Homeostasis: Unit Review

Stimulus: body temperature rises. Receptor: thermoreceptors (skin, hypothalamus). Control centre: hypothalamus. Effector: sweat glands / skin arterioles. Response: sweating and vasodilation cool the body.

Negative: the response reverses the change (e.g., insulin lowering high glucose). Positive: the response increases the change until an end event (e.g., oxytocin in childbirth, LH surge, blood clotting).

Because of time delays between sensing and response, the variable overshoots and is corrected repeatedly: a dynamic equilibrium.

Any two: vasoconstriction (less warm blood near the surface, less heat lost); shivering (muscle contractions release heat); brown fat (releases heat directly); behaviour (warm clothes).

600 g × 2.4 kJ/g = 1440 kJ.

Pyrogens raise the set point; the body is below the new set point, so warming responses (shivering) are triggered.

Warm blood flowing out runs beside cold blood flowing back, so heat passes into the returning blood instead of being lost (e.g., in a goose's legs).

Glomerulus / Bowman's capsule → proximal tubule → loop of Henle → distal tubule → collecting duct.

Glucose and amino acids.

(175 − 1.4) ÷ 175 × 100 = 173.6 ÷ 175 × 100 ≈ 99.2%.

Ammonia is very toxic and needs lots of water; urea is much less toxic, so it can be carried in blood and stored.

Released by the posterior pituitary when blood is too concentrated, ADH causes aquaporins to be inserted in the collecting ducts, so more water is reabsorbed by osmosis.

Low blood pressure → renin → angiotensin I → angiotensin II → aldosterone.

Released by stretched atria, it reduces Na⁺ reabsorption and inhibits renin and aldosterone, so more salt and water are excreted.

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻. Added H⁺ combines with HCO₃⁻; the equilibrium shifts left, so pH changes little.

0.03 × 50 = 1.5; 24 ÷ 1.5 = 16; log 16 = 1.204; pH = 6.1 + 1.204 ≈ 7.30 (acidosis).

Respiratory alkalosis: too much CO₂ is breathed out, removing H⁺, so pH rises.

Blood glucose above the renal threshold (about 10 mmol/L), usually from untreated or poorly controlled diabetes.

So there is no gradient for glucose (no loss) but a steep gradient for urea (it diffuses out).

Making hormones such as EPO or renin (or activating vitamin D).

Steroid: lipid-soluble, crosses the membrane, binds an intracellular receptor, changes gene expression (slow, long-lasting). Peptide: water-soluble, binds a membrane receptor, acts through a second messenger (fast).

A hormone that stimulates another endocrine gland: e.g., TSH, ACTH, FSH, LH.

PTH raises it; calcitonin lowers it.

Insulin (beta cells) lowers glucose: cells take it up (GLUT4), liver and muscle make glycogen. Glucagon (alpha cells) raises glucose: liver breaks down glycogen and makes new glucose.

Type 1: autoimmune destruction of beta cells (little or no insulin). Type 2: insulin resistance, later with too little insulin.

At or above 11.1 mmol/L, it is in the diabetes range (to be confirmed by a doctor).

Epinephrine (adrenal medulla, via sympathetic nerves) acts in seconds, short-lived. Cortisol (adrenal cortex, via CRH → ACTH) acts over hours to days, raises glucose, reduces inflammation.

Low iodine → low T₄ → weak negative feedback → high TSH → thyroid is overstimulated and enlarges.

It suppresses ACTH by negative feedback, so the adrenal cortex needs time to resume making cortisol.

LH: interstitial (Leydig) cells make testosterone. FSH (with testosterone): Sertoli cells support sperm production (and release inhibin).

Sustained high estrogen switches to positive feedback, causing the LH surge, which triggers ovulation.

The corpus luteum breaks down, progesterone and estrogen fall, and the endometrium is shed.

It acts like LH to keep the corpus luteum alive, so progesterone stays high.

Receptor → sensory neuron → interneuron (spinal cord) → motor neuron → effector.

Any two: heart rate up/down, pupils dilate/constrict, airways widen/narrow, digestion slowed/stimulated.

√(0.30 ÷ 9.8) = √0.0306 ≈ 0.17 s.

The Na⁺/K⁺ pump (3 Na⁺ out, 2 K⁺ in), K⁺ leak channels (K⁺ diffuses out) and trapped negative proteins.

Depolarization: voltage-gated Na⁺ channels open, Na⁺ flows in. Repolarization: Na⁺ channels inactivate, K⁺ channels open, K⁺ flows out.

The impulse jumps from node to node (saltatory conduction); myelin insulates the membrane between nodes.

Action potential arrives → Ca²⁺ enters → vesicles release neurotransmitter → it diffuses across the cleft → binds receptors → ion channels open → removed by enzymes/reuptake.

4 × 5 − 4 = +16 mV → −54 mV, which is above −55 mV, so yes.

It breaks down ACh in the cleft. If inhibited, ACh stays and overstimulates the muscle (twitching, then paralysis).

Taxis: directed movement toward/away from a stimulus. Kinesis: non-directed change in speed or turning.

To check for side bias (other factors affecting where the animals go).

(6² ÷ 10) + (6² ÷ 10) = 3.6 + 3.6 = 7.2 > 3.84: significant.

Agonist activates a receptor (e.g., nicotine at ACh receptors, opioids at opioid receptors). Antagonist blocks a receptor (e.g., naloxone at opioid receptors, caffeine at adenosine receptors).

With repeated drug use, the body adapts (e.g., fewer receptors) to restore normal activity, so the same dose has less effect.

It inhibits ADH, so less water is reabsorbed and more urine is produced.

Methylmercury is stored and excreted slowly, so each predator keeps the mercury from all its prey; concentration increases at each level of the food chain.

It attacks rapidly dividing cells, including bone marrow (fewer white blood cells) and hair follicles.

Examples: heat waves overwhelm thermoregulation; wildfire smoke (PM2.5) inflames the lungs; endocrine disruptors (e.g., BPA) bind hormone receptors; lead/mercury damage the nervous system.