Blood Diseases Important Question and Answers

Diseases Of Blood

Question. Discuss in short Neutropenia.

Answer. The presence of abnormally small number of neutrophils in the blood usually less than 1500 to 2000 per micro liter.

Causes Of Neutropenia

• Starvation and *debility.
• Overwhelming infections and toxemia in older people.
• Infections: Typhoid, measles, malaria, kala­azar, hepatitis,inflenza, HIV and miliary TB.
• Hypersplenism, liver cirrhosis.
• Bone marrow failure: In aplastic anemia, leukemia and myelofiroma
• Drugs: Sulfonamides, antibiotic, analgesics, anti­thyroids,anti­convulsants, etc.
• Anaphylactic shock.

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Clinical Manifestations Of Neutropenia

• Females are more commonly affcted as compared to males
• Early manifestations of agranulocytosis are may be in form of sore throat or pain.
• There may be fever going up to 130°F, sometimes coming with rigor chills, body ache and pain and extreme degree of prostration.
• In large number of cases ulceromembranous lesions appear on throat, tonsils, gum, tongue and genitalia
• These are often covered with grayish black exudates and may become gangrenous.
• Lymph gland generally cervical groups and in some, there are generalized lymphadenopathy
• Liver and spleen may become enlarged.
• As disease progresses severe toxemia develops and patient may go into shock.

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Investigations Of Neutropenia

• Peripheral blood film shows a complete absence of neutrophils.
• Bone marrow is normocellular and show decrease mature neutrophils.

Management Of Neutropenia

• Firstly, the cause is removable, which is identifiable.
• Secondly, the infection is controlled, and the patient is put on the isolation ward and barrier nursing is done.
• Anti­bacterial drugs such as penicillin 5 mega units IM or IV 4 hourly or ciproflxacin 500 mg IV 4 hourly is started immediately.
• In addition, metrogyl 500 mg every 6 hours is taken to take care of the infection
• Anabolic steroids are also given.
• In cases where toxemia is severe, corticosteroids are employed, i.e. injection n dexamethasone 4 mg IV 6 hourly.
• Granulocyte transfusion is given to tide over the crisis. This is given daily for 5 to 7 days.

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Clinical Features Of Acute Leukemia

Following are the clinical features of acute leukemia:

1. Due To Bone Marrow Failure

• Constitutional symptoms: Fever, malaise and prostration
  Due to anemia: Tiredness, fatigue, pallor, weakness and dyspnea.
• Bleeding manifestations: Bruises, Petechiae, bleeding from gums and nose, purpura, gastrointestinal, renal and bleeding in nervous system.
• Infections: Infective lesions of oral cavity and throat, ulcers in oral cavity and pharynx, herpes simplex infection, Infections of respiratory tract such as bronchitis and pneumonia, infections of skin such as cellulitis and boils.

2. Due To Organ Infitration

• CNS: Hemorrhage, meningeal infitration and multiple cranial nerve palsies.
• Skin: Bluish nodules or dusky red patches.
• Kidneys: Renal failure
• Heart: Cardiomyopathy and pericarditis
• Fundus: Roth spots and papilledema
• Testes: Swelling present in acute lymphoid leukemia
• Bony tenderness is present especially in sternum
• Presence of hepatosplenomegaly and lymphadenopathy.

Due To Leukemic Cells

• Tissue deposits of leukemic cells leads to gum hypertrophy.
• Symptoms of cellular hyperviscosity are headache,confusion, fis, focal neurological signs and coma.
• In promyelocytic variant of acute myeloid leukemia the release of cytoplasmic granular contents activates coagulation and firinolytic systems which leads to acute hemostatic failure.

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Folic Acid

Folic acid is a combination of glutamic acid, para-aminobenzoic acid and pteridine nucleus.

Folic acid  Sources

Sources of folic acid are yeast, fresh green vegetables, cereals,liver, kidney, meat.

Folic acid  Daily Requirement
50 to 100 μg.

Deficiency of Folic Acid

Deficiency of folic acid leads to megaloblastic anemia, glossitis,diarrhea, weight loss and weakness.

Folic acid  Indications

• In megaloblastic anemia caused due to folate defiiency,folic acid is given in dose of 1–5 mg/day and is continued till 3–4 months.
• In pregnancy due to increase demand, it is given 0.5 mg/day from fist trimester.
• Folic acid antagonizes methotrexate toxicity.

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Common Coagulation Disorders

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Coagulation disorders deal with disruption of the body’s ability to control blood clottng.

Common Coagulation Disorders are:

• Hemophilia, orhemophiliaA (FactorVIIIdefiiency),an inherited coagulation disorder. This genetic disorder is carried by females but most often affcts males.
• Christmas disease, also known as hemophilia B or
  Factor IX defiiency, is less common than hemophilia
  A with similar in symptoms.
• Disseminated intravascular coagulation disorder,also known as consumption coagulopathy, occurs as a result of other diseases and conditions. This disease accelerates clottng, which can actually cause hemorrhage.
• Thrombocytopenia is the most common cause of coagulation disorder. It is characterized by a lack of circulating platelets in the blood. This disease also includes idiopathic thrombocytopenia.
• Von Willebrand’s disease is a hereditary disorder with prolonged bleeding time due to a clottng factor defiiency and impaired platelet function. It is the most common hereditary coagulation disorder.
• Hypoprothrombinemia is a congenital defiiency of clottng factors that can lead to hemorrhage.
• Other coagulation disorders include factor XI deficiency, also known as hemophilia C, and factor VII defiiency. Hemophilia C afflts one in
  100,000 people and is the second most common bleeding disorder among women. Factor VII is also called serum prothrombin conversion accelerator (SPCA) defiiency. One in 500,000 people may be afflted with this disorder that is often diagnosed in newborns because of bleeding into the brain as a result of traumatic delivery.

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Idiopathic Thrombocytopenic Purpura

It is considered to be the autoimmune disease of platelets.

Idiopathic Thrombocytopenic Purpura Clinical Features

Acute Idiopathic Thrombocytopenic Purpura

• It is seen commonly in children who are recovering from the viral disease.
• Onset of the disorder is sudden and symptoms are seen 2 to 3 weeks after the viral infection with appearance of purpura or at times epistaxis.

Chronic Idiopathic Thrombocytopenic Purpura

• This is seen during 2nd to 4th decades of life.
• It has female predilection.
• Patient has purpura or epistaxis.
• There is presence of ecchymoses and menorrhagia
• Internal bleeding can also be present.
• Splenomegaly can be present.

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Chronic Idiopathic Thrombocytopenic Purpura Investigations

• Bleeding time becomes prolonged.
• Platelet count get decreased
• Bone marrow examination reveals increase in the number of megakaryocytes indicating peripheral destruction of platelets.

Chronic Idiopathic Thrombocytopenic Purpura Management

Chronic Idiopathic Thrombocytopenic Purpura In children

• Mild idiopathic thrombocytopenic purpura requires no treatment.
• In moderate­to­severe idiopathic thrombocytopenic purpura prednisolone, 2 mg/kg daily oral administration is advised.
• Platelet transfusion can be given.
  After giving steroidal therapy, if bleeding persist
• immunoglobulins should be given.

Chronic Idiopathic Thrombocytopenic Purpura In adults

• In adults prednisolone should be given 1 mg/kg as standard regimen and is continued for 2 to 4 weeks, after this drug should be slowly withdrawn.
• If bleeding is high platelet infusion should be done.
• IV immunoglobulin should be given, i.e. 1 g/kg. This is to be given in the patients who are not responding to prednisolone therapy.
• If patient has more than two remissions of the disease splenectomy should be done.

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 Treatment of Anemias

Treatment of Anemias Etiology

1. Due to increased blood loss:

• Gastrointestinal: Peptic ulcer, piles, hookworm manifestation,
• Carcinoma of stomach, acute erosive gastritis, ulcerative colitis
• Lung: Due to hemoptysis
• Renal: Haemoglobinuria and hematuria
• Uterine: Menorrhagia, post menopausal uterine bleeding.
• Nose: Epistaxis

2. Due to increased body demands:

• In adolescence
• During prematurity
• In pregnancy and lactation.

3. Due to inadequate dietary intake:

• In low socioeconomic status
• In elder patients with loss of teeth
• Anorexia of pregnancy.

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4. Decreased absorption:

• In achlorhydria
• In patients with malabsorption
• In cases with gastrectomy.

1. Anemias – Vitamin B12 defiiency

• Inadequate intake:
• In strict vegetarians
• In poor diet.

Anemias – Due to malabsorption:

• Gastric:
• Pernicious anemia
• Congenital intrinsic factor defiiency
• Gastrectomy.
• Small intestinal disease:
• Topical and Non­topical sprue
• Crohn’s disease
• Fish tapeworm.
• Increased requirement
• In pregnancy.

Folic Acid Defiiency

1. Inadequate intake

• Infancy
• Old age
• Poverty
• Alcoholism
• Kwashiorkor.

2. Malabsorption

• Coeliac Disease
• Topical sprue
• Congenital folate malabsorption.

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3. Increased utilization or loss

1. Physiological

• Prematurity
• Pregnancy and lactation.

2. Pathological

• Blood disorders
• Malignancy
• Dialysis.

3. Anti­folate Drugs

• Methotrexate
• Pyrimethamine
• Trimethoprim
• Anti­convulsant drugs.

1. Acquired or Extracorpuscular

1. Immunohemolytic anemia:

• Autoimmunohemolytic anemia
• Warm antibody autoimmune hemolytic anemia
• Cold antibody autoimmune hemolytic anemia
• Drug induced immunohemolytic anemia
• Iso immune hemolytic anemia.

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2. Mechanical trauma: Micro­angiopathic hemolytic anemia

3. Direct toxic effct: Malaria, bacteria, infection and other agents

4. Acquired red cell membrane abnormalities: Paroxysmal nocturnal hemoglobinuria.

5. Splenomegaly.

2. Hereditary or Intracorpuscular

1. Abnormalities ofred cell membrane:

• Hereditary spherocytosis
• Hereditary elliptocytosis
• Hereditary stomatocytosis.

2. Disorders ofred cell interior:

• Red cell enzyme defect:
• Defects in HMP shunt: G6PD defiiency
• Defects in glycolytic pathway: Pyruvate kinase defiiency.

3. Disorders ofhemoglobin:

• Structurally abnormal hemoglobin, sickle syndrome and other hemoglobinopathies.
• Reduced globin chain synthesis: Thalassemias.

Treatment of Anemias: Clinical Features

Anemias Symptoms

• Tiredness
• Weakness
• Lethargy
• Loss of appetite
• Headache and bodyache
• Inability to concentrate, giddiness
• Breathlessness
• Epigastric discomfort.

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Anemias Signs

• Pallor
• Palpitation
• Angular stomatitis
• Atrophic gastritis
• Flattning or spoon-shaped nails, i.e. platynychia and koilonychia
• Tongue is pale and smooth
• Glossitis
• Hepatosplenomegaly
• Pulmmer­Vinson syndrome, i.e. dysphagia and cricoid webs.

• Due to anemia: Shortness of breadth, anemia and pallor.
• Gastrointestinal: Diarrhea, loss of weight and apetite
• Neurological: Vitamin B12 neuropathy and neural tube defects due to defiiency of folic acid.
• Gonadal dysfunction: It is due to deficiency of both Vitamin B12 and folic acid
• Epithelial cell changes: Glossitis and other epithelial surfaces show cellular abnormalities.

• There is presence of high fever, toxemia, marked*prostration, shock and hemoglobinuria
• Acute renal failure may develop
• Chronic form includes jaundice varying from mild to severe form, mongoloid faces, splenomegaly, chronic leg ulcers and pigment stones in gallbladder.

Anemias Approach To Diagnosis

Anemias Diagnosis

It is based on the clinical signs and symptoms and investigations

Anemias Clinical Signs And Symptoms

Anemias Investigations

Blood picture and red cell indices

• Hemoglobin: Fall on hemoglobin concentration.
• Red cells: The RBCs in blood fim are hypochromatic and microcytic and there is anisocytosis, poikilocytosis and elliptocytosis
• Reticulocyte count: Normal or reduced.
• Absolute values: MCV, MCH and MCHC are decreased.
• Leukocytes: Usually normal
• Platelets: Usually normal but raised if bleeding is cause of anemia
• ESR: value of ESR is low

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Bone marrow fidings:

• Marrow cellularity: The marrow cellularity is increased due to erythroid hyperplasia.
• Erythropoiesis: Normoblastic erythropoiesis.
• Marrow iron is defiient.

Biochemical fidings:

• Serum iron level is low.
• Total iron binding capacity is high.
• Serum ferritin is very low.

Anemias Treatment

• Proper physical and mental rest.
• Good nourishing diet with supplementation of foods rich in iron.
• Oral iron therapy: Ferrous sulphate 200 mg TID is given in between the meals. If after taking the drug, there is any abdominal pain, nausea, vomiting or constipation, the salt is changed to ferrous gluconate or ferrous fumarate. Oral iron therapy should be given for 6 months.
• Parenteral iron therapy: Iron sorbitol ciric acid complex 1.5 mg/kg body weight is given as IM or Iron dextran in 5% glucose is given as IV
• Blood transfusion: Packed red cells are transfused.

Vitamin B12 Defiiency:

• Hydroxycobalamine 1000 µg IM is given, i.e. 6 injections in 2 to 3 weeks.
• Since rapid regeneration of blood deplete marrow iron stores, so ferrous sulphate 200 mg daily is given after starting the therapy.
• Maintenance dose of 500–1000 μg IM is given for every 3 months.

Folic acid defiiency:

• InitiallyFolicacid 5 mgdailyorallyfor4months isgiven.
• Maintenance dose is 5 mg folic acid once a week.

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Iron Defiiency Anemia Underfollowing Headings

• Iron metabolism
• Investigations
• Treatment

 Iron metabolism: Average diet consists of 10–15 mg of iron out of which 5–10% is normally absorbed.

Iron required for hemoglobin synthesis is derived from two primary sources, i.e. ingestion of food containing iron and recycling of iron from senescent red cells.

Iron is absorbed from duodenum and upper jejunum in ferrous form (Fe2+) and plays role in absorption.

Iron absorbs better from heme diet. Iron from heme is released in mucosa of small intestine after absorption for its utilization.

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Iron is consumed from the diet and recycling of iron released is done by catabolism of hemoglobin derived from destroyed senescent red cells.

Transfer of iron to bone marrow is by iron­binding globulin, i.e. transferrin. Iron is stored in reticuloendothelial cells, hepatocytes and skeletal muscle cells as two iron protein complexes, i.e. ferritin which is water soluble and hemosiderin which is water insoluble. Iron is also present in myoglobin and cytochrome enzymes.

Total of 0.5–2 mg of iron is absorbed daily by normal human male or non­menstruating female.

Out of which 0.5–1 mg of iron is lost in sweat, urine, stool and in mensis. 2 mg of iron is utilized in pregnancy. 0.5 mg is utilized in growth and lactation women.