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Why large organisms need exchange surfaces and mass transport?
Smaller SA:V; diffusion distance too long to supply all cells
SA:V scaling?
Surface area ∝ length², volume ∝ length³, so SA:V falls as size increases
SA:V and metabolic rate?
Small animals have a larger SA:V, so lose more heat per gram; faster respiration releases heat to replace it, so a higher metabolic rate
Single-celled organisms?
Large SA:V, short diffusion distance; gases diffuse across the cell-surface membrane
Insect tracheal system?
Spiracles → tracheae → tracheoles; gases diffuse directly to and from cells
Tracheole adaptations?
Highly branched, so large surface area; thin walls and reach the tissues, so short diffusion pathway; abdominal pumping ventilates
Insects limiting water loss?
Waxy waterproof cuticle; spiracles close; hairs around spiracles; small SA:V
Fish gills?
Gill filaments covered in lamellae: large surface area, thin epithelium, many capillaries
Counter-current flow?
Blood and water flow in opposite directions, so a concentration gradient is kept along the whole lamella
Leaf gas exchange?
Many stomata; air spaces in spongy mesophyll; large surface area of mesophyll cells; thin leaf, short diffusion pathway
Xerophyte adaptations?
Sunken stomata, hairs, rolled leaves (trap moist air, reduce water potential gradient); thick waxy cuticle; fewer stomata
Human airways?
Trachea → bronchi → bronchioles → alveoli
Alveolar epithelium?
One thin, flat cell thick; many alveoli give a large surface area; close to capillaries, short pathway; ventilation and blood flow keep the gradient
Oxygen's route into blood?
Across the alveolar epithelium, then the capillary endothelium
Inspiration?
Diaphragm contracts and flattens; external intercostals contract, internal relax; ribcage up and out; volume up, pressure below atmospheric; air moves in
Expiration?
Diaphragm relaxes and domes; external intercostals relax (internal contract when forced); ribcage down and in; volume down, pressure up; air moves out
Pulmonary ventilation?
Tidal volume × breathing rate
Lung disease effects?
Reduced surface area, thicker epithelium or lost elasticity → slower diffusion, lower FEV₁
Correlation vs causation?
Correlation shows an association; it doesn't prove cause, as other factors may be involved
Carbohydrate digestion?
Amylase hydrolyses starch to maltose; membrane-bound disaccharidases (maltase, sucrase, lactase) hydrolyse disaccharides to monosaccharides
Lipid digestion?
Bile salts emulsify lipids into droplets (larger surface area); lipase hydrolyses ester bonds → monoglycerides and fatty acids
Micelles?
Bile salts + monoglycerides + fatty acids; carry them to the epithelium, keeping their concentration high; they diffuse in
Lipids after absorption?
Triglycerides re-formed in the ER; combined with proteins in the Golgi as chylomicrons; leave by exocytosis into lacteals
Protein digestion?
Endopeptidases: internal peptide bonds. Exopeptidases: terminal bonds. Membrane-bound dipeptidases: dipeptides → amino acids
Amino acid absorption?
Co-transport with Na⁺, as for glucose
Haemoglobin structure?
Quaternary: four polypeptides (two α, two β), each with a haem group containing Fe²⁺; carries four O₂
Loading and unloading?
High pO₂ (lungs): high affinity, loads. Low pO₂ (respiring tissues): lower affinity, unloads
Why is the curve S-shaped?
Cooperative binding: the first O₂ changes haemoglobin's shape, making the next ones bind more easily
Bohr effect?
Higher CO₂ lowers pH, reducing haemoglobin's affinity; curve shifts right; more O₂ unloaded in respiring tissues
Curve shifted left?
Higher affinity; loads at low pO₂ (e.g. fetal haemoglobin, animals in low-oxygen environments)
Curve shifted right?
Lower affinity; unloads more readily (e.g. small or active mammals with a high respiration rate)
Mammalian circulation?
Closed double circulation: pulmonary and systemic
Named vessels?
Coronary arteries; vena cava and aorta; pulmonary artery and vein; renal artery and vein
Route through the heart?
Vena cava → right atrium → AV valve → right ventricle → SL valve → pulmonary artery → lungs → pulmonary vein → left atrium → AV valve → left ventricle → SL valve → aorta
Why is the left ventricle wall thicker?
More muscle to generate the higher pressure needed for the systemic circulation
Atrial systole?
Atria contract; atrial pressure > ventricular; AV valves open; blood into ventricles
Ventricular systole?
Ventricles contract; pressure > atria, so AV valves close; pressure > arteries, so SL valves open; blood ejected
Diastole?
Muscle relaxes; ventricular pressure < arteries, so SL valves close; atria and ventricles fill
Valve rule?
Open when pressure behind is higher; close when pressure in front is higher; prevent backflow
Cardiac output?
Stroke volume × heart rate (heart rate = 60 ÷ time for one cycle)
Arteries?
Thick muscle and elastic tissue (stretch and recoil, smooth flow, maintain pressure); thick wall resists high pressure; narrow lumen
Arterioles?
More muscle; constrict or dilate to control blood flow to tissues
Veins?
Wide lumen; thin wall, little muscle and elastic tissue; valves prevent backflow; low pressure
Capillaries?
Wall one cell thick (short diffusion pathway); narrow lumen; many and branched (large surface area)
Tissue fluid formation?
High hydrostatic pressure at the arteriole end forces water and small molecules out; proteins and cells stay in the blood
Tissue fluid return?
At the venule end, plasma proteins give the blood a lower water potential; water returns by osmosis; excess drains into the lymph
Xylem?
Long, hollow dead cells with no end walls, strengthened with lignin; a continuous water column
Cohesion-tension?
Water evaporates from leaves, creating tension; hydrogen bonds give cohesion, so a continuous column is pulled up; adhesion to xylem walls
Evidence for cohesion-tension?
Trunk diameter narrows in the day (tension); a broken xylem vessel draws air in rather than leaking water
Factors affecting transpiration?
Light (stomata open), temperature (more evaporation), humidity (lower = steeper gradient), wind (removes moist air)
Phloem?
Sieve tube elements (no nucleus, sieve plates) and companion cells (many mitochondria)
Mass flow?
Source: sucrose actively loaded (co-transport with H⁺ via companion cells); water potential lowered; water enters by osmosis; high hydrostatic pressure. Sink: sucrose unloaded and used; water leaves; lower pressure. Flow source → sink
Ringing experiment?
Remove a ring of bark and phloem; sugars build up above the ring, tissue below dies, so phloem carries sugars
Tracer experiment?
Supply ¹⁴CO₂; autoradiography shows labelled sugars in the phloem moving to sinks
Evidence against mass flow?
Sugars travel to different sinks at different rates; sieve plates would slow flow
Oxygen dissociation curve axes?
x: partial pressure of oxygen (pO₂). y: % saturation of haemoglobin with oxygen
Insect tracheoles during exercise?
Muscle cells respire anaerobically, making lactate, which lowers their water potential; water moves out of the tracheoles into cells by osmosis, drawing air further in
Heart valves?
Atrioventricular valves (tricuspid right, bicuspid left) between atria and ventricles; semilunar valves at the base of the aorta and pulmonary artery
Bile?
Made in the liver, stored in the gall bladder; bile salts emulsify lipids. It contains no enzymes