What Is Blood?
Blood is a specialised connective tissue — yes, connective tissue, not just a fluid. It consists of living cells (formed elements) suspended in a non-living fluid matrix called plasma. About 8% of your body weight is blood; an average adult has 5–6 litres.
Blood is not just a transport medium. It is simultaneously a heat distributor, an immune army, a wound-sealer, and a pH buffer. Understanding its composition explains all these roles.
Composition of Blood
Blood has two major components:
Plasma (55% of blood volume):
- 90–92% water
- Proteins: fibrinogen, globulins (antibodies), albumin (maintains osmotic pressure)
- Nutrients: glucose, amino acids, fatty acids, vitamins
- Waste products: urea, uric acid, CO₂
- Hormones, enzymes, inorganic salts
Plasma without clotting factors (fibrinogen) is called serum.
Formed Elements (45% of blood volume): Three types of cells float in plasma:
Red Blood Cells (Erythrocytes, RBCs)
RBCs are the most abundant cells in blood — about 5 million per mm³ in males, 4.5 million in females.
Key features:
- Biconcave disc shape — increases surface area for gas exchange without increasing volume
- No nucleus in mature RBCs (in mammals) — more space for haemoglobin
- Contain haemoglobin (Hb): an iron-containing protein that carries O₂ (as oxyhaemoglobin) and CO₂
- Life span: ~120 days; destroyed in spleen (the “graveyard of RBCs”)
- Made in red bone marrow
Haemoglobin: Each Hb molecule has 4 globin chains, each with a heme group containing Fe²⁺. One Hb molecule can carry 4 O₂ molecules. Adult haemoglobin (HbA) differs from fetal haemoglobin (HbF) — HbF has higher O₂ affinity, allowing the fetus to extract O₂ from maternal blood.
White Blood Cells (Leucocytes, WBCs)
WBCs are the soldiers of the immune system. Count: 6000–8000 per mm³ (much fewer than RBCs). Lifespan varies from hours (neutrophils) to years (memory lymphocytes).
Two main categories:
Granulocytes (have visible granules in cytoplasm):
- Neutrophils (60–65%): First responders to bacterial infection; phagocytose bacteria; pus contains dead neutrophils
- Eosinophils (2–3%): Fight parasitic infections; involved in allergic reactions
- Basophils (<1%): Release histamine and heparin; involved in inflammation
Agranulocytes (no visible granules):
- Monocytes (6–8%): Largest WBCs; differentiate into macrophages in tissues; phagocytose large particles
- Lymphocytes (20–25%): B lymphocytes (antibody production), T lymphocytes (cell-mediated immunity)
NEET loves questions about which WBC type is most abundant (neutrophils), largest (monocyte), smallest (lymphocyte), and which is involved in allergies (eosinophil) vs histamine release (basophil). Memorise these comparisons.
Platelets (Thrombocytes)
Platelets are not true cells — they are cell fragments pinched off from large cells called megakaryocytes in bone marrow. Count: 1.5–3.5 lakh per mm³. They are essential for blood clotting.
Blood Groups — ABO and Rh System
ABO Blood Group System
Blood groups are determined by the presence or absence of specific antigens on the surface of RBCs, and corresponding antibodies in the plasma.
| Blood Group | Antigen on RBCs | Antibody in Plasma | Can Donate To | Can Receive From |
|---|---|---|---|---|
| A | A antigen | Anti-B | A, AB | A, O |
| B | B antigen | Anti-A | B, AB | B, O |
| AB | A + B antigens | None | AB only | A, B, AB, O |
| O | None | Anti-A and Anti-B | A, B, AB, O | O only |
Group O is the universal donor (no antigens to trigger reaction).
Group AB is the universal recipient (no antibodies to react with donor antigens).
Remember: the antibody in plasma is always against the antigens you DON’T have on your RBCs. Group A has anti-B antibodies; Group B has anti-A antibodies; Group O has both (you’re “missing” both antigens); Group AB has neither (you already have both antigens, so no need for antibodies against them).
Rh Blood Group System
Rh factor is another antigen system. About 80% of Indians are Rh+ (have Rh antigen). Rh⁻ individuals develop anti-Rh antibodies only after exposure to Rh⁺ blood.
Erythroblastosis foetalis (Haemolytic Disease of the Newborn):
- Mother is Rh⁻, Father is Rh⁺, Baby is Rh⁺
- First pregnancy: Rh⁺ fetal blood may leak into Rh⁻ mother’s blood during delivery → mother develops anti-Rh antibodies
- Second pregnancy with Rh⁺ fetus: mother’s anti-Rh antibodies cross the placenta → attack fetal RBCs → severe anaemia in fetus
- Prevention: give anti-Rh antibodies (Rho-GAM) to Rh⁻ mother within 72 hours of first delivery — prevents her from developing the antibodies
Blood Clotting (Coagulation)
When you cut yourself, blood vessels constrict, platelets aggregate, and a cascade of reactions forms a clot to stop bleeding. This is haemostasis.
Injury → Platelet aggregation
Damaged tissue releases thromboplastin (tissue factor)
Thromboplastin + Ca²⁺ + Clotting factors → activates Prothrombin activator
Prothrombin (inactive) → Thrombin (active enzyme)
Thrombin acts on Fibrinogen (soluble protein in plasma)
→ Fibrin (insoluble threads form a mesh)
Fibrin mesh traps RBCs and platelets → Blood clot
Key clotting factors:
- Vitamin K is required for synthesis of several clotting factors (II, VII, IX, X)
- Ca²⁺ is essential at multiple steps — this is why blood banks store blood with citrate or EDTA (calcium chelators that prevent clotting)
- Factor VIII deficiency causes Haemophilia A (the most common haemophilia)
- Factor IX deficiency causes Haemophilia B (Christmas disease)
CBSE Class 12 and NEET ask: “Why is blood stored with sodium citrate?” Answer: Citrate chelates Ca²⁺ ions, preventing the clotting cascade. Without calcium, blood cannot clot even after storage.
Disorders of Blood
Anaemia: Reduced haemoglobin or RBC count. Most common cause in India: iron deficiency (iron is needed for heme synthesis).
Sickle Cell Anaemia: Mutation in the β-globin gene (valine replaces glutamate at position 6). Causes HbS to polymerise under low oxygen conditions, distorting RBCs into a sickle shape. Sickle cells clog capillaries and are destroyed faster, causing anaemia and painful crises.
Haemophilia: X-linked recessive disorder. Males (XY) are more commonly affected. The disease is “royal” — it ran in the European royal families descended from Queen Victoria.
Leukaemia: Cancer of blood-forming tissues; abnormal WBC proliferation. White blood cell count rises dramatically (sometimes > 100,000/mm³).
Thalassaemia: Reduced synthesis of globin chains (α or β). Very common in India, especially in tribal populations.
Solved Examples
Example 1 (CBSE Level): A person has blood group A. What antigens and antibodies do they have?
Antigens on RBCs: A antigens
Antibodies in plasma: Anti-B antibodies
They can donate blood to: Group A and Group AB
They can receive blood from: Group A and Group O
Example 2 (NEET Level): An Rh⁻ mother delivers her second Rh⁺ baby. What complication may arise?
During the first pregnancy, the Rh⁻ mother may have been sensitised to the Rh⁺ antigen from the first baby’s blood. She now has anti-Rh antibodies. In the second pregnancy, these IgG antibodies cross the placenta and attack the Rh⁺ fetal RBCs, causing haemolytic anaemia — erythroblastosis foetalis. Treatment: blood transfusion to the fetus; prevention via Rho-GAM injection to the mother after the first delivery.
Common Mistakes to Avoid
Mistake 1: Saying plasma = serum. Serum is plasma minus fibrinogen and other clotting proteins. Plasma contains fibrinogen; serum does not. This distinction appears every year in CBSE.
Mistake 2: Confusing the clotting sequence. Fibrinogen comes before fibrin; prothrombin comes before thrombin. Fibrinogen → fibrin (the end product); prothrombin → thrombin (the enzyme that acts on fibrinogen). Don’t reverse these.
Mistake 3: Writing that Group AB is the universal donor. Group O is the universal donor. Group AB is the universal recipient. This is a 1-mark reversal error that commonly occurs.
Practice Questions
Q1. Which type of WBC is most abundant in blood?
Neutrophils (60–65% of all WBCs). They are the first line of defence against bacterial infections and are the main component of pus.
Q2. Why don’t mature RBCs in humans have mitochondria?
Mature RBCs eject not just the nucleus but also organelles including mitochondria, to maximise space for haemoglobin. They produce ATP via anaerobic glycolysis instead. The absence of mitochondria means RBCs do not consume the O₂ they are transporting.
Q3. What is the role of Vitamin K in blood clotting?
Vitamin K is required for the synthesis (specifically, the gamma-carboxylation) of clotting factors II (prothrombin), VII, IX, and X in the liver. Without vitamin K, these factors are synthesised but inactive. Deficiency leads to prolonged bleeding (haemorrhage). Warfarin, a blood thinner, works by blocking vitamin K action.
Q4. A person’s blood coagulates in 15–20 minutes instead of the normal 2–8 minutes. Which disease do they likely have?
Haemophilia. Delayed clotting indicates a deficiency in one of the clotting factors. Haemophilia A (Factor VIII deficiency) is the most common form. The person’s blood eventually clots but takes much longer because of the missing factor.
Differential WBC Count — Clinical Significance
Understanding which WBC type is elevated helps diagnose infections and diseases. This is tested in NEET under “body fluids and circulation.”
| Condition | WBC Change | Clinical Significance |
|---|---|---|
| Bacterial infection | Neutrophilia (high neutrophils) | Body’s first-line response to bacteria |
| Parasitic infection | Eosinophilia (high eosinophils) | Eosinophils target parasites |
| Allergic reaction | Eosinophilia + Basophilia | Histamine release triggers immune cascade |
| Viral infection | Lymphocytosis (high lymphocytes) | T and B cells fight viral infections |
| Chronic infection | Monocytosis (high monocytes) | Macrophages clean up persistent infections |
| Leukaemia | Extremely high total WBC | Uncontrolled proliferation of abnormal WBCs |
NEET 2023 asked: “A patient shows eosinophilia. What is the most likely cause?” The answer choices included bacterial infection, viral infection, allergic reaction, and cancer. Correct answer: allergic reaction (or parasitic infection). Eosinophils are specifically associated with allergies and parasites, not bacteria or viruses.
Oxygen-Haemoglobin Dissociation Curve
The relationship between oxygen partial pressure and haemoglobin saturation follows a sigmoid (S-shaped) curve. This shape has important physiological implications:
At the lungs (high pO₂ ~100 mmHg): Hb is nearly 100% saturated — it loads oxygen efficiently.
At the tissues (low pO₂ ~40 mmHg): Hb releases a large proportion of its oxygen — it unloads efficiently.
The Bohr effect: increased CO₂ and decreased pH (more acidic conditions, as in actively metabolising tissues) shift the curve to the RIGHT — meaning Hb releases oxygen more readily where it is most needed.
Fetal haemoglobin (HbF) has a curve shifted to the LEFT of adult HbA — it has higher oxygen affinity, allowing the fetus to extract O₂ from maternal blood in the placenta.
Q5. Why is carbon monoxide (CO) poisoning so dangerous?
CO binds to haemoglobin with an affinity about 200 times greater than oxygen, forming carboxyhaemoglobin (HbCO). Once bound, CO does not easily dissociate. This means: (1) the CO-occupied haemoglobin cannot carry oxygen, and (2) the remaining haemoglobin holds onto its oxygen more tightly (the dissociation curve shifts left), making it harder for tissues to extract even the little oxygen available. The combination of reduced oxygen-carrying capacity and impaired oxygen release makes CO poisoning lethal even at relatively low CO concentrations.
Q6. Explain why stored blood is mixed with sodium citrate or EDTA, not with heparin for long-term storage.
Sodium citrate and EDTA are calcium chelators — they bind and sequester Ca²⁺ ions, which are essential for multiple steps in the clotting cascade. Without free Ca²⁺, the cascade cannot proceed and blood remains unclotted. Heparin works differently — it activates antithrombin III, which inhibits thrombin. While heparin is used for short-term anticoagulation (during surgery), citrate is preferred for blood bank storage because it is less expensive, easy to reverse (by adding calcium back), and does not interfere with subsequent transfusion compatibility testing.
FAQs
What makes blood red? The iron in haemoglobin (specifically Fe²⁺ in the heme group) gives blood its red colour. Oxyhaemoglobin (with O₂) is bright red; deoxyhaemoglobin is darker red (not blue — veins appear blue due to light absorption by skin, but venous blood is dark red, not blue).
Why does blood type matter for transfusions? Transfusing incompatible blood causes agglutination — the donor’s RBC antigens react with the recipient’s plasma antibodies, forming clumps. These clumps block capillaries and trigger immune reactions that can be fatal.
Why is haemophilia rare in females? Haemophilia is X-linked recessive. Females (XX) need two defective copies to show the disease. Males (XY) only have one X chromosome — one defective copy is sufficient. Females usually carry one defective X and one normal X (carrier females) and don’t show symptoms but can pass the defective gene to sons.
What is the normal clotting time? Normal blood clotting time is 2–8 minutes (Lee-White method) or 1–2 minutes (Duke’s method). Platelet count and clotting factor levels both affect this.