SBPM SSN Multiple Choice Answers #5
April 1, 2003
1. c
2. b (Cobalamin is another name for Vitamin B12. Yes, it’s important to know both.)
3. a
4. b
5. Conjugated primary bile salt then primary bile salt then secondary bile salt then cholesterol
6. D. While hepatocytes are metabolizing drugs, the drugs are mostly compartmentalized, and do not freely float in the cytosol
7. b) The excretion of K+ in the urine results primarily from the secretion of K+ by the distal segments. The rate of K+ secretion is
modified primarily by aldosterone and the urinary flow rate. Almost all of the filtered K+ is reabsorbed along the nephron.
8. c) Since the pH is > 7.4 this is an alkalosis. The bicarbonate is high so the cause of the alkalosis must be metabolic. The high
pCO2 indicates there has been respiratory compensation, by hypoventilation. The ↓ [H+] in the blood  extrusion of H+ from
cells and driving of K+ into cells. The patient’s low BP and dry mucous membranes indicates volume depletion (low ECFV) which
would stimulate aldosterone secretion  increased K+ secretion by the distal tubules. The patient will be secreting less H+ into
the urine so the ratio of H2PO4- to HPO4-2 in the urine will be decreased.
9. d) β-blockers are associated with hyperkalemia. All foods contain large amounts of potassium. β-blockers inhibit the ability of
epinephrine (released after meals) to increase the activity of the β-adrenergic receptor which would then be able to ↑ K+ uptake
by liver and muscle cells.
10. a, b, c
11.a, b, c
12. c. SERT mutations can cause a failure to take up synaptic serotonin for intracellular breakdown, leading to a synaptic buildup
of the transmitter. As a result, the excitatory effect of serotonin will cause hyperactivity of the bowel (diarrhea). However,
periodically, there will be desensitization of the synapse (as with other hyperactive synaptic transmissions) leading to inactivity of
the bowel (constipation).
13. C
The afferent limb of this system includes volume sensors in the left atrium of the heart, ventricles, carotid arteries, aortic arch,
renal circulation, and hepatic circulation.
Efferent mechanisms included the following:
Angiotensin II, a polypeptide that is made in response to increased renin, which in turn is released from the juxtaglomerular
apparatus in when ECV is decreased. AII is a vasoconstrictor, especially of the efferent arteriole, which causes increased
sodium reabsorption and decreased renal plasma flow but increased filtration fraction. It also acts on the brain to increase thirst
and salt appetite and causes the release of aldosterone.
Aldosterone is a steroid hormone made in the adrenal cortex that increases the reabsorption of sodium in the collecting duct.
ANP is released from granules in atrial myocytes in response to increased volume. It causes afferent arteriole dilatation and
inhibits sodium reabsorption in the collecting duct. It also inhibits release of renin and aldosterone and decreases thirst and salt
appetite.
Norepinephrine, released from sympathetic nerve terminals, and epinephrine, produced in the adrenal cortex, are released when
the sympathetic nervous system is stimulated by volume depletion or decreased blood pressure. They directly stimulate the
kidney to reabsorb salt and water and cause increased renin production. Norepinephrine also causes vasoconstriction of both
the afferent and efferent arterioles.
ADH regulates water balance by increasing the permeability of the collecting duct to water and allowing more water to be
reabsorbed. It is made in the hypothalamus and released from the posterior pituitary.
14. C
The afferent limb of this system includes volume sensors in the left atrium of the heart, ventricles, carotid arteries, aortic arch,
renal circulation, and hepatic circulation.
Efferent mechanisms included the following:
Angiotensin II, a polypeptide that is made in response to increased renin, which in turn is released from the juxtaglomerular
apparatus in when ECV is decreased. AII is a vasoconstrictor, especially of the efferent arteriole, which causes increased
sodium reabsorption and decreased renal plasma flow but increased filtration fraction. It also acts on the brain to increase thirst
and salt appetite and causes the release of aldosterone.
Aldosterone is a steroid hormone made in the adrenal cortex that increases the reabsorption of sodium in the collecting duct.
ANP is released from granules in atrial myocytes in response to increased volume. It causes afferent arteriole dilatation and
inhibits sodium reabsorption in the collecting duct. It also inhibits release of renin and aldosterone and decreases thirst and salt
appetite.
Norepinephrine, released from sympathetic nerve terminals, and epinephrine, produced in the adrenal cortex, are released when
the sympathetic nervous system is stimulated by volume depletion or decreased blood pressure. They directly stimulate the
kidney to reabsorb salt and water and cause increased renin production. Norepinephrine also causes vasoconstriction of both
the afferent and efferent arterioles.
ADH regulates water balance by increasing the permeability of the collecting duct to water and allowing more water to be
reabsorbed. It is made in the hypothalamus and released from the posterior pituitary.
15. D The glomerular filtration barrier is a trilaminar structure. The first layer is the fenestrated capillary endothelium. Under that
is the basement membrane, which is composed of type IV collagen and negatively charged proteoglycans. The final layer is the
visceral epithelium, which is composed of podocytes. Mesangial cells influence the structure of the filtration barrier, but are not
actually part of the barrier.
16. C
GFR = UCr x V/PCr
UCr = 70 mg/ml
V = 1.2 L/24 hours = 1200 ml/24 hours = .83 ml/min
PCr = 0.6 mg/ml
GFR = (70 mg/ml) x (.83 ml/min)/(0.6 mg/ml) = 97 ml/min
.
17.d
18. d