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USMLE Step 1 > Endocrine > Flashcards

Endocrine Flashcards

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1
Q

Which endocrine hormones are IP3 linked? T/F: Hormones from the posterior pituitary are IP3-linked.

A 
GGOAT "butts" you:
GnRH
GHRH
Oxytocin
ADH
TRH
Oxytocin / ADH are from the posterior pituitary and are IP3-linked.
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2
Q

Which endocrine hormones are cAMP linked? (12)

A 
FLAT ChAMP
FSH
LH
ACTH
TSH
CRH
hCG
ADH
MSH
PTH
calcitonin / GHRH / glucagon too!
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3
Q

Hormones in the anterior pitiutary tend to be linked to which signaling pathway? Can you name 4?

A

cAMP. These include FSH, LH, ACTH, TSH.

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4
Q

Endocrine hormones which signal through steroid receptors (6):

A

VET3 CAP

Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone

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5
Q

Effect of too much SHBG in men? Too little in women?

A

Men: Gynecomastia with high SHBG.
Women: Hirsutism with low SHBG.

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6
Q

What kind of signaling path does prolactin use?

A

Tyrosine kinase

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7
Q

What kind of signaling path does oxytocin use?

A

IP3

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8
Q

What signaling path does insulin use?

A

Tyrosine kinase

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9
Q

GH is secreted from:

A

Anterior pituitary

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10
Q

Glucocorticoids are secreted from:

A

The adrenal cortex, zona fasciculata

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11
Q

Progesterone is secreted from (2):

A

Ovaries, placenta

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12
Q

Prolactin comes from the:

A

Anterior pituitary

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13
Q

Oxytocin comes from the:

A

Posterior pituitary

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14
Q

Glucagon comes from the:
Insulin comes from:
Somatostatin comes from:

A

Glucagon from alpha cells of pancreas
Insulin from beta cells
Somatostatin from delta cells

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15
Q

FSH comes from the:

A

Anterior pituitary

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16
Q

Vasopressin (ADH) comes from:

A

The hypothalamus (supraoptic nucleus), is stored in the posterior pituitary

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17
Q

TSH comes from the:

A

Anterior pituitary

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18
Q

Estradiol comes from the:

A

Ovaries

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19
Q

Estriol comes from the:

A

Placenta

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20
Q

Estrone is made by:

A

Fat

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21
Q

Lutenizing hormone comes from the:

A

Anterior pituitary

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22
Q

Mineralocorticoids / aldosterone comes from the:

A

Zona glomerulosa of the adrenal cortex

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23
Q

ACTH is excreted by the:

A

Anterior pituitary

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24
Q

This molecule is the precursor to ACTH, lipotropins, MSH, and the beta-endorphins:

A

Pro-opiomelanocortin

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25
Q

Four main causes of hyperprolactinemia:

A
  1. Pregnancy / nipple stimulation
  2. Stress
  3. Prolactinoma
  4. Dopamine antagonists
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26
Q

Where is somatostatin made?

A

In the GI tract, mostly D cells in gut mucosa, pancreatic delta cells make it too.

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27
Q

What does somatostatin do?

A

Inhibits secretion of GI hormones, decreases endocrine / exocrine secretion, reduces GI motility and GB contraction.

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28
Q

Three somatostatin analogues that are used clinically:

A

Octreotide
Somatostatin LAR
Lanreotide-P

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29
Q

In the fetus, this hormone is secreted late in gestation and is responsible for lung maturation:

A

Cortisol

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30
Q

Most common tumor of adrenal medulla in adults:

A

Pheo

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31
Q

Most common tumor of adrenal medulla in chidren:

T/F this tumor causes episodic HTN.

A

Neuroblastoma. Does not cause episodic HTN.

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32
Q

The posterior pituitary is derived from this tissue layer:

A

Neuroectoderm

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33
Q

The anterior pituitary is derived from this tissue in embryonic development:

A

Surface ectoderm (Rathke’s pouch)

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34
Q

Hormones secreted by the anterior pituitary:

A

FSH, LH, ACTH, TSH, prolactin, GH, MSH

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35
Q

There are three cell types in the islets of the pancreas. What are they, where are they, and what do they make?

A

a on the outside make glucagon
b on the INSide make INSulin
d are throughout and they make somatostatin

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36
Q

The adrenal cortex is derived from this germ layer:

A

Mesoderm

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37
Q

The adrenal medulla derives from this cell lineage:

A

Neural crest

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38
Q

Is it the L or R adrenal vein that drains directly into the IVC?

A

The R. The left drains into the L renal vein then to the IVC.

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39
Q

What are the three zones of the adrenal cortex?

A

Glomerulosa
Fasciculata
Reticularis

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40
Q

This zone of the adrenal cortex is under control of the renin-angiotensin system.

A

The glomerulosa, this is where aldosterone is made.

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41
Q

Zone of the adrenal cortex that makes cortisol:

A

Zona fasciculata

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42
Q

Where does the thyroid gland come from?

A

Floor of the pharynx, it descends into the neck and leaves behind the foramen cecum = remnant of the thyroglossal duct.

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43
Q

The hypothalamus releases this hormone to stimulate prolactin release. What other hormone is stimulated by this substance?

A

TRH causes prolactin and TSH release from the anterior pituitary

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44
Q

This molecule released from the hypothalamus causes ACTH, MSH, and b-endorphin release from the anterior pituitary:

A

CRH

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45
Q

This hormone inhibits GH release from the anterior pituitary:

A

Somatostatin

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46
Q

Somatostatin inhibits these two hormones:

A

GH, TSH

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47
Q

What happens if you give someone a good whopping dose of GnRH?

A

GnRH in a steady dose will inhibit LH and FSH. It is PULSATILE secretion that drives FSH and LH production.

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48
Q

What effect does prolactin have on GnRH?

A

Inhibits its release

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49
Q

ACTH is released from the anterior pituitary in response to two major things:

A
  1. CRH from the hypothalamus

2. Stress

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50
Q

T/F: You would measure growth hormone levels to dx acromegaly.

A

F. Measure IGF-1.

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51
Q

T/F: GH increases insulin resistance.

A

T

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52
Q

Two things inhibit the secretion of growth hormone:

A

Somatostatin

Glucose

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53
Q

5 main effects of cortisol on the body:

A
  1. Maintains BP (increase in a1 receptors)
  2. Decreases bone formation
  3. Anti-inflammatory
  4. Insulin resistance
  5. Increases energy release (gluconeogenesis, lipolysis, proteolysis)
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54
Q

Primary adrenal insufficiency is defined as decrease in cortisol secondary to what kind of difficulty?
Secondary and tertiary, where are they?

A

Primary adrenal insufficiency = problem with the adrenal gland itself.
Secondary = problem with the pituitary.
Tertiary = problem with the hypothalamus.

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55
Q

How is iodine transported into cells?

A

Sodium gradient is used to drive it in.

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56
Q

This hormone binds most of the thyroid hormone in the blood:

A

Thyroxine-binding globulin

57
Q

When would you see TBG decreased? Increased?

A

TBG is decreased in hepatic failure, increased in pregnancy and OCP use (estrogen upregulates it).

58
Q

The enzyme that converts T4 -> T3:

A

5’ deiodonase

59
Q

This drug works both to inhibit thyroid synthesis and to inhibit the conversion of T4 to T3:

A

Propylthiouracil

60
Q

This anti-thyroid drug works only to inhibit the conversion of one thyroid hormone precursor to another. What is the enzyme this drug inhibits? The other drug that has the same effect?

A

Methimazole inhibits peroxidase, PTU works here too.

61
Q

If you give someone a crazy excess of I2 you may see a paradoxical decrease in T4 production. What is this effect called?

A

Wolff-Chaikoff effect

62
Q

This thyroid hormone feeds back to the anterior pituitary to cause a decrease in sensitivity to TRH:

A

T3

63
Q

Thyroid hormone upregulates which adrenergic receptors?

A

b1, responsible for increase in cardiac contractility, HR, and stroke volume.

64
Q

What hormone is elevated in Cushing syndrome?

A

Cortisol

65
Q

What is Cushing disease?

A

Hypercortisol state 2/2 pituitary adenoma (ACTH-secreting pituitary tumor)

66
Q

Second most common cause of Cushing syndrome:

A

Ha! Trick question!
Most common: Iatrogenic
Second: Pituitary adenoma
Third: Ectopic ACTH-producing tumor

67
Q

Dexamethasone suppression test: In what case will a low dose of dex suppress cortisol? A high dose? When will there be no suppression?

A

Low dose suppresses a normal pituitary.
High dose suppresses a pituitary tumor.
Failure to suppress = the thing makes what it wants anyway without any input, ie it is an ectopic source of ACTH (lung CA) or an adrenal tumor making cortisol directly.

68
Q

How do you tell an ectopic ACTH-producing tumor from an adrenal tumor making cortisol?

A

The ectopic tumor (usually small cell lung CA, bronchial carcinoid) will make ACTH. The adrenal tumor doesn’t.

69
Q

What hormone is affected in Conn syndrome?

A

Conn syndrome = primary hyperaldosteronism

70
Q

What is primary hyperaldosteronism caused by?

Secondary?

A

Primary hyperaldo = Conn syndrome = adrenal problem.
Secondary hyperaldo = overactivity of the RAA system (such as one kidney receiving low blood flow and flooding the system with renin)

71
Q

T/F: Conn syndrome is associated with high plasma renin.

A

F. Renin is low, kidneys know they are getting enough blood and that there is HTN. Renin is high in secondary hyperaldosteronism.

72
Q

Tx for Conn syndrome:

A
  1. Remove tumor

2. Spironolactone or epleronone (K+ sparing)

73
Q

Hypertension / salt retention, low potassium, met. alkalosis… first thing that should come to mind:

A

Hyperaldosteronism

74
Q

What effect should a rise in serum potassium have on aldosterone?

A

Should stimulate it, want to dump the K+

75
Q

Hormone affected in Addison disease:

A

Aldosterone and cortisol

76
Q

Most common cause of Addison disease:

A

Autoimmunity

77
Q

T/F: The medulla of the adrenal gland is affected in Addison disease:

A

F. All three layers of the cortex get hit, but the medulla is untouched.

78
Q

What is secondary adrenal insufficiency?

A

Secondary adrenal insufficiency occurs at the level of the pituitary.

79
Q

In which case of adrenal insufficiency – primary or secondary – would you see skin hyperpigmentation and why?

A

Primary = problem with the gland = pituitary making loads of ACTH = POMC activation and MSH made = skin hyperpigmentation. Secondary = pitutary failure, no ACTH, no skin pigmentation.

80
Q

What is tertiary adrenal insufficiency, and what usually causes it?

A

Tertiary adrenal insufficiency = HTH thinking there is still cortisol when there is not, ie in cases of steroid w/d that are too abrupt. HTH will make no CRH, so the pituitary will make no ACTH, so you get no cortisol / aldo. Need to taper.

81
Q

Metabolic abnormalities in Addison disease:

A

Hyponatremic volume contraction, hyperkalemia, acidosis.

82
Q

In secondary adrenal insufficency, do you see hyperkalemia?

A

No! There is no ACTH, but your adrenals still make aldosterone, so salt / H2O / K+ balance is normal.

83
Q

With what three syndromes are pheochromocytomas associated?

A

NF-1
MEN-2A
MEN-2B

84
Q

Medical treatment of a pheo prior to surgical removal?

A

a-block first: Phenoxybenzamine or phentolamine, then follow with b-block. Don’t want to b-block first, you leave Epi unopposed in the body to hit a1 receptors and cause through the roof HTN.

85
Q

Pheochromocytomas can secrete epo. Three other tumors that do this:

A

Renal cell CA
Hemangioblastoma
Hepatocellular carcinoma

86
Q

Most common tumor of adrenal medulla in adults? Kids?

A

Pheo in adults, adrenal neuroblastoma in kids.

87
Q

Which oncogene is implcated in adrenal neuroblastoma?

A

N-myc

88
Q

T/F: A pheo can calcify

A

T. Rule of 10’s:

10% calcified, malignant, bilateral, extra-adrenal, and 10% in kids.

89
Q

HLA associated with Hashimoto thyroiditis (2):

A

HLA-DR5

HLA-B5

90
Q

Endocrine disease that is a risk for B cell lymphoma:

A

Hashimoto

91
Q

Severe fetal hypothyroidism, 5 Ps in addition to the mental retardation and FTT:

A 
Pot-bellied
Pale
Protrubent tongue
Puffy-faced
Protruding umbilicus
92
Q

HLA type associated with de Quervain’s thyroiditis:

A

HLA B35

93
Q

What is Reidel’s thyroiditis? What do you see in there histologically?

A

Replacement of the thyroid with fibrous tissue. See macrophages and eosinophils in fibrous base.

94
Q

Name for what happens when you give someone with a goiter or excess thyroid tissue who is iodine deficient a ton of iodine suddenly:

A

Jod-Basedow thyrotoxicosis

95
Q

Three things that can cause Jod-Basedow:

A

Amiodarone
Contrast
Ppl w/ Graves who are iodine deficient getting iodine suddenly

96
Q

Which anti-thyroid agent is preferred in pregnancy?

A

PTU. Methymazole causes fetal cutis aplasia.

97
Q

Both PTU and methimazole cause this problem with WBCs:

A

Agranulocytosis

98
Q

T/F: PTU, the preferred anti-thyroid drug in pregnancy, crosses the placenta:

A

T.

99
Q

Tx for thyroid storm:

A

b-block aggressively, PTU

100
Q

Autoimmune thyroid disease with thyroid stimulating Ab? With thyroid destruction?

A

Graves, Hashimoto

101
Q

HLA subtypes associated with Graves disease:

A

HLA DR3

HLA B8

102
Q

Most common thyroid cancer:

A

Papillary

103
Q

Thyroid cancers with RET mutations:

A

Papillary, medullary

104
Q

Thyroid cancer with Ras mutation:

A

Papillary

105
Q

Thyroid cancer that likes to spread hematogenously:

A

Follicular

106
Q

Sheets of cells in an amyloid base, hyperthyroidism:

A

Medullary thyroid CA

107
Q

Disease in which you see an increased resin radioactive T3 uptake:

A

Graves. TBG is all occupied by endogenous thyroid hormone, give people a radiolabeled one and everything you give them will bind your test resin.

108
Q

This teratoma has functional thyroid tissue:

A

Struma ovarii teratoma

109
Q

Treatment for acromegaly:

A

Resect pituitary if you can

Octreotide or other somatostatin analogue

110
Q

Three ways of diagnosing acromegaly:

A
  1. High serum IGF-1
  2. Fail to suppress GH with oral glucose
  3. Mass on MRI
111
Q

What is Sheehan’s syndrome?

A

Postpartum bleeding drops BP so much that the pituitary gets damaged, can be any hormone affected. Most commonly presents with failure to lactate.

112
Q

GH excess is called _____ in adults but is called _____ in children.

A

Acromegaly

Gigantism

113
Q

Common presentation of MEN 1:

A 
Renal stones (hyper PT)
Ulcers in the stomach (ZE or another pancreatic endocrine tumor)
114
Q

MEN 1 tumors:

A

Parathyroid
Pituitary
Pancreatic endocrine

115
Q

MEN 2A and 2B tumors:

A

Medullary thyroid cancer & pheo in both.
2A = parathyroid
2B = mucosal neuromas, marfanoid habitus

116
Q

MEN associated with 11q13

A

MEN 1

117
Q

MEN syndromes associated with a problem on chromosome 10:

A

MEN 2 (RET)

118
Q

What form of inheritance do all the MEN syndromes share?

A

Autosomal dominant

119
Q

Glucocorticoid medication that is virtually the same molecule as cortisol:

A

Hydrocortisone

120
Q

This drug is used in the treatment of aldosterone deficiency. Why?

A

Fludracortisone.

This drug has the highest mineralocorticoid effect of all the glucocorticoids.

121
Q

How do the glucocorticoids work to decrease the production of leukotrienes and prostaglandins?

A

They block phospholipase A2 and inhibit COX-2.

122
Q

T/F: Empty sella syndrome is most often sub-clinical.

A

T, usually there is some pituitary tissue glued to the sella somewhere. Can present with any deficiency.

123
Q

These hormones share a common alpha sub-unit:

A

TSH, LH, FSH, b-HCG

Think pregnancy

124
Q

This hormone increases blood glucose level and decreases protein synthesis:

A

Cortisol

125
Q

These two cancers are associated with RET gene mutations:

A

MEN 2

Medullary thyroid cancer

126
Q

Four clinical uses for somatostatin:

A

Inhibits GH, TSH, ACTH
Decreases sphlancnic circ. (can help control bleeding)
Tones down GI endocrine excess
Can be used for refractory diarrhea

127
Q

Thyroid cancer associated with RAS or PAX8-PPAR gamma:

A

Follicular

128
Q

Thyroid cancer associated with RET or NTRK1:

A

Papillary thyroid CA

129
Q

Thyroid cancer associated with BRAF:

A

Papillary

130
Q

Starting molecule for steroid synthesis:

A

Cholesterol

131
Q

Cholesterol is converted to pregnolone, first step of steroid synthesis, by this enzyme. What drug inhibits this enzyme?

A

Desmolase

Ketoconazole inhibits desmolase

132
Q

From pregnenolone, in order to make aldosterone, you need to first make this molecule. What is the enzyme?

A

To get to mineralocorticoids, you make progesterone with 3b-OH dehydrogenase.

133
Q

What is the one arm of the steroid synthesis path that does not require 17a-hydroxylase?

A

Synthesis of mineralocorticoids, eg aldosterone.

134
Q

What is the one arm of the steroid synthesis path that does not require 21-hydroxylase?

A

Synthesis of sex hormones.

135
Q

Precursor molecule to the synthesis of sex hormones:

A

DHEA, which is made into androstenedione.

136
Q

What is the main difference between 21-hydroxylase and 11b-hydroxylase deficiency?

A

The paths are really very close together. 11b-hydroxylase acts a little later in the path, so you get one extra product backing up. This product is 11-deoxycorticosterone, which causes HTN. Both syndromes = high sex hormones, 11b also has HTN.

137
Q

Mnemonic involving 1’s for adrenal steroid synthesis:

A

1 in the first digit = HTN

1 in the second digit = masculinization

138
Q

What would a male with 17a-hydroxylase deficiency look like? A female? Why?

A

17a-hydroxylase needed everywhere but the path that makes aldosterone, so you have no sex hormones. The little boy will have testes but ambiguous genitalia (no testosterone around). A little girl will look normal until puberty, at which point she will not develop secondary sex chars.

USMLE Step 1 (18 decks)

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