Internal-Medicine

76 3: Endocrinology
also be caused by psychologic disturbance, but
may indicate androgen deficiency or drug
effect. (Kasper, pp. 271–274)
79. (E) Failure of detumescence—priapism—can
be caused by sickle cell anemia or chronic granulocytic
leukemia. Priapism must be treated
promptly to preserve future erectile functioning.
(Kasper, p. 272)
80. (B) Vascular disease, by itself or in conjunction
with peripheral neuropathy in DM, is a
common cause of erectile dysfunction. The
lesions can be in large vessels (aortic occlusion,
Leriche syndrome), small arteries, or even in
the sinusoidal spaces. (Kasper, pp. 271–274)
81. (E) Idiopathic hirsutism may simply represent
an extreme of normal androgen production. It
is diagnosed by demonstrating minimal elevation
of androgens and exclusion of other
causes. Management is primarily by cosmetic
therapy, although drugs to suppress androgen
production and/or androgen effects on the hair
follicle can be used. (Kasper, pp. 275–278)
82. (C) The most severe form of PCOD, Stein-
Leventhal syndrome, is associated with chronic
anovulation, hirsutism, enlarged cystic ovaries,
obesity, and amenorrhea. The spectrum of disease,
however, is quite wide, and some patients
have only mild hirsutism. (Kasper, pp. 275–277)
83. (F) Krukenberg’s tumors of the ovary stimulate
surrounding ovarian stromal tissue to produce
excess androgen. When onset of hair growth
(with or without frank virilization) is very
rapid, a neoplastic source of androgen is suggested.
As well as ovarian tumors, the potential
neoplasms include adenomas and carcinomas
of the adrenal gland. (Kasper, pp. 275–278)
84. (D) Attenuated forms of adrenal hyperplasia
can present with hirsutism at puberty or in
adulthood. Elevated levels of a precursor of
cortisol biosynthesis such as 17-hydroxyprogesterone,
17-hydroxypregnenolone, or 11-
deoxycortisol can present. ACTH infusion will
increase the precursor level, and dexamethasone
will suppress it. (Kasper, pp. 275–278)
85. (A) Salivary gland enlargement occurs both in
anorexia nervosa (AN) and bulimia (BN). Other
common findings in AN include constipation,
bradycardia, hypotension, hypercarotinemia,
and soft downy hair growth (lanugo). Menses
are usually absent. (Kasper, p. 430)
86. (D) Hyperglycemia is not seen in eating disorders,
and would suggest an alternate diagnosis for
the weight loss such as diabetes. Hypoglycemia
and low estrogens and gonadotropins are frequently
seen in anorexia nervosa (AN). BUN
and creatinine may be elevated. Hypochloremia,
hypokalemia, and alkalosis are frequently seen
in BN. (Kasper, p. 430)
87. (E) Low QRS voltages, sinus bradycardia, and
ST-T changes are common. However, the presence
of a prolonged QT interval is most suggestive
of serious cardiac arrhythmias. (Kasper,
p. 431)
88. (B) Hospitalization should be considered when
the body weight dips below 75% of the
expected. The goal is to achieve a weight of
90% of that expected. Vomiting is more characteristic
of bulimia than anorexia nervosa
(AN). (Kasper, p. 432)
89. (B) Recurrent vomiting and exposure of the
teeth to stomach acid leads to loss of dental
enamel and eventual chipping and erosion of
the teeth. The vomiting may be manually
induced, but eventually most patients with
bulimia (BN) are able to trigger vomiting at
will. (Kasper, p. 433)
90. (C) The patient is most likely to develop
glomerulosclerosis. This can be diffuse or
nodular (Kimmelstiel-Wilson nodules). Poor
metabolic control is probably a major factor in
the progression of diabetic nephropathy. (Felig,
pp. 900–901)
91. (B) AN has one of the highest mortality rates of
any psychiatric illness at 5% per decade. The
mortality for BN is very low, and 50% have a
full recovery within 10 years. Only 25% have
persistent symptoms of BN over many years,