ENDOCRINE Flashcards

1
Q

How to treat hyperthyroidism in first trimester preg

A

PTU

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2
Q

How to treat hyperthyroid in 2nd and 3rd trimester pregnancy

A

Methimazole

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3
Q

Teratogenic effects of methimazole when used during first trimester of pregnancy

A

Aplasia cutis
Scalp defects
Omphalocele
TE fistula

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4
Q

Cause of 60-90% of congenital heart block

A

Neonatal lupus

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5
Q

Girl missed her period for 2 months and prig test is negative. Next step?

A

TSH or prolactin.

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6
Q

Treatment for heart failure and/or a fib in thyroid storm

A

Digoxin

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7
Q

If pt is hyperthyroid based on TSH and thyroid sono, next step?

A

radionucleotide uptake scan

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8
Q

If radio nucleotide uptake scan shows a hot nodule?

A

Treat as hyperthyroid

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9
Q

If radio nucleotide uptake scan shows a cold nodule?

A

FNA

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10
Q

If hypothyroid based on thyroid sono and TSH, next step?

A

Replace thyroid hormone and monitor for decrease in nodule size. If nodule persists AFTER thyroid replacement, do an FNA.

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11
Q

What to do if FNA of thyroid is non diagnostic

A

Repeat FNA.

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12
Q

If FNA of thyroid is benign …

A

Repeat sono q 6m-1 yr to make sure no increase in size. If size does end up increasing, repeat FNA.

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13
Q

Somogyi effect

A

Evening NPH is too high so pt ends up bottoming out overnight and the release of stress hormone GREATLY increases morning glucose.

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14
Q

Treatment of somogyi effect

A

Decrease nighttime dose of NPH or give it later.

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15
Q

What is the dawn phenomenon?

A

Too low dose of evening NPH so glucose creeps up throughout the night, causing very high morning glucose.

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16
Q

Treatment of dawn phenomenon

A

Increase nighttime dose of NPH.

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17
Q

How to distinguish between dawn and smoggy effect

A

Check a 3am glucose.

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18
Q

Which 2 oral DM agents have the most common SE of hypoglycemia

A

Sulfonylurea, meglutinides

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19
Q

Which is the oldest and cheapest of DM oral agents?

A

Sulfonylureas

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20
Q

Which oral DM agent also helps lower TG and LDL

A

Metformin

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21
Q

Which oral DM agent is not safe in settings of CHF

A

TZD

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22
Q

Which 2 oral DM agents should not be used in pts with elevated serum creatinine

A

Metformin, sulfonylureas

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23
Q

Which oral DM agent should not be used in pts with IBD

A

Alpha glucosidase inhibitors (acarbose)

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24
Q

Hepatic serum transaminase levels should b carefully monitored when using these oral DM agents.

A

Metformin or TZDs

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25
Q

Which oral DM agent is metabolized by the liver and is thus an excellent choice in pts with renal disease

A

TZD

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26
Q

MOA of exenatide

A

Glucagon like peptide-1 derived from Gila monster saliva. It prolongs incretin secretion, which decreases glucagon secretion and increases insulin secretion. It also delays gastric emptying.

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27
Q

SE of exenatide

A

Acute pancreatitis.

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28
Q

MOA of Sitagliptin

A

Inhibitor of dipeptidyl peptidase IV which affects GLP-1 among other hormones. Therefore it prolongs uncertain secretion which decreases glucagon secretion and increases insulin secretion. It also delays gastric emptying.

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29
Q

How is eventide administered

A

SQ twice daily at morning and evening meals

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30
Q

MOA of Pramlintide

A

Amylin analog, normally secreted with insulin, decreases glucagon secretion and gastric emptying. USED ONLY IN PTS TAKING INSULIN.

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31
Q

How is pramlintide administered

A

IM prior to meals.

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32
Q

Anti-islet Abs seen in pts with Type 1 DM

A

Anti insulin
Anti islet cell cytoplasm
Anti glutamic acid decarboxylase
Anti tyrosine phosphatase

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33
Q

Criteria for diagnosis of metabolic syndrome

A
Any 3 of following:
Abdominal obesity with waist circum >40 in in men or >35 in in women
TG >150
HDL  130/85
Glc > 100 or 2 hr post oral glucose >140
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34
Q

Tx options for diabetic gastroparesis

A

Metoclopramide
Cisapride
Erythromycin

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35
Q

What medications should never be taken with cisapride due to risk of cardiac arrhythmias?

A

Drugs metabolized by CYP 450 - 3A4 system. MACROCODES, antifungals, phenothiazines like prochlorperazine and chlorpromazine.

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36
Q

How often should HbA1c be checked if >7? >6?

A

If >7, q3 months.

If >6, q6 months.

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37
Q

Goal LDL in diabetics

A
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38
Q

Which anti - HLD agent can worsen insulin resistance

A

Niacin

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39
Q

How often is a dilated eye exam performed in a diabetic?

A

annually

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40
Q

How often are chem 8 and UA performed in diabeticcs

A

annually

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41
Q

If pt has a pituitary adenoma and surgery is indicated, which glands removed?

A

Removal of only the gland containing the adenoma and biopsy of 1-3 others.

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42
Q

If pt has pituitary hyperplasia and surgery is indicated, which glands are removed?

A

Remove 3.5 glands and mark the remaining half with a surgical clip (or forearm autotransplantation of the gland to remain in cases where recurrence is likely, such as MEN type 1)

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43
Q

Meds to avoid in hyperparathyroidism

A

Thiazides
Lithium
Calcium ingestion >1000 mg/day

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44
Q

How often is serum calcium monitored in pts with hyperparathyroidism? serum creatinine? bone density?

A

Calcium q6 mos
Creatinine q12 mos
Bone density q12 mos

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45
Q

3 oral phosphate binders

A

Calcium carb or acetate (most commonly used)
Sevelamer (can be taken with calcium)
Lanthanum

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46
Q

Tx of hyperparathyroidism due to renal osteodystrophy

A

Calcitriol, other vitamin D analog, or cinacalcet (calcimimetic) to suppress PTH secretion

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47
Q

Tx for prolactinoma

A

DA agonsit. CABERGOLINE > bromocriptine or pergolide.

If ineffective, switch to a 2nd DA agonist.

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48
Q

If a female with prolactinoma >3 cm and a desire to become pregnant …

A

Transphenoidal surgery, even if DA agonist is effective.

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49
Q

How to screen for acromegaly

A

Measure serum IGF-1

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50
Q

How to confirm dx of acromegaly

A

oral glucsoe suppression test. If GH concentration is >1ng/mL = acromegaly.

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51
Q

What do you do if your pt has acromegaly and your somatostatin analog ineffective

A

Cabergoline, a DA agonist that inhibits GH secretion.

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52
Q

What is pegvisomant

A

GH receptor antagonist

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53
Q

A pt with elevated BP, palpitations, headache, excessive perspiration is found to have elevated urine VMA. What effect would giving a beta blocker have on this pt?

A

Would increase BP.

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54
Q

Of DHEA, DHEA-S and testosterone, which is made by the ADRENALS ONLY is a more specific marker for an androgen producing adrenal tumor in a woman

A

DHEA-S

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55
Q

Most specific lab finding in making dx of primary hyperaldosteronism

A

Aldosterone renin ratio

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56
Q

Most likely cause of increased PTH and decreased serum calcium and increased serum phosphate

A

Renal failure with vitamin D deficiency

57
Q

Next step in mgmt of pt found to have an absent pituitary on MRI (empty sella)

A

Reassurance. If symptomatic, treat the hormone deficiency.

58
Q

Pituitary adenoma’s response to high dose dexamethasone

A

Suppressed.

59
Q

Drugs known for causing elevated prolactin

A

Phenothiazines
Anti psychotics
Methyldopa

60
Q

Pages disease lab levels

A

Increased alk phos.

61
Q

Labs in osteomalacia/rickets

A

Decreased serum calcium and phosphate. Normal/increased alk phos.
Increased PTH.

62
Q

Labs in osteoporosis

A

Normal.

63
Q

Labs in osteopetrosis

A

Normal

64
Q

Labs in pseudohypoparathyroidism

A

This is a receptor problem (not responding to PTH).

Thus calcium is low, phosphate is high, and PTH is high.

65
Q

Indications for surgical parathyroidectomy

A
Ca > 1 mg/dL above ULN
CrCl decreased by 30%
24 hr urine calcium >400 mg
Symptomatic
Bone min density ..
66
Q

How do you calculate a corrected HCO3 ?

A

(Measured anion gap - normal anion gap of 12 ) + HCO3.

If corrected is greater than a normal HCO3 of about 24, you probably have a concomitant metabolic alkalosis.

67
Q

MOA of Glyburide and glipizide

A

Second gen sulfonylureas which reduce serum glucose levels by increasing insulin secretion from beta cells.

68
Q

Thyroid peroxidase is also known as?

A

Microsomal antigen

69
Q

Which thyroid autoimmune disease has higher levels of thyroid peroxidase antibody?

A

Hasimotos. Note, they BOTH HAVE THEM!!

70
Q

What is thyroglobulin

A

Protein produced by the follicular cells of the thyroid gland and stored as colloid. When stimulated by TSH, it produces the thyroid hormones. Its also responsible for storing iodine.

71
Q

High levels of anti thyroglobulin antibody are more diagnostic of which autoimmune disease?

A

Hashimotos. It can be elevated in many other autoimmune disorders though including graves.

72
Q

Thyroid stimulating hormone receptor antibody is the direct cause of ?

A

Graves disease. There are 3 types of TSH receptor antibodies and these Abs stimulate the production of thyroid hormones in addition to the thyroid gland. As a result, 15% of pts with a positive TSH-R Ab assay develop a diffuse multi nodular goiter.

73
Q

Regular insulin onset and duration

A

Onset 30-60 min

Diration 5-8 hours

74
Q

Insulin detemir onset and duration

A

Onset 1-2 hours

Duration 24 hours

75
Q

NPH insulin onset and duration

A

Onset 1-2 hours

Duration 18-24 hrs

76
Q

Glargine insulin onset and duration

A

Onset 1-4 hours

Duration 24-28 hours

77
Q

Fastest onset of action for insulin

A

Insulin lispro, 5-10 minutes.

78
Q

How do bile acid resins work

A

Prevent intestinal reabsorption of bile acids. Therefore, the liver must use cholesterol to make more. Increases the LDL receptor expression.

79
Q

How does niacin work

A

Inhibits lipolysis in adipose tissue and reduces hepatic VLDL secretion into circulation.

80
Q

How do fibrates work

A

Upregulate LPL, leading to increased TG clearance.

81
Q

Nitrates cause what effect on contractility and heart rate

A

Increase. Its a reflex.

82
Q

Beta blockers do what to EDV

A

Increase! They affect after load.

83
Q

Beta blockers do what to ejection time

A

Increase

84
Q

Tx of malignant hypertension

A

NITROPRUSSIDE. It increases cGMP via direct release of NO. However it can cause CYANIDE TOXICITY!!

Can also use fenoldapam.

85
Q

What hormone is increased in 17 a hydroxyls deficiency?

A

Mineralocorticoids. Therefore you have HTN but hypokalemia. decreased sex hormones.

86
Q

What hormone is increased in 21 hydroxyls deficiency

A

SEX. HYPOtension, HYPERkalemia and increased renin activity due to the lack of aldosterone. Leads to masculinization.

87
Q

Which hormones are increased in 11 B hydroxylase deficiency

A

11 deoxycorticosterone and sex hormones. Though you’re low in aldosterone, the corticosterone is a mineralocorticoid and secreted in excess.

88
Q

Why does CAH cause enlargement of both adrenal glands?

A

Increased ACTH stimulation due to decreased cortisol.

89
Q

How does GH affect insulin?

A

Increases insulin resistance.

90
Q

Secretion of GH is inhibited by what 2 things

A

Glucose

Somatostatin.

91
Q

What does TRH do to prolactin

A

Increases secretion.

92
Q

How does prolactin affect GnRH

A

INHIBITS

93
Q

How does cortisol affect BP?

A

Maintains by up regulating alpha 1 receptors on arterioles, increasing the sensitivity to NE and epinephrine.

94
Q

What does cortisol do to bone formation

A

Decreases via inhibition of osteoBLasts and DECREASING intestinal calcium absorption.

95
Q

What causes the abdominal striae in cushion syndrome

A

Cortisol inhibits fibroblasts.

96
Q

Regulation of cholecalciferol

A

This is vitamin D.

Increased PTH, decreased calcium and phosphate cause increased 1,25 OH2 production.

97
Q

What happens if a man has increased sex hormone binding globulin

A

Lowered free testosterone – > gynecomastia

98
Q

What happens if a woman has decreased sex hormone binding globulin

A

Raises our free testosterone.

99
Q

In conns syndrome, what happens to renin?

A

Low (increased aldosterone will obviously negatively FB)

100
Q

In renal artery stenosis, what happens to renin?

A

HIGH plasma renin. The renal perception of a low intravascular volume results in an overactive renin-angiotensin system

101
Q

Pheochromocytoma is associated with which 3 problems

A

NF 1
Men 2A
Men 2B

102
Q

Elevated homovanillic acid in the urine indicates ?

A

Neuroblastoma.

103
Q

Bombesin is the tumor marker for ?

A

Neuroblastoma!

104
Q

RAdial arrangement of cells around fibrils on histology

A

Neuroblastoma

105
Q

3 causes of addison disease

A

autoimmune
TB
mets

106
Q

How does metyrapone work

A

Decreases cortisol synthesis thus stimulating ACTH secretion and increasing plasma deoxycortisol.

107
Q

Thyroid replaced by fibrous tissue, causing hypothyroidism.

A

Riedels thyroiditis

108
Q

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

A

CRETINISM!

109
Q

Subacute thyroidits causes hypo or hyper ?

A

Hyperthyroid early in course (basically thyroid fractures and releases a bunch of T4. But then it might exhaust itself and necrose causing later hypothyroidism.)

110
Q

Orphan annie nuclei

A

Papillary carcinoma. Also a/w psammoma bodies, increased risk with childhood irradiation.

111
Q

Medullary CA a/w what 2 dz?

A

MEN 2A, 2B

112
Q

What CA a/w hashimotos?

A

Lymphoma.

113
Q

Osteitis fibrosa cystica

A

Cystic bone spaces filled with brown fibrous tissue, causing bone pain.

114
Q

Renal osteodystrophy

A

Bone lesions due to secondary or tertiary hyper PTH due in turn to renal disease.

115
Q

Wich type of DM a/w islet amyloid deposit ?

A

Type II

116
Q

Which DM is a/w HLA system?

A

Type 1. DR3 and DR4.

117
Q

Kidney stones and stomach ulcers

A

MEN 1 – WERMERSE syndrome

118
Q

What kind of heart dz a/w carcinoid syndrome

A

Tricuspid stenosed by serotonin action.

119
Q

What vitamin might be deficient in carcinoid syndrome

A

Niacin. Tryptophan is the precursor for serotonin and niacin and if most is being used to make serotonin a niacin deficiency may result.

120
Q

Which diabetes drug decreases gluconeogenesis

A

Biguanides (METFORMIN). Also increases glycolysis and peripheral glucose uptake.

121
Q

What class of drugs are tolbutamide and chlorpropamide

A

FIRST gen sulfonylureas which cause DISULFIRAM LIKE EFFECTS !!!!

122
Q

Which class of DM drugs trigger insulin release via increased calcium influx?

A

Sulfonylureas. They close the potassium channel in Beta cell membrane so the cell depolarizes.

123
Q

What class of drugs are glyburide, glimepiride, and glipizide

A

Second gen sulfonylureas, a/w HYPOglycemia

124
Q

Why are sulfonylureas useless in type 1 DM

A

Require some islet function as they stimulate the release of endogenous insulin

125
Q

MOA of TZD

A

Increases insulin sensitivity in peripheral tissue by binding to PPAR-gamma nuclear transcription regulator.

126
Q

4 toxicities of the glitazones

A

These are TZDs and they cause weight gain! edema. Hepatotoxicity and HEART FAILURE.

127
Q

Which class of DM drugs decrease postprandial hyperglycemia

A

Alpha glucosidase inhibitors.

128
Q

What class of med is Miglitol

A

Alpha glucosidase inhibitor

129
Q

What class of med is pramlintide

A

Amylin analog

130
Q

What is the MOA of pramlintide

A

Decreaes glucagon and gastric emptying

131
Q

Exenatide and liraglutide are what class of drugs

A

GLP-1 analogs

132
Q

How do GLP-1 analogs and DPP-4 inhibitors work

A

Increase insulin and decrease glucagon release.

133
Q

What class of drugs are the gliptins

A

DPP-4 inhibitors.

134
Q

Which DM drugs may cause pancreatitis as a SE?

A

Exenatide

Liraglutide (GLP-1 analogs)

135
Q

Turner syndrome can use what kind of pituitary drug

A

GH!

136
Q

SE of octreotide

A

Inhibit GH release from AP which is similar to ADH ..as in it can cause hyponatremia and seizures!

137
Q

MOA of glucocorticoids

A

Decreases production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2

138
Q

Which thyroid med also decreases peripheral conversion of T4 to T3

A

PTU

139
Q

Which endocrine drug can cause agranulocytosis

A

PTU