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Free STEP1 Exam Braindumps (page: 58)

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PDF with 845 Questions

Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder in which autoantibodies attack voltage-gated calcium channels in the presynaptic nerve terminal. A characteristic manifestation of LEMS is limb muscle weakness. A decrease in which of the following would you expect to see in LEMS?

  1. activation threshold for the action potential
  2. amplitude of the action potential
  3. amplitude of the miniature end-plate potential (MEPP)
  4. magnitude of the end-plate potential (EPP)
  5. quantal content

Answer(s): D

Explanation:

At the neuromuscular junction, an invading action potential opens voltage-gated calcium channels and enters the presynaptic terminal. Elevated cytoplasmic causes release of vesicles
containing acetylcholine. Acetylcholine diffuses across the cleft and activates postsynaptic acetylcholine receptors with a resultant depolarization (the EPP). Lack of presynaptic calcium channels in LEMS means that less enters the terminal of the presynaptic membrane--therefore less transmitter is released and the size of the EPP is decreased. Postsynaptic properties, neither action potential threshold nor size are altered due to the deficit of presynaptic calcium channels in LEMS (choices A and B). The MEPP is due to spontaneous transmitter release. The amplitude depends on the amount of transmitter in each vesicle. Lack of presynaptic calcium channels will not affect the size of the MEPP, since each vesicle still has the same amount of transmitter (choice C). Quantal content is the amount of transmitter per vesicle which, as described above, will not be altered in LEMS (choice E).



A newlywed 23-year-old woman and her 28-year-old husband are evaluated for infertility. They have been unable to conceive a child despite regular intercourse for the past 12 months. The first step of this couple's infertility workup is to determine whether ovulation occurs regularly. Which of the following hormones is directly responsible for ovulation?

  1. estradiol
  2. estriol
  3. follicle-stimulating hormone (FSH)
  4. inhibin
  5. luteinizing hormone (LH)

Answer(s): E

Explanation:

Although the early maturation of an ovarian follicle depends on the presence of FSH, ovulation is induced by a surge of LH. Although estrogens (choices A and B) usually have a negative feedback effect on LH and FSH secretion, the LH surge seems to be a response to elevated estrogen levels. In concert with FSH, LH induces rapid follicular swelling. LH also acts directly on the granulose cells, causing them to decrease estrogen production, as well as initiating production of small amounts of progesterone. These changes lead to ovulation. FSH (choice C) causes follicle maturation, and is also required for Sertoli cells to mediate the development of spermatids into mature sperm cells. Inhibin (choice D) is a polypeptide secreted by the testes and ovaries that inhibits FSH secretion.



The electrocardiogram of a 66-year-old male with a history of atherosclerotic heart disease reveals an irregular, but rapid heart rate. The QRS complexes are normal but no P-waves can be seen. What is the most likely reason for these findings?

  1. atrial fibrillation
  2. Paroxysmal ventricular tachycardia
  3. Right bundle branch block
  4. Sinus tachycardia
  5. Wolff-Parkinson-White syndrome

Answer(s): A

Explanation:

Atrial fibrillation is a continuous, chaotic reentry of electrical impulses within the atrial myocardium that arises in a diseased or stretched left atrium. The chaotic patterns of atrial excitation prevent P- waves from being seen in the electrocardiogram. The ventricular response is rapid and irregular. In all the other alternatives (choices BE), a P-wave should be distinguishable in some part of the electrocardiogram, although not necessary in a constant relationship to the QRS complex.



Which of the following diseases will result in left ventricular hypertrophy?

  1. Aortic valve stenosis
  2. mitral valve stenosis
  3. pulmonary valve regurgitation
  4. tricuspid valve regurgitation
  5. tricuspid valve stenosis

Answer(s): A

Explanation:

Stenosis of the outlet valve of the left ventricle greatly increases the work of the ventricle in ejecting blood and will result in left ventricular hypertrophy. Mitral valve stenosis (choice B) will impede filling of the left ventricle and will not cause left ventricular hypertrophy. Tricuspid valve regurgitation (choice D), pulmonary valve regurgitation (choice C), and tricuspid valve stenosis (choice E) cause congestion of the right atria and/or right ventricles and impede flow of blood toward the left ventricle and thus will not result in left ventricular hypertrophy.






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