Blood

Blood

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Blood is a specialized fluid connective tissue with plasma (55%) and formed elements (45%). Total blood volume ≈ 70 mL/kg (≈5L males, ≈4.5L females). Hemoglobin: 14–18 g/dL (males), 12–16 g/dL (females). Hematocrit: ~45% males, ~40% females. Platelets: 150,000–400,000/μL. Total WBC: 4,000–11,000/μL.

Key formulas: O₂ carrying capacity = Hb × 1.34 mL O₂/g; RPI = (Retic% / maturation factor) × (Patient Hct / 45).

INI CET high-yield pointers: ABO naturally occurring antibodies are IgM (not IgG) — a classic trap. Rh-negative hemolytic disease occurs post-sensitization only. Vitamin K-dependent factors: II, VII, IX, X. ESR rises primarily due to fibrinogen (not only immunoglobulins). Blood indices: MCV distinguishes micro/normo/macrocytic; MCHC detects hypochromia.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Composition

Blood consists of plasma and formed elements. Plasma is 91–92% water with plasma proteins: albumin (4–5 g/dL) — principal determinant of colloid osmotic pressure; globulin (2–3 g/dL) — includes immunoglobulins and transport proteins; fibrinogen (0.3 g/dL) — essential for coagulation. Serum is plasma without fibrinogen (clotted blood). Formed elements include erythrocytes, leukocytes, and platelets.

Erythrocytes

RBCs are biconcave discs (7.2 μm diameter) with no nucleus, maximizing surface area for gas exchange. Lifespan is 120 days, after which senescent RBCs are phagocytosed by splenic macrophages. Hemoglobin (Hb) carries oxygen — each Hb molecule binds up to 4 O₂ molecules via iron in heme. RBC production (erythropoiesis) is driven by erythropoietin from kidney peritubular cells in response to hypoxia.

RBC Indices (diagnostic cornerstone)

Index	Formula	Normal
MCV (Mean Corpuscular Volume)	PCV/RBC count	80–100 fL
MCH (Mean Corpuscular Hemoglobin)	Hb/RBC count	27–33 pg
MCHC (Mean Corpuscular Hemoglobin Concentration)	Hb/PCV	32–36 g/dL

MCV classifies anemias: microcytic (<80 fL), normocytic (80–100 fL), macrocytic (>100 fL). MCHC <32 g/dL indicates hypochromia. These indices appear frequently in INI CET data-interpretation questions.

Leukocytes

Total WBC count: 4,000–11,000/μL. Differential: Neutrophils 60–70% (first responders to bacterial infection); Lymphocytes 20–25% (adaptive immunity — T cells and B cells); Monocytes 3–8% (transform to macrophages); Eosinophils 1–4% (parasitic infections, allergic reactions); Basophils <1% (mast cell equivalents, histamine release).

Platelets

Derived from megakaryocytes in bone marrow. Count: 150,000–400,000/μL. Lifespan: 7–10 days. Platelets contain alpha granules (fibrinogen, PDGF, vWF) and dense bodies (ADP, serotonin, calcium) — essential for hemostasis.

ABO Blood Group System

Group	Antigen on RBC	Antibody in plasma
A	A antigen	Anti-B (IgM)
B	B antigen	Anti-A (IgM)
AB	Both A and B	Neither
O	Neither	Both anti-A and anti-B

Group O is universal donor; Group AB is universal recipient. Naturally occurring ABO antibodies are IgM (present by 6 months of age without prior exposure) — clinically relevant because IgM does not cross the placenta.

Rh System

Rh antigen (D antigen) is the most immunogenic. Rh-negative individuals do not have anti-D antibodies until sensitized (transfusion, pregnancy, childbirth). Hemolytic disease of the newborn (HDN) occurs when an Rh-negative mother develops anti-D IgG antibodies in a subsequent pregnancy with an Rh-positive fetus — these IgG antibodies cross the placenta causing fetal hemolysis. Prevention: Rho(D) immunoglobulin given to the mother at 28 weeks gestation and within 72 hours of delivery.

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🔴 Extended — Deep Study (3mo+)

Comprehensive coverage for students on a longer study timeline.

Hemostasis: Primary and Secondary

Primary hemostasis (platelet plug formation): vascular injury triggers vasospasm → platelet adhesion to exposed subendothelial collagen via von Willebrand factor (vWF) → platelet activation (shape change, granule release) → platelet aggregation (GP IIb/IIIa binds fibrinogen) forming a temporary platelet plug. Takes 3–7 minutes.

Secondary hemostasis (coagulation cascade): propagates through enzymatic reactions forming fibrin mesh. Two pathways converge:

• Extrinsic pathway: Tissue Factor (Factor III) released from damaged tissue binds Factor VII → activates Factor X. Measured by PT (Prothrombin Time) — screens extrinsic and common pathway. Prolonged PT indicates deficiency in Factor VII, X, V, II, or fibrinogen.
• Intrinsic pathway: Contact activation (exposure to negatively charged surfaces/glass) activates Factor XII → Factor XI → Factor IX (requires Factor VIII as cofactor) → Factor X. Measured by aPTT (Activated Partial Thromboplastin Time) — screens intrinsic and common pathway. Prolonged aPTT indicates Factor XII, XI, IX, VIII, X, V, II, or fibrinogen deficiency.

Both pathways converge at Factor X → Factor Xa (with Factor Va) converts prothrombin (Factor II) → thrombin (Factor IIa) → thrombin cleaves fibrinogen → fibrin monomer → Factor XIIIa cross-links fibrin stabilizes the clot. Vitamin K-dependent factors: II, VII, IX, X (also Protein C and S). Warfarin inhibits vitamin K epoxide reductase, reducing synthesis of these factors — monitoring via INR (International Normalized Ratio).

Reticulocyte Production Index (RPI)

Reticulocytes are immature RBCs released from bone marrow (normal: 0.5–2.5%). RPI corrects for the degree of anemia and reticulocyte maturation time (shorter at lower hematocrit). RPI = (Retic% × Patient Hct) / (Maturation factor × 45). RPI >2 indicates adequate marrow response (hyperproliferative anemia); RPI <2 indicates inadequate response (hypoproliferative anemia) — guides distinction between production defect vs. destruction/loss.

Blood Volume Calculation

Blood volume (BV) = body weight (kg) × 70 mL/kg. For a 70 kg male: BV ≈ 4.9–5 L. Plasma volume = BV × (1 − Hct). In anemia, the body compensates by increasing plasma volume (dilutional effect), masking the true RBC deficit — always interpret Hct in clinical context.

Common INI CET Traps

1. Serum vs. plasma confusion: Serum lacks fibrinogen (removed during clotting) — relevant in coagulation questions.
2. ABO antibodies are IgM: Many candidates answer IgG — a high-frequency trap. Remember IgM does not cross placenta (hence ABO HDN is rare; Rh HDN is the major concern).
3. PT vs. aPTT: Prolonged aPTT = intrinsic pathway defect (Hemophilia A/B — Factor VIII/IX deficiency); prolonged PT = extrinsic pathway defect (Factor VII deficiency, warfarin effect). Both prolonged = common pathway/coagulation factor problem.
4. Erythropoietin source: Primarily kidney (not liver) — relevant in chronic kidney disease anemia.
5. ESR mechanism: Elevated fibrinogen (acute phase reactant) increases ESR by increasing RBC stacking (rouleaux formation) — not primarily due to immunoglobulins.

Practice Prompts

1. A patient with aPT T of 65 seconds (normal 25–35 sec) and normal PT undergoes factor assay which reveals Factor VIII deficiency. What is the diagnosis, and what is the physiological role of Factor VIII in the intrinsic pathway?

2. A Rh-negative mother delivered a Rh-positive baby. She did not receive RhoGAM. In her second pregnancy, the fetus is Rh-positive. Describe the sequence of events leading to hemolytic disease of the newborn, specifying the antibody class involved and the mechanism of fetal red cell destruction.

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