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Free STEP1 Exam Braindumps (page: 49)

Page 48 of 213
PDF with 845 Questions

A 53-year-old man is being treated for hypertension and diabetes. His medications include insulin and propranolol. He presents at his physician's office complaining of muscle weakness. Blood tests reveal hyperkalemia (elevated serum potassium) as well as elevated BUN (blood urea nitrogen). Propranolol is gradually eliminated and his insulin dosage is adjusted. His serum potassium normalizes and his muscle weakness is alleviated. What probably caused his muscle weakness?

  1. high potassium-mediated block of acetylcholine receptors
  2. high potassium-mediated block of skeletal muscle calcium channels
  3. motor neuron hyperpolarization
  4. skeletal muscle depolarization with resultant Na-channel inactivation
  5. skeletal muscle hyperpolarization with resultant Na-channel blockade

Answer(s): D

Explanation:

Elevated serum potassium levels cause membrane depolarization with a resulting Na-channel inactivation.
Fibers are thus less able to fire action potentials, leading to impaired excitation contraction coupling, with muscle weakness (choice D is correct). Though hyperpolarization would also impede action potential generation, by moving the Na-channel away from its activation threshold, choices C and E are incorrect since high potassium causes membrane depolarization. Calcium required for skeletal muscle contraction is derived from internal stores (the sarcoplasmic reticulum) and is not dependent on calcium influx through surface membrane channels (choice B). There is no evidence that potassium interferes with the acetylcholine receptor (choice A). Hyperkalemia in this patient is probably due to multiple factors. Since insulin promotes potassium uptake into cells, too low an insulin dosage in the diabetic can lead to hyperkalemia. In addition, propranolol can cause a shift of potassium from cell to blood. Finally, the elevated BUN indicates some renal failure, and failing kidneys cannot efficiently excrete potassium into the urine.



A 30-year-old male seeks help because he lost weight and feels full after eating only a small amount of food. He is diagnosed with a delay in gastric emptying. Which of the following hormones has at physiological levels the strongest effect in inhibiting gastric emptying?

  1. cholecystokinin
  2. gastrin
  3. glucose-dependent insulinotropic peptide
  4. motilin
  5. pancreatic polypeptide

Answer(s): A

Explanation:

The major control mechanism for gastric emptying involves duodenal gastric feedback, hormonal as well as neural. The major hormone involved in the inhibition of gastric emptying is cholecystokinin (CCK), which is released by fat and protein digestion products. Gastrin (choice B) stimulates hydrochloric acid secretion and exerts a trophic effect on the gastric and intestinal mucosa. When the gastrin concentration is elevated to supraphysiologic levels, various other actions can be demonstrated including inhibition of gastric emptying. However, the physiologic importance of these actions is uncertain. Glucose-dependent insulinotropic peptide (GIP, choice C) is released from the intestinal mucosa by acid, fat, or hyperosmolarity and acts to some extent by inhibiting stomach functions including gastric motility. Although this function gave GIP its initial name (gastric inhibitory peptide), GIP's action as an enterogastrone is now controversial.
The major physiologic action of GIP is to cause insulin release. Motilin (choice D) stimulates gastric motor activity, especially during the interdigestive phase, when it regulates contractions that serve to empty the GI residual contents. Pancreatic polypeptide (choice E) is a negative feedback regulator for pancreatic enzymes and bicarbonate secretion. It is considered to be a candidate hormone since it satisfies some, but not all of the criteria for hormonal status.



A 4-year-old child with signs of precocious (early onset) puberty is brought to a clinic for evaluation and found to have a congenital deficiency of 21--hydroxylase. Feedback inhibition of the pituitary gland is lost and excess ACTH is secreted. As a result, which of the following happens?

  1. adrenal cortical atrophy occurs
  2. adrenal medullary hypertrophy occurs
  3. excess cortisol is released
  4. precursors to cortisol synthesis increase
  5. serum cholesterol falls dramatically

Answer(s): D

Explanation:

In the adrenogenital syndrome, the failure to make cortisol due to lack of the adrenal enzyme 21-- hydroxylase results in an inability to provide negative feedback suppression of ACTH production. As a result, the adrenal glands are under constant stimulation to maximize steroidogenesis. Substrates that cannot reach cortisol flow down other pathways and by mass action drive the massive overproduction of androgens, which can also be peripherally aromatized to estrogens. No significant change in serum cholesterol is observed (choice E), probably because the cholesterol reservoir in the body is large, even compared to the massive levels of steroids being synthesized in this syndrome. Cortical atrophy (choice A) and release of excess cortisol (choice C) are the opposite of what is observed. There is no mechanism to achieve selective hypertrophy of the adrenal medulla (choice B) because the action of ACTH to drive adrenal hypertrophy is limited to the cortex.



A 59-year-old Caucasian female is self-donating blood in preparation for a hip replacement surgery in the near future. Shortly after her third session of donating a unit (pint) of whole blood, her mean arterial pressure remains unchanged, even though the venous return of blood to her heart is diminished. Which of the following is the most likely reason for the preservation of arterial pressure?

  1. cardiac output rises to compensate for the reduced venous return
  2. end-diastolic ventricular filling pressure rises during hemorrhage
  3. fall in venous return is offset by an increase in total peripheral resistance
  4. heart rate rises to compensate for a reduced venous return
  5. venous return and blood pressure are unrelated

Answer(s): C

Explanation:

By Ohm's law, a reduction in flow should also reduce pressure if resistance is constant. Therefore a rise in total peripheral resistance in the face of reduced flow would account for the preservation of arterial pressure. Choice A is incorrect since cardiac output and venous return must rise and fall together. Choice B is incorrect since end-diastolic ventricular filling pressure falls with decreased venous return. Choice D is incorrect since heart rate can maintain pressure only if venous return is also maintained. Choice E is incorrect since Ohm's law states the inverse relationship of venous return and pressure.






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