Physiology
Medical physiology for MBBS: cell and body fluids, blood, nerve and muscle, and the cardiovascular, respiratory, gastrointestinal, renal, endocrine, reproductive and nervous systems, special senses and integrative physiology.
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Definition
Blood is a specialised fluid connective tissue (~5–6 L; ~8% of body weight) made of plasma (55%) and formed elements (45%).
Composition
- Plasma (55%) — water 90–92%, proteins, salts, glucose, hormones, wastes
- Formed elements (45%) — RBCs, WBCs, platelets
- Cell-to-blood ratio = haematocrit (~45%)
Plasma Proteins
- Albumin — osmotic pressure, transport
- Globulins — antibodies, transport
- Fibrinogen — clotting
- Total 6–8 g/dL; A:G ratio ~2:1
Functions
- Transport — O₂, CO₂, nutrients, hormones, waste
- Regulation — temperature, pH (buffers), water balance
- Protection — immunity (WBC, antibodies) and clotting
Spun blood separates into an upper plasma layer and lower formed elements. Parameter Normal value Blood volume 5–6 L (~8% body weight) Haematocrit M 40–50%, F 36–46% Plasma proteins 6–8 g/dL Blood pH 7.35–7.45 Applied
- ↓ Albumin → oedema
- Blood is the ‘mirror of the body’ — key diagnostic fluid
🔑KEY POINTS TO REMEMBER- Blood = fluid connective tissue; plasma 55% + formed elements 45%.
- Plasma proteins: albumin, globulin, fibrinogen (6–8 g/dL, A:G 2:1).
- Functions: transport, regulation, protection.
- Haematocrit ~45%; pH 7.35–7.45.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Erythrocytes (RBCs) are biconcave, non-nucleated oxygen-carrying cells (~5 million/mm³); erythropoiesis is their formation in red bone marrow, driven by erythropoietin.
RBC — Features
- Biconcave, non-nucleated, no mitochondria
- Diameter ~7.2 µm; life span ~120 days
- Haemoglobin 13–17 g/dL (M), 12–15 (F)
- Destroyed in the spleen (‘graveyard of RBCs’)
Erythropoiesis — Stages
- Proerythroblast → early normoblast → late normoblast
- → reticulocyte (nucleus lost) → mature RBC
- Site: red bone marrow (fetus: liver, spleen, marrow)
Factors Required
- Erythropoietin (from the kidney)
- Iron, vitamin B12, folic acid
- Proteins, vitamin C, copper, thyroxine
Erythropoietin drives a marrow stem cell through normoblast and reticulocyte to a mature RBC. Regulation
- Hypoxia → ↑ erythropoietin (kidney) → ↑ RBC production
Applied
- Renal failure → ↓ erythropoietin → anaemia
- ↑ Reticulocyte count → active marrow (after bleeding/treatment)
- Polycythaemia — excess RBCs
Parameter Normal value RBC count 4.5–5.5 million/mm³ Haemoglobin M 13–17, F 12–15 g/dL MCV 80–96 fl Life span 120 days Reticulocyte 0.5–2% Fate of Old RBCs
- Destroyed in the spleen after ~120 days
- Haem → iron (recycled) + bilirubin
- Globin → amino acids reused
- Excess breakdown → jaundice
🔑KEY POINTS TO REMEMBER- RBC: biconcave, non-nucleated, ~5 million/mm³, life 120 days.
- Erythropoiesis in red marrow; needs EPO, iron, B12, folate.
- EPO from kidney ↑ with hypoxia.
- Renal failure → anaemia; reticulocyte count = marrow activity.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Haemostasis is the arrest of bleeding from an injured vessel, in three steps: vascular spasm, platelet plug and blood coagulation.
Stages of Haemostasis
- 1. Vascular spasm — vessel constricts, reduces blood loss
- 2. Platelet plug — platelets adhere, activate, aggregate
- 3. Coagulation — fibrin clot forms
- 4. Clot retraction & fibrinolysis — healing and clearance
Coagulation Pathways
- Intrinsic — activated within blood (tested by aPTT)
- Extrinsic — tissue factor from injured tissue (tested by PT)
- Both → common pathway: prothrombin → thrombin → fibrinogen → fibrin
- Requires Ca²⁺ (factor IV) and vitamin K
Bleeding is stopped by spasm, then a platelet plug, then a fibrin clot. Test What it checks Bleeding time Platelet function PT / INR Extrinsic pathway aPTT Intrinsic pathway Clotting time Overall coagulation Applied
- Haemophilia A (factor VIII), B (factor IX)
- Warfarin blocks vitamin K; heparin activates antithrombin
- Vitamin K deficiency → bleeding tendency
🔑KEY POINTS TO REMEMBER- Haemostasis: spasm → platelet plug → coagulation → fibrinolysis.
- Intrinsic (aPTT) + extrinsic (PT) → common path → fibrin.
- Needs Ca²⁺ and vitamin K.
- Haemophilia A = factor VIII deficiency.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Leucocytes (WBCs) are nucleated blood cells of the defence system (total count 4,000–11,000/mm³), classified into granulocytes and agranulocytes.
Classification (with normal %)
- Granulocytes — neutrophil 40–75%, eosinophil 1–6%, basophil <1%
- Agranulocytes — lymphocyte 20–45%, monocyte 2–8%
Functions
- Neutrophil — phagocytose bacteria (first line)
- Eosinophil — parasites and allergy
- Basophil — release histamine and heparin (allergy)
- Lymphocyte — specific immunity (B → antibodies, T → cell-mediated)
- Monocyte → macrophage — phagocytosis, antigen presentation
Two families: granulocytes (with granules) and agranulocytes. Cell % Main role Neutrophil 40–75 Bacteria Lymphocyte 20–45 Immunity Monocyte 2–8 Macrophage Eosinophil 1–6 Parasite/allergy Basophil <1 Histamine Applied
- Neutrophilia — bacterial infection; Lymphocytosis — viral
- Eosinophilia — allergy/parasite
- Leukaemia — malignant ↑ WBC; Leucopenia — ↓ WBC
💡Order of frequency (Never Let Monkeys Eat Bananas): Neutrophil > Lymphocyte > Monocyte > Eosinophil > Basophil.🔑KEY POINTS TO REMEMBER- WBC 4,000–11,000/mm³; granulocytes + agranulocytes.
- Neutrophil = bacteria; lymphocyte = immunity; monocyte = macrophage.
- Eosinophil = allergy/parasite; basophil = histamine.
- Neutrophilia (bacterial), lymphocytosis (viral), eosinophilia (allergy).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Blood groups are determined by antigens on the RBC surface; the two major systems are ABO and Rh.
ABO System
- A — A antigen, anti-B antibody
- B — B antigen, anti-A antibody
- AB — A & B antigens, no antibody (universal recipient)
- O — no antigen, anti-A & anti-B (universal donor)
Rh System
- Rh (D) antigen present = Rh positive
- Absent = Rh negative
- Important in pregnancy (erythroblastosis fetalis)
Group Antigen Antibody Can receive A A anti-B A, O B B anti-A B, O AB A, B none all O none anti-A,B O Transfusion needs ABO match, Rh match and a cross-match to avoid a reaction. Transfusion Reaction
- Mismatch → agglutination + haemolysis
- Fever, chills, jaundice, renal failure
- Always cross-match before transfusion
Applied
- Rh– mother + Rh+ fetus → HDN; prevent with anti-D
- O negative = universal donor; AB positive = universal recipient
🔑KEY POINTS TO REMEMBER- Blood group = RBC surface antigen; ABO & Rh are major.
- O = universal donor; AB = universal recipient.
- Antibody is against the absent antigen (A has anti-B).
- Rh– mother + Rh+ fetus → HDN (prevent with anti-D).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Plasma proteins are proteins in plasma (total 6–8 g/dL), mostly made by the liver: albumin, globulins and fibrinogen.
Types & Functions
- Albumin (3.5–5 g/dL) — osmotic pressure, transport
- Globulins (2–3.5 g/dL) — γ: antibodies; α,β: transport
- Fibrinogen — blood clotting
- A:G ratio ~2:1
General Functions
- Colloid osmotic (oncotic) pressure
- Immunity (antibodies)
- Clotting; acid-base buffering
- Transport of hormones, drugs, ions
- Suspension stability (affects ESR)
Three groups with three key roles: oncotic pressure, immunity and clotting. Applied
- ↓ Albumin → oedema (liver/kidney disease)
- A:G reversal → chronic infection, multiple myeloma
Protein Value (g/dL) Function Albumin 3.5–5 Oncotic pressure, transport Globulin 2–3.5 Immunity, transport Fibrinogen 0.2–0.4 Clotting 🔑KEY POINTS TO REMEMBER- Plasma proteins 6–8 g/dL: albumin, globulin, fibrinogen.
- Albumin = oncotic pressure; globulin = immunity; fibrinogen = clotting.
- ↓ Albumin → oedema; A:G ratio ~2:1.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Platelets (thrombocytes) are small non-nucleated cell fragments (1.5–4 lakh/mm³) derived from megakaryocytes, essential for haemostasis.
Features
- Non-nucleated fragments of megakaryocytes
- Count 1.5–4 lakh/mm³; life span 7–10 days
- Formation controlled by thrombopoietin
- About one-third stored in the spleen
Functions
- Adhesion → activation → aggregation → platelet plug
- Release ADP, thromboxane A2, serotonin
- Clot retraction
- Release growth factors (wound healing)
Platelets adhere, activate and aggregate to form the first plug. Applied
- ↓ Platelets (thrombocytopenia) → petechiae, bleeding
- Aspirin inhibits platelet aggregation (antiplatelet)
Parameter Value Count 1.5–4 lakh/mm³ Life span 7–10 days Source Megakaryocyte Control Thrombopoietin 🔑KEY POINTS TO REMEMBER- Platelets 1.5–4 lakh/mm³, from megakaryocytes, life 7–10 days.
- Function: adhesion → activation → aggregation → plug.
- Thrombocytopenia → bleeding; aspirin → antiplatelet.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Anaemia is a reduction in blood haemoglobin below normal (M <13, F <12, pregnancy <11 g/dL), lowering the oxygen-carrying capacity.
Morphological Classification (by MCV)
- Microcytic hypochromic — iron deficiency, thalassaemia
- Normocytic normochromic — acute blood loss, chronic disease
- Macrocytic — vitamin B12 / folate deficiency
Etiological Classification
- Blood loss (haemorrhagic)
- ↓ Production (nutritional, marrow failure)
- ↑ Destruction (haemolytic)
Grouping by cell size quickly points to the cause. Features & Applied
- Pallor, fatigue, dyspnoea, palpitation
- Commonest in India = iron-deficiency anaemia
- Investigate: Hb, MCV, peripheral smear
Type (MCV) Cause Example Microcytic (<80) ↓ Hb synthesis Iron deficiency, thalassaemia Normocytic (80–96) Blood loss Haemorrhage, chronic disease Macrocytic (>96) ↓ DNA synthesis B12 / folate deficiency 🔑KEY POINTS TO REMEMBER- Anaemia = ↓ Hb (M<13, F<12, pregnancy<11 g/dL).
- By MCV: microcytic (iron), normocytic (blood loss), macrocytic (B12/folate).
- Commonest = iron deficiency.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Immunity is the body’s ability to resist and eliminate foreign agents. It is of two types — innate (non-specific) and acquired (specific).
Innate (Inborn) Immunity
- Present from birth; non-specific; immediate
- Barriers — skin, mucous membranes, acid
- Cells — neutrophils, macrophages, NK cells
- No memory
Acquired (Adaptive) Immunity
- Develops after exposure; specific; has memory
- Humoral — B lymphocytes → antibodies
- Cell-mediated — T lymphocytes
Active vs Passive
- Active — body makes its own antibodies (infection, vaccine); slow, long-lasting
- Passive — ready-made antibodies given (placenta, serum); quick, short-lived
Innate acts at once and generally; acquired is specific and remembers. Applied
- Vaccination → active immunity
- Anti-tetanus / anti-rabies serum → passive immunity
Feature Innate Acquired Onset Immediate Delayed Specificity Non-specific Specific Memory Absent Present Cells Neutrophil, macrophage B & T lymphocytes 🔑KEY POINTS TO REMEMBER- Immunity: innate (non-specific, no memory) + acquired (specific, memory).
- Acquired: humoral (B cells, antibodies) + cell-mediated (T cells).
- Active (vaccine, lasting) vs passive (serum, quick, short).
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus; maternal anti-Rh antibodies destroy fetal RBCs — haemolytic disease of the newborn (erythroblastosis fetalis).
Mechanism
- 1st pregnancy: fetal Rh+ cells enter mother at delivery → sensitisation
- Mother forms anti-D (IgG) antibodies
- Next Rh+ pregnancy: anti-D crosses the placenta
- Destroys fetal RBCs → haemolysis
Effects on the Baby
- Anaemia and jaundice
- Hydrops fetalis (severe oedema)
- Kernicterus (bilirubin brain damage)
First pregnancy sensitises; later ones are attacked — anti-D prevents it. Prevention & Treatment
- Anti-D immunoglobulin within 72 h of delivery/abortion/bleeding
- Treatment: phototherapy, exchange transfusion
1st Rh+ pregnancy Later Rh+ pregnancy Fetal risk Usually safe At risk (HDN) Reason Sensitisation only Anti-D crosses placenta 🔑KEY POINTS TO REMEMBER- Rh– mother + Rh+ fetus → sensitisation → HDN in next pregnancy.
- 1st pregnancy usually safe; risk rises later.
- Prevent with anti-D within 72 h; treat with phototherapy/exchange transfusion.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
The erythrocyte sedimentation rate (ESR) is the rate at which RBCs settle in an anticoagulated vertical column of blood in one hour — a non-specific marker of inflammation.
Normal Values & Methods
- Male 0–15 mm/hr, Female 0–20 mm/hr
- Methods: Westergren (standard), Wintrobe
Mechanism (why it rises)
- Inflammation → ↑ fibrinogen and globulins
- → RBCs stack into rouleaux
- Heavier rouleaux settle faster → ↑ ESR
Inflammatory proteins make RBCs stack and fall faster, raising the ESR. Causes of ↑ ESR / Applied
- TB, chronic infection, malignancy, multiple myeloma
- Also ↑ in anaemia, pregnancy, old age
- Non-specific — used to monitor disease activity
ESR Causes Increased TB, infection, malignancy, myeloma, anaemia, pregnancy Decreased Polycythaemia, sickle-cell disease, heart failure 🔑KEY POINTS TO REMEMBER- ESR = rate of RBC settling in 1 hr; Westergren method.
- Normal: M 0–15, F 0–20 mm/hr.
- Rises via ↑ fibrinogen → rouleaux; non-specific.
- High in TB, myeloma, infection.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).Definition
Anticoagulants are agents that prevent blood clotting, used in vivo (treatment) and in vitro (laboratory).
In Vivo (Therapeutic)
- Heparin — fast, parenteral; activates antithrombin; monitored by aPTT
- Warfarin — slow, oral; blocks vitamin K; monitored by PT/INR
In Vitro (Laboratory)
- EDTA — blood counts (chelates Ca²⁺)
- Sodium citrate — coagulation tests, blood bank
- Oxalate, heparin — various tests
In the body: heparin/warfarin. In the lab: calcium-removing agents. Applied
- Used in DVT, pulmonary embolism, dialysis, stored blood
- Reversal: heparin → protamine; warfarin → vitamin K
Agent Action Use Heparin Activates antithrombin Rapid, in vivo Warfarin Blocks vitamin K Oral, long-term Citrate Removes Ca²⁺ Blood bank EDTA Chelates Ca²⁺ Blood counts 🔑KEY POINTS TO REMEMBER- In vivo: heparin (fast, aPTT), warfarin (slow, PT/INR).
- In vitro: EDTA (counts), citrate (coagulation/blood bank).
- Lab agents work by removing Ca²⁺.
📚SOURCES: Guyton & Hall Textbook of Medical Physiology; Ganong’s Review of Medical Physiology; Textbook of Physiology (A.K. Jain).