FMGE Physiology Flashcards

24 sample cards from the Physiology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Where is most of the filtered Na+ and water reabsorbed, and what is the main active transporter driving it?

   About 65-67% is reabsorbed in the proximal convoluted tubule. The basolateral Na+/K+ ATPase creates the gradient that drives Na+ (and coupled solute/water) reabsorption.

2. Explain the countercurrent multiplier mechanism for concentrating urine.

   The loop of Henle creates a hyperosmotic medullary interstitium: the thick ascending limb actively pumps out NaCl (impermeable to water) while the descending limb is permeable to water, multiplying the osmotic gradient so that collecting duct fluid can be concentrated.

3. How does ADH (vasopressin) act on the kidney to concentrate urine?

   ADH increases insertion of aquaporin-2 water channels in the collecting duct principal cells, increasing water reabsorption and producing concentrated urine. Absence of ADH yields dilute urine (as in diabetes insipidus).

4. Write the Henderson-Hasselbalch equation for the bicarbonate buffer system and normal arterial pH.

   pH = 6.1 + log10([HCO3−] / (0.03 × PCO2)). Normal arterial pH is 7.35-7.45, with HCO3− ~24 mEq/L and PCO2 ~40 mmHg.

5. Classify the four primary acid-base disorders by pH, PCO2, and HCO3−.

   Respiratory acidosis: low pH, high PCO2. Respiratory alkalosis: high pH, low PCO2. Metabolic acidosis: low pH, low HCO3−. Metabolic alkalosis: high pH, high HCO3−.

6. Name the cells of the gastric mucosa and their secretions.

   Parietal (oxyntic) cells secrete HCl and intrinsic factor; chief cells secrete pepsinogen; mucous neck cells secrete mucus; G cells (antrum) secrete gastrin; ECL cells secrete histamine.

7. List the three phases of gastric secretion and their main triggers.

   Cephalic phase (sight/smell/thought of food, vagal), gastric phase (distension and peptides in stomach, gastrin), and intestinal phase (chyme entering duodenum, initially stimulatory then inhibitory).

8. State the actions of secretin and cholecystokinin (CCK).

   Secretin (from S cells, triggered by acid) stimulates bicarbonate-rich pancreatic/biliary secretion and inhibits gastric acid. CCK (from I cells, triggered by fat/protein) stimulates pancreatic enzyme secretion, gallbladder contraction, and relaxes the sphincter of Oddi.

9. Name the final products of carbohydrate, protein, and fat digestion that are absorbed.

   Carbohydrates: monosaccharides (glucose, galactose, fructose). Proteins: amino acids and small di/tripeptides. Fats: free fatty acids, monoglycerides, and glycerol (absorbed via micelles, re-formed into chylomicrons).

10. How is glucose absorbed across the intestinal epithelium?

    Glucose enters the enterocyte apical membrane via SGLT1 (secondary active transport with Na+) and exits the basolateral membrane into blood via GLUT2 (facilitated diffusion). Fructose enters via GLUT5.

11. List the hormones secreted by the anterior pituitary.

    Growth hormone (GH), prolactin, ACTH, TSH, FSH, and LH. (The posterior pituitary stores/releases ADH and oxytocin made in the hypothalamus.)

12. How does the hypothalamus control anterior versus posterior pituitary hormone release?

    It controls the anterior pituitary via releasing/inhibiting hormones carried in the hypothalamo-hypophyseal portal system. It controls the posterior pituitary directly via neuronal axons that release ADH and oxytocin (made in supraoptic and paraventricular nuclei).

13. Describe sequential events of neuromuscular transmission at the NMJ.

    Action potential reaches the axon terminal → voltage-gated Ca2+ channels open → ACh released by exocytosis → ACh binds nicotinic receptors on the motor end plate → end-plate potential → muscle action potential. ACh is broken down by acetylcholinesterase.

14. Differentiate an EPSP from an IPSP at a synapse.

    An EPSP (excitatory postsynaptic potential) is a depolarization (e.g., Na+ influx) that brings the neuron toward threshold. An IPSP (inhibitory postsynaptic potential) is a hyperpolarization (e.g., Cl− influx or K+ efflux) moving it away from threshold.

15. Outline the steps of skeletal muscle excitation-contraction coupling.

    Action potential travels down T-tubules → activates DHP receptors → triggers Ca2+ release from sarcoplasmic reticulum via ryanodine receptors → Ca2+ binds troponin C → tropomyosin moves → myosin binds actin → cross-bridge cycling (sliding filament) → contraction.

16. Compare skeletal, cardiac, and smooth muscle for striations, control, and pacemaker activity.

    Skeletal: striated, voluntary, no pacemaker. Cardiac: striated, involuntary, has pacemaker (autorhythmic), with intercalated discs/syncytium. Smooth: non-striated, involuntary, often has pacemaker activity (single-unit).

17. Name the cutaneous mechanoreceptors and what each detects.

    Meissner's corpuscles (light touch, rapidly adapting), Merkel discs (sustained touch/pressure, slowly adapting), Pacinian corpuscles (vibration/deep pressure, rapidly adapting), Ruffini endings (sustained stretch).

18. Compare the dorsal column-medial lemniscus and spinothalamic (anterolateral) pathways.

    Dorsal column-medial lemniscus carries fine touch, vibration, and proprioception; it crosses (decussates) in the medulla. The spinothalamic tract carries pain and temperature; it crosses at the spinal cord segmental level.

19. Describe the components of the stretch (myotatic) reflex.

    A monosynaptic reflex: muscle stretch activates the muscle spindle (Ia afferent) → synapses directly on the alpha motor neuron in the spinal cord → contraction of the same (agonist) muscle. Example: the knee-jerk reflex.

20. Distinguish upper motor neuron from lower motor neuron lesion signs.

    Upper motor neuron lesion: spastic paralysis, hyperreflexia, increased tone, positive Babinski sign, no significant atrophy. Lower motor neuron lesion: flaccid paralysis, hyporeflexia/areflexia, decreased tone, marked atrophy, and fasciculations.

21. Compare the sympathetic and parasympathetic divisions by outflow and neurotransmitters.

    Sympathetic: thoracolumbar outflow (T1-L2), short preganglionic/long postganglionic; postganglionic releases noradrenaline (except sweat glands). Parasympathetic: craniosacral outflow, long preganglionic/short postganglionic; both pre- and postganglionic release ACh. All preganglionic fibers release ACh (nicotinic).

22. List the major effects of sympathetic activation (fight-or-flight).

    Increased heart rate and contractility, bronchodilation, pupillary dilation (mydriasis), decreased GI motility/secretion, glycogenolysis, sweating, and vasoconstriction in skin/gut with vasodilation in skeletal muscle.

23. Match the EEG waves (alpha, beta, theta, delta) to their states.

    Beta (>13 Hz): alert/active mental activity. Alpha (8-13 Hz): awake, relaxed, eyes closed. Theta (4-7 Hz): drowsiness, light sleep, children. Delta (<4 Hz): deep sleep (slow-wave sleep).

24. Differentiate REM sleep from non-REM (slow-wave) sleep.

    REM (paradoxical) sleep: low-voltage fast EEG resembling wakefulness, rapid eye movements, dreaming, skeletal muscle atonia, irregular heart rate/respiration. Non-REM sleep: progressive slowing of EEG (high-voltage slow delta waves in deep stages), reduced metabolic rate, restorative.

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