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Step 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What receptors on what cells lead to NO release when stimulated?

A

Muscarinic receptors on endothelial cells

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2
Q

Most pituitary hormones act via cAMP-linked receptors. Which ones dont and how do they work?

A

GnRH, Oxytocin, and ADH act via IP3 system. Prolactin and GH act via JAK/STAT tyrosine kinases

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3
Q

Steroid hormones bind their receptors in the cytoplasm and translocate to the nucleus. What is the exception to this?

A

Thyroid hormones bind their receptor in the nucleus

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4
Q

What inhibits uptake and organification of iodide?

A

Anions (perchlorate, pertechnetate) inhibit uptake and excess iodine (Wolff-Chaikoff effect) inhibits organification

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5
Q

Why are beta blockers helpful in hyperthyroidism?

A

Combat sympathetic effects (except increased o2 demand and weight loss) and they decrease peripheral T4 to T3 conversion

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6
Q

Give the change in cortisol levels in the following conditions during a dexamethasone test (give low dose first then high dose): normal, ACTH-pituitary tumor, ectopic ACTH-producing tumor, cortisol-producing tumor

A

Normal - up (high dose not done). ACTH-pituitary tumor - up down. Ectopic ACTH-producing tumor - up up. Cortisol producing tumor - up up.

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7
Q

Conns syndrome

A

Primary hyperaldosteronism

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8
Q

Causes of waterhouse-friederichsen syndrome

A

Neisseria meningitidis septicemia, DIC, endotoxic shock

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9
Q

Test of choice to diagnose pheochromocytoma

A

Urinary VMA or metanephrines

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10
Q

Treatment for pheochromocytoma

A

Alpha antagonists (esp phenoxybenzamine) and surgery

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11
Q

Most common extracranial neoplasm in children

A

Neuroblastoma

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12
Q

Non-rhythmic eye movements with myoclonus (opsoclonus-myoclonus) in child

A

Neuroblastoma

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13
Q

Test of choice for neuroblastoma

A

HVA (breakdown product of dopamine)

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14
Q

What genetic change is associated with neuroblastoma

A

N-myc overexpression signals rapid tumor progression

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15
Q

Spinal cord compression, pancytopenia, hepatomegaly, palpable nodules, proptosis, truncal ataxia

A

Neuroblastoma

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16
Q

Hypotension, tachycardia, hypoglycemia, with existing history of vomiting abdominal pain and weight loss

A

Acute adrenal crisis (will occur in patients with adrenal insufficiency during stress)

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17
Q

Increased risk of what cancer in hashimotos thyroiditis

A

Non-hodgkin lymphoma

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18
Q

Histology of Hashimotos thyroiditis

A

Lymphocytic infiltrate with germinal centers with Hurthle cells. Thyroid will be moderately enlarged and nontender

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19
Q

Cretinism

A

Defect in T4 formation or developmental failure in thyroid formation

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20
Q

Pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue

A

Cretinism

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21
Q

Self-limited hypothyroidism following flulike illness

A

Subacute (de Quervain) thyroiditis. Will see granulomatous inflammtion, jaw pain, tender thyroid

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22
Q

Riedels thyroiditis

A

Thyroid replaced by fibrous tissue (hypothyroid). Will find fixed, hard painless goiter

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23
Q

What do you have to rule out if you suspect Riedels thyroiditis?

A

Iodine deficiency, thyroglossal duct cyst, goitrogens, Wolff-Chaikoff effect

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24
Q

Treatment for Graves

A

Glucocorticoids to reduce inflammation

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25
Q

What is another name for De Quervains Thyroiditis?

A

Granulomatous thyroiditis. (also subacute thyroiditis)

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26
Q

Give the histology of each of the following thyroid cancers: papillary, follicular, medullary

A

Papillary - ground glass nuclei, psammoma bodies, nuclear grooves. Follicular - uniform follicles. Medullary - sheets of cells in amyloid stroma

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27
Q

What type of bone changes do you see in hyperparathyroidism?

A

Subperiosteal reabsorption with cystic degeneration

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28
Q

What is osteitis fibrosa cystica associated with?

A

Primary hyperparathyroidism

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29
Q

What GI abnormality is primary hyperparathyroidism associated with?

A

Constipation

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30
Q

What is required to diagnose complete central DI?

A

An increase of 50 percent or greater in urine osmolality on DDAVP administration

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31
Q

Lab findings in prolactinoma

A

Decreased GnRH, decreased LH, decreased testosterone

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32
Q

One difference in symptoms between pheochromocytoma and neuroblastoma

A

Pheochromocytoma causes episodic hypertension

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33
Q

To where do the left and right adrenal veins respectively drain?

A

Left - left renal. Right - IVC

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34
Q

What do neurophysins do and what does their deficiency cause?

A

Carry ADH and oxytocin from hypothalamus to posterior pituitary. Deficiency leads to central DI

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35
Q

What are the posterior and anterior pituitary respectively derived from?

A

Posterior (neurohypophysis) - Neuroectoderm, Anterior (adenohypophysis) - Oral ectoderm (Rathkes pouch)

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36
Q

What do the acidophils and basophils of the pituitary gland make?

A

Acidophils - GH, prolactin. Basophils - FSH, LH, ACTH, TSH

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37
Q

What organs dont need insulin for glucose uptake?

A

Brain, RBCs, Intestine, Cornea, Kidney, Liver

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38
Q

What type of transport do GLUT transporters carry out, and what is their specificity for?

A

Facilitated diffuse for D-glucose

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39
Q

What type of receptor is the insulin receptor?

A

RTK

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40
Q

What protein gets activated as a result of insulin receptor stimulation in hepatocytes?

A

Protein phosphatase (which phosphorylates glycogen synthase)

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41
Q

Which glucose transporter is insulin dependent?

A

GLUT-4

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42
Q

Give the pituitary hormones secreted or inhibited by each of the following hypothalamic secretions: TRH, Dopamine, Somatostatin, Prolactin

A

TRH - stim TSH and prolactin. Dopamine - inhibits prolactin. Somatostatin - inhibits GH and TSH. Prolactin - Inhibits GnRH

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43
Q

What substance acts counter to ACTH in synthesis of adrenal hormones?

A

Ketoconazole (inhibits cholesterol to pregenolone conversion by desmolase, which is stimulated by ACTH)

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44
Q

Metyrapol

A

Inhibits cortisol formation by 11B-hydroxylase. Leads to decreased cortisol and increased ACTH (reflexively)

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45
Q

Relative levels of mineralocorticoids, cortisol, and sex hormones in 17a-hydroxylase deficiency

A

MC - high, cortisol - low, sex hormones - low

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46
Q

Relative levels of mineralocorticoids, cortisol, and sex hormones in 21-hydroxylase deficiency

A

MC - low, cortisol - low, sex hormones - high

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47
Q

Relative levels of mineralocorticoids, cortisol, and sex hormones in 11b-hydroxylase deficiency

A

MC - Aldosterone low but 11-deoxycorticosterone high, cortisol - low, sex hormones - high

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48
Q

Hypertension, hypokalemia, male pseudohermaphroditism if XY or female with lacking secondary sex characteristics if XX

A

17a-hydroxylase deficiency

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49
Q

Hypotension, hyperkalemia, increased renin, volume depletion, masculinization, female pseudohermaphroditism

A

21-hydroxylase deficiency

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50
Q

Hypertension, masculinization

A

11b-hydroxylase deficiency. Contrast with 21-hydroxylase deficiency, which is masculinization with HYPOtension

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51
Q

What is the most common congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

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52
Q

What does prolonged ACTH stimulation do to the adrenal gland histologically?

A

Causes hyperplasia of the fasiculata

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53
Q

Treatment of congenital adrenal hyperplasias

A

Suppress ACTH with exogenous corticosteroids

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54
Q

What effect does GH have on IGF-1 production?

A

Stimulates IGF-1 production in liver (no effect on hypothalamic activity)

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55
Q

Amenorrhea, galactorrhea, low libido, infertility

A

Prolactinoma (pituitary adenoma)

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56
Q

What secondary effect can a prolactinoma have in women?

A

Hypogonadism which leads to osteoporosis (prolactin inhibits GnRH release)

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57
Q

Medical treatment for prolactinomas

A

Bromocriptine or cabergoline (dopamine agonists)

58
Q

Medical treatment for acromegaly

A

Octreotide

59
Q

What factors cause increased GH release

A

Stress, exercise, and hypoglycemia

60
Q

Serum sodium in DI

A

Greater than 142

61
Q

Water deprivation test results in DI

A

Urine osmolality fails to increase (stays less than 300-500)

62
Q

Treatment for DI

A

Central - desmopressin. Nephrogenic - HCTZ, indomethacin, or amilioride

63
Q

Typically where is the dysfunction in central DI?

A

Hypothalamus. Usually posterior pituitary problems only cause transient DI

64
Q

Treatment for SIADH

A

Demeclocycline or water restriction

65
Q

Causes of SIADH (4)

A

Ectopic ADH (small cell), 2) CNS disorders/head trauma, 3) Pulmonary disease, 4) Drugs (eg cyclophosphamide)

66
Q

Complication of pituitary adenoma

A

Pituitary apoplexy (bleeding into existing pituitary adenoma)

67
Q

What type of insulin is the preferred treatment for DKA?

A

Regular (not short acting)

68
Q

What factors tend to increase or decrease blood glucose in type 1 diabetics?

A

Infection, pain, and sleep deprivation tend to increase blood glucose. Exercise decreases blood glucose

69
Q

What compounds are central in the pathogenesis of T2DM?

A

FFAs and serum TGs

70
Q

What are the tests of choice for T1DM, T2DM, and gestational diabetes respectively?

A

T1 and T2 DM - fasting blood sugar (in the US). Gestational - OGTT

71
Q

What are potassium levels like in DKA?

A

Hyperkalemia is present, but intracellular levels of K are very low due to transcellular shift from decreased insulin

72
Q

What is your first step in management if you suspect mucormycosis in a DKA patient?

A

Biopsy and look at it under the microscope

73
Q

Pathogenesis of fetal macrosomia in gestational diabetes

A

Maternal glucose crosses placenta, hyperplasia of fetal islets, fetal hyperinsulinemia followed by fetal hypoglycemia, fetal macrosomia

74
Q

Rule of thirds for carcinoid

A

One third metastasize, One third present with second malignancy, one third present as multiple

75
Q

Treatment for carcinoid syndrome

A

Octreotide

76
Q

Test of choice for Zollinger-Ellison

A

Infusion of secretin (will see increased gastrin secretion in Z-E syndrome)

77
Q

MEN 1

A

Pituitary (prolactin or GH), Parathyroid, Pancreas (ZES, insulinoma, VIPoma, glucagonoma). Kidney stones and stomach ulcers. Draw a diamond

78
Q

MEN 2A

A

Medullary thyroid carcinoma (calcitonin), Pheochromocytoma, Parathyroid tumors. Draw a square

79
Q

MEN 2B

A

Medullary thyroid carcinoma (calcitonin), pheochromocytoma, oral/intestinal ganglioneuromatosis (neuromas). Marfinoid habitus. Draw a triangle.

80
Q

How does pheochromocytoma often present

A

Headache

81
Q

Genetic mutation associated with MEN 2A and 2B

A

Ret mutation

82
Q

List the insulins and include their duration of action

A

Rapid - lispro and aspart. Short acting - insulin. Intermediate - NPH. Long-acting - Glargine and detemir

83
Q

Treatment for gestational diabetes

A

Insulin

84
Q

Tolbutamide

A

Sulfonylurea (first generation)

85
Q

Chlorpropamide

A

Sulfonylurea (first generation)

86
Q

Glyburide

A

Sulfonylurea (second generation)

87
Q

Glimepiride

A

Sulfonylurea (second generation)

88
Q

Glipizide

A

Sulfonylurea (second generation)

89
Q

Metformin

A

Biguanide

90
Q

Pioglitazone

A

Glitazone (aka thiazolidinedione)

91
Q

Rosiglitazone

A

Glitazone (aka thiazolidinedione)

92
Q

Acarbose

A

Alpha-glucosidase inhibitor

93
Q

Miglitol

A

Alpha-glucosidase inhibitor

94
Q

Pramlinitide

A

Mimetic (diabetes drug)

95
Q

Exenatide

A

GLP-1 Analog

96
Q

Sulfonylurea mechanism

A

Closes K channel in beta cell membrane, triggering insulin release via increased Ca influx

97
Q

Mechanism of biguanides (metformin)

A

Unknown. Decreased gluconeogenesis, increased glycolysis, increased peripheral insulin sensitivity

98
Q

Mechanism of Glitazones/Thiazolidinediones

A

Increased insulin sensitivity via PPAR-gamma binding

99
Q

Alpha-glucosidase inhibitor mechanism

A

Inhibits intestinal brush border alpha-glucosidases leading to decreased glucose absorption

100
Q

Mimetics (pramlinitide) action

A

Amylin analogue. Leads to decreased glucagon secretion and delayed gastric emptying and promotes satiety

101
Q

Exenatide (GLP-1 analog) effects

A

Increased insulin, decreased glucagon release

102
Q

What does activation of PPAR-gamma do and what drugs activate it?

A

Increases insulin sensitivity and levels of adiponectin. Glitazones/thiazolidinediones

103
Q

Contraindications of metformin

A

Renal failure (can cause lactic acidosis)

104
Q

Toxicities of glitazones/thiazolidinediones

A

Weight gain, edema, hepatotoxicity, heart failure

105
Q

PTU and methimazole

A

Block peroxidase and inhibit iodide organification. PTU also blocks 5-deiodinase (decreasing peripheral conversion of T4 to T3).

106
Q

Toxicities of PTU and methimazole

A

Rash, agranulocytosis, aplastic anemia, hepatotoxicity (PTU), teratogen (methimazole)

107
Q

Necrolytic migratory erythema, elevated erethematous rash on groin, hyperglycemia, stomatitis, cheilosis, abdominal pain, anemia

A

Glucagonoma

108
Q

Uses of GH

A

GH deficiency and Turner syndrome

109
Q

Uses of octreotide

A

Acromegaly, carcinoid, gastrinoma, glucagonoma, hepatorenal syndrome

110
Q

Uses of oxytocin

A

Stimulate labor, uterine contractions, milk let down, and controlling uterine hemorrhage

111
Q

Demeclocycline

A

ADH anatgonist, use in SIADH. May cause nephrogenic DI, photosensitivity, abnormalities of bone and teeth

112
Q

What effect do glucocorticoids have on liver sugar metabolism?

A

Stimulate gluconeogenesis (have an anti-insulin effect)

113
Q

Uses of glucocorticoids

A

Addisons, inflammation, immune suppression, asthma, Graves

114
Q

What is the bone finding in Cushings?

A

Osteoporosis

115
Q

3 tumors secreting stuff you cannot suppress

A

Parathyroid adenoma making PTH, adrenal adenoma making cortisol, adrenal tumor secreting aldosterone

116
Q

Most common cause of hypopituitarism in adults

A

Nonfunctioning pituitary adenoma

117
Q

What type of necrosis occurs in Sheehans syndrome?

A

Coagulative (pituitary is not part of the brain)

118
Q

Second most common cause of hypopituitarism in adults

A

Sheehans syndrome

119
Q

Most common cause of hypopituitarism in kids

A

Craniopharyngioma

120
Q

First signs of hypopituitarism

A

Amenorrhea or impotence (due to loss of gonadotropins)

121
Q

Test of choice for pituitary dwarfism

A

Sleep GH and IGF-1 levels

122
Q

What amino acids stimulate growth hormone release?

A

Histidine and arginine

123
Q

Order in which hormone production disappears in hypopituitarism

A

(first to go) Gonadotropins, GH, TSH, ACTH, prolactin (last to go)

124
Q

Stimulators of prolactin synthesis

A

OCPs, hydralazine, Ca channel blockers, psychotropic drugs, primary hypothyroidism

125
Q

What non-thyroid related symptom is seen in women with primary hypothyroidism and why?

A

Galactorrhea. Low thyroid hormones levels increase synthesis of TSH and TRH. TRH stimulates prolactin synthesis

126
Q

Prolactin level above what value always means prolactinoma?

A

200

127
Q

Increased T4 with a normal TSH

A

Estrogens such as OCPs or pregnancy (due to increase in TBG)

128
Q

Use of I-131 test

A

Distinguishes Graves from exogenous thyroid supplementation

129
Q

Cardiac abnormality associated with Graves

A

A-fib

130
Q

Most common symptom of hypothyroidism

A

Proximal muscle weakness (cannot get out of chairs, serum CK will be high)

131
Q

Give the rule for cold thyroid nodules

A

Any cold nodule in a man or child is cancer until proven otherwise. Cold nodules in (esp older) women are often benign

132
Q

Thyroid cancer prognosis

A

(Best) Papillary then follicular then medullary (worst)

133
Q

Most common cause of hypocalcemia

A

Hypoalbuminemia (albumin carries about 40 percent of total Ca)

134
Q

Why is alkalosis associated with tetany?

A

Because albumin is made of acidic AAs, and thus will bind more free calcium (lowering ionized calcium levels) in alkalotic state. Will not have hypocalcemia on labs but will have tetany and functional hypocalcemia

135
Q

Purple striae, obesity, thin extremities

A

Cushings

136
Q

What type of Cushings can you suppress with high dose dexamethasone?

A

Pituitary

137
Q

What will the low dose dexamethasone suppression test result be in all types of Cushings?

A

Failure to suppress. You will, however, see suppression at low doses in normal patients

138
Q

Why do Cushings patients have thin exremities and central obesity?

A

Cortisol encourages protein (muscle) breakdown, but leads to hyperglycemia, which leads to insulin release, which causes fat and sugar storage centrally. Essentially we are moving tissue from our muscles centrally

139
Q

Why are the striae in Cushings purple?

A

Cortisol decreases collagen synthesis

140
Q

Why will patients with Conns syndrome have tetany?

A

Metabolic alkalosis causes functional hypocalcemia

141
Q

Patient with neurofibromatosis and HTN

A

Suspect pheochromocytoma. Check VMA and metanephrines

142
Q

Only meningitis with petechial lesions

A

N meningitidis

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