HBY 531
MEDICAL PHYSIOLOGY
2003
Section 1: Answer the following using:
A = increase
B = remain the same
C = decrease
1.
During
the gastric phase of acid secretion, distension of the stomach will cause
plasma levels of gastrin to ___A_____.
2.
CCK
concentrations in the blood will ____A____ with
the introduction of H+ into the duodenum.
3.
Chief
cell secretion of pepsinogen will____A____ as
CCK levels increase in the blood.
4.
The
concentration of chylomicra within plasma will ____A____
during the absorptive state.
5.
Segmentation
and peristalsis, within the small intestine will ____A____
in the presence of substance P.
6.
In
Hirshbrung’s disease, the colon luminal diameter within the region lacking
Auerbach’s plexuses will ____C____ when compared
to an otherwise healthy individual.
7.
During the growth of a
secondary follicle, during the later portion of the follicular phase, FSH
secretion by the pituitary will
___ C ____.
8.
After degeneration of
the corpus luteum in the absence of pregnancy, plasma levels of progesterone
will ____ C
___.
9.
After degeneration of
the corpus luteum during pregnancy, plasma levels of progesterone will ____A
___.
10.
With the advent of
menopause, bone resorption will ____A ___.
Section
2:
For each of the following, choose the single best response.
11. Achalasia:
a. is the result of an incompetent
cardio-esophageal sphincter (CES, also known as the LES).
b. is the result of a chronically
constricted CES.
c. results in adenocaricinoma of the squamous
epithelium of the esophagus.
d. Both a and c are correct.
12. Lactose intolerance:
a. is the result of inflammatory diarrhea.
b. results in secretory diarrhea.
c. arises from the lack of the fructose
transporter.
d. None of the above is correct
13. A lack of enterokinase:
a. could cause diarrhea.
b. would affect the conversion of pepsinogen
into pepsin.
c. would decrease lipase activation.
d. would not affect the conversion of
trypsinogen to trypsin.
14. Intracellular elevation of cAMP:
a. promotes acid secretion in parietal cells.
b. alters the activity of chloride channels in
crypt cells.
c. does not affect chylomicra formation
d. all of the above are correct.
15. Elevation of intracellular Na+ in a columnar
absorptive cell of the small intestine
a. will not affect monosaccharide uptake.
b. will affect fructose uptake.
c. will not affect dipeptide uptake.
d. None of the above is correct.
16. Gastrin levels
a. will decrease as plasma
somatostatin concentrations are elevated.
b. Are not affected by VIP.
c. Are unaffected by H+ levels in the stomach.
d. Cause a decrease in the diameter of the
sphincter of Oddi.
17. The gastroileal reflex
a. is triggered during the cephalic phase of
acid secretion.
b. Is triggered during the gastric
phase of acid secretion.
c. Is a short reflex
d. Both a and c are correct.
18. Hypersecretion of acid by parietal cells can
occur as a result of
a. Blockade of gastrin receptors
b. lowered prostaglandin levels
c. cutting the vagus nerve
d. due to distension of the duodenum
19. Chloride ion flux from Crypt cells
a. will be outward if the resting potential is
less negative than the chloride equilibrium potential.
b. will be inward if the resting potential is
more negative than the chloride equilibrium potential.
c. is modulated by PKA activity.
d. determines the resting potential of the crypt
cell.
20. Salivary gland secretion
a. is always hyposmotic relative to
plasma.
b. produces a constant Cl- concentration
regardless of flow rate.
c. Rate produces ~0.5L/day.
d. Is always hyperosmotic relative to plasma.
21. Damage to the 12th cranial nerve
a. will affect the oral phase of swallowing.
b. can result in dysphagia.
c. will not affect the esophageal phase of
swallowing.
d. all of the above are correct.
22. During receptive relaxation,
a. stomach motility is reduced or lacking.
b. acid secretion by parietal cells is mediated
by factors such as gastrin and wall distension.
c. chief cell secretion of pepsinogen is
ongoing.
d. All of the above are correct
23. A female patient was admitted with frequent
morning spells of dizziness, complaining of fatigue and nausea. Fasting blood
glucose was found to be lower than normal, but a glucose tolerance test was
otherwise normal. The patient could be diagnosed with Addison’s disease if
a. she had low levels of circulating
cortisol, and high levels of circulating ACTH.
b. there was hyperpigmentation of her skin due
to excess cortisol secretion.
c. a CAT scan of her adrenal gland showed bilateral
hypertrophy.
d. glycosuria was abnormally high because of
high ACTH levels.
24. Non-shivering thermogenesis is how human
newborns and certain rodents increases their body temperature when exposed to
cold, and is characterized by
a. increased white adipose tissue metabolism in
response a-adrenergic stimulation.
b. atropine-sensitive b-adrenergic stimulation of brown
adipose tissue.
c. increased glycolytic rates and decreased O2
consumption.
d. the T3-dependent suppression of Na+/K+
ATPase transcription and activity.
25. The processing of insulin in the pancreatic
islet b-cell
a. is stimulated by sympathetic nerve activation
to the pancreas.
b. is completed only after glucose or amino acid
dependent accumulation of ATP.
c. starts with the action of signal
peptidase and ends with the separation of the C-peptide.
d. is stimulated by glucose but not by amino
acids.
26. The glucose sensitivity of the endocrine
pancreas is determined by a combination of
a. the high affinity glucose transporter
(GLUT-2) and low Km enzyme Glucokinase.
b. the low affinity glucose transporter (GLUT-2)
and the ATP-sensitive Ca2+-channel.
c. the low affinity enzyme Glucokinase and high
Km glucose transporter (GLUT-2).
d. an inhibition of the voltage-sensitive Ca2+-channel
and the Kreb’s cycle.
27. A teen-aged patient has an enlarged thyroid
gland (Goiter). Which of the following
would distinguish between Grave’s disease and Hashimoto’s thyroiditis?
a. Increased levels of TSH in Grave’s but not in Hashimoto’s.
b. The presence of TSH receptor stimulating
immunoglobulins in Grave’s.
c. Higher levels of circulating T4 levels in Hashimoto’s.
d. Increased levels of T4 and TSH in Grave’s,
but only T4 in Hashimoto’s.
28. Thyroid and steroid hormones
a. both bind to intracellular receptors but only
steroid hormones affect transcription rates.
b. both bind to intracellular
receptors but only steroids displace heat shock proteins.
c. both depend on essential dietary precursors
for proper biosynthesis in their respective glands.
d. both increase progressively during waking
hours and are lowest during deep sleep.
29. The secretion of Prolactin from the anterior
pituitary is regulated by hypothalamic dopamine
a. which increases during suckling.
b. which increases intracellular cyclic AMP
levels and stimulates prolactin synthesis.
c. which also decreases Luteinizing and Follicle-stimulating
hormones (LH & FSH) secretion from the anterior pituitary.
d. which decreases after childbirth,
relieving the inhibition of prolactin secretion.
30. Growth hormone is synthesized and secreted
from the anterior pituitary
a. in response to an as-inhibition of adenylyl cyclase.
b. as a large polypeptide that is cleaved to
give the biologically active dimer.
c. and acts by binding to intracellular
receptors that increase gene transcription.
d. in a pulsatile manner with highest
levels observed during sleeping hours.
31. Gonadotropin Relasing hormone (GnRH) and
Follicle stimulating hormone (FSH)
a. both act by binding to intracellular
receptors.
b. both bind to G-protein coupled
receptors with 7 transmembrane domains.
c. both stimulate hormone granule fusion with
the plasma membrane of their target tissues.
d. oppose each other’s action in regulating
estrogen release from the ovary
32. The biosynthesis of ACTH takes place in the
corticotrophs of the anterior pituitary,
a. in response to episodic stimulation
from the hypothalamus, with maxima observed in late sleep and early morning.
b. where it is derived from a large precursor
that also encodes Luteinizing hormone and b-endorphin.
c. and its secretion controls the synthesis of
adrenal cortisol but not of adrenal androgens.
d. and in ectopic adrenal tumors resulting in
hyperpigmentation.
33. The human adult relies predominantly on sweat
to cool the body because
a. adrenergic stimulation can increase rates of
sweat formation 50 fold to more than 2 liters/hour .
b. apocrine gland blood supply is very sensitive
to small changes in acetyl choline levels.
c. sweat gland blood flow is independent of
hypothalamic control.
d. cholinergic stimulation results in
increased production of a hypotonic protein-free solution.
34. Growth hormone and insulin are considered
anabolic hormones because
a. they both promote glucose uptake and
utilization.
b. they both activate intracellular
tyrosine kinases.
c. they both stimulate insulin-like growth
factor (IGF) synthesis in liver and secretion.
d. they both bind to dimeric receptors composed
of two a and two b
subunits.
35. The catecholamine hormones epinephrine and nor-epinephrine act on liver
as follows:
a. Epinephrine binds to an a-adrenergic membrane receptor, while
nor-epinephrine binds to an intracellular a-adrenergic receptor.
b. Epinephrine activates glycogen synthesis
while nor-epinephrine increases glycogen hydrolysis.
c. Nor-epinephrine decreases intracellular cAMP
levels, and epinephrine decreases intracellular Ca2+ levels.
d. Each binds to a unique G-protein
coupled receptor, but both stimulate gluconeogenesis.
36. The
amino acid tyrosine is the precursor of several hormones including
a. cortisol, thyroxine (T4) and catecholamines.
b. thyroid releasing hormone (TRH), thyroxine
(T4) and cortisol.
c. glucagon, insulin and cortisol.
d. thyroxine (T4), epinephrine and
dopamine.
37. The post-absorptive state of metabolism, following a 12 hr fast, is characterized
by
a. the induction of liver glucokinase, and the
dephosphorylation of pyruvate dehydrogenase.
b. the phosphorylation and activation
of adipose triglyceride lipase and increased blood ketones.
c. a decrease in muscle protein catabolism and
in urine urea levels.
d. an increase in hepatic Fru-2,6-P2
levels and gluconeogenesis from Acetyl CoA.
38. A 2-year old child in a hypoglycemic (low blood glucose) coma is
immediately given glucagon intravenously. After 10 minutes, blood glucose levels
have still not returned to normal. Possible explanations are:
a. The patient has inherited a constitutively active as G-protein subunit.
b. The patient has eaten only protein for
several days before the coma.
c. The patient has a pancreatic islet tumor that
over secretes insulin.
d. The patient has inherited a
defective glucose-6-phosphatase gene.
39. The synthesis and
secretion of glucagon from
pancreatic islet a-cells in response to
amino acids from the diet
a. is simultaneous with insulin release, only
when glucose in the blood is above normal.
b. is potentiated by insulin secretion from the b-cells, when glucose levels are high.
c. decreases the level of urea in urine, because
of decreased de-amination by the liver.
d. allows for gluconeogenesis from
amino acids even in the absorptive phase.
40. A Non-Insulin Dependent Diabetic (NIDDM) has decreased rates of blood
glucose clearance most probably because
a. there is a down-regulation of
insulin receptors associated with increased body weight.
b. there is an increased rate of IRS-1
de-phosphorylation and proteolysis associated with obesity.
c. the expression of insulin processing
proteases (PC2 and PC3) decreases with age and obesity.
d. hepatic expression of glucagon receptors
increases with age and obesity.
41. An orally administered synthetic compound
that mimics the structure of Fructose-2,6-bisphosphate (Fru-2,6-P2)
and is quantitatively removed from portal circulation by the liver would be
expected to
a. decrease glycolytic rates by inhibiting
phosphofructo-1-kinase.
b. decrease gluconeogenic rates by decreasing
PEPCK activity.
c. decrease gluconeogenic rates by
inhibition of Fructose-1,6-bisphosphatase.
d. increase glycolytic rates by activating
phosphofructo-2-kinase.
42. An untreated Insulin-Dependent Diabetic (IDDM)
a. would test Islet-cell Antibody
(ICA) positive early during the progression of diabetes.
b. would show decreased levels of lipoprotein
lipase expression in adipose endothelia.
c. would have decreased levels of circulating fatty
acids and ketones in the blood.
d. can be treated by daily administration of
oral hypoglycemic agents and by exercise.
43. A 1 year old infant was brought in by his
parents, who described symptoms of weight loss, frequent urination and general
malaise that seem to follow shortly after weaning and switching to less
frequent larger meals. Subsequent blood
analysis revealed a fasting blood glucose level of 210 mg/dL and an abnormal
glucose tolerance curve (blood glucose >300 mg/dL after 2 hr).
Radioimmunoassay revealed that the patient had a normal, to slightly elevated,
insulin response to the glucose load.
Which of the following is NOT a
likely explanation?
a. The patient may have inherited a mutation in
the insulin gene, which decreases the insulin’s binding affinity to the
receptor.
b. The patient may have inherited a mutated
insulin receptor with decreased insulin binding affinity.
c. The patient may have a pituitary adenoma that
secretes high levels of growth hormone
d. The patient may have inherited
an abnormal glucose transporter GLUT-2
with a lower Km for glucose.
44. If the patient in #43 were assayed for a
C-peptide to insulin ratio during the glucose tolerance curve and it was found
to be high, it could be concluded that
a. The mutation is definitely in the sequence of
the insulin gene.
b. Sequencing of the patient’s insulin receptor
should reveal a decrease in insulin binding.
c. The patient may have inherited a
mutation in the sequence of the IRS-1 protein.
d. The patient may have a mutation in either of
the insulin converting proteases, PC2 or PC3.
45. Administration
of GnRH in a non-pulsatile manner would cause
a. suppression of gonadal steroid secretion.
b. a high
non-pulsatile release of gonadotropins.
c. no effect
on either pituitary or gonadal secretion.
d. upregulation
of GnRH receptors in the pituitary gonadotropin-secreting cells.
e. b and d.
46. The LH
surge
a. is
essential for ovulation.
b. occurs at
the end of the Luteal phase.
c. is caused
by the estrogen positive feedback on the pituitary.
d. is caused by the estrogen positive feedback on the
pituitary and on the hypothalamus.
e. a and d.
47. The
corpus luteum
a. produces
progesterone but no estrogens, under the influence of LH.
b. produces progesterone and estrogens, under the influence of LH.
c. produces
only estrogens, under the influence of FSH.
d. has a
life span of 4 days.
e. none of
the above.
48. During
the first week after implantation of the blastocyst in the uterus:
a. Nutrition
is provided to the embryo by the decidual cells.
b. Nutrition
is provided to the embryo by the trophoblast cells.
c. The placenta
is able to sustain pregnancy by secreting progesterone.
d. The
corpus luteum is no longer needed and finally degenerates.
e. a and b.
49. Milk
secretion:
a. is
inhibited by estrogens and progesterone.
b. requires
the action of estrogens and progesterone on the mammary gland.
c. requires
a decrease in the hypothalamic secretion of dopamine.
d. requires
the action of prolactin.
e. all of the above.
50. What is
the best medical intervention in case of a placenta previa?
a. Administration
of oxytocin to induce parturition as soon as possible.
b. Treatment
of the patient with anti-hemorrhagic agents.
c. To perform a cesarean birth.
d. To
prescribe bed rest and anti-hypertensive agents.
e. None of
the above.
Section 3: Clinical
Scenario questions. Choose the single
best response based on the following case studies:
Clinical Scenario 1: A patient complains of
diarrhea, which has been persistent for the last two weeks. He is not diabetic
but does drink heavily. He complains of developing a “beer gut” over the last 5
months and swelling in his legs, which you determine is peripheral edema. His blood pressure is 80/60 and his pulse is
100 beats/minute. The patient also complains that he is very fatigued. He is
admitted to the hospital and subsequently his stool volume is revealed to be
2L/day based void volumes collected within the first 12 hours. Upon admission,
rehydration via intravenous feed was administered.
51. At this point, the most likely diagnosis is,
a. This patient is suffering from secretory
diarrhea.
b. Osmotic diarrhea is the cause.
c. Malabsorption is the cause.
d. It is impossible to unequivocally
determine which type of diarrhea the patient is suffering from.
52. Further tests reveal that the patient’s serum
electrolytes are normal with the exception of K+ (2.9 mM vs 4.0 mM). Gastrin
and VIP are normal. By day two, the
stool volume is 0.8L/day.
a. This patient is suffering from secretory
diarrhea.
b. Osmotic diarrhea is a better
candidate than secretory diarrhea based on the reduced stool volume.
c. This patient is suffering from irritable
bowel syndrome .
d. None of the above is applicable.
53. The blood tests also indicate that the
patient has compromised liver function and urine analysis shows elevated
aldosterone levels. Analysis of the
stool reveals no white cells and cultures are negative. The patient tells you
that he has recently (over the last month) started a new diet in which he
consumes large amounts of legumes. A mainstay of his diet is dried chick pea
which is rich in nutrients and minerals including magnesium (110 mg/100ml). He
has also began using an un-absorbable
artificial sweetener (sorbitol) in an attempt to reduce his “beer gut”.
a. The dietary change is the cause of the
secretory diarrhea.
b. Osmotic diarrhea is implicated because of the
magnesium intake.
c. Sorbitol is the source of the osmotic
diarrhea.
d. Both b and c are possible.
54. The lowered serum K+
a. arises primarily as a consequence of the
diarrhea.
b. is a consequence aldosterone
mediated K+ secretion.
c. Is due to reduced acid secretion in the
stomach
d. Is the cause of the rapid heart rate.
55. The “beer gut” and peripheral edema:
a. Are most likely due to the new diet.
b. are most likely due to compromised
liver function leading to fluid retention.
c. are coincidental with regard to the patient’s
conditions.
d. None of the above is relevant
Clinical Scenario 2: The
patient is a 48-year-old woman who sees her physician because her friends have
noted that she now appears to be “bent over,”, and she has noted increased back
pain and that she is now shorter than she had been.
Her
past medical history is significant because as a young adult she had been told
she was hypothyroid due to an auto-immune destruction of her thyroid gland. She
has been treated with one pill of thyroid hormone a day that she religiously
takes. When she was about 35, she noted pain in her joints associated with
objective inflammation and swelling of the affected joints. She was diagnosed
as having rheumatoid arthritis on the basis of her clinical picture and
diagnostic laboratory tests. Her flare-ups of the disease were treated with
anti-inflammatory agents (aspirin and ibuprophen), and for severe flare ups
prednisone in pharmacologic-dose would be added to her regimen for a brief
period of time. During the last 10 years of her rheumatoid arthritis, she has
been increasingly cavalier about her prednisone usage and now frequently doses
herself without physician monitoring for her joint discomfort. In the last 6
months because of a particularly prolonged bout of joint pain, swelling and
inflammation, she has treated herself with 20 mg/OD of prednisone (about four
times the normal physiologic amount of glucocorticoid that would be produced by
a normally functioning adrenal cortex). She has recently noted that she must
get up three to four time a night to urinate and she suffers from a moderate puritius
of the vaginal region.
After
six months of this self-directed prednisone therapy, and because of feeling
fatigued and weak, she saw her family physician. The physician noted that the
patient appeared to have a round and full face that appeared red and to exhibit
mild acne, have a fullness to her upper back and an enlargement to her
abdominal girth. She noted that small vessels were easily visible on her
abdominal waist and her upper leg muscles appeared wasted. Her reflexes were
normal.
Her blood pressure
was 155/100 with a pulse of 80.
Her CBC was normal
but her urine showed 1+ to 2+ glucose without ketonuria and 1+ protein.
WBC were plentiful
on urinalysis.
Serum Sodium 140mEq/L nl 1350145 mEq/L
Serum potassium 3.5 mEq/L nl
3.5-5.0 mEq/L
glucose fasting 170 mg/dL nl
70-110 mg/dL
Glucose 2 h after meal 200 mg/dL nl
less than 140 mg/dL
BUN and creatinine nl
T4 7
mg/dL 5-12 mg/dL
TSH 3.0
mU/L 0.3-5.0 mU/L
56. The patient’s clinical presentation and laboratory data are consistent
with the diagnosis(es) of:
a. Hypothyroidism and acromegaly.