced hypoglycemia, neuropathy, poor control of glucose and lipids, or obesity.
• Vitamins, minerals and antioxidants: intake should be encouraged.

Forbidden foods: Sugar, jam, jellies, honey, jaggery, tinned fruits and juices, sweets, chocolate, ice creams, pastries, glucose drinks, foods made with sugar, pudding, sauces.

Foods allowed in moderation: Bread of all kinds and chapatts made from wheat or millets, plain biscuits, all fresh fruits, baked beans, breakfast cereals.

Free foods: All meat, fih, eggs (not fried), clear soup or meat extracts; tea or coffe; vegetables such as cabbage, cauliflwer, spinach, pumpkin, brinjal, lady’s figer, turnip, French beans,cucumber, lettce, tomato, spring onions, radish, asparagus.
Spices, salt, pepper and mustard; buttr and margarine. Sugar substitutes for sweetening.

Oral Hypoglycemics

These drugs are used in patients of Type II diabetes mellitus(NIDDM) who do not respond to dietary management and who would otherwise require treatment with insulin in later situation, so they are also used as adjuvant drugs to insulin in overweight diabetes patients.

Insulin secretagogues i.e. drugs increasing secretion of insulin

Sulfonyl ureas

Meglitinides:

• Repaglinide, i.e. 0.5–4 mg three times a day
• Netaglinide, i.e. 60–120 mg three times a day 15 to 30 min before each meal
• Voglibose, i.e. 0.2–0.3 mg, 15–30 min before each meal.

Insulin sensitizers, i.e.drugs sensitizing action of insulin and overcome insulin resistance

• Biguanides, i.e. metformin should be given 1.5–2.5 g/day in three divided doses after meals.
• Thiozolidinediones, i.e.rosiglitazone should be given 2–8 mg or pioglitazone 15–45 mg in a single or two divided doses.
  They can be combined with sulfonyl ureas or metformin

• Alpha glucosidase inhibitors, i.e. Acarbose 25 to 100 mg TDS or Voglibose 0.2–5 mg TDS taken orally in three main meals.
• It can be given in combination with metformin 500 mg for increased effiency.
• DPP-4 inhibitor: Vildagliptin 50–100 mg daily in two dived doses with meals ot saxagliptin 2.5 to 5mg OD.
• Pramlinide: Initial dose is 15 μg before each meals in Type I diabetes mellitus and 60 μg in Type II diabetes mellitus.

“How does phenylketonuria (PKU) affect metabolism? FAQ explained”

Question.9. Write short note on insulin.

Answer. Insulin is required for proper control of diabetes and to keep blood sugar within limits.

Following are the indications for insulin therapy:

• In type I diabetes mellitus
• In gestational diabetes
• Hyperglycemia despite maximum doses of oral agents
• Decompensation due to intercurrent events such as infection, acute injury or stress
• Development of severe hyperglycemia with ketosis
• Perioperative in patients undergoing surgery
• Kidney or hepatic disease

Various insulin preparations

Treatment Strategies with Insulin

• Single dose regimen: Daily injection of intermediate acting
  insulin given before breakfast.
  The starting dose 0.3–0.4 U/Kg/ day; increased gradually to obtain glucose values in acceptable range.
  Regular insulin can be added to decrease the glucose level that follows breakfast.
• Twice daily regimen: Combination of regular and intermediate acting insulin BD, i.e. before breakfast and before dinner (“Split mix” regimen).
• Multiple daily injections: For achievement of more tight control of blood glucose which requires administration of at least 3 injections per day.
  These can be given with use of mixture of intermediate­ and short acting insulins (pre­mixed insulin) in the morning before breakfast, with regular insulin before supper­ and intermediateacting at bedtime; or again a combination of regular and intermediate acting before dinner.
  Divide the total daily into 2 equal doses following 1:1 transfer from basal insulin.
  Give half before breakfast and other half before dinner.
  The largest meal will require larger proportion of insulin.
  Reduce total dose by 20%, if patient experiences recurrent hypoglycemia.
• Insulin concentrations: The insulins are available in many concentrations. In India, the commonly used is 40 U/mL
• Insulin purity: The impurities which may be contained are proinsulin, insulin intermediates and contaminating proteins from islet tissue or exocrine pancreas such as glucagon, somatostatin and pancreatic polypeptides.
• Standard insulins currently have only 10–20 PPM of proinsulin and purifid monocomponent insulins less than 1 PPM.

Site of Insulin Injection

Best sites for the insulin injection are subcutaneous fat on abdomen, buttck, anterior thigh and dorsal area of arm.

Insulin Delivery System

• Insulin pens are used in both Type I and Type II diabetes mellitus.
• Continuous insulin infusion systems are used in Type II diabetes mellitus.

Complications

Following are the complications of insulin therapy:

• Hypoglycemia: It is the most frequent and most serious reaction. Hypoglycemia can occur in any diabetic following inadvertent injection of large doses, by missing a meal or by performing various exercises
• Local reaction: Swelling, erythema and stinging sometimes occurs especially in beginning. *Lipodystrophy occurs at injection site after long usage.
• Insulin allergy: This is infrequent and is due to contaminating proteins. Urticaria, angiedema and anaphylaxis are manifestations.
• Edema: Some patients develop short­lived dependent edema when insulin therapy is started.
• Weight gain: Patients on long­term insulin therapy gain weight.

Question.10. Outline management of diabetic comma.

Answer. Diabetic ketoacidosis or diabetic comma is the exaggeration or deranged energy metabolism due to defiiency of insulin which results in accumulation of acid metabolites and ketone bodies.

Management

Following is the management of diabetic comma

Admission of patient

• Diagnosis is confirmed by examination of blood glucose and ketone measurements.
• Initial assessment of dehydration, hyperosmolality, serum potassium, acidosis and kidney function is done.
• Fluid loss is measured by subtracting admission weight by last known stable weight.
• Patient should be evaluated for sepsis.

Management during hour 1

• If patient is hypovolemic and hypotensive fluid administration is done, i.e. normal saline is administered and if necessary colloids should be given.
  Rate of administration is necessary to restore circulatory function.
  As blood pressure become normal and urine output becomes adequate rate of administration of normal saline is 1000 mL/hour.
• Continuous I.V. infusion of regular insulin 5–10 units/hour is given.
• I.V, infusion of potassium is done at 10–40 mmol/ hour during initiation of insulin therapy.
• Sodium bicarbonate IV is given in cases with acidosis.
  Dose is 50–100 mmol/L sodium bicarbonate in 0.45% saline for 30–60 minutes. Additional potassium should also be given with bicarbonate therapy.

Management during hour 2

• Normal saline should be continued at 500 mL/ hour.
  Plasma osmolality should be greater than 285 mmol/ L during fist 12 hours. If serum sodium is greater than 150 mmol/L switch to 0.45% saline.
• Blood glucose should be checked and insulin is adjusted to 5 mmol/litre/hour. Blood glucose should not fall below 11.1–14.0 mmol/L. Anion gap is decreasing and blood pH is increasing.
• Serum potassium should be maintained at 4–5 mmol/litre by addition of potassium to IV flids.

Management during hours 3 to 4

• Management should be continued as given in second hour.
• Cognitive and neurological symptoms should be observed for 12 hours.

Management during hours 5 to 8

• Normal saline should be continued at 250 mL/ hour.
• As blood glucose reaches 11.1–14 mmol/ L, change IV flid to 500 mL/hour normal saline with 5% glucose.
  Insulin should be continued at maintenance dose until ketoacidosis is cleared.
• Potassium should be continued at 10–40 mmol/ hour,since ketoacidosis is cleared.
• Phosphate replacement is done at 6 hours, if serum phosphate is < 2 mg/dL

Management during hours 8 to 24

• IV repletion is continued with 0.45% saline with or without 2.5% or 5% glucose as needed.
• As diabetic comma is subsided, patient should be switched to subcutaneous insulin and stop IV and IM insulin.

“Early warning signs of gaps in understanding metabolic defect basics: Common questions”

Question.11. Differentiate between diabetic comma and hypoglycemic comma.

Answer

Question.12. Write short note on hypoglycemia.

Answer.

Hypoglycemia is defined as fall in blood glucose concentration below 2.5 mmol/L.

It can be present as asymptomatic, mild, severe or may be present as coma.

Etiology

• Postprandial
• Alcohol ingestion
• Starvation, prolonged exercise, infection
• Non­islet cell tumors, e.g. hepatoma, adrenal carcinoma,mesothelioma, etc
• Iatrogenic, i.e. drug induced due to oral hypoglycemic,salicylism, due to propranolol.

Clinical Features

• Cardiovascular system: Palpitation, tachycardia, anxiety,cardiac arrhythmias
• Central nervous system: Tremors, confusion, headache,tiredness, difficulty in concentration, in cordination,slurred speech, drowsiness, convulsion and coma.
• Gastrointestinal tract: Nausea and vomiting
• Skin: Sweating and hypothermia

Diagnosis

1. In hypoglycemia state:

• Suggestive history
• Dramatic response to IV glucose during attck
• Low plasma level glucose during attck
• C-peptide concentration > 200pmL/L

2. Ofcause:

• Clinical: Exclude hypopituitarism, Addison’s disease,liver cirrhosis or failure, sarcoma, alcohol ingestion after fasting, self administration of insulin or sulphonylurea.
• Investigations for insulinomas:

• Overnight fasting plasma glucose and insulin measurements will demonstrate spontaneous hvpoglycemia and raised plasma insulin
• Low plasma C­peptide with high plasma insulin.
• High fasting plasma proinsulin.

Management

1. In acute attck:

• Administration of rapidly absorbable carbohydrate
• In mild reaction, orange juice (100 mL) or corn syrup or candy taken orally suffient.
• In unconscious or uncooperative patients 50 mL of 50% glucose IV if vein not available glucagon 1 mg SC or IM will cause suffient increase in blood sugar to allow the patient to become rational and cooperative.
• When recovery is slow, e.g. after overdose of insulin or sulphonylurea therapy, constant infusion of 10–20% dextrose is given to maintain the blood sugar.

2. Conservative treatment and prevention ofacute attcks

• Diet: Carbohydrate not more than 150 gms in slowly absorbable form like cereals, bread, fruits and vegetables.
  Liberal protein because glucose derived from it is liberated slowly; fat to make up calories.
  In hepatogenic type bedtime meal to prevent early morning hypoglycemia.
• Restriction of physical exercise.

3. Surgical measures:

• Removal of islet cell tumors, or partial resection of pancreas

• In fulminating cases where convulsions are not controlled by glucose.
• In severe, chronic cases not controlled by diet.
• Patients with marked, neuropsychiatric syrnptoms.

4. Drugs

• Glucagon: The efficy depends on size of hepatic glycogen stores. The drug has litte effct on blood glucose in patients who have been fasting or are hypoglycemic for long periods. IM injection of 1mL of glucagon is given, if hypoglycemia is insulin induced.
• Diazoxide and Octreotide may be used to control symptoms while the patient is awaiting surgery or when the patient is not a candidate for surgery.

Question.13.Write short note on vitamin B12 defiiency.

Answer. It is also known as Wonder vitamin and cyanocobalamin.

Causes of Vitamin B12 Defiiency

• Due to inadequate dietary intake
• Due to malabsorption
• Intrinsic factor deficiency in pernicious anemia,gastrectomy, congenital lack of intrinsic factor
• Intestinal causes, i.e. tropical sprue, Ileal resection,
  Crohn’s disease
• Removal of vitamin B12 from intestines i.e. In tapeworm infestation and due to bacterial proliferation in intestinal blind loop syndrome
• Drugs such as neomycin, PAS and colchicine.

Clinical Features

• Blood: Megaloblastic anemia
• General features: Pallor, anorexia, diarrhea
• Oral manifestations: Glossitis, Glossodynia, Angular stomatitis, xerostomia
• Nervous system manifestations:

• Subjective sensory disturbances: Paraesthesia, Tingling and numbness in toes, tips of fingers, rarely simultaneously in both upper and lower extremities.
  Sometimes burning or stabbing pains or even lightning pains like tabes.
• Objective sensory loss: Sense ofvibration, posture and passive movement affcted fist in lower, later in upper limbs. Glove and stocking type of superfiial sensory loss. Tenderness of calf muscles.
• Motor symptoms: Pyramidal weakness and ataxia develop at variable interval after onset of sensory disturbances.
• Reflxes: Ankle jerks lost, knee jerks may be absent. Both exaggerated, if lateral column lesion predominates.
  Plantars extensor.
• Sphincter disturbances: First diffilt or precipitate micturition, later retention of urine or incontinence.
  Impotence is early.
• Mental changes: Mild dementia, impaired memory.
  Confusional psychosis or irritability or depression.
• Bilateral primary optic atrophy in 5%.

Diagnosis

• Presence of low hemoglobin
• Macrocytosis,
• High MCHC
• Megaloblastic bone marrow
• Gastric achlorhyclria
• Serum vitamin B12 less than 100 pg/mL
• Elevated homocysteine

Treatment

• Vitamin B12 defiiency especially in those with megaloblastic anemia is treated by giving hydroxycobalamin 1000 microgram IM twice a week for fist week.
  This is followed by 1000 µg weekly for 6 weeks.
• Replacement therapy is given throughout the life in dosage of hydroxycobalamin 1000 µg IM for every three months.
• For patients sensitive to injections, Oral B12 in large daily doses is given, i.e. 100 µg or more.

Question.14. Write short note on scurvy.

Answer. Deficiency of vitamin C leads to scurvy.

Due to vitamin C defiiency, there is defective collagen formation.

Etiology

• In artifiially fed infants
• It is precipitated by febrile disease, infections and diarrhea

Clinical Features

• Onset of the disease is usually gradual, there is fretfulness and increasing pallor, or tenderness of legs which causes child to cry whenever touched, anorexia and loss of weight. First symptom is inability of the child to use his legs.
• Symptoms due to hemorrhages:
• Under periosteum of long bones: “Pithed frog posture”with thighs flxed and abducted and knees flxed,sometimes diffse swelling above or below the knee;in severe cases, infitration of muscles with blood causing edematous limbs, i.e woody leg; hemorrhage between diaphysis and epiphysis causes separation of epiphysis from shaft.
• Perifollicular hemorrhage.
• In orbit, there is proptosis with swelling of eyelids
• Hematuria: May be an early symptom and is only microscopic.
• Scorbutic beading of the ribs
• Presence of anemia
• Keratosis of hair follicles with ‘corkscrew’ hair
• Failure of wound healing

“Asymptomatic vs symptomatic effects of ignoring nutritional principles: Q&A”

Oral Manifestations

• It chiefl affcts the gingival and periodontal region.
• The interdental and marginal gingiva becomes bright red,swollen, smooth, shiny producing appearance known as scurvy bud. In fully developed scurvy, gingiva becomes boggy, ulcerated and bleeds easily
• There is a typical fetid breath of a patient with fusospirochetal stomatitis.
• Color of the gingiva changes to violaceous red.
• In severe cases, hemorrhage and swelling of periodontal
  ligament membrane occur followed by loss of bone and loosening of teeth which are exfoliated.

Diagnosis

• Low ascorbic acid level in platelets and plasma
• Anemia is mild­to­moderate but may be severe.
• X­ray shows characteristic features such as

• Pencilled cortex
• White lines of Frankel
• Zone of Trummerfeld
• Halo sign of Wimberger
• Subperiosteal hematoma
• Joint effsion
• Scorbutic rosary

Management

• About 3 to 4 ounces of fresh orange juice or tomato juice daily.
• Ascorbic acid 100 mg or more orally or parenterally twice or thrice daily for 10 to 15 days.

Question.15. Write short note on balanced diet.
Or
Write notes on balanced diet.
Or
Write about balanced diet.

Answer. A diet adequate in energy providing substances, i.e.carbohydrates and fats, tissue building compounds,i.e. proteins, inorganic chemical, i.e. water and mineral salts, agents that regulate or catalyze metabolic process,i.e. vitamins and substances for certain physiological processes such as bulk for promoting peristaltic movement of digestive tract known as balanced diet.

• For proper growth, maintenance and development of our body an ideal combination of essential nutrient, vitamins and minerals should be aimed.
• An average Indian diet is poor in quality as well as quantity in meeting the daily needs.
• A balanced diet should contain 30 cal/kg optimum body weight.
• Balanced diet should contain 60–70% carbohydrates of total calories, 12–18% protein of total calories,20–25% fats of total calories.
• Diet should contain as much as of fresh fruits,vegetables which provide nutrients.
• Fiber is an important part of the food.
• Milk is an ideal food and contains or proximate the principles of balanced diet.
• A balanced diet not only looks after the well-being of person but may have role to play in prevention of certain diseases.
• So while planning a balanced diet, care should be taken that all essential ingredient in diet are adequately incorporated with fresh fruits, vegetables and fier diet.
• Food should be palatable, properly cooked and well balanced providing a balance between food intake and energy output.

Question16. Write note on pellagra.

Answer. It is the clinical condition produced due to the defiiency of nicotinic acid or niacin.

Etiology

• Inadequate intake or absorption of niacin.
• Restricted or limited diet in which single serial grain, i.e.corn is consumed without consumption of wheat, eggs, beef and another niacin rich food.
  In chronic alcoholism.

Clinical Features

• Pellagra is triad of dermatitis, diarrhea and dementia.
• Dermatitis is bilaterally symmetrical and occur in parts exposed to sunlight. In acute cases skin lesions may produce vesiculation, cracking, exudation, crusting with ulceration and desquamation. In chronic cases, dermatitis occurs.
• Gastrointestinal manifestations: Presence of anorexia,nausea, dysphagia. Glossitis precede the skin lesions.
  Diarrhoea is also present.
• Mental features consists of apathy, insomnia, fatigue followed by encephalopathy characterized by confusion,disorientation, loss of memory and hallucination.
• Other features: Loss of appetite, irritability and burning sensation in diffrent areas of body.

Oral Manifestations

• Oral mucosa is firy red and is painful.
• Glossitis is present. Tongue is red, swollen and beefy. In early stage, only the tip and margins of tongue are swollen and red but in advance cases, tongue looses the papillae and reddening is intense.
• Presence of angular stomatitis
• Superimposed acute necrotizing ulcerative gingivitis is present involving gingiva, tongue and mucosa.

Diagnosis

• NAD and NADP levels are low in RBCs in patients with pellagra.
• Plasma tryptophan is low.

Treatment

• Initially by injection nicotinamide 50–100 mg IM daily for a week. Maintenance dose of 50 mg orally per day.

Question.17. Write in brief clinical features and management of diabetic ketoacidosis.

Answer. Diabetic ketoacidosis or diabetic comma is the exaggeration or deranged energy metabolism due to defiiency of insulin which results in accumulation of acid metabolites and ketone bodies.

Clinical Features

Symptoms

• Polyuria
• Thirst
• Weight loss
• Weakness
• Nausea
• Vomiting
• Leg cramps
• Blurred vision
• Abdominal pain.

signs

• Dehydration
• Hypotension
• Tachycardia
• Confusion
• Drowsiness
• Comma.

Management

Following is the management of diabetic comma

Admission of patient

• Diagnosis is confirmed by examination of blood glucose and ketone measurements.
• Initial assessment of dehydration, hyperosmolality, serum potassium, acidosis and kidney function is done.
• Fluid loss is measured by subtracting admission weight by last known stable weight.
• Patient should be evaluated for sepsis.

Management during hour 1

• If patient is hypovolemic and hypotensive fluid administration is done, i.e. normal saline is administered and if necessary colloids should be given.
  Rate of administration is necessary to restore circulatory function.
  As blood pressure become normal and urine output becomes adequate rate of administration of normal saline is 1000 mL/hour.
• Continuous I.V. infusion of regular insulin 5–10 units/hour is given.
• I.V, infusion of potassium is done at 10–40 mmol/ hour during initiation of insulin therapy.
• Sodium bicarbonate IV is given in cases with acidosis.
  Dose is 50–100 mmol/L sodium bicarbonate in 0.45% saline for 30–60 minutes. Additional potassium should also be given with bicarbonate therapy.

Management during hour 2

• Normal saline should be continued at 500 mL/ hour.
  Plasma osmolality should be greater than 285 mmol/ L during fist 12 hours. If serum sodium is greater than 150 mmol/L switch to 0.45% saline.
• Blood glucose should be checked and insulin is adjusted to 5 mmol/litre/hour. Blood glucose should not fall below 11.1–14.0 mmol/L. Anion gap is decreasing and blood pH is increasing.
• Serum potassium should be maintained at 4–5 mmol/litre by addition of potassium to IV flids.

Management during hours 3 to 4

• Management should be continued as given in second hour.
• Cognitive and neurological symptoms should be observed for 12 hours.

Management during hours 5 to 8

• Normal saline should be continued at 250 mL/ hour.
• As blood glucose reaches 11.1–14 mmol/ L, change IV flid to 500 mL/hour normal saline with 5% glucose.
  Insulin should be continued at maintenance dose until ketoacidosis is cleared.
• Potassium should be continued at 10–40 mmol/ hour,since ketoacidosis is cleared.
• Phosphate replacement is done at 6 hours, if serum phosphate is < 2 mg/dL

Management during hours 8 to 24

• IV repletion is continued with 0.45% saline with or without 2.5% or 5% glucose as needed.
• As diabetic comma is subsided, patient should be switched to subcutaneous insulin and stop IV and IM insulin.

“Can targeted interventions improve outcomes for metabolic defect patients? FAQs provided”

Question.18. Write short note on metabolic syndrome X /dysmetabolic syndrome.

Answer. Metabolic syndrome is a combination of medical disorders that increase one’s risk for cardiovascular disease and diabetes.

It affcts a large number of people in a clustered fashion.

It is known under various other names, such as (metabolic) syndrome X, insulin resistance syndrome,Reaven’s syndrome or CHAOS.

Clinical Features

Symptoms

• Fasting hyperglycemia
• High blood pressure
• Central obesity (also known as visceral, male pattrn or apple­shaped adiposity), overweight with fat deposits mainly around the waist.
• Weakness, fatigue and restlessness.

Signs

• Fatt liver (especially in concurrent obesity),
• Non-alcoholic fatt liver disease
• Polycystic ovarian syndrome
• Hemochromatosis (iron overload);
• Acanthosis nigricans (a skin condition featuring dark patches).

Treatment

The main treatment is lifestyle, i.e. caloric restriction and physical activity.

However, drug treatment may occasionally be necessary.

Generally, the individual diseases that comprise the metabolic syndrome are treated separately, e.g. diuretics and ACE inhibitors for hypertension.

Cholesterol drugs may be used to lower LDL cholesterol and triglyceride levels, if they are elevated.

Question.19. Write short note on diabetic ketoacidosis.

Answer. Diabetic ketoacidosis a state of acidemia induced by excess production of ketoacids.

Dehydration and hyperglycemia are the rule and lactic acidosis may also be present.

Pathophysiology

Diabetic ketoacidosis is caused by severe insulin defiiency and is accentuated by excessive glucagon secretion.

This leads to major clinical and laboratory abnormalities seen in diabetic ketoacidosis, which includes excess mobilization of free acids from adipose tissue, increased glucose production from the liver, impaired glucose uptake and utilization by muscle.

The two major effcts of uncontrolled diabetes are:

• Increased glucose production which causes hyperglycemia,osmotic diuresis, electrolyte depletion and dehydration
• Increased ketogenesis, resulting in metabolic acidosis

Precipitating causes

• Acute infection viral or bacterial single most common cause.
• Omission of insulin or inadequate dosage.
• Vomiting.
• Diarrhea.
• Prolonged neglect of diabetes.
• Indiscretions in diet.
• Surgical operations.
• Trauma.
• Myocardial infarction.
• Pregnancy.
• Thyrotoxicosis.
• Resistance to insulin.
• Unnoticed interruption of insulin delivery in diabetics treated with continuous subcutaneous insulin infusion.

Clinical Features

Symptoms

• Polyuria
• Thirst
• Weight loss
• Weakness
• Nausea
• Vomiting
• Leg cramps
• Blurred vision
• Abdominal pain.

signs

• Dehydration
• Hypotension
• Tachycardia
• Confusion
• Drowsiness
• Comma.

Diagnosis

The cardinal features are:

• Acidosis, i.e. arterial pH ≤ 7.3
• Plasma anion gap ≥ 16 mmol/L
• Serum ketone is positive
• Serum bicarbonate ≥ 15 mmol/L
• Hyperglycemia, i.e. Plasma glucose ≥ 11.1 mmol/L

Management

Following is the management of diabetic ketoacidosis

1. Admission of patient

• Diagnosis is confimed by examination of blood glucose and ketone measurements.
• Initial assessment of dehydration, hyperosmolality, serum potassium, acidosis and kidney function is done.
• Fluid loss is measured by subtracting admission weight by last known stable weight.
• Patient should be evaluated for sepsis.

2. Management during hour 1

• If patient is hypovolemic and hypotensive flid administration is done, i.e. normal saline is administered and if necessary colloids should be given.
  Rate of administration is necessary to restore circulatory function.
  As blood pressure become normal and urine output becomes
  adequate rate of administration of normal saline is 1000 mL/hour.
• Continuous IV infusion of regular insulin 5–10 units/hour is given.
• IV infusion of potassium is done at 10–40 mmol/hour during initiation of insulin therapy.
• Sodium bicarbonate IV is given in cases with acidosis. Dose is 50–100 mmol/L sodium bicarbonate in 0.45% saline for 30–60 minutes.
  Additional potassium should also be given with bicarbonate therapy.

3. Management during hour 2

• Normal saline should be continued at 500 mL/hour.
  Plasma osmolality should be greater than 285 mosmol / L during fist 12 hours.
  If serum sodium is greater than 150 mmol/L switch to 0.45% saline.
• Blood glucose should be checked and insulin is adjusted to 5 mmol/L/hour.
  Blood glucose should not fall below 11.1–14.0 mmol/L. Anion
  gap is decreasing and blood pH is increasing.
• Serum potassium should be maintained at 4–5 mmol/L by addition of potassium to IV flids.

4. Management during hours 3 to 4

• Management should be continued as given in second hour.
• Cognitive and neurological symptoms should be observed for 12 hours.

5. Management during hours 5 to 8

• Normal saline should be continued at 250 mL/hour. As blood glucose reaches 11.1–14 mmol/
  lt, change IV flid to 500 mL/hour normal saline with 5% glucose.
• Insulin should be continued at maintenance dose until ketoacidosis is cleared.
• Potassium should be continued at 10–40 mmol/hour since ketoacidosis is cleared.
• Phosphate replacement is done at 6 hours if serum phosphate is < 2 mg/dL

6. Management during hours 8 to 24

• IV repletion is continued with 0.45% saline with or without 2.5% or 5% glucose as needed.
• As ketoacidosis is subsided patient should be switched to sub­cutaneous insulin and stop IV and IM insulin.

“Treatment scope in children vs adults for metabolic defects: FAQs”

Question.20. Write short note on vitamin D.

Answer. Vitamin D are a group of sterol and commonly found in animals mainly there are two types of active form:

D2 – Ergosterol/Ergocalciferol

D3 – 7- dehydrocholesterol.

Source

Fish liver oil, egg yolk, buttr milk, the cheapest source is sun light which forms vitamin D3 from its precursor present in the skin.

Physiological Functions

• Vitamin D increases the absorption of Ca and P.
• It increases the calcifiation of bones in children and adult.
• So, it is essential for the development of bones and normal growth of body.
• It increases the excretion of phosphate by kidney and helps in lowering of serum phosphate concentration.
• It increase the citrate levels of blood, bone, kidney and heart tissues.
• It decreases the pH in the lower intestinal tract which helps in increasing the absorption of calcium and phosphate.

Daily Requirements

• Infants and children:400 IU
• Adult: 200 IU
• Pregnant and lactating women:400 IU

Defiiency of Vitamin D

• Rickets: Due to defect in bone growth and calcifiation of long bones in children.
• Osteomalacia: Due to defective calcifiation of steroid tissue in adult.

Causes of Defiiency of Vitamin D

• Dietary insuffiency or insuffient exposure to sunlight.
• Gastrointestinal disorder.
• Chronic obstructive jaundice.
• Prolonged treatment with anticonvulsant drugs.

Toxicity or excess of vitamin D

There is presence of anorexia, lassitude, vomiting, diarrhea,profuse sweating, polydipsia, polyuria and headache.

Hypercalcemia causes calcium deposition in tissues and kidneys which leads to renal failure.

Question.21. Write short note on vitamin C.

Answer. Vitamin C was named ascorbic acid owing to its antiascorbic properties.

Ascorbic acid is a white crystalline water­soluble substance with sour taste.

It is easily destroyed by cooking.

Absorption And Storage

• Ascorbic acid is easily absorbed from the small intestine,peritoneum and subcutaneous tissues.
• It is not stored in any particular organ and is spread throughout the body.

Sources

Amla, citrus fruits, tomatoes, guava, green peppers.

Physiological Functions

• It is involved in oxidation reaction of cell.
• It is required for the metabolism of amino acid, e.g. tyrosine and tryptophan.
• It is also involved in conversion of folic acid into its active coenzyme.
• It is required for iron absorption and also for the formation of collagen fiers and mucopolysaccharides of connective tissue.

Daily Requirements

• Infants: 35 mg
• Children: 40 mg
• Adults: 45 mg
• Pregnant and lactating women 80 mg.

Defiiency Manifestations

• Severe ascorbic acid defiiency produces—Scurvy.

Deficiency of vitamin C leads to scurvy.

Due to vitamin C defiiency, there is defective collagen formation.

Etiology

• In artifiially fed infants
• It is precipitated by febrile disease, infections and diarrhea

Clinical Features

• Onset of the disease is usually gradual, there is fretfulness and increasing pallor, or tenderness of legs which causes child to cry whenever touched, anorexia and loss of weight. First symptom is inability of the child to use his legs.
• Symptoms due to hemorrhages:
• Under periosteum of long bones: “Pithed frog posture”with thighs flxed and abducted and knees flxed,sometimes diffse swelling above or below the knee;in severe cases, infitration of muscles with blood causing edematous limbs, i.e woody leg; hemorrhage between diaphysis and epiphysis causes separation of epiphysis from shaft.
• Perifollicular hemorrhage.
• In orbit, there is proptosis with swelling of eyelids
• Hematuria: May be an early symptom and is only microscopic.
• Scorbutic beading of the ribs
• Presence of anemia
• Keratosis of hair follicles with ‘corkscrew’ hair
• Failure of wound healing

Oral Manifestations

• It chiefl affcts the gingival and periodontal region.
• The interdental and marginal gingiva becomes bright red,swollen, smooth, shiny producing appearance known as scurvy bud. In fully developed scurvy, gingiva becomes boggy, ulcerated and bleeds easily
• There is a typical fetid breath of a patient with fusospirochetal stomatitis.
• Color of the gingiva changes to violaceous red.
• In severe cases, hemorrhage and swelling of periodontal
  ligament membrane occur followed by loss of bone and loosening of teeth which are exfoliated.

Diagnosis

• Low ascorbic acid level in platelets and plasma
• Anemia is mild­to­moderate but may be severe.
• X­ray shows characteristic features such as

• Pencilled cortex
• White lines of Frankel
• Zone of Trummerfeld
• Halo sign of Wimberger
• Subperiosteal hematoma
• Joint effsion
• Scorbutic rosary

Management

• About 3 to 4 ounces of fresh orange juice or tomato juice daily.
• Ascorbic acid 100 mg or more orally or parenterally twice or thrice daily for 10 to 15 days.

“Differential applications of inherited vs acquired metabolic defects: Questions answered”

Question.22. Write short note on Thiamin (Vitamin B1).

Answer.

Thiamine (vitamin B1)

Synonyms: Anti­beriberi factor, anti­neuritic vitamin, aneurin.

Properties

• Thiamine is readily soluble in water
• It is stable in acid medium.
• It is destroyed when autoclave at 120°C for 30 minutes.

Source

• Rich sources: Polishing rice, wheat jaw and yeast
• Good source: Cereals, pulses, nuts, oil seeds
• Fair sources: Meat, fih, egg, milk, vegetable and fruit.

Daily requirement

• Infants: 0.3 to 0.5 mg
• Children: 0.7 to 1.2 mg
• Adults: 1 to 1.5 mg
• Pregnant woman: 1.3 to 1.5 mg.

Physiological role

• Thiamine is essential for growth.
• It is essential for maintaining the nerves in normal condition.

Defiiency Manifestations

• Beri-beri: It is a nutritional disorder.
• Wet-beriberi
• Edema is the most prominent feature
  Anorexia and dyspepsia are present.
• Dry beriberi
• Essential feature is polyneuropathy
• Muscles become wasted and weak and diffilty in walking.
• Infantile Beriberi.
• Wernick’s encephalopathy: There is involvement of brain which is characterized by ataxia, ophthalmoplegia,confusion and disorientation.
• Korsakoff psychosis: It occurs due to involvement of mammilary bodies and confabulates with amnesia.

Presence of angular stomatitis.

Question.23. Write short note on diabetic diet.

Answer. The golden rule for a diabetic on diet therapy should be to eat litte and more often.

• A heavy meal is not desirable since it gives rise to rise in blood lipids.
• One must time the meals, food must have variety and monotony in diet be avoided.
• Foods should be adjusted in such a way that they form part of the family ratios.

Requirements are determined by the patient’s activity

• Overweight NIDDM should be encouraged to establish their weight within a desirable range.
  A reduction of approximately 500 kcal/ day can result in loss of 1–2 kg/month.
• Carbohydrates: Carbohydrates should be taken in form of starch and complex sugars.
  100–300 gm of carbohydrates should be spreaded over 3 meals, i.e. 60 gm each and 3 snacks, i.e. 30 gm each with half liter of milk.
  Unrefied carbohydrates should be substituted by refied carbohydrates to the extent possible.
• Proteins: Recommended dietary allowance of 0.85 g/kg body weight for adult is an appropriate guide.
• Fat: Fat intake should be 50 to 150 gm daily divided between the meals.
  Replacement of saturated with polyunsaturated fat is desirable to reduce cardiovascular risk.
  Cholesterol intake should be < 300 mg/day.
• Fiber: Increased consumption of dietary fier especially soluble fier are associated with lower levels of blood glucose and serum lipids.
  The water insoluble fiers such as cellulose, lignin and most hemicelluloses found in whole grain breads, cereals and wheat bran affct gastrointestinal transit time and faecal bulk with litte impact on plasma glucose.
  However, highly viscous water soluble fiers such as pectins, gums and storage polysaccharide found in fruits, legumes, lentils roots, tubers, oat and oat bran, when eaten in purifid form, reduce serum levels of glucose and insulin.
  Ideal recommended amount of fier in patient’s diet is 35–40 g/day.
• Alternative sweeteners: Both nutritive and non­nutritive sweeteners are acceptable in diabetes management.
• Sodium: It should be restricted to 1000 mg/1000 kcal, not to exceed 3000 mg/day to minimize symptoms of hypertension.
• Alcohol: It should be taken in moderation and may need to be restricted entirely by person with diabetes and insulin—induced hypoglycemia, neuropathy, poor control of glucose and lipids, or obesity.
• Vitamins, minerals and antioxidants — intake should be encouraged.

Forbidden foods: Sugar, jam, jellies, honey, jaggery, tinned fruits and juices, sweets, chocolate, ice creams, pastries, glucose drinks, foods made with sugar, pudding, sauces.

Foods allowed in moderation: Bread of all kinds and chapatts made from wheat or millets, plain biscuits, all fresh fruits, baked beans, breakfast cereals.

Free foods: All meat, fih, eggs (not fried), clear soup or meat extracts; tea or coffe; vegetables such as cabbage, cauliflwer, spinach, pumpkin, brinjal, lady’s figer, turnip, French beans, cucumber, lettce, tomato, spring onions, radish, asparagus.
Spices, salt, pepper and mustard; buttr and margarine. Sugar substitutes for sweetening.

Question.24. G ive defiition, etiology, sign, symptoms, complication and management of diabetes mellitus.

Answer. Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both.

Etiology

• Heredity: It is inherited as mendelian type of recessive trait and is predominant in children born to parents who are diabetic.
  Every person who has a history of diabetes in his or her family is a carrier of disease.
  The risk percentage in fist degree relatives is generally up to 20% while in second degree relatives it is about 5 % and the overall percentage of diabetes among the children of diabetics goes up to 10 %. Identical twins of a diabetic have almost 40 % chances of developing the disease.
• Obesity: Obese people are more prone to suffer from diabetes probably because obesity imposes strain on the islets of Langerhans and there is a relative defiiency of insulin.
  Obese also show a relative resistance to insulin due to reduction in the number of insulin receptors on target cells. Obesity results due to uninhibited indulgence in food and lack of physical activity and imposes a constant stress on the pancreas.
  Thus these people are more prone to get diabetes.
• Race: All races are involved and suffer from diabetes though a number of factors operate in one ethnic group or the other. Jewish race has been known to be more commonly affcted than others.
  Some communities are known to have less incidence of diabetes as compared to others, but here the role of diet, physical exercise and environmental factors come into play.
  A certain community in Japan (Ainus) was known to have practically no or litte diabetes probably due to undernourishment and poverty, but with the rapid industrialization and boom in the economy of the community, the incidence of diabetes among them has gone up.
• Social and environmental factors: Diabetes has been considered a disease of civilization and its prevalence is closely related to the economic afflnce.
  Diabetes occurs more in richer and afflnt classes of society though the poorer class of people are equally liable to suffr from early onset diabetes.
  Diabetes in richer class of people is closely related to their eating habits, lack of physical effrt and obesity.
• Exercise: Lack of physical effrt and exercise promotes obesity and indirectly predisposes to diabetes.
  Physical effrt and leading an active life goes a long way in keeping one self trim and helps in the proper utilization of body glucose and maintains a homeostatic balance.
• Diet: Excessive intake of carbohydrates and refied sugars produces strain on the pancreas and this combined with sedentary occupation goes a long way in predisposing to diabetes.
• Parity: Women with repeated pregnancies are more liable to develop diabetes since too many pregnancies are a strain on the carbohydrate metabolism and often there is hormonal imbalance.

Sign and symptoms/ clinical Features

In type I diabetes Mellitus

Symptoms

• Polydypsia, polyuria and polyphagia
• Weight loss
• Weakness and lassitude.

Sign

• Severe emaciation with wastening of muscles
• Ribs are prominent.
• In such patients if diabetic ketoacidosis is severe patient develop mental apathy, confusion and undergo coma.

In type II diabetes Mellitus

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess.
• Nervous system: Autonomic neuropathy and peripheral neuritis.
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritis vulvae, menstrual irregularity and infertility.

Complications

Acute Or Immediate Complications

• Diabetic ketoacidosis or coma
• Hypoglycemia or hypoglycemic coma
• Non­ketotic hyperosmolar diabetic coma
• Lactic acidosis

First two complications occur in Type I diabetes mellitus and other two occur in Type II diabetes mellitus.

Diabetic Ketoacidosis

• It is an exclusive complication of type I diabetes. It can develop in patients with severe insulin defiiency combined with glucagon excess.
  Failure to take insulin and exposure to stress are precipitating causes.
• As the ketogenesis continues the excess ketone bodies produced cannot be degraded by the muscles and other tissues resulting in ketosis, which manifests as anorexia, nausea, vomiting, deep and fast breathing, mental confusion and coma. However, most of the patients recover.

Hypoglycemia

• It is defied as fall in blood glucose concentration below 3.1 mmol/L.
• It is seen in type I diabetes patients due to excessive administration of insulin, missing a meal or due to stress.
• As the hypoglycemia continues, it can lead to comma,cardiac arrhythmias and is fatal.
• This can lead to worsening of control of diabetes and rebound hyperglycemia.

Nonketotic Hyperosmolar Diabetic Coma

• It is common in type II diabetes mellitus.
• The clinical hallmark is hyperglycemia, hyperosmolality and dehydration without ketoacidosis.
• Precipitating features are infection, myocardial infarction,drugs such as thiazides, steroids, diphenylhydantoin.
• Loss of glucose in urine is so intense that the patient is unable to drink suffient water to maintain urinary flid loss.
• Because of high viscosity of blood, thrombotic and bleeding complications are frequent. Mortality rate is high in this complication.

Lactic Acidosis

• It is seen in type II diabetes mellitus.
• It is caused due to excess lactate production and/or inadequate utilization.
• This can be precipitated by metformin or other systemic disorders such as liver or renal failure, pancreatitis or leukemia.
• Cardiovascular collapse leads to mortality.

Chronic or late-onset complications

These complications are due to changes in small blood vessels i.e.microangiopathy or in large blood vessels, i.e. macroangiopathy.

Microvascular are retinopathy, neuropathy, nephropathy and miscellaneous

Macrovascular are atherosclerosis, hypertension, peripheral vascular disease and diabetic foot ulcer

The chronic complications occur more frequently in Type II diabetes mellitus rather than Type I diabetes mellitus.

Diabetic Retinopathy

• This is the very important cause of blindness in diabetic patients.
• Dilatation of retinal capillaries is earliest sign. Besides these there is also presence of microaneurysms, retinal hemorrhage, neovascularization, hard and soft exudates,vitreous hemorrhage and firosis.
• Frequency, onset and severity of retinopathy vary in diabetic patients.
• Background retinopathy is most common and proliferative retinopathy is less common.

Diabetic Neuropathy

• It can involve any part of nervous system except the brain.
• Neuropathy is an early and common complication which leads to morbidity and disability.
• Poor glycemic control and long duration of diabetes is associated with high incidence of neuropathy.
• Sign and symptoms are of peripheral nervous system.
• Main pathological changes in peripheral nerves are axonal degeneration of myelinated and non-myelinated fiers,
  Segmental demyelination, Schwann cell injury.

Diabetic Nephropathy

• This is the most common cause of mortality and morbidity in diabetic patients.
• 40 to 50% of type II diabetes patient develop it and 25% patients with type I diabetes develop end stage renal disease and die of it.
• It is divided into three stages, in fist stage patient is asymptomatic but has high GFR, in next stage there is renal hypertrophy which leads to microalbuminuria.
• In advance stage, patient develop macroproteinuria and passes onto nephrotic syndrome.
• 25% of patients with diabetic nephropathy can go directly at end stage renal disease with hypertension and undergo chronic renal failure.

Miscellaneous

It consists of various infections, gastroparesis, arthropathy.

Atherosclerosis

• In diabetic patient development of athroma is faster as compared to normal individual.
• Hyperlipidemia, decreased HDL levels, increased platelet adhesiveness, obesity and associated hypertension are contributory factors for athrosclerosis.
• Atherosclerosis leads to coronary artery disease, silent myocardial infarction, cerebral stroke and gangrene of toes and feet.

Diabetic Foot Ulcer

• This is the frequent site of complication in diabetes.
• Pathogenic components of diabetic foot are neuropathy,peripheral vascular disease causing ischemia and secondary infection causing ulceration.

“Steps to apply nutrition and metabolic defect knowledge in clinical practice: Diagnosis vs treatment: Q&A guide”

Management

Diet Management

• Restoration of normal blood glucose and optimum levels.
• Maintenance of blood glucose levels as near to physiologic levels to prevent onset or progression of complications.
• Maintenance of normal growth rate in children and adolescents as well as attinment and maintenance of reasonable body weight in adolescents and children.
• Provision of adequate nutrition for pregnant women and fetus during lactation.
• Consistency in timing of meals and snacks to prevent inordinate swings in blood glucose level.
• Motivation to have small frequent meals.
• Determination of meal plan appropriate for individual and based on dietary history to have good compliance.
• Management of weight reduction for obese individuals with NIDDM.
• Improvement in the overall health of patients with diabetes through optimal nutrition.

Total Calories

Requirements are determined by the patients activity:

• Overweight NIDDM should be encouraged to establish their weight within a desirable range. A reduction of approximately 500 kcal/ day can result in loss of 1–2 kg/month.
• Carbohydrates: Carbohydrates should be taken in form of starch and complex sugars. 100–300 g of carbohydrates should be spreaded over 3 meals, i.e. 60g each and 3 snacks,i.e. 30 geachwithhalflitre ofmilk. Unrefied carbohydrates should be substituted by refied carbohydrates to the extent possible.
• Proteins: Recommended dietary allowance of 0.85 g/kg body weight for adult is an appropriate guide.
• Fat: Fat intake should be 50–150 g daily divided between the meals. Replacement of saturated with polyunsaturated fat is desirable to reduce cardiovascular risk. Cholesterol intake should be < 300 mg/day.
• Fiber: Increased consumption of dietary fier especially soluble fier are associated with lower levels of blood glucose and serum lipids. The water insoluble fiers such as cellulose, lignin and most hemicelluloses found in whole grain breads, cereals and wheat bran affct gastrointestinal transit time and fecal bulk with litte impact on plasma glucose. However highly viscous water soluble fiers such
  as pectins, gums and storage polysaccharide found in fruits, legumes, lentils roots, tubers, oat and oat bran, when eaten in purifid form, reduce serum levels of glucose and insulin. Ideal recommended amount of fier in patient’s diet is 35–40 g/day.
• Alternative sweeteners: Both nutritive and non­nutritive sweeteners are acceptable in diabetes management.
• Sodium: It should be restricted to 1000 mg/1000 kcal, not to exceed 3000 mg/day to minimize symptoms of hypertension.
• Alcohol: It should be taken in moderation and may need to be restricted entirely by person with diabetes and insulin—induced hypoglycemia, neuropathy, poor control of glucose and lipids, or obesity.
• Vitamins, minerals and antioxidants: intake should be encouraged.

Forbidden foods: Sugar, jam, jellies, honey, jaggery, tinned fruits and juices, sweets, chocolate, ice creams, pastries, glucose drinks, foods made with sugar, pudding, sauces.

Foods allowed in moderation: Bread of all kinds and chapatts made from wheat or millets, plain biscuits, all fresh fruits, baked beans, breakfast cereals.

Free foods: All meat, fih, eggs (not fried), clear soup or meat extracts; tea or coffe; vegetables such as cabbage, cauliflwer, spinach, pumpkin, brinjal, lady’s figer, turnip, French beans,cucumber, lettce, tomato, spring onions, radish, asparagus.
Spices, salt, pepper and mustard; buttr and margarine. Sugar substitutes for sweetening.

Oral Hypoglycemics

These drugs are used in patients of Type II diabetes mellitus(NIDDM) who do not respond to dietary management and who would otherwise require treatment with insulin in later situation, so they are also used as adjuvant drugs to insulin in overweight diabetes patients.

Insulin secretagogues i.e. drugs increasing secretion of insulin Sulfonyl ureas

Meglitinides:

• Repaglinide, i.e. 0.5–4 mg three times a day
• Netaglinide, i.e. 60–120 mg three times a day 15 to 30 min before each meal
• Voglibose, i.e. 0.2–0.3 mg, 15–30 min before each meal.

Insulin sensitizers, i.e.drugs sensitizing action of insulin and overcome insulin resistance

• Biguanides, i.e. metformin should be given 1.5–2.5 g/day in three divided doses after meals.
• Thiozolidinediones, i.e.rosiglitazone should be given 2–8 mg or pioglitazone 15–45 mg in a single or two divided doses.
  They can be combined with sulfonyl ureas or metformin

• Alpha glucosidase inhibitors, i.e. Acarbose 25 to 100 mg TDS or Voglibose 0.2–5 mg TDS taken orally in three main meals.
• It can be given in combination with metformin 500 mg for increased effiency.
• DPP-4 inhibitor: Vildagliptin 50–100 mg daily in two dived doses with meals ot saxagliptin 2.5 to 5mg OD.
• Pramlinide: Initial dose is 15 μg before each meals in Type I diabetes mellitus and 60 μg in Type II diabetes mellitus.

Question.25.Write briefl on sign, symptoms and treatment of protein malnutrition.

Answer. Protein malnutrition is caused due to deficiency of proteins in body.

Symptoms

• Patient has high urge for food and water.
• Patient becomes weak, exhausted and fatigued.
• Presence of loss of libido
• Patient feels cold
• Amenorrhea is present.
• Patient looks old and mature and face is expressionless.
• Diarrhea may occur.
• Patient in inactive and is depressed.
• There is loss of libido

Signs

• Muscle wastening is present.
• Extremities of patient are cold.
• Skin is dry, lustureless and become fisured.
• Subcutaneous fat is absent and bony prominences are prominent.
• Circumference of arm is subnormal.
• In females edema is present which is not due to hypoalbuminemia.
• Body temperature is subnormal
• Tendon jerks become diminished.
• Pulse of patient is slow and blood pressure becomes low.
• Abdominal distention is commonly present.

Treatment

In adults

• For mild starvation adequate supplementation of nutrients is necessary
• In moderately starved people extra­feeding is needed
• In severely starved persons food is given in small amount at frequent intervals.
  Food should be staple meal, i.e. cereal with some sugar, milk and oils, salt is restricted.
  Potassium,magnesium and vitamins are adequately given. This is continued till patient feel active.

In children

1. Diet

• Diet for mild to moderate cases: Diet should be easily digestable. It should be rich in proteins, minerals and vitamins with extra calories. Milk should be given.
  Egg is a good flp with milk and water as a source of fist class protein.
  Plant protein mixtures such as corn,soya, diet milk can be given. Additional fats should be included.
  If there is lactose intolerance dal, rice and buttr can be given.
• Diet for acute cases: Protein intake should be 3 to 4g/kg/day and energy intake of 150kcal/Kg/day.
  If child is unable to take diet from mouth go for nasogastric intubation.
  Care must be taken to take sufficient amount of plant, animal proteins and fats to maintain the weight.

2. Vitamins and mineral supplementations:

• Vitamin A, D, B complex and C are given at therapeutic dosages.
• In vitamin A defiiency 30 mg of vitamin A should be given for 3 days.
• 0.5 to 1gm of potassium chloride dissolve in feeds or water should be given daily in divided dosages.

“Role of blood tests in diagnosing metabolic defect severity: Questions answered”

3. Maintainence of body temperature

For maintainence of body temperature at night blankets or room heaters are useful.

4. Skincare

In cases of dermatoses skin should be kept clean and protected.

In-hospital treatment:

• Correction of dehydration, electrolyte disturbances, hypoglycemia, acidosis and hypothermia.
• Parenteral therapy with half of saline and 2.5% glucose before diet therapy.
• In anemia packed erythrocyte infusion is given.

Question.26. Discuss the clinical features, diagnosis diabetes mellitus.

Answer.

Sign and symptoms/ clinical Features

In type I diabetes Mellitus

Symptoms

• Polydypsia, polyuria and polyphagia
• Weight loss
• Weakness and lassitude.

Sign

• Severe emaciation with wastening of muscles
• Ribs are prominent.
• In such patients if diabetic ketoacidosis is severe patient develop mental apathy, confusion and undergo coma.

In type II diabetes Mellitus

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess.
• Nervous system: Autonomic neuropathy and peripheral neuritis.
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritis vulvae, menstrual irregularity and infertility.

Diagnosis

Diagnosis is based on symptoms, signs and laboratory tests.
In presence ofsigns and symptoms confimation is done by fiding random blood glucose higher than 200 mg/dL.

Investigations

• Blood sugar estimation: Both fasting and post­prandial (2 hours after a meal) levels of blood sugar be estimated.
  Mean value of blood sugar in healthy adults is 70 to 80 mg%. When fasting blood sugar level exceeds 110 mg% diagnosis is clear.
  Post­prandial blood sugar level is further screening test, if value exceeds 120 mg% it is strongly suggestive of diabetes mellitus.
  Random blood sugar estimation is not of much help as screening test.
  Value exceeding 160 mg% in presence of glycosuria is suggestive but values about 200 mg% is diagnostic.
• Oral glucose tolerance test: In this fist sample is taken after an overnight fast of 8 hours following which patient is given glucose 1g/kg body weight.
  Blood is then collected at 30, 60, 120 and 180 minutes.
  In diminished glucose tolerance, level of blood glucose is raised at 180 minutes.
• Glycosylated hemoglobin: It measures the long­term glycemic control.
  Slow non­enzymatic attachment of glucose to hemoglobin result in formation of glycosylated hemoglobin.
• Microalbumin: Patients with microalbumineria are on greater risk in developing kidney failure as well as cardiovascular damage.
• Urine protein/creatinine ratio: It provides information of proteinuria in patients with diabetic nephropathy.
  More is the ratio greater is the damage.
• Insulin levels: Elevated blood glucose levels with low insulin levels indicate insufficient insulin levels for adequate control of blood glucose.
  High insulin levels with low blood glucose indicate change in dosage of drug.
• Insulin antibody test: In this there is quantitative determination of antibodies against insulin in serum.
• GAD 65 antibody: These antibodies are common in newly diagnosed diabetic patient and often appear years before clinical onset in the disease. Presence of this antibody is the strong predictive marker for onset of type I diabetes mellitus.

Criterias Given By WHo In 1999

• Presence of classic symptoms of diabetes and causal plasma glucose greater than or equal to 200 mg/dL.
  Causal is any time of day without regard to time since last meal.
  Classic symptoms of diabetes include polyuria, polydypsia and unexplained weight loss.
  Or
• Fasting plasma glucose greater than or equal to 126 mg/dL.
  Fasting is defied as no caloric intake for 8 hours.
  Or
• Twohoursplasmaglucosegreaterthanorequalto200 mg/dL during an oral glucose tolerance test.
  Test is performed as described by World Health Organization by using glucose load containing equivalent of 75 gm anhydrous glucose dissolved in water.

In absence of unequivocal hyperglycemia with acute metabolic decompensation above criterias are confimed by repeated testing on other days.

Question.27. Write sign and symptoms of diabetes mellitus.
Or
Describle clinical features of diabetes mellitus.

Answer.

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both.

Etiology

• Heredity: It is inherited as mendelian type of recessive trait and is predominant in children born to parents who are diabetic.
  Every person who has a history of diabetes in his or her family is a carrier of disease.
  The risk percentage in fist degree relatives is generally up to 20% while in second degree relatives it is about 5 % and the overall percentage of diabetes among the children of diabetics goes up to 10 %. Identical twins of a diabetic have almost 40 % chances of developing the disease.
• Obesity: Obese people are more prone to suffer from diabetes probably because obesity imposes strain on the islets of Langerhans and there is a relative defiiency of insulin.
  Obese also show a relative resistance to insulin due to reduction in the number of insulin receptors on target cells. Obesity results due to uninhibited indulgence in food and lack of physical activity and imposes a constant stress on the pancreas.
  Thus these people are more prone to get diabetes.
• Race: All races are involved and suffer from diabetes though a number of factors operate in one ethnic group or the other. Jewish race has been known to be more commonly affcted than others.
  Some communities are known to have less incidence of diabetes as compared to others, but here the role of diet, physical exercise and environmental factors come into play.
  A certain community in Japan (Ainus) was known to have practically no or litte diabetes probably due to undernourishment and poverty, but with the rapid industrialization and boom in the economy of the community, the incidence of diabetes among them has gone up.
• Social and environmental factors: Diabetes has been considered a disease of civilization and its prevalence is closely related to the economic afflnce.
  Diabetes occurs more in richer and afflnt classes of society though the poorer class of people are equally liable to suffr from early onset diabetes.
  Diabetes in richer class of people is closely related to their eating habits, lack of physical effrt and obesity.
• Exercise: Lack of physical effrt and exercise promotes obesity and indirectly predisposes to diabetes.
  Physical effrt and leading an active life goes a long way in keeping one self trim and helps in the proper utilization of body glucose and maintains a homeostatic balance.
• Diet: Excessive intake of carbohydrates and refied sugars produces strain on the pancreas and this combined with sedentary occupation goes a long way in predisposing to diabetes.
• Parity: Women with repeated pregnancies are more liable to develop diabetes since too many pregnancies are a strain on the carbohydrate metabolism and often there is hormonal imbalance.

Sign and symptoms/ clinical Features

In type I diabetes Mellitus

Symptoms

• Polydypsia, polyuria and polyphagia
• Weight loss
• Weakness and lassitude.

Sign

• Severe emaciation with wastening of muscles
• Ribs are prominent.
• In such patients if diabetic ketoacidosis is severe patient develop mental apathy, confusion and undergo coma.

In type II diabetes Mellitus

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess.
• Nervous system: Autonomic neuropathy and peripheral neuritis.
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritis vulvae, menstrual irregularity and infertility.

Complications

Acute Or Immediate Complications

• Diabetic ketoacidosis or coma
• Hypoglycemia or hypoglycemic coma
• Non­ketotic hyperosmolar diabetic coma
• Lactic acidosis

First two complications occur in Type I diabetes mellitus and other two occur in Type II diabetes mellitus.

Diabetic Ketoacidosis

• It is an exclusive complication of type I diabetes. It can develop in patients with severe insulin defiiency combined with glucagon excess.
  Failure to take insulin and exposure to stress are precipitating causes.
• As the ketogenesis continues the excess ketone bodies produced cannot be degraded by the muscles and other tissues resulting in ketosis, which manifests as anorexia, nausea, vomiting, deep and fast breathing, mental confusion and coma. However, most of the patients recover.

Hypoglycemia

• It is defied as fall in blood glucose concentration below 3.1 mmol/L.
• It is seen in type I diabetes patients due to excessive administration of insulin, missing a meal or due to stress.
• As the hypoglycemia continues, it can lead to comma,cardiac arrhythmias and is fatal.
• This can lead to worsening of control of diabetes and rebound hyperglycemia.

Nonketotic Hyperosmolar Diabetic Coma

• It is common in type II diabetes mellitus.
• The clinical hallmark is hyperglycemia, hyperosmolality and dehydration without ketoacidosis.
• Precipitating features are infection, myocardial infarction,drugs such as thiazides, steroids, diphenylhydantoin.
• Loss of glucose in urine is so intense that the patient is unable to drink suffient water to maintain urinary flid loss.
• Because of high viscosity of blood, thrombotic and bleeding complications are frequent. Mortality rate is high in this complication.

Lactic Acidosis

• It is seen in type II diabetes mellitus.
• It is caused due to excess lactate production and/or inadequate utilization.
• This can be precipitated by metformin or other systemic disorders such as liver or renal failure, pancreatitis or leukemia.
• Cardiovascular collapse leads to mortality.

Chronic or late-onset complications

These complications are due to changes in small blood vessels i.e.microangiopathy or in large blood vessels, i.e. macroangiopathy.

Microvascular are retinopathy, neuropathy, nephropathy and miscellaneous

Macrovascular are atherosclerosis, hypertension, peripheral vascular disease and diabetic foot ulcer

The chronic complications occur more frequently in Type II diabetes mellitus rather than Type I diabetes mellitus.

Diabetic Retinopathy

• This is the very important cause of blindness in diabetic patients.
• Dilatation of retinal capillaries is earliest sign. Besides these there is also presence of microaneurysms, retinal hemorrhage, neovascularization, hard and soft exudates,vitreous hemorrhage and firosis.
• Frequency, onset and severity of retinopathy vary in diabetic patients.
• Background retinopathy is most common and proliferative retinopathy is less common.

“How does untreated malnutrition lead to severe complications like growth retardation? FAQ explained”

Diabetic Neuropathy

• It can involve any part of nervous system except the brain.
• Neuropathy is an early and common complication which leads to morbidity and disability.
• Poor glycemic control and long duration of diabetes is associated with high incidence of neuropathy.
• Sign and symptoms are of peripheral nervous system.
• Main pathological changes in peripheral nerves are axonal degeneration of myelinated and non-myelinated fiers,
  Segmental demyelination, Schwann cell injury.

Diabetic Nephropathy

• This is the most common cause of mortality and morbidity in diabetic patients.
• 40 to 50% of type II diabetes patient develop it and 25% patients with type I diabetes develop end stage renal disease and die of it.
• It is divided into three stages, in fist stage patient is asymptomatic but has high GFR, in next stage there is renal hypertrophy which leads to microalbuminuria.
• In advance stage, patient develop macroproteinuria and passes onto nephrotic syndrome.
• 25% of patients with diabetic nephropathy can go directly at end stage renal disease with hypertension and undergo chronic renal failure.

Miscellaneous

It consists of various infections, gastroparesis, arthropathy.

Atherosclerosis

• In diabetic patient development of athroma is faster as compared to normal individual.
• Hyperlipidemia, decreased HDL levels, increased platelet adhesiveness, obesity and associated hypertension are contributory factors for athrosclerosis.
• Atherosclerosis leads to coronary artery disease, silent myocardial infarction, cerebral stroke and gangrene of toes and feet.

Diabetic Foot Ulcer

• This is the frequent site of complication in diabetes.
• Pathogenic components of diabetic foot are neuropathy,peripheral vascular disease causing ischemia and secondary infection causing ulceration.

Question.28. Write management of diabetic ketoacidosis.

Answer. Following is the management of diabetic ketoacidosis

1. Admission of patient

• Diagnosis is confimed by examination of blood glucose and ketone measurements.
• Initial assessment of dehydration, hyperosmolality, serum potassium, acidosis and kidney function is done.
• Fluid loss is measured by subtracting admission weight by last known stable weight.
• Patient should be evaluated for sepsis.

2. Management during hour 1

• If patient is hypovolemic and hypotensive flid administration is done, i.e. normal saline is administered and if necessary colloids should be given.
  Rate of administration is necessary to restore circulatory function.
  As blood pressure become normal and urine output becomes
  adequate rate of administration of normal saline is 1000 mL/hour.
• Continuous IV infusion of regular insulin 5–10 units/hour is given.
• IV infusion of potassium is done at 10–40 mmol/hour during initiation of insulin therapy.
• Sodium bicarbonate IV is given in cases with acidosis. Dose is 50–100 mmol/L sodium bicarbonate in 0.45% saline for 30–60 minutes.
  Additional potassium should also be given with bicarbonate therapy.

3. Management during hour 2

• Normal saline should be continued at 500 mL/hour.
  Plasma osmolality should be greater than 285 mosmol / L during fist 12 hours.
  If serum sodium is greater than 150 mmol/L switch to 0.45% saline.
• Blood glucose should be checked and insulin is adjusted to 5 mmol/L/hour.
  Blood glucose should not fall below 11.1–14.0 mmol/L. Anion
  gap is decreasing and blood pH is increasing.
• Serum potassium should be maintained at 4–5 mmol/L by addition of potassium to IV flids.

4. Management during hours 3 to 4

• Management should be continued as given in second hour.
• Cognitive and neurological symptoms should be observed for 12 hours.

5. Management during hours 5 to 8

• Normal saline should be continued at 250 mL/hour. As blood glucose reaches 11.1–14 mmol/
  lt, change IV flid to 500 mL/hour normal saline with 5% glucose.
• Insulin should be continued at maintenance dose until ketoacidosis is cleared.
• Potassium should be continued at 10–40 mmol/hour since ketoacidosis is cleared.
• Phosphate replacement is done at 6 hours if serum phosphate is < 2 mg/dL

6. Management during hours 8 to 24

• IV repletion is continued with 0.45% saline with or without 2.5% or 5% glucose as needed.
• As ketoacidosis is subsided patient should be switched to sub­cutaneous insulin and stop IV and IM insulin.

Question.29.Write classifiation, clinical features, investigations and treatment of diabetes mellitus.

Answer. Diabetes mellitus is a clinical syndrome of hyperglycemia with glycosuria due to lack of insulin or insulin resistance is termed as diabetes mellitus.

Classification

Primary diabetes

1. Type I insulin dependent diabetes mellitus (IDDM). It is sub­divided:

• Immuned mediated (islet cell antibodies).
• Non­immune (no antibody).

2. Type II non­insulin dependent diabetes mellitus (NIDDM)
It is sub­divided:

• Obese (insulin resistance with relative insulin defiiency).
• Non­obese (insulin secretory detect with insulin resistance).

Secondary Diabetes

• Pancreatic diabetes due to pancreatitis.
• Hormonal or endocrinal abnormalities, i.e., acromegaly,shing’s syndrome, pheochromocytoma, etc.
• Drugs induced (Iatrogenic) due to steroids and thiazides.
• Insulin receptors antibodies.
• Genetic syndromes, i.e., Lipodystrophies, muscular dystrophies, Klinefelter’s syndrome, Turner’s syndrome,
• Down’s syndrome, DIDMOAD (Diabetes insipidus,diabetes mellitus, optic atrophy and deafness) syndrome.

Clinical Features

In type I diabetes Mellitus

Symptoms

• Polydypsia, polyuria and polyphagia
• Weight loss
• Weakness and lassitude.

Sign

• Severe emaciation with wastening of muscles
• Ribs are prominent.
• In such patients if diabetic ketoacidosis is severe patient develop mental apathy, confusion and undergo coma.

In type II diabetes Mellitus

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess.
• Nervous system: Autonomic neuropathy and peripheral neuritis.
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritis vulvae, menstrual irregularity and infertility.

Investigations

• Blood sugar estimation: Both fasting and post­prandial (2 hours after a meal) levels of blood sugar be estimated.
  Mean value of blood sugar in healthy adults is 70 to 80 mg%. When fasting blood sugar level exceeds 110 mg% diagnosis is clear.
  Post­prandial blood sugar level is further screening test, if value exceeds 120 mg% it is strongly suggestive of diabetes mellitus.
  Random blood sugar estimation is not of much help as screening test.
  Value exceeding 160 mg% in presence of glycosuria is suggestive but values about 200 mg% is diagnostic.
• Oral glucose tolerance test: In this fist sample is taken after an overnight fast of 8 hours following which patient is given glucose 1 g/kg body weight.
  Blood is then collected at 30, 60, 120 and 180 minutes. In diminished glucose tolerance, level of blood glucose is raised at 180 minutes.
• Glycosylated hemoglobin: It measures the long­term glycemic control. Slow non­enzymatic attachment of glucose to hemoglobin result in formation of glycosylated hemoglobin.
• Microalbumin: Patients with microalbuminria are on greater risk in developing kidney failure as well as cardiovascular damage.
• Urine protein/Creatinine ratio: It provides information of proteinuria in patients with diabetic nephropathy. More is the ratio greater is the damage.
• Insulin levels: Elevated blood glucose levels with low insulin levels indicate insufficient insulin levels for adequate control of blood glucose.
  High insulin levels with low blood glucose indicate change in dosage of drug.
• Insulin antibody test: In this there is quantitative determination of antibodies against insulin in serum.
• GAD 65 antibody: These antibodies are common in newly diagnosed diabetic patient and often appear years before clinical onset in the disease. Presence of this antibody is the strong predictive marker for onset of type I diabetes mellitus.

“Early warning signs of complications from ignoring metabolic defect care: Common questions”

Treatment

Treatment Strategies with Insulin

• Single dose regimen: Daily injection of intermediate act ing insulin given before breakfast.
  The starting dose 0.3–0.4 U/Kg/ day; increased gradually to obtain glucose values in acceptable range.
  Regular insulin can be added to decrease the glucose level that follows breakfast.
• Twice daily regimen: Combination of regular and intermediate acting insulin BD, i.e. before breakfast and before dinner (“Split mix” regimen).
• Multiple daily injections: For achievement of more tight control of blood glucose which requires administration of at least 3 injections per day.
  These can be given with use of mixture of intermediate­ and short­acting insulins (pre­mixed insulin) in the morning before breakfast, with regular insulin before supper­ and intermediateacting at bedtime; or again a combination of regular and intermediate­acting before dinner.
  Divide the total daily into 2 equal doses following 1:1 transfer from basal insulin.
  Give half before breakfast and other half before dinner.
  The largest meal will require larger proportion of insulin.
  Reduce total dose by 20%, if patient experiences recurrent hypoglycemia.
• Insulin concentrations: The insulins are available in many concentrations. In India the commonly used is 40 U/mL
• Insulin purity: The impurities which may be contained are proinsulin, insulin intermediates and contaminating proteins from islet tissue or exocrine pancreas such as glucagon, somatostatin and pancreatic polypeptides.
  Standard insulins currently have only 10–20 PPM of proinsulin and purifid monocomponent insulins less than 1 PPM.

Best sites for the insulin injection are subcutaneous fat on abdomen, buttck, anterior thigh and dorsal area of ar

Question.30. Write short note on obesity.

Answer.

Obesity is the condition in which there is excessive accumulation of body fat.

Obesity is the common disorder of the nutrition of afflnt societies.

Etiology

• GeneticandEnvironmentalfactors: Genetic and environmental factors play important role in causing the obesity.
  Familial predisposition is also seen.
  Overeating and other factors also cause obesity.
  If both the parents of a child are overweight then chances of child being obese are 80%.
• Socioeconomic status: Obesity is the disorder of afflnt societies.
  Some occupations also predisposes to obesity, such as cooks.
  In some of the societies obesity is considered as the sign of heritage.
• Energy intake: Minute excess of calories causes accumulation of fat. If there is lag of physical activity, this also causes obesity.
• Drugs: Various drugs such as steroids, oral contraceptives,etc causes increase in apetite, this leads to weight gain.
• Endocrine: During pregnancy there is increase in the body fat which is under hormonal inflence.
  Obesity can also occur in hypothyroidism due to decrease calorie demands.

Clinical Features

• Type II diabetes mellitus, gallbladder stones, gout and various other metabolic disorders are associated with obesity.
• Varicose vein, hernia and osteoarthritis are the mechanical disorders associated with obesity.
• Various respiratory infections are also associated with the obesity along with the sleep disorders.
• Hypertension, atherosclerosis and ischemic heart diseases are the cardiovascular diseases which are associated with the obesity.

Management

• Diet: Calories uptake should depend on the age, sex,occupation and urgency of the weight reduction.
  An obese person should spare from fats, buttr, ghee, cream dryfruits (nuts) vegetables (potatoes and peas).
  Person should follow strict diet regime and maintain discipline in choice of foods to which he/she takes and the amount ofcalories consumed per day.
  Food should be taken in intervals, chewed slowly.
• Exercise: Habit of regular physical exercise should be cultivated by an obese person.
  An obese person should do morning and evening walks, jogging, stretch exercise and taking part in outdoor games.
• Drug therapy: In this recent era serotonergic drugs are used.
  DL-fenflramine which was the fist generation drug was used to reduce weight.
  These days it is replaced by second generation drugs dL-fenflramine, floxetine which is a slow releasing serotonin antagonist, sibutramine which is a slow serotonin and noradrenaline reuptake inhibitor.
  These drugs increase the satiety and potentiate serotonin in hypothalamus.
• Surgical treatment: This method is employed in the persons having severe obesity. The surgical methods employed are:

• Wiring ofjaws: This is carried out to prevent eating and only taking liquids.
  This method is good but as wires are removed patient regains the weight.
• Gastric plcation: In this stomach is reduced by creating a small pouch due to stapling of stomach to abdominal wall. Good results can be attined.
• Bariatric surgery: It is done in persons with extreme obesity.

Question.31. Write short note on gestational diabetes.

Answer. Gestational diabetes is defined as development of hyperglycemia, fist time in pregnancy.

• It occurs in women who are genetically predisposed to type 1 and type 2 diabetes.
• The condition is asymptomatic.
• Repeated hyperglycemia in every pregnancy lead the women to undergo suffring from permanent diabetes.
• Gestational diabetes can occur in any women, so at the time of pregnancy during each trimester random blood sugar screening is done by oral glucose tolerance test.
  In this test blood glucose is more than 126 mg%.

Obstetric Complications Associated With Gestational

Diabetes Mellitus

1. Maternal risk

• Maternal hypertension
• Eclampsia
• Nephropathy, retinopathy and vascular complications can worsen.

2. Fetal risk

• Stillbirth
• Neonatal hypoglycemia
• Neonatal hypocalcemia
• Macrosome
• Hyaline membrane disease
• Growth retardation
• Congenital anomalies diagnostic criteria

“Asymptomatic vs symptomatic effects of outdated metabolic defect practices: Answered”

A two-step strategy has been proposed for establishment of diagnosis of gestational diabetes.

First step is to give 50 mg oral glucose and measure serum glucose at 60 min; if glucose is found less than 140 mg then test is normal and if found greater than140 mg, then it warrants second step of administration of 100 g glucose and measure the serum glucose in fasting state and at 1, 2 and 3 hrs. Normal plasma glucose concentration is given below:

• Fasting <105 mg/L.
• At 1 hr < 190 mg/L.
• At 2 hr <165 mg/L
• At 3 hr <145 mg/L.

Deviations from the normal indicate gestational diabetes mellitus.

Management

• High dietary protein intake. Salt restriction if edema is present.
• Exercise should be done regularly
• Insulin therapy is essential.
• Oral hypoglycemic should be avoided except metformin which is effctive in women with PCOD to aid conception.

Question.32.Describe briefl on Type II diabetes.

Answer. Type II diabetes is also known as non­ insulin dependent diabetes mellitus.

Etiology

• Genetic: It is inherited as mendelian type of recessive trait and is predominant in children born to parents who are diabetic.
  Every person who has a history of diabetes in his or her family is a carrier of disease.
  The risk percentage in fist degree relatives is generally up to 20 %t while in second degree relatives it is about 5 %.
  Type II diabetes is caused due to abnormal insulin secretion and insulin resistance.
• Due to pancreatic beta cell failure: In Type II diabetes there is reduction of pancreatic beta cell mass with reduction in insulin levels.
  As beta cells decreases alpha cells secrete glucagon and this causes hyperglycemia.
• Environmental factors: Physical inactivity and obesity are the factor leading to type II diabetes in genetically susceptible individuals.
• Age: Type II diabetes occur after age of 30 years.

Clinical Features

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess
• Nervous system: Autonomic neuropathy and peripheral neuritis
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritus vulvae, menstrual irregularity and infertility.

Management

• Low energy and weight reducing diet is given to the patient of obese type II diabetes mellitus.
• Non­obese type II diabetes should have to maintain their weight, so they have to take weight maintenance diet.

Meglitinides

• Repaglinide, i.e. 0.5 to 4 mg three times a day
• Netaglinide, i.e. 60 to 120 mg three times a day 15 to 30 min before each meal
• Voglibose, i.e. 0.2 to 0.3 mg, 15 to 30 min before each meal.
• Insulin sensitizers, i.e.drugs sensitizing action of insulin and overcome insulin resistance
• Biguanides, i.e. metformin should be given 1.5 to .5gm/day in three divided doses after meals.
• Thiozolidinediones, i.e.Rosiglitazone should be given 2 to 8mg or pioglitazone 15 to 45 mg in a single or two divided doses.
  They can be combined with sulfonyl ureas or metformin.
• Alpha-glucosidase inhibitors, i.e. Acarbose 25 to 100 mg
  TDS or Voglibose 0.2 to 5 mg TDS taken orally in three main meals.
  It can be given in combination with metformin 500 mg for increased effiency.
• DPP 4 inhibitor: Vildagliptin 50 to 100 mg daily in two dived doses with meals ot saxagliptin 2.5 to 5 mg OD.
• Pramlinide: Initial dose is 15μg before each meals in Type I diabetes mellitus and 60 μg in Type II diabetes mellitus.

“Can preventive measures reduce risks of metabolic defect progression? FAQs provided”

Question.33. Write short note on tetany.

Answer: Tetany is a clinical condition with low levels of ionized calcium causing increased neuromuscular excitability.

Etiology

Low levels of calcium, potassium, magnesium causes tetany.

• Hypocalcemia: This is due to following factors, i.e. malabsorption of calcium, osteomalacia, hypoparathyroidism,acute pancreatitis, anti­convulsant drugs.
• Hypokalemia: This is caused due to repeated vomiting,excessive intake of alkali, due to acute anion load, primary hyperaldosteronism, due to acute anion load.
• Acute hypocalcemia is caused by sepsis, burns, alkalosis,parathyroid surgery, malignancy, hypomagnesemia, etc.

Clinical Features

• In children there is presence of triad of symptoms, i.e.
  carpopedal spasm, stridor and convulsion.
• In carpopedal spasm the hands adopt a posture in which flxion occurs at metacarpophalangeal joint and extension at interphalangeal joint and opposition of thumb occur.
• Stridor occurs due to closure of glotts.
• In case of adults tingling sensation occur in peripheral part of limbs and around the mouth.
• Trousseau’s sign: Increasing the blood pressure by the infltion of sphygmomanometer cuf at above the systolic level leads to carpopedal spasm in 2 to 5 minutes.

Chvostek’s sign: Tapping at the facial nerve especially at angle of mandible leads to twitching of facial muscles.

Management

In management etiological factor leading to tetany is eliminated and hypocalcemia and alkalosis should be treated.

Treatment Of Hypocalcemia

10% calcium gluconate 20 mL IM is given. For long lasting effct 10 mL of drug is given additionally.

Treatment Of Alkalosis

• If vomiting is present IV isotonic saline should be given.
• If alkali is the etiological factor, alkalis should be withdrawn, after withdrawal if effect is not proper ammonium chloride 2 gm orally is given after every 4 hours.
• If hyperventilation is the etiological factor, patient is asked to inhale 5% carbon dioxide in oxygen.

Question.34. What are the non-communicable disease type-2 diabetes mellitus.

Answer.

Non­communicable disease is a medical condition or
disease that is non­infectious or non­transmissible.

Non­communicable disease can refer to chronic diseases which last for long periods of time and progress slowly.

The most non­communicable diseases are obesity,diabetes, cancer, cardiovascular, chronic respiratory and neurological diseases.

Diagnosis

Diagnosis is based on symptoms, signs and laboratory tests.
In presence ofsigns and symptoms confimation is done by fiding random blood glucose higher than 200 mg/dL.

Investigations

• Blood sugar estimation: Both fasting and post­prandial (2 hours after a meal) levels of blood sugar be estimated.
  Mean value of blood sugar in healthy adults is 70 to 80 mg%. When fasting blood sugar level exceeds 110 mg% diagnosis is clear.
  Post­prandial blood sugar level is further screening test, if value exceeds 120 mg% it is strongly suggestive of diabetes mellitus.
  Random blood sugar estimation is not of much help as screening test.
  Value exceeding 160 mg% in presence of glycosuria is suggestive but values about 200 mg% is diagnostic.
• Oral glucose tolerance test: In this fist sample is taken after an overnight fast of 8 hours following which patient is given glucose 1g/kg body weight.
  Blood is then collected at 30, 60, 120 and 180 minutes.
  In diminished glucose tolerance, level of blood glucose is raised at 180 minutes.
• Glycosylated hemoglobin: It measures the long­term glycemic control.
  Slow non­enzymatic attachment of glucose to hemoglobin result in formation of glycosylated hemoglobin.
• Microalbumin: Patients with microalbumineria are on greater risk in developing kidney failure as well as cardiovascular damage.
• Urine protein/creatinine ratio: It provides information of proteinuria in patients with diabetic nephropathy.
  More is the ratio greater is the damage.
• Insulin levels: Elevated blood glucose levels with low insulin levels indicate insufficient insulin levels for adequate control of blood glucose.
  High insulin levels with low blood glucose indicate change in dosage of drug.
• Insulin antibody test: In this there is quantitative determination of antibodies against insulin in serum.
• GAD 65 antibody: These antibodies are common in newly diagnosed diabetic patient and often appear years before clinical onset in the disease. Presence of this antibody is the strong predictive marker for onset of type I diabetes mellitus.

“Differential applications of dietary changes vs enzyme therapy in metabolic defects: Q&A”

Criterias Given By WHo In 1999

• Presence of classic symptoms of diabetes and causal plasma glucose greater than or equal to 200 mg/dL.
  Causal is any time of day without regard to time since last meal.
  Classic symptoms of diabetes include polyuria, polydypsia and unexplained weight loss.
  Or
• Fasting plasma glucose greater than or equal to 126 mg/dL.
  Fasting is defied as no caloric intake for 8 hours.
  Or
• Twohoursplasmaglucosegreaterthanorequalto200 mg/dL during an oral glucose tolerance test.
  Test is performed as described by World Health Organization by using glucose load containing equivalent of 75 gm anhydrous glucose dissolved in water.

In absence of unequivocal hyperglycemia with acute metabolic decompensation above criterias are confimed by repeated testing on other days.

Complications

Acute Or Immediate Complications

• Diabetic ketoacidosis or coma
• Hypoglycemia or hypoglycemic coma
• Non­ketotic hyperosmolar diabetic coma
• Lactic acidosis

First two complications occur in Type I diabetes mellitus and other two occur in Type II diabetes mellitus.

Diabetic Ketoacidosis

• It is an exclusive complication of type I diabetes. It can develop in patients with severe insulin defiiency combined with glucagon excess.
  Failure to take insulin and exposure to stress are precipitating causes.
• As the ketogenesis continues the excess ketone bodies produced cannot be degraded by the muscles and other tissues resulting in ketosis, which manifests as anorexia, nausea, vomiting, deep and fast breathing, mental confusion and coma. However, most of the patients recover.

Hypoglycemia

• It is defied as fall in blood glucose concentration below 3.1 mmol/L.
• It is seen in type I diabetes patients due to excessive administration of insulin, missing a meal or due to stress.
• As the hypoglycemia continues, it can lead to comma,cardiac arrhythmias and is fatal.
• This can lead to worsening of control of diabetes and rebound hyperglycemia.

Nonketotic Hyperosmolar Diabetic Coma

• It is common in type II diabetes mellitus.
• The clinical hallmark is hyperglycemia, hyperosmolality and dehydration without ketoacidosis.
• Precipitating features are infection, myocardial infarction,drugs such as thiazides, steroids, diphenylhydantoin.
• Loss of glucose in urine is so intense that the patient is unable to drink suffient water to maintain urinary flid loss.
• Because of high viscosity of blood, thrombotic and bleeding complications are frequent. Mortality rate is high in this complication.

Lactic Acidosis

• It is seen in type II diabetes mellitus.
• It is caused due to excess lactate production and/or inadequate utilization.
• This can be precipitated by metformin or other systemic disorders such as liver or renal failure, pancreatitis or leukemia.
• Cardiovascular collapse leads to mortality.

Chronic or late-onset complications

These complications are due to changes in small blood vessels i.e.microangiopathy or in large blood vessels, i.e. macroangiopathy.

Microvascular are retinopathy, neuropathy, nephropathy and miscellaneous

Macrovascular are atherosclerosis, hypertension, peripheral vascular disease and diabetic foot ulcer

The chronic complications occur more frequently in Type II diabetes mellitus rather than Type I diabetes mellitus.

Diabetic Retinopathy

• This is the very important cause of blindness in diabetic patients.
• Dilatation of retinal capillaries is earliest sign. Besides these there is also presence of microaneurysms, retinal hemorrhage, neovascularization, hard and soft exudates,vitreous hemorrhage and firosis.
• Frequency, onset and severity of retinopathy vary in diabetic patients.
• Background retinopathy is most common and proliferative retinopathy is less common.

Diabetic Neuropathy

• It can involve any part of nervous system except the brain.
• Neuropathy is an early and common complication which leads to morbidity and disability.
• Poor glycemic control and long duration of diabetes is associated with high incidence of neuropathy.
• Sign and symptoms are of peripheral nervous system.
• Main pathological changes in peripheral nerves are axonal degeneration of myelinated and non-myelinated fiers,
  Segmental demyelination, Schwann cell injury.

“Difference between inherited and acquired metabolic defects: Q&A explained”

Diabetic Nephropathy

• This is the most common cause of mortality and morbidity in diabetic patients.
• 40 to 50% of type II diabetes patient develop it and 25% patients with type I diabetes develop end stage renal disease and die of it.
• It is divided into three stages, in fist stage patient is asymptomatic but has high GFR, in next stage there is renal hypertrophy which leads to microalbuminuria.
• In advance stage, patient develop macroproteinuria and passes onto nephrotic syndrome.
• 25% of patients with diabetic nephropathy can go directly at end stage renal disease with hypertension and undergo chronic renal failure.

Question.35. Write diagnosis, clinical features and complications of diabetes mellitus.

Answer. Diagnosis is based on investigations,

Investigations

• Blood sugar estimation: Both fasting and post­prandial (2 hours after a meal) levels of blood sugar be estimated.
  Mean value of blood sugar in healthy adults is 70 to 80 mg%. When fasting blood sugar level exceeds 110 mg% diagnosis is clear.
  Post­prandial blood sugar level is further screening test, if value exceeds 120 mg% it is strongly suggestive of diabetes mellitus.
  Random blood sugar estimation is not of much help as screening test.
  Value exceeding 160 mg% in presence of glycosuria is suggestive but values about 200 mg% is diagnostic.
• Oral glucose tolerance test: In this fist sample is taken after an overnight fast of 8 hours following which patient is given glucose 1 g/kg body weight.
  Blood is then collected at 30, 60, 120 and 180 minutes. In diminished glucose tolerance, level of blood glucose is raised at 180 minutes.
• Glycosylated hemoglobin: It measures the long­term glycemic control. Slow non­enzymatic attachment of glucose to hemoglobin result in formation of glycosylated hemoglobin.
• Microalbumin: Patients with microalbuminria are on greater risk in developing kidney failure as well as cardiovascular damage.
• Urine protein/Creatinine ratio: It provides information of proteinuria in patients with diabetic nephropathy. More is the ratio greater is the damage.
• Insulin levels: Elevated blood glucose levels with low insulin levels indicate insufficient insulin levels for adequate control of blood glucose.
  High insulin levels with low blood glucose indicate change in dosage of drug.
• Insulin antibody test: In this there is quantitative determination of antibodies against insulin in serum.
• GAD 65 antibody: These antibodies are common in newly diagnosed diabetic patient and often appear years before clinical onset in the disease. Presence of this antibody is the strong predictive marker for onset of type I diabetes mellitus.

Diagnosis

Diagnosis is based on symptoms, signs and laboratory tests.
In presence ofsigns and symptoms confimation is done by fiding random blood glucose higher than 200 mg/dL.

Investigations

• Blood sugar estimation: Both fasting and post­prandial (2 hours after a meal) levels of blood sugar be estimated.
  Mean value of blood sugar in healthy adults is 70 to 80 mg%. When fasting blood sugar level exceeds 110 mg% diagnosis is clear.
  Post­prandial blood sugar level is further screening test, if value exceeds 120 mg% it is strongly suggestive of diabetes mellitus.
  Random blood sugar estimation is not of much help as screening test.
  Value exceeding 160 mg% in presence of glycosuria is suggestive but values about 200 mg% is diagnostic.
• Oral glucose tolerance test: In this fist sample is taken after an overnight fast of 8 hours following which patient is given glucose 1g/kg body weight.
  Blood is then collected at 30, 60, 120 and 180 minutes.
  In diminished glucose tolerance, level of blood glucose is raised at 180 minutes.
• Glycosylated hemoglobin: It measures the long­term glycemic control.
  Slow non­enzymatic attachment of glucose to hemoglobin result in formation of glycosylated hemoglobin.
• Microalbumin: Patients with microalbumineria are on greater risk in developing kidney failure as well as cardiovascular damage.
• Urine protein/creatinine ratio: It provides information of proteinuria in patients with diabetic nephropathy.
  More is the ratio greater is the damage.
• Insulin levels: Elevated blood glucose levels with low insulin levels indicate insufficient insulin levels for adequate control of blood glucose.
  High insulin levels with low blood glucose indicate change in dosage of drug.
• Insulin antibody test: In this there is quantitative determination of antibodies against insulin in serum.
• GAD 65 antibody: These antibodies are common in newly diagnosed diabetic patient and often appear years before clinical onset in the disease. Presence of this antibody is the strong predictive marker for onset of type I diabetes mellitus.

Criterias Given By WHo In 1999

• Presence of classic symptoms of diabetes and causal plasma glucose greater than or equal to 200 mg/dL.
  Causal is any time of day without regard to time since last meal.
  Classic symptoms of diabetes include polyuria, polydypsia and unexplained weight loss.
  Or
• Fasting plasma glucose greater than or equal to 126 mg/dL.
  Fasting is defied as no caloric intake for 8 hours.
  Or
• Twohoursplasmaglucosegreaterthanorequalto200 mg/dL during an oral glucose tolerance test.
  Test is performed as described by World Health Organization by using glucose load containing equivalent of 75 gm anhydrous glucose dissolved in water.

In absence of unequivocal hyperglycemia with acute metabolic decompensation above criterias are confimed by repeated testing on other days.

clinical Features

In type I diabetes Mellitus

Symptoms

• Polydypsia, polyuria and polyphagia
• Weight loss
• Weakness and lassitude.

Sign

• Severe emaciation with wastening of muscles
• Ribs are prominent.
• In such patients if diabetic ketoacidosis is severe patient develop mental apathy, confusion and undergo coma.

In type II diabetes Mellitus

Symptoms

Patient remains asymptomatic in the beginning. Disease is detected during routine check up.

Sign

In this multiple systems are affcted, so considering this various signs are:

• Eyes: Errors of refraction leads to frequent change in spectacles, premature formation of cataract, retinopathy,recurrent sty.
• Skin: Abscess, carbuncle, boils, non­healing wounds.
• Gastrointestinal tract: Chronic diarrhea, malabsorption and dilatation of stomach.
• Cardiovascular system: Hypertension, ischemic heart disease, diabetic foot, cold extremities.
• Respiratory system: Pneumonia, tuberculosis and lung abscess.
• Nervous system: Autonomic neuropathy and peripheral neuritis.
• Urinary tract: Nephrotic syndrome, urinary tract infection.
• Genital tract: Pruritis vulvae, menstrual irregularity and infertility.

Complications

Acute Or Immediate Complications

• Diabetic ketoacidosis or coma
• Hypoglycemia or hypoglycemic coma
• Non­ketotic hyperosmolar diabetic coma
• Lactic acidosis

First two complications occur in Type I diabetes mellitus and other two occur in Type II diabetes mellitus.

Diabetic Ketoacidosis

• It is an exclusive complication of type I diabetes. It can develop in patients with severe insulin defiiency combined with glucagon excess.
  Failure to take insulin and exposure to stress are precipitating causes.
• As the ketogenesis continues the excess ketone bodies produced cannot be degraded by the muscles and other tissues resulting in ketosis, which manifests as anorexia, nausea, vomiting, deep and fast breathing, mental confusion and coma. However, most of the patients recover.

Hypoglycemia

• It is defied as fall in blood glucose concentration below 3.1 mmol/L.
• It is seen in type I diabetes patients due to excessive administration of insulin, missing a meal or due to stress.
• As the hypoglycemia continues, it can lead to comma,cardiac arrhythmias and is fatal.
• This can lead to worsening of control of diabetes and rebound hyperglycemia.

Nonketotic Hyperosmolar Diabetic Coma

• It is common in type II diabetes mellitus.
• The clinical hallmark is hyperglycemia, hyperosmolality and dehydration without ketoacidosis.
• Precipitating features are infection, myocardial infarction,drugs such as thiazides, steroids, diphenylhydantoin.
• Loss of glucose in urine is so intense that the patient is unable to drink suffient water to maintain urinary flid loss.
• Because of high viscosity of blood, thrombotic and bleeding complications are frequent. Mortality rate is high in this complication.

Lactic Acidosis

• It is seen in type II diabetes mellitus.
• It is caused due to excess lactate production and/or inadequate utilization.
• This can be precipitated by metformin or other systemic disorders such as liver or renal failure, pancreatitis or leukemia.
• Cardiovascular collapse leads to mortality.

Chronic or late-onset complications

These complications are due to changes in small blood vessels i.e.microangiopathy or in large blood vessels, i.e. macroangiopathy.

Microvascular are retinopathy, neuropathy, nephropathy and miscellaneous

Macrovascular are atherosclerosis, hypertension, peripheral vascular disease and diabetic foot ulcer

The chronic complications occur more frequently in Type II diabetes mellitus rather than Type I diabetes mellitus.

“Most common complications of poorly understood metabolic defect concepts: FAQs”

Diabetic Retinopathy

• This is the very important cause of blindness in diabetic patients.
• Dilatation of retinal capillaries is earliest sign. Besides these there is also presence of microaneurysms, retinal hemorrhage, neovascularization, hard and soft exudates,vitreous hemorrhage and firosis.
• Frequency, onset and severity of retinopathy vary in diabetic patients.
• Background retinopathy is most common and proliferative retinopathy is less common.

Diabetic Neuropathy

• It can involve any part of nervous system except the brain.
• Neuropathy is an early and common complication which leads to morbidity and disability.
• Poor glycemic control and long duration of diabetes is associated with high incidence of neuropathy.
• Sign and symptoms are of peripheral nervous system.
• Main pathological changes in peripheral nerves are axonal degeneration of myelinated and non-myelinated fiers,
  Segmental demyelination, Schwann cell injury.

Diabetic Nephropathy

• This is the most common cause of mortality and morbidity in diabetic patients.
• 40 to 50% of type II diabetes patient develop it and 25% patients with type I diabetes develop end stage renal disease and die of it.
• It is divided into three stages, in fist stage patient is asymptomatic but has high GFR, in next stage there is renal hypertrophy which leads to microalbuminuria.
• In advance stage, patient develop macroproteinuria and passes onto nephrotic syndrome.
• 25% of patients with diabetic nephropathy can go directly at end stage renal disease with hypertension and undergo chronic renal failure.

Miscellaneous

It consists of various infections, gastroparesis, arthropathy.

Atherosclerosis

• In diabetic patient development of athroma is faster as compared to normal individual.
• Hyperlipidemia, decreased HDL levels, increased platelet adhesiveness, obesity and associated hypertension are contributory factors for athrosclerosis.
• Atherosclerosis leads to coronary artery disease, silent myocardial infarction, cerebral stroke and gangrene of toes and feet.

Diabetic Foot Ulcer

• This is the frequent site of complication in diabetes.
• Pathogenic components of diabetic foot are neuropathy,peripheral vascular disease causing ischemia and secondary infection causing ulceration.

The post Nutrition and Metabolic Defects Important Question and Answers appeared first on BDS Notes.

Question.1. Enumerate causes of facial pain.

Answer. Causes of facial pain are:

• Neuritis of cutaneous nerves of face and scalp.
• Arthralgia of temporomandibular joint
• Trigeminal neuralgia.
• Post herpetic neuralgia.
• Temporal arthritis.
• Miscellaneous causes:

“Understanding nervous system diseases through FAQs: Causes, symptoms, and treatments explained”

• Facial neuralgia: It is a form of inflmmation of nerve of face and scalp.
  It generally occurs as complication of septic state or due to involvement of neurotrophic virus. The pain is confied to face and scalp.
• Arthralgia of TMJ: It is in the form of rheumatic arthritis or ankylosing spondylitis (a chronic progressive inflmmatory disorder unlike other rheumatological disorders) when there is pain and swelling of joint.
• Trigeminal neuralgia: This is a disease seen commonly in middle and elderly individuals and is characterized by attcks of sever pain in distribution of trigeminal nerve and its branches especially in maxillary and mandibular branches.

• Postherpetic neuralgia: Herpes zoster commonly involves the ophthalmic division of 5th nerve,characterized by vesicular eruption on the face.
• Temporal arthritis: It is a form of collagen disorder of unknown etiology which involves mainly the arteries. It occurs in elderly age group.
  Patient may complain of pain on the face, jaw,mouth and tongue in distribution of branches of external carotid artery.
• Miscellaneous causes: These include lesions of trigeminal nerve in brain stem, *syringobulbia and thrombosis of posterior inferior cerebellar artery.
  Tabes dorsalis is another cause of pain coming in attcks over the face.

“How do degenerative disorders affect the nervous system? FAQ answered”

Read And Learn More: General Medicine Question And Answers

Question.2. Write short note on trigeminal neuralgia.

Answer. Trigeminal Neuralgia is also called as Tic Douloureux.

A disorder characterized by the *paroxysmal attcks of neuralgic pain with affction of one or more division of trigeminal nerve.

The pain involves the third and second divisions equally and rarely the fist.

Trigeminal Neuralgia Clinical Features or Trigeminal Neuralgia Treatment

• Pain is unilateral and is confined to one of the three divisions of nerve. Pain is sharp and onset is sudden. The pain is only of a few seconds.
• During the attcks there is flshing of face, i.e. redness of the face.
• Dilatation of pupil is present.
• There is excessive lacrimation
• After repeated attcks skin becomes shiny and hair in the area becomes gray.
• Sometimes secretion of nasal mucus and saliva may occur in the side of pain.

Trigeminal Neuralgia Etiology

Trigeminal neuralgia is spontaneous and following exposure to cold wind, blow on face, or chewing or eating, drinking hot or cold flid and washing the face.

Trigeminal Neuralgia Management or  Trigeminal Neuralgia Treatment

• Elimination of all possible sources of infection.
• Drugs:

• Analgesics: Potent analgesics must be used with caution because of danger of habituation.
• Carbamazepine: 100–200 mg BD a day and increasing the dose to 600–800 mg per day.
• Phenytoin sodium: 0.1 gm TDS when carbamazepine is not tolerated.
• Vitamin B12: 1000 μg IM daily for two weeks.
• Injection ofalcohol: It is given in affcted nerve, or gasserian ganglion.
  If more than one division is affcted inject 10 minims of 90% alcohol after local anesthesia with 2–3 drops of procaine.
• Microvascular decompression: In this there is separation of blood vessels is done which are in contact with trigeminal nerve roots.
  There is also insertion of non absorbable sponge which provide relief of pain in most of the patients.
• Radiofrequency thermocoagulation: This procedure is carried out at the trigger spot or site of pain origin which is localized by electric stimulation of needle inserted in trigeminal ganglion and leads to permanent relief.
• Surgery: In this selective or complete preganglionic section of trigeminal root is done.
  This technique can lead to disadvantages such as permanent dysesthesiae.
  Another bettr technique is percutaneous electrocoagulation of preganglionic rootlets corresponding to trigger zone, the temperature of probe being so regulated as to coagulate small thinly myelinated pain fiers but preserving most heavily myelinated touch fiers.

Trigeminal Neuralgia Treatment

“Importance of studying nervous system diseases for healthcare professionals: Questions explained”

Question.5. Write short note on Migraine.

Answer. Migraine is defied as recurrent attcks of headache varied in intensity frequency and duration and is commonly unilateral in onset and is associated with anorexia and sometimes with nausea and vomiting.

Migraine Clinical Features

• The headache follows and the pain is confied on one side by occasionally it may be bilateral.
• Nausea and vomiting may be present and last for the few hours.
• Light and noise sensitivity is present.
• Fatigue and stress are present in the case.
• There is presence of polyuria.

Simplifid Diagnostic Criteria for Migraine

Repeated attcks of headaches lasting for 4 to 72 hours which have features:

• Normal physical examination
• No other reasonable cause for headache
• At least two of:
• Unilateral pain
• Throbbing pain
• Aggravation of pain by movement
• Moderate or severe intensity
• At least one of:
• Nausea or vomiting
• Photophobia or phonophobia

Migraine Management

Migraine During attack

• Analgesics: NSAIDs, e.g. diclofenac can be given orally or im and is particularly useful when severe vomiting is a feature. Sublingual Piroxicam has significant analgesic effcts in acute migraine without aura with excellent tolerability.
• Ergotamine: Ergotamine tartrate 0.25 to 0.5 mg IM or orally 1–2 mg. tablet preferably in combination with 100 mg caffine –2 tablets at onset followed by l tablet after 30 minutes, if necessary, or Dihydroergotamine 1 mg IM, or 1–2 mg by mouth.
  Whichever preparation is used, a high dose often causes nausea and vomiting.
  These may be prevented by giving cyclizine 50 mg.or chlorpromazine 25 mg.
• 5-HT1 agonists: Sumatriptan 6 mg s.c. gives relief from headache in 60 minutes, with corresponding improvement in nausea, vomiting and photophobia.
  Oral dose of 100 mg provides relief within 2 hours.
  Headaches recur within 48 hours in litte less than half the patients.
  Rizatriptan given orally acts faster than sumatriptan. Zolmitriptan nasal spray 5 mg gives relief in 5 minutes.
• General: Lying in a darkened and quiet room and ice pack to the head may help.

“Common challenges in diagnosing and treating nervous system diseases effectively: FAQs provided”

Reducing frequency and severity of subsequent attcks

• Elimination oftrigger factors: Sleeping late, irregular and hurried meals, certain foods, especially chocolate and fried food, or missing of meals, psychological stress,contraceptive pills.
  Treatment of cervical spondylosis
• Relaxation exercises: They may include biofeedback from a temporalis electromyogram. Yoga, Pranayama.

Drugs:

• Serotonin (5-HT) inhibitors: Calcium antagonists suchas Flunarizine 10 mg/day Or Cyproheptadine 4 mg tds. Or Pizotifen 0.5 mg tds or 1.5 mg nocte.
  Or Methysergide 1–2 mg t,d.s. is the most effctive drug in this group, but should be used under supervision in courses not exceeding 3–4 months.
• Topiramate: It is an antiepileptic drug used in prophylaxis of migraine, Dose: 2.5 to 5 mg BD
• Divalproex (valproic acid) 200 mg BD
• Tricyciic agents: Amitryptiline 25 mg TDS may be effective irrespective of the presence of depression.
• Ergotamine tartrate: For histamine cephalgia 1 mg by mouth or 0.25 mg by self­administered injection or by suppository used regularly last thing at night can be continued for many weeks without harmful effcts, 2 days being left without treatment each week.
• Hormones: Progesterone given for last eight days may be useful for migraine occurring in the immediate premenstrual period or at beginning of catamenia.
  When migraine begins or becomes worse at the time of menopause, estrin, given in small doses as continuous therapy sometimes helpful.

Schedule:

• Propranolol 40–160 mg/day or Flunarizine 5–10 mg/day as fist line of therapy.
• In patients with episodic and chronic migraine
• Topiramate 50–100 mg/day.
• In patients with episodic migraine Divalproex
  250–750 mg/day.
• For mixed migraine and tension type headache:
  Amitryptiline 10–25 mg/ day.
  After 6–12 months of prophylaxis gradual
  withdrawal should be considered.

Question.6. Classify headache. Discuss etiology, symptoms, signs,pathogenesis of cluster headache.

Answer.

Classification of Headache

The classifiation is given by International Headache Society,which is as follows:

• Migraine (Classical common, opthalmoplegic and basilarartery)
• Tension type, headache (e.g. episodic or chronic)
• Cluster headache and chronic hemicrania
• Miscellaneous headache not associated with structural lesion (e.g., cold stimulus induced, cough headache,idiopathic, sexual activity induced)
• Traumatic headache
• Headache associated with vascular disorders (e.g. CVA,intracranial hemorrhage or hematoma, arteritis, venoussinus thrombosis and other vascular disorders).
• Hedache associated with nonvascular intracranial diseases(e.g. high or low CSF pressure, intracranial infections orneoplasm).
• Headache associated with substance abuse or their withdrawal.
• Headache associated with systemic infection (e.g. viral and bacterial).
• Headache associated with metabolic diseases (e.g. hypoxia, hypercapnia, hypoglycemia, dialysis, etc.)
• Headache due to referred pain (e.g., disorders of eyes, ear,nose and sinuses, teeth, jaw and temporomandibular joint)
• Cranial neuralgia (e.g., trigeminal, glossopharyngeal or occipital neuralgia).
• Unclassifid headache.

Cluster Headache/Migranous Neuralgia

This is distinctive and treatable vascular headache syndrome which is characterized by one to three short lived attcks of periorbital pain per day over 4 to 8 weeks.

Migranous Neuralgia Etiology

Headache associated with at least one of the following on the painful site namely:

• Conjunctival injection
• Nasal *congestion
• Forehead and facial flshing
• *Miosis
• *Ptosis
• Eyelid edema
• Rhinorrhea.

Migranous Neuralgia Symptoms

• There is periodic, severe and unilateral periorbital pain.
• Reddening of eye is present.
• Nasal *stuffiss is present.
• Nausea is present.
• Pain occur after 1 or 2 hours when patient fallen asleep.

Migranous Neuralgia Signs

• Conjunctiva infection
• Rhinorrhea
• Nasal congestion
• Lacrimation
• Miosis
• Ptosis
• Flushing, sweating
• Edema of face.

“Why is early detection critical for preventing nervous system disease complications? Answered”

Migranous Neuralgia Pathogenesis

Carotid body plays major role in cluster headache.

• Disturbance in some specific areas in hypothalamus due to cyclic cluster periods which causes disturbances in sympathetic and parasympathetic supplies to body.
  It causes increase in vasomotor tone which activate peripheral chemoreceptors.
• It induces attacks with oxygen desaturation which reaches the threshold level of oxygen causing activation of chemoreceptor and stimulate the nuclei of 7th and 10th cranial nerve in respiratory center.
• It results in stimulation of peripheral secretory and other receptors innervated by the cranial nerves causing cluster headache.

Question.7. Outline the management of Headache.

Answer. The management of headache is as follows:

• Mild headache responds to rest, massage,acetaminophen or listening to relaxing music.
• Moderate headache typically requires NSAID therapy
  Caffine helps ameliorate many mild-to-moderate headache.
• Antiemetics such as prochlorperazine or metoclopramide helps to relieve moderate to severe headache especially those accompanied by nausea.
  Ergotamine and triptan drugs are suited to treating migraine.
  Cluster headache often resolves after treatment with corticosteroid or high flw oxygen.
  The headache of temporal arteritis also responds to high dose steroids, but these agents must be continued for months or years until syndrome remits.

Question.9. Write short note on Temporal Epilepsy.

Answer. Temporal epilepsy is the form of epilepsy where aura (A subjective, but recognizable sensation that precedes and signals the onset convulsion) is either auditory, visual, olfactory or gustatory.

Temporal Epilepsy Clinical Features

• There is feeling of unusual smell, an emotional feeling or*hallucinations.
• Motor activity stops and patient looks vacant.
• There is unilateral dystonic posturing of the limb.
• There is temporary cessation of the activity followed by lip smoking, chewing movements or the patient may walk aimlessly. When seizure and amnesia is present.

Temporal Epilepsy Management

General:

• Avoid physical exertion, regular habits of eating and sleeping.
• Avoid alcohol.

Pharmacological:

• Clonazepam 1.5 mg/day reduces excitability of neurons.
• Methsuximide 500 mg daily is effctive.
• Clobazam 10 to 20 mg has antiepileptic activity.
• Gabapentin 300 mg TDS is used to control epilepsy.
• Lamotrigine 50 mg daily for two weeks followed by 100 mg/day given in two divided doses for 2 weeks.
• After dose is increased by 100 mg every 1 to 2 weeks till response is obtained.

Question.11. Write short note on Brown-Sequard’s syndrome.

Answer. Brown­Sequard’s syndrome is a spinal cord lesion. In it hemisection (Bisection) of spinal cord is present.

Brown-Sequard’s syndrome Etiology

• Compression of cord
• Intramedullary neoplasm
• Due to *stab in back
• Bullet wounds
• Vertebral fracture and caries
• Vascular causes, i.e. *arachnoiditis.

Brown-Sequard’s syndrome Clinical Features

Below the site of lesion

• Motor changes: Spastic paralysis, i.e.
• Positive Babinski’s sign
• Clasp knife rigidity
• Exaggerated tender jerks and loss of voluntary power. All the above features are seen in unilateral side of lesion. The sign are due to interruption of already crossed pyramidal tract.
• Sensory changes:
• Loss of fie touch, tactile sensation and vibration sense is loss in ipsilateral side. This is due to loss of lemniscal fiers.
• Loss of crude touch, pressure, pain and temperature sense on contralateral side. This is due to loss of spinothalamic tract fier.

At the site of lesion

• Motor changes: Lower motor neuron paralysis is segment corresponding to level of lesion on ipsilateral side, due to loss of anterior horn cells of segment.
• Sensory changes: There is anesthesia or ipsilateral *dermatomes due to loss of posterior root of corresponding spinal cord segment.

“Factors influencing success with nervous system disease knowledge: Q&A”

Question.12. Enumerate the cause of Epilepsy.

Answer. The causes ofepilepsy are:

Follwing are the causes of epilepsy in diffrent age groups.

In neonates (0 to 2 years)

• Perinatal hypoxia, or ischemia
• Birth injury
• Acute infections, i.e., meningitis, encephalitis metabolic d isturbance, i.e hypoglycemia, hypocalcemia,hypomagnesemia structural lesions such as congenital vascular malformations
• Familial or genetic disorders.

In chidren (2 to 12 years)

• Idiopathic
• Acute infections, i.e., meningitis, encephalitis,toxoplasmosis, cerebral abscess
• Head injury or trauma
• Febrile convulsions

In adolescents (12 to 18 years)

• Idiopathic
• Head trauma
• Drugs, i.e., amphetamines, antidepressants, phenothiazines,etc.
• Alcohol withdrawal
• Arteriovenous malformations
• Infections, i.e., meningitis, encephalitis, cerebral abscess,toxoplasmosis

In Person of age 18 to 35 years

• Head injury or trauma
• Alcoholism
• Brain tumors, cysts, hydrocephalus, aneurysms, AV malformations
• Inflammatory disorders such as sarcoidosis, multiple sclerosis, SLE.

In older adults and old Persons

• Brain tumours
• Cerebrovascular accidents (thrombosis, infarction,hemorrhage)
• Alcoholism
• Uremia
• Hepatic encephalopathy
• Hypertensive encephalopathy
• Electrolyte disturbances
• Hypoglycemia

Question.14. Enumerate the etiological factors of Bacterial Meningitis. Describe clinical features, complications and management of a case of meningococcal meningitis.

Answer. Etiology of Bacterial Meningitis

Bacterial meningitis is caused by various bacteria which are as follows:

• In neonates or infants
• Gram negative bacilli, i.e. E. coli and B. proteus
• Group B streptococci
• Listeria monocytogenes

In adolescents or adults

• Streptococcus pneumoniae
• Neisseria meningitidis
• Mycobacterium tuberculosis
• Staphococcus aureus
• Hephilus inflenzae

In old age

• Hemophilus inflenzae
• Neisseria meningitides
• Streptococcus pneumoniae
• Mycobacterium tuberculosis

In immunocompromised

• Listeria monocytogenes
• Gram negative bacilli
• Streptococcus pneumoniae
• Mycobacterium tuberculosis
• Cryptococcus neoformans

Clinical Features Of Meningococcal Meningitis

• Meningococcal rash, petechial rash on skin, mucus membrane and conjunctiva.
• Acute fulminant illness with adrenal insuffiency.
• Hypotension, shock and patient go quickly in comma. This is called as Water house–Friderichsen syndrome.
• It is due to necrosis in adrenal gland during course of meningococcal septicemia.
• Signs of meningeal irritation, i.e. Kernig’s and Brudzinski’s sign are positive.
• In children and adults it is mainly present.
• Neck rigidity
• Vomiting
• Fever with rigor
• Dilatation of pupil.

Complications of Meningococcal Meningitis

• Neurological defect like hemiplegia, aphasia, ocular nateor, hemianopia, blindness and deafness.
• Mental deterioration
• Cerebritis, brain abscess
• Focal fis
• Auditory impairment
• Sub­dural empyema
• Internal hydrocephalus
• Spinal cord compression due to arachnoiditis.

“Steps to explain nervous system diseases: Causes vs symptoms vs treatment: Q&A guide”

Management of Meningococcal Meningitis

• For adult patients penicillin G 5 to 10 million units IV 6 hourly.
• Cephalosporins, i.e. cefotaxime 2 gm IV or ceftriaxone
  2 gm IV OD is also effctive.
• Patients allergic to penicillin are treated with chloramphenicol 1 gm IV 6 hourly
• Treatment is continued for 7 to 10 days.
• For raised intracranial tension IV mannitol is given which is accompanied by high doses of dexamethasone 4 mg IV 6 hourly. The supportive treatment is to maintain nutrition, flid and electrolytic balance.

Question.15. Describe the management of tubercular meningitis.

Answer.

Management of Tubercular Meningitis

General management:

• Maintenance of nutrition, hydration and electrolyte balance.
• Case of bowel and bladder
• Nursing should be good
• If there are convulsions, anticonvulsants are given.

Tubercular Meningitis Treatment:

• Antitubercular drugs: Rifampicin 600 mg/day + Isoniazide (600 to 900 mg/day) + Pyrazinamide(1.5 gm) should be given. Treatment with this regimen is given for 2 months.
  This is followed by rifampicin 600 mg/day + Isoniazide (600 to 900 mg/day) for 12 to 18 months.
• Steroids: Prednisolone 40–60 mg/day to reduce toxicity, pia­arachnoid adhesions and felling of well­being.

Question.16. Describe clinical features and evaluate management of Meningitis.

Answer.

Meningitis Clinical Features

Meningitis Symptoms

• Fever coming with rigors.
• Headache which is very severe (bursting in character) mainly in frontal region radiating down to back.
• Vomiting
• Convulsion in children
• Malaise
• Severe photophobia
• Ptosis: Due to raised intracranial tension
• Stiffess in neck and back
• Pain in neck
• Impairment of consciousness i.e. confusion, delirium and coma.

Meningitis Signs

• Head retraction is present in infants and children.
• Neck rigidity, i.e. bending of neck causes pain and spasm of neck muscles or it is diffilt to bend the neck.
• Kernig’s sign is positive
• Brudzinski’s sign is also positive if patient is conscious.
• Presence of papilledema
• Presence of cranial nerve palsies

Clinical Features Of Tuberculous Meningitis

Meningitis Symptoms

• Headache
• Vomiting
• Low grade fever
• Lassitude, i.e. weariness or exhaustion
• Depression
• Confusion
• Behavior changes.

Meningitis Signs

• Meningism may be present
• Occulomotor palsies
• Papilledema
• Depression of conscious level
• Focal hemisphere signs.
  Management
  • Cholinesterase inhibitors, i.e. pyridostigmine 30 to 120 mg or neostigmine 15 to 45 mg TDS is given.
  • Thymectomy is performed as soon as feasible in any antibody positive patient with symptoms not confied to extraocular muscles.
  • Plasma exchange is done
  • IV immunoglobin 0.4 gm/kg/day for 5 days is given.
  • Immunosuppressant: Azathioprine 2.5 mg/kg body weight
    is helpful in reducing dosage of steroids necessary and allows steroids to withdraw.

“Role of infections in causing nervous system diseases: Questions answered”

Question.17.Diffrentiate between Tubercular Meningitis and Pyogenic Meningitis.

Answer.

Question.18.Write briefl on Myasthenia Gravis.

Answer. An acquired autoimmune disorder causing skeletal muscle fatigability and weakness which can be present at any age is called as myasthenia gravis.

Myasthenia Gravis Symptoms And Signs

Muscular weakness: There is repetitive contraction with tendency to recovery of motor power after inactivity

• Ocular muscles: The ocular muscles are fist to be involved.
  There is presence of double vision or Ptosis. Symptoms are asymmetrical.
• Limb weakness: It may involve proximal or distal limbs.
• Bulbar muscle weakness: It leads to the loss of facial expression, inability to whistle, diffilty with speech,chewing and swallowing.
• Respiratory muscle involvement: It leads to shortness of breath and ventilatory failure.

Myasthenia Gravis Management

• Cholinesterase inhibitors, i.e. pyridostigmine 30 to 120 mg or neostigmine 15 to 45 mg TDS is given.
• Thymectomy is performed as soon as feasible in any antibody positive patient with symptoms not confied to extraocular muscles.
• Plasma exchange is done
• IV immunoglobin 0.4 gm/kg/day for 5 days is given.
• Immunosuppressant: Azathioprine 2.5 mg/kg body weight is helpful in reducing dosage of steroids necessary and allows steroids to withdraw.

Question.19. Describe the clinical and diagnostic features of Tberculous Meningitis.

Answer.

Tberculous Meningitis Clinical Features

Tberculous Meningitis Symptoms

• Fever coming with rigors.
• Headache which is very severe (bursting in character) mainly in frontal region radiating down to back.
• Vomiting
• Convulsion in children
• Malaise
• Severe photophobia
• Ptosis: Due to raised intracranial tension
• Stiffess in neck and back
• Pain in neck
• Impairment of consciousness i.e. confusion, delirium and coma.

Tberculous Meningitis Signs

• Head retraction is present in infants and children.
• Neck rigidity, i.e. bending of neck causes pain and spasm of neck muscles or it is diffilt to bend the neck.
• Kernig’s sign is positive
• Brudzinski’s sign is also positive if patient is conscious.
• Presence of papilledema
• Presence of cranial nerve palsies

Tberculous Meningitis Diagnostic Features

• Person with history of contact with tubercular patient presenting with low grade fever, ill health, weight loss, odd behavior, headache should make one suspect tubercular meningitis.
• Diagnosis shall be confimed by the lumbar puncture.

CSF examination reveals following results:

• CSF is straw colored, clear but when allowed to stand, a fie clot, i.e. spider web is formed.
• Lymphocyte count is high
• Protein content is high
• Glucose is low
• In acute cases, polymorphs may predominate AFB stain can be positive. Culture or AFB is positive in 80% of cases
  CT or MRI brain may show meningeal enhancement or hydrocephalous

Question.21. Describe causes, clinical features, treatment and complication of meningitis.

Answer.Inflmmation of the meninges is called as meningitis.

Meningitis Causes

Infectious causes:

Bacterial:

• Common: N. meningitides, S. pneumoniae, H.inflenza, M tuberculosis
• Neonatal: Group B streptococcus, E. coli, L.monocytogenes
• Uncommon: S. aureus, Ps. Areuginosa
• Rare: Salmonella, Shigella, N. gonorrhea

Viral:

• Common: Mumps, Echovirus, Coxsackie virus A and B, Genital herpes virus 1 and 2
• Neonatal: Other herpes virus, Epstein­Barr virus,
  Varicella zoster virus
• Uncommon: Cytomegalovirus, HIV, Lymphocytic choriomeningitis virus
• Rare: Adenovirus Types 3 and 7, Arbovirus

• Protozoa: Naegleria
• Fungal: Cryptococcus neoformans, Candida
• Spirochaetal: Leptospirosis, Syphilis and Lyme disease
• Ricketssial: Typhus fever

Non­infectious causes

• Malignant: Leukemic meningitis Other non-infectious causes:
• Sarcoidosis, connective tissue disease, systemic lupus erythematosus,
  Sjögren’s syndrome
• Vasculitis: Granulomatous polyangiitis, Eosinophilic granulomatous polyangiitis, CNS vasculitis

Meningitis Clinical Features

Meningitis Symptoms

• Fever coming with rigors
• Headache which is severe mainly in frontal region radiating down to back
• Vomiting
• Convulsion in children
• Malaise
• Severe photophobia
• Ptosis due to raised intra cranial tension
• Stiffess in neck and back
• Pain in neck
• Impairment of consciousness, i.e. confusion, delirium and coma

Meningitis Signs

• Head retraction is present in infants and children.
• Neck rigidity, i.e. bending of neck causes pain and spasm of neck muscles or it is diffilt to bend the neck.
• Kernig’s sign is positive
• Brudzinski’s sign is also positive if patient is conscious.
• Presence of papilledema
• Presence of cranial nerve palsies

Meningitis Treatment

Empirical treatment should be given before CSF culture and
Gram stain report.

Treatment should be directed to the most common microorganism present in particular age group.

Meningitis Antibiotic treatment

• Ceftriaxone or cefotaxime is given against S. pneumonia,H. inflenzae, Group B streptococci and N. meningitides.
  In this vancomycin can be added to cover cephalosporin resistant S. pneumonia. Ampicillin can be added to cover L. monocytogens in neonates of less than 3 months and more than 55 years of age.
• Ceftazidime is active against P. aeuroginosa and is preferred over ceftriaxone or cefotaxime in hospital acquired meningitis.
• Choice of empirical antibiotics in pyogenic meningitis is:
• In neonates or infants of less than 3 months: Ampicillin 100 to 50 mg/dL + Ceftriaxone 500 to 1000 mg/kg/day or cefotaxime 50 mg/kg
• In children and adults: Ceftriaxone 500 to 1000 mg/kg/day or cefotaxime 50 mg/kg + vancomycin 60 mg/Kg
• Adults more than 55 years: Ampicillin 3 gm TDS or QDS + Ceftriaxone 2gm BD or cefotaxime 50 mg/kg + vancomycin 1gm 8 hourly
• In hospital acquired meningitis, post­traumatic or postsurgical, immunocompromised patients: Ampicillin 3 gm TDS or QDS + Ceftazidime 2 gm 8 hourly + vancomycin 1gm 8 hourly.

“How does Alzheimer’s disease impact the nervous system? FAQ explained”

Duration Of Antibiotic Therapy

• One week for H. inflenzae and N. meningitides infection
• S. pneumoniae for two weeks
• L. monocytogenes and Gram­negative bacilli infections for 3 weeks

Adjunctive Therapy

Dexamethasone 0.4 mg/kg BD for 4 days with fist dose of antibiotic.

Supportive Therapy

• Patients having raised intra­cranial pressure should be treated in ICU.
• IV mannitol, hyperventilation and elevation of patient’s head to 30° is done to decrease raised intracranial pressure.

Treatment

Emperical treatment should be given before CSF culture and Gram stain report.

Treatment should be directed to the most common microorganism present in particular age group.

Antibiotic Treatment

• Ceftriaxone or cefotaxime is given against S. pneumonia,H. inflenz, Group B streptococci and N. meningitides.
  In this vancomycin can be added to cover cephalosporin resistant S. pneumonia. Ampicillin can be added to cover L.monocytogens in neonates of less than 3 months and more than 55 years of age.
• Ceftazidime is active against P. aeuroginosa and is preferred over ceftriaxone or cefotaxime in hospital acquired meningitis.
• Choice of empirical antibiotics in pyogenic meningitis is:

• In neonates or infants ofless than 3 months: Ampicillin 100 to 50 mg/dL + Ceftriaxone 500 to 1000 mg/kg/day or cefotaxime 50 mg/kg
• In children and adults: Ceftriaxone 500 to 1000 mg/kg/ day or cefotaxime 50 mg/kg + vancomycin 60 mg/kg
• Adults more than 55 years: Ampicillin 3 gm tds or QDS + Ceftriaxone 2 gm BD or cefotaxime 50mg/kg + vancomycin 1gm 8 hourly
• In hospital acquired meningitis, post­traumatic or post­surgical, immunocompromised patients—Ampicillin 3 gm tds or qds + Ceftazidime 2gm 8 hourly+ vancomycin 1 gm 8 hourly.

Duration of Antibiotic Therapy

• One week for H. inflenzae and N. meningitides infection
• S. pneumonia for two weeks
• L. monocytogenes and Gram­negative bacilli infections for 3 weeks.

Adjunctive Therapy

Dexamethasone 0.4mg/kg BD for 4 days with fist dose of antibiotic.

Supportive Therapy

• Patients having raised intra­cranial pressure should be treated in ICU.
• IV mannitol, hyperventilation and elevation of patient’s head to 30° is done to decrease raised intra-cranial pressure.

Complications

• Neurological defiiencies: Hemiplegia, aphasia, hemianopia,blindness, deafness.
• Mental deterioration
• Cerebritis, brain abscess, focal fis, auditory impairments,sub­dural empyema, internal hydrocephalus.

Question.22. Discuss causes and management of unconsciousness.

Answer. Causes of Unconsciousness

Decrease in the cerebral perfusion:

Inadequate vasoconstriction mechanism

• Postural hypotension
• Vasovagal shock
• Anti­hypertensive drugs
• Carotid sinus syncope.

Hypovolemia:

• Addison’s disease
• Due to blood loss i.e. hemorrhage.

Decrease in the venous return

• Mediastinal compression
• Micturition
• Cough
• Straining during defecation.

Decrease in cardiac output

• Myocardial infarction
• Pulmonary embolism
• Aortic stenosis
• Cardiac temponade.

Arrhythmias

• In AV blocks
• Supraventricular tachycardia
• Ventricular asystole
• Ventricular tachycardia.

Cerebrovascular disturbances

• Hypertension
• Transitory ischemic attck
• Vertebrobasilar insuffiency.

Non-circulatory causes:

• Anemia
• Anxiety neurosis
• Hypoxia.

Management

• All the medical/dental procedure or treatment is stopped.
• Remove instruments from oral cavity such as rubber dam,gauze, cottn etc.
• Patient is kept in Trendelenburg position, i.e. patient is kept in a head low and feet up position.
• Loose tighten clothing of patient.
• Aromatic fumes inhalation is given or sprinkle cold water on face of patient for reflx stimulation.
• If recovery is gained escort patient home.
• If recovery is not gained Injection Atropine 0.6 mg IM or I.V. is given.
• If still recovery is not gained look for hypoglycemia and Addison’s crisis
• Start basic life support
• Summon medical help.

Question.23. Describe the CSF picture of pyogenic meningitis and tubercular meningitis.

Answer.

“Early warning signs of gaps in understanding nervous system disease basics: Common questions”

Question.24. Discuss the causes of headache.

Answer. The causes of headache are:

Intracranial and local extracranial

• Trauma leads to contusional or post­traumatic headache
• Intracranial inflmmations: Meningitis, encephalitis, cerebral abscess.
• Vascular headaches: Hypertension, cerebral or subarachnoid hemorrhage, intracranial aneurysm;vasodilator drugs like nitrites and histamine,adrenaline.
• Menopausal: Alcohol hangover or withdrawal, coffe withdrawal. Giant cell arteritis (temporal arteritis),thrombosis of intracranial venous sinus.
• Traction headache: Pain produced by intracranial arterial displacement and distortion of the dura, usually caused by space occupying lesions or raised intracranial pressure or low intracranial pressure (intracranial hypotension).
• Post-lumbar puncture headache: Low CSF pressure headache.
• Cough headache: A benign syndrome of severe headache which accompanies coughing, straining or sneezing can be due to posterior fossa tumour.

• Cranial neuritis and neuralgias: This is of sensory nerves of scalp, e.g. orbital neuralgia, or neuralgia of auriculotemporal, posterior auricular or great occpital nerves, herpes of Gasserian ganglion.

General Or Systemic Causes

• Anoxemia: Anemia, carbon monoxide or carbon dioxide poisoning.
• Toxic: Fevers, uremia, eclampsia, metallic poisoning,”alcoholic” hangover, postconvulsive, drugs like quinine, tobacco, cocaine, morphine, sulphonamides.
  Pelvic or gallbladder disease, constipation, intestinal stasis. Nervous exhaustion.
• Metabolic factors: Hypoglycemia, alkalosis or acidosis.
• Hemopoietic factors: Essential polycythemia,thromobasthenia.

Referred pain

• Eyes: Errors ofrefraction, glaucoma, iritis, etc.
• Ears: Otitis, mastoiditis, vestibular nerve lesions,
• Eustachian tube block, tumors of middle and inner ear.
  Teeth: Impacted teeth, infected tooth sockets and dental roots.
• Paranasal sinuses: Infection of paranasal sinuses may cause localized pain.
• Neck: Diseases of upper cervical spine may be associated with both occipital and frontal pain.
• Psychogenic: Common cause of headache in depression.
• Tension (muscle contraction) headache:
• Pain resulting from sustained contraction of skeletal muscles of the neck, frontalis, occipital muscles due to emotional tension.
• Exertional headache:
  Headache may come on during exertion and persist for few hours afterwards.

Other primary headaches:

• Hypnic headache syndrome is a late onset disorder and usually wakes up the patient from sleep at around the same time every night.
  The headache is usually treatable with flnarizine and lithium.
• Exploding head syndrome can occur any time during day or night.

Question.25.Write short note on defiition and classifiation of epilepsy.

Answer. Epilepsy is defied as condition characterized by the recurrent episodes primarily of cerebral origin in which there is disturbance of movement, sensation, behavior and consciousness.

Classifiation

Classifiation of epileptic seizures modifid in 1981 Partial or focal seizures:

Simple partial seizures (awareness preserved)
Depending on the concomitant signs, they are:

• Motor
• Sensory
• Visual
• Versive
• Psychomotor

Complex partial seizures (awareness lost)

Depending on the area involved due to spread, they are:

• Temporal lobe
• Frontal lobe

Secondary generalized partial seizures

Primary generalized seizures:

• Tonic clonic (grand mal)
• Tonic
• Absence (petit mal)
• Akinetic
• Myoclonic
• Infantile spasms

Unclassifid seizures:

Seizures which do not fi into above two categories;

• Neonatal seizures
• Infantile spasms

Question.26.Write short note on panic attck.

Answer.

Panic attacks are discrete episodes of paroxysmal severe anxiety and are characterized by severe and frightening autonomic symptoms, i.e. shortness of breadth, palpitations, excessive perspiration; dizziness,faintness and chest pain.
Many patients believe they are in immediate danger of death or collapse and seek urgent medical attntion.

Typical Feature Of Panic Attack

• It is of sudden onset and short duration
• It shows rapidly escalating physical and psychological
  Symptoms
• Presence of incapacitating symptoms of breadthness and/or palpitations
• Fear of impending death, collapse or loss of control
• Rapid escape from situation where attck is occurred
• Sometimes panic attcks are labeled nocturnal when they occur at night only
• Panic attck in social phobia is restricted to feared social situations
• Panic attck in panic disorder occurs unexpectedly in social encounters and when person is alone.

Diagnostic Guideline For Panic Attack

• A panic attck is characterized by all ofthe following:
• A discrete episode of intense fear or discomfort
• It starts abruptly
• It reaches maximum intensity within a few minutes
• It lasts for at least several minutes
• At least four symptoms are present (including at least one autonomic symptom)
• The attack is not caused by a physical disease, an organic mental disorder, or another condition such as schizophrenia, mood disorder or somatoform disorder.
• Panic attck may accompany any anxiety disorder, but a specifi diagnosis of panic disorder can be made if they occur frequently and unexpectedly.

Management

Psychological:

• Helping patients to understand that their symptoms are not caused by serious physical ailment.
• Relaxation training can be helpful, but severely ill patients are more likely to benefi from cognitive behavior therapy.
• Exposure therapy can be formed under supervision of a behavior therapist.

Drugs:

• High dose benzodiazepines, e.g. alprazolam are effctive but can cause substantial depression and should be prescribed in severely ill patients who have not responded to other treatment approaches.
• Anti­depressant drugs, i.e. imipramine, clomipramine and selective serotonin re­uptake inhibitors, i.e. paroxetine are as efficacious in reducing anxiety symptoms, lessening agoraphobia and minimizing overall impairment.

Question.27. Write short note on depression.

Answer. Depression is defied as depressed mood on a daily basis for a minimum duration of two weeks.

Depression is present in a quarter to half of all mental patients.

Etiology

• Genetic factors: They play a major role in mood disorders and their effct is stronger in patients with more severe biological symptoms.
  In twin studies of bipolar disorder, average concordance rate is 65% in monozygotic twins and 14% in dizygotic twins.
• Social factors: Events associated with depression are generally ’loss events’ such as loss of a job, relative or tend, money, health or status.
  Other factors that adversely affct the response to the events can be, a working class background, lack of confiing relationship with a spouse, unemployment, loss of a parent before l l years of age.
• Biological markers for depression: They show strong associations, particularly with the somatic (endogenous) syndrome.
  False­positive results occur in the presence of various medical disorders.
  Dexamethasone suppression test is the most important biological marker.
• Circadian rhythms and related markers: They have also been found abnormal in depression.
  This is suggested by the diurnal variations in mood, early morning waking and the sometimes periodic course, for example, yearly attcks of illness.
• Psychological factors: Repeated trauma, stressful life events and disturbed marital and interpersonal relationships.

Clinical Features

• General: Hopelessness, helplessness, low mood, low self esteem, reduced energy, suicidal thoughts, loss of interest,poor concentration, guilt, pessimism, depersonalization.
• Somatic: Appetite disturbance, weight change, constipation,amenorrhea, low libido, sleep disturbance
• Anxiety: Tension, apprehension, phobias.

Management

• Antidepressants are used in all phases of the treatment of major depression, acute management, continuation therapy and maintenance or prophylactic treatment.
• Tricyclic drugs: They increase recovery rate signifiantly,but have a wide range of side effcts. These lead to noncompliance and limit usefulness in illnesses of mild to moderate severity.
  The dose of tricyclics should be initially low and increased gradually.
• Selective serotonin re-uptake inhibitors: They are effctive drugs and are bettr tolerated at therapeutic doses than other compounds.
• If patient is not responding to anti­depressant drugs ECT treatment should be given. Usually 6 to 10 ECTs are effctive in resolving acute depression.
  As course is completed prophylactic treatment should be given to prevent relapse
• Congenitive psychotherapy should also be done

“Asymptomatic vs symptomatic effects of ignoring nervous system disease principles: Q&A”

Question.28. Write short note on anxiety neurosis.

Answer.

Anxiety is a normal response to threat or stressful events and is usually short lived and controllable.

It probably functions as an ‘alarm mechanism’ to prepare an individual for a physical response to perceived danger (the fiht or—flght’ response).

Anxiety symptoms are considered clinically signifiant when they:

• Are abnormally severe
• Are unusually prolonged
• Occur in absence of stressful circumstances
• Impair physical, social or occupational functioning

Features of anxiety neurosis

Anxiety Neurosis Psychological

• Fear and apprehension
• Inner tension and restlessness
• Irritability
• Impaired ability to concentrate
• Increased startle response
• Increased sensitivity to physical sensations
• Disturbed sleep

Anxiety Neurosis Physical

• Increased muscle tension
• Tremor
• Sweating
• Palpitations
• Chest tightness and discomfort
• Shortness of breath
• Dry mouth
• Diffilty in swallowing
• Diarrhea
• Frequency of micturition
• Loss of sexual interest
• Dizziness
• Numbness and tingling
• Faintness

Anxiety Neurosis Management

Defiitive need for treatment depends on severity of symptoms,degree of personal distress, level of occupational and social impairment.

• Benzodiazepines are effctive anxiolytic drugs but can cause sedation and have potential for dependence.
  They should be given in short courses.
• Other drugs include certain tricyclic antidepressants e.g.imipramine (50 300 mg/d), buspirone (15–45 mg/d) and venlafaxine (serotonin—noradrenaline re uptake inhibitor 75 mg/d) none of which have same potential for psychological or physical dependence.
• Behavior therapy in form of relaxation training, systemic desensitization and cognitive therapy.
  Psychotherapy and family education is must.

Question.29. Describe clinical features, diagnosis and management of tubercular meningitis.

Answer.

Tubercular Meningitis Clinical Features

Tubercular Meningitis Symptoms

• Headache
• Vomiting
• Low grade fever
• Lassitude, i.e. weariness or exhaustion
• Depression
• Confusion
• Behavior changes.

Tubercular Meningitis Signs

• Meningism may be present:
• Oculomotor palsies
• Papilledema
• Depression of conscious level
• Focal hemisphere signs.

Tubercular Meningitis Diagnosis

• Person with history of contact with tubercular patient presenting with low grade fever, ill health, weight loss, odd behavior, headache should make one suspect tubercular meningitis.
• Diagnosis shall be confimed by the lumbar puncture. CSF examination reveals following results:

• CSF is straw colored, clear but when allowed to stand,a fie clot, i.e. spider web is formed.
• Lymphocyte count is high
• Protein content is high
• Glucose is low
• In acute cases, polymorphs may predominate
• AFB stain can be positive. Culture or AFB is positive in 80% of cases
• CT or MRI brain may show meningeal enhancement or hydrocephalous

Tubercular Meningitis Management

General management

• Maintenance of nutrition, hydration and electrolyte balance.
• Case of bowel and bladder
• Nursing should be good
• If there are convulsions, anticonvulsants are given.

Tubercular Meningitis Treatment

• Antitubercular drugs: Antitubercular drugs—
  Rifampicin 600 mg/day + Isoniazide (600 to 900 mg/day) + Pyrazinamide (1.5 gm) should be given.
  Treatment with this regimen is given for 2 months.
  This is followed by rifampicin 600 mg/day + Isoniazide (600 to 900 mg/day) for 12 to 18 months.
• Steroids: Prednisolone 40–60 mg/day to reduce toxicity, pia­arachnoid adhesions and felling of well­being.

Question.30. Write short note on examination of cerebrospinal flid.

Answer.

Normal CSF is colorless, clear.

• Presence of blood indicates either local trauma or subarachnoid hemorrhage especially fresh.
• Xanthochromia or yellowish coloration of CSF is found in cerebral hemorrhage and when pus is present in CSF in considerable amount.
• Turbidity when present indicates excess of polymorphonuclear cells (meningitis).
• A clot or cob web may form in cases of tuberculous meningitis.
• Of the biochemical tests, protein content is 30–40 mg/dL and sugar 80 mg/DL.
• Normal CSF contains a small number of cells mostly lymphocytes (0–5/cumm).
• Excess of cells in the CSF indicate meningeal irritation.
• In cases of meningitis, CSF is examined for bacteria by gram’s staining.
• A culture examination of CSF is often carried out in suspected infective process for identifying the causal organism.
• CSF examination has animportant role indiagnosing bacterial and viral diseases, but its role in cases of cerebral hemorrhage is now being taken over by CT scan because of hazards involved.
• Colloidal reactions in the form of colloidal gold reaction is of value in cases of general paralysis of insane (GPI) and diffrentiates it from other form of neurosyphilis.
• Serological reactions like wasserman reaction are also of help in cases of neurosyphilis.

Question.31. Diffrentiate between syncope and epilepsy.

Answer.

“Can targeted interventions improve outcomes for nervous system disease patients? FAQs provided”

Question.33.Write short note on transient ischemic attck.

Answer.

These are transient attcks of loss of function of one part of the brain coming suddenly and lasting for variable period of time ranging from minutes to hours.

• Since arteries supplying the brain are end arteries so any pathology which produces obstruction to the flw of that vessel shall produce symptoms in the distribution of that blood vessel.
• Internal carotid artery is one of the commonest cerebral vessel which is involved by atherosclerosis and patient complains of transient disturbances due to localized cortical ischemia in the form of confusion contralateral hemiparesis and sensory loss.
  There may be aphasia (if lesion on left side) and hemianopic visual loss.
• Most commonly occlusion is in the common carotid artery and one may be able to appreciate diminished pulsation in the vessel in the neck.
  When obstruction is severe a bruit may be auscultated at the site.
• Obstruction of other arteries like anterior cerebral artery, middle cerebral artery and posterior cerebral artery produce picture almost like above except for litte variations depending on the occlusion site.
• On the other hand involvement of posterior circulation (basilar artery, vertebral artery, postinferior cerebellar artery) produces a picture of crossed hemiplegia, hemisensory loss and hemianopic visual loss. In addition patient has impairment of consciousness, small fied pupils,pseudobulbar palsy and quadriplegia seen mainly.
• In basilar artery lesions while cases with posterior inferior cerebellar artery involvement are associated with severe vertigo, vomiting, dysphasia and diplopia. In addition there is some degree of cerebellar defiiency with hypotonia and incoordination on the side of lesion, analgesia and thermoanesthesia on the face on the side of lesion and on the trunk and limbs on opposite side.
• Again neurological defiits shall be depending on which branch of the vessel is involved.

Question.34. Write short note on facial pain.

Answer. Various number of conditions are involved in the pain localized to face.
These may range from pain arising from diseases of teeth, gums, sinuses, temporomandibular joint to various causes.

Facial neuritis

• It is a form of inflmmation of the nerve of the face and scalp.
• It generally occurs as a complication of a septicemic estate or due to involvement by a neurotropic virus.
• Onset is usually acute and pain is confied to the face and scalp, occurring in paroxysms lasting for several hours and very often till the end of the day when the patient is exhausted.
• If the character ofpain is dull aching which is intensifid by exposure to cold and often occurs in the form of shooting pains in the distribution of the nerve.
  Sometimes the pain is so severe that the patient is unable to sleep.
• Physical examination shows presence of hyperalgesia in the distribution of nerves including face and scalp.
  Nerve trunk is tender on pressure.

Myofascial Pain

• It is a form of dull constant pain with local tenderness of the muscles of jaw.
• There is often pain and diffilty in opening the mouth.
• This pain is related to bad and improper habits of clenching and grinding of teeth. This type of habit is present amongst hysterical persons especially women who often clench and grind their teeth.
• There is no physical fiding in such people except that these people have an emotionally labile personality and often suffr from depression.
• Treatment consists in giving them assurance, analgesics and tricyclic antidepressants.

Trigeminal Neuralgia

Trigeminal neuralgia is also called as Tic Douloureux.

A disorder characterized by the *paroxysmal attcks of neuralgic pain with affction of one or more division of trigeminal nerve.

The pain involves the third and second divisions equally and rarely the fist.

Clinical Features

• Pain is unilateral and is confined to one of the three divisions of nerve. Pain is sharp and onset is sudden. The pain is only of a few seconds.
• During the attcks there is flshing of face, i.e. redness of the face.
• Dilatation of pupil is present.
• There is excessive lacrimation
• After repeated attcks skin becomes shiny and hair in the area becomes gray.
• Sometimes secretion of nasal mucus and saliva may occur in the side of pain.

Etiology

Trigeminal neuralgia is spontaneous and following exposure to cold wind, blow on face, or chewing or eating, drinking hot or cold flid and washing the face.

Management

• Elimination of all possible sources of infection.
• Drugs:

• Analgesics: Potent analgesics must be used with caution because of danger of habituation.
• Carbamazepine: 100–200 mg BD a day and increasing the dose to 600–800 mg per day.
• Phenytoin sodium: 0.1 gm TDS when carbamazepine is not tolerated.
• Vitamin B12: 1000 μg IM daily for two weeks.
• Injection ofalcohol: It is given in affcted nerve, or gasserian ganglion.
  If more than one division is affcted inject 10 minims of 90% alcohol after local anesthesia with 2–3 drops of procaine.
• Microvascular decompression: In this there is separation of blood vessels is done which are in contact with trigeminal nerve roots.
  There is also insertion of non absorbable sponge which provide relief of pain in most of the patients.
• Radiofrequency thermocoagulation: This procedure is carried out at the trigger spot or site of pain origin which is localized by electric stimulation of needle inserted in trigeminal ganglion and leads to permanent relief.
• Surgery: In this selective or complete preganglionic section of trigeminal root is done.
  This technique can lead to disadvantages such as permanent dysesthesiae.
  Another bettr technique is percutaneous electrocoagulation of preganglionic rootlets corresponding to trigger zone, the temperature of probe being so regulated as to coagulate small thinly myelinated pain fiers but preserving most heavily myelinated touch fiers.

Post Herpetic neuralgia

• Herpes zoster commonly involves the ophthalmic division of the 5th nerve characterized by vesicular eruption on the face and pain.
  When herpes heals it leave behind neuralgic pain in the distribution of previous eruptions.
• It is a form of continuous aching or burning pain at that site on face and patient is often in great agony.
• Treatment is by analgesics. Sometimes codeine phosphate may have to be given.
• In some severe cases the course of post herpetic neuralgia may be prolonged one.

Migrainous neuralgia

• It is often called ‘Facio plegic migraine’ where there are attcks of severe pain especially at night and the pain is confied to face and around one eye.
  This form of disease is common in men especially middle aged and the attck may be brought on after a bout of alcohol.
• The pain may last for our. Because of associated vomiting and paroxysmal nature of disease it is called ‘migrainous neuralgia’ or ‘facioplegic migraine.
  There is headache and patient complains of some degree of congestion in the face.
• Treatment is by analgesics but response is poor.

Arthralgia Of Temporomandibular Joint

• It may be in the form of rheumatoid arthritis or ankylosing spondylitis when there is pain and swelling of the joint.
• Movements at the joint are limited and patient complains of pain at the site as well as along the jaw confied to face.
  Involvement of other joints in the body shall favor the diagnosis.
• Treatment is by heat and anti-inflmmatory drugs as well as by exercises of the joint involved with adequate periods of rest.

Temporal Arteritis

• It is a form of collagen disorder of unknown etiology which involves mainly the arteries.
• It commonly occurs in elderly age group.
• Patient may complain of pain on the face, jaw, mouth and tongue in the distribution of branches of external carotid artery.
• This pain worsens of if on eating and opening of the mouth.
• Since temporal arteritis is a collagen disorder there is a form of inflmmation of the arteries.

Question.35. Write short note on temporal lobe epilepsy.

Answer.

Temporal lobe epilepsy is a form of focal epilepsy,a chronic neurological condition characterized by recurrent seizures.

Temporal lobe epilepsy (TLE) is the most common single form causing refractory epilepsy.

Temporal lobe epilepsies are a group of medical disorders in which humans and animals experience recurrent epileptic seizures arising from one or both temporal lobes of the brain.

Types

• Two main types are internationally recognized:
  Medial temporal lobe epilepsy (MTLE): arises in the hippocampus,parahippocampal gyrus and amygdala which are located in the inner aspect of the temporal lobe.
• Lateral temporal lobe epilepsy (LTLE): arises in the neocortex on the outer surface of the temporal lobe of the brain.

Symptoms And Signs

• Simple partial seizures (SPS) involve small areas of the temporal lobe such as the amygdala or the hippocampus.
  The term “simple” means that consciousness is not altered.
  In temporal lobe epilepsy SPS usually only cause sensations. These sensations may be mnestic such as déjà vu (a feeling of familiarity), jamais vu (a feeling of unfamiliarity), a specifi single or set of memories, or amnesia.
  The sensations may be auditory such as a sound or tune, gustatory such as a taste, or olfactory such as a smell that is not physically present.
  Sensations can also be visual, involve feelings on the skin or in the internal organs.
  The lattr feelings may seem to move over the body.
  Dysphoric or euphoric feelings, fear, anger, and other sensations can also occur during SPS.
  Often, it is hard for persons with SPS of TLE to describe the feeling.
  SPS are often called “auras” by lay persons who mistake them for a warning sign of a subsequent seizure.
  In fact, they are actual seizures in and of themselves.
  Persons experiencing only SPS may not recognize what they are or seek medical advice about them.
  SPS may or may not progress to the seizure types listed below.
• Complex partial seizures (CPS) by defiition are seizures which impair consciousness to some extent.
  This is to say that they alter the person’s ability to interact with his or her environment.
  They usually begin with an SPS, but then the seizure spreads to a larger portion of the temporal lobe resulting in impaired consciousness.
  Signs may include motionless staring, automatic movements of the hands or mouth, altered ability to respond to others, unusual speech,or unusual behaviors.
• Seizures which begin in the temporal lobe but then spread to the whole brain are known as secondarily generalized
  Tonic­Clonic Seizures (SGTCS).

Treatment

• In temporal lobe epilepsy, the most commonly used drugs are phenytoin, carbamazepine, primidone, valproate and phenobarbital.
• Newer drugs, such as gabapentin, topiramate, levetiracetam,lamotrigine, pregabalin, tiagabine, lacosamide, and zonisamide promise similar effctiveness, possibly with fewer side-effcts.
• For patients with medial TLE whose seizures remain uncontrolled after trials of several antiepileptic drugs,resective surgery should be considered.

“Differential applications of central vs peripheral nervous system diseases: Questions answered”

Question.36. Write in brief signs, symptoms and treatment of epilepsy.
Or
Write short note on epilepsy.

Answer. Epilepsy is defied as the group of disorders in which there are recurrent episodes of altered cerebral functions associated with paroxysmal and hypersynchronous electrical discharge of cerebral neurons.

Symptoms

• Aura is present which means there is warning of the attck.
• Loss of consciousness
• Patient fall over the ground
• Irritability
• Depression and abnormal feelings
• Giddiness and abdominal cramps
• When patient awakes he complains of headache

Signs

• Tonic contraction of muscles and epileptic cry produced by forceful expiration through the partly closed vocal cords.
• Tonic convulsions of two sides of the body occur with head and eyes rotated to one side.
• Tonic phase followed by clonic phase, i.e. after completion of tonic phase patient remain unconscious for few minutes to half an hour.
• Frothing of mouth and increased salivation from the mouth.
• During clonic phase patient may bite his tongue and pass urine and stools.

Treatment

Treatment of epilepsy is directed at the elimination of the cause of seizures, suppressing the expression of seizures and dealing with psychosocial consequences.

Immediate treatment ofa seizure:

• Patient should always be migrated to the safer place.
• Loose the clothes around the neck and move people away from the place so that patient can breathe fresh air easily.
• At the time of convulsion, helpers are not allowed to put the figers inside the mouth. Tongue biting should be prevented by puttng tightly rolled piece of cloth in mouth.
• As convulsion ceases, patient is turned into semiplane position and make air passage clear.
• Patient is advised to consult the doctor for medical advice.

Drug therapy:

Choice of the drug depends on type of seizure.

• In localization related epilepsy fist line prophylactics are lamotrigine, carbamazepine (slow­release),oxcarbamazepine, levetiracetam.
• In primary generalized, symptomatic generalized and unclassifid epilepsies, initial therapy should be lamotrigine or valproate (broad spectrum gents).
  Valproic acid is useful in absences and benzodiazepines in myoclonic jerks.
• Patients with refractory generalized epilepsy may benefi from adjunctive treatment with topiramate or levetiracetam, zonisamide, clonazepam, pregabalin.

Various anti­epileptic drugs along with their dosages used in epilepsy are:

Plan of treatment

• Initial regimen: The drug selected must be used in monotherapy.
  The drug should be introduced in small doses, since rapid introduction may cause side effcts.
• Maintenance treatment: The aim should be to find the lowest dose which achieves complete seizure control without side effcts which may be either idiosyncratic or due to intoxication, or chronic.
  Serum anticonvulsant levels are a useful guide to therapy phenytoin (40–80) carbamazepine (20–50), phenobarbitone (40–170),ethosuximide (20–600).
  Valproate 300-600, oxcarbazepine 50–125, lamotrigine 4–60 mmol/L.
  If the optimum level of a single, fist line drug does not control seizures, or if side-effcts develop, the initial drug should be substituted with another fist line anticonvulsant.
  If the second drug also fails to control seizures monotherapy with a third anticonvulsant, or combination therapy with two fist line drugs should be tried.

If a combination of two fist-line drugs is unsuccessful, one of the second­line drugs may be considered.

Drug Withdrawl

It should take place slowly over 2 to 3 months. If patient is receiving more than one drug, each drug should be withdrawn individually.

Question.37. Write in brief signs, symptoms and treatment of facial palsy.
Or
Write signs and symptoms of facial palsy.

Answer. It is the paralysis of the facial nerve.

Symptoms

• Post auricular pain is common and may precede paralysis by 2 days.
• Spontaneous complains of loss of taste sensation,hyperacusis and watering of eyes.
• Sweating is less over the affcted side.

Signs

• Forehead cannot be wrinkled; frowning lost.
• Eye of affcted cannot be closed.
  On attmpting closure,eyeball turns upwards and outwards (Bell’s phenomena).
• On showing the teeth, the lips do not separate on affcted side. Whistling not possible.
  Articulation of labial components diffilt. Naso-labial fold flttned out.
  Angle of mouth on affcted side droops with dribbling of saliva.
• Cheek puff out with expiration because of buccinator paralysis.
  Food collects between teeth and paralyzed cheek.
  Fluid runs out while drinking.
• Base of tongue is lowered.
• Vesicles within the external auditory meatus and ear drum in Ramsay Hunt syndrome.
  Pain may precede facial weakness. Deafness may result.

Treatment

• Local heat: Infrared or moist heat over the face or parotid region or both if there is tenderness of nerve trunk.
• Local treatment ofmuscles: The patient should massage the facial muscles with bland oil for twice a day for 5 min.
  The massaging movements should start from the chin and lower lip and are directed upwards.
  With return offunction the patient should practice movements of various muscles of face before a mirror.
• Prevention offacial sagging: Application of strips of adhesive tape is done to lift up the angle of mouth.
  Tape is attched to the temple and extends down in a V shaped fashion to upper and lower lips.
• Protection of eye: It is done with dark glass or eye patch.
  Mild zinc boric solution is used to wash the eye to prevent conjunctivitis.
• Corticosteroids: If seen under a week of onset. Prednisolone 40 mg/day for 4 days and in tapering doses for over next 6 days helps by reducing secondary edema.
• Anti-virals: Acyclovir, Valacyclovir or Famciclovir in combination with steroids, ifstrated within 3 days ofonset.
• Surgery: Decompression of facial nerve in second or third week cannot inflence favorably natural course of Bell’s palsy. Cases which fail to recover after 9 months in them anastomosis of facial nerve with accessory or preferably hypoglossal nerve is considered, or plastic surgery in cases of total paralysis with atrophy of muscle.

“Steps to master nervous system diseases for exams: Study plans vs mock tests: Q&A guide”

Question.38. Write on causes of meningitis and discuss in detail bacterial meningitis.
Or
Describe the etiology, clinical features and management of bacterial meningitis.

Answer.

Following are the causes of meningitis:

• Neonates: E.coli

Children:

• H. inflenzae
• S. pneumoniae
• N. meningitidis.

Adults:

• Young people: Meningococcus
• Older people: S. pneumonia.

Elderly and immunocompromised persons:

• Pneumococcus
• Listeria
• Tuberculosis
• Gram­negative organism
• Cryptococcus.

Viral:

• Enterovirus
• Herpes simplex virus
• Mumps virus
• Inflenza virus
• Japanese encephalitis virus
• Arbo viruses
• Rabies virus
• HIV.

Nosocomial and post-traumatic meningitis:

• Klebsiella pneumonia
• E.coli
• Pseudomonas aeruginosa
• S. aureus.

Meningitis in special situation:

• CSF shunts staphylococcal
• Spinal procedurespseudomonas.

Bacterial Meningitis

Pathophysiology Involves

• Transmission, colonization and invasion of nasopharyngeal epithelium.
• Survival in the blood stream by evading host immune response.
• Meningeal invasion. Bacteremia may be rapidly followed by seeding of meningeal pathogens and secondary infection of the meninges.
• CSF inflmmatory response.
• Cerebral edema and thrombosis.
• Bacterial meningitis causes loss of cerebrovascular anticoagulation.

Clinical Features

Symptoms

• Fever, malaise headache and vomiting.
• Pain over the neck
• Stiffess over the neck
• Confusion, delirium and coma.

Signs

• Kernig’s sign is positive.
• Neck rigidity, i.e. when neck is bended there is presence of pain and there is spasm of neck muscles.
• Brudzinski’s sign is also positive.
• Photophobia is present
• Cranial nerve palsies most commonly IIIrd, IVth, VIth and VIIth.
• Focal neurological defiits such as nystagmus, aphasia, ataxia and peripheral nerve palsies.
• Partial or generalized seizures tend to be more common in Strep. pneumoniae and HIV meningitis.
• Purpura or petechiae in meningococcal meningitis, with or without features of septic shock.

Diagnosis

• Examination of CSF
  Typical CSF fidings in acute bacterial meningitis:
• Raised WBC count (usually 100–60,000 cells/mL (predominantly neutrophils)
• Reduced CSF glucose (30–40% serum glucose level)
• Raised CSF protein (0.5–5 g/L)
• Gram­staining of CSF is positive in over 90% of cases of hematologically acquired meningitis.
• Blood culture should be performed in all patients with suspected meningitis, and latex agglutination bacterial antigen test or polymerase chain reaction analysis (to detect bacterial DNA) may be performed on blood or CSF to try to obtain a diagnosis.
  Such tests remain positive for several days after administration of antibiotics.
  Laboratory markers of poor prognosis include low peripheral WBC count, thromobocytopenia, absence of CSF pleocytosis and high CSF protein levels.

Management

• For adult patients penicillin G 5 to 10 million units IV 6 hourly.
• Cephalosporins, i.e. cefotaxime 2 gm IV or ceftriaxone 2 gm IV OD is also effctive.
• Patients allergic to penicillin are treated with chloramphenicol 1 gm IV 6 hourly
• Treatment is continued for 7 to 10 days.
• For raised intracranial tension IV mannitol is given which is accompanied by high doses of dexamethasone 4 mg IV 6 hourly.
  The supportive treatment is to maintain nutrition, flid and electrolytic balance.

Question.39.Enumerate fie causes of headache.
Or
Enumerate causes of headache.

Answer. Following are the causes ofheadache:

Intracranial and local extracranial

• Trauma
• Intracranial inflmmations
• Vascular headaches: Hypertension, cerebral or subarachnoid haemorrhage, intracranial aneurysm, vasodilator drugs like nitrites and histamine, adrenaline.
• Traction headache: Pain produced by intracranial arterial displacement and distortion of the dura
• Post­lumbar puncture headache: Low CSF pressure headache.
• Cough headache: A benign syndrome of severe headache which accompanies coughing,straining or sneezing can be due to posterior fossa tumor.
• Cranial neuritis and neuralgias of sensory nerves of scalp, e.g. orbital neuralgia, neuralgia of auriculotemporal, posterior auricular or great occipital nerves.

General or systemic causes:

• Anoxemia: Anaemia, carbon monoxide or carbon dioxide poisoning.
• Toxic: Fever, uremia, metallic poisoning,“alcoholic” hangover etc
• Metabolic factors: Hypoglycemia, alkalosis oracidosis
• Hemopoietic factors: Essential polycythemia,thrombasthenia.

Referred pain

• Eyes: Errors of refraction, glaucoma, iritis, etc.
• Ears: Otitis, mastoiditis, vestibular nerve lesions,
  Teeth: Impacted teeth, infected tooth sockets and dental roots
• Paranasal sinuses: Infection of paranasal sinuses may cause localised pain
• Neck: Diseases of upper cervical spine may be associated with both occipital and frontal pain.

Psychogenic:

• Common Cause Of Headache In Depression.
• Tension (muscle contraction) headache: Pain resulting from sustained contraction of skeletal muscles of the neck, frontalis, occipital muscles due to emotional tension.
• Exertional headache: Headache may come on during exertion and persist for few hours afterwards.

Question.40. Write in brief sign, symptoms and treatment of bacterial meningitis.

Answer.

Following are the causes of meningitis:

• Neonates: E.coli

Children:

• H. inflenzae
• S. pneumoniae
• N. meningitidis.

Adults:

• Young people: Meningococcus
• Older people: S. pneumonia.

Elderly and immunocompromised persons:

• Pneumococcus
• Listeria
• Tuberculosis
• Gram­negative organism
• Cryptococcus.

Viral:

• Enterovirus
• Herpes simplex virus
• Mumps virus
• Inflenza virus
• Japanese encephalitis virus
• Arbo viruses
• Rabies virus
• HIV.

Nosocomial and post-traumatic meningitis:

• Klebsiella pneumonia
• E.coli
• Pseudomonas aeruginosa
• S. aureus.

Meningitis in special situation:

• CSF shunts staphylococcal
• Spinal procedurespseudomonas.

Bacterial Meningitis

Pathophysiology Involves

• Transmission, colonization and invasion of nasopharyngeal epithelium.
• Survival in the blood stream by evading host immune response.
• Meningeal invasion. Bacteremia may be rapidly followed by seeding of meningeal pathogens and secondary infection of the meninges.
• CSF inflmmatory response.
• Cerebral edema and thrombosis.
• Bacterial meningitis causes loss of cerebrovascular anticoagulation.

Clinical Features

Symptoms

• Fever, malaise headache and vomiting.
• Pain over the neck
• Stiffess over the neck
• Confusion, delirium and coma.

Signs

• Kernig’s sign is positive.
• Neck rigidity, i.e. when neck is bended there is presence of pain and there is spasm of neck muscles.
• Brudzinski’s sign is also positive.
• Photophobia is present
• Cranial nerve palsies most commonly IIIrd, IVth, VIth and VIIth.
• Focal neurological defiits such as nystagmus, aphasia, ataxia and peripheral nerve palsies.
• Partial or generalized seizures tend to be more common in Strep. pneumoniae and HIV meningitis.
• Purpura or petechiae in meningococcal meningitis, with or without features of septic shock.

Diagnosis

• Examination of CSF
  Typical CSF fidings in acute bacterial meningitis:
• Raised WBC count (usually 100–60,000 cells/mL (predominantly neutrophils)
• Reduced CSF glucose (30–40% serum glucose level)
• Raised CSF protein (0.5–5 g/L)
• Gram­staining of CSF is positive in over 90% of cases of hematologically acquired meningitis.
• Blood culture should be performed in all patients with suspected meningitis, and latex agglutination bacterial antigen test or polymerase chain reaction analysis (to detect bacterial DNA) may be performed on blood or CSF to try to obtain a diagnosis.
  Such tests remain positive for several days after administration of antibiotics.
  Laboratory markers of poor prognosis include low peripheral WBC count, thromobocytopenia, absence of CSF pleocytosis and high CSF protein levels.

Management

• For adult patients penicillin G 5 to 10 million units IV 6 hourly.
• Cephalosporins, i.e. cefotaxime 2 gm IV or ceftriaxone 2 gm IV OD is also effctive.
• Patients allergic to penicillin are treated with chloramphenicol 1 gm IV 6 hourly
• Treatment is continued for 7 to 10 days.
• For raised intracranial tension IV mannitol is given which is accompanied by high doses of dexamethasone 4 mg IV 6 hourly.
  The supportive treatment is to maintain nutrition, flid and electrolytic balance.

“Role of diagrams in understanding nervous system anatomy: Questions answered”

Question.41. Enumerate causes of meningitis and describe clinical features, complications and treatment of tubercular meningitis.

Answer.

Following are the causes of meningitis:

• Neonates: E.coli

Children:

• H. inflenzae
• S. pneumoniae
• N. meningitidis.

Adults:

• Young people: Meningococcus
• Older people: S. pneumonia.

Elderly and immunocompromised persons:

• Pneumococcus
• Listeria
• Tuberculosis
• Gram­negative organism
• Cryptococcus.

Viral:

• Enterovirus
• Herpes simplex virus
• Mumps virus
• Inflenza virus
• Japanese encephalitis virus
• Arbo viruses
• Rabies virus
• HIV.

Nosocomial and post-traumatic meningitis:

• Klebsiella pneumonia
• E.coli
• Pseudomonas aeruginosa
• S. aureus.

Meningitis in special situation:

• CSF shunts staphylococcal
• Spinal procedurespseudomonas.

Clinical Features

Symptoms

• Fever coming with rigors.
• Headache which is very severe (bursting in character) mainly in frontal region radiating down to back.
• Vomiting
• Convulsion in children
• Malaise
• Severe photophobia
• Ptosis: Due to raised intracranial tension
• Stiffess in neck and back
• Pain in neck
• Impairment of consciousness i.e. confusion, delirium and coma.

Signs

• Head retraction is present in infants and children.
• Neck rigidity, i.e. bending of neck causes pain and spasm of neck muscles or it is diffilt to bend the neck.
• Kernig’s sign is positive
• Brudzinski’s sign is also positive if patient is conscious.
• Presence of papilledema
• Presence of cranial nerve palsies

Clinical Features Of Tuberculous Meningitis

Symptoms

• Headache
• Vomiting
• Low grade fever
• Lassitude, i.e. weariness or exhaustion
• Depression
• Confusion
• Behavior changes.

Signs

• Meningism may be present
• Occulomotor palsies
• Papilledema
• Depression of conscious level
• Focal hemisphere signs.

Management of Tubercular Meningitis

General management:

• Maintenance of nutrition, hydration and electrolyte balance.
• Case of bowel and bladder
• Nursing should be good
• If there are convulsions, anticonvulsants are given.

Complications

• Infection spreads in parenchyma of brain causing meningoencephalitis.
• Involvement of cerebral vessel causes obliterative endarteritis
• Thrombosis of cerebral vessels lead to cerebral infarction
• Delayed complications are development of hydrocephalus optic atrophy, spinal cord compression and cranial nerve palsy.

“Can advanced tools supplement nervous system disease exam preparation? FAQs provided”

Question.42. Write notes on facial pain.

Answer.

Various number of conditions are involved in the pain localized to face.
These may range from pain arising from diseases of teeth, gums, sinuses, temporomandibular joint to various causes.

Facial neuritis

• It is a form of inflmmation of the nerve of the face and scalp.
• It generally occurs as a complication of a septicemic estate or due to involvement by a neurotropic virus.
• Onset is usually acute and pain is confied to the face and scalp, occurring in paroxysms lasting for several hours and very often till the end of the day when the patient is exhausted.
• If the character ofpain is dull aching which is intensifid by exposure to cold and often occurs in the form of shooting pains in the distribution of the nerve.
  Sometimes the pain is so severe that the patient is unable to sleep.
• Physical examination shows presence of hyperalgesia in the distribution of nerves including face and scalp.
  Nerve trunk is tender on pressure.

Myofascial Pain

• It is a form of dull constant pain with local tenderness of the muscles of jaw.
• There is often pain and diffilty in opening the mouth.
• This pain is related to bad and improper habits of clenching and grinding of teeth. This type of habit is present amongst hysterical persons especially women who often clench and grind their teeth.
• There is no physical fiding in such people except that these people have an emotionally labile personality and often suffr from depression.
• Treatment consists in giving them assurance, analgesics and tricyclic antidepressants.

Trigeminal Neuralgia

Trigeminal neuralgia is also called as Tic Douloureux.

A disorder characterized by the *paroxysmal attcks of neuralgic pain with affction of one or more division of trigeminal nerve.

The pain involves the third and second divisions equally and rarely the fist.

“Asymptomatic vs symptomatic effects of outdated study methods: Answered”

Differential Diagnosis Of Facial Pain

Symptomatic trigeminal neuralgia

• Neuralgia indistinguishable from the idiopathic variety may occur as a result of compression of trigeminal root or ganglion, e.g. meningioma, acoustic neuroma, aneurysm of basilar artery, arteriovenous malformations, basilar invagination, epidermoid cholesteatomas in the cerebellopontine angle, as a result of Paget’s disease or osteomalacia.
• Paratrigeminal neuralgia (Raeder’s syndrome): Severe pain in and around one eye accompanied by Horner’s syndrome on the affcted side.
  It is continuous and progressive and is usually caused by a structural lesion, often malignant in the base of the skull involving the paratrigeminal region.
• Multiple sclerosis: Diagnosis of multiple sclerosis should always be suspected in a young patient with trigeminal neuralgia.
• Syringobulbia.
• Painful superior orbital fisure syndrome (TolosaHunt syndrome) caused by granulomatous tissue involving nerves III, IV and VI. Pain with development of ocular palsies and loss of fist division trigeminal sensation.

• Referred pain: Paranasal sinuses, toothache, aural infection.
  Temporomandibular joint dysfunction (Costen’s syndrome)
• abnormality of bite and aggravated by chewing.

Vascular pain:

• Migraine: Episodes of severe and continuous pain,often burning in character in or behind one eye, or in cheek, forehead and temple.
  Often suffsion of conjunctiva and blocking of nostril on that side.
• Temporal arteritis: Pain of dull, throbbing nature with associated scalp tenderness.
  Thickened temporal arteries with reduced or absent pulsations.

Other neuralgias

• Post-herpetic neuralgia: Pain is continuous in nature.
  Vesicles and scars of herpetic infection.
• Glossopharyngeal neuralgia: Pain in tonsillar fossa, back of throat and larynx; may radiate to ear on affcted side. Swallowing is the stimulus most likely to produce pain.

Atypical facial pain

Intermittnt but long lasting pain of aching character which affcts the cheek and upper jaw, often bilateral and occurs almost exclusively in young and middle—aged women.
Generally believed to be a manifestation of depression or anxiety.

Miscellaneous

• Clonic facial spasm: Sometimes painful, usually associated with intermittent twitching of eyelid and face on one side.
• Platysma usually involved in twitching.
• Neuralgic pain: Occasionally associated with facial hemiatrophy.
• Idiopathic trigeminal neuropathy: It is commonly associated with muscle wasting of masseter.

“Early warning signs of poor performance in nervous system disease exams: Common questions”

Question.43. Write short note Grand-mal epilepsy.

Answer. It is a type of a primary generalized seizure.

• It is a true seizure.
• It is also known as tonic clonic seizure.
• Grand mal epilepsy comes suddenly without warning in some patients while in others it is preceded by various phases or symptoms.
• Following are the phases:

• Prodromal phase: In this phase patient become uneasy and irritable for some hours to days before an attck.
• Aura: It is seen when partial seizure become generalized so the symptoms of partial seizures such as flashing of light, hallucination of
  hearing words or sounds, Tingling or numbness sensation, pain in epigastrium and unnatural sensations in some part of the body. Aura is
  warning of an attack and is produce by an activation of epileptic discharge in brain. It remains for some seconds or minutes.
• Tonic clonic phase: Tonic convulsions of two side of body occur with head and eyes rotated to one side. Tonic Phase occur for 10–30 seconds and there is presence of flxion of arms, tonic contraction of muscles, a cry due to spasm of respiratory muscles and extension of legs. Tonic phase is followed by clonic phase which last for 1–5 minutes. In clonic phase there is violent jerking of face and limbs, biting of tongue and passing of urine and stools. Clonic phase is followed by unconsciousness which lasts for few minutes to half an hour.
• Postictal phase: This phase last for few minutes to hours. There is presence of unconsciousness with flccid limbs, corneal reflxes are lost and plantar extensor response may occur during this phase. In this patient has severe headache,confusion and automatic behavior.

Diagnosis Of Grand Mal Epilepsy

• Diagnosis of grand mal epilepsy is made by careful assessment of patient’s history documented by the diagnostic studies.
• These include blood test to assess for the metabolic disarray, brain imaging using MRI or CT scan and EEG. Normally EEG shows series of small alpha waves about 10per second and occasionally small beta waves,but during attck in Grand mal epilepsy series of sharp spikes is present. Between the attcks 3 Hz 5W interictal epileptiform activity there is presence of intermittnt irregular slow waves in grand mal epilepsy.
• It also depends upon its onset and symptoms like biting of tongue, passing of urine in clothes, injury to the patient,loss of consciousness and postepileptic features.

Management

Immediate treatment of an attck of fit.

• Patient should be protected from the injury. He should be moved away from fie and sharp and hard object.
• Padded mouth gag is inserted between the teeth to avoid tongue injury.
• Clear airway should be maintained.
• Diazepam 5 to 10 mg slow IV injection is given.

“How do case studies enhance comprehension of nervous system disease complications? FAQ explained

Long-term drug therapy.

• Phenytoin sodium 200 to 400 mg daily.
• Carbamazepine 600 to 1800 mg daily in divided dose.
• Sodium valproate 0.25 to 1 mg daily.
• Phenobarbitone 60 to 180 mg daily.
• Primidone 750 to 1500 mg daily in divided dose.

Social and psychological aspects.

• Patients and relatives should be told about the illness,its precipitating factors and consequences.
• Restriction should be in children as they are more likely to be in danger. Cycling, driving and swimming is avoided.
• Patient should be advised to take occupation in which neither he nor the community is on risk.

The post Nervous System Diseases Important Question and Answers appeared first on BDS Notes.

Question. Write short note on coarctation of aorta.

Answer. Coarctation of aorta is defied as the narrowing of aorta at or distal to the subclavian artery.

“Role of hypertension in causing cardiovascular diseases: Questions answered”

“Understanding cardiovascular diseases through FAQs: Causes, symptoms, and treatments explained”

Clinical Features Coarctation Of Aorta.

1. In uncomplicated cases the onlysymptoms are *intermittent claudication, pain, weakness and dyspnea on running.
2. Headache and nose bleed
3. Hypertension in upper limb
4. Physical examination shows weak or impalpable femorals in comparison to strong radial acting pulsation.
5. Heart size remains normal with left ventricular forcible apex.

“Importance of studying cardiovascular diseases for healthcare professionals: Questions explained”

“Common challenges in managing cardiovascular diseases effectively: FAQs provided”

On auscultation:

• S1 is accentuated
• S2 normal splittng delayed A2
• S3 with left ventricular filing
• S4 with hypertension.

Read And Learn More: General Medicine Question And Answers

“Steps to explain cardiovascular diseases: Causes vs symptoms vs treatment: Q&A guide”

Investigation Coarctation Of Aorta.

1. ECG: It shows left axis deviation representing left ventricular failure.
2. X-ray: Normal sized heart with prominent ascending aorta.
3. Barium swallow shows characteristic E sign.
4. Aortography: Show usually short narrow segment.

“Factors influencing success with cardiovascular disease knowledge: Q&A”

Treatment Coarctation Of Aorta.

1. Medical management consists of control of congestive cardiac failure in infancy.
2. Defiitive management is operative.
3. Operation can be done at any age, but lowest risk is between 1–10 years.
4. Resection of narrow segment is done in operation.

The post DIseases Of CardIovascular System Question And Answers appeared first on BDS Notes.

Question 1. Write a short note on tender hepatomegaly.

Answer. The term tender hepatomegaly itself means there is an enlargement of the liver with tenderness present in it.

Causes of  Tender Hepatomegaly

1. Infections of  Tender Hepatomegaly
   • Viral hepatitis
   • Amoebic abscess
   • Acute alcoholic hepatitis
   • Autoimmune hepatitis
   • Actinomycosis of liver
   • Weil’s disease
   • Malaria
2. Disturbances of  Tender Hepatomegaly
   • Congestive heart failure
   • Hepatic vein occlusion
3. Tumors of  Tender Hepatomegaly
   • Hepatocellular carcinoma
   • Angiosarcoma
4. Budd­Chiari syndrome of  Tender Hepatomegaly

“Understanding liver diseases through FAQs: Causes, symptoms, and treatments explained”

Read And Learn More: General Medicine Question And Answers

Hepatitis Of Tender Hepatomegaly

• Viral hepatitis: Inflammation of the liver due to viral hepatitis is a common cause of tender hepatomegaly.
  • There is a moderate enlargement of the liver which is smooth with consistency varying from soft to firm.
• Amoebic liver abscess: This liver is enlarged and is tender and tenderness present on the lower costal cartilage on the right side.
• Bacterial liver abscess: Multiple small pyogenic abscesses or a single large abscess involves the liver mainly the right lobe producing an enlarged tender liver.
• Acute alcoholic hepatitis: This follows the period of heavy drinking. There is the presence of right upper abdominal pain, anorexia, nausea and vomiting, profound weakness.
  • The liver becomes enlarged and tender.

“Steps to explain liver diseases: Causes vs symptoms vs treatment: Q&A guide”

• Autoimmune hepatitis: Prevalence is in young females.
  • Presence of enlarged and tender liver, spider naevi, and enlarged spleen.
• Actinomycosis of the liver: Here liver becomes enlarged and tender.
• Weil’s disease: Spirochetes causes Weil’s disease. There is the presence of an enlarged and tender liver.
• Malaria: In the malignant form of malaria there is hepatomegaly and tenderness over the liver.
• The liver is palpable in half of the cases. The spleen is always palpable.

“Importance of studying liver diseases for healthcare professionals: Questions explained”

“Common challenges in diagnosing and treating liver diseases effectively: FAQs provided”

General Medicine BDS 3rd Year Question and Answers

Circulatory disturbances Of Tender Hepatomegaly

• Congestive heart failure: Congestive heart failure is an important cause of hepatomegaly moderate to massive.
• The liver is firm and tender.
• Hepatic vein occlusion: It is an uncommon condition and there is the presence of an enlarged and tender liver.

“Factors influencing success with liver disease knowledge: Q&A”

Tumors Of Tender Hepatomegaly

• Hepatocellular carcinoma: Liver becomes enlarged but sometimes it is tender.
• Angiosarcoma: In patients with exposure to gaseous chemicals, the liver becomes enlarged and tender.

Budd-Chiari syndrome Here liver is enlarged and tender. There is the failure of the jugular vein to fill when the liver is pressed.

The post Liver Disease Important Question And Answers appeared first on BDS Notes.

Question 1. Enumerate white lesions of orofacial region. Describe etiology, histopathology and clinical features of leukoplakia.
Or
Enumerate white lesions of oral cavity. Describe leukoplakia in detail.

Answer. The white lesions of oral cavity/orofacial region are as follows:

• Hereditary condition:
  • Leukoedema
  • White sponge nevus
  • Hereditary benign intraepithelial dyskeratosis
  • Keratosis follicularis
  • Ptylosis syndrome.
• Leukoplakia and malignancies:
  • Chronic cheek biting
  • Friction or trauma-associated leukoplakia
  • Tobacco associated leukoplakia
  • Carcinoma in situ
  • Squamous cell carcinoma
  • Verrucous carcinoma.

“Understanding the role of tumors in oral health: Benign vs malignant Q&A explained”

Read And Learn More: Oral Pathology Question And Answers

• Dermatosis:
  • Lichen planus
  • Lupus erythematous.
• Inflammation:
  • Mucous patches of syphilis
  • Candidiasis
  • Koplik spots of measles.
• Miscellaneous conditions:
  • Oral submucous firosis
  • Papilloma
  • Lipoma
  • Hairy tongue
  • Geographic tongue
  • Fordyce’s granules.

“Importance of studying benign and malignant tumors for better diagnostic outcomes: Questions explained”

Leukoplakia is defied as “a white patch or plaque that cannot be characterized, clinically or pathologically as any other disease and is not associated with any other physical or chemical causative agent except the use of tobacco”.

Axell et al, 1984 Leukoplakia is defied as a predominantly white lesion of the oral mucosa that cannot be characterized as any other defiable lesion. WHO (1997)

Leukoplakia should be used to recognize white plaques of questionable risk having excluded (other ) known diseases or disorders that carry no increased risk for cancer.

“Common challenges in diagnosing benign and malignant tumors effectively: FAQs provided”

Warnakulasuriya et al (2008).

Etiology Of Leukoplakia

The common predisposing factors of leukoplakia are:

• Tobacco: It is used by large number of people in various forms such as smoking of cigarett, cigar, biddies and pipes.
  All these types of tobacco habits are important for development of leukoplakia.
  It is believed that during smoking a large amount of tobacco end products are produced in oral cavity.
  The products in association with heat cause severe irritation to oral mucus membrane and finally result in development of leukoplakia.
• Alcohol: Alcohol leads to the entry of carcinogen into exposed cells and thus alters oral epithelium as well as its metabolism.
• Candidiasis: Chronic candidal infections are associated with leukoplakia.
• Dietary deficiency: Deficiency of vitamin A causes metaplasia and hyperkeratinization of epithelium which may result in development of leukoplakia.
• Syphilis: Syphilitic infections play minor role in causation of leukoplakia.
• Hormonal imbalance: Imbalance or dysfunction of both male and female sex hormones causes keratogenic changes in oral epithelium. These changes lead to the development of leukoplakia.

“Factors influencing success with treatment of oral cavity tumors: Q&A”

Modifid Classifiation of Leukoplakia

“Steps to explain the causes of benign and malignant tumors in the oral cavity: Genetics vs environmental factors: Q&A guide”

Oral Leukoplakia Staging System

Stage 1 L1P0
Stage 2 L2P0
Stage 3 L3P0 Or L1L2P1
Stage 4 L3P1

Histopathology

During leukoplakia variety of histologic changes are present which are related to:

• Keratinization pattern
• Changes in cellular layer
• Thickness of epithelium
• Alteration in underlying connective tissue stroma.

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Keratinization pattern

• Leukoplakia generally presents hyperorthokeratinization or hyperparakeratinization or both with or without the presence of epithelial dysplasia.
• In case of leukoplakia an abnormal increase in the thickness of orthokeratin layer is seen in area of epithelium which is usually keratinized.
• An important histological criterion of leukoplakia is presence of hyperkeratinization of normally keratinized epithelium or some amount of parakeratin deposition in area of epithelium which are usually not keratinized.
• Epithelium dysplasia is more frequently associated with hyperkeratinized lesion.

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Changes in Cellular layer

Epithelial dysplasia is the hallmark of histologic changes seen in epithelium in case of leukoplakia. The criteria for epithelial dysplasia are:

Architecture and Cytologic Criteria for Grading Epithelial Dysplasia Given by WHO (2005)

Architecture Criteria

• Irregular epithelial stratifiation
• Loss of polarity of basal cells
• Basal cell hyperplasia
• Drop shaped rete pegs
• Increased number of mitotic fiures
• Abnormally superfiial mitosis
• Dyskeratosis i.e. premature keratinization in the cell
• Keratin pearls within rete ridges

Cytologic Criteria

• Anisonucleosis: Abnormal variation in nuclear size
• Nuclear pleomorphism: Abnormal variation in nuclear shape
• Anisocytosis: Abnormal variation in cell size
• Cellular pleomorphism: Abnormal variation in cell shape
• Increased nuclear cytoplasmic ratio
• Increased nuclear size
• Atypical mitotic fiures
• Increase in the number and size of nucleoli
• Hyperchromatism

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Histopathology

• Classification of epithelial dysplasia is done on basis of its severity which is:
  • Mild epithelial dysplasia: It refers to the alteration which is limited to basal and parabasal cell layers.
  • Moderate epithelial dysplasia: It shows involvement from basal layer to mid portion of spinous cell layer.
  • Severe epithelial dysplasia: It shows alterations from basal layer to the level above mid portion of epithelium.
  • When complete thickness of epithelium, term carcinoma in situ is used.
• Histopathological report of leukoplakia should include a statement on absence or presence of epithelial dysplasia.

Thickness Of The Epithelium

In leukoplakia, the thickness of epithelium is altered and it occurs in epithelial atrophy or acanthosis.

Alteration In Underlying Connective Tissue

In leukoplakia there is often variable degree of destruction of collagen fiers and moreover chronic inflammatory cell infitrate is also present in underlying connective tissue stroma.

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Clinical Features

• Usually the lesion occurs in 4th, 5th, 6th and 7th decades of life.
• Buccal mucosa and commissural areas are most frequent affcted sites followed by alveolar ridge, tongue, hard and soft palate, etc.
• Oral leukoplakia often present solitary or multiple white patches.
• Size of lesion may vary from small well localized patch measuring few millimeters in diameter.
• The surface of lesion may be smooth or fiely wrinkled or even rough on palpation and lesion cannot be removed by scrapping.
• Lesion is whitish or greyish or in some cases it is brownish yellow in color due to heavy use of tobacco.
• In most of the cases these lesion are asymptomatic, however in some cases they may cause pain, feeling of thickness and burning sensation, etc.

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Question 14.Defie premalignant lesion and condition. Describe etiology, clinical features, and histopathology of oral submucous firosis.
Or
Define precancerous condition and precancerous lesion. Discuss about etiology and histopathology of OSMF.

Answer. The premalignant lesions are defied as morphologically altered tissue in which cancer is more likely to occur then in its apparently normal counter part, e.g. leukoplakia, erythroplakia, nicotiana palati, stomatitis, dyskeratosis congenita, etc.

• The premalignant condition is defied as generalized state of body, which is associated with significantly increased risk of cancer, e.g. oral sub- mucus firosis, syphilis, lichen planus, etc.

The post Benign And Malignant Tumors Of Oral Cavity Important Question And Answers appeared first on BDS Notes.

Describe the clinical features and treatment of carotid body tumors.

Answer. It is also called chemodectoma or potato tumor.

Definition: It is a non-chromaffin paraganglioma.

It most commonly arises near the bifurcation of the common carotid artery.

It is a benign tumor.

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Carotid Body Tumor Clinical Features

• It is usually unilateral.
• More common in middle age.
• Swelling (75%) in the carotid region of the neck which is smooth, firm, pulsatil,e and moves only side to side but not in vertical direction.
• It can often compress over the esophagus and larynx.
• Headache, neck pain, dysphagia, and syncope are other presentations.

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• It can present with unilateral vocal cord palsy; which can cause Horner’s syndrome.
• Features of transient ischemic attacks due to compression over the carotids, “carotid body syncope. “
• Thrill may be felt and bruit may be heard.
• It is located at the level of hyoid bone deep to the anterior edge of the sternomastoid muscle in an anterior triangle, vertically placed, round, firm ‘potato-like swelling.
• Often tumors may extend into the cranial cavity along with the internal carotid artery as a dumbbell tumor.

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Carotid Body Tumor Treatment

• If it is small, it can be excised easily as the tumor is situated in the adventitia.
• When it is large, as commonly observed, complete excision has to be done followed by placing a vascular graft.
• During resection, a temporary shunt is placed between the common carotid below and the internal carotid above to safeguard cerebral perfusion;the external carotid artery is ligated. The venous or prosthetic graft is placed between the common carotid and internal carotid arteries.

The post Carotid Body Tumors: Clinical Features, Diagnosis, and Surgical Management appeared first on BDS Notes.