Raul's Lab
NYMC · PHYM 1010 · Mammalian Physiology

Hard Exam — Cell & Muscle Physiology

An independent practice exam covering Section 1, written to graduate-school standard: harder than what Wednesday will actually ask, so the real thing feels easy.
Covers S1.1–S1.6 (Basics → ANS → Skeletal Muscle) Length 44 items + 5 integrative cases (49 total) Exam date Wed Sept 9, 2026 Built by Cody, 2026-09-08
Fill in a bubble for every question, then hit Submit Exam — each question reveals right where it sits: your answer, the correct one, and why every option (not just the right one) is right or wrong. No peeking ahead; nothing reveals until you submit.
01Physiology Basics & Homeostasis
04Synaptic Transmission
02Ions & Membrane Transport
05Autonomic Nervous System
03Excitable Membranes & APs
06Skeletal Muscle
Integrative Cases
Answer Key Grid
MODULE 1

Physiology Basics & Homeostasis

Dr. Ratliff, S1.1. The foundational vocabulary — regulated variables, gain, feedback loops — that every later module quietly assumes you already have.

Field note This module is the reason "regulated variable" language shows up again in Module 5 (ANS) and everywhere in your future cardio/renal blocks. The set-point framing is the same one behind why you treat a septic patient's fever and a heat-stroke patient's fever completely differently: one is a reset set-point (the hypothalamus is doing its job, just aimed higher), the other is a failure of the control system itself.
MODULE 2

Ions & Membrane Transport

Dr. Fisher, S1.2. Diffusion, carriers, channels, and the Nernst/Goldman math that everything electrical in Modules 3–4 is built on top of.

Nernst equation — single ion, 37 °C Eion = 61 mVz · log₁₀ ([ion]out[ion]in)
Goldman equation — two permeant ions, cations shown Vm = 61 mV · log₁₀ ( PK[K⁺]out + PNa[Na⁺]out PK[K⁺]in + PNa[Na⁺]in )
Memory hook "Carriers get tired, channels don't." Anything that requires a protein to physically change shape and reset (carriers, pumps, symporters/antiporters) has a ceiling — a Vmax — because the protein can only flip back and forth so fast. Ion channels are just a hole; more driving force, more flux, no ceiling (within physiologic ranges). If a question mentions saturation kinetics, it's never simple diffusion and never an open channel.
MODULE 3

Excitable Membranes & Action Potentials

Dr. Fisher, S1.3. Threshold fixed at −55 mV throughout, per the correction above.

Field note This is the physiology under the peaked T-waves and widened QRS you're taught to recognize on a 12-lead in crush injuries, renal failure, and rhabdomyolysis. You already know the pattern-recognition; this module is why it happens.
Worked Nernst check — [Na⁺]out = 145 mM, [Na⁺]in = 14.5 mM
ENa = 61 · log₁₀(145 mM14.5 mM)
= 61 · log₁₀(10)
= 61 · 1
= +61 mV
MODULE 4

Synaptic Transmission

Dr. Fisher, S1.4. The chemical-synapse sequence, EPSPs/IPSPs, and the pharmacology that hangs off every step of it.

MODULE 5

Autonomic Nervous System

Dr. Ratliff, S1.5. Receptor pharmacology throughout — including two facts worth knowing cold: α1 spares the brain, and β3 is real and testable.

Adrenergic receptors — effector & dominant action
ReceptorMajor locationsDominant effect
α1Skin, GI, kidney, splanchnic vasculatureVasoconstriction (spares brain & heart — local autoregulation dominates there)
α2Presynaptic terminals; pancreatic β-cellsNegative feedback: ↓ NE release, ↓ insulin release
β1Heart (SA/AV node, myocardium); kidney JG cells↑ HR, ↑ contractility, ↑ renin release
β2Bronchial, vascular, GI, bladder, uterine smooth muscleSmooth-muscle relaxation (bronchodilation, vasodilation, tocolysis); ↑ insulin secretion
β3Adipose tissue; bladder detrusorLipolysis; detrusor relaxation — real drug target (mirabegron), not in Costanzo
Field note Atropine's dose ceiling in organophosphate poisoning is functionally "until secretions dry up," far higher than the cardiac-arrest dose you're used to — because you're titrating against a massive, ongoing muscarinic flood, not a single bradycardic event.
MODULE 6

Skeletal Muscle

Dr. Ratliff, S1.6. Excitation-contraction coupling, the cross-bridge cycle, fiber typing, and the mechanical properties that follow from them.

Skeletal muscle fiber types
Type IType IIaType IIb/IIx
MetabolismOxidativeOxidative-glycolyticGlycolytic
Fatigue resistanceHighIntermediateLow
Contraction speedSlowFastFastest
Motor unit sizeSmallIntermediateLarge
Recruitment orderFirstSecondLast
Mitochondria / myoglobinHighModerateLow
Memory hook "DHP talks, RYR listens, SR pours." The DHP (voltage) receptor on the T-tubule doesn't move ions itself — it undergoes a conformational change that mechanically tugs open the ryanodine receptor sitting on the adjacent SR membrane, which is the actual Ca²⁺ release channel. Skeletal muscle EC coupling is mechanical (DHP–RYR physically linked); cardiac muscle EC coupling is chemical (Ca²⁺-induced Ca²⁺ release) — a favorite place for exam writers to swap the two.
CASES

Integrative Cases

Cross-module vignettes — the kind that reward actually understanding the mechanism rather than pattern-matching a keyword.

Review Grid

Click a cell to jump to that question. Never shows the correct answer — just what's answered, flagged, and (once checked or revealed) right or wrong.

not answered answered, not graded correct incorrect ⚑ flagged