Molecules, transport and health
Carbohydrates and lipids
Monosaccharides (glucose, fructose, galactose, ribose) join by condensation to form glycosidic bonds, releasing water; hydrolysis breaks them. Disaccharides: maltose (glucose + glucose), sucrose (glucose + fructose), lactose (glucose + galactose). α-glucose polymers store energy: amylose (unbranched, 1,4, helical, compact), amylopectin and glycogen (1,4 and 1,6 branches, many ends for rapid hydrolysis); insoluble, so no osmotic effect. β-glucose forms cellulose: straight chains, alternate glucose flipped, linked by hydrogen bonds into microfibrils: high tensile strength. Triglycerides = glycerol + 3 fatty acids (ester bonds): energy store, insulation. Phospholipids have a hydrophilic phosphate head and hydrophobic tails: membranes. Tests: Benedict's (reducing sugars), acid hydrolysis then Benedict's (non-reducing), iodine (starch), ethanol emulsion (lipids).
≈ 50 minBlood vessels and haemoglobin
Arteries: thick muscle and elastic tissue, narrow lumen, high pressure. Veins: wide lumen, thin walls, valves, low pressure. Capillaries: one-cell-thick endothelium, short diffusion distance. Tissue fluid forms at the arterial end of capillaries where hydrostatic pressure exceeds the water potential effect of plasma proteins; it returns at the venous end and via lymph. Haemoglobin binds O₂ cooperatively, giving an S-shaped (sigmoid) dissociation curve: high saturation in lungs, unloading in respiring tissues. Bohr shift: more CO₂ lowers affinity (curve shifts right), so more O₂ is released where it's needed. Fetal haemoglobin has higher affinity (curve left). CO₂ is carried mostly as HCO₃⁻ (carbonic anhydrase in red cells), with the chloride shift balancing charge.
≈ 50 minThe heart and cardiac cycle
Mammals have a double circulation: pulmonary (right ventricle → lungs) and systemic (left ventricle → body). The left ventricle wall is thickest to pump blood at high pressure. Cardiac cycle: atrial systole (atria contract, AV valves open), ventricular systole (ventricles contract; pressure rises; AV valves close when ventricular pressure exceeds atrial; semilunar valves open when it exceeds arterial), diastole (relaxation; semilunar valves close; atria fill). Valves open and close only due to pressure differences. Heartbeat is myogenic: the SAN (pacemaker) sends a wave of excitation over the atria; the AVN delays it, then passes it down the bundle of His and Purkyne fibres so ventricles contract from the apex up. Cardiac output = stroke volume × heart rate.
≈ 45 minCardiovascular disease and risk
Atherosclerosis: damage to the artery endothelium (e.g. high blood pressure, smoking) triggers an inflammatory response; white cells and LDL cholesterol build up as an atheroma (plaque), which hardens and narrows the artery. Plaques can rupture, triggering blood clotting: platelets release thromboplastin → prothrombin → thrombin (needs Ca²⁺, vitamin K) → fibrinogen → fibrin mesh traps cells → thrombus. A clot in a coronary artery causes a heart attack (myocardial infarction); in the brain, a stroke. Risk factors: genes, age, male sex, high blood pressure, smoking, high LDL, obesity, inactivity, high salt. Measures: BMI = mass (kg) ÷ height² (m²), waist-to-hip ratio, energy budget. Treatments: antihypertensives (lower pressure), statins (lower LDL), anticoagulants and platelet inhibitors (reduce clotting; risk of bleeding).
≈ 45 min