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USMLE > Endocrine > Flashcards

Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

Embryological origin of thyroid, parathyroid and pancreas

A

Endoderm

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2
Q

Embryological origin of hypothalamus, anterior pituitary, posterior pituitary, adrenal medulla, and C cells of thyroid

A

Ectoderm

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3
Q

Embryological origin of adrenal cortex and gonads

A

Mesoderm

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4
Q

Zona glomerulosa responds to and secretes

A

Renin-angiotensin; Aldosterone

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5
Q

Zona Fasciculata responds to and secretes

A

ACTH, CRH; Cortisol

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6
Q

Zona Reticularis responds to and secretes

A

ACTH, CRH; sex hormones (androgens)

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7
Q

Chromaffin cells of adrenal medulla respond to and secrete

A

Preganglionic sympathetic fibers; Catecholamines (Epinephrine)

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8
Q

Which four hormones share a common alpha subunit?

A

TSH, FSH, LH, hCG

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9
Q

Which anterior pituitary hormones are basophiles?

A

FSH, LH, ACTH, TSH

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10
Q

Which part of the hypothalamus produces vasopressin (AVP/ADH)?

A

Supraoptic nucleus

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11
Q

Paraventricular nucleus of hypothalamus forms which hormone

A

Oxytocin

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12
Q

Which Glucose transporter is Insulin-dependent

A

GLUT-4

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13
Q

Where are GLUT-4 transporters located

A

Adipose tissue and striated muscle tissue

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14
Q

Name the Insulin-independent GLUT transporters

A

GLUT-1, 2, 3, 5

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15
Q

Where is GLUT-1 found

A

Brain, RBCs, cornea, placenta

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16
Q

Where is GLUT-2 found and why is it special

A

pancreatic beta cells, liver, kidney, small intestine; bidirectional glucose transport

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17
Q

Where is GLUT-3 found

A

brain, placenta

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18
Q

Where is GLUT-5 (Fructose) found

A

spermatocytes, GI tract

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19
Q

What are the insulin-independent glucose organs

A

Brian, RBCs, Intestine, Cornea, Kidney and Liver

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20
Q

does insulin cross the placenta

A

No

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21
Q

Does glucagon cross placenta

A

yes

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22
Q

Why do you have greater insulin release with oral intake of glucose?

A

Incretins like GLP-1 are released after meals ad increase beta cell sensitivity to glucose via GLUT-2

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23
Q

Which hormone increases release of ACTH, MSH and beta-endorphins

A

CRH released by hypothalamus

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24
Q

Which hormone is inhibited by chronic steroid use

A

CRH

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25
Q

Which hormone decreases prolactin and TSH

A

Dopamine

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26
Q

How do dopamine antagonists (anti-psychotics) cause galactorrhea?

A

They decrease inhibition of prolactin

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27
Q

Where in the hypothalamus is CRH synthesized

A

paraventricular nucleus

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28
Q

Where in hypothalamus are dopamine and GHRH synthesized

A

Arcuate nucleus

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29
Q

Function of GHRH

A

Stimulate release of GH from Anterior pituitary

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30
Q

The analog (tesamorelin) of which hormone is used to treat HIV-associated lipodystrophy?

A

GHRH

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31
Q

From where is GnRH released?

A

medial-preoptic nucleus

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32
Q

What is the difference between tonic and pulsatile release of GnRH

A

Tonic release suppresses HPG axis while pulsatile leads to puberty and fertility by increasing FSH and LH release

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33
Q

Which hormone inhibits GnRH

A

Prolactin

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34
Q

Signs of pituitary prolactinoma

A

amenorrhea, osteoporosis, hypogonadism and galactorrhea

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35
Q

Which hormone decreases release of GH and TSH

A

Somatostatin

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36
Q

Which hormone increases release of TSH and prolactin

A

TRH

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37
Q

Which hormone is prolactin structurally similar to

A

Growth hormone

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38
Q

Stimulates milk production, inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH

A

Prolactin

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39
Q

Excess is associated with decreased libido

A

Prolactin

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40
Q

How can primary or secondary hypothyroidism cause prolactinemia?

A

TRH stimulates prolactin secretion

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41
Q

GH + IGF-1 lead to which changes

A

increaesd linear and muscle growth, increased insulin resistance

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42
Q

When is growth hormone secretion increased

A

Exercise, deep sleep, puberty, hypoglycemia

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43
Q

Where is Ghrelin-produced

A

stomach

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44
Q

Which two conditions increase Ghrelin production

A

sleep deprivation and Prader-Willi syndrome

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45
Q

Which tissue produces leptin

A

Adipose tissue

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46
Q

Where do endocannabinoids act

A

Hypothalamus or nucleus accumbens (food intake)

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47
Q

How can exogenous corticosteroids cause reactivation of TB and candidiasis

A

Decrease IL-2 secretion and suppress immune response

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48
Q

How does cortisol suppress the immune response

A

Inhibits LTE and PGE release, inhibits WBC adhesion, inhibits Histamine release from mast cells, decreases eosinophils, inhibits IL-2 production

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49
Q

How does alkalosis cause hypocalcemia

A

Increases affinity of serum Ca+2 for albumin

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50
Q

Symptoms of hypocalcemia

A

cramps pain, parasthesia, carpopedal spasms, Chvostek and Trosseau sign

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51
Q

What is the function of Active Vitamin D (1,25-OH2)

A

Increase absorption of Ca+2 and PO4 in gut

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52
Q

What is the source of PTH?

A

Chief cells of parathyroid

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53
Q

Four common causes of Magnesium loss

A

Aminoglycasides, diarrhea, alcohol abuse and diuretics

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54
Q

Four functions of PTH

A

Increse bone resorption of Ca+2 and PO4
Increase kidney reabsorption of Ca+2 in DCT
decrease reabsorption of PO4 in PCT
increase calcitriol production by stimulating kidney 1 alpha-hydroxylase in PCT

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55
Q

Which three factors increase PTH secretion?

A

decrease Ca+2, decrease Mg+2(initially, substantial decrease inhibits it), increase PO4

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56
Q

What is the source of calcitonin

A

Parafollicular (C) cells of thyroid

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57
Q

What is the function of calcitonin

A

oppose actions of PTH by decreasing bone resorption of Ca+2

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58
Q

What is the major function of thyroid hormone

A

Regulate body’s metabolic rate

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59
Q

Which factors increase and decrease TBG respectively

A

increase: pregnancy and OCP (estrogen)
decrease: hepatic failure, steroids

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60
Q

What is the Wolff-Chaikoff effect

A

excess iodine temporarily inhibits TPO leading to decreased T3/T4

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61
Q

Which hormones use the cAMP signaling pathway (FLAT ChAMP)

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHRH, glucagon

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62
Q

Which hormones use the cGMP pathway BAD GraMPa

A

BNP, ANP, EDRF (NO)

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63
Q

Which hormones use the IP3 pathway? (GOAT HAG)

A

GnRH, Oxytosin, ADH (V1R), TRH, Histamine, Angiotensin II, Gastrin

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64
Q

Which hormones use Receptor Tyrosine Kinase? (MAP kinase pathway)

A

Insulin, IGF-1, FGF, PDGF, EGF (growth factors)

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65
Q

Which hormones use Nonreceptor Tyrosine Kinase (PIGGlET- acidophiles and cytokines) – JAK/STAT pathway

A

Prolactin, immunomodulators (cytokines IL-2, IL-6, IFN), GH, G-CSF, EPO, TPO

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66
Q

What does increased sex hormone binding globulin cause in men?

A

Gynecomastia

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67
Q

What does decreased sex hormone binding globlulin cause in women?

A

Hirsuitism

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68
Q

Symptoms of Sheehan syndrome

A

Fatigue, loss of pubic hair, and poor lactation after giving birth (preceded by blood loss)

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69
Q

Etiology of Sheehan Syndrome

A

Pituitary grows in pregnancy, blood supply cannot meet demand and leads to pituitary infarct

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70
Q

Which drugs can cause nephrogenic diabetes insipidus?

A

Lithium and demeclocycline

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71
Q

Most common cause of SIADH

A

Small cell carcinoma in the lung

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72
Q

What condition does demecocyline treat?

A

SIADH

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73
Q

Clinical features of SIADH

A

Hypertension, Isovolemic hyponatremia and low serum osmolality
Mental status changes and seizure s

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74
Q

Which part of the neck does thyroglossal duct cyst present

A

Anterior neck mass

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75
Q

Thyrogloossal duct cyst is a failure of

A

Involution

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76
Q

Where does lingual thyroid present

A

Base of tongue

77
Q

Four Bs of thyroid function

A

Basal metabolic rate
Brain growth
Bone growth
beta-adrenergic receptor expression increase

78
Q

What causes increased BMR in hyperthyroidism?

A

Excess thyroid hormone causes production of more Na+/K+ ATPase

79
Q

Lid lag is specific for which thyroid condition

A

Graves disease

80
Q

What is thyrotoxic myopathy

A

Proximal muscle weakness with normal CK, seen in hyperthyroidism

81
Q

Four causes of nodular goiter

A

Toxic multinodular goiter
Thyroid adenoma
Thyroid cancer
Thyroid cyst

82
Q

Four causes of smooth/diffuse goiter

A

Graves disease
Hashimoto Thyroiditis
Iodine deficiency
TSH-secreting pituitary adenoma

83
Q

What cause exophthalmos and pretibial myxedema in Graves disease

A

Fibroblasts behind orbit and shin express TSH receptor, which is overstimulated and produces GAGs, fibrosis and edema buildup

84
Q

What causes hypcholesterolemia in hypothyroidism

A

Increase bile excretion and increased LDL gene receptor activity (even though HMG CoA Reductase activity increases)

85
Q

Common clinical features of hyperthyroidism

A

Heat intolerance, weight loss, increase appetite, hyperactivity, anxiety, insomnia, hand tremor
brisk reflexes, diarrhea, myxedma, chest palpitations/arrhythmias, hypocholesterolemia

86
Q

Lab findings of hyperthyroidism

A

Decreased TSH if primary (Graves), increased free or total T3, T4; hypocholesterolemia

87
Q

What causes diffuse goiter appearance in Graves disease

A

Constant TSH stimulation by IgG leads to thyroid hyperplasia and hypertrophy

88
Q

What type of hypersensitivity reaction is Graves disease

A

Type II

89
Q

How does pregnancy affect thyroid levels

A

Increases TBG so increases total thyroid levels since more T4 binds to it, but does not increase free T3 or T4

90
Q

How does Graves cause hyperglycemia

A

Stimulates gluconeogenesis and glycolysis

91
Q

What causes a thyroid storm and what is its treatment

A

Elevated catecholamines in hyperthyroid patient during stress (surgery, childbirth); tx is PTU

92
Q

Symptoms of thyroid storm

A

Arrhythmia, hyperthermia, vomiting and hypovolemic shock

93
Q

Which test is best for screening thyroid dysfunction?

A

TSH

94
Q

Usual cause for nodular goiter

A

Iodine deficiency

95
Q

What is the function of Iodine-123 uptake test?

A

Evaluate acitivity of thyroid gland
Increased uptake = hot nodule (increased TH synthesis)
Decreased uptake = cold nodule

96
Q

Mental retardation, enlarged tongue, short stature, skeletal abnormalities and short stature in a child are indiicative of

A

Cretinism

97
Q

What causes cretinism in neonates and infants

A

Hypothyroidism of mother in early pregnancy; need thyroid hormone for normal brain devo and skeletal devo

98
Q

Clinical feature of myxedema in hypothyroidism

A

Deep voice, large tongue (GAG accumulation in soft tissue and skin)

99
Q

General symptoms of hypothyroidism

A

cold intolerance, weight gain, constipation, facial/periorbital myxedema, dry skin and brittle hair, bradycardia

100
Q

What is hypothyroid myopathy

A

proximal muscle weakness with increased CK

101
Q

Lab findings in hypothyroidism

A

increased TSH (if primary.. Hashimoto); decreased free T3, T4, hypercholesterolemia

102
Q

Presentation of myxedema coma

A

Progressive stupor, hypothermia, bradycardia, hypoglycemia, hypocortisolism, SIADH

103
Q

Findings of pheochromocytoma

A

increased catecholamines and metanephrines in urine and plasma

104
Q

Treatment for Pheochromocytoma

A

Phenoxybenzamine (irreversible alpha antagonist) followed by beta-blocker

105
Q

What type of hypersensitivity reaction is Hashimoto thyroiditis

A

Type 2 or Type 4

106
Q

3 clinical features of Hashimoto Thyroiditis

A

Initial presentation of hyperthyroidism due to follicle damage
Progresses to hypothyroidism; decreased T4, increased TSH
Anti-thyroglobulin and antiTPO antibodies

107
Q

Hurthle cells are inidicative of which condition

A

Hashimoto thyroiditis

108
Q

Hashimoto thyroiditis increases risk of which lymphoma

A

B cell marginal zone lymphoma (presents as enlarging thyroid gland in late disease)

109
Q

Characteristic feature of De Quearvain (Acute) Thyroiditis

A

Tender thyroid with symptoms of hyperthyroidism following a viral infection; self-resolving

110
Q

Histology of Hashimoto

A

Lymphocytic germinal centers/infiltration with Hurthle cells (eosinophilic large cells)

111
Q

Histology of De Quervain thyroiditis

A

Granulomatous inflammation with multinucleated giant cells, decreased I-123 uptake

112
Q

“Hard as wood” nontender thyroid gland is indicative of

A

Riedel fibrosiing thyroiditis

113
Q

What is the risk of Riedel fibrosing thyroiditis

A

Fibrosis may extend to airway and lead to shortness of breath; treat wit corticosteroids or tamoxifen

114
Q

What causes Hashimoto thyroiditis?

A

Autoimmune destruction of thyroid gland; associated with HLA-DR5

115
Q

Most commmon cause of Cretinism in US

A

Thyroid dysgenesis

116
Q

6 Ps of cretinism

A

Pot-bellied, Pale, Puffy face, Protruding uumbilicus, Protruding tongue, Poor brain development

117
Q

4Ps to treat Thyroid Storm

A

Propanolol, PTU, Prednisolone, Potassium iodide

118
Q

What is Jod-Besedown phenomenon

A

Giving iodine to pt who has iodine deficiency but hot thyroid nodule causes thyrotoxicosis

119
Q

Why do cold nodules warrant biopsy

A

They are usually seen in adenoma or carcinoma

120
Q

What is Orphan Annie Eye cell and what is it indicative of?

A

Cell with white clearing center of nucleus and nuclear groove; indicates Papillary carcinoma

121
Q

What are Psammoma bodies indicative of

A

Papillary carcinoma

122
Q

How does follicular thyroid carcinoma spread

A

Hematogenously

123
Q

Medullary carcinoma of thyroid is associated with which gene mutation?

A

RET (MEN2A, MEN2B)

124
Q

What is the MEN2A triad

A

Medullary carcinoma, pheochromocytoma, parathyroid adenoma

125
Q

What is the MEN2B triad

A

Medullary carcinoma, pheochromocytoma, ganglioneuroma of oral mucosa

126
Q

Medullary carcinoma is malignant spread of which cells

A

Parafollicular C cells (Secrete calcitonin, lowers serum calcium)

127
Q

Histology of medullary carcinoma of thyroid

A

Calcitonin cell deposits in amyloid stroma (a bunch of purple cells surrounded by pink)

128
Q

Anaplastic carcinoma is a poor prognosis malignant thyroid cancer seen in which population

A

Elderly (prsents as dysphagia or respiratory compromise)

129
Q

Lab findings for primary hyperparathyroidism

A

Increased: PTH, calcium, urine CAMP, alkaline phosphatase
Decreased: phosphate

130
Q

Potential complications of hyperparathyroidism due to hypercalcemia

A

Nephrolithiasis (calcium oxalate), nephrocalcinosis (renal insufficiency and polyuria)
CNS disturbances, constipation, acute pancreatitis, steitis fibrosa cystica

131
Q

How can hyperparathyroidism lead to acute pancreatitis

A

Ca+2 activates pancreatic enzymes (zymogens) within pancreas, causing damage

132
Q

Autosomal dominant Pseudohypoparathyroidism presents as

A

Hypocalcemia, increased PTH, mutation in Gs, short stature, short 4th and 5th digits

133
Q

Short 4th and 5th digits with hypocalcemia likely indicate

A

Pseudohypoparathyroidism

134
Q

“Stones, bones, groans and psychatric overtones” applies to

A

Primary hyperparathyroidism

135
Q

Osteoclasts and deposited hemosiderin from hemorrhages “brown tumor” is indicative of

A

Osteitis fibrosa cystica from hyperparathyroidism

136
Q

What causes type 1 diabetes mellitus

A

Autoimmune destruction of beta cells (antibodies against glutamic acid decarboxyalse)

137
Q

What type of hypersensitivy reaction is T1DM

A

Type IV

138
Q

Best diet advice for T2DM

A

Control fat intake and weight control

139
Q

Clinical findings of MEN1

A

Pituitary adenoma, hyperparathyroidism, pancreatic tumors

140
Q

Tumor of islet cells is associated with which condition

A

MEN1

141
Q

Watery diarrhea, hypokalemia and achlorydia suggest which pancreatic neoplasm

A

VIPoma

142
Q

Treatment-resistant ulcers extending into jejunum suggest which pancreatic neoplasm

A

gastrinoma

143
Q

Achlorydia and cholelithiasis with steatorrhea are suggestive of which pancreatic neoplasm?

A

Somatostatinoma

144
Q

Hypertension, hypokalemia and metabolic alkalosis suggest which condition

A

Hyperaldosteronism

145
Q

Aldosterone function

A

Increase sodium reabsorption in PCT, increase K+ secretion in DCT/CCT

146
Q

Most common cause of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia, and adrenal adenoma (Connn syndrome)

147
Q

Difference between primary and secondary hyperaldosteronism

A

Primary has low renin and high aldosterone, secondary has high renin and high aldosterone

148
Q

AD excess expression of aldosterone synthase in fasciculata

A

Familial hyperadosteronism

149
Q

Clinical presentation of familial hyperaldosteronism

A

HTN, hypokalemia and high aldosterone with low renin in children. Responds to dexamethasone

150
Q

Why do you get diffuse skin pigmentation in 21-hydroxylase deficiency?

A

Body isn’t producing cortisol or aldosterone, so increased ACTH activity

151
Q

Males with ambiguous genitalia at birth and hypokalemic hypertension suggest which CAH

A

17-alpha-hydroxylase deficiency

152
Q

A girl who has no secondary sexual development and presents with hypokalemic hypertension most likely has

A

17-alpha-hyrdoxylase deficiency

153
Q

Which CAH is most common

A

21-hydroxylase deficiency

154
Q

Decreased mineralocorticoids and decreased glucocorticoids with increased sex hormones indicates which CAH

A

21 hydroxylase deficiency

155
Q

Ambiguous female genitalia and precocious puberty in both sexes implies which two CAHs

A

11-beta-hydroxylase deficiency or 21-hydroxylase deficiency

156
Q

Why is edema absent in hyperaldosteronism induced hypertension?

A

Aldosterone escape mechanism causes natriuresis

157
Q

First-line treatment for hyperaldosteronism

A

Spironolactone or eplerenone

158
Q

What is Liddle syndrome

A

AD, decreased degradation of Na channels in collecting duct, leading to hyperaldosteronism-like symptoms (hypokalemia, hypernatremia, hypertension, metabolic alkalosis in young patient)

159
Q

Lab values of aldosterone and renin in Liddle syndrome

A

low aldosterone and low renin

160
Q

Treatment for Liddle syndrome

A

Potassium-sparing diuretics (triamterene and amiloride), block Na+ channels in CCT

161
Q

Which gene mutations increase risk of papillary carcinoma?

A

RET and BRAF

162
Q

How is pseudohypoparathyroidism inherited?

A

Through mother by imprinting

163
Q

How is pseudopseudohypoparathyroidism inherited and how is it different from pseudohypoparathyroidism?

A

Inherited from father due to imprinting. No end-organ PTH resistance

164
Q

How does hypercortisolism lead to hypertension and hypokalemia

A

Cortisol increases peripheral vascular sensitivity to catecholamines (constriction) and at high levels can cross react with aldosterone receptors

165
Q

Muscle weakness with thin extremities, moon facies, buffalo hump, purple striae, truncal obesity, hypertension with metabolic alkalosis, oosteoporsis and immune suppression indicate

A

Hypercortisolism

166
Q

How does hypercortisolism (Cushing syndrome) lead to immune suppression?

A

Inhibits phospholipase A2, IL-2 and Histamine

167
Q

Diagnosis of Cushing syndrome

A

1) 24-hour urine cortisol (increased)
2) late-night salivary cortisol level (increased)
3) Low-dose dexamethosone suppression test

168
Q

What is the purpose of plasma ACTH test

A

Distinguishes ACTH-dependent causes of Cushing syndrome from ACTH-independent

169
Q

Difference between low-dose and high-dose dexamethosone test

A

Low-dose suppresses cortisol in normal individuals

High-dose suppresses ACTH production by pituitary adenoma but not by ectopic source

170
Q

Difference between Cushing syndrome and Cushing disease

A

Cushing syndrome is hypercortisolism in general, Cushing disease is hypercortisolism caused by pituitary adenoma

171
Q

Why does hypercortisolism cause weak, thin extremities

A

Breaks down muscle to release amino acids for gluconeogenesis

172
Q

Why does hypercortisolism cause buffalo hump, moon facies, and truncal obesity?

A

Increases insulin resistance, and storage of fat centrally

173
Q

Why does hypercortisolism cause purple striae?

A

Impaired collagen synthesis leads to thinning of skin

174
Q

Hypotension, hyperpigmentation, vomiting, diarrhea and hyperkalemia and hyponatremia suggest which adrenal insufficiency disorder?

A

Addison disease (destruction of adrenal glands)

175
Q

Most common cause of Addison disease in developing world

A

TB

176
Q

Which three hormones does POMC produce?

A

beta-endorphins, ACTH, MSH (melanin)

177
Q

3 gene mutations associated with pheochromocytoma

A

MEN2, VHL, NF1

178
Q

What is the mechanism of phenoxybenzamine?

A

irreversible alpha blocker

179
Q

Why is phenoxybenzamine used before adrenal medulla excision

A

catecholamines can leak out during excision surgery and cause hypertensive crisis so phenoxybezamine prevents this

180
Q

Inheritance of MEN syndromes

A

Autosomal dominant

181
Q

Pheochromocytoma, Medullary thyroid carcinoma, Mucosal neuromas

A

MEN2B

182
Q

Which MEN is associated with marfanoid habitus

A

MEN2B

183
Q

Parathyroid hyperplasia, pheochromocytoma, Medullary thyroid carcinoma

A

MEN2A

184
Q

Pituitary tumors, Pancreatic endocrine tumors (ZE syndrome, insulinomas, VIPomas), Parathyroid adenomas

A

MEN1

185
Q

Diagnosis of acromegaly

A

Increased serum IG-1, failure to suppress GH with oral glucose tolerance test, pituitary mass on MRI

186
Q

Laron syndrome features

A

Saddle nose, prominent forehead, small head circumference, short height, small genitalia, delayed skeletal maturation
increase GH but decreased IGF-1

187
Q

What is the most common cause of death in children with Gigantism?

A

heart failure

188
Q

A patient comes in complaining of a painful rash involving her groin and legs that has been worsening over time. Her PMH includes diabetes mellitus and occasional loose stools (GI sx). The rashes are erythematous plaques with crusting and scaling at borders. They are necrolytic and migratory. This suggests which condition?

A

Glucagonoma (pt will have hyperglycemia)

USMLE (36 decks)

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