Homeostasis Study Guide
Study Guide
📖 Core Concepts
Homeostasis – maintenance of stable internal physical & chemical conditions (temperature, pH, ion concentrations, glucose, etc.).
Control System Triad – Receptor (sensor) → Control Center (integrator) → Effector (response organ).
Negative Feedback – effector action reduces the original stimulus, turning the loop off.
Set Point – the target value for a variable; can shift (circadian rhythm, fever, acclimatization).
Allostasis – behavioral or anticipatory adjustments made before physiological mechanisms engage (e.g., seeking shade, predictive insulin release).
📌 Must Remember
Key variables: temperature, extracellular pH, Na⁺, K⁺, Ca²⁺, glucose, iron, water.
Temperature: vasoconstriction conserves heat; shivering & non‑shivering thermogenesis generate heat; sweating & panting dissipate heat.
Glucose: ↑ blood glucose → β‑cells release insulin → ↑ GLUT4 uptake, glycogen synthesis, lipogenesis. ↓ glucose → α‑cells release glucagon → hepatic glycogenolysis & gluconeogenesis.
Calcium: low Ca²⁺ → PTH → bone resorption, renal ↓ phosphate, ↑ 1,25‑OH₂ vitamin D → ↑ intestinal Ca²⁺ absorption. High Ca²⁺ → calcitonin → bone deposition.
Sodium: low Na⁺/BP → juxtaglomerular cells release renin → Ang I → ACE → Ang II → vasoconstriction + aldosterone → Na⁺ reabsorption.
Potassium: high K⁺ → zona glomerulosa depolarization → aldosterone release → renal K⁺ secretion.
Water: ↑ osmolality → hypothalamic ADH release → collecting duct water reabsorption + thirst. ↓ osmolality → ADH suppression → dilute urine.
pH (Henderson–Hasselbalch):
$$\text{pH}=pKa+\log\frac{[\text{HCO}3^-]}{0.03\,P{CO2}}$$
Normal ratio = 1:20 → pH ≈ 7.4.
Renal‑Respiratory Compensation – lungs adjust CO₂ (acute), kidneys adjust HCO₃⁻ (chronic).
🔄 Key Processes
Negative‑Feedback Loop (generic)
Stimulus → Receptor → Control Center → Effector → Response → ↓ Stimulus → Receptor activity stops.
Thermoregulation (cold)
↓ core temp → thermoreceptors → hypothalamic center → sympathetic → vasoconstriction + shivering → heat production.
Thermoregulation (heat)
↑ core temp → thermoreceptors → hypothalamus → sympathetic → vasodilation + sweat gland activation → evaporative cooling.
Insulin‑Glucagon Glucose Control
↑ glucose → β‑cell → insulin → ↑ GLUT4, glycogen synthase, lipogenesis → ↓ glucose.
↓ glucose → α‑cell → glucagon → hepatic glycogenolysis + gluconeogenesis → ↑ glucose.
Renin‑Angiotensin‑Aldosterone System (RAAS)
↓ Na⁺/BP → JGA → renin → Ang I → ACE → Ang II → vasoconstriction + aldosterone → Na⁺ reabsorption, K⁺ excretion.
ADH‑Mediated Water Retention
↑ plasma osmolality → osmoreceptors → posterior pituitary → ADH → V2 receptors in collecting duct → aquaporin‑2 insertion → water reabsorption.
🔍 Key Comparisons
Insulin vs. Glucagon – insulin ↓ blood glucose; glucagon ↑ blood glucose.
PTH vs. Calcitonin – PTH raises plasma Ca²⁺; calcitonin lowers plasma Ca²⁺.
Renin‑Angiotensin vs. ADH – RAAS primarily restores Na⁺/volume & BP; ADH primarily restores water balance/osmolality.
Peripheral vs. Central Chemoreceptors – peripheral detect O₂ & CO₂ Pa; central detect CSF pH (driven by CO₂).
Shivering vs. Non‑shivering Thermogenesis – shivering = rapid muscular contractions; non‑shivering = ↑ metabolic rate (brown fat, thyroid hormones).
⚠️ Common Misunderstandings
“Set point is fixed.” – It shifts with circadian rhythms, menstrual cycle, fever, acclimatization.
“Insulin always lowers glucose instantly.” – Predictive (anticipatory) insulin release occurs before glucose rise; negative feedback still needed.
“ADH only acts on kidneys.” – It also triggers thirst via hypothalamic centers.
“Calcitonin is a major regulator of calcium.” – Its effect is modest; PTH dominates calcium homeostasis.
“Hyperventilation always improves oxygenation.” – At altitude it helps O₂ but lowers CO₂, causing respiratory alkalosis; renal compensation follows.
🧠 Mental Models / Intuition
Thermostat Analogy – The hypothalamus = thermostat; receptors = temperature probes; effectors = heater (shivering) or AC (sweating).
Bank Account – Homeostatic variables are “balances.” Negative feedback = deposits/withdrawals that keep the balance near a target; “interest” (allostatic/anticipatory) adds money before a known expense.
Push‑Pull Levers – RAAS pushes (vasoconstriction, Na⁺ reabsorption) when volume drops; ADH pulls water back when osmolality rises.
🚩 Exceptions & Edge Cases
Fever – Set point is deliberately raised by cytokines → body generates heat (chill) until new point reached.
High Altitude – Chronic hypoxia → ↑ EPO → polycythemia; also renal bicarbonate loss → compensatory respiratory alkalosis.
Hemochromatosis – Hepcidin deficiency → excess iron absorption despite adequate stores.
Type 1 Diabetes – No insulin → unopposed glucagon → severe hyperglycemia & ketoacidosis.
📍 When to Use Which
Diagnosing hypercalcemia → check PTH (high → primary hyperparathyroidism; low → malignancy, vitamin D excess).
Hyponatremia with low ADH → consider diabetes insipidus (ADH deficiency) vs. excessive water intake.
Acute metabolic acidosis → expect respiratory compensation: ↑ ventilation (hyperventilation) to lower PaCO₂.
Persistent hypertension → assess RAAS activity (renin, aldosterone levels) before prescribing ACE inhibitors.
👀 Patterns to Recognize
“Low → hormone ↑ → opposite effect” – Low Na⁺ → renin ↑ → Ang II ↑ → BP ↑.
“High → opposite hormone ↓” – High Ca²⁺ → calcitonin ↑ → bone deposition.
“Combined sensor‑effector response” – Any deviation in temperature, glucose, or osmolality triggers a three‑part cascade (sensor → center → effector).
🗂️ Exam Traps
Mistaking peripheral chemoreceptor stimulus – they respond to low O₂ and high CO₂, not just O₂.
Confusing aldosterone’s primary target – it acts on distal tubule & collecting duct (Na⁺ reabsorption, K⁺ secretion), not the proximal tubule.
Assuming ADH acts on all nephron segments – only the collecting duct expresses V2 receptors.
Over‑attributing calcium regulation to calcitonin – most long‑term calcium balance is via PTH & vitamin D.
Equating hyperventilation with “more O₂” – primary effect is CO₂ washout → pH rise; O₂ increase is secondary and limited by hemoglobin saturation.
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Use this guide to scan quickly before the exam – focus on the triad, feedback loops, and the hormone‑target relationships that drive each variable back to its set point.
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