Physiology Final Exam Study Deck

A cell loses its ability to regulate internal balance when its membrane is damaged. Explain why this happens based on membrane structure and function.

The membrane is selectively permeable and controls what enters and exits; damage disrupts this control, leading to loss of homeostasis.

If a cell’s shape is altered due to mutation, how might this affect its function?

Since form = function, a change in shape can impair the cell’s ability to perform its specific role

A drug destroys extracellular matrix proteins. What effect would this have on surrounding cells?

Cells would lose structural support and communication signals, leading to impaired tissue integrity

A membrane protein that normally transports glucose is blocked. What happens to glucose movement?

Glucose transport decreases because it relies on facilitated diffusion through carrier proteins

A membrane becomes less permeable to ions. How would this affect cell function?

Ion movement would decrease, disrupting gradients and affecting processes like membrane potential

A molecule moves from high to low conc. without energy but requires a protein. What type of transport is this and why?

Facilitated diffusion, because it utilizes a transport protein to assist the process.

A cell needs to move sodium ions into an area where sodium conc. is already high. What transport method is required and why?

Active transport, because it moves against the concentration gradient and requires energy

Temperature increases in a cell environment. Predict how diffusion rate changes and explain why.

Diffusion rate increases because molecules move faster at higher temperatures

A large molecule diffuses slower than a small one. Explain why using diffusion principles.

Larger molecules have more resistance and move more slowly, reducing diffusion rate.

A membrane channel becomes saturated with ions. What happens to transport rate and why?

Transport reaches a maximum because all channels are occupied

A competitor molecule binds to a transport protein. How does this affect transport of the original molecule?

Transport decreases because the competitor blocks binding sites

A cell is placed in a hypertonic solution. Predict what happens to the cell and explain why

The cell will lose water and shrink because the concentration of solutes outside the cell is higher than inside, causing water to move out of the cell to balance the solute concentrations.

A cell swells and bursts after being placed in a solution. What type of solution was it in and why?

Hypotonic, because water moved into the cell causing it to lyse

Two solutions have the same osmolarity, but one changes cell shape and the other does not. Why?

Not all isoosmotic are isotonic, if solutes can cross the membrane, they affect water movement differently

An ion is more concentrated outside the cell but negatively charged inside. Which direction will it move and why?

It depends on the electrochemical gradient, concentration pulls it in, but electrical forces may oppose or enhance movement

A hormone is released and travels through the bloodstream, but only certain cells respond. Explain why using receptor and signaling principles.

Only cells with the correct receptor can bind the hormone and activate signal transduction pathways, so response is target-cell specific.

A mutation prevents a peptide hormone from being stored in vesicles. Predict how this affects its secretion and function.

Peptide hormones must be synthesized and stored before release; without storage, secretion would be impaired or delayed, reducing signaling efficiency.

A lipid-soluble hormone is injected into the bloodstream. Describe how it travels and enters target cells compared to a peptide hormone.

It binds carrier proteins in blood, diffuses through the membrane, and binds intracellular receptors, unlike peptides which bind membrane receptors.

A drug blocks cholesterol synthesis. Predict which class of hormones is most affected and why.

Steroid hormones, because they are synthesized from cholesterol.

A signaling molecule is rapidly degraded in extracellular fluid. What type of signaling is this most likely and why?

Paracrine signaling (like eicosanoids), because they act locally and have short half-lives.

A ligand binds its receptor but no cellular response occurs. Identify two possible points of failure in the signaling pathway.

Signal transduction pathway may be inactive, or receptor may be inactivated or unable to activate downstream proteins.

If a ligand concentration increases significantly, explain how the law of mass action affects receptor binding and response.

More ligand increases receptor binding, increasing response until receptors become saturated.

A cell stops responding to a hormone after prolonged exposure. Explain how receptor regulation could cause this.

Receptors may be internalized, inactivated, or degraded, reducing sensitivity to the ligand.

A mutation prevents G-proteins from dissociating after activation. What happens to the cAMP signaling pathway?

Adenylyl cyclase remains active, producing excessive cAMP and prolonged signaling.

ATP levels drop in a cell. Predict how this affects the cAMP pathway.

Reduced ATP limits cAMP production, decreasing activation of protein kinase A and downstream responses.

A drug blocks phospholipase C. What happens to the PIP2/IP3 signaling pathway?

PIP2 cannot be split into DAG and IP3, so Ca²⁺ release and protein kinase activation are reduced.

Calcium release from intracellular stores is inhibited. Which signaling pathway is most directly affected and why?

The PIP2/IP3 pathway, because IP3 normally triggers Ca²⁺ release.

A patient has constantly high blood glucose despite insulin release. Identify a likely issue in the signaling pathway.

Insulin receptor (tyrosine kinase) or downstream signaling may be impaired, preventing glucose uptake.

During childbirth, contractions become stronger over time. Explain why this is a positive feedback loop.

Oxytocin increases contractions, which increase stimulus, causing more oxytocin release and further contractions.

Tubulin concentration suddenly drops in a cell. Predict how this affects microtubule dynamics and intracellular transport.

Microtubules shrink (dynamic instability), disrupting transport of vesicles and organelles.

A patient has low blood calcium levels but fails to release parathyroid hormone. What type of stimulus is involved, and where is the likely problem?

This is a humoral stimulus; the issue is likely in the parathyroid gland’s ability to detect or respond to low Ca²⁺.

A tumor causes continuous sympathetic stimulation of the adrenal gland. Predict the hormonal and physiological effects.

Increased catecholamine release, causing elevated heart rate, blood pressure, and prolonged stress response.

A patient is exposed to high hormone levels for a long time and shows decreased response. What cellular mechanism explains this?

Down-regulation—receptors are removed or become less sensitive, reducing the response.

A hormone has a short half-life but is secreted rapidly and continuously. How does this affect its blood concentration?

Levels may remain stable because rapid release balances rapid degradation.

Action potentials from the hypothalamus to the pituitary are blocked. Which hormones are most affected and why?

Oxytocin and vasopressin, because their release from the posterior pituitary depends on neural signaling.

A mutation prevents neurophysin from binding hormones. Predict the effect on hormone release.

Oxytocin and vasopressin cannot be transported properly, leading to reduced release.

A patient has impaired IP3 signaling in uterine smooth muscle. How does this affect labor?

Reduced Ca²⁺ release leads to weaker contractions, impairing oxytocin’s positive feedback loop.

A patient has high blood osmolarity but produces very dilute urine. Identify the hormone and likely issue.

Vasopressin (ADH) is involved; likely impaired signaling (cAMP) or failure to insert aquaporin channels.

Vasopressin receptors in the kidney are blocked. Predict the effect on water balance.

Decreased water reabsorption → increased urine output → dehydration risk.

Growth hormone levels are low despite high growth hormone releasing hormone. Where is the dysfunction?

The anterior pituitary is not responding properly.

A mutation disrupts the MAPK pathway. Which hormone’s major function is most affected and why?

Growth hormone, because its effects are mediated through IGFs using the MAPK pathway.

A patient has high ACTH but low cortisol levels. What does this indicate?

The adrenal cortex is not responding to ACTH.

Dopamine levels increase significantly. Predict the effect on prolactin and explain.

Prolactin decreases, because dopamine inhibits its release.

A patient has elevated potassium levels. Which hormone is released, and what is the outcome?

Aldosterone is released → increases Na⁺ reabsorption and K⁺ excretion → affects fluid balance.

ATP-sensitive K⁺ channels in pancreatic cells are blocked. Predict how this affects insulin release.

Channels close → depolarization → Ca²⁺ influx → increased insulin secretion

A patient is unable to sense temperature changes in the skin. Which division of the nervous system is affected, and which type of fibers carry the signal?

The sensory (afferent) division of the PNS; somatic sensory fibers carry the information to the CNS.

A virus infects a neuron and moves retrograde to the cell body. Which type of axonal transport is it using, and why is this clinically significant?

Retrograde transport; allows pathogens like rabies and herpes to reach the cell body and evade immune detection.

A patient has a mutation that keeps their K⁺ leak channels constantly closed. Predict the effect on their resting membrane potential.

Membrane potential would depolarize, as the normal K⁺ efflux that maintains RMP is reduced.

A graded potential is initiated by a weak neurotransmitter signal that does not reach threshold. What happens next, and why?

No action potential occurs; graded potentials decay over distance and must reach threshold at the axon hillock to trigger an AP.

A neuron is exposed to a strong depolarizing stimulus repeatedly. How does temporal summation influence action potential generation?

Multiple graded potentials in quick succession can combine to reach threshold, triggering an action potential.

During an action potential, Na⁺ channels are inactivated and K⁺ channels are open. What refractory period is this, and can another AP be generated?

Absolute refractory period; no action potential can be generated regardless of stimulus.

A demyelinating disease slows action potential conduction. Which type of conduction is most affected and why?

Saltatory conduction; myelin insulates the axon and allows rapid AP propagation between Nodes of Ranvier.

An axon with a larger diameter conducts impulses faster than a smaller one. Explain using Ohm’s law.

Larger diameter reduces axonal resistance, increasing current flow (I = V/R), so action potentials propagate faster.

A patient has defective voltage-gated Ca²⁺ channels in presynaptic terminals. Predict the effect on neurotransmitter release.

Reduced or absent neurotransmitter release, impairing chemical synapse communication.

A postsynaptic neuron receives simultaneous excitatory and inhibitory inputs. How is the overall membrane potential determined?

Through spatial and temporal summation of graded potentials; the net effect determines if threshold is reached.

A patient has a mutation causing slow inactivation of Na⁺ channels. Predict changes in action potential shape and refractory periods.

APs would last longer, repolarization delayed, absolute refractory period prolonged, and relative refractory period shifted.

A neuron receives a strong stimulus frequently. How does the nervous system code for stimulus intensity?

By increasing the frequency of action potentials (frequency coding), not amplitude.

A patient’s axosomatic synapses are damaged, but axodendritic synapses are intact. Which neuron functions are most affected?

Integration at the soma is impaired; fewer inputs influence AP initiation at the axon hillock.

Gap junctions between two neurons are blocked. How are electrical synapses affected?

Rapid conduction is lost, as ions can no longer diffuse directly between neurons

A toxin selectively opens ligand-gated Cl- channels on postsynaptic neurons. Predict the effect on AP generation

Hyperpolarization, neuron moves further from threshold, making it less likely to fire on action potential

A patient has damage to the cornea that prevents proper light refraction. Predict how this affects vision even if the lens is functioning normally.

Light will not be properly bent toward the lens, so it will not converge correctly on the retina, leading to a blurred image.

A patient’s ciliary muscles cannot contract. How does this affect their ability to see nearby objects?

The lens cannot become more bulbous, so light focuses behind the retina, impairing near vision (accommodation fails).

A patient has damage to the iris muscles and cannot constrict their pupil. How does this impact image clarity?

More stray light enters the eye, increasing “noise” and causing a less focused, blurrier image.

An object is moved closer to the eye but the lens does not adjust. Where will the focal point be and why?

Behind the retina, because additional refraction is needed but not achieved.

A patient has degeneration of the choroid layer. Predict the impact on retinal function.

Reduced nutrient supply and increased light scatter (less absorption of stray light), impairing visual clarity.

A patient loses rod function but retains cone function. Describe their vision in low-light and bright conditions

Poor night vision (rods needed for low light) but relatively normal color vision in bright light.

Multiple rods converge onto one bipolar cell, while cones do not. How does this affect visual sensitivity vs detail?

Rods increase sensitivity (better in dim light), but cones provide higher resolution and detail.

Light hits the retina, but rhodopsin cannot activate transducin. Predict what happens to the photoreceptor response.

cGMP is not broken down → Na⁺ channels stay open → cell remains depolarized → glutamate continues to be released → no signal sent.

A toxin prevents cGMP breakdown in photoreceptors. How does this affect vision in light conditions?

Na⁺ channels remain open → no hyperpolarization → glutamate release continues → bipolar cells inhibited → impaired vision.

A lesion occurs at the optic chiasm affecting crossing fibers. Which visual field is most likely lost?

Temporal visual fields (because nasal retinal fibers, which carry temporal field info, cross here).

A patient cannot detect odorants despite normal airflow. Identify a likely molecular issue in olfaction.

Dysfunction in G-protein (GOLF), cAMP production, or cation channels, preventing depolarization.

A mutation prevents Ca²⁺ from opening Cl⁻ channels in olfactory neurons. How does this affect signal strength?

Reduced depolarization, since Cl⁻ efflux is a major contributor to membrane potential change.

A patient can detect salty and sour tastes but not sweet or bitter. What type of signaling pathway is likely impaired?

G-protein–mediated pathways, since sweet and bitter rely on them.

A patient has damage to the basilar membrane. How does this affect hearing?

Hair cells cannot properly vibrate, preventing stereocilia bending and reducing sound signal transduction.

A patient’s stereocilia cannot stretch tip-links. What happens to auditory signal generation?

K⁺ channels do not open → no depolarization → no signal sent → hearing loss.

A patient experiences dizziness when moving their head but not during acceleration. Which structure is likely affected?

Semicircular canals, which detect rotational movement (not linear acceleration).

A sensory receptor detects a stimulus, but no response occurs. Identify two possible failures along the neural pathway.

Failure could occur in the afferent neuron (signal not transmitted) or the integration center (no processing/decision made).

A postsynaptic neuron receives input but does not reach threshold unless another signal arrives shortly after. Which zone is this neuron in and why?

The facilitated zone, because it is partially depolarized and more likely to reach threshold with additional input.

A reflex occurs immediately without conscious thought. What type of neural processing is this and why?

Serial processing, because the signal follows a single, rapid pathway (reflex arc).

You smell food and simultaneously recall a memory and feel hungry. What type of processing is occurring and why?

Parallel processing, because multiple pathways are activated simultaneously for perception, memory, and emotion.

A patient has damage to the blood-brain barrier. Predict how this affects neural function.

Harmful substances can enter the CNS, disrupting neuronal signaling and homeostasis.

A lesion affects white matter in the brain. What function is most impaired and why?

Signal transmission between regions, because white matter contains myelinated axons.

A patient cannot regulate heart rate or breathing after brain injury. Which brain region is likely damaged?

The medulla oblongata, which controls vital autonomic functions.

A patient has poor coordination and cannot integrate sensory input with movement. Which structure is affected?

The cerebellum, responsible for coordinating motor activity with sensory input.

A patient loses the ability to coordinate communication between the left and right hemispheres. What structure is damaged?

The corpus callosum, which connects the two hemispheres.

A patient shows abnormal hunger, aggression, and sexual behavior. Which brain region is most likely involved?

The hypothalamus, which regulates the “four F’s.”

A reflex arc is tested and the sensory neuron works, but no response occurs in the muscle. Identify the most likely failure point.

The motor (efferent) neuron or effector (muscle) is not functioning properly.

A reflex involves multiple interneurons between sensory and motor neurons. What type of reflex is this and why?

A polysynaptic reflex, because more than one synapse is involved.

A patient has damage to postganglionic neurons in the autonomic nervous system. How does this affect effector organs?

Signals cannot reach target organs, impairing involuntary functions like gland secretion or smooth muscle activity.

A drug blocks nicotinic receptors. Predict the effect on somatic and autonomic signaling.

Both are affected because nicotinic receptors are used in somatic neuromuscular junctions and autonomic ganglia, reducing excitation.

A patient is given a drug that stimulates β1 receptors. Predict the physiological effects.

Increased heart rate and contractility, and increased renin release.

A patient experiences bronchodilation after drug administration. Which receptor was likely activated and why?

β2 receptors, which inhibit smooth muscle in the respiratory tract.

A patient has high sympathetic tone. Predict the general physiological state and why.

Fight-or-flight state: increased heart rate, blood glucose, and alertness due to sympathetic dominance.

A toxin blocks voltage-gated Ca²⁺ channels in the synaptic bulb of a motor neuron. Predict the downstream effects on muscle contraction and explain why contraction fails.

Ca²⁺ cannot enter the synaptic bulb, so acetylcholine (ACh) vesicles cannot fuse with the membrane. No ACh is released → no depolarization of the motor end plate → no muscle action potential → no contraction.

If acetylcholinesterase is inhibited, how would this affect muscle contraction and why might this lead to paralysis?

ACh remains in the synaptic cleft, continuously stimulating Na⁺ channels → persistent depolarization → inability to repolarize → muscle cannot relax → leads to spastic paralysis.

A mutation prevents the DHP receptor from changing shape during depolarization. How does this affect excitation-contraction coupling?

RyR channels on the sarcoplasmic reticulum (SR) are not activated → Ca²⁺ is not released → troponin is not activated → no cross-bridge formation → no contraction.

If Ca²⁺ ATPase pumps in the SR stop working, predict what happens to muscle contraction and relaxation cycles.

Ca²⁺ cannot be pumped back into the SR → remains in cytoplasm → troponin stays activated → continuous contraction (rigor-like state) → inability to relax.

A mutation causes tropomyosin to permanently block myosin binding sites on actin. What happens to muscle contraction?

Myosin cannot bind actin → no cross-bridges → no contraction, even if Ca²⁺ is present.

During extreme fatigue, ATP levels drop significantly. Explain how this affects cross-bridge cycling.

ATP is required for myosin to detach from actin → without ATP, myosin remains bound → muscle becomes stiff (rigor) and cannot continue cycling.

If titin is damaged, how would this affect muscle extensibility and recoil after stretching?

Titin provides elasticity and recoil → without it, muscle loses passive elasticity → overstretching and reduced ability to return to resting length.