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Lecture iii anaemia
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- 2. 2 ANAEMIA • Quantitative/qualitative decrease inRBC count • Leading to decreased O2 carrying capacity Features • Tiredness • Easy fatigability • Gen. muscular weakness • Pallor – nail beds, skin, conjunctiva, mucous membrane • Dyspnoea on exertion with palpitations • Murmurs • Amenorrhoea
- 3. 3 Aetiological classification ofAnaemia Decrease production • Nutrient deficiency – Iron, B12, Folate • Inactive bone marrow – Irradiation, drugs • Chronic renal disease • Chronic inflammatory disease • Hypothyroidism Increased destruction • Corpuscular defect – Sickle cell anaemia – Thalassemia – Spherocytosis – G6PD deficiency • Extracorpuscular defect – Splenomegaly – Drugs & Poisons – Antibodies Increased blood Loss • Acute Blood loss-RBC LESS, NCYTIC, NCHROMIC. • Chronic Blood loss – heavy Menstrual loss, piles, hook worm infection---HCHROMIC, MCYTIC
- 4. 4 IRON DEFICIENCY ANAEMIA •Most common type • RBC small & ↓ Hb • Microcytic, Hypochromic Anaemia CAUSE ↓ supply or ↑demand Growing children Menstruating, lactating, pregnant women FEATURES ↓ RBC count, size Hb ↓ MCV, MCH, MCHC Pallor TREATMENT Iron Oral/Intramuscular TESTS Serum Iron Total Iron binding capacity Serum ferritin
- 5. 5 MEGALOBLASTIC ANAEMIA • B12& FOLIC ACID DEFICIENCY • INCOMPLETE DNA SYNTHESIS • DECREASED RBC, WBC & PLATELETS • INCREASED RBC DIAMETER (> 8µm) • SHORT RBC LIFE SPAN • MEGALOBLASTS ACCUMULATES • MCV & MCH ↑, MCHC NORMAL • MACROCYTIC, NORMOCHROMIC
- 6. 6 MACROCYTIC-NORMOCHROMIC ANAEMIA VITAMIN B12 • ACTSAS A CO-ENZYME • ABSORBED IN ILEUM • INTRINSIC FACTOR REQUIRED FOR ABSORPTION • INTRINSIC FACTOR DEFICIENCY – PERNICIOUS ANAEMIA • DEFICIENCY ALSO AFFECTS NERVOUS SYSTEM • SUBACUTE COMBINED DEGENERATION OF SPINAL CORD & PERIPHERAL NEUROPATHY FOLIC ACID • ABSORBED FROM THE JEJUNUM • DEFICIENCY DUE TO ↓ ABSORPTION • ↑DEMAND-PREGNANCY • FEATURES: SIMILAR TO B12 • BUT NO NEUROLOGICAL SIGNS TREATMENT • VITAMIN B12 – FOR BOTH • PARENTERAL B12 FOR PERNICIOUS ANAEMIA
- 7. 7 APLASTIC ANAEMIA • DECREASEDBONE MARROW ACTIVITY • DUE TO – DRUG TOXICITY – IRRADIATION • ALL CELL COUNTS DECREASE (EXCEPT AGRANULOCYTES) • NORMOCHROMIC, NORMOCYTIC ANAEMIA
- 8. 8 OTHERS CAUSES CHRONIC RENALDISEASE • DECREASED ERYTHROPOIETIN – DECREASED RBC PRODUCTION • NORMOCHROMIC, NORMOCYTIC ANAEMIA HYPOTHYROIDISM • DECREASED METABOLIC RATE • DECREASED RBC PRODUCTION
- 9. 9 ↑ RBC DESTRUCTION CORPUSCULARDEFECTS SICKLE CELL ANAEMIA THALASSEMIA SPHEROCYTOSIS G6PD DEFICIENCY METHAEMO GLOBINAEMIA
- 10. 10 SICKLE CELL ANAEMIA-HBs •α chain is normal,β CHAIN – VALINE INSTEAD OF GLUTAMIC ACID. • Hb-s.(abnormal- sickle cell). Congenital. • Hb POLYMERISES WHEN O2 DECREASES – RBC SICKLES • PRONE FOR INTRAVASCULAR HEMOLYSIS • INHERITED AS AN AUTOSOMAL RECESSIVE TRAIT • HETEROZYGOUS – SICKLE CELL TRAIT ONLY
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- 12. 12 NORMAL vs SICKLECELL • DISC SHAPE • FLEXIBLE • EASILY FLOW THRO VESSELS • LIFE SPAN 120 DAYS • SICKLE SHAPE • HARD • OFTEN GETS STUCK TO VESSELS • LIFE SPAN 20 DAYS
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- 14. 14 TREATMENT • DAILY FOLICACID • AVOID TOO HOT/COLD TEMP • AVOID STRESS • BLOOD TRANSFUSION • GENE THERAPY
- 15. 15 THALASSEMIA • COOLEY’S ANAEMIA •IMPAIRED SYNTHESIS OF GLOBIN CHAINS in α and β chains. ∀ α (polypeptide chain) ∀ β THALASSEMIA – (MAJOR/MINOR) – COMMON β THALASSEMIA MAJOR – FATAL IN CHILDREN • IMPAIRED O2 TRANSPORT • TREATMENT : Blood transfusion, Gene therapy
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- 17. 17 SPHEROCYTOSIS • RBC MEMBRANEPERMEABLE TO SODIUM • DUE TO DEFECT IN MEMBRANE PROTEIN SPECTRIN(CONTRACTILE LIPO PROTEIN) • SUFFERS FROM ENLARGEMENT OF SPLEEN • RBC BECOMES BICONVEX • HENCE EASILY DESTROYED
- 18. 18 NORMAL RBC &SPHEROCYTE
- 19. 19 GLUCOSE 6 PHOSPHATE DEFICIENCY •G6PD REQUIRED FOR PENTOSE PHOSPHATE SHUNT • FOR NADPH GENERATION • NADPH NEEDED FOR MAINTAINING REDUCED GLUTATHIONE CONCENTRATION) ∀ ↓ REDUCED GLUTATHIONE – OXIDATIVE STRESS – PRONE TO HEMOLYSIS – Damaged to RBC membrane. – ↓ RBC LIFE SPAN
- 20. PERNICIOUS ANEMIA • Atrophyof gastric mucosa- intrinsic factor production poor absorption of VIT B12, • Macrocytic , normochromic . • Associated with diff. Auto immune disease • Yellow color skin. Red sore tongue, • Neurological disorder 20
- 21. 21 EXTRACORPUSCULAR DEFECTS • ANTI-RBC ANTIBODIES •OVER ACTIVE SPLEEN- HYPERSPLENISM • DRUGS • SNAKE VENOM
- 22. 22 BLOOD INDICES INANAEMIA HYPOCHROMIC MICROCYTIC ANAEMIA MEGALOBLASTIC ANAEMIA NORMOCYTIC NORMOCHROMIC ANAEMIA PCV ↓ ↓ ↓ Hb ↓ ↓ ↓ RBC DIA ↓ ↑ N MCV ↓ ↑ N MCH ↓ ↑ N MCHC ↓ N N
- 23. 23 POLYCYTHEMIA • INCREASE INRBC COUNT • RELATIVE INCREASE IN RBC COUNT – ↓ IN PLASMA VOLUME WITH NORMAL RBC COUNT – DEHYDRATION – REDISTRIBUTION OF BODY FLUIDS • ABSOLUTE INCREASE IN RBC COUNT – PRIMARY – SECONDARY
- 24. 24 ABSOLUTE POLYCYTHEMIA PRIMARY • POLYCYTHEMIAVERA • SECONDARY TO INAPPROPRIATE ERYTHROPOIETIN • KIDNEY TUMOR • LIVER TUMOR • PHAEOCHROMOCYTOMA SECONDARY TO TISSUE HYPOXIA • HIGH ALTITUDE • CORONARY HEART DISEASE • CHRONIC PULMONARY DISEASE • SECONDARY TO HORMONAL STIMULUS • CUSHING’S SYNDROME • ANDROGENS
- 25. 25 HYPOXIA & ERYTHROPOIESIS •EVIDENCE • HIGH ALTITUDE ↑ RBC PRODUCTION • RENAL DISEASE • NEPHRECTOMY ↓RBC PRODUCTION KIDNEY LIVER ERYTHROPOIETIN BM ↑RBC production HYPOXIA
- 26. 26 EFFECTS OF POLYCYTHEMIA •↑ IN RBC COUNT RESULTS IN ↑ BLOOD VISCOCITY • WHICH LEADS TO – ↓ RATE OF BLOOD FLOW – ↓ VENOUS RETURN – ↓ CARDIAC OUT PUT – ↑ BLOOD PRESSURE • CYANOSIS