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Internal Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

MOA & SE of Insulin

A

Decrease hepatic glucose production
Increase peripheral glucose uptake

hypoglycemia

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2
Q

Sulfonylureas MOA & SE

A

stimulate insulin secretion

MIDE/RIDE/ZIDE
tolbutamide, chlorporpamide, glipizide, glyburide, gliclazide, glimepiride

wt gain, hypoglycemia

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3
Q

Biguanides MOA & SE

A

decrease hepatic glucose production
increase insulin-mediated uptake of glucose in muscles

Metformin

GI

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4
Q

Alpha-glucosidase inhibitor MOA & SE

A

inhibit polysaccharide absorption

Acarbose, miglitol, voglibose

Flatulance, GI

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5
Q

Thiazolidinediones MOA & SE

A

increase peripheral uptake of glucose
Decreased hepatic glucose production

GLITAZONE
Rosiglitazone, pioglitazone

wt gain, fluid retention, HF, macular edema, osteo, bladder cancer with pioglitazone

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6
Q

Which class of oral anti-diabetic medicine should NOT be used in pts with HF? And which other single specific drug and drug class?

A

Thiazolidinediones

Saxagliptin (DPP-4)

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7
Q

Meglitinides MOA & SE

A

stimulate insulin increase

Repaglinide, Nateflinide

wt gain, hypoglycemia

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8
Q

Amylinomimetics MOA & SE

A

slow gastric emptying, suppress glucagon secretion, increase satiety

PramlinTIDE

wt loss, nausea, vomiting, increased hypoglycemic risk if used with insulin

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9
Q

GLP-1 MOA & SE

A

slow gastric emptying, suppress glucagon secretion, increase satiety

Exenatide & liraglutide

wt loss, hypoglycemia when used with sylfonylureas, nausea & vomiting, possible increased PANCREATITIS and CKD

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10
Q

DPP-4 MOA & SE

A

slow gastric emptying
Suppress glucagon secretion

sitaGLIPTIN, saxaGLIPTIN, vildaGLIPTIN, linaGLIPTIN, aloGLIPTIN

hypoglycemia with sulfonylureas, nausea, increased risk of INFECTIONS & possible PANCREATITIS

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11
Q

SGLT-2 MOA & SE

A

increase kidney excretion of glucose

DapaGLIFLOZIN & canaGLIFLOZIN

wt loss, hypoglycemia with insulin, & insulin secretagogues. kidney impairment. Hypersensitivity rx. Increased candidal genital infx and UTI.

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12
Q

What is the Whipple triad in glucose control

A
  1. Symptomatic hypoglycemia
  2. documented hypoglycemia 55mg/dl
  3. prompt symptomatic relief with correction of hypoglycemia
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13
Q

Causes of hypoglycemia w/o DM

A
  1. Insulinoma
  2. surreptitious use of sulfonylureas/meglitinides
  3. Surreptitious use of insulin
  4. Insulin autoimmune hypoglycemia
  5. Alcohol
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14
Q

Hypoglycemic patient with decreased c-peptide, ddx?

A

Surreptitious insulin use

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15
Q

How to test for surreptitious use of sulfonylureas/meglitinides

A

Urine or blood metabolites

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16
Q

How do you do a “Fasting Challenge”?

A

Measure blood glucose while fasting every 6 hours until below 60, then every 1-2 hours. Then obtain serum insulin, plasma c-peptide, plasma pro-insulin, b-hydroxybutyrate (should be normal if no excessive insulin). Then administer GLUCAGON (should bring it up if it’s physiologic)

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17
Q

Indication for giving sodium bicarb?

A

DKA/HHS with pH <6.9

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18
Q

When to start screening for retinopathy (T1DM vs. T2DM)

A

T1DM: after 5 years
T2DM: at diagnosis
gDM: 1st trimester

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19
Q

BP goal for pts with DM

A

<140/80

SBP <130 in young pts with long life expectancy or increased risk of stroke)

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20
Q

When to start statin

A

In DM:
High dose if LDL >190, ASCVD risk >7.5%
Mod-high if ASCVF >7.5%
or in <40yo with LDL >100

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21
Q

When to screen for nephropathy (T1 v T2)

A

T1: after 5 years
T2: at diagnosis

> 30mg/g

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22
Q

Hormones of the Anterior Pituitary (6)

A
  1. ACTH
  2. TSH
  3. LH
  4. FSH
  5. GH
    6 Prolactin
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23
Q

Hormones of Posterior Pituitary (2)

A

ADH and Oxytocin

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24
Q

Tests for ADH

  1. Excess
  2. Deficiency (DI)
A

Same for both: Serum and urine sodium, and urine Osm

In deficiency: also do WATER DEPRIVATION TEST

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25
Q

Tests for Excess Growth Hormone

A

IGF-1

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26
Q

Tests for Excess/deficiency in Growth Hormone

A

Excess: glucose tolerance test (would normally suppress GH/IGF-1) –> then MRI
Deficiency: IGF-1 response to serum GH on stimulatory test (insulin tolerance test)

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27
Q

Test for LH and FSH deficiency

A

LF, FSH, testosterone (male), estriol (female)

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28
Q

What can cause enlargement of pituitary gland? (at which time it would make it difficult to see whether there is a mass and thus imaging should be avoided)

A

pregnancy and hypothyroidism

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29
Q

Name 3 benign sellar masses and 2 malignant

A

Benign: craniopharyngioma, meningioma, Rathke’s cleft cyst

Malignant: metastatic disease and pituitary carcinoma

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30
Q

What is lymphocytic hypophysitis & how do you treat it?

A

inflammatory pituitary lymphocytic infiltration common in pregnant and post-partum women. May cause pituitary insufficiency (could be transient or permanent).

Tx: glucocorticoids

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31
Q

How do you evaluate a sellar mass?

A

(mass effect? hormone producing? will it grow?)

Initial labs: 8am cortisol, TSH, FT4, prolactin, IGF-1.

If not causing mass effect, and not secreting hormones, repeat MRI in 6 mo for macroadenoma (>1cm) or 12mo for micro adenoma (<1cm)

If no growth, repeat imaging q1-2year for the next 3 years.

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32
Q

How do you evaluate an Empty Sella

A
  1. look for 2ndary cause (prior surgery? radiation? infarction? incr. CSF?)
  2. Look for signs of pituitary hormone deficiency.
  3. If none, screen for cortisol, TSH, 8am cortisol, FT4

No need for repeat imaging

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33
Q

What cranial nerves pass through the Cavernous sinus?

A

III, IV, VI

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34
Q

Indication for surgery of pituitary mass

A
  1. mass effect (visual field defect) (or tumor close to optic chiasm in pt who wants to get pregnant)
  2. tumor that abuts optic chiasm
  3. tumor growth
  4. invasive tumor (invading brain/cavernous sinus)
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35
Q

Pituitary apoplexy vs. Sheehan sd

Treatment?

A 
Apoplexy = bleed
Sheehan = infarct/hypoperfusion due to hemorrhage

stress dose steroids & surgery

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36
Q

What hormones are damaged first after pit gland injury (radiation/surgery, etc), what hormones are damaged later?

A

Early: GH (somatotrophs) and gonadotropin (LH, FSH) – deficiency

Late: THS and ACTH deficiency

Can also increase prolactin (compression of stalk = blocking dopaminergic inhibition of prolactin secretion)

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37
Q

Secondary cortisol deficiency (as compared to primary). Cause, symptoms.

A

Likely 2/2 excessive steroid use

Sx: n/v lightheaded, hypoglycemia, hypotension, hyponatremia. Less than primary adrenal issues (no mineralocorticoid deficiency).

No hyperpigmentation (cuz low ACTH)

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38
Q

When do you need to taper steroids

A

If HD for 3wk
–> before stopping, test AM cortisol (should be greater than 11 ). Then, after 36-48h, do ACTH stimulation test with cosyntropin. If appropriate response, can keep off. May need stress dose steroids during illness for 1 year.

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39
Q

Difference bw primary and secondary hypothyroidism

A

Primary: TSH high, FT4 low

Secondary (central): TSH low, FT4 low – must monitor FT4, not TSH

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40
Q

Diagnosis of DI

A 
Water deprivation test
Stop test when one is achieved:
1. Urine Osm >600 (no DI)
2. Patient lost 5% of weight
3. Urine Osm is stable while serum osm rises over 2-3h
4. Plasma Osm >295
5. Serum Na >145

Desmopressin challenge if Urine Osm <600
- If 100% increase in urine Osm = CENTRAL DI
- if 0% increase then nephrogenic DI
(and then in between)

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41
Q

Diagnosis of Acromegaly (growth hormone excess)

A

Glucose tolerance test

75g oral glucose –> measure glucose at 0, 30, 60, 90, 120 and 150 m
If GH <0.2 (LOW) = normal
If GH >1.0 (NOT SUPPRESSED) = acromegaly

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42
Q

Most common cause of gonadotropin deficiency in women

A

hypothalamic amenorrhea (excessive exercise, illness, anorexia)

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43
Q

Tx of hypogonadotropic hypogonadism

A

Premenopausal women:
Estrogen & progesterone containing OCP
- RECOMMENDED to preserve bone density

Postmenopausal women:
- No Tx

Men:
Testosterone, only if they don’t desire fertility

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44
Q

Syndrome associated with hypogonadotropic hypogonadism

A

Kallman

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45
Q

Growth Hormone Deficiency sx

A

Pre-pubertal: decreased linear growth

Adult: fatigue, loss of muscle mass, increased ratio of fatty tissue to lean tissue, increased risk of osteoporosis

46
Q

GH deficiency tx

A

GH injections

47
Q

Definition of polyuria

A

> 3L urine a day

48
Q

Tx for panhypopit

A

levothyroxine, cortisol, ADH (+/- gonadotropin depending on age/fertility wants)

49
Q

Causes of hyperprolactinemia

A

Most common: physiologic (postpartum, nipple stimulation, exercise, coitus, stress, nipple piercing)

Drugs (mild elevation): antipsychotics (anti-dopamine), metoclopramide

  • Prolactinoma (>100)
  • Primary hypothyroidism (increased TRH can increase prolactin)
  • Non-functioning adenoma (compress stalk to decrease inhibitory dopamine
50
Q

Sx of hyperprolactinemia

A

cause hypogonadotropic hypogonadism (prolactin inhibits GnRH therefore decrease LH, FSH)

  • amenorrhea
  • early menopause
  • infertile, high risk of osteoporosis
51
Q

Management of Prolactinoma

A

Microprolactinoma (if asymptomatic, ntd). Repeat MRI after 12 mo of medical therapy. If shrunk, no need to repeat.

Macroprolactinomas >250 or >10,000: oral contraceptive pills or dopamine agonist (bromocriptine and cabergoline). Hormone replacement if pre-menopausal. Repeat MRI after 3 mo of medical therapy, then q6-12mo until stable.

Surgery is NOT first line, even with mass effect

Check prolactin level after 1 mo of tx then q3-4mo. Can taper Bromocriptine once prolactin lvl is normal after 2 years. After stopping check prolactin q1mo, then q3mo for 1 year, then annually.

52
Q

SE of bromocriptine

A

orthostasis and lightheadedness, dizziness, nausea, headache

53
Q

Acromegaly (GH excess) sx

A
  1. excessive growth (tall) - due to continued opening of epiphyseal growth plates
  2. Prominent bbrow or jawline, enlarged skull, large nose,
  3. facial edema,
  4. excessive spacing between teeth
  5. macroglossia
  6. large hands and feet
  7. skin tags
  8. arthritis
  9. DM, HTN, colon polyps, thickened skin, excessive perspiration
  10. LVH and cardiomyopathy, valvular heart dz
  11. increased cancer
54
Q

Tx of acromegaly

A
  1. transsphenoidal tumor resection
  2. If no response, injectable SOMATOSTATIN (inhibits GH secretion)
  3. if no response, High dose dopamine agonist therapy
  4. if no response, PEGVISOMANT (GH receptor blocker) –> but has high risk of tumor growth since it’s a peripheral receptor inhibitor, doesn’t decrease GH

Gamma knife radiosurgery can be offered

55
Q

TSH-secreting tumor

A

RARE - can also secrete prolactin or GH

First line = neurosurgery
May need medication if co-secretes above

56
Q

Cushing Disease vs. Cushing Syndrome

A

Disease: ACTH-secreting pit adenoma
Syndrome: hypercortisolism from any cause (ACTH-dependent or not)

57
Q

How to differentiate ectopic source or central cause of Cushing

A

Measure ACTH on 2 separate occasions

  1. MRI brain. If <6mm then,
  2. 8 mg dexamethasone suppression test (non-specific/sensitive)
  3. Intrapetrosal sinus sampling while administering CRH is recommended (high sensitivity) prior to surgery. Central to peripheral gradient >2 prior to CRH or >3 after is diagnostic of Cushing DISEASE

Ectopic sources: pancreas, lung, thymus (all rare)

58
Q

Tx of Cushing

A

transsphenoidal surgery –> then glucocorticoid

Medical options: ketoconazole, inhibitors of adrenal enzyme synthesis of cortisol, metyrapone, cabergoline (DA ag), pasireotide (somatostatin analogue)

Last resort: bilateral adrenalectomy – will need life long glucocorticoid and mineralocorticoid

59
Q

4 zones of the adrenals and what they produce

A

Outer: glomerulosa (aldosterone)
Middle: Fasciculata (glucocorticoid)
Inner: Reticularis (androgens – DHEA and DHEAS, androstenedione)

Medulla (chromaffin cells): catecholamines –> norepinephrine, epinephrine,

60
Q

Lab tests to diagnose Cushing

A
  1. Overnight low dose suppression test (1mg dexamethasone)
  2. 24h Urine free cortisol (w/ UCr)
  3. Late night salivary cortisol

do this twice

61
Q

When is dexamethasone suppression test unreliable?

A

Malnutrition/cirrhosis/nephrotic sd (low cortisol-binding globulin)

Using OCP or pregnant

Taking CYP450 activator (phenytoin, phenobarb, carbamazepine, rifampin, pioglitazone)

shift work

62
Q

First line treatment of adrenal adenoma

A

surgical resection

63
Q

Classic triad of pheochromocytoma

…and other sx

A

Triad: diaphoresis, HA, tachycardia
Sx: palpitations, tremor, pallor, anxiety

64
Q

What syndrome is pheochromocytoma associated with (4)

A

MEN 2A
MEN 2B
Neurofibromatosis 1
von Hippel-Lindau Sd (VHL)

65
Q

MEN1 manifestation

A

3Ps
Parathhyroid adenoma
Pancreatic islet cell and enteric tumors (gastrinoma, insulinoma)
Pituitary adenoma

Other (carcinoid tumor, adrenocortical adenoma)

66
Q

MEN 2A & 2B

A

RET mutations
Medullary thyroid carcinoma)
Pheochromocytoma
Parathyroid hyperplasia

2B = marfinoid
+ mucosal neuroma, GI ganglinoneuroma

67
Q

Diagnosis of Pheochromocytoma

A
  1. Plasma free metanephrines (very sensitive, low 85-89% specificity)
  2. Urine fractionated metanephrines and catecholamines (if pre-test probability is low, because there is low false positive rate)

If hospitalized due to critical illness –> abd imaging rather than lab (as would not be reliable)

68
Q

Imaging to localize pheochromocytoma & for mets

A

Initial: CT or MRI of abdomen
if negative…

THEN: Iodine 123 (MIBG) scanning & head and chest imaging

Mets: Fluorine18-fluorodeoxyglucose (FDG) pet scanning

69
Q

First-line, pre-operative therapy for pheochromocytoma

A

phenoxybenzamine (to block alpha adrenoceptors) –> titrate to BP <130/80 seated and SBP >90 standing

B-blockers added AFTER to decrease reflex tacychardia

70
Q

When to stop surveillance for pheo once it is treated surgically

A

NEVER

High rate of metastasis and recurrence.

71
Q

Signs of primary hyperaldosteronism

A

High BP
Low K (can be diuretic induced)
Metabolic ALKALOSIS

72
Q

Causes of secondary hyperaldosteronism

A
  1. Renal artery stenosis
  2. Liddle sd (AD pseudoaldosteronism)
  3. renin-secreting tumors
  4. Congenital adrenal hyperplasia
  5. Licorice
73
Q

How to test for primary hyperaldosteronism

A

Midmorning plasma renin activity (PRA) and plasma aldosterone conc (PAC)

(stop ACE-i, b-blocker, NSAIDs, MRA, SSRI prior to testing if possible. Can use hydralazine, doxazosin, verapamil)

Positive if PAC >15, PRA is suppressed, and PAC/PRA ratio is >20

Confirmatory testing: oral and IV salt loading and fludrocortisone suppression, and captopril challenge test

If confirmed –> CT abd –> adrenal vein sampling if imaging unrevealing & to confirm lateralization

74
Q

Goal of tx of PA and method

A
  1. Improve HTN (will not be resolved)
  2. Improve hypokalemia
  3. Decrease serum aldosterone conc (to decrease CV events)

Method: lap adrenalectomy
If not a surgical candidate or bilateral adrenals, MRA (spironolacotone, eplerenone). Amiloride is second line.

75
Q

Common cause of primary adrenal failure

A

Most: autoimmune adrenalitis (70-80%)

Addison Dz: tuberculosis infiltration of adrenal glands(7-20%)
Metastatic cancer
Autoimmune polyglandular syndromes (APS) Type 1&s
CAH
X-Linked adrenoleukodystrophy
Antiphospholipid syndrome/DIC/Systemic Anticoagulation –> hemorrhage

76
Q

Clinical hallmark of primary adrenal failure

A

hyperpigmentation

77
Q

Labs to send if there are signs of hirsutism, deepening of voice, precocious adrenarche

A

DHEA & DHEAS

mild elevation is typical. PCOS.
–> CT adrenals to find tumor

78
Q

DIff in tx in primary vs. secondary adrenal insufficiency

A

Primary: glucocorticoid + fludrocortisone (not if >50mg/d of glucocorticoid is given) (mineralocorticoid)
Secondary: just glucocorticoid

79
Q

Workup of incidental adrenal mass (Imaging)

A

Favors benign:
<4 cm
Density <10 HU
Contrast washout >50% (10 m)

Suspicious:
>4m
Density >10 HU
Contrast washout <50% (10 m)

80
Q

Workup of Incidental Adrenal Mass (Hormonal)

A
  • Cortisol - all pts
  • Aldosterone - pts with HTN or low K
  • Catecholamines - all pts
  • Androgens - women with hirsutism, virilization, irregular menses
81
Q

Follow up schedule for incidental adrenal mass

A
  • CT/MRI in 3-6 mo then annually for 1-2 years

- Hormonal evaluation yearly for 4 years

82
Q

Indications for adrenalectomy

A

Suspicious imaging
Growth >1cm/year
Functioning tumors (pheochromocytoma, aldosterone-producing adrenal tumor, subclinical CS with complications)

83
Q

Labs for Hashimoto’s (chronic lymphocytic thyroiditis)

A

TPO (thyroid peroxidase)

84
Q

Grave’s disease Labs and is it hyper or hypo

A

TSI (thyroid-stimulating immunoglobulins)
TRAb against TSH receptor
HYPERthyroidism

85
Q

What labs to test for thyroid cancer

A

Serum Tg (thyroglobulin) and TgAb (thyroglobulin antibody)

86
Q

Specific serum lab to test for Medullary Thyroid Carcinoma besides thyroid function tests

A

Calcitonin

87
Q

When is radioactive iodine uptake (RAIU) test contraindicated

A

pregnancy and breastfeeding

88
Q

Most common cause of hyperthyroidism

A

Graves disease and toxic adenoma

89
Q

What is apathetic hyperthyroidism

A

no symptoms but will have afib and heart failure

90
Q

Normal or high TSH in the setting of T3/T4

A

TSH-secreting pituitary adenoma

91
Q

First line therapy for thyrotoxicosis

A
  1. Methimazole/PTU
  2. B-blocker

Then definitively –> radioactive iodine and surgery

92
Q

Side effects of both PTU and methimazole

A

rash
agranulocytosis
liver dysfunction (cholestasis in Methimazole, fatal hepatotoxicity in PTU)
Methimazole - teratogenic

93
Q

Physical exam in Graves Disease

A

Widened pule pressure
Thyroid bruit
lid retraction (proptosis), scleral injection, periorbital edema

94
Q

Causes & Tx of PAINFULL thyroiditis

A

Most common: subacute thyroiditis - post-viral inflammatory process

  1. Inflammatory (de Quervain or subacute granulomatous tyroiditis)
  2. Infectious (suppurative; staph & strep)
  3. Radiation induced

Tx: NSAID & glucorticoids if severe

95
Q

Causes & Tx of PAINLESS thyroiditis

A
  1. Postpartum thyroiditis (up to 1yr post delivery)
  2. Silent thyroiditis
  3. Drug-Induced thyroiditis

TPO antibodies?

96
Q

Course of thyroiditis

A

thyrotoxicosis for 2-6 wks

hypothyroid 6-12 weeks

97
Q

Indication for treatment of subclinical hyperthyroidism

A

If TSH <0.1

98
Q

Indication for treatment of subclinical hypothyroidism

A

+TPO Antibodies

or large goiter

99
Q

Type 1 Amiodarone-induced thyrotoxicosis vs Type 2 AIT

A

Type 1: caused from iodine in amiodarone

type 2: from cytotoxicity of amiodarone itself

100
Q

Indication to screen pregnant women & how often. What medication to treat with and when.

A

If >30 yo, if there is history of autoimmune disorder, previous thyroid hormone replacement, those living in iodine-deficient areas, known + TPO or TSI Ab.

q6 weeks if abnormal

PTU 1st trimester
Methimazole 2nd and 3rd trimester

101
Q

When do fetal thyroid tissue become functional

A

10-12 weeks

102
Q

What causes fluctuation in T3 and T4 in pregnancy?

A

Increased thyroxine-binding globulin

103
Q

Early and late Euthyroid Sick Syndrome labs

A

Early: normal to high TSH, Low T3, Low T4
Late: low everything

104
Q

Tx for thyroid storm

A
  1. PTU and propranolol
  2. HD glucocorticoids
  3. iodine drops
105
Q

Management of myxedema coma

A

Labs: TSH, T4, CORTISOL

Tx: give HD steroids
then IV levothyroxine (200-500 mcg) –> maintenance 50-100 mcg IV)

106
Q

Diagnosis pathway to thyroid nodules and goiters

A
  1. TSH
  2. High/normal TSH
    a. Ultrasound
    b. If >1cm, FNA
    c. If <1cm, repeat US in 6-24 mo
  3. Low TSH
    a. Thyroid scan, FT4, FT3
    i. “Hot” –> No FNA –> Tx hyperthyroid
    ii. “Cold” –> US and FNA
107
Q

Radiographic findings of thyroid that are suspicious for cancer (70% specificity)

A

microcalcifications
marked hypoechogenicity
Irregular borders
Taller-than-wide shape

108
Q

When is hemithyroidectomy indicated

A

<45 yo

<4 cm nodule

109
Q

Management of large multinodular goiter with compressive symptoms

A

Surgical removal

110
Q

Most common types of thyroid cancer and the most aggressive

A
  1. Papillary
  2. Follicular
  3. Medullary

Aggressive: Anaplastic thyroid cancer

111
Q

If you find medullary thyroid cancer, what should you screen patient with

A

RET proto-oncogene

Biochemical screening for pheochromocytoma with plasma fractionated metanephrine levels

Internal Medicine (6 decks)

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