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BLOOD PHYSIOLOGY - University Exam Pattern Answers

The image shows a question paper with LAQ (Long Answer Questions), SAQ (Short Answer Questions), and VSAQ (Very Short Answer Questions) on Blood Physiology. Below are brief but complete answers written in university exam style.

LAQ SECTION


1. Erythropoiesis - Definition, Stages & Factors Affecting ⭐⭐⭐⭐⭐ (Most Important)

Definition: Erythropoiesis is the process of formation of red blood cells (erythrocytes) from stem cells, occurring primarily in the red bone marrow.
Site: Red bone marrow (in adults); liver and spleen in fetal life.
Stages of Erythropoiesis (in order):
StageFeature
1. Pluripotent stem cellUncommitted progenitor
2. CFU-GEMMMixed myeloid progenitor
3. BFU-EBurst-forming unit - erythroid
4. CFU-EColony-forming unit - erythroid
5. Pronormoblast (Proerythroblast)First recognizable RBC precursor
6. Basophilic normoblastBasophilic cytoplasm; active Hb synthesis
7. Polychromatophilic normoblastMixed staining; Hb increasing
8. Orthochromatic normoblastPink cytoplasm; nucleus condenses
9. ReticulocyteNucleus extruded; released to blood; matures in spleen in 1-2 days
10. Mature RBC (Erythrocyte)Biconcave disc; no nucleus; lifespan ~120 days
Factors Affecting Erythropoiesis:
Stimulating factors:
  • Erythropoietin (EPO) - produced by kidney in response to hypoxia (key regulator)
  • Testosterone, thyroxine, growth hormone, cortisol
  • Vitamins: B12, B6, folic acid, Vitamin C, Vitamin E
  • Minerals: Iron (essential for Hb), Copper, Cobalt
  • Hypoxia - at high altitude
Inhibiting factors:
  • Estrogen
  • Chronic renal disease (reduced EPO)
  • Malnutrition, chronic infection
Draw diagram: Stem cell → CFU-GEMM → BFU-E → CFU-E → Pronormoblast → Normoblasts → Reticulocyte → RBC
(Guyton and Hall Textbook of Medical Physiology; Basic Medical Biochemistry - A Clinical Approach)

2. Physiology of Clotting + Bleeding Disorders + Note on Anticoagulants ⭐⭐⭐⭐⭐

Hemostasis is the process by which bleeding is stopped. It occurs in 3 steps:
Step 1 - Vascular Spasm: Injury → smooth muscle contraction → reduces blood flow.
Step 2 - Primary Hemostasis (Platelet Plug):
  • Platelets adhere to exposed collagen (via vWF)
  • Platelet activation + aggregation → Platelet plug
Step 3 - Coagulation Cascade (Secondary Hemostasis):
Extrinsic Pathway:
  • Tissue factor (Factor III) + Factor VII → activates Factor X
Intrinsic Pathway:
  • Contact activation: XII → XI → IX → VIII → activates Factor X
Common Pathway:
  • Factor X + V → Prothrombin (II) → Thrombin
  • Thrombin → Fibrinogen (I) → Fibrin clot
Clot Retraction & Fibrinolysis: Plasmin dissolves the clot via fibrinolysis.
Bleeding Disorders:
DisorderMechanism
Hemophilia AFactor VIII deficiency
Hemophilia BFactor IX deficiency
Von Willebrand diseaseDefective platelet adhesion
ITPAutoimmune platelet destruction
Vitamin K deficiencyImpaired II, VII, IX, X synthesis
DICWidespread clotting + bleeding
Anticoagulants:
TypeExampleMechanism
NaturalAntithrombin IIIInhibits thrombin + Factor X
NaturalProtein C, Protein SDegrades Va and VIIIa
NaturalTissue factor pathway inhibitor (TFPI)Inhibits extrinsic pathway
ClinicalHeparinActivates antithrombin III
ClinicalWarfarinAntagonizes Vitamin K (inhibits II, VII, IX, X)
ClinicalAspirinInhibits platelet aggregation (COX-1)

3. Blood Grouping + Note on Erythroblastosis Foetalis ⭐⭐⭐

ABO Blood Grouping (Landsteiner's Law):
Blood GroupAntigen on RBCAntibody in Plasma
AAAnti-B
BBAnti-A
ABA & BNone
ONoneAnti-A & Anti-B
Rh System:
  • Rh+: Rh antigen present
  • Rh-: Rh antigen absent
  • Important in blood transfusion and pregnancy
Erythroblastosis Foetalis (Haemolytic Disease of Newborn):
  • Rh- mother carries Rh+ fetus
  • During 1st delivery, fetal RBCs enter maternal blood → mother forms Anti-Rh antibodies
  • In 2nd Rh+ pregnancy, maternal IgG antibodies cross placenta → destroy fetal RBCs → hemolytic anemia, jaundice, hydrops foetalis
  • Prevention: Anti-D immunoglobulin (RhoGAM) given to Rh- mother within 72 hours of delivery

SAQ SECTION


1. Types of Jaundice & Causes ⭐⭐⭐⭐⭐

Jaundice = yellowish discoloration of skin/sclerae due to elevated bilirubin (normal: 0.5 mg/dL; jaundice appears >1.5 mg/dL).
3 Types:
TypeCauseBilirubinUrineStool
Hemolytic (Pre-hepatic)Excess RBC destruction (malaria, sickle cell)Unconjugated ↑Urobilinogen ↑Dark
Hepatocellular (Hepatic)Liver damage (hepatitis, cirrhosis)Both ↑Both ↑Pale
Obstructive (Post-hepatic)Bile duct obstruction (gallstones, cancer)Conjugated ↑Bilirubin ↑, Urobilinogen absentClay-colored
Neonatal Jaundice: Due to immature liver (reduced UDP-glucuronyl transferase) → unconjugated hyperbilirubinemia; treated with phototherapy.
(Guyton and Hall Textbook of Medical Physiology)

2. Functions of Plasma Proteins ⭐⭐⭐⭐⭐

Three major fractions: Albumin, Globulin, Fibrinogen
Albumin (synthesized in liver):
  • Maintains colloid osmotic pressure (oncotic pressure) → prevents edema
  • Transport protein (fatty acids, bilirubin, drugs, hormones)
  • Protein reservoir (amino acid source during starvation)
Globulins:
  • Alpha: Transport (ceruloplasmin, transcortin, haptoglobin)
  • Beta: Transport (transferrin, LDL)
  • Gamma: Immunoglobulins (antibodies) → immunity
Fibrinogen:
  • Converted to fibrin by thrombin → blood clotting
Other functions:
  • Buffer action (maintains pH)
  • Viscosity of blood
  • Acute-phase proteins (CRP, complement) - inflammation response
(Ganong's Review of Medical Physiology; Guyton and Hall)

3. Types of Leucocytes & Their Functions ⭐⭐⭐

Total WBC count: 4,000 - 11,000/mm³
Granulocytes:
  • Neutrophils (60-70%): Phagocytosis of bacteria; first responders
  • Eosinophils (2-4%): Allergic reactions; antiparasitic
  • Basophils (0.5-1%): Release histamine and heparin; mediate allergy
Agranulocytes:
  • Lymphocytes (20-30%): T cells (cell-mediated immunity), B cells (antibody production)
  • Monocytes (2-8%): Become macrophages; phagocytosis; antigen presentation

4. Anticoagulants & Mechanisms of Action ⭐⭐⭐

(See table above in LAQ-2. For SAQ, list and briefly explain each one.)

7. Indications & Complications of Blood Transfusion ⭐⭐⭐⭐⭐

Indications:
  • Severe anemia (Hb <7 g/dL)
  • Acute blood loss (>30% volume)
  • Thrombocytopenia with bleeding
  • Coagulation factor deficiency
  • Exchange transfusion in erythroblastosis foetalis
Complications (TRIM = Transfusion-Related Immunomodulation):
  • Hemolytic reaction (ABO mismatch) - fever, chills, hemoglobinuria
  • Febrile non-hemolytic reaction (most common)
  • Allergic/anaphylactic reaction
  • Transfusion-transmitted infections (HIV, HBV, HCV)
  • Circulatory overload (TACO)
  • Transfusion-related acute lung injury (TRALI)
  • Hypothermia, hypocalcemia, hyperkalemia (massive transfusion)

8. Fibrinolytic System ⭐⭐⭐⭐⭐

Fibrinolysis is the process of dissolving clots after healing.
  • Plasminogen (inactive) → activated to Plasmin by tissue plasminogen activator (tPA) and urokinase
  • Plasmin degrades fibrin → fibrin degradation products (D-dimers)
  • Regulated by: Alpha-2-antiplasmin, PAI-1 (plasminogen activator inhibitor)
Clinical Use:
  • tPA (alteplase), Streptokinase, Urokinase are used as thrombolytic agents in MI and stroke

10. Differentiate Folic Acid Deficiency vs Pernicious Anaemia ⭐⭐⭐

FeatureFolic Acid DeficiencyPernicious Anaemia
CausePoor diet, malabsorption, pregnancy, alcoholAbsence of intrinsic factor (autoimmune)
Deficient factorFolateVitamin B12
Blood pictureMegaloblastic anaemiaMegaloblastic anaemia
Neurological signsAbsentPresent (subacute combined degeneration of spinal cord)
Site of absorptionJejunumTerminal ileum
Schilling testNormalAbnormal
TreatmentFolic acid supplementsIM Vitamin B12 (cyanocobalamin)

VSAQ SECTION


1. A:G Ratio ⭐⭐⭐

  • Albumin to Globulin ratio
  • Normal: 1.2 - 1.7:1
  • Reversed in: chronic liver disease, nephrotic syndrome, myeloma, chronic infections

2. Landsteiner's Law ⭐⭐⭐⭐⭐

  • If an antigen is present on RBC, the corresponding antibody is absent from plasma
  • If an antigen is absent from RBC, the corresponding antibody is present in plasma
  • Example: Blood group A → Anti-B in plasma; Blood group B → Anti-A in plasma

3. Functions of Lymph

  • Returns plasma proteins and fluid to blood
  • Absorption of fat from intestine (lacteals)
  • Immune surveillance (lymphocytes)
  • Transport of fat-soluble vitamins (A, D, E, K)

4. ESR ⭐⭐⭐

  • Erythrocyte Sedimentation Rate = rate at which RBCs settle in 1 hour
  • Normal: Males 0-15 mm/hr; Females 0-20 mm/hr (Westergren method)
  • Increased in: infections, inflammation, pregnancy, malignancy, anemia
  • Decreased in: polycythemia, sickle cell disease

5. RBC Indices ⭐⭐⭐

IndexNormal ValueSignificance
MCV80-100 fLMicro/normo/macrocytic
MCH27-32 pgHypochromic vs normochromic
MCHC32-36 g/dLHypochromic anemia if low

6. Variants of Haemoglobin ⭐⭐⭐

  • HbA: Normal adult (α2β2)
  • HbA2: Minor adult (α2δ2), elevated in β-thalassemia trait
  • HbF: Fetal (α2γ2), has high O2 affinity
  • HbS: Sickle cell (β-chain mutation Val→Glu)
  • HbC, HbE: Other abnormal variants

7. Blood Banking ⭐⭐⭐

  • Collection, testing, processing, and storage of donated blood
  • Key tests: ABO/Rh typing, crossmatch, screening for HIV, HBV, HCV, syphilis
  • Storage: Whole blood at 2-6°C; RBCs up to 42 days; FFP at -18°C

8. BT & CT ⭐⭐⭐

TestNormalMeasures
Bleeding Time (BT)1-6 minutesPlatelet plug (primary hemostasis)
Clotting Time (CT)5-11 minutesIntrinsic coagulation cascade

9. Osmotic Fragility of RBCs ⭐⭐⭐

  • Ability of RBCs to resist hemolysis in hypotonic solutions
  • Increased osmotic fragility (lyse easily): Hereditary spherocytosis
  • Decreased osmotic fragility (resist lysis): Thalassemia, iron deficiency anemia, sickle cell disease
  • Normal: RBCs begin hemolysis at 0.45% NaCl; complete at 0.30% NaCl

Exam Writing Tips

  1. LAQ format: Definition → Classification/Types → Mechanism/Stages (with diagram if applicable) → Clinical significance → Summary (10-15 marks, ~1.5-2 pages)
  2. SAQ format: Definition → Key points in tabular/point format → Clinical note (5 marks, ~half page)
  3. VSAQ format: 2-4 crisp sentences or a small table (2 marks, 4-6 lines)
  4. Always draw a flowchart or table wherever possible - examiners value diagrams
  5. Bold the key terms in your answer
  6. End LAQs with a brief clinical significance line
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