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USMLE Endocrine

Study online at https://quizlet.com/_33yr8j

1. thyroid development: floor of primitive pharynx


thyroid diverticulum arises from ___ and neck
descends into ___

2. the thyroid, in development, is connect- thyroglossal duct


ed to tongue by ___. what is the fate of normally disappears but may
this structure? persist as pyramidal lobe of thy-
roid

3. what is the normal remnant of the thy- foramen cecum


roglossal duct?

4. most common ectopic thyroid tissue tongue


site

5. thyroglossal duct cyst presents as anterior midline


neck mass that moves with swal-
lowing or protrusion of tongue
(vs. persistent cervical sinus
leading to branchial cleft cyst in
lateral neck)

6. adrenal cortex is derived from what mesoderm


germ layer?

7. adrenal medulla embryologic dericative neural crest

8. adrenal cortex: zona reticularis


layers from innermost to outer zona fasciculata
zona glomerulosa

9. zona glomerulosa: renin-angiotensin


primary regulatory control and secreto- aldosterone
ry products

10. zona reticularis: ACTH, CRH


primary regulatory control and secreto- sex hormones (e.g. androgens)
ry products

11.
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zona fasciculata: ACTH, CRH
primary regulatory control and secreto- cortisol, sex hormones
ry products

12. endocrine cells of adrenal medulla Chromaffin cells

13. Chromaffin cells: preganglionic sympathetic fibers


primary regulatory control and secreto- catecholamines (epi, NE)
ry products

14. adrenal cortex layers mnemonic "deeper you go, the sweeter it
gets"
GFR corresponds with Salt
(Na+), Sugar (glucocorticoids),
Sex (androgens)

15. pheochromocytoma most common tumor of adrenal


who, where, what (effects) medulla in adults
episodic hypertension

16. neuroblastoma most common tumor of adrenal


who, where, what (effects) medulla in children
rarely causes hypertension

17. anterior pituitary hormones mnemonic B-FLAT:


Basophils: FSH, LH, ACTH, TSH
and
FLAT PiG:
FSH, LH, ACTH, TSH, Prolactin,
GH

18. acidophils of anterior pituitary secrete GH


what hormones? prolactin

19. from where is melanotropin secreted? intermediate lobe of pituitary

20. anterior pituitary is derived from ___ oral ectoderm (Rathke pouch)

21. hormonal subunit common to TSH, LH, alpha


FSH, GH

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22. hormonal subunit that determines pitu- beta
itary hormone specificity

23. posterior pituitary hormones vasopressin (ADH)


oxytocin

24. site of vasopressin (ADH) synthesis supraoptic nuclei of hypothala-


mus

25. site of oxytocin synthesis paraventricular nuclei of hypo-


thalamus

26. hormones from the hypothalamus are neurophysins (carrier proteins)


transported to the posterior pituitary
via___

27. posterior pituitary is derived from___ neuroectoderm

28. pancreatic islets arise from ___ pancreatic buds

29. pancreatic islet cells: secretion and lo- glucagon


cation peripheral
alpha

30. pancreatic islet cells: secretion and lo- insulin


cation central
beta

31. pancreatic islet cells: secretion and lo- somatostatin


cation interspersed
delta

32. insulin synthesis preproinsulin synth. in


RER--->cleavage of presig-
nal-->proinsulin (stored in se-
cretory granules)--->proinsulin
cleavage--->exocytosis of in-
sulin and C-peptide equally

33.
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2 conditions in which insulin and C-pep- insulinoma
tide are both increased sulfonylurea use

34. exogenous insulin lacks ___ C-peptide

35. insulin anabolic functions inc glucose transport in skeletal


muscle, adipose tissue
inc glycogen synth, storage
inc triglyceride synth
inc Na+ retention (kidneys)
inc protein synth (muscles)
inc K+, AA uptake by cells
dec glucagon release

36. does insulin cross placenta? glucose? no


yes

37. insulin binding to receptors stimulates... tyrosine kinase activity--->glu-


cose uptake via carrier-mediat-
ed transport into insulin-depen-
dent tissue
and
--->gene transcription

38. insulin-dependent glucose transporters GLUT-4: adipose tissue, striated


muscle

39. insulin and ___ can increase GLUT-4 ex- exercise


pression

40. insulin-independent transporters GLUT-1: RBCs, brain, cornea


GLUT-2 (bidirectional): beta islet
cells, liver, kidney, SI
GLUT-3: brain
GLUT-5 (fructose): spermato-
cytes, GI tract

41. brain's energy source during starvation, ketone bodies


when glucose is not available

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42. why do RBCs always (only) utilize glu- lack mitochondria for aerobic
cose? metabolism

43. insulin-independent glucose uptake BRICK-L:


mnemonic brain
RBCs
intestine
cornea
kidney
liver

44. insulin regulation: increase insulin


GH, beta2-agonists

45. GH causes ___ resistance insulin

46. insulin regulation by glucose (pathway) glucose enters beta cells--->inc


ATP generated via glucose me-
tabolism--->K+ channels close
(sulfonylurea target)--->beta cell
membrane depolarizes--->volt-
age-gated Ca2+ channels
open--->Ca2+ influx--->stimula-
tion of insulin exocytosis

47. glucagon catabolic function glycogenolysis


gluconeogenesis
lipolysis
ketone production

48. glucagon release: stimulation and inhi- stimulation: hypoglycemia


bition inhibition: insulin, hyper-
glycemia, somatostatin

49. hypothalmic-pituitary hormones: func- inc ACTH, NSH, beta-endorphin


tion and clinical notes: dec in chronic exogenous
CRH steroid use

50. dec prolactin


dopamine antagonists (e.g. an-
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hypothalmic-pituitary hormones: func- tipsychotics) can cause galact-
tion and clinical notes: orrhea due to hyperprolactine-
dopamine mia

51. hypothalmic-pituitary hormones: func- inc GH


tion and clinical notes: analog (tesamorelin) used to
GHRH treat HIV-associated lipodystro-
phy

52. hypothalmic-pituitary hormones: func- inc LH, FSH


tion and clinical notes: regulated by prolactin
GnRH tonic GnRH suppressed HPA
axis
pulsatile GnRH--->puberty, fer-
tility

53. hypothalmic-pituitary hormones: func- dec GnRH


tion and clinical notes: pituitary prolactinoma--->amen-
prolactin orrhea, osteoporosis, hypogo-
nadism, galactorrhea

54. hypothalmic-pituitary hormones: func- dec GH, TSH


tion and clinical notes: analogs used to treat
somatostatin acromegaly

55. hypothalmic-pituitary hormones: func- inc TSH, prolactin


tion and clinical notes:
TRH

56. prolactin source mainly anterior pituitary

57. prolactin function stimulation of milk production


ovulation, spermatogenesis inhi-
bition
(GnRH synth/release inhibition)

58. excessive prolactin is associated with libido


dec ___

59.
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prolactin secretion from ant. pit. is toni- dopamine
cally inhibited by ___ from ____ hypothalamus

60. how does prolactin inhibit its own secre- inc dopamine synthesis and se-
tion? cretion from hypothalamus

61. effect of TRH on prolactin secretion increase


(e.g. in primary or secondary hy-
pothyroidism)

62. effect of dopamine agonists (e.g. inhibit


bromocriptine) on prolactin secretion can be used to treat prolactino-
ma

63. effect of dopamine antagonisms (e.g. stimulation


most antipsychotics) and estrogens
(e.g. OCPs, pregnancy) on prolactin se-
cretion

64. somatotropin is aka GH

65. GH source ant. pit.

66. GH function stimulates linear growth and


muscle mass via IGF-1 (so-
matomedin C)
inc. insulin resistance (diabeto-
genic)

67. GHRH stimulates ___ pulsatile release of GH from ant.


pit.

68. secretion of GH ___ during exercise and inc


sleep

69. inhibitors of GH secretion glucose


somatostatin release
(via negative feedback by so-
matomedin)

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70. excess secretion of GH (e.g. pituitary acromegaly
adenoma) causes what in adults? in chil- gigantism
dren?

71. ghrelin function stimulates hunger (orexigenic


effect) and GH release (via GH
secretagog receptor

72. ghrelin production location stomach

73. 2 causes of increased ghrelin produc- sleep loss


tion Prader-Willi syndrome

74. leptin function satiety hormone


dec during starvation

75. where is leptin produced? adipose tissue

76. effect of sleep deprivation on leptin pro- decreased


duction

77. mutation of leptin gene is associated congenital obesity


with what?

78. andocanabinoids function stimulate cortical reward cen-


ters--->inc desire for high-fat
foods

79. ADH source synthesized in supraoptic nuclei


of hypothalamus
released by post. pit.

80. ADH function primary function: dec serum os-


molarity, inc urine osmolarity
(V2 receptors) via regulation of
aquiporin channel insertion in
principal cells of CD
secondary: regulation of BP (V1
receptors)

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81. ADH levels in central diabetes insipidus dec
(DI)? nephrogenic DI? inc

82. nephrogenic DI can be caused by a mu- V2


tation in what receptor?

83. desmopressin acetate is a ___ analog ADH


and is used to treat ___ central DI

84. adrenal steroids and congenital adrenal + ACTH


hyperplasia: - ketoconazole
+ and - regulator of cholesterol desmo-
lase

85. adrenal steroids and congenital adrenal cholesterol desmolase


hyperplasia: zona glomerulosa
enzyme and location:
cholesterol--->pregnenolone

86. products of zona glomerulosa mineralcorticoids

87. products of zona fasciculata glucocorticoids

88. products of zona reticularis androgens

89. adrenal steroids and congenital adrenal 3beta hydroxysteroid dehydro-


hyperplasia: genase
enzyme and location: zona gomerulosa
pregnenolone--->progesterone

90. adrenal steroids and congenital adrenal 21-hydroxylase


hyperplasia: zona glomerulosa
enzyme and location:
progesterone--->11-deoxycorticos-
terone

91. adrenal steroids and congenital adrenal 11-beta-hydroxylase


hyperplasia: zona glomerulosa
enzyme and location:

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11-deoxycorticosterone--->corticos-
terone

92. adrenal steroids and congenital adrenal aldosterone synthase


hyperplasia: zona glomerulosa
enzyme and location:
corticosterone--->aldosterone

93. + regulator of aldosterone synthase angiotensin II

94. adrenal steroids and congenital adrenal 17-alpha-hydroxylase


hyperplasia: glomerulosa--->fasciculata
enzyme and location:
pregnenolone--->17-hydroxypre-
nenolone

95. adrenal steroids and congenital adrenal 17-alpha-hydroxylase


hyperplasia: glomerulosa--->fasciculata
enzyme and location:
progesterone--->17-hydroxyproges-
terone

96. adrenal steroids and congenital adrenal 3beta-hyroxysteroid dehydroge-


hyperplasia: nase
enzyme and location: zona fasciculata
17-hydroxypregnenolone--->17-hydrox-
yprogesterone

97. adrenal steroids and congenital adrenal 21-hydroxylase


hyperplasia: zona fasciculata
enzyme and location:
17-hyroxyprogesterone--->11-deoxycor-
tisol

98. adrenal steroids and congenital adrenal 11beta-hydroxylase


hyperplasia: zona fasciculata
enzyme and location:
11-deoxycortisol--->cortisol

99. fasciculata--->reticularis
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adrenal steroids and congenital adrenal
hyperplasia:
enzyme and location:
12-hydroxypregnenolone--->dehy-
droepiandrosterone (DHEA)

100. adrenal steroids and congenital adrenal fasciculata--->reticularis


hyperplasia:
enzyme and location:
17-hydroxyprogesterone--->androstene-
dione

101. adrenal steroids and congenital adrenal 3beta-hydroxysteroid dehydro-


hyperplasia: genase
enzyme and location: zona reticularis
DHEA--->androstenedione

102. adrenal steroids and congenital adrenal zona reticularis


hyperplasia:
enzyme and location:
androstenedione--->testosterone

103. adrenal steroids and congenital adrenal aromatase


hyperplasia: zona reticularis--->peripheral
enzyme and location: tissues
androstenedione--->estrone

104. adrenal steroids and congenital adrenal aromatase


hyperplasia: zona reticularis--->peripheral
enzyme and location: tissues
testosterone--->estradiol

105. adrenal steroids and congenital adrenal 5-alpha-reductase


hyperplasia: zona reticularis--->peripheral
enzyme and location: tissues
testosterone--->dihydrotestosterone
(DHT)

106.

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all congenital adrenal enzyme deficien- both adrenal glands
cies are characterized by enlargement of inc ACTH stimulation (due to dec
___ due to ___ cortisol_

107. adrenal enzyme deficiencies: 17-al- inc


pha-hydroxylase:
mineralocorticoids

108. adrenal enzyme deficiencies: 17-al- dec


pha-hydroxylase
cortisol

109. adrenal enzyme deficiencies: 17-al- dec


pha-hydroxylase
sex hormones

110. adrenal enzyme deficiencies: 17-al- inc


pha-hydroxylase
BP

111. adrenal enzyme deficiencies: 17-al- dec


pha-hydroxylase
[K+]

112. adrenal enzyme deficiencies: 17-al- dec androstenedione


pha-hydroxylase
labs

113. adrenal enzyme deficiencies: 17-al- XY: pseudohermaphrodism (am-


pha-hydroxylase biguous genitalia, undescended
presentation testes)
XX: lack secondary sexual de-
velopment

114. adrenal enzyme deficiencies: 21-hydrox- dec


ylase
mineralocorticoids

115. dec

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adrenal enzyme deficiencies: 21-hydrox-
ylase
cortisol

116. adrenal enzyme deficiencies: 21-hydrox- inc


ylase
sex hormones

117. adrenal enzyme deficiencies: 21-hydrox- dec


ylase
BP

118. adrenal enzyme deficiencies: 21-hydrox- inc


ylase
[K+]

119. adrenal enzyme deficiencies: 21-hydrox- inc renin activity


ylase inc 17-hydroxyprogesterone
labs

120. adrenal enzyme deficiencies: 21-hydrox- most common adrenal enzyme


ylase deficiency
presentation presents in infancy (salt wasting)
or childhood (precocious puber-
ty)
XX: virilization

121. adrenal enzyme deficiencies: dec aldosterone


11-beta-hydroxylase inc 11-deoxycorticosterone (re-
mienralocorticoids sult: inc BP)

122. adrenal enzyme deficiencies: dec


11-beta-hydroxylase
cortisol

123. adrenal enzyme deficiencies: inc


11-beta-hydroxylase
sex hormones

124. inc
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adrenal enzyme deficiencies:
11-beta-hydroxylase
BP

125. adrenal enzyme deficiencies: dec


11-beta-hydroxylase
[K+]

126. adrenal enzyme deficiencies: dec renin activity


11-beta-hydroxylase
labs

127. adrenal enzyme deficiencies: XX: virilization


11-beta-hydroxylase
presentation

128. cortisol adrenal zona fasciculata


source bound to corticosteroid-binding
globulin

129. cortisol BIG FIB:


function inc BP
inc Insulin resistance (diabeto-
genic)
dec Glucogenesis, lipolysis, pro-
teolysis
dec Fibroblast activity (causing
striae)
dec Inflammatory, Immune re-
sponses
dec Bone formation (dec os-
teoblast activity)

130. how does cortisol inc BP? upregulates alpha1 receptors


on arterioles--->inc sensitivity to
NE, epi
at high conc. can bind to min-
eralocorticoid (aldosterone) re-
ceptors

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131. how does cortisol dec inflammatory and inhibits production of
immune responses? leukotrienes, prostaglandins
inhibits WBC adhesion--->neu-
trophilia
blocks histamine release from
mast cells
reduces eosinophils
blocks IL-2 production

132. exogenous corticosteroids can cause TB


reactivation of ___ and ___ by blocking candidiasis
IL-2 production

133. cortisol regulation: CRH (hypothalamus)--->ACTH


stimulation release (pit)--->cortisol produc-
tion in z. fasciculata

134. excess cortisol causes what to happen dec


to CRH? (= dec ACTH = dec cortisol se-
cretion)

135. chronic stress does what to cortisol se- induces prolonged secretion
cretion?

136. 3 forms of plasma calcium ionized (45%)


bound to albumin (40%)
bound to anions (15%)

137. affect of inc plasma pH on Ca2+ in plas- inc affinity of albumin


ma for Ca2+ (inc nega-
tive charge)--->hypocalcemia
(cramps, pain, parasthesias,
carpopedal spasm)

138. Vit D source D3 from sun exposure in skin


D2 ingested from plants

139. vit D3 and D2 are both converted to ___ 25-OH (liver)


in liver and ___ in kindey 1,25-OH2 (active form; kidney)

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140. Vit D deficiency causes what in kids? rickets
adults? osteomlacia
(malabsorption, dec sunlight,
poor diet, chronic kidney failure)

141. Vit D function inc absorption of dietary Ca2+


and phosphate
inc bone reabsorption--->inc
Ca2+ and phosphate

142. Vit D regulation: inc PTH = dec [Ca2+], dec phos-


PTH effect phate--->inc 1,25OH2 produc-
tion

143. Vit D regulation: feedback inhibition on its own


effect of 1,25-OH2 production

144. 24,25-OH2 D3 inactive form of vit D

145. effect of PTH in kidney inc Ca2+ and dec phosphate re-
absorption

146. effect of 1,25-OH2 in gut inc Ca2+ and phosphate ab-


sorption

147. calcium and phosphate homeostasis


diagram

148. PTH source chief cells of parathyroid

149. PTH function inc bone reabsorption of Ca and


Ph
inc kidney reab. of Ca in DCT
dec kindey reab. of Ph on PCT
inc 1,25-OH2 D3 (calcitriol) pro-
duction (by stimulating kidney
1alpha-hydroxylase in PCT)

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inc macrophage CSF and
RANK-L

150. RANK-L receptor activator of NF-KB lig-


and)

151. RANK-L (ligand) is secreted by___ and osteoblasts


____ binds RANK (receptor) on ___ and octeocytes
their precursors to stimulate ___ and inc osteoclasts
Ca2+ osteoclasts

152. intermittent PTH release can stimulate bone formation


___

153. PTH-related peptide (PTHrP) function functions like PTH


and when increased increased in many malignancies

154. PTH regulation: inc PTH secretion


dec serium Ca2+ =

155. PTH regulation: inc PTH secretion


inc serum phosphate =

156. PTH regulation: inc PTH secretion


dec serum Mg2+ =

157. PTH regulation: dec PTH production


big dec serum Mg2+ =

158. common causes of Mg2+ decrease diarrhea


aminoglycosides
diuretics
alcohol abuse

159. calcitonin source parafollicular (C) cells of thyroid

160. calcitonin function dec bone reabsorption of Ca2+


opposes actions of PTH
not important in normal Ca2+
homeostasis

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161. calcitonin regulation: calcitonin secretion
inc serum Ca2+ =

162. signaling pathways of endocrine hor- FLAT ChAMP:


mones: FSH
cAMP LH
ACTH
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH
calcitonin
GHRH
glucagon

163. signaling pathways of endocrine hor- (think vasodilators)


mones: ANP
cGMP BNP
NO
(EDRF)

164. signaling pathways of endocrine hor- GOAT HAG:


mones: GnRH
IP3 Oxytocin
ADH (V1 receptor)
TRH
Histamine (H1 receptor)
Angiotensin II
Gastrin

165. signaling pathways of endocrine hor- VETTT CAP:


mones: Vit D
intracellular receptor Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
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166. signaling pathways of endocrine hor- insulin


mones: IGF-1
intrinsic tyrosine kinase FGF
PDGF
EGF
(think growth factors; MAP ki-
nase pathway)

167. signaling pathways of endocrine hor- PIGGlET:


mones: Prolactin
receptor-associated tyrosine kinase Immunomodulators (e.g. cy-
tokines, IL-2, IL-6, IFN)
GH
G-CSF
Erythropoietin
Thrombopoietin

168. signaling pathway of steroid hormones


diagram

169. how to steroid hormones circulate? are lipophilic, so must be bound


to specific binding globulins to
inc their solubility

170. men: inc ____-binding globulin (SHBG) sex hormone


lowers free ___--->gynecomastia testosterone

171. in women: dec ____ raises free testos- SHBG


terone, resulting in ____ hirstutism

172. OCPs, pregnancy ____ SHBG levels; SHBG


free estrogen levels remain ____ unchanged

173. T3/T4 functions control body's metabolic rate

174. thyroid hormone source follicles of thyroid


most T3 formed in target tissues

175. T3 functions
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4 B's:
Brain (CNS) maturation
Bone growth
Beta-adrenergic effects
Basal metabolic rate inc
(inc glycogenolysis, gluconeo-
genesis, lipolysis)

176. the bone growth stimulation of thyroid GH


hormones is a result of synergy with
what other hormone?

177. thyroid hormone action on heart inc beta1 receptors in heart--->


inc CO
inc HR
inc SV
inc contractility

178. how does T3 increase basal metabolic inc NA+/K+ ATPase activi-
rate? ty--->inc O2 consumption, RR,
body temp

179. what binds most T3/T4 in blood and ren- thyroxine-binding globulin (TBG)
ders it inactive? only free hormone is active

180. what results in dec. TBG? hepatic failure


steroids

181. what results in inc. TBG? pergnancy


OCP use
(inc estrogen = inc TBG)

182. enzyme that converts T4 (the major thy- 5'-deiodinase


roid product) to T3 in peripheral tissue?

183. does nuclear receptor have greater affin- T3


ity for T3 or T4?

184. what enzyme is responsible for oxida- peroxidase


tion and organification of iodine, as well
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as coupling of monoiodotyrosine (MIT)
to di-iodotyrosine (DIT)?

185. what inhibits both peroxidase and propylthiouracil


5'-deiodinase?

186. methimazole inhibits peroxidase in what oxidation and organification of


pathway? iodine, as well as coupling
of monoiodotyrosine (MIT) to
di-iodotyrosine (DIT)

187. thyroid hormone regulation TRH (hypothalamus)-->TSH (pi-


(+) tuitary)-->stimulation of follicular
cells of thyroid

188. thyroid hormone regulation free T3/T4--->acts on ant pit to


(-) dec sensitivity to TRH

189. thyroid-stimulating Igs (e.g. TSH) stimu- Graves disease


late follicular cells in what diseases (an
example)?

190. Wolff-Chaikoff effect excess iodine temporarily in-


hibits thyroid peroxidase--->
dec iodine organification--->dec
T3/T4 production

191. anions that have a negative regulatory perchlorate


effect on iodine oxidation to I2 in the pertechnetate
thyroid thiocyanate

192. Cushing syndrome inc cortisol due to variety of


etiology causes:
1. exogenous corticosteroids
2. primary adrenal adenoma, hy-
perplasia, carcinoma
3. pseudohyperaldosteronism
4. ACTH-secreting pituitary ade-
noma (Cushing disease)
5. paraneoplastic ACTH secre-
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tion (e.g. small cell lung cancer,
bronchial carcinoids)

193. what is responsible for the majority Cushing disease (ACTH-secret-


of endogenous cases of Cushing syn- ing pituitary adenoma)
drome?

194. how do exogenous corticosteroids dec ACTH, bilateral adremal at-


cause Cushing syndrome? rophy

195. most common cause of Cushing syn- exogenous corticosteroids


drome

196. how do primary adrenal ademona, hy- dec ACTH-->atrophy of unin-


perplasia, carcinoma, and pseudohy- volved adrenal gland
peraldosteronism cause Cushing syn-
drome?

197. how do Cushing disease (ACTH-secret- inc ACTH--->bilateral adrenal


ing pituitary adenoma) and paraneo- hyperplasia
plastic ACTH secretion result in Cush-
ing syndrome?

198. Cushing syndrome findings hypertension


weight gain
moon facies
truncal obesity
buffalo hum
skin changes (thinning, striae)
osteoporosis
hyperglycemia (insulin resis-
tance)
amenorrhea
immunosuppression

199. Cushing syndrome diagnosis: inc free cortisol on 24-hr urinaly-


screening tests sis
inc midnight salivary cortisol
no suppression with overnight
low-dose dexamethasone test
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200. Cushing syndrome diagnosis: adrenal tumor


what to suspect if ACTH is dec

201. Cushing syndrome diagnosis: Cushing disease or ectopic


what to suspect if ACTH is inc ACTH secretion

202. tests used to distinguish Cushing dis- 1. high-dose (8mg) dexametha-


ease from ectopic ACTH secretion sone suppression test
2. CRH stimulation test

203. Cushing syndrome diagnosis: ectopic ACTH secretion


if ACTH is not decreased with high-dose (source is resistant to negative
(8mg) dexamethasone test___ feedback)

204. Cushing syndrome diagnosis: ectopic ACTH secretion


if ACTH is not increased with CRH stim- (pituitary ACTH is suppressed)
ulation test ___

205. adrenal insufficiency inability of adrenal glands to


generate enough mineralo- +/-
glucocorticoids

206. adrenal insufficiency symptoms weakness


fatigue
orthostatic hypotension
muscle aches
weight loss
GI disurbances
sugar and/or salt cravings

207. adrenal insufficiency diagnosis measurement of serum elec-


trolytes
morning/random serum cortisol
and ACTH
response to ACTH stimulation
test

208. metyrapone stimulation test for adrenal insufficiency diagno-


sis
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metyrapone blocks last step of
cortisol synthesis (11-deoxycor-
tisol-->cortisol)
normal: dec cortisol, compen-
satory inc ACTH
+: ACTH remains dec after test

209. primary adrenal insufficiency loss of gland function =


dec aldosterone and cor-
tisol--->hypotension (hypona-
tremic vol contraction), hy-
perkalemia, metabolic acido-
sis, skin/mucosal hyperpigmen-
tation

210. what causes hyperpigmentation of MSH, a byproduct of inc ACTH


skin/mucosa in primary adrenal insuffi- production from pro-opiome-
ciency? lanocortin

211. primary adrenal insufficiency sudden onset (e.g. due to mas-


acture sive hemorrhage)
may present with sock and acute
adrenal crisis

212. primary adrenal insufficiency autoimmunity


most common cause in Western worls esp. associated with autoim-
mune polyglandular syndromes

213. primary adrenal insufficiency aka - Addison disease


chronic

214. Addison disease chronic primary adrenal insuffi-


ciency
due to adrenal atrophy or de-
struction due to disease (e.g. au-
toimmune, TB, metastasis)

215. Waterhouse-Friderichsen syndrome acute primary adrenal insuffi-


ciency due to adrenal hem-
orrhage associated with sep-
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ticemia (usually N. meningitidis),
DIC, endotoxic shock

216. secondary adrenal insufficiency dec pituitary ACTH production


no skin/mucosal hyperpigmen-
tation
no hyperkalemia (aldosterone
synthesis preserved)

217. tertiary adrenal insufficiency in patients with chronic exoge-


nous steroid use, precipitated by
abrupt withdrawal
aldosterone synthesis unaffect-
ed

218. neuroblastoma most common adrenal tumor in


children <4yo
originates in neural crest cells
Homer-Wright rosettes charac-
teristic
occurs anywhere along sympa-
thetic chain

219. neuroblastoma presentation abdominal distension with firm,


irregular mass that can cross
midline (vs. Wilms tumor -
smooth and unilateral)
opsoclonus-myoclonus syn-
drome (dancing eyes-dancing
feet)
bombesin and neuron-specific
enolase +

220. there is an increased presence of what 1. homovanillic acid (HVA; prod-


in urine associated with a neuroblas- uct of dopamine breakdown)
toma? 2. vanillylmandelic acid (VMA);
NE breaskdown product)

221. neuroblastoma is associated with over- N-myc oncogene


expression of what gene?
25 / 52
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222. neuroblastoma is associated with de- hypertension


creased likelihood to develop what?

223. pheochromocytoma most common tumor of adrenal


etiology gland in adults
derived from chromaffin cells
(arise from neural crest)
rule of 10s

224. pheochromocytoma 10% malignant


etiology: rule of 10s 10% bilateral
10% extra-adrenal
10% calcify
10% kids

225. pheochromocytoma most tumors secrete epi, NE,


symptoms dopamine-->episodic hyperten-
sion
associated with neurofibromato-
sis type 1, von Hippel Lindau dis-
ease, MEN 2a,2B,
symptoms occur in spells
episodic hyperadrenergic symp-
toms

226. pheochromocytoma 5 Ps:


episodic hyperadrenergic symptoms Pressure (in BP)
Pain (headache)
Perspiration
Palpitations (tachycardia)
Pallor

227. pheochromocytoma inc catecholamines and


findings metanephrines in urine and
plasma

228. pheochromocytoma irreversible alpha-agonists (e.g.


treatment phenoxybenzamine) followed by
beta-blockers prior to tumor re-
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section
(must be alpha then beta to
avoid hypertensive crisis)

229. hypothyroidism cold intolerance (dec heat pro-


signs/symptoms duction)
weight gain, dec appetite
hypoactivity, lethargy, fatigue,
weakness
constipation
dec reflexes
myxedema (facial, periorbital)
dry, cool skin; coarse, brittle hair
bradycardia, dyspnea on exer-
tion

230. hypothyroidism inc TSH (sensitive test for prima-


lab findings ry hypothyroidism)
dec free T3, T4
hypercholesterolemia (dec LDL
receptor expression)

231. hyperthyroidism heat intolerance (inc heat pro-


signs/symptoms duction)
weight loss, inc appetite
hyperactivity
diarrhea
inc reflexes
pretibial myxedema (Graves dis-
ease); periorbital edema
warm, moist skin; fine hair
chest pain, palpitations, arrhyth-
mias
inc #/sensitivity of beta-adrener-
gic receptors

232. hyperthyroidism dec TSH (if primary)


lab findings inc free or total T3, T4
hypocholesterolemia (inc LDL
receptor expression)
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233. hypothyroidism: Hashimoto thyroiditis most common cause of hypothy-


roidism in iodine-deficient re-
gions
autoimmune (anti-thyroid perox-
idase, antimicrosomal, antithy-
roglobulin Abs)
associated with HLA-DR5 and
inc risk non-Hodgkin lymphoma
may be hyperthyroid early due
to thyrotoxicosis during follicular
rupture

234. hypothyroidism: Hashimoto thyroiditis Hurthle cells


histologic findings lymphoid aggregate with germi-
nal centers

235. hypothyroidism: Hashimoto thyroiditis moderately enlarged, nontender


findings thyroid

236. hypothyroidism: congenital (cretinism) severe fetal hypothyroidism due


to maternal hyperthyroidism,
thyroid agenesis, thyroid dysge-
nesis (most common cause in
US), I deficiency, dyshormono-
genetic disorder

237. hypothyroidism: congenital (cretinism) 6 P's:


findings Pot-bellied
Pale
Puffy-faced child
Protruding umbilicus
Protuberant tongue
Poor brain development

238. hypothyroidism: subacute thyroiditis self-limiting


(de Quervain) follows flu-like illness
may be hyperthyroid early in
course

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239. hypothyroidism: subacute thyroiditis granulomatous inflammation
(de Quervain)
histology

240. hypothyroidism: subacute thyroiditis inc ESR


(de Quervain) jaw pain
findings early inflammation
tender thyroid

241. hypothyroidism: Riedel thyroiditis thyroid replaced by fibrous tis-


sue (hypothyroid), which may ex-
tend to local structures (e.g. air-
way)
mimics anaplastic carcinoma
is a manifestation of
IgG4-related systemic disease
(e.g. autoimmune pancreatitis,
retroperitoneal fibrosis, nonin-
fectious aortitis)

242. hypothyroidism: Riedel thyroiditis fixed, hard (rock-like), painless


findings goiter

243. hypothyroidism: other causes iodine insufficiency


goitrogens
Wolff-Chaikoff effect (thyroid
gland downregulation due to inc
iodine)

244. hyperthyroidism: most common cause Graves disease

245. hypertyroidism: Graves disease IgG stimulates TSH receptors


on...
1. thyroid (hyperthyroidism and
diffuse goiter)
2. retro-orbital fibroblasts (ex-
ophthalmos proptosis, extraocu-
lar muscle swelling)
3. dermal fibroblasts 9pretibial
myxedema)
29 / 52
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often presents during stress
(e.g. childbirth)

246. hyperthyroidism: toxic multinodular hoi- focal patches of hyperfunction-


ter ing follicular cells working in-
depenedently of TSH (mutated
TSH receptor)
inc T3, T4 release
hot nodules are rarely malignant

247. hyperthyroidism: thyroid storm stress-induced catecholamine


surge as serious complication
of thyrotoxicosis due to disease
and o/ hyperthyroid disorders

248. thyroid storm presentation agitation


delirium
fever
diarrhea
coma
tachyarrhythmia (cause of
death)
inc ALP due to inc bone turnover

249. thyroid storm treatment 3 P's:


beta-blockers (e.g. Propranolol)
Propylthiouracil
corticosteroids (e.g. Prenisone)

250. hyperthyroidism: Jod-Basedow phe- thyrotoxicosis if patient with io-


nomenon dine defiency goiter is made io-
dine replete

251. thyroidectomy is an option for___ thyroid cancer and hyperthy-


roidism

252. complications of thyroidectomy hoarseness (recurrent laryngeal


nerve damage)
hypocalcemia (parathyroid
gland removal)
30 / 52
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transection of recurrent and su-
perior laryngeal nerves (during
ligation of inferior thyroid artery
and superior laryngeal artery, re-
spectively)

253. papillary carcinoma most common thyroid cancer;


excellent prognosis
empty-appearing nuclei with
central clearing (Orphan Annie
eyes)
psammoma bodies
nuclear grooves
lymphatic invasion common
inc risk w/ childhood radiation,
RET and BRAF mutations

254. follicular carcinoma thyroid cancer w/ excellent prog-


nosis
invades capsule (unlike follicular
adenoma)
uniform follicles

255. medullary carcinoma a thyroid cancer


from parafollicular "C"
cells--->produces calcitonin,
sheets of cells in an amyloid
stroma
hematogenous spread common
associated with MEN 2A and 2B
(RET mutations)

256. undifferentiated/aplastic carcinoma of older patients


thyroid local structures
very poor prognosis

257. lymphoma of thyroid associated with Hashimoto thy-


roiditis

258.
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hypoparathyroidism
diagram

259. hypoparathyroidism causes accidental surgical excision


autoimmune destruction
DiGeorge syndrome

260. hypoparathyroidism findings hypocalcemia


tetany
Chvostek sign
Trousseau sign

261. Chvostek sign tapping facial nerve (tap Cheek)


-->facial muscle contraction

262. Trousseau sign occlusion of brachial artery with


BP cuff--->carpal spasm

263. pseudohypoparathyroidism aka - Albright hereditary os-


teodystrophy
unresponsiveness to kidney
PTH
hypocalcemia, shortened
4th/5th digits, short stature
AD

264. familial hypocalciuric hypercalcemia defective Ca2+-sensing recep-


tor on parathyroid cells
PTH cannot be suppressed
by inc [Ca2+]---->mild hypercal-
cemia with normal/inc PTH lev-
els

265. PTH and Ca2+ pathologies: hypoparathyroidism


low calcium, low PTH

266.

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PTH and Ca2+ pathologies: secondary hyperparathyroidism
low calcium, high PTH (Vit D deficiency, chronic renal
failure)

267. PTH and Ca2+ pathologies: PTH-independent hypercal-


high calcium, low PTH cemia
(excess Ca2+ ingestion, cancer)

268. PTH and Ca2+ pathologies: primary hyperparathyroidism


high calcium, high PTH (hyperplasia, adenoma, carcino-
ma)

269. hyperparathyroidism: primary parathyroid adenoma or hyper-


causes plasia

270. hyperparathyroidism: primary hypercalcemia


presentation hypercalciuria (renal stones)
hypophosphatemia
inc PTH
inc ALP
inc cAMP in urine
weakness and constipation
abdominal/flank pain (kidney
stones, acute pancreatitis)
depression

271. osteoitis fibrosa cystica cystic bone spaces filled with fi-
brous brown tissue
("brown tumor of deposited he-
mosiderin from hemorrhages;
bone pain)
associated with primary hyper-
parathyroidism

272. hyperparathyroidism: secondary secondary hyperplasia due to


causes dec Ca2+ absorption or inc
phosphate
Add... most often chronic renal dis-
ease (causes hypovitaminosis
D-->dec Ca2+ absorption)
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273. hyperparathyroidism: secondary hypocalcemia


presentation hyperphosphatemia in chronic
renal failure (hypophasphatemia
in most other causes)
inc ALP
inc PTH

274. renal osteodystrophy one lesions due to secondary


or tertiary hyperparathyroidism
(mainly due, in turn, to renal dis-
ease)

275. pituitary adenoma most commonly benign prolac-


toma
adenoma may be hormone-pro-
ducing (functional) or silent
(non-functional)

276. presentation of nonfunctional tumors mass effect (bitemporal


associated with pituitary adenoma hemianopia, hypopituitarism,
headache)

277. presentation of functional tumors asso- based on hormone produced,


ciated with pituitary adenoma e.g.:
1. prolactinoma: amenorrhea,
galactorrhea, low libido, infertility
2. somatotropic adenoma:
acromegaly

278. hyperparathyroidism: tertiary refractory (autonomous)


resulting from chronic renal dis-
ease
big inc PTH
inc Ca2+

279. acromegaly excess GH in adults

280. gigantism excess H in children


inc linear bone growth
34 / 52
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281. most common cause of death associat- HF


ed with gigantism

282. acromegaly large tongue with deep furrows


findings deep voice
large hands, feet
coarse facial features
impaired glucose toelrance (in-
sulin resistance)
increased risk colorectal polyps,
cancer

283. acromegaly inc serum IGF-1


diagnosis failure to suppress serum GH
following oral glucose tolerance
test
pituitary mass on brain MRI

284. acromegaly resection of pituitary adenoma


treatment of not cured: octreotide (somato-
statin analog) or pegvisomant
(GH receptor antagonist)

285. diabetes insipidus characteristics intense thirst


polyuria
inability to concentrate urine
lack of ADH (central) or failure
to respond to circulating ADH
(nephrogenic)

286. central DI: pituitary tumor


etiology autoimmune
trauma
surgery
ischemic encephalopathy
idiopathic

287. central DI: dec ADH


findings urine SG < 1.006
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serum osmolality: >290
mOsm/kg
hyperosmotic volume contrac-
tion

288. central DI: >50% inc in urine osmolality only


water deprivation test after ADH analog administration

289. central DI: intranasla desmopressin ac-


treatment etate
hydration

290. water deprivation test for diagnosis of DI


no water intake 2-3 hours fol-
lowed by hourly measurements
of uring vol/oslmolarity and plas-
ma Na+ conc. and osmolarity
if normal values are not clearly
reached: administer ADH analog
(desmopressin acetate)

291. nephrogenic DI: hereditary (ADH receptor muta-


etiology tion)
secondary to hypercalcemia,
lithium, demeclocycline (ADH
antagonist)

292. nephrogenic DI: normal ADH levels


findings urine SG< 1.006
serum osmolality > 290
mOsm/kg
hyperosmotic volume contrac-
tion

293. nephrogenic DI: minimal change in urine osmo-


water deprivation test lality, even after administration of
ADH analog

294. nephrogenic DI: HCTZ, indomethacin, amiloride


treatment hydration
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295. SIADH syndrome of inappropriate ADH


secretion:
excessive water retention
euvolemic hyponatremia with
continued urinary Na+ excretion
urine osmolality > serum osmo-
lality

296. SIADH causes extopic ADH (e.g. small cell lung


cancer)
CNS disorders/head trauma
pulmonary disease
drugs (e.g. cyclophosphamide)

297. SIADH treatment fluid restriction


IV hypertonic saline
conivaptan
tolvaptan
demeclocycline

298. SIADH: dec aldosterone (hyponatremia)


body response to the abnormal ADH se- to maintain near-normal volume
cretion and consequences of response --->cerebral edema, seizures

299. SIADH slowly


correct slowly or quickly? why? need to prevent osmotic de-
myelination syndrome (aka cen-
tral pontine myelinosis)

300. hypopituitarism causes nonsecreting pituitary adenoma


craniopharyngioma
Sheehan syndrome
Empty Sella syndrome
Pituitry Apoplexy
brain injury
radiation

301. hypopituitarism treatment hormone replacement therapy:


corticosteroids
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thyroxine
sex steroids
human GH

302. Sheehan syndome ischemic infarct of pituitary fol-


lowing postpartum bleeding
failure to lactate, absent men-
struation, cold intolerance
(cause of hypopituitarism)

303. empty sella syndrome atrophy or compression of pitu-


itary
often idiopathic
common in obese women
(cause of hypopituitarism)

304. pituitary apoplexy sudden hemorrhage of pituitary,


often in presence of existing pi-
tuitary adenoma
(cause of hypopituitarism)

305. acute manifestations of diabetes melli-


tus
diagram

306. maifestations of diabetes mellitus polydipsia


polyuria
polyphagia
weight loss
DKA (type I)
hyperosmolar coma (type 2)
rarely: unopposed GH and epi
secretion

307. what two conditions may cause unop- diabetes mellitus (rarely)
posed secretion of GH and epi? glucocorticoid therapy (steroid
diabetes)

308. 1. small vessel disease


--->retinopathy (hemorrhage,
38 / 52
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chronic complications of diabetes melli- exudates, microaneurysms, ves-
tus: sel proliferation), glaucoma,
nonenzymatic glycation neuropathy, nephropathy
2. large vessel atheroscle-
rosis, CAD, peripheral vas-
cular occlusive disease, an-
grene--->limb loss, cerebrovas-
cular disease--->MI/death (most
commonly)

309. nephropathy due to diabetes mellitus nodular goleruloscerosis (Kim-


causes____ melsteil-Wilson nodules)--->pro-
gressive proteinuria and ather-
osclerosis--->hypertension and
chronic renal failure

310. diabetes mellitus diagnosis fasting serum glucose


oral glucose tolerance test
HbA1c (reflects average blood
glucose over prior 3 months)

311. Diabetes mellitus: type 1 vs. type 2: 1. autoimmune beta cell dstruc-
primary defect tion
2. increased insulin resistance;
progressive pancreatic beta cell
failure

312. Diabetes mellitus: type 1 vs. type 2: 1. always


insulin necessary for treatment? 2. sometimes

313. Diabetes mellitus: type 1 vs. type 2: 1. <30 yrs


age (exceptions common) 2. >40 yrs

314. Diabetes mellitus: type 1 vs. type 2: 1. no


obesity association? 2. yes

315. Diabetes mellitus: type 1 vs. type 2: 1. weak (50% concordance w/


genetic predisposition identical twins); polygenic
2. strong (90% " "), polygenic

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316. Diabetes mellitus: type 1 vs. type 2: 1. yes (HLA-DR3, -DR4)
association w/ HLA system 2. no

317. Diabetes mellitus: type 1 vs. type 2: 1. severe


glucose intolerance 2. mild-moderate

318. Diabetes mellitus: type 1 vs. type 2: 1. high


insulin sensitivity 2. low

319. Diabetes mellitus: type 1 vs. type 2: 1. common


ketoacidosis 2. rare

320. Diabetes mellitus: type 1 vs. type 2: 1. dec


beta cell #s in islets 2. variable (with amyloid de-
posits)

321. Diabetes mellitus: type 1 vs. type 2: 1. dec


serum insulin level 2. variable

322. Diabetes mellitus: type 1 vs. type 2: 1. common


classic symptoms (polyuria, polydipsia, 2. sometimes
polyphagia, weight loss)

323. Diabetes mellitus: type 1 vs. type 2: 1. islet leukocytic infiltrate


histology 2. islet amyloid polypeptide
(IAPP) deposits

324. diabetic ketoacidosis inc insulin requirements from inc


causes stress (e.g. infection)
excess fat breakdown, ketogen-
esis from inc FAs--->ketone bod-
ies
usually type 1 diabetes (endoge-
nous insulin in type 2 prevents
lipolysis usually)

325. ketone bodies beta-hydroxybutyrate


acetoacetate

326.
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diabetic ketoacidosis Kussmaul respirations (rapid,
signs/symptoms deep breathing)
nausea/vomiting
abdominal pain
psychosis/delirium
dehydration
fruity breath odor (due to ex-
haled acetone)

327. diabetic ketoacidosis hyperglycemia


labs inc H+
dec HCO3- (inc anion gap meta-
bolic acidosis)
inc blood ketone levels
leokocytosis
kyperkalemia (depleted intracel-
lular K+ due to shift from dec
insulin; so total body is actually
K+ depleted)

328. diabetic ketoacidosis life-threatening mucormycosis


complications (usually Thizopus infection)
cerebral edema
cardiac arrhythmias
HF

329. diabetic ketoacidosis IV fluids


treatment IV insulin
K+ (to replete intracellular
stores)
glucose if necessary to prevent
hypoglycemia

330. glucagonoma (cause and signs/symp- tumor of pancreatic alpha


toms) cells--->
glucagon overproduction
dermatitis (necrolytic migrato-
ry erythema), diabetes (hyper-
glycemia), DVT, depression

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331. insulinoma tumor of pancreatic beta
cells-->insulin overproduc-
tion--->hypoglycemia
may see Whipple triad
dec. blood glucose, inc C-pep-
tide levels (vs. exogenous insulin
use)

332. Whipple triad 1. low blood glucose


2. symptoms of hypoglycemia
(e.g. lethargy, syncope, diplopia)
3. resolution of symptoms after
normalization of glucose levels

333. insulinoma treatment surgical resection

334. carcinoid syndrome caused by carcinoid tumors


causes (neuroendocrine cells), esp
metastatic bowel tumors, which
secrete hig levels of serotonin
(5-HT)
not seen if tumor is only in GI
tract (5-HT undergoes first-pass
metabolism in liver)

335. carcinoid syndrome recurrent disrrhea


presentation cutaneous flushing
asthmatic wheezing
right-sided valvular disease
inc 5-hydroxyindoleacetic acid
(5-HIAA) in urine
niacin deficiency (pellagra)

336. carcinoid syndrome treatment surgical resection


somatostatin analog (e.g. oc-
treotide)

337. most common malignancy of SI carcinoid syndrome

338.
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carcinoid syndrome: 1/3 metastasize
rule of 1/3s 1/3 present with 2nd malignancy
1/3 are multiple

339. Zollinger-Ellison syndrome gastrin-secreting tumor (gastri-


noma) of pancreas or duodenum
acid hypersecretion--->recurrent
ulcers in duodenum, jejunum
abdominal pain (peptic ulcer dis-
ease, distal ulcers)
darrhea (malabsorption)
+ secretin stimulation test
may be associated with MEN-1

340. secretin stimulation test for Zollinger-Ellison syndomre


+ if gastrin levels remain ele-
vated after secretin administra-
tion (normally inhibits gastrin re-
lease)

341. multiple endocrine neoplasias (MEN) in- AD


heritance

342. MEN-1 3 P's:


characteristics Parathyroid tumors
Pituitary tumors (prolactin or
GH)
Pancreatic endocrine tu-
mors (Zollinger-Ellison syn-
drome, insulinomas, VIPomas,
glucagonomas (rare)
MEN1 gene mutation

343. MEN1 gene function menin (tumor suppressor) en-


coded

344. MEN2A 2P's:


characteristics Parathyroid hyperplasia
Pheochromocytoma
medullary thyroid carcinoma
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(secretes calcitonin)
RET gene mutation (tyrosine ki-
nase receptor)

345. MEN2A and 2B are associated with ___ marfanoid habitus

346. MEN2B 1 P:
characteristics Pheochromocytoma
medullary thyroid carcinoma
(secretes calcitonin)
oral/intestinal ganglioneuro-
matosis (mucosal neuromas)
RET gene mutation (tyrosine ki-
nase receptor)

347. MEN 2A vs 2B (medullary thyroid cancer at


center of both shapes)

348. diabetes treatment: low-carb diet


type 1 insulin replacement

349. diabetes treatment: dietary modification and exer-


type 2 cise for weight loss
if lifestyle changes fail: insulin re-
placement

350. diabetes treatment: dietary modifications


gestational diabetes mellitus (GDM) exercise
insulin replacement if lifestyle
changes fail

351. insulin preparations: rapid acting


examples
44 / 52
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aspart
glulisine
lispro

352. insulin preparations: rapid acting binds insulin receptor (tyrosine


action kinase activity)
Liver: inc glucose stored as
glycogen
Muscle: inc glycogen, protein
synthesis, K+ uptake
Fat: TG storage

353. insulin preparations: rapid acting type 1 DM


clinical use type 2 DM
DM (postprandial glucose con-
trol)

354. insulin preparations: rapid acting hypoglycemia


toxicities rare hypersensitivity rxn

355. insulin preparations: short acting (regu- type 1 DM


lar) type 2 DM
clinical use GDM
DKA (IV)
hyperkalemia (+glucose)
stress hyperglycemia

356. insulin preparations: intermediate act- type 1 DM


ing (NPH) type 2 DM
clinical use GDM

357. insulin preparations: long acting detemir


examples glargine

358. insulin preparations: long acting type 1 DM


clinical use type 2 DM
GDM (basal glucose control)

359. oral hypoglycemia drugs: biguanides metformin


examples
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360. oral hypoglycemia drugs: biguanides exact mechanism unknown


acting dec gluconeogenesis
inc glycolysis
inc peripheral glucose uptake
(inc insulin sensitivity)

361. oral hypoglycemia drugs: biguanides oral


clinical use first-line therapy in type 2 DM
causes modest weight loss
can be used in pts without islet
function

362. oral hypoglycemia drugs: biguanides GI upset


toxicities lactic acidosis (contraindicated
in renal insufficiency; most seri-
ous side-effect)

363. oral hypoglycemia drugs: sulfonylureas First generation: chloro-


examples propamide, tolbutamide
Second generation: glimepiride,
glipizide, glyburide

364. oral hypoglycemia drugs: sulfonylureas close K+ channel in beta


action cell membrane--->depolariza-
tion--->insulin release via inc
Ca2+ influx

365. oral hypoglycemia drugs: sulfonylureas stimulate release of endoge-


clinical use nous insulin in type 2 DM
cannot be used for type 1 DM
because some islet cell function
is required

366. oral hypoglycemia drugs: sulfonylureas risk of hypoglycemia inc in renal


toxicities failure
1st generation: disulfiram-like ef-
fects
2nd generation: hypoglycemia

46 / 52
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367. oral hypoglycemia drugs: glitazones/thi- piolitazone
azolidinediones: rosiglitazone
examples

368. oral hypoglycemia drugs: glitazones/thi- inc insulin sensitivity in peripher-


azolidinediones: al tissue
action binds PPAR-gamma nuclear
transcription regulator

369. oral hypoglycemia drugs: glitazones/thi- monotherapy for type 2 DM or


azolidinediones: combined with biguanides/sul-
clinical use fonylureas

370. oral hypoglycemia drugs: glitazones/thi- weight gain


azolidinediones: edema
toxicity hepatotoxicity
HF
inc fracture risk

371. PPAR-gamma genes encode transcrip- FA storage


tion factors that activate genes for ___ glucose metabolism

372. PPAR-gamma activation causes inc ___ insulin


sensitivity and inc levels of ___ adiponectin

373. oral hypoglycemia drugs: GLP-1 exenatide


analogs liraglutide
examples

374. oral hypoglycemia drugs: GLP-1 dec insulin relase


analogs inc glucagon release
action

375. oral hypoglycemia drugs: GLP-1 type 2 DM


analogs
clinical use

376. oral hypoglycemia drugs: GLP-1 nausea


analogs vomiting
toxicities pancreatitis
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377. oral hypoglycemia drugs: DPP-4 in- linagliptin


hibitors sexagliptin
examples sitagliptin

378. oral hypoglycemia drugs: DPP-4 in- inc insulin release


hibitors dec glucagonrelease
action

379. oral hypoglycemia drugs: DPP-4 in- type 2 DM


hibitors
clinical use

380. oral hypoglycemia drugs: DPP-4 in- mild urinary or respiratory infec-
hibitors tions
toxicities

381. oral hypoglycemia drugs: amylin pramlinitide


analogs
example

382. oral hypoglycemia drugs: amylin dec gastric emptying


analogs dec glucagon
action

383. oral hypoglycemia drugs: amylin types 1 and 2 DM


analogs
clinical use

384. oral hypoglycemia drugs: amylin hypoglycemia


analogs nausea
toxicities diarrhea

385. oral hypoglycemia drugs: SGLT-2 in- canagliflozin


hibitors
example

386. oral hypoglycemia drugs: SGLT-2 in- block glucose reabsorption in


hibitors PCT
action

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387. oral hypoglycemia drugs: SGLT-2 in- type 2 DM
hibitors
clinical use

388. oral hypoglycemia drugs: SGLT-2 in- glucosuria


hibitors UTIs
toxicities vaginal yeast infections

389. oral hypoglycemia drugs: alpha-glucosi- acarose


dase inhibitors miglitol
examples

390. oral hypoglycemia drugs: alpha-glucosi- inhibit brush border alpha-glu-


dase inhibitors cosidases
action delayed carb hydrolysis and glu-
cose absortion---> dec post-
prandial hyperglycemia

391. oral hypoglycemia drugs: alpha-glucosi- monotherapy for type 2 DM or


dase inhibitors combined with other oral hypo-
clinical use glycemic drugs

392. oral hypoglycemia drugs: alpha-glucosi- GI disturances


dase inhibitors
toxicities

393. propylthiouracil, methimazole: block thyroid peroxidase-->I ox-


mechanism idation/organification (coupling)
inhibited--->inhibition of thyroid
hormone synthesis
propylthiouracil also blocks
5'-deiodinase--->dec T4 to T3
conversion in peripheral tissues

394. propylthiouracil, methimazole: hyperthyroidism


clinical use propylthiouracil used in preg-
nancy

395. propylthiouracil, methimazole: skin rash


toxicities agranulocytosis (rare)
49 / 52
USMLE Endocrine
Study online at https://quizlet.com/_33yr8j
aplastic anemia
hepatotoxicity (propylthiouracil)
teratogen (methimazole; aplasia
cutis)

396. levothyroxine (T4), triiodothyronine (T3): thyroid hormone replacement


mechanism

397. levothyroxine (T4), triiodothyronine (T3): hypothyroidism


clinical use myxedema
used off-label as weight-loss
supplements

398. levothyroxine (T4), triiodothyronine (T3): tachycardia


toxcitity heat intolerance
tremors
arrhythmias

399. hypothalamic/pituitary drugs: ADH ago- conivaptan


nists tolvaptan
examples

400. hypothalamic/pituitary drugs: ADH ago- SIADH


nists block action of ADH at V2 recep-
clinical use tor

401. hypothalamic/pituitary drugs: desmo- central (not nephrogenic) DI


pressin acetate
clinical use

402. hypothalamic/pituitary drugs: GH GH deficiency


clinical use Turner syndrome

403. hypothalamic/pituitary drugs: oxytocin stimulates labor, uterine contrac-


clinical use tions, milk let-down
controls uterine hemorrhage

404. hypothalamic/pituitary drugs: somato- acromegaly


statin (octreotide) carcinoid syndrome
clinical use gastrinoma
50 / 52
USMLE Endocrine
Study online at https://quizlet.com/_33yr8j
glucagonoma
esophageal varices

405. demeclocycline: ADH antagonist (member of


mechanism tetracycline family)

406. demeclocycline: SIADH


clinical use

407. demeclocycline: nephrogenic DI


toxicity photosensitivity
bone/teeth abnormalities

408. glucocorticoids: beclomethasone


examples dexamethasone
fludrocortisone (also has miner-
alcorticoid activity)
hydrocortisone
methylprednisone
prednisone
triamcinolone

409. glucocorticoids: metabolic, catabolic, anti-inflam-


mechanism matory, immunosuppresive ef-
fects mediated by interactions
w/ glucocorticoid response ele-
ments
phospholipase A2 inhibition
inhibition of transcription factors
such as NK-kB

410. glucocorticoids: Addison disease


clinical use inflammation
immunosuppression
asthma

411. glucocorticoids: Iatrogenic Cushing syndrome


toxicity adrenalcortical atrophy
peptic ulcers
steroid diabetes
51 / 52
USMLE Endocrine
Study online at https://quizlet.com/_33yr8j
steroid psychosis
adrenal insufficiency (when drug
stopped abruptly after chronic
use)

412. presentation of Iatrogenic Cushing syn- hypertension


drome weight gain
moon facies
truncal obesity
buffalo hump
thinning of skin
striae
osteoporosis
hyperglycemia
amenorrhea
immunosuppression

413. cinacalcet: sensitizes Ca2+-sensing recep-


mechanism tor (CaSR) in parathyroid gland
to circulated Ca2+ ---> dec PTH

414. cinacalcet hypercalcemia due to primary or


clinical use secondary hyperparathyroidism

415. cinacalcet hypocalcemia


toxicity

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