Study Guide - Physiology Course
A comprehensive review of every topic covered in the physiology course. Use this guide for exam prep, quick revision, or as a reference while studying.
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Use this loop when a vignette gives vitals, labs, or imaging - trace backward to the broken physiological step.
Parse the disturbance
Hypoxemia, hypotension, acidemia, osmolar gap, etc.
Name the regulated variable
MAP, PaO2, pH, osmolality, K+, glucose…
Identify sensor and effector arms
Which reflexes or hormones should respond?
Compare expected vs observed compensation
Winter formula, anion gap, A-a gradient, FeNa…
Localize organ-system pathology
Heart, lungs, kidneys, or integration - then read deeper in that chapter.
| Term | Definition |
|---|---|
| Homeostasis | Stable internal environment despite external change; regulated by feedback |
| Negative feedback | Response opposes the stimulus; dominant pattern for MAP, temperature, glucose |
| Set point | Target value a regulated variable is driven toward (with normal variation) |
| Afterload | Resistance the ventricle must overcome to eject blood (arterial pressure, impedance) |
| Preload | End-diastolic fiber stretch; major determinant of stroke volume via Frank-Starling |
| Cardiac output (CO) | HR x SV; liters per minute delivered to the circulation |
| Stroke volume (SV) | Blood ejected per beat; depends on preload, contractility, afterload |
| Frank-Starling law | Greater ventricular filling increases force of contraction (healthy heart) |
| Baroreflex | Arterial baroreceptor loop adjusting HR and vascular tone to buffer MAP |
| Systemic vascular resistance (SVR) | Opposition to flow in arterioles; sets diastolic pressure trends |
| Alveolar ventilation | Portion of minute ventilation that reaches gas-exchanging alveoli |
| V/Q ratio | Ventilation-perfusion matching; near 1 in healthy alveolar-capillary units |
| Bohr effect | H+ and CO2 shift oxyhemoglobin curve right; favors O2 unloading in tissues |
| P50 | PO2 at 50% Hb saturation; tracks left/right shifts of the dissociation curve |
| GFR | Volume of plasma ultrafiltrate formed per unit time across glomerular barrier |
| RAAS | Renin-angiotensin-aldosterone system; defends perfusion and Na+ retention |
| ADH (vasopressin) | Increases collecting duct water permeability; concentrates urine |
| Titratable acid / NH4+ | Renal mechanisms for net acid excretion and HCO3- regeneration |
Introduction
Homeostasis, feedback, delivery chain across organ systems
Membrane & resting potential
Gradients, pumps, channels, Vm near EK at rest
Cardiovascular
Cardiac cycle, CO, Starling curve, MAP, baroreflex
Respiratory
Ventilation, diffusion, Hb binding, chemoreceptor drive
Renal & fluids
Nephron transport, GFR, RAAS, ADH, acid-base integration
| Topic | Relationship |
|---|---|
| Cardiac output | CO = HR x SV; SV from preload, contractility, afterload |
| Membrane potential | Ion gradients plus relative permeabilities (Nernst per ion; GHK combined) |
| Alveolar ventilation | Minute ventilation minus dead space; drives alveolar PO2 and PCO2 trends |
| Filtration | GFR from net filtration pressure, Kf, and renal plasma flow |
| Category | Energy | Examples |
|---|---|---|
| Passive | Down electrochemical gradient | Leak channels, GLUT-facilitated glucose, aquaporins |
| Primary active | ATP on transporter | Na/K-ATPase, H+-ATPase, Ca-ATPase |
| Secondary active | Ion gradient (often Na+) | SGLT, Na/H exchange, many renal/apical cotransporters |
| Presentation focus | Physiology lens | First-pass differentials |
|---|---|---|
| Hypoxemia + high A-a gradient | V/Q mismatch, shunt, diffusion | PE, pneumonia, ARDS, intracardiac shunt |
| Hypoxemia + normal A-a | Hypoventilation, low PiO2 | Opioids, neuromuscular weakness, altitude |
| Low cardiac output state | SV and/or HR failure | HF, tamponade, massive PE, hemorrhagic shock |
| Prerenal AKI | Perfusion to GFR without parenchymal necrosis | Hypovolemia, low effective arterial volume, renal artery stenosis |
| Metabolic acidosis | Low HCO3- buffer; respiratory compensation | AG gap (keto, lactate, toxins) vs non-AG (GI, RTA) |
Q1.Why is resting membrane potential in many excitable cells closer to EK than to ENa at rest?
At rest, permeability to K+ through leak channels usually dominates over Na+ permeability. The membrane voltage is therefore weighted toward the potassium equilibrium potential. The Na/K-ATPase maintains the underlying gradients but the dominant resting conductance is typically K+.
Q2.State the Frank-Starling mechanism and one clinical situation where preload rises without a compensatory increase in forward output.
Frank-Starling: within physiological limits, increased end-diastolic volume (preload) increases stroke volume because sarcomeres are stretched toward optimal overlap. In decompensated systolic heart failure, elevated filling pressures may not translate into higher stroke volume because the ventricle is on the flat or descending limb of the function curve and contractility is impaired.
Q3.Contrast the primary roles of central versus peripheral chemoreceptors in ventilatory control.
Central chemoreceptors (medulla) respond chiefly to H+ in brain interstitial fluid, which reflects CO2 diffusion and bicarbonate buffering. They are central to steady-state CO2 regulation. Peripheral chemoreceptors (carotid bodies) are important for hypoxic drive and also sense hypercapnia and acidemia, especially acute changes.
Q4.How does aldosterone modify collecting duct function, and what electrolyte side effect is classic?
Aldosterone increases epithelial sodium channel activity in principal cells, promoting Na+ reabsorption and lumen-negative voltage that favors K+ secretion. Hypokalemia and metabolic alkalosis are classic associations when aldosterone is inappropriately high.
Q5.A patient has hypotension and tachycardia. Outline how the arterial baroreflex attempts to restore MAP.
Reduced stretch on carotid sinus and aortic arch baroreceptors lowers afferent firing to the medulla. The reflex increases sympathetic outflow to increase heart rate and contractility and causes vasoconstriction; parasympathetic tone to the SA node falls. The integrated response raises SVR and CO to oppose the hypotensive stimulus (negative feedback).
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