Components of Blood
and Their Functions
An interactive e-learning module for B.Sc. Zoology students following the UGC Four Quadrant approach
🎯 Learning Objectives
- Describe the composition and properties of blood plasma.
- Distinguish the structural and functional characteristics of erythrocytes, leukocytes, and thrombocytes.
- Explain the role of haemoglobin in oxygen and carbon dioxide transport.
- Outline the process of haemostasis and blood clotting.
- Relate disruptions in blood composition to specific clinical disorders.
Introduction to Blood
Blood is a specialised connective tissue — and yes, it truly is a tissue — that circulates continuously through the cardiovascular system of vertebrates. It is the body's indispensable courier service: delivering oxygen and nutrients, whisking away metabolic waste, broadcasting hormonal signals, and mounting defence whenever pathogens dare to invade. In an adult human, approximately 5–6 litres of blood course through roughly 96,000 km of blood vessels, working tirelessly every second of life.
Blood is not a simple fluid. It is a dynamic, living mixture of cells suspended in a protein-rich liquid medium. Understanding its components is foundational to the entire study of animal physiology.
📊 Composition of Whole Blood (Approximate Volume %)
The fraction of blood occupied by red blood cells is called the haematocrit (PCV). Normal haematocrit: ~45% in males, ~40% in females.
Tap on a cell type to explore it
Plasma constitutes about 55% of total blood volume. It is a pale-yellow, slightly alkaline fluid (pH 7.35–7.45) consisting of approximately 91–92% water, the remainder being dissolved solutes.
- Plasma proteins (6–8 g/dL): Albumin (maintains oncotic pressure), globulins (immunoglobulins for immunity; transport proteins), fibrinogen (clotting precursor).
- Electrolytes: Na⁺, K⁺, Ca²⁺, Mg²⁺, Cl⁻, HCO₃⁻ — essential for membrane potential and acid-base balance.
- Nutrients: Glucose (80–120 mg/dL fasting), amino acids, fatty acids, vitamins.
- Gases: O₂, CO₂, N₂ in dissolved form.
- Waste products: Urea, creatinine, bilirubin — all en route to excretory organs.
- Hormones and enzymes in trace amounts.
When fibrinogen and other clotting factors are removed from plasma, the remaining fluid is called serum.
Erythrocytes are the most abundant formed elements of blood — a single microlitre of human blood contains roughly 4.5–5.5 million RBCs in males and 4.0–5.0 million in females.
Structural adaptations:
- Biconcave disc shape: increases surface area-to-volume ratio, optimising gas diffusion.
- Anucleate (in mammals): the absence of a nucleus and organelles maximises interior space for haemoglobin (~280 million molecules per cell).
- Flexible membrane: enables deformation when squeezing through capillaries as narrow as 3–4 µm.
- Diameter ~7–8 µm; thickness ~2 µm at periphery, ~1 µm at centre.
Haemoglobin: A quaternary protein with 4 globin subunits (2α + 2β in adult HbA), each bearing a haem group containing Fe²⁺. One haemoglobin molecule binds 4 O₂ molecules cooperatively (sigmoidal O₂ dissociation curve). CO₂ is transported as carbaminohaemoglobin (~23%) and dissolved in plasma (~7%), with the majority (~70%) as HCO₃⁻ via the carbonic anhydrase reaction inside RBCs.
Erythropoiesis (RBC production) occurs in red bone marrow, regulated by the hormone erythropoietin (EPO) secreted by the kidneys in response to hypoxia. The lifespan of an RBC is approximately 120 days; senescent RBCs are phagocytosed by macrophages in the spleen and liver.
Leukocytes are the sentinel cells of the immune system. Normal count: 4,000–11,000 cells/µL. They are nucleated and do not contain haemoglobin. They are broadly classified into granulocytes and agranulocytes.
Granulocytes (contain cytoplasmic granules):
- Neutrophils (50–70%): First responders; highly phagocytic; multi-lobed nucleus; release antimicrobial enzymes and form neutrophil extracellular traps (NETs).
- Eosinophils (2–4%): Combat helminth parasites; modulate allergic responses; contain major basic protein toxic to parasites.
- Basophils (<1%): Release histamine and heparin; mediate immediate hypersensitivity reactions (allergies).
Agranulocytes:
- Lymphocytes (20–35%): B lymphocytes (antibody production / humoral immunity); T lymphocytes (cell-mediated immunity); Natural Killer (NK) cells (innate cytotoxicity).
- Monocytes (3–8%): Migrate into tissues and differentiate into macrophages and dendritic cells; powerful phagocytes; antigen presentation.
Platelets are small (2–4 µm), anucleate cell fragments derived from the fragmentation of megakaryocytes in bone marrow. Normal count: 150,000–400,000/µL. Lifespan: 7–10 days.
Haemostasis — the four-step response to vascular injury:
- 1. Vascular spasm: Immediate vasoconstriction of the damaged vessel, mediated by thromboxane A₂ and endothelin.
- 2. Primary haemostatic plug: Platelets adhere to exposed collagen via von Willebrand factor (vWF) and GPIb receptor, then aggregate through GPIIb/IIIa receptor binding fibrinogen, forming a loose plug.
- 3. Coagulation cascade: Intrinsic pathway (contact activation, Factor XII) and extrinsic pathway (tissue factor + Factor VIIa) converge on Factor X → prothrombin → thrombin → converts soluble fibrinogen to insoluble fibrin strands, reinforcing the clot.
- 4. Fibrinolysis: Plasmin (activated by tPA) gradually dissolves the clot once tissue repair is complete.
Vitamin K is essential for the synthesis of clotting factors II, VII, IX, and X in the liver.
Functions of Blood & Clinical Significance
Blood does far more than simply flow. Every millilitre performs a cascade of functions simultaneously, and disruptions — even minor ones — ripple across multiple organ systems. Let us explore these functions systematically and then understand what happens when things go wrong.
Transportation
Blood is the body's primary transport highway. It carries O₂ from the lungs, nutrients from the gut, hormones from endocrine glands, and CO₂ and nitrogenous waste to excretory organs — all simultaneously.
Respiratory Gas Exchange
Haemoglobin in RBCs binds O₂ in the lungs (forming oxyhaemoglobin, HbO₂) and releases it in metabolically active tissues. CO₂ returns primarily as HCO₃⁻ (bicarbonate), maintaining a crucial buffer system (Henderson–Hasselbalch equilibrium).
Immune Defence
Leukocytes patrol relentlessly. Neutrophils phagocytose bacteria; lymphocytes mount specific responses via antibodies and cytotoxic T cells; NK cells destroy virus-infected cells without prior sensitisation. Complement proteins in plasma also lyse pathogens.
Homeostasis
Blood buffers pH (7.35–7.45) through the bicarbonate system. It distributes heat generated by active muscles, regulating core body temperature. Osmotic pressure is maintained by plasma proteins (chiefly albumin), preventing oedema.
Haemostasis (Clotting)
Platelets and the coagulation cascade arrest bleeding within minutes of vascular injury. This prevents exsanguination and creates a scaffold for tissue repair. Uncontrolled, the same system can produce life-threatening thrombosis.
Clinical Disorders Related to Blood Components
Pathological disruptions in blood composition are a window into disease. The table below summarises key disorders relevant to undergraduate study.
| Disorder | Component Affected | Pathophysiology | Key Clinical Features |
|---|---|---|---|
| Iron-Deficiency Anaemia | RBC / Hb | Insufficient Fe²⁺ impairs haem synthesis → microcytic, hypochromic RBCs with reduced O₂-carrying capacity. | Fatigue, pallor, dyspnoea, koilonychia (spoon nails) |
| Sickle Cell Disease | RBC / Hb | Point mutation (Glu→Val in β-globin) → HbS polymerises under low O₂ → rigid, sickle-shaped RBCs that obstruct microvasculature. | Vaso-occlusive crises, haemolytic anaemia, splenomegaly, stroke risk |
| Polycythaemia Vera | RBC | Myeloproliferative disorder with uncontrolled RBC production (JAK2 mutation) → hyperviscous blood. | Headache, pruritus after bathing, thrombosis risk, plethoric face |
| Leukaemia | WBC | Malignant proliferation of immature leukocytes (blasts) in bone marrow → crowding out normal haematopoiesis → anaemia, thrombocytopaenia, immunosuppression. | Fatigue, frequent infections, bleeding, lymphadenopathy |
| Neutropaenia | WBC | Absolute neutrophil count <1500/µL (severe: <500) → loss of first-line bacterial defence. | Recurrent severe bacterial infections, fever, oral ulcers |
| Haemophilia A | Clotting | X-linked deficiency of Factor VIII → intrinsic coagulation pathway fails → prolonged bleeding after minor trauma. | Haemarthrosis, deep muscle bleeds, excessive bruising, prolonged aPTT |
| Immune Thrombocytopaenia (ITP) | Platelets | Autoantibodies (anti-GPIIb/IIIa, anti-GPIb) tag platelets for splenic destruction → platelet count <100,000/µL. | Petechiae, purpura, mucosal bleeding, risk of intracranial haemorrhage |
| Deep Vein Thrombosis (DVT) | Clotting | Virchow's Triad: stasis + hypercoagulability + endothelial damage → fibrin-platelet thrombus in deep veins. | Unilateral leg pain, swelling, warmth; risk of pulmonary embolism |
📚 Further Reading & Reference Topics
ABO & Rh Blood Groups
The ABO system involves A and B antigens on RBC surface and corresponding antibodies in plasma. The Rh system (Rh D antigen) is critical in transfusion medicine and haemolytic disease of the newborn.
Haematopoiesis
All blood cells originate from pluripotent haematopoietic stem cells (HSCs) in red bone marrow. Regulated by colony-stimulating factors (CSFs), erythropoietin, and thrombopoietin.
Structure & Function of Haemoglobin
Cooperative O₂ binding, Bohr effect (pH ↓ → O₂ release), Haldane effect, 2,3-BPG modulation — all pivotal for understanding respiratory physiology at the molecular level.
Complement System
A cascade of plasma proteins that lyse pathogens, opsonise bacteria, and recruit inflammatory cells — integrating innate immunity with the formed elements of blood.
Test Your Understanding
Answer all questions carefully. Immediate feedback is provided after each response. Your score is tracked throughout.
Analytical Discussion Questions
These questions encourage higher-order thinking — analysis, application, and synthesis. Expand the hints to guide your reasoning, then attempt a full written answer in your notebook.
1 Why do mature mammalian erythrocytes lack a nucleus, whereas fish and amphibian RBCs retain their nucleus?
This is one of the most elegant design questions in comparative vertebrate physiology. Consider what the nucleus contributes metabolically and spatially, and weigh this against the extreme functional demands placed on mammalian erythrocytes.
- Enucleation in mammals (and to some extent birds) maximises interior volume for haemoglobin, increasing oxygen-carrying capacity per cell.
- Without a nucleus and mitochondria, the mammalian RBC relies exclusively on anaerobic glycolysis (Embden–Meyerhof pathway) for ATP — it cannot consume the O₂ it carries, ensuring maximum delivery to tissues.
- Fish and amphibians are ectotherms with lower metabolic demands; retaining the nucleus allows RBCs to remain longer-lived and capable of limited gene expression.
- Consider: the spleen as the "graveyard" of RBCs — how does enucleation affect recognition and destruction of senescent RBCs?
2 Explain how the oxygen–haemoglobin dissociation curve facilitates both O₂ loading in the lungs and O₂ unloading in actively respiring tissues.
The sigmoidal shape of the O₂-Hb dissociation curve is no accident — it is the result of cooperative binding among four haem groups. Think about how partial pressures and pH differ between the lungs and muscle tissue, and what these differences do to the curve.
- Lungs: High pO₂ (~100 mmHg) → haemoglobin is ~97–98% saturated. Flat upper portion of the curve means saturation is maintained even with mild drops in alveolar pO₂.
- Resting tissues: Tissue pO₂ ~40 mmHg → steep portion of the curve → ~25% of O₂ is unloaded.
- Active tissues: pO₂ drops to ~20 mmHg, CO₂ rises, pH falls → Bohr effect shifts the curve rightward → even more O₂ unloaded (~50–75%).
- 2,3-Bisphosphoglycerate (2,3-BPG): Synthesised in RBCs via the Rapoport–Luebering shunt; stabilises deoxy-Hb, rightward shift, promotes O₂ delivery.
- Fetal haemoglobin (HbF) has higher O₂ affinity than adult HbA — relate this to placental O₂ transfer.
3 A patient presents with petechiae (pin-point haemorrhages), a platelet count of 30,000/µL, and a normal coagulation profile (PT and aPTT). Suggest a differential diagnosis and explain the underlying mechanism.
This is a clinical application question. Normal coagulation tests in the presence of thrombocytopaenia tell you something very specific about which arm of haemostasis is defective. Think systematically — primary vs. secondary haemostasis.
- Normal PT and aPTT → secondary haemostasis (coagulation cascade, Factors I–XIII) is intact → the problem is in primary haemostasis (platelet plug formation).
- Thrombocytopaenia causes: ↓ production (aplastic anaemia, bone marrow infiltration), ↑ destruction (ITP, TTP, DIC), ↑ sequestration (hypersplenism).
- Most likely: Immune Thrombocytopaenic Purpura (ITP) — autoantibodies against platelet surface glycoproteins → splenic macrophages destroy antibody-coated platelets.
- Petechiae (not ecchymoses) are characteristic of platelet disorders; large bruises/haemarthroses suggest coagulation factor deficiency.
- Additional investigations: peripheral smear (absent platelet clumping, large platelets suggesting compensatory megakaryocyte activity), antiplatelet antibodies, bone marrow biopsy.
4 What is the biological significance of having five distinct types of white blood cells rather than a single, multipotent immune cell type?
Evolution has driven specialisation. Consider how different pathogens present fundamentally different challenges to the immune system, and how each WBC type is adapted to address a specific category of threat.
- Neutrophils: rapid, non-specific first response to bacteria and fungi — speed over specificity.
- Eosinophils: evolved specifically against multicellular parasites (helminths) that are too large for phagocytosis — release extracellular toxic granules.
- Basophils/Mast cells: coordinate tissue-level inflammatory and allergic responses, important in early parasite expulsion.
- B lymphocytes: immunological memory + antibody diversity through VDJ recombination — millions of antigen specificities encoded.
- T lymphocytes (CD4⁺ and CD8⁺): orchestrate adaptive immunity; CD8⁺ cytotoxic T cells kill intracellular pathogens (viruses) that antibodies cannot reach.
- Discuss: why does HIV target CD4⁺ T-helper cells, and why does this eventually collapse the entire immune response?
5 Critically evaluate the statement: "Anaemia is always caused by a lack of iron."
This is a common misconception. Anaemia is defined by reduced haemoglobin concentration or reduced RBC count, but the causes are diverse. Use your knowledge of haemoglobin synthesis, erythropoiesis, and RBC lifespan to construct a systematic argument.
- Nutritional causes beyond iron: Vitamin B₁₂ deficiency (pernicious anaemia – megaloblastic), folate deficiency (megaloblastic anaemia).
- Haemolytic anaemias: G6PD deficiency, hereditary spherocytosis, sickle cell disease, autoimmune haemolysis — none involve iron deficiency.
- Bone marrow failure: Aplastic anaemia, leukaemic infiltration, chemotherapy effects.
- Anaemia of chronic disease: Inflammatory cytokines (IL-6) upregulate hepcidin → functional iron sequestration even when iron stores are adequate.
- Renal anaemia: Decreased erythropoietin (EPO) production in chronic kidney disease.
- Conclude: Anaemia is a syndrome with many causes; iron deficiency is the most common worldwide, but far from the only one.
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