2. Hemoglobin Large protein MW 64000 4 polypeptides
2  chains and 2 β chains
Each chain heme, an iron-containing pigment
The iron ion in heme is able to reversibly bind an oxygen molecule.
O2 can bind to Hb at the lungs and then be released at the tissues

3. Hemoglobin Synthesis Normal hemoglobin production dependent upon
Adequate iron supply
iron is delivered to the RBC precursor by transferrin. It goes to the mitochondria where it is inserted into protoporphyrin to form heme.
Adequate synthesis of protoporphyrins
In the mitochondria
Adequate globin synthesis.
Ribosomes

4. Hemoglobin synthesis 2 succinyl CoA +2 glycine → Pyrrole
4 pyrroles → Protoporphyrin IX
Protoporphyrin IX + Fe++→ Heme
Polypeptide chains of globin are
produced by ribosomes
Heme + Polypeptide → Hemoglobin chain (Alpha chain or beta chain)
2 alpha chains + 2 beta chains → Hemoglobin A

5. Hemoglobin

6. Hemoglobin

7. Hemoglobin
92-95% Hb A
 3-5% Hb A1c
 2-3% Hb A2
 1-2% Hb F

8. Absolute values Total count Size Hemoglobin contents
♂ 5000,000 ± 300,000
♀ 4700,000 ± 300,000
Size
Diameter =7.8 µ
Outer edges = 2.5 µ
Centre = 1 µ
Hemoglobin contents
34 % of cell volume
♂ g/dl of whole blood
♀12-15 g/dl of whole blood

9. Absolute values Hematocrit O2 carrying capacity MCV 80-100 fl
♂ %
♀ %
O2 carrying capacity
Each molecule carries 4 O2
1 G Hb ml
100 ml of blood
♂ 20 ml
♀ 19 ml
MCV fl
MCH pg
MCHC g/dl

10. Anemia

11. Anemia means deficiency of hemoglobin in blood either due to few RBCs in blood or too little hemoglobin in the cells.

12. Anemia
anemia is a functional inability of the blood to supply the tissue with adequate O2 for proper metabolic function.
anemia is not a disease, but rather the expression of an underlying disorder or disease.

13. Anemia Quantitative and/or qualitative deficiency of RBC ↓ No of RBCs
↓ Amount of Hb
↓ O2 carrying capacity

14. Anemia Anemia may develop:
When RBC loss or destruction exceeds the maximal capacity of bone marrow RBC production
When bone marrow production is impaired

15. Anemia
Various diseases and disorders are associated with anemia include:
Nutritional deficiencies
External or internal blood loss
Increased destruction of RBCs
Ineffective or decreased production of RBCs
Abnormal hemoglobin synthesis
Bone marrow suppression by toxins, chemicals, radiation, Infection
Bone marrow replacement by malignant cells

16. Normal RBCs

17. Types of Anemia Blood loss anemia Aplastic anemia Megaloblastic anemia
Hemolytic anemia

18. Classification of Anemia
Nutritional anemia
Pernicious anemia
Aplastic anemia
Renal anemia
Blood loss anemia
Hemolytic anemia
Congenital anemia

19. Classification of anemias
Anemias may be classified morphologically based on the average size of the cells and the hemoglobin concentration into:
Macrocytic
Normochromic, normocytic
Hypochromic, microcytic

20. Nutritional Anemia Iron deficiency anemia ↓ intake of iron
↓ absorption of iron
Chronic blood loss
↑ demand of iron (e.g. pregnancy)
No of cells may be normal
↓ iron → ↓ Hb → ↓ size of cells (microcytic)
↓ iron → ↓ Hb → ↓ colour (Hypo chromic)
(brittle spoon shaped nails- koilonychias- is a common feature)

21. Microcytic RBC

22. Micocytic Hypochromic anemia

23. Nutritional Anemia Magaloblastic anemia ↓ dietary Vitamin B12
↓ intrinsic factor
↓Folic acid
Maturation failure
Cells- bigger ( megaloblasts)
Cell membrane – fragile → easy rupture
Hb contents - normal

24. Pernicious Anemia Maturation failure anemia
↓ Vit. B12 due to poor absorption from GIT
↓ intrinsic factor in the stomach
Autoimmune destruction of parietal cells
Atrophy of gastric mucosa
Gastrectomy
Megaloblastic anemia
Cell membrane fragile → easy rupture

25. Macro ovalocyte

26. Aplastic Anemia Failure of bone marrow to produce RBCs
Aplasia of the bone marrow
Bone marrow may be destroyed
Radiation e.g X-rays, gamma rays, nuclear bomb explosion
Chemicals e.g.benzene, arsenic, chloramphenicol. quinine, gold salts, benzene, radium etc
Bacterial toxins
Tuberculous invasion
HIV infections
Invasion of bone marrow by cancer cells
Chemotherapy for cancer

27. Renal Anemia Renal diseases (CRF) → ↓ Erythropoietin
↓ Erythropoietin → → ↓ Production of erythrocytes

28. Hemorrhagic Anemia Acute blood loss anemia Chronic blood loss anemia
Normocytic
Normochromic
↓ RBC count
↓ Hb/cmm of blood
Chronic blood loss anemia
Microcytic
Hypochromic

29. Normocytic RBC

30. Normochromic & Hypochromic cells

31. Hemolytic Anemia Erythroblastosis Fetalis Sickle cell anemia
Congenital spherocytosis
Hemolysis due to
Infections like malaria, septicemia
Chemicals like lead, hemolysins
Agglutinins
(Jaundice is common feature in hemolytic anemia)

32. Erythroblastosis fetalis
Rh negative mother
Rh positive fetus
Mother exposed to positive cells during first delivery
Antibodies formed against positive cells
Severe anemia in subsequent fetus
Blast cells in the blood

33. Erythroblastosis fetalis

34. Erythroblastosis fetalis

35. Sickle cell anemia
Sickle-cell anemia – results from a defective gene coding for an abnormal hemoglobin called hemoglobin S (Hb S)
Alpha chains are normal, beta chain is defective
Hb S has a single amino acid substitution in the beta chain
Valine is substituted for Glutamic acid at position 6
Low oxygen → Precipitation and crystallization of Hb S → Sickling & hemolysis of RBC
Sickle cell disease crises – a vicious cycle
Hb S precipitate and cells aggregate may block small blood vessels leading to necrosis

36. Sickle cells

37. Hereditary spherocytosis
One of the congenital anemia
RBC are spherical instead of being biconcave
Decreased deformability
Cannot withstand compression
Hemolysis in tight vascular beds

38. Spherocytes

39. Thalassemia Cooley’s anemia or Mediterranean anemia
Impaired α or β chain synthesis due to genetic abnormality
α thalassemia
Decreased, defective or absent α chain
β thalassemia (more common)
Decreased, defective or absent β chain

40. Effects of anemia ↓ viscosity Easy flow of blood
↑ blood flow in all the tissues
↓O2 →vasodilatation
↑ COP
↑ work load on heart
May → cardiac failure

41. Common clinical features in anemia
Pale skin, lips, conjunctiva, mucous membrane, koilonychias etc
Increased HR, COP, murmurs
Increased Respiration rate, breathlessness
Anorexia, nausea , vomiting,
Headache, lack of concentration, irritability, lethargy, lack of energy, fatigue
Menstrual disturbances, menorrhagia, oligomenorrhea, amenorrhea

42. Summary of variations in color and size

43. Polycythemia
An increase in RBC mass is called polycythemia and it may lead to an increase in blood viscosity.
Polycythemia
Relative polycythemia due to decreased plasma volume e.g. in dehydration.
Absolute polycythemia due to actual increase in RBC mass.
This may occur in disorders that prevent adequate tissue oxygenation

44. failure of oxygen delivery to the tissues (cardiac failure)
Secondary Polycythemia
tissues become hypoxic because of too little oxygen in the breathed air
high altitudes,
failure of oxygen delivery to the tissues (cardiac failure)
RBC count commonly rises to 6 to 7 million/ mm 3
30 percent above normal.

45. Physiological polycythemia
occurs in natives who live at altitudes of 14,000 to 17,000 feet, where the atmospheric oxygen is very low
The blood count -- 6 to 7 million/mm3
to perform continuous work even in a rarefied atmosphere

46. Polycythemia Vera (Erythremia)
Pathological condition/tumorous condition
RBC count to 8 million/mm3
hematocrit to 70 percent instead of the normal 40 to 45 percent
genetic aberration in the hemocytoblastic cells
blast cells no longer stop producing RBCs when too many cells are already present
viscosity of the blood increases to10 times that of water---engorgement of capillaries

47. EFFECT OF POLYCYTHEMIA ON THE CIRCULATORY SYSTEM
greatly increased viscosity of the blood ---
blood flow very sluggish---decreases venous return to the heart
blood volume is greatly increased in polycythemia which tends to increase venous return
cardiac output in polycythemia is normal because these two factors more or less neutralize each other

48. The arterial pressure is also normal
(1/3, the arterial pressure is elevated)
The color of the skin depends to a great extent on the quantity of blood in the skin subpapillary venous plexus
blood passes sluggishly through the skin capillaries
deoxygenated hemoglobin ---bluish coloration

49. Chronic blood loss leads to which type of anemia a) megaloblastic anemia b)microcytic hypochromic anemia c) normocytic, normochromic anemia

50. Megaloblastic anemia is due to which of the following a) folic acid deficiency b) Iron deficiency c)Vitamin C deficiency

51. In sickle cell anemia, a)Alpha chains are faulty b)Beta chains are faulty c)Gamma chains are faulty

52. Thank-you
Questions ??