Anemia Pathology Question And Answers

Common Types Of Anemia And Their Pathology Anemia

Question 1. Write a short note on the classification of anemia.
Answer: 

Classification of Anemia

• Pathophysiologic
  • Anemia due to increased blood loss
    1. Acute post-hemorrhagic anemia
    2. Chronic blood loss.
  • Anemia due to impaired red cell function:
    • Cytoplasmic maturation defect:
      1. Deficient heme synthesis, i.e., iron deficiency anemia
      2. Defective globin synthesis, i.e., thalassemic syndrome.
    • Nuclear maturation defect, i.e., vitamin B12 or folic acid deficiency, For Example. megaloblastic anemia
    • Defects in stem cell proliferation and differentiation
      1. Aplastic anemia
      2. Pure red cell aplasia.
    • Anemia of chronic disorders
    • Bone marrow infiltration
    • Congenital anemia.
  • Hemolytic anemia:
    1. Acquired or extracorpuscular
    2. Hereditary or intracorpuscular.

Read And Learn More: Pathology Questions and Answers

• Morphologic
  • Microcytic hypochromic
  • Normocytic normochromic
  • Macrocytic normochromic.

Question 2. Write a brief on iron deficiency anemia.
Or
Write a short note on iron deficiency anemia.
Or
Mention the causes, clinical features, and laboratory diagnosis of iron deficiency anemia.
Answer:

Iron deficiency anemia is caused by a deficiency of iron in the body. 20% of the world’s population is suffering from iron deficiency anemia.

Iron deficiency anemia Pathogenesis

It develops when the supply of iron is insufficient for the requirement of hemoglobin synthesis. Three major factors in the pathogenesis of iron deficiency anemia are:

• Increased Physiologic Demand, i.e., growing children, pregnancy, lactation, and menstruating females.
• Pathological Blood Loss, i.e., hemorrhage from GIT and urinary tract.
• Inadequate Intake, i.e., nutritional deficiency or impaired malabsorption.

Iron Deficiency anemia Etiology

• Due to increased blood loss
  • Uterine, For Example. Excessive menstruation in reproductive years, repeated miscarriages at the onset of menarche, postmenopausal uterine bleeding
  • Gastrointestinal, For Example. Peptic ulcer, hemorrhoids, hookworm infestation, cancer of the stomach and large bowel, esophageal varices, hiatus hernia, chronic aspirin ingestion, ulcerative colitis, diverticulosis
  • Renal tract, For Example. hematuria, hemoglobinuria
  • Nose, For Example. repeated epistaxis
  • Lungs, For Example. hemoptysis
• Due to increased requirements
  • Spurts of growth in infancy, childhood, and adolescence
  • Prematurity
  • Pregnancy and lactation
• Due to inadequate dietary intake
  • Poor economic status
  • Anorexia, For Example. in pregnancy
  • Elderly individuals due to poor dentition, apathy, and financial constraints
• Due to decreased absorption
  • Partial or total gastrectomy
  • Achlorhydria
  • Intestinal malabsorption, such as in coeliac disease.

Iron deficiency anemia Clinical Features

• Anemia: Lassitude, weakness, fatigue, dyspnea, palpitations, angina, congestive cardiac failure, and pallor.
• Epithelial tissue changes
  • Nails: Thin, lustreless, brittle, show ridging and flattening; the presence of koilonychia.
  • Tongue: Atrophy of papillae, shiny or glazed tongue, glossitis, and angular stomatitis.
  • Plummer-Vinson syndrome: It is characterized by chronic iron deficiency, dysphagia, and glossitis.
• Pica: It is defined as a craving to eat substances like dirt, clay, salt, and hair and is a typical manifestation of iron deficiency.
• Recurrent infections: Iron deficiency leads to defective lymphocyte-mediated immunity and impaired bacterial killing by phagocytes, leading to impaired immunity and recurrent infections.

Iron Deficiency Anemia Laboratory Diagnosis

• General blood parameters
  • Hemoglobin is decreased
  • RBC count is decreased
  • RBC indices, i.e., MCV, MCH, and MCHC, are reduced or low

Iron Deficiency Anemia Diagnosis And Treatment Question

Peripheral blood smear

It shows the following features, i.e.

• Microcytic hypochromic cells, i.e., red cells, are smaller than normal and have increased central pallor.
• Anisocytosis or variation in size of the cell. This is indicated by increased red cell distribution width and is more marked in iron deficiency anemia.
• Poikilocytosis or variation in the shape of the cell, i.e., the presence of a tailed variety of RBC, elliptical form, is common.
• In severe anemia, there is the presence of normoblasts, elliptocytes, pencil-shaped cells, and target cells.
• There is the presence of normal, increased, or decreased platelet count and unremarkable WBCs.

Reticulocyte count: It is normal or decreased.

Bone marrow

• There is the presence of erythroid hyperplasia, due to which marrow cellularity is increased.
• In the bone marrow, the prominent cell is polychromatic normoblast, which is smaller than normal.
• Cytoplasm shows ragged borders
• Cytoplasmic maturation lags behind that of the nucleus
• Prussian blue stain shows a decrease in iron stores

Iron studies

• There is a decrease in the serum iron
• Total iron binding capacity is high and rises to give less than 10% saturation.
• Serum ferritin is very low, which is indicative of poor tissue iron stores
• Red cell protoporphyrin is very low
• Serum transferrin receptor protein, which is normally present in developing erythroid cells and reflects total red cell mass, is raised in iron deficiency due to its release in circulation.

Question 3. Write a short note on peripheral blood pictures in iron deficiency anemia.
Answer:

Examination of Peripheral Blood Picture

It shows the following features, i.e.

• Microcytic hypochromic cells, i.e., red cells, are smaller than normal and have increased central pallor.
• Anisocytosis or variation in size of the cell.
• Poikilocytosis or variation in the shape of the cell, i.e., the presence of a tailed variety of RBC, elliptical form, is common.
• In severe anemia, there is the presence of normoblasts, elliptocytes, pencil-shaped cells, and target cells.
• There is the presence of normal, increased, or decreased platelet count and unremarkable WBCs.

Question 4. Write in brief on megaloblastic anemia.
Or
Write a short note on megaloblastic anemia
Or
Describe the peripheral and bone marrow pictures of anyone.
Or
Write a short note on laboratory diagnosis of megaloblastic anemia.
Answer:

Megaloblastic anemia Pathology

It is caused by impaired DNA synthesis and is characterized by the distinctive abnormality in the hemopoietic precursors in bone marrow in which maturation of the nucleus is delayed related to the cytoplasm. Defective DNA synthesis is due to a deficiency of vitamin B₁₂ and folic acid.

Megaloblastic anemia Etiology

1. Vitamin B₁₂ deficiency

• Inadequate dietary intake, For Example. Strict vegetarians, breastfed infants.
• Malabsorption

Gastric causes: Pernicious anemia, gastrectomy, congenital lack of intrinsic factor.

Intestinal causes: Tropical sprue, ileal resection, Crohn’s disease, intestinal blind loop syndrome, fish-tapeworm infestation.

2. Folate deficiency

• Inadequate dietary intake, For Example. in alcoholics, teenagers, infants, old age, and poverty.
• Malabsorption, For Example. in tropical sprue, coeliac disease, partial gastrectomy, jejunal resection, and Crohn’s disease.
• Excess demand in
  • Physiological: pregnancy, lactation, infancy.
  • Pathological: malignancy, increased hematopoiesis, chronic exfoliative skin disorders, tuberculosis, rheumatoid arthritis.
• Excess urinary folate loss, For Example. in active liver disease and congestive heart failure.

3. Other causes

• Impaired metabolism, For Example. Inhibitors of dihydrofolate reductase such as methotrexate and pyrimethamine; alcohol, congenital enzyme deficiencies.
• Unknown etiology, For Example. in Di Guglielmo’s syndrome, congenital dyserythropoietic anemia, and refractory megaloblastic anemia.

Clinical Features And Causes Of Anemia Questions For Medical Exams

Laboratory Diagnosis of Megaloblastic Anemia

1. General Blood Parameters

• Decrease in RBC count and hemoglobin levels
• Increase in MCV and decrease in MCH.
• Reticulocyte count is normal

2. Peripheral Smear

• Red cells show anisopokilocytosis with the presence of macrocytes and macro ovalocytes, i.e., large oval RBCs.
• Presence of Howell-Jolly bodies, i.e., nuclear remnants left after the nucleus is extruded and Cabot rings (abnormal histone synthesis causes arginine-rich histone to accumulate as rings in red cells)
• Neutrophil hypersegmentation is seen, i.e., greater than 5% of neutrophils with more than five lobes or the presence of at least one fixed lobe cell.

3. Bone Marrow Examination

• It shows megaloblastic hyperplasia. The nuclei of erythroblasts are large with fine and open sieve-like chromatin. Hemoglobinization of cytoplasm is of normal rate, while nuclear maturation lags behind that of cytoplasm. This is known as nuclear-cytoplasmic asynchrony.
• Giant metamyelocytes and stab form are seen.
• Megakaryocytes may be large and abnormal.

4. Biochemical Tests

• Serum vitamin B₁₂ levels less than 200 pg/ml are indicative of vitamin B₁₂ deficiency, and serum folate levels less than six ng/ml indicate folate deficiency. Two methods are used to measure serum B₁₂ microbiological and radioisotope assay. Radioisotope assay is the preferred method.
• Holotranscobalamin is considered active B₁₂ and is the earliest biomarker for vitamin B₁₂ deficiency.
• Elevated methylmalonic acid level indicates a depletion of vitamin B₁₂ stores.
• Isolated decreased levels of holo transcobalamin support vitamin B₁₂ deficiency, and a combination of decreased Holotranscobalamin and increased methylmalonic acid
  and homocysteine indicate a metabolically manifest B₁₂ deficiency.
• Schilling test: It is useful for diagnosing intrinsic factor deficiency. It measures the absorption of free radiolabelled vitamin B₁₂.
• Radiolabelled vitamin B₁₂ is given orally, followed in 1 to 6 hours by 1000 mg of parenteral vitamin B12, which reduces the uptake of radiolabelled vitamin B₁₂ by the liver.
• Absorbed radiolabelled vitamin B12 is excreted in the urine, which is collected for 24 hours. The amount excreted is measured, and the percentage of radiolabelled vitamin B₁₂ is determined.
• If absorption is normal, i.e.,≥ 9% of the dose given appears in the urine. Reduced urinary excretion (if kidney function is normal) indicates inadequate vitamin B₁₂ absorption.

Question 5. Write a short note on the classification of hemolytic anemia.
Answer:

Classification of hemolytic anemia

• Acquired or extracorpuscular.
• Hereditary or intracorpuscular.

Hemolytic anemia Acquired or Extracorpuscular

• Immunohemolytic anemia
  • Autoimmune hemolytic anemia
    1. Warm antibody autoimmune hemolytic anemia
    2. Cold antibody autoimmune hemolytic anemia
  • Drug-induced immune hemolytic anemia
  • Isoimmune hemolytic anemia.
• Mechanical trauma: Microangiopathic hemolytic anemia
• Direct toxic effect: Malaria, bacteria, infection, and other agents
• Acquired red cell membrane abnormalities: Paroxysmal nocturnal hemoglobinuria.
• Splenomegaly.

Hemolytic anemia Hereditary or Intracorpuscular

• Abnormalities of red cell membrane:
  • Hereditary spherocytosis
  • Hereditary elliptocytosis
  • Hereditary stomatocytosis.
• Disorders of red cell interior:
  • Red cell enzyme defect
    1. Defects in HMP shunt: G6PD deficiency
    2. Defects in the glycolytic pathway: Pyruvate kinase deficiency
  • Disorders of hemoglobin
    1. Structurally abnormal hemoglobin, sickle syndrome, and other hemoglobinopathies
    2. Reduced globin chain synthesis: Thalassemias.

A Plastic Anemia Diagnosis And Management Questions

Question 6. Classifymorphological anemia.
Or
Write notes on morphological Anemia classification of anemias.
Answer:

Classification of Morphological Anemia

Based on red cell size, hemoglobin content, and red cell indices.

Microcytic hypochromic: MCV, MCH, and MCHC are all reduced For Example. in iron deficiency anemia and certain non-iron deficiency anemias, i.e., sideroblastic anemia, thalassemia, and anemia of chronic disorders.

Normocytic normochromic: MCV, MCH, and MCHC are all normal, For Example. after acute blood loss, hemolytic anemias, bone marrow failure, and anemia of chronic disorders.

Macrocytic: MCV is raised, For Example. in megaloblastic anemia due to a deficiency of vitamin B₁₂ and folic acid.

Question 7. Describe in brief peripheral and bone marrow pictures of megaloblastic anemia.
Answer:

• Peripheral picture
  • Red cells show anisopokilo cytosis with the presence of macrocytes and macro ovalocytes, i.e., large oval RBCs.
  • Presence of Howell-Jolly bodies, i.e., Nuclear remnants left after the nucleus is extruded and Cabot rings (abnormal histone synthesis causes arginine-rich histone to accumulate as rings in red cells)
  • Neutrophil hypersegmentation is seen, i.,e. greater than 5% of neutrophils with more than five lobes or the presence of at least one six-lobe cell.
• Bone marrow picture
  • It shows megaloblastic hyperplasia. The nuclei of erythroblasts are large with fine and open sieve-like chromatin. Hemoglobinization of cytoplasm is of normal rate, while nuclear maturation lags behind that of cytoplasm. This is known as nuclear-cytoplasmic asynchrony.
  • Giant metamyelocytes and stab form are seen.
  • Megakaryocytes may be large and abnormal.

Question 8. Write a short note on the causes and lab findings of microcytic hypochromic anemia.
Answer:

Microcytic hypochromic anemia

Microcytic hypochromic anemia Etiology/Causes

1. Iron deficiency anemia

• Due to increased blood loss
  • Uterine, For Example. Excessive menstruation in reproductive years, repeated miscarriages at the onset of menarche, postmenopausal uterine bleeding
  • Gastrointestinal, For Example. peptic ulcer, hemorrhoids, hookworm infestation, cancer of the stomach and large bowel, esophageal varices, hiatus hernia, chronic aspirin ingestion, ulcerative colitis, diverticulosis
  • Renal tract, For Example. hematuria, hemoglobinuria
  • Nose, For Example. repeated epistaxis
  • Lungs, For Example. hemoptysis
• Due to increased requirements
  • Spurts of growth in infancy, childhood, and adolescence
  • Prematurity
  • Pregnancy and lactation
• Due to inadequate dietary intake
  • Poor economic status
  • Anorexia, For Example. in pregnancy
  • Elderly individuals due to poor dentition, apathy, and financial constraints
• Due to decreased absorption
  • Partial or total gastrectomy
  • Achlorhydria
  • Intestinal malabsorption, such as in coeliac disease

2. Sideroblastic anemia

3. Thalassemia

4. Anemia of chronic disorders

• Defective red cell production
• Reduce red cell life span.

5. Isoniazide, pyrizinamide therapy.

Microcytic Hypochromic Anemia Lab Findings

1. General blood parameters

• Hemoglobin is decreased
• RBC count is decreased
• RBC indices, i.e., MCV, M, C, H and M, C HC are reduced or low

2. Peripheral blood smear

It shows the following features, i.e.

• Microcytic hypochromic cells, i.e., red cells, are smaller than normal and have increased central pallor.
• Anisocytosis or variation in size of the cell. This is indicated by increased red cell distribution width and is more marked in iron deficiency anemia.
• Poikilocytosis or variation in the shape of the cell, i.e., the presence of a tailed variety of RBC, elliptical form, is common.
• In severe anemia, there is the presence of normoblasts, elliptocytes, pencil-shaped cells, and target cells.
• There is the presence of normal, increased, or decreased platelet count and unremarkable WBCs.

3. Reticulocyte count: It is normal or decreased.

4. Bone marrow

• There is the presence of erythroid hyperplasia,  due to which marrow cellularity is increased.
• In the bone marrow, the prominent cell is polychromatic normoblasts, which is smaller than nor. Mall.
• Cytoplasm shows ragged borders.
• Cytoplasmic maturation lags behind that of the nucleus.
• Prussian blue stain shows a decrease in iron stores.

4. Iron studies

• There is a decrease in the serum iron.
• Total iron binding capacity is high and rises to give less than 10% saturation.
• Serum ferritin is very low,w which is indicative of poor tissue iron stores.
• Red cell protoporphyrin is very low.
• Serum transferrin receptor protein, which is normally present in developing erythroid cells and reflects total red cell mass, is raised in iron deficiency due to its release in circulation.

Anemia Treatment Options For Medical Students

Question 9. Write a short note on the blood group.
Answer:

Blood groups are genetically determined antigens that can be detected on the RBC surface by specific antibodies.

Name of the Blood Group with Antigens

ABO Blood Group

• The ABO system is the product of one gene locus situated on chromosome 9, which determines the expression of ABO blood groups on RBCs, endothelial cells, and some epithelial cells.
• The basic precursor substance in antigens has a short chain of sugars.
• There are two types of chains;  Type 1 and Type 2 chains, which differ from each other in the way the terminal galactose joins the N-acetylglucosamine residue.
• The basic precursor substance is converted to an H substance by L-fucosyltransferase
• A gene codes for a transferase that attaches N-acetylgalactosamine to the precursor substance, thereby producing A antigen (blood group A).
• B gene codes for a transferase that attaches galactose to the precursor substance to produce B antigen (blood group B).
• O gene is inactive; hence, neither A nor B antigens are present on the surface of blood group O RBCs.
• Group AB individuals have H antigen that carries both A or B active sugars.
• An individual receives one blood group antigen from the mother and one from the father.
• Antibodies belonging to the ABO system are naturally occurring, IgM-type, complete antibodies.
• The A group contains about twenty subgroups, of which Al and A2 are the most common. A1 makes up 80% of all A-type blood,d while A2 makes up for the rest.

Bombay Blood Group (hh)

Some individuals do not inherit the H gene and are not able to express substance H on their RBCs, and thus, do not produce A or B antigens. Instead, they produce antibodies to substance H and both A and B antigens. They can receive blood only from other donors but can donate like group O individuals.

Blood Group Rh Antigen System

• Rh antigen system has three closely linked gene loci, coding for D antigen (there is no d antigen), C and/or c antigen, and E and/or e antigen. Thus, the antigens produced are C, D, E, c, and e.
• An individual may have similar or different sets of these three Rh antigens on each chromosome; for example, CDE/cde, cde/cde, or CdE/cdE (each person inherits one trio
  gene from each parent).
• Individuals who are positive for D antigen are considered Rh-positive (85% of the population), and those who lack it are Rh-negative.
• Individuals with a weak variant of D antigen, called the Du variant, are also considered Rh-positive.
• Alloimmunization, i.e., the formation of an antibody against an antigen,n occurs if a person is exposed to an Rh antigen that is not on the patient’s RBCs.
• The majority of clinically important antibodies that produce a transfusion reaction are warm-reacting (IgG) antibodies (For Example. anti-D, anti-Kell) rather than cold-reacting (IgM) antibodies.

Blood Group Duffy Antigen System

African–Americans commonly lack Duff (Fy) antigens on their RBCs, which protects their cells from Plasmodium vivax infestation, since P. vivex requires Duff antigen as a receptor to bind to the RBCs.

Blood Group Lewis Antigens

They are closely related to ABH antigens and are produced in body secretions. Naturally occurring IgM antibodies develop against these antigens, but they are generally weak antibodies of no clinical importance.

Question 9. Write a short note on normoblast.
Answer:

Normoblast is divided into three stages, i.e.

• Early normoblast
• Intermediate normoblast
• Late normoblast.
  • Early
  • Late.

Early Normoblast

• It is 14-16µm in size.
• The size of the nucleus is small. No nucleoli is present. Condensation of chromatin is present.
• The cytoplasm is more in amount and is less basophilic.
• Active mitosis is present.

Intermediate Normoblast

• It is 10-14 µm in size.
• The size of the nucleus decreases as compared to early normoblast. There is more condensation of chromatin as compared to early normoblast.
• The cytoplasm is present in good amounts and is present with polychromatophilic staining.
• Hemoglobin starts appearing.
• Active mitosis is present.

Late Normoblast

• Early:
  • It is 8-10 µm in size.
  • The nucleus is very small with a chromatin dot and appears cart-wheel-shaped.
  • Cytoplasm staining increases markedly.
  • Hemoglobin further increases in amount.
  • Mitosis stops here.
• Late:
  • It is 7-8 µm in size.
  • The nucleus gets degenerated, is deeply stained, and is pyknotic.
  • Staining of cytoplasm increases and is more acidic.
  • Hemoglobin further increases in amount.
  • Mitosis is absent.

Question 10. Write notes on laboratory diagnosis of iron deficiency anemia.
Or
Write a brief lab diagnosis of iron deficiency anemia.
Or
Write a short note on lab diagnosis of Iron deficiency anemia.
Answer:

• General blood parameters
  • Hemoglobin is decreased
  • RBC count is decreased
  • RBC indices, i.e., MCV, MCH, and MCH, C, are reduced or low
• Peripheral blood smear
  • It shows the following features, i.e.
  • Microcytic hypochromic cells, i.e., red cells,s are smaller than normal and have increased central pallor.
  • Anisocytosis or variation in size of the cell. This is indicated by increased red cell distribution width and is more marked in iron deficiency anemia.
  • Poikilocytosis or variation in the shape of the cell, i., the presence of a tailed variety of RBC, elliptical form, is common.
  • In severe anemia, there is the presence of normoblasts, elliptocytes, pencil-shaped cells, and target cells.
  • There is the presence of normal, increased, or decreased platelet count and unremarkable WBCs.
• Reticulocyte count: It is normal or decreased.
• Bone marrow
  • There is the presence of erythroid hyperplasia, due to which marrow cellularity is increased.
  • In the bone marrow, the prominent cell is polychromatic normoblast, which is smaller than normal.
  • Cytoplasm shows ragged borders
  • Cytoplasmic maturation lags behind that of the nucleus
  • Prussian blue stain shows a decrease in iron stores.
• Iron studies
  • There is a decrease in the serum iron.
  • Total iron binding capacity is high and rises to give less than 10% saturation.
  • Serum ferritin is very low, which is indicative of poor tissue iron stores.
  • Red cell protoporphyrin is very low.
  • Serum transferrin receptor protein,n, which is normally present in developing erythroid cells and reflects total red cell ma, ss, is raised in iron deficiency due to its release in circulation.

Question 11. Define and classify anemias.
Answer:

Anemia is defined as reduced hemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual.

As per WHO, the lower extreme of normal hemoglobin is taken as 13 g/dl for adult males and 12 g/dl for adult females.

11 g/dl in pregnant females. At birth, the lower limit of normal hemoglobin level is 13 g/dl is taken as the lower limit at birth, whereas at 0 to 6 mon, the normal lower level is 10.5 g/dl.

Question 12. Write a short note on Hb estimation.
Or
Write a short note on the estimation of Hb%.
Answer:

Hb estimation means hemoglobin estimation.

This is done to check the levels of hemoglobin in the body.

Following are the meththathich undergo Hb estimation.

• Visual methods:
  • Sahli’s method
  • Dare’s method
  • Haden’s method
  • Wint robe’s method
  • Halden’s method
  • Tallquist’s method.
• Gasometric method.
• Spectrophotometric method:
  • Oxyhemoglobin method
  • Cyanomethamoglobin method.
• Automated hemoglobinopathy.
• Non-automated hemoglobinopathy.

Other methods:

• Alkaline-hematin method
• Specific gravity method
• Comparator method.

Sahli’s (Acid Hematin) Method for Hb Estimation

Principle

When blood is added to 0.1 N HCl, hemoglobin is converted to brown color acid hematin. The resulting color after dilution is compared with standard brown glass reference blocks of Sahli’s hemoglobinometer.

Specimen

Capillary blood or thoroughly mixed anti-coagulated venous blood.

Apparatus

• Sahli’s hemoglobinometer: This consists of:
  • A standard brown glass mounted on a comparator
  • A graduated tube
  • Hb-pipette (0.02 ml).
• 0.1 N HCl
• Distilled water
• Pasteur pipettes.

Procedure

• By using a Pasteur pipette, add 0.1 N HCl in the tube up to the lowest mark, i.e., 20% mark.
• Draw blood upto 20µl mark in Hb pipette. Adjust the blood column carefully without bubbles. Wipe excess blood on the sides of the pipette by using a dry piece of cotton.
• Transfer blood to the acid in the graduated tube, rinse the pipette well, mix the reaction mixture, and allow the tube to stand for 10 minutes.
• Dilute the solution with distilled water by adding a few drops at a time carefully and by mixing the reaction mixture until the color matches with the glass plate in the
  comparator.
• Matching should be done only against the natural light. The level of fluid is noted at its lower meniscus, and the reading corresponding to this level on the scale is recorded in gm/dl.

Understanding Anemia Pathophysiology And Clinical Cases

Question 17. Discuss etiopathogenesis of anemia.
Answer:

Anemia Etiopathogenesis

The development of iron deficiency depends upon one or more of the following factors:

• Increased blood loss
• Increased requirements
• Inadequate dietary intake
• Decreased intestinal absorption.
• Iron deficiency anemia develops when the supply of iron is inadequate for the requirement of hemoglobin synthesis.

Initially, the negative iron balance is made good by mobilization from the tissue storestoo maintain hemoglobin synthesis.

It is only after the tissue stores of iron are exhausted that the supply of iron to the marrow becomes insufficient for hemoglobin formation, so a state of iron deficiency anemia develops.

Question 18. Define anemia.
Answer:

Anemia is defined as reduced hemoglobin concentration in blood below the lower limit of the normal range for the age and sex of the individual.

As per WHO, the lower extreme of normal hemoglobin is taken as 13 g/dl for adult males and 12 g/dl for adult females. 11 g/dl in pregnant females.

At birth, the lower limit normal hemoglobin level is 13 g/dl is taken as lower limit at birth, whereas at 0 to 6 months hee normal lower level is 10.5 g/dl.