Sec 4 Biology Homeostasis & Response notes

Homeostasis is the maintenance of a constant internal environment — blood glucose, core temperature, water and ion levels — despite swings outside. Cells depend on it: enzymes (chapter 3) have narrow optimal conditions, and drifting outside them means slowed metabolism or death.

Every homeostatic control runs the same negative feedback loop: a stimulus (a level rises or falls away from the set point) is detected by a receptor; a control centre (often the hypothalamus, or a gland) compares it with the ideal and triggers a corrective mechanism that pushes the level the opposite way. Because the correction cancels the original change, the loop is called negative feedback — the level oscillates gently around the set point instead of running away.

Temperature receptors in the skin detect the outside, and the hypothalamus in the brain monitors the temperature of the blood itself — it is the body’s thermostat. If the core temperature climbs above about 37 °C, the hypothalamus triggers two corrections: vasodilation — arterioles supplying skin capillaries widen, flooding the surface with warm blood so more heat radiates away — and sweating, where water evaporating from the skin carries heat off with it.

If the core temperature falls, the corrections reverse: vasoconstriction narrows the skin arterioles, keeping warm blood in the body core and away from the radiating surface, and shivering — rapid involuntary muscle contraction — releases the heat of respiration to warm the blood.

A hormone is a chemical messenger produced by an endocrine (ductless) gland and transported in the blood to its target organ. Compared with nerves, hormones act more slowly but over longer periods. The blood glucose pair come from the islets of Langerhans, clusters of cells in the pancreas: insulin and glucagon.

After a carbohydrate-rich meal, blood glucose rises above the set point. The islets respond by releasing insulin, which makes liver and muscle cells convert glucose into glycogen (and tissues to use glucose faster in respiration) — the level falls back. During fasting or exercise, glucose falls below the set point and the islets release glucagon, which makes the liver convert stored glycogen back into glucose. Insulin and glucagon are antagonistic — one lowers, the other raises — which is precisely what negative feedback needs.

In type 2 diabetes, the feedback loop falters at the effector: body cells become resistant to insulin (or too little is produced), so glucose cannot be moved into storage efficiently and blood glucose stays dangerously high after meals. The main risk factors are an unhealthy diet, obesity, a sedentary lifestyle — plus age and family history. Unlike type 1, it is usually managed without insulin injections: a balanced diet with controlled carbohydrate, regular exercise, weight loss and medication if needed.

ADH (antidiuretic hormone) runs the water loop. Osmoreceptors in the hypothalamus monitor the water concentration of the blood; the pituitary gland releases more or less ADH accordingly. When you are dehydrated, more ADH makes the kidney’s collecting duct more permeable to water, so more is reabsorbed into the blood — producing a small volume of concentrated urine. When you are over-hydrated, ADH release drops, less water is reabsorbed, and urine becomes a large volume of dilute fluid. (The kidney chapters of chapter 7 supply the plumbing; ADH is the dial that tunes it.)

The nervous system divides into the central nervous system (CNS) — the brain and spinal cord — and the nerves that carry signals to and from it. Electrical impulses travel along neurones at high speed, making the nervous system the body’s rapid coordination system, opposite in style to the slow, blood-borne hormones.

A reflex is a rapid, automatic, protective response that bypasses conscious thinking. Its five-step pathway is the reflex arc: a receptor detects the stimulus → a sensory neurone carries the impulse into the CNS → a relay neurone passes it across the spinal cord (and usually informs the brain afterwards) → a motor neurone carries the command outward → an effector (a muscle or gland) responds. Touch a hot pan and your hand withdraws before the pain report reaches your brain.

Light enters through the cornea, which does most of the bending (refraction), passes through the pupil — a hole whose size the pigmented iris adjusts — and is fine-focused by the lens onto the retina, where light-sensitive cells fire impulses along the optic nerve to the brain.

Accommodation is the lens changing shape to focus. To focus on a near object, the ciliary muscles contract, slackening the suspensory ligaments, so the elastic lens springs fatter and rounder — more curved, more refractive. For a distant object the ciliary muscles relax, the ligaments pull taut, and the lens is drawn thin and flat. The muscles work against the lens’s own elasticity — an antagonistic pair, again.

The pupil reflex protects the retina. In bright light, circular muscles of the iris contract while radial muscles relax, shrinking the pupil (constriction) so less light enters. In dim light the radial muscles contract and the circular relax, widening the pupil (dilation) to catch what light there is. It is a reflex: the retina is the receptor, the optic nerve carries the news, and the iris muscles are the effectors.