Physiology Flashcards

1
Q

What allows for the voluntary retention of urin once a full bladder has induced an increase in bladder parasympathetic tone?
A. Inhibition of S2-S4 α-motor neurons causing relaxation of the external urethral sphincter striated muscle fibers
B. Inhibition of pelvic splanchnic nerves causing a compensatory increase in bladder sympathetic activity
C. Activation of S2-S4 α-motor neurons causing contraction of the external urethral sphincter striated muscle fibers
D. Activation of neurons in the inferior mesenteric ganglion and subsequent contraction of the internal urethral sphincter
E. Activation of neurons in the inferior mesenteric ganglion and subsequent contraction of the external urethral sphincter

A

C. Activation of S2-S4 α-motor neurons causing contraction of the external urethral sphincter striated muscle fibers

The external urethral sphincter is under voluntary (somatic) control, and muscle fiber contraction causes closure of the sphincter. A full bladder sends afferent signals causing inhibition of sympathetic tone and an increase in parasympathetic activity to the bladder through the pelvic splanchnic nerves. The parasympathetic activity relaxes the internal urethral sphincter and induces bladder contraction.

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2
Q

What neurotransmitter is used by preganglionic sympathetic fibers?
A. Norepinephrine
B. Epinephrine
C.Glutamate
D.Acetylcholine
E. GABA

A

D. Acetylcholine

Acetylcholine acts through nicotinic receptors at the ganglionic synapse. (A) Norepinephrine is the neurotransmitter used in most postganglionic sympathetic fibers.

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3
Q

This toxin inhibits vesicle fusion in the presynaptic terminal at the neuromuscular junction.
A. Botulism toxin
B.Tetanus toxin
C. Diphtheria toxin
D.Alpha bungarotoxin
E. Tetrodotoxin

A

Botulism toxin

(B) Tetanus toxin inhibits the release of GABA and glycine in the spinal cord. (D) Alpha bungarotoxin inhibits acetylcholine from binding to its receptors at the neuromuscular junction. (E) Tetrodotoxin blocks action potentials by binding to and inhibiting fast, voltage-gated sodium channels.

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4
Q

This toxin inhibits RNA translation.
A. Botulism toxin
B. Tetanus toxin
C. Diphtheria toxin
D. Alpha bungarotoxin
E. Tetrodotoxin

A

C. Diphtheria toxin

(B) Tetanus toxin inhibits the release of GABA and glycine in the spinal cord. (D) Alpha bungarotoxin inhibits acetylcholine from binding to its receptors at the neuromuscular junction. (E) Tetrodotoxin blocks action potentials by binding to and inhibiting fast, voltage-gated sodium channels.

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5
Q

What decreases the rate of degradation of a passively conducted electrical signal in an axon?
A. Decreasing axonal diameter
B. Demyelinating an axon
C. Increasing axonal membrane resistance
D. Increasing extracellular resistance

A

C. Increasing axonal membrane resistance

The length constant (λ) describes the distance over which a passively conducted electrical signal decays to 37% of its initial voltage. A larger length constant means a slower rate of degradation. The equation is: λ = √(rm/(ri +ro )) where rm is the membrane resistance, ri is the internal axonal resistance, and ro is the extracellular resistance. Increasing myelination increases membrane resistance, and internal axonal resistance is decreased with increasing axonal cross-sectional area (i.e., diameter).

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6
Q

What substance releases factor VIII from von Willebrand factor?
A. Fibrinogen
B. Platelets
C. Factor IX
D. Antithrombin III
E. Thrombin

A

E. Thrombin

Factor VIII is bound to von Willebrand factor (vWF) and inactive in circulation. Under the action of thrombin, factor VIII is released form vWF and thus activated. When not bound to vWF, factor VIII quickly degrades.

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7
Q

In brain death, what happens to the intracranial pressure (ICP) as the mean arterial pressure (MAP) rises?
A. Cerebral autoregulation increases ICP.
B. Cerebral autoregulation decreases ICP.
C. The lack of cerebral autoregulation causes an increase in ICP.
D. The lack of cerebral autoregulation causes a decrease in ICP.
E. Cerebral autoregulation maintains a relatively constant ICP.

A

C. The lack of cerebral autoregulation causes an increase in ICP.

With brain death, there is a loss of cerebral autoregulation, so the brain’s normal response of maintaining a vascular tone sufficient to counteract increases in mean arterial pressure (MAP) is lost. The brain experiences the increases in MAP, which translate to increases in intracranial pressure.

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8
Q

The sensory nerves originating in the extremities with cell bodies in the dorsal root ganglia are examples of what classification of neuron?
A. Unipolar
B. Bipolar
C. Multipolar
D. Pyramidal
E. Multiaxonic

A

A. Unipolar

Sensory neurons are classified as unipolar with an axon and dendrites on each end and a cell body branching from some point along the axon. (B) Bipolar neurons have an axon with dendrites on each end with a cell body along the axon. They are found as interneurons, like in the retina. (C) Multipolar neurons have dendrites surrounding a cell body from which a single axon originates. They are found as motor neurons. (D) Pyramidal neurons appear as bipolar neurons with numerous arboretic dendritic processes extending from the cell body and axons. Prime examples are found in the cerebellum as Purkinje cells. (E) Multiaxonic neurons do not exist.

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8
Q

To what type of motion/activity will the utricle respond?
A. Injecting cold water into the ear of a person sitting upright
B. Sleeping
C. Stopping at a stop sign in a motor vehicle
D. Beginning to spin in an office chair
E. Falling at terminal velocity while skydiving

A

C. Stopping at a stop sign in a motor vehicle

Both the utricle and saccule respond to changes in linear acceleration with the utricle being oriented horizontally and the saccule vertically. Deceleration in a motor vehicle traveling straight or a head tilt downward each causes anterior displacement of the otoliths in the macula of the utricle and excites hair cells that respond to movement in that direction. In contrast, the act of jump roping mainly would be sensed by action in the saccule. (A, D) Both of these activities cause a shift of endolymph in the semicircular canals that is detected in the ampulla of each canal. The ampullae respond to angular acceleration. (B, E) The vestibular system only responds to changes in acceleration and will adapt with no or constant motion in the same direction.

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9
Q

A patient has a hormone-producing pituitary microadenoma that puts him at risk (if left untreated) for peripheral neuropathies, cardiac arrhythmias, and sleep apnea. What hormone is the adenoma producing?
A. Adrenocorticotropic hormone (ACTH)
B. Growth hormone
C. Prolactin
D. Thyroid-stimulating hormone
E. Follicle-stimulating hormone

A

B. Growth hormone

Excess growth hormone in adults results in arthropathy, paresthesias, polyneuropathy, cardiomyopathy, arrhythmias, upper airway obstruction due to palatal/pharyngeal tissue overgrowth, increased risk for malignancies and colon polyps, and diabetes. (A) Excess adrenocorticotropic hormone (ACTH) secretion results in Cushing disease, characterized by weight gain, hypertension, mood changes, hypertelorism, fatigue, and “moon face.” (C) High prolactin levels are associated with infertility, spontaneous lactation, loss of libido, erectile dysfunction, and abnormal menstrual cycles. (D) Excess thyroid-stimulating hormone results in hyperthyroidism with symptoms of tremors, anxiety, weight loss, heat intolerance, brittle hair, and insomnia. (E) Excess follicle-stimulating hormone results in infertility

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10
Q

What are the major proinflammatory cytokines?
A. TGF- α and VEGF
B. IL-1 and TNF-α
C. IL-6 and TGF-α
D. IL-6 and IL-13
E. IFN-γ and IL-10

A

B. IL-1 and TNF-α

The major proinflammatory cytokines are the interleukins (IL) IL-1, IL-6, IL-8, TNF-α (tumor necrosis factor-alpha), and IFN-γ (interferongamma). These produce fever, tissue destruction, and inflammation. The major anti-inflammatory cytokines include IL-4, IL-6, IL-10, IL-11, and IL-13. Of note, IL-6 can be anti- or proinflammatory depending on how it is used in a signaling cascade. (A) TGF-α and VEGF are examples of growth factors.

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11
Q

What is a miniature end-plate potential?
A. Inhibitory postsynaptic potential
B. Excitatory postsynaptic potential
C. Response of the postsynaptic terminal caused by the release of a single vesicle into the synaptic cleft
D. Response of the postsynaptic terminal caused by the release of a single molecule of neurotransmitter into the synaptic cleft
E. Response of the postsynaptic terminal caused by the release of the neurotransmitters from a single neuron only

A

C. Response of the postsynaptic terminal caused by the release of a single vesicle into the synaptic cleft

Response of the postsynaptic terminal caused by the release of a single vesicle into the synaptic cleft
MEPs summate in the postsynaptic terminal to induce a response of either hyperpolarization or depolarization. (A, B) Miniature end-plate poten- tials (MEPs) can be excitatory or inhibitory.

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12
Q

When do T-type calcium channels open during the action potential?
A. At the resting potential
B. Between the resting and threshold potentials
C. Between the threshold potential and maximal depolarization
D. Between maximal depolarization and the resting potential
E. Between the resting potential and “overshoot” phase (hyperpolarization)

A

B. Between the resting and threshold potentials

Between the resting and threshold potentials
Found initially in cardiac smooth muscle cells, T-type calcium channels are unique voltage-gated calcium channels that open at around –55 mV, which is slightly higher than the resting potential in cardiac cells of –60 mV. T-type calcium channels open to allow a large calcium flux into the cell to aid in the depolarization required to reach the trig- gering threshold for an action potential.

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13
Q

How do class 3 cardiac antiarrhythmics (potassium channel blockers) affect action potentials and conduction velocity?
A. Shorten action potential refractory period and increase conduction velocity
B. Shorten action potential duration and maintain normal conduction velocity
C. Prolong action potential refractory period and slow conduction velocity
D. Prolong action potential duration and maintain normal conduction velocity
E. Shorten action potential refractory period and slow conduction velocity

A

D. Prolong action potential duration and maintain normal conduction velocity

Prolong action potential duration and maintain normal conduction velocity
By blocking only potassium channels (notably the inward rectifier channels), hyperpolarization (returning to a negative resting potential) is inhib- ited, and cardiac cells remain depolarized longer. This prolongs the action potential and the refrac- tory period. Conduction velocity is unaffected, as there is no prevention of the opening of subsequent sodium channels and depolarizing adjacent mem- brane segments.

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14
Q

What neurotransmitters never can be used to upregulate action downstream in a neural network?
A. GABA and glycine
B. Glutamate and acetylcholine
C. Norepinephrine and epinephrine
D. Dopamine and substance P
E. All neurotransmitters can be used to upregulate downstream neural network activation

A

E. All neurotransmitters can be used to upregulate downstream neural network activation

All neurotransmitters can be used to upregulate downstream neural network activation
Although neurotransmitters are labeled as excit- atory or inhibitory, this refers only to the effect of a neurotransmitter on a specific type of receptor at a specific synapse. It is how the various receptors and neurons containing the receptors are organized that causes a downstream effect. For example, the basal ganglia circuitry is full of circuits that inhibit inhibitory circuits so that an inhibitory synapse/ receptor on an inhibitory neuron could result in the activation of a downstream neuron.

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15
Q

How does caffeine exert its effects?
A. GABA receptor antagonism
B. Phosphodiesterase inhibition
C. Adenosine receptor agonism
D. Acetylcholinesterase activation
E. Ryanodine receptor antagonist

A

B. Phosphodiesterase inhibition

Phosphodiesterase inhibition
By inhibiting phosphodiesterase, cAMP degrada- tion is reduced. All of the actions of caffeine serve to upregulate the nervous system in a stimulatory manner. (A) Caffeine competitively inhibits glycine receptors. (C) Caffeine competitively inhibits ade- nosine receptors. Activation of adenosine receptors leads to the sensation of drowsiness. (D) Caffeine competitively inhibits acetylcholinesterase. (E) Caf- feine is an agonist for the ryanodine receptor.

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16
Q

How does cocaine affect neurotransmission at the synaptic cleft?
A. Inhibition of the presynaptic uptake of monoamines
B. Induction of the release of monoamines
C. Prevention of the degradation of monoamines in the synaptic cleft
D. Blockade of the postsynaptic uptake of monoamines
E. Induction of the postsynaptic uptake of monoamines

A

A. Inhibition of the presynaptic uptake of monoamines

Inhibition of the presynaptic uptake of monoamines
Cocaine blocks the monoamine transporter pro- teins on the presynaptic cleft, thus preventing monoamine reuptake and vesicular storage in the presynaptic terminal. (B) Amphetamines both block the reuptake of monoamines into the presynaptic terminal and induce the release of monoamines into the synaptic cleft.

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17
Q

What are the degradation products of the reaction between acetylcholine and acetylcholinesterase on the postsynaptic membrane?
A. Phosphatidylcholine and choline
B. Phosphatidylcholine and acetate
C. Acetyl CoA and acetate
D. Choline and acetate
E. Choline and acetyl CoA

A

D. Choline and acetate

Choline and acetate
Following the breakdown of acetylcholine by acetylcholinesterase in the extracellular space, acetate is transported into the intracellular space, where it is converted to acetyl CoA, which then can combine with choline to reform acetylcholine.

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18
Q

What role do caspases play in necrosis?
A. Caspases signal and regulate the orderly fragmentation of DNA.
B. Caspases signal a cell to undergo necrosis.
C. Caspases typically are not part of necrosis.
D. Caspases inhibit necrosis and cell death.

A

C. Caspases typically are not part of necrosis.

aspases typically are not part of necrosis
Caspases are proteases necessary for apoptosis. They signal and regulate the controlled process by which DNA and cellular components are frag- mented and degraded. In contrast, necrosis is un- controlled cell death and results in inflammation. Caspases typically play little to no role in necrosis.

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18
Q

What molecules are needed to activate the ligandgated component of NMDA receptors?
A Glutamate and glycine
B. Magnesium and glycine
C. Magnesium and serine
D. Aspartate and zinc
E. Zinc and glycine

A

A. Glutamate and glycine

Glutamate and glycine
Two molecules of either glutamate or aspartate and two molecules of either glycine or serine need to bind to an NMDA receptor in order to activate it. The receptor also has a voltage-gated component requiring depolarization of the neuron on which it is located. The voltage-gated component of the receptor is controlled by the calcium channel being blocked by either a zinc or magnesium ion when the receptor is inactive.

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19
Q

What is the mechanism of action of bisphosphonates?
A. Increasing the body stores of calcium
B. Activation of osteocytes
C. Inhibition of osteocytes
D. Inhibition of osteoclasts
E. Recruitment of osteoblasts

A

D. Inhibition of osteoclasts

Inhibition of osteoclasts
Bisphosphonates bind to calcium and are taken up by osteoclasts. Bisphosphonates then induce apoptosis of these bone-reabsorbing cells. These are useful agents in osteopenia and osteoporosis. (A) Bisphosphonates have no effect on the body total stores of calcium. (B) Osteocytes are osteo- blasts that have entrapped themselves in their secretory bony matrix. They do not divide, but they do play a role in the turnover and maintenance of the bony matrix. They express TGF-β to suppress bone resorption. (C) Inhibition of osteocytes would lead to increased bone resorption. (E) Osteoblasts form new, nonmineralized bony matrix on the sur- face of mature, mineralized bone. They are regu- lated and recruited in part by osteocytes

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20
Q

Where does GABA bind on the GABAA receptor?
A. On the α subunit
B. On the β subunit
C. Between the α and β subunits
D. On the γ subunit
E. Between the α and γ subunits

A

C. Between the α and β subunits

Between the α and β subunits
(E) The benzodiazepine binding site on the GABAA receptor is between the α and γ subunits

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21
Q

A patient with a complete spinal cord injury has a patellar reflex in the acute period following his injury. What circuitry component must be intact?
A. Cell bodies in the midthoracic spinal cord
B. Dorsal columns between the brain and lumbar spinal cord
C. Cell bodies in the lumbar prominence of the spinal cord
D. Anterior horn cells between the brain and lumbar spinal cord

A

C. Cell bodies in the lumbar prominence of the spinal cord

Cell bodies in the lumbar prominence of the spi- nal cord
The patellar reflex occurs independently of input from the brain; however, the brain does work to suppress the reflex when all spinal circuitry is in- tact. This is why hyperreflexia and clonus can be seen with significant spinal cord compression. The actual reflex only requires the sensory nerves from the patellar tendon to be intact and synapse on cell bodies within the lumbar spinal cord. The reflex arc then stimulates motor neurons at that same level to provide the motor component of the reflex.

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22
Q

What is the mechanism of action for temozolomide (Temodar)?
A. Microtubule inhibitor
B. DNA cross-linking
C. Anti-VEGF antibody
D. DNA alkylation
E. Topoisomerase inhibitor

A

D. DNA alkylation

DNA alkylation
Temozolomide and procarbazine are DNA alky- lating (methylating) agents that interfere with protein synthesis. (A) Microtubule function inhibi- tors include vincristine and vinblastine. (B) DNA cross-links by carbamylation of amino groups are formed by the nitrosoureas such as BCNU and CCNU. (C) Bevacizumab (Avastin) is an anti-VEGF anti- body. (E) Tamoxifen is a topoisomerase inhibitor.

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23
What are the first cleavage products of proopiomelanocortin? A. β-lipotrophin, α-MSH, and γ-MSH B. ACTH, α-MSH, and γ-MSH C. α-MSH, β-MSH, β-endorphin D. ACTH, β-lipotrophin, and γ-MSH E. α-MSH, β-MSH, and γ-MSH
D. ACTH, β-lipotrophin, and γ-MSH ## Footnote ACTH, β-lipotrophin, and γ-MSH Following the initial cleavage of pro-opiomela- nocortin into ACTH, β-lipotrophin, and γ-MSH, ACTH can be processed further to α-MSH and CLIP. β-lipotrophin can be processed into β-endorphin and γ-lipotrophin with the latter eventually becoming β-MSH.
24
What happens during testing of the H-reflex in electrophysiological studies when stimulation is increased to a supramaximal level? A. The H-wave disappears B. The M-wave disappears. C. The H-wave increases. D. The M-wave decreases. E. The F-wave remains constant.
A. The H-wave disappears ## Footnote The H-wave disappears The H-wave is the electrophysiological equiva- lent of the stretch reflex and represents the mus- cle’s electrical response to a square wave stimulus to the skin that first propagates in the antidromic direction (away from the muscle) to the cell bodies. The reflex arc continues with an electrical signal sent in the orthodromic direction (toward the mus- cle) to elicit a response. This response is the H-wave. As stimulation amplitude increases, the H-wave diminishes and disappears with supramaximal stimulation. It is most useful for evaluating the Ia sensory afferents. (B, D) The M-wave is the ortho- dromic response recorded in the muscle to electri- cal stimulation of the skin overlying the muscle. It bypasses the reflex arc and increases with increas- ing stimulation amplitude. (E) The F-wave increases with increases in amplitude but not to the extent seen in the M-wave. The F-wave is the result of alpha-fiber stimulation and is useful to evaluate proximal (near the spinal cord) nerve conduction velocities.
25
What is the substrate for nitric oxide synthetase? A. Tyrosine B. NADP C. Citrulline D. Arginine E. Asparagine
D. Arginine ## Footnote Arginine along with cofactors NADPH and oxy- gen react in the presence of nitric oxide synthe- tase to produce nitric oxide, NADP, and citrulline. (A, E) Tyrosine and asparagine are not involved in nitric oxide synthesis. (B, C) NADP and citrulline are products in the reaction creating nitric oxide.
26
How does the isometric tension-length curve of smooth muscle compare to the curve of skeletal muscle? A. Smooth muscle force is maximal in the tension trough. B. The curve is wider with smooth muscle C. Maximal tension occurs at the point of maximal contraction in smooth muscle. D. There is only a single peak of maximal tension with smooth muscle.
B. The curve is wider with smooth muscle ## Footnote The curve is wider with smooth muscle, as shown in this image. (A) Tension equals the force of the muscle. (C) Tension increases to its maximum as the mus- cle is stretched beyond its ideal working length (at the point of maximal myosin and actin overlap). Tension will increase indefinitely at the far right of the tension–length curve until muscle tissues begin to tear. (D) When the single peak of active muscle tension versus length is added to the exponential relationship of tension to length in resting muscle, there is a tension peak, followed by a trough, fol- lowed by a continued rise in tension with both smooth and skeletal muscle
26
What substance in excess in the extracellular space induces increased calcium ion flux through NMDA receptors on oligodendrocytes to cause excitotoxic damage? A. Calcium B. Glutamate C. Acetylcholine D. GABA E. Epinephrine
B. Glutamate ## Footnote Glutamate triggers the activation of NMDA receptors. When the magnesium ion is displaced from its channel-blocking site, there is calcium influx into the cytosol. Elevated calcium levels trigger apoptotic changes in the affected cells.
27
What component of the blood–brain barrier is most responsible for its integrity, creation, and maintenance? A. Astrocytic foot processes B. Arachnoid “cap” cells C. Pericytes D. Endothelial cells
C. Pericytes ## Footnote Pericytes are the cells surrounding the endothelial cells of capillaries and venules throughout the body. In the brain, pericytes create and maintain the tight junctions between endothelial cells and regulate vesicle trafficking between endothelial cells. It is this role that creates the selectivity of the blood–brain barrier. Pericytes also inhibit the expression of endothelial markers that increase vascular permeability. (A) Astrocytic foot processes historically were thought to be the key component creating the blood–brain barrier; however, their role is to provide biochemical support to the endothelial cells creating the barrier. (B) Arachnoid “cap” cells are cells of the arachnoid villi from which meningiomas originate. (D) The endothelial cells themselves are not the key component to the blood–brain barrier. Instead, the highly selective tight junctions between endothelial cells allow for the specialized function of the blood–brain barrier.
28
How do organophosphates cause accumulation of acetylcholine in the synaptic cleft? A. Irreversible binding to and inhibition of acetylcholinesterase B. Blockade of postsynaptic acetylcholine receptors C. Blockade of presynaptic acetylcholine receptors D. Stimulation of release of presynaptic acetylcholine E. Temporary reduction in binding affinity for acetylcholine and acetylcholinesterase
A. Irreversible binding to and inhibition of acetylcholinesterase ## Footnote Organophosphates irreversibly bind to acetylcholinesterase and inactivate this acetylcholine-degrading enzyme. Pralidoxime can be used as an antidote in organophosphate poisoning, as it is able to reactivate the enzyme prior to degradation.
29
How does hemoglobin’s affinity for oxygen change as blood passes through a capillary, and what shift occurs with the oxygen-hemoglobin dissociation curve? A. The affinity of hemoglobin for oxygen decreases, and the oxygen-hemoglobin dissociation curve shifts to the left. B. The affinity of hemoglobin for oxygen decreases, and the oxygen-hemoglobin dissociation curve shifts to the right. C. The affinity of hemoglobin for oxygen increases, and the oxygen-hemoglobin dissociation curve shifts to the left. D. The affinity of hemoglobin for oxygen increases, and the oxygen-hemoglobin dissociation curve shifts to the right. E. The affinity of hemoglobin for oxygen remains the same, and the oxygen-hemoglobin dissociation curve does not shift.
B. The affinity of hemoglobin for oxygen decreases, and the oxygen-hemoglobin dissociation curve shifts to the right. ## Footnote The affinity of hemoglobin for oxygen decreases, and the oxygen-hemoglobin dissociation curve shifts to the right, as shown in this image. Increasing temperature, carbon dioxide, and 2,3-DPG along with decreasing pH all decrease the binding affinity of hemoglobin for oxygen and thus shift the hemoglobin-oxygen dissociation curve to the right. Conditions opposite to these will increase binding affinity and shift the curve to the left. As blood passes through a capillary, metabolically active tissues release 2,3-DPG, which induces an allosteric change in hemoglobin and leads to oxygen unbinding. Oxygen is taken up by tissues, and carbon dioxide enters the blood. The partial pressure of oxygen thus is reduced as is the pH causing subsequent oxygen unbinding from hemoglobin. A decrease in the partial pressure of oxygen causes a shift along the curve to the left.
30
What is the approximate resting membrane potential of a neuron, and conductance of what ion is most responsible for determining this potential? A. –65 mV; potassium B. –60 mV; sodium C. +60 mV; chloride D. –90 mV; potassium E. +20 mV; calcium
A. –65 mV; potassium ## Footnote All ions considered, the actual resting membrane potential for a neuron is between –60 and –70 mV. This is due in large part to the flux of potassium ions from inside to outside the neuron through open channels along the concentration gradient. The equilibrium potential for potassium is around –90 mV. (B) Sodium flux is from the extracellular to the intracellular space when a membrane is at rest, but there are far fewer sodium than potassium channels open when a neuron is at rest. (C) The equilibrium potential for sodium is around +60 mV, whereas it is around –60 mV for chloride. (D) Although the resting membrane potential is based largely on potassium conductance, it is more positive than the equilibrium potential for potassium alone. (E) The equilibrium potential for calcium is around +20 mV, but the ion plays little role in the membrane resting potential.
31
Secretion of what proteins from the notochord establishes the ventral pole of the dorsal-ventral axis in the developing nervous system? A. Bone morphogenic proteins B. Wnt family proteins C. Sonic hedgehog proteins D. Patched proteins E. Ras proteins
C. Sonic hedgehog proteins ## Footnote Sonic hedgehog proteins are secreted from the notochord and signal the development of the floor plate and motor neurons in a concentration-dependent fashion. (A, B) Bone morphogenic proteins from the ectoderm overlying the notochord and Wnt family proteins establish the dorsal axis. (D) The patched gene (Ptc) expresses the ligand-binding domain for the sonic hedgehog proteins. (E) The Ras family proteins are GTPases involved cell signal transduction and can signal aberrantly in cancers.
32
How will a patient with severe myasthenia gravis affecting a particular neuromuscular junction react to organophosphate poisoning at that same junction? A. No effect on postsynaptic activity B. Increased postsynaptic activity C. Decreased postsynaptic activity D. Increased presynaptic activity E. Decreased presynaptic activity
B. Increased postsynaptic activity ## Footnote Myasthenia gravis is a condition characterized by antibodies that bind to postsynaptic acetylcholine receptors and inhibit acetylcholine binding. This reduces the postsynaptic activity. Medications for myasthenia gravis act by competitively inhibiting acetylcholinesterase, thus decreasing acetylcholine breakdown and increasing acetylcholine in the synaptic cleft. Organophosphates irreversibly bind to and inhibit acetylcholinesterase and have a similar end result on the postsynaptic activity.
33
If a resting neuron with only potassium permeability was taken from its normal extracellular space and placed in endolymph, what would happen to its resting state? A. Its resting state would become more positive. B. Its resting state would become more negative. C. Its resting state would remain the same. D. Its resting state would be too variable to predict.
A. Its resting state would become more positive. ## Footnote Due to its high potassium relative to sodium concentration compared with perilymph and normal neuronal extracellular fluid, endolymph has a potential of 80 to 120 mV. The normal resting concentration of potassium in a neuron is about 150 mmol, which is the same concentration of potassium in endolymph. This means that there essentially would be almost no passive flow of potassium ions in this situation, and according to the Nernst equation, the resting potential due to potassium flux would be about 0 mV.
34
What is the mechanism of action of strychnine? A. Blockade of GABA receptors B. Activation of acetylcholine receptors on neurons in the spinal cord C. Inhibition of neurons through activation of GABA receptors D. Inhibition of glycine receptors E. Potentiation of neurons through activation of glycine receptors
D. Inhibition of glycine receptors ## Footnote Strychnine is a rodenticide that works by binding to, and thus blocking, glycine and acetylcholine receptors on motor neurons in the spinal cord. This leads to a hyperactivation of skeletal musculature and death by asphyxiation due to tonic contraction of the respiratory muscles.
35
What is the hourly rate of production of cerebrospinal fluid in the adult brain? A. 10 mL/h B. 14 mL/h C. 18 mL/h D. 22 mL/h E. 26 mL/h
C. 18 mL/h ## Footnote Cerebrospinal fluid (CSF) is produced at an average rate of 18 mL/h, yielding a total daily production of 400 to 500 mL. The total CSF volume in an adult is approximately 140 mL at any given time. Seventy percent of CSF is produced by the choroid plexus.
36
What role do gamma motor neurons play in the muscle spindle? A. Shorten the muscle spindles with skeletal muscle fiber contraction B. Regulate beta motor neurons C. Inhibit alpha motor neurons D. Allow for the adaptation of type 2 afferents E. Shorten the Golgi tendon organs with muscle contraction
A. Shorten the muscle spindles with skeletal muscle fiber contraction ## Footnote The cells bodies of gamma motor neurons are located in the anterior horns of the spinal cord. They are activated along with their corresponding alpha motor neurons and contract the intrafusal muscle fibers to keep the muscle spindles taut regardless of extrafusal muscle fiber length. (B) Beta motor neurons activate both extrafusal and intrafusal muscle fibers, thus shortening muscle length and keeping muscle spindles taut. They greatly are outnumbered by gamma motor neurons. (C) Gamma and alpha motor neurons are activated simultaneously in a given muscle. (D) Type 2 afferents are highly myelinated stretch receptors in the muscle that, unlike type 1a afferents, are non-adapting and thus fire continuously with a stable muscle length. (E) The Golgi tendon organs are proprioceptive sensory receptors oriented in series with skeletal muscle fibers. They are located where skeletal muscles join their tendons and sense the force on the muscles. With signaling through 1b afferents, the Golgi tendon reflex can be initiated, which inhibits further contraction of the muscle involved through inhibitory interneurons in the spinal cord.
37
What enzyme promotes the conversion of 5¬hydroxy-tryptophan to serotonin? A. Tyramine β-hydroxylase B. Aromatic amino acid decarboxylase C. Tryptophan hydroxylase D. Tyrosine hydroxylase E. Catechol-O-methyl transferase
B. Aromatic amino acid decarboxylase ## Footnote Aromatic amino acid decarboxylase uses activated B6 as a cofactor. (A) Tyramine β-hydroxylase converts tyramine to octopamine (an amine that acts in place of norepinephrine in sympathetic neurons with chronic monoamine oxidase inhibitors). (C) Tryptophan hydroxylase converts tryptophan to 5-hydroxy-tryptophan during serotonin synthesis. (D) Tyrosine hydroxylase converts tyrosine to levodopa during dopamine synthesis. (E) Catechol-O-methyl transferase inactivates catecholamine neurotransmitters including dopamine, levodopa, norepinephrine, and epinephrine
38
How is presynaptic hyperpolarization of a neuron advantageous over postsynaptic hyperpolarization? A. It allows for inhibition of the entire presynaptic and postsynaptic neuronal chain. B. It allows for more precise temporal summation. C. It reduces the amount of neurotransmitter degradation occurring in the synapse. D. It allows for more precise spatial resolution.
D. It allows for more precise spatial resolution. ## Footnote Presynaptic inhibition has an advantage over postsynaptic inhibition in that presynaptic inhibition downregulates only one synapse acting on the postsynaptic cell. The entire neuronal chain thus does not simply become inhibited based on one postsynaptic action. In addition, the multiple miniature end-plate potentials (MEPPs) from several presynaptic terminals (whether inhibitory or excitatory) can be grouped together at the postsynaptic cell to induce or inhibit an action potential (spatial resolution). (B) Temporal summation involves the grouping of MEPPs together in a temporal fashion to induce an action potential postsynaptically. (C) With presynaptic inhibition, there are fewer quanta of neurotransmitters entering the synaptic cleft.
39
What role do L-type voltage-dependent calcium channels play in muscle contraction? A. Release calcium from the sarcoplasmic reticulum B. Allow for depolarization of the postsynaptic terminal C. Reuptake calcium into the presynaptic terminal D. Respond to depolarization and activate calcium channels on the sarcoplasmic reticulum E. Binds to troponin to induce an allosteric change
D. Respond to depolarization and activate calcium channels on the sarcoplasmic reticulum ## Footnote As the action potential at the neuromuscular junction occurs, depolarization propagates through the T-tubules in the muscle fiber. L-type voltage-dependent calcium channels are activated, and they open ryanodine receptors in the adjacent sarcoplasmic reticulum. The calcium that then is released binds to troponin C on the myofibrils to start sarcomere contraction. (A) Once activated, calcium-release channels (ryanodine receptors) on the sarcoplasmic reticulum allow for stored calcium to be released within the muscle cells’ cytoplasm. (E) This is the role of calcium and not a channel.
40
How does parathyroid hormone increase the serum calcium level? A. Inhibits calcitonin production B. Inhibits osteoblasts C. Increases phosphate reabsorption in the kidneys D. Blocks the formation of vitamin D E. Inhibits osteoclasts
B. Inhibits osteoblasts ## Footnote By inhibiting osteoblasts, parathyroid hormone (PTH) is not able to inhibit osteoclasts and reduce bone reabsorption. As bone is reabsorbed, calcium is released into the circulation. (A) Calcitonin is secreted by the thyroid and inhibits intestinal calcium absorption of calcium, inhibits osteoclast activity, stimulates osteoblast activity, and promotes renal secretion of calcium. All of these effects work to reduce the serum calcium concentration. Calcitonin can be thought of as having the opposite activity of PTH. (C) PTH promotes the reabsorption of calcium from the distal tubules and thick ascending limbs in the kidneys and reduces phosphate reabsorption. This leads to an increase in the calcium/ phosphate ratio, meaning that more calcium is free in the serum. Increasing renal phosphate reabsorption would have the opposite effect. (D) PTH upregulates the enzyme responsible for activating vitamin D, which in turn increases the intestinal reabsorption of calcium. (E) Osteoclast inhibition would reduce bone turnover and calcium release from the bony matrix.
41
A particular inhibitor is found to prevent the formation of L-dopa from tyrosine. Further studies show that the inhibitor only works once tyrosine hydroxylase has interacted with tyrosine. The inhibitor is a(n): A. Competitive inhibitor B. Noncompetitive inhibitor C. Uncompetitive inhibitor D. Mixed inhibitor
C. Uncompetitive inhibitor ## Footnote An uncompetitive inhibitor binds to an enzyme/ substrate complex to reduce or inhibit its activity. The enzyme/substrate must first form for this type of inhibition to take place. (A) In a simple form, a competitive inhibitor binds to an enzyme and, when bound, prevents the enzyme from binding to its substrate. In other words, the enzyme may either be bound to its inhibitor or substrate but not both at the same time. (B) A noncompetitive inhibitor binds to and acts on an enzyme to reduce its activity and interaction with its substrate. A noncompetitive inhibitor binds to an enzyme equally well whether or not the enzyme is bound to its substrate. The substrate does not have to be present for a noncompetitive inhibitor to act. (D) A mixed inhibitor is a type of noncompetitive inhibitor that has a higher affinity for the enzyme in a particular state (e.g., bound to its substrate).
42
What feature of excitatory synapses forces them to transmit in only one direction? A. Absolute refractory period across the synaptic cleft B. Postsynaptic clefts residing on multiple postsynaptic neurons C. Presynaptic neurotransmitter reuptake receptors D. Vesicles and corresponding receptors each on only one side of the synaptic cleft
D. Vesicles and corresponding receptors each on only one side of the synaptic cleft ## Footnote Excitatory synapses have vesicles and corresponding receptors each on only one side of the synaptic cleft; thus, there always is a “signaling” end and a “receiving” end for vesicular traffic. (A) The absolute refractory period forces axons to propagate action potentials in only one direction. (C) Presynaptic neurotransmitter reuptake receptors exist but do not play a role in signal direction across a synapse.
43
What is the brain’s response to a rising PCO2 with regard to cerebral blow flow (CBF) and intracranial pressure (ICP)? A. Decrease CBF and increase ICP. B. Increase CBF and decrease ICP. C. Decrease CBF and decrease ICP. D. Increase CBF and keep ICP constant. E. Increase CBF and increase ICP.
E. Increase CBF and increase ICP. ## Footnote When the brain detects a rising carbon dioxide level in the blood, the cerebrovasculature dilates to increase cerebral blood flow (CBF) and thus increase the clearance of carbon dioxide. In turn, this raises intracranial pressure. With the increase in CBF, the PO2 the brain experiences also increases. This mechanism is impaired in brain death and severe stroke.
44
What makes an action potential propagate in only one direction once it has been initiated? A. Absolute refractory period B. Unidirectional protein transport C. Saltatory conduction D. Relative refractory period E. Temporal summation
A. Absolute refractory period ## Footnote The absolute refractory period is determined by the inability of voltage-gated sodium channels to open for a period of time once they have opened and closed during an action potential. Without a large sodium flux from outside to inside the axon, there can be no depolarization and thus no subsequent action potential. The action potential thus must propagate in an anterograde fashion to a portion of the axon where the sodium channels have not been activated and closed recently. (B) Protein transport goes in both an anterograde and retrograde fashion in axons but is not the mechanism behind action potential direction. (C) Saltatory conduction describes the process by which the action potential “leaps” between nodes of Ranvier in a design that speeds signal conduction along axons. Action potentials are triggered only in the unmyelinated nodes, and the voltage differential produced at one node must be transmitted at a sufficient level to the next node to trigger another action potential. (D) The relative refractory period promotes an action potential to propagate in one direction but is not the absolute mechanism. The relative refractory period refers to the point at which a neuron is hyperpolarized by potassium flux with voltage-gated sodium channels that are not inactivated. The neuron is resistant to depolarization, but a sufficient depolarization would trigger an action potential. If the relative refractory period was the only mechanism present, a large depolarization would send an action potential propagating in two directions along an axon. (E) Temporal summation refers to the summation of multiple small depolarizations in the postsynaptic terminal over a given period of time with each small depolarization alone not being sufficient to trigger an action potential. It requires the summation of signal to initiate the action potential.
45
How would hexamethonium administration affect postsynaptic parasympathetic neurons? A. Reduction of the depolarization threshold B. Favoring temporal instead of spatial summation C. Selective inhibition of the parasympathetic nervous system D. No postsynaptic blockade E. Augmentation of the postsynaptic response
D. No postsynaptic blockade ## Footnote Hexamethonium is an antagonist of nicotinic acetylcholine receptors and thus is a ganglionic blocker in the autonomic nervous system. It binds to the nicotinic acetylcholine receptors but not in the binding site for acetylcholine. Hexamethonium has no effect on the postsynaptic muscarinic acetylcholine receptors. (C) Hexamethonium administration will decrease signaling in both the sympathetic and parasympathetic nervous systems.
46
How do steroid hormones pass through cell membranes? A. Through membrane steroid channels B. By simple diffusion C. By facilitated diffusion D. Through G proteins E. By active transport
B. By simple diffusion ## Footnote Steroids are lipophilic and thus can pass through lipophilic cell membranes without the use of channels or receptors. (A) Membrane channels for steroids do not exist. (C) Facilitated diffusion relies on membrane channels to allow molecules to pass through cell membranes along their electrochemical and/or osmotic gradients. (D) G proteins allow extracellular molecules to induce cell signaling within cells, without signaling molecules passing through the membranes. (E) Active transport requires the use of energy (usually in the form of ATP) for molecules to pass through membrane channels against a gradient.
47
What is the result of light falling upon the photoreceptor cells of the retina? A. Phosphodiesterases inhibit the phototransduction cascade. B. Retinal is converted from the trans to the cis isomer. C. Molecules of cAMP are hydrolyzed. D. Hyperpolarization of the retinal cells results in phototransduction
D. Hyperpolarization of the retinal cells results in phototransduction ## Footnote As in the auditory and vestibular systems, the stimulus (light) induces hyperpolarization of the retinal cells, which is due to the closure of sodium channels and reduction of the inward sodium flux of sodium in the case of phototransduction. (A) Phosphodiesterases are essential for continuing the phototransduction cascade. (B) Rhodopsin contains retinal in the 11-cis conformation until light evokes a configuration change to the all-trans form. This change makes rhodopsin no longer fit into the opsin-binding site, and upon disengagement, opsin changes forms, continuing the phototransduction cascade. (C) Molecules of cGMP are hydrolyzed, which causes the closure of cGMP dependent sodium channels.
48
In which stage of the cell cycle does growth arrest by p53 occur? A. G1 phase B. S phase C. G2 phase D. M phase E. G0 phase
A. G1 phase ## Footnote The G1 (growth 1) phase is characterized by cell growth and synthesis of mRNA and proteins in preparation for DNA replication in S phase. Various checkpoint systems like the p53 tumor-suppressor protein prevent progression to S phase and DNA replication if errors are present. (B) During the S (synthetic) phase, cells replicate their DNA and are resistant to radiation due to the numerous DNA proofreading and repair mechanisms at play. (C) The G2 (growth 2) phase is characterized by cell growth and protein synthesis after cell DNA has replicated. Some rapidly dividing cells (e.g., cancer cells) may skip the G2 phase. There exist checkpoints in the G2 phase that induce cell arrest if errors are detected. (D) The M (mitotic) phase is characterized by division and separation of the cellular nuclear material and division of cells into two daughter cells. Cells are very sensitive to radiation during the M phase. (E) The G0 (resting) phase occurs when cells are in a quiescent state. Cells can enter the G0 phase due to a variety of conditions including nutrient deficiency and lack of growth factors. Most neurons in the central nervous system are in the G0 phase of the cell cycle.
48
A motor unit is composed of: A. A motor neuron and all of the muscle fibers innervated by that neuron B. A muscle fiber and all of the motor neurons that innervate that fiber C. All of the motor neurons within a peripheral nerve D. A single motor neuron and a single muscle fiber innervated by that neuron E. The motor and sensory neurons along with the muscle spindles associated with a single muscle fiber
A. A motor neuron and all of the muscle fibers innervated by that neuron ## Footnote Each motor neuron innervates several muscle fibers. There are numerous motor neurons in each peripheral nerve.
48
Where is norepinephrine synthesized? A. Cytoplasm B. Postsynaptic terminal C. Neuronal membrane D. Synaptic vesicle E. Synaptic cleft
D. Synaptic vesicle ## Footnote During the process of conversion of dopamine to norepinephrine, the latter is transported into synaptic vesicles by the vesicular monoamine transporter. The actual synthesis of norepinephrine mostly takes place in the synaptic vesicle. (A) Dopamine synthesis from tyrosine takes place in the neuronal cytoplasm. (E) The synaptic cleft is where acetylcholine is degraded by acetylcholinesterase.
48
How do cytotoxic and vasogenic edema differ? A. Cytotoxic edema responds better to steroids than does vasogenic edema. B. The blood–brain barrier is closed in cytotoxic edema and disrupted in vasogenic edema C. Cells shrink in vasogenic edema but expand in cytotoxic edema. D. Cytotoxic but not vasogenic edema occurs after ischemic injury. E. Proteins expand the extracellular space in cytotoxic edema
B. The blood–brain barrier is closed in cytotoxic edema and disrupted in vasogenic edema ## Footnote The blood–brain barrier (BBB) becomes disrupted in vasogenic edema, as breakdown of the endothelial tight junctions occurs. In addition, gliomas and certain brain tumors can secrete vascular endothelial growth factors that increase permeability. Proteins and molecules leave the intravascular space and create an oncotic force driving fluid into the extracellular space. Fluid spreads along white matter tracts, creating a large area of edema. In cytotoxic edema, alteration of cellular metabolism leads to a failure of ion pumps (notably the sodium-potassium pumps), which in turn creates an osmotic gradient and increased fluid in the intracellular space. (A) Vasogenic edema responds better to steroids, in that steroids decrease endothelial permeability by various means. (C) Cytotoxic edema is characterized by cell swelling, whereas cells remain of similar size in pure vasogenic edema. (D) Although ischemic injury initially is characterized by cytotoxic edema, when cells die and the BBB breaks down, elements of vasogenic edema arise. (E) Proteins expand the extracellular space in vasogenic edema due to disruption of the BBB.
48
In rigor mortis, in what state are the myosin heads? A. Myosin heads are unbound from actin with their heads uncocked. B. Myosin heads are bound to actin following the power stroke C. Myosin heads are bound to actin before the power stroke. D. Myosin heads are unbound from actin with their heads cocked.
B. Myosin heads are bound to actin following the power stroke ## Footnote The power stroke occurs as phosphate is released from the cocked myosin heads, and they change conformation to move relative to the actin thin filaments. Without the addition of ATP, the myosin heads cannot unbind actin. This accounts for the rigid muscles and tonic sarcomere length seen in rigor mortis. (A) The myosin heads are able to unbind from actin thin filaments with the addition of ATP and return to their resting (uncocked) positions. (C) Once cocked, myosin heads bind actin. (D) Myosin heads cock in a high-energy, ready position as ATP is hydrolyzed into ADP and phosphate.
48
What enzyme is necessary for conversion of norepinephrine to epinephrine? A. Monoamine oxidase B. Tyrosine hydroxylase C. Aromatic L-amino acid decarboxylase D. Dopamine β-hydroxylase E. Phenylethanolamine N-methyltransferase
E. Phenylethanolamine N-methyltransferase ## Footnote Phenylethanolamine N-methyltransferase converts norepinephrine to epinephrine creating homocysteine in the process. (A) Monoamine oxidase degrades monoamines like dopamine. (B) Tyrosine hydroxylase converts tyrosine to L-dopa in dopamine synthesis. It is the rate-limiting factor in dopamine synthesis. (C) Aromatic L-amino acid decarboxylase converts L-dopa to dopamine in dopamine synthesis. (D) Dopamine β-hydroxylase converts dopamine to norepinephrine.
49
How would an isolated vitamin K deficiency affect the clotting cascade? A. Upregulation of antithrombin activity B. Reduced activity of factors XI and XII C. Inhibition of synthesis of proteins C, S, and Z D. Prolongation of bleeding time E. Prolongation of the partial thromboplastin time without affecting the prothrombin time
C. Inhibition of synthesis of proteins C, S, and Z ## Footnote Vitamin K is required for the complete synthesis of the coagulation factors prothrombin (factor II), factor VII, factor IX, factor X, protein C, protein S, and protein Z. These factors are present (in the classic coagulation model) in the intrinsic, extrinsic, and common pathways. (A) Antithrombin inhibits several factors in the clotting cascade, and its effects on factors II and X are inhibited by heparin. (B) Factor XII acts on factor XI to begin the clotting cascade in the intrinsic pathway. (D) Bleeding time and platelet function are unaffected by a vitamin K deficiency. (E) With a vitamin K deficiency, prothrombin time (a measure of the extrinsic pathway) and partial thromboplastin time (a measure of the intrinsic pathway) both are prolonged, with the former being affected to a greater extent.
50
What typically prevents axonal regeneration in the central nervous system? A. Reduced axonal growth factors following injury B. Astrocytic scarring C. Lack of progenitor cells D. Lack of directional markers and/or architecture
B. Astrocytic scarring ## Footnote Astrocytic scarring disrupts the axonal tracts following wallerian degeneration, and astrocytes secrete axonal growth inhibitory proteins in the central nervous system. (A) There is a relative paucity of axonal growth–promoting factors in the central nervous system, but this is not due to, nor does it change relative to, the presence of axonal injury. (C) There is a lack of progenitor cells in the central nervous system, but axons in the peripheral nervous system regenerate without such progenitor cells. (D) Directional markers and signaling molecules do degrade following neurogenesis, but axons still can regenerate in the peripheral nervous system along axon tracts following the supporting matrix (e.g., endoneurium and other such components) after wallerian degeneration.
51
During the action potential, what does closing of the sodium channels cause? A. Membrane depolarization B. Opening of the potassium channels C. The beginning of the relative refractory period D. Membrane repolarization E. Opening of the voltage-gated calcium channels
D. Membrane repolarization ## Footnote As the sodium channels close, the open potassium channels are able to keep the net flux of positive ions out of the cell, resulting in membrane repolarization toward the resting membrane potential of potassium. (B) Potassium channels are open at this point, which allows for cellular repolarization and eventual hyperpolarization as the sodium channels close. (C) The relative refractory period is the time at which the cell is hyperpolarized so that the membrane depolarization required to trigger a subsequent action potential is greater than it is when the cell is at its resting membrane potential. (E) Voltage-gated calcium channels open with depolarization and not repolarization.
52
What is the mechanism of action of hydrochlorothiazide? A. Promotion of aquaporin channels in the distal convoluted tubules and collecting ducts B. Inhibition of the sodium-potassium cotransporters in the distal tubules C. Inhibition of the sodium-potassium-chloride symporters in the thick ascending limb of the loops of Henle D. Reduction of sodium chloride and bicarbonate reabsorption in the proximal tubules E. Inhibition of the sodium-chloride cotransporters in the distal tubules
E. Inhibition of the sodium-chloride cotransporters in the distal tubules ## Footnote By competing for the chloride-binding site and blocking the sodium-chloride transporters, hydrochlorothiazide prevents the reabsorption of sodium in the distal convoluted tubules. This maintains the osmotic gradient in the tubules, thus promoting natriuresis. In addition, hydrochlorothiazide increases calcium reabsorption in the tubules through an unrelated mechanism. (A) One mechanism by which vasopressin acts is by promoting the insertion of aquaporin channels in the apical membrane of the distal convoluted tubules and collecting ducts, allowing water to be reabsorbed into the blood along its osmotic gradient. This creates an antidiuretic effect. (B) Spironolactone acts on the distal nephron on the distal convoluted tubules where it inhibits the sodium-potassium exchangers. This prevents the exchangers from reabsorbing sodium and excreting potassium, resulting in a diuretic effect. It is considered a potassium-sparing diuretic. (C) Furosemide is a loop diuretic that works by inhibiting the sodium-potassium-chloride symporters in the thick ascending limb of the loops of Henle. Blockade of the transporter prevents reabsorption of sodium, chloride, and potassium. (D) Carbonic anhydrase inhibitors reduce sodium chloride and bicarbonate reabsorption in the proximal tubules by blocking the luminal conversion of bicarbonate to carbon dioxide. Without the inhibitors, carbon dioxide diffuses passively back into the cells of the proximal tubules. Without the conversion, sodium remains with the bicarbonate ions in the lumen due to their electrochemical attraction.
53
What are the two major characteristics of/associated with protein molecules that prevent them from being filtered into the Bowman capsule in the renal glomerulus? A. Large size and negative charge B. Low oncotic pressure and positive charge C. Small size and negative charge D. High hydrostatic pressure and positive charge E. High hydrostatic pressure and negative charge
A. Large size and negative charge ## Footnote The basement membrane and podocytic epithelium in the glomerulus have a positive charge and thus resist passage of negatively charged molecules. In addition, the effective pore size in the glomerular wall is about 8 nm, preventing passage of most proteins and other large molecules. The oncotic pressure in the glomerular capillaries increases as blood passes through as proteins are retained while ions and small molecules are filtered through the wall. This causes a gradient of flow back into the capillaries at their distal ends as oncotic pressure builds. Finally, the hydrostatic pressure in the glomerular capillaries is low relative to capillaries elsewhere in the body. This resists filtration through the capillary walls.
54
Lateral geniculate cells have what type of receptive fields? A. Concentric B. Rectangular C. Motion D. Direction E. No receptive fields
A. Concentric ## Footnote Lateral geniculate nucleus cells have concentric (center-surround) receptive fields that are either on-center or off-center, with the surrounding region being antagonistic. Similar receptive fields are seen in retinal ganglion cells. (B) Rectangular receptive fields are seen in simple cells of the visual cortex. (C, D) Motion, direction, and orientation receptive fields are seen in complex cells of the visual cortex. Cells are dedicated and specialized to respond to certain aspects of visual stimuli.
54
What ion entering neurons during the secondary phase of traumatic brain injury accounts for the majority of the mitochondrial malfunctioning and damage? A. Glutamate B. Sodium C. Potassium D. Calcium
D. Calcium ## Footnote During the secondary (delayed) phase of traumatic brain injury, neurons spill the neurotransmitter glutamate that in turn causes a large calcium flux into neurons. Excess intracellular calcium can initiate apoptosis and open mitochondrial pores, leading to metabolic dysfunction. (A) Glutamate is the neurotransmitter involved in excitotoxic brain injury, but the molecule only activates the receptor that opens calcium channels. (B, C) During the primary phase of traumatic brain injury, there is cell damage and cellular membrane damage due to the direct forces involved. Cellular membrane damage can allow numerous ions and molecules to pass freely along their concentration and electrochemical gradients.
55
What is the role of dynein in axoplasmic transport? A. Slow anterograde transport B. Both anterograde and retrograde transport C. Fast anterograde transport D. Inhibits transport E. Retrograde transport
E. Retrograde transport ## Footnote Retrograde transport of vesicles using dynein is an ATP-dependent process. (A) There are two types of slow anterograde transport. The slower mode carries microtubules and neurofilaments, whereas the faster slow transport mechanism carries actin and a variety of other proteins. (B) There is no single carrier protein that serves bidirectional axoplasmic transport. (C) Both slow and fast anterograde transport of molecules in vesicles are mediated by kinesins along microtubules
55
What structure in the sarcomere is composed of myosin and actin filaments? A. C-band B. A-band C. I-band D. H-band E. M-band
A. C-band ## Footnote The C-band enlarges with sarcomere shortening, as shown in this image. It is the region of the A-band not including the H-band. (B) The A-band is the region of the sarcomere containing myosin thick filaments with actin thin filament overlaps at the ends of the band. The A-band remains the same size during sarcomere contraction. (C) The I-band is the portion of the sarcomere with actin thin filaments that are not overlapping with myosin thick filaments. It decreases in size with sarcomere contraction. (D) The H-band is the portion of the sarcomere containing myosin thick filaments that are not overlapping actin thin filaments. It shortens with contraction. (E) The M-band is the center anchoring point of the myosin thick filaments and does not change in size as sarcomere length changes.
55
What enzymes allow retroviruses to produce DNA from their RNA genomes? A. RNA polymerases B. DNA polymerases C. Reverse transcriptases D. Integrases E. Helicases
C. Reverse transcriptases ## Footnote Reverse transcriptases create cDNA from RNA templates in the very error-prone process of reverse transcription. (A) RNA polymerases are involved in RNA translation from DNA. (B) DNA polymerases are involved in transcription and DNA replication. (D) Integrases allow the DNA created from retroviruses to be incorporated into host cell genomes. (E) Helicases separate two annealed strands of DNA, RNA, or DNA-RNA hybrids, and are involved in the processes of transcription and translation among other roles that they play.
55
What is the rate-limiting step in dopamine synthesis? A. Tyrosine availability B. Tyrosine hydroxylase C. Dopa decarboxylase D. Dopamine β-hydroxylase E. Tetrahydrobiopterin
B. Tyrosine hydroxylase ## Footnote Tyrosine hydroxylase converts tyrosine to L-dopa. (A) Tyrosine is abundant and does not limit the rate of dopamine synthesis. (C) Dopa decarboxylase converts L-dopa to dopamine. (D) Dopamine β-hydroxylase converts dopamine to norepinephrine. (E) Tetrahydrobiopterin is a cofactor for the conversion of tyrosine to L-dopa, but being widely available, it does not limit the reaction.
56
In addition to being synthesized in the neuron and being deactivated at the site of action, what other criterion is necessary to label a substance a neurotransmitter? A. Released nonspecifically from the presynaptic terminal B. Exogenous administration that mimics the endogenous activity C. Presence throughout the nervous system D. Ubiquitous effect throughout all neural networks E. Exerting an effect at a distant site in the body
B. Exogenous administration that mimics the endogenous activity ## Footnote To prove that the action seen in a neuronal chain is due to signaling by a neurotransmitter, the effect from exogenous administration must be the same as endogenous activity. (A) Neurotransmitters are present in the presynaptic terminal and only released in a controlled amount and fashion to exert a particular effect. (C) Some neurotransmitters can be seen throughout the nervous system, whereas others are found in only a few select locations. (D) Although a neurotransmitter may be excitatory or inhibitory at a particular synapse, the downstream effects can vary depending on the arrangement of the neural network. (E) An effect distant from the site of production/release is part of the definition of a hormone.
57
What is the main role of orexin/hypocretin in the human body? A. Promoting arousal B. Promoting sleep C. Inhibiting pain D. Appetite suppression E. Decreasing thermogenesis
A. Promoting arousal ## Footnote Orexin/hypocretin is a neurotransmitter that promotes arousal and wakefulness along with appetite. Despite decreased levels of production in the brains of narcoleptics, narcoleptics tend to have higher body mass indices, highlighting that the chemical plays more of a role in arousal and thermogenesis than in promoting that appetite. The weight gain effect is due to the lowered metabolic rate in orexin-deficient individuals.
58
A patient receives an overdose of intravenous potassium. How would muscle action potentials be affected? A. Resting membrane potential would increase, and the threshold to trigger an action potential would be reached with more miniature end-plate potentials (MEPPs) B. Resting membrane potential would decrease, and the threshold to trigger an action potential would be reached with fewer MEPPs C. Resting membrane potential would increase, and the threshold to trigger an action potential would be reached with fewer MEPPs D. The threshold to trigger an action potential would become more negative E. The threshold to trigger an action potential would become more positive
C. Resting membrane potential would increase, and the threshold to trigger an action potential would be reached with fewer MEPPs ## Footnote The equilibrium potential for an ion is determined by the relative concentration of the ion outside compared with inside the neuron. If the extracellular concentration of potassium increases and the intracellular concentration remains constant, the equilibrium potential would become more positive. Because the resting membrane potential for a neuron is determined mainly by potassium ions, it also would increase. The threshold for trigging an action potential would remain the same but now would be closer to the resting potential.