endocrine uworld Flashcards

1
Q

what vitamin deficiency might see in carcinoid syndrome?

A

niacin

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2
Q

low urine osmolality < 300 mOsm
low urine specific gravity < 1.006
high serum osmolality > 250 mOsm

THEN
Low serum Na vs High serum Na >145

A

diluted urine
pointing towards diabetes insipidus

low: primary polydipsia

high: diabetes insipidus

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3
Q

wt loss, DM, diarrhea, painful, pruritic rash

necrolytic migratory erythema: erythematous papule that coalesce to form large, indurated plaques with central clearing

dx w/:

A

glucagonoma

dx w/: abdominal imaging MRI or CT scan

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4
Q

decreased libido, ED, no morning eretions, DM, joint pain, hepatomegaly

A

hereditary hemochromatosis

d/t excessive absorption of iron and deposition of excess iron in the tissues

can cause secondary hypogonadism

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5
Q

young girl with rapidly progressive (<1year) hirsutism and virilization (clitoromegaly)

dheas
testosterone
LH levels

A

androgen secretion tumor

androgens will be high

dheas: high
testosterone: high
LH: low d/t negative feedback from testosterone

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6
Q

Female with hirsuitism, rapid onset (<1year), virilization(temporal balding, clitoromegaly) suggests:

A

androgen secreting neoplasm

High TESTOSTERON with normal dheas –> ovarian source

high DHEAS suggests adrenal tumor

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7
Q

propylthioruracil and methimazole adverse effect:

A

agranulocytosis

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8
Q

TSH - low
Free T4 - high
RAIU - low

next step?

A

measure thyroglobulin

if low: then exogenous hormone (weight loss supplement)

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9
Q

graves disease treatment that worsens ophthalmopathy

A

radioactive iodine

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10
Q

Patient takes OCP’s and then elevation in T4 but normal TSH

A

estrogen induced increase in T4-binding globulin
(increased thyroid hormone binding protein)

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11
Q

thyrotoxicosis (lid retraction, fine tremor) with HTN
what’s causing the HTN?

A

increased myocardial contractility

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12
Q

muscle weakness, muscle atrophy, with anxiety, tachycardia, wt loss

A

thyrotoxic myopathy

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12
Q

muscle weakness, muscle atrophy, with anxiety, tachycardia, wt loss

A

thyrotoxic myopathy

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13
Q

treatment management of Graves hyperthyroidism

A

**INITIAL: b-blocker
1) anti-thyroid drugs :
Propylthiouracil or Methimazole
2)^^if still no results then Radioactive iodine (more definitive treatment)
3) thyroidectomy (if they have a large goiter or coexisting thyroid nodule suspicious for cancer or have severe ophthalmopathy (since RAIU is contraindicated)

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14
Q

untreated hyperthyroidism can cause:

A

bone loss leading to osteoporosis
(increase osteoclast activity)

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15
Q

hypoglycemia + high insulin + LOW c-peptide

A

exogenous insulin

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16
Q

hypoglycemia + high insulin + high c-peptide + high pro-insulin >5pmol/L

A

beta cell tumor (insulinoma)

or

surreptitious use of insulin or sulfonylurea (but you will see sulfonylurea in the plasma)

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17
Q

chronic glucocorticoid therapy effects on:
cortisol:
aldosterone:
ACTH:

A

cortisol: LOW
aldosterone: normal
ACTH: LOW

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17
Q

chronic glucocorticoid therapy effects on:
cortisol:
aldosterone:
ACTH:

A

cortisol: LOW
aldosterone: normal
ACTH: LOW

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18
Q

euthyroid sick syndrome: why will you see low T3

A

decreased peripheral conversion of T4 to T3

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19
Q

cool, dry ski, metabolic slowing, cognitive (difficulty concentrating) psychiatric depression, irritability, + abnormal uterine bleeding

TSH:
prolactin:
FSH:
LH:

A

hypothyroidism

THS: HIGH
PROLACTIN: HIGH
FSH: low
LH: low

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20
Q

PCOS treatment

A

weight loss
OCP’s
letrozole for ovulation induction

21
Q

hemorrhage during child birth can cause ____
ACTH:
Serum sodium:
serum potassium:

A

Sheehan syndrome
pituitary infarction (central AI) causing adrenal insufficiency

AI causes cortisol deficiency
cortisol acts as an inhibitor of Anti-diuretic hormone –> so you will see SIADH –> hyponatremia

ACTH: LOW
SERUM NA: LOW
K: normal (vs Primary AI destroyed cortex Addisons: hyperkalemia)

22
Q

29F generalized weakness, fatigue, nausea, abdominal pain, dry and pigmented buccal mucous membranes, eosinophilia

A

primary adrenal insufficiency: autoimmune response (Addisons)

23
Q

pt with Addisons: hypotension, hyperpigmentation, also called: ____

what are the labs:
Na:
K:
____
morning cortisol
ACTH

A

autoimmune adrenalitis

hypo-Na
Hyper-K
Eosinophilia

Low morning cortisol
High ACTH

tx: Glucocorticoids (prednisone) or mineralocorticoids (fludrocortisone)

24
Q

PAI - Addisons
what tests?

A

8 am cortisol
or
cosyntropin (synthetic ACTH analogue) ACTH stimulation

25
Q

PAI - Addisons
what tests?

A

8 am cortisol
or
cosyntropin (synthetic ACTH analogue) ACTH stimulation

26
Q

initial tests for Cushing syndrome:

A

24 hr urinary cortisol excretion

late night salivary cortisol assay

low-dose dexamethasone suppression test

27
Q

38F with hirsuitim, weight gain, bone demineralization, HTN, muscle weakness:
d/t :

A

Cushing syndrome d/t excess cortisol from either
1)exogenous glucorticoid use
2)endogenous cortisol secretions:
A) ACTH-Producing pituitary tumor (Cushing dx)
B) ectopic ACTH production (small cell lung cancer)
C) Primary adrenal disease (adenoma)

either way: causes breakdown of muscles, painless with normal ck values

muscle atrophy

28
Q

diabetes medication that:
induces weight loss, decrease of atherosclerotic cardiovascular disease, heart failure, and slow progression of albuminuria in diabetic nephropathy

A

SGLT-2 inhibitors

and GLP-1 receptor agonists

29
Q

diabetes med: reduces cardiovascular mortality, induce weight loss, and has low risk for hypoglycemia

A

glucagon-like peptide 1 receptor agonist GLP-1

30
Q

management for DKA

A
31
Q

in DKA why do you see hyperkalemia

A

insulin deficiency impairs cellular ENTRY of potassium

impaired cellular uptake

32
Q

HHS management

A

replenish K ***** since giving insulin can cause hypokalemia

33
Q

drugs for neuropathy

A

pregabalin

34
Q

diabetic neuropathy:
proprioception loss (negative symptoms)

vs

pain/paresthesia (positive symptoms

A

large

small

35
Q

diabetic gastroparesis

dx:

tx:

A
36
Q

HTN, hypokalemia, metabolic alkalosis, elevated plasma aldosteron:renin ratio>20

dx:

tx: (2)

A

primary hyperaldosteronism Conn syndrome

dx: plasma aldosterone/renin ratio
CT scan
absence of aldosterone suppression with oral saline laid

tx: bilateral adrenal hyperplasia MRA spironolactone epilreone(doesnt have the gyno decreased libido effects)
unilateral adenoma: surgical resection

37
Q

primary hyperaldosteroneism chart

A
38
Q

adrenocortical causes of HTN

A
39
Q

pulmonary embolism with hyperventilation and respiratory alkalosis –> hypocalcemia sxms:
why low calcium

vs
if in state of acidosis what would drive Ca towards

A

alkalosis: hydrogen ions dissociate from albumin, allowing na increase in binding to calcium (causing hypocalcemia since ionized calcium is the active form)

vs

acidosis: increASED LEVELS OF IONIZED calcium

40
Q

Acromegaly:
what test?
if positive what next test?
if inadequate GH suppression, what next?
treatment options?

A

1) Insulin-like Growth Factor-1 (IGF-1 from liver) level
2) Oral glucose suppression test –> normally: should suppress GH
3) MRI of brain for pituitary adenoma

tx options:
transphenoidal surgical resection
or
somatostatin analogue: octreotide
or
GH receptor antagonist: Pegvisomant

41
Q

water deprivation test

A
42
Q

pt with DM2, better glycemic control will reduce the risk of ____ complications within 5 years?

A

MICRO-vascular complications like nephropathy or retinopathy

macro-vascular complications like MI, stroke, all-mortality has no change

43
Q

muscle weakness, fatigue, HTN, mild hypernatremia, low potassium, 3cm mass in left adrenal gland

what is it?
bicarb level?

A

Primary Hyperaldosteronism

increase in aldosterone causing wasting of potassium –> HYPO-kalemia

Aldosterone stimulates nephron to secrete H+ resulting in increased reabsorption of bicarb (elevated bicarb metabolic alkalosis)

increase in Na reabsorption leading to HTN but d/t aldosterone escape: [you will see increased Renal Blood flow, increased GFR, increased atrial natriuretic peptide] WHICH all lead to some increase in Na excretion (which is why you see mild hypernatremia)

44
Q

60M with dry cough, fatigue, anorexia, 20lb weight loss over 3 mo, smoking, now with hypercalemia due to:

A

elevated Parathyroid hormone-related protein
PTH-RP

45
Q

pt has hypercalcemia, next best test/step?

A

measure parathyroid level:

determines if it is PTH-independent (suppressed PTH) d/t malignancy, vit-D toxicity etc.

or PTH dependent (elevated PTH) D/T primary hyperparathyroidism

46
Q

pituitary microadenoma (>1cm) OR symptomatic (prolactinoma with galactorhea amenorrhea etc.)
treatment?

tumor size of >3cm or refractory to medication, treatment?

A

dopamine agonist cabergoline or bromocriptine – normalize prolactin levels and reduce tumor size

large 3cm+ transphenoidal resection

47
Q

post-viral painful tender goiter

tx?

A

subacute thyroiditis

tx: symptomatic with b-blockers and nsaids

48
Q

post partum thyroiditis (will see positive thyroid peroxidase assay marker for autoimmune thyroid disease) and negative thyrotropin receptor antibody assay (marker for graves)
treatment?

A

self limited
you can do symptomatic with b-blocker but nothing else

49
Q

pt with symptomatic hypocalcemia: you’ve rule out hypoparathyroidism, what is the next step?

A

rule out vitamin d deficiency with measuring serum 25-hydroxyvitamin D

50
Q

causes of primary hypoparathyroidism (hypocalcemia)

A

post-surgical**
autoimmune
congenital absence or maldevelopment of parathyroid (di Georges)
defective calcium sensing receptor on the parathyroid glands
infiltrative disease hemochromatosis, Wilsons or neck radiation

51
Q

bone pain, fatigue, hypo-phosphatemia, with malabsorptiv disorder (celiac)

what are the impt lab values

A

osteomalacia
elevated alk-phos, PTH
LOW Ca, Phos, AND urinary Ca
Low 25(OH)D

impaired osteoid matrix mineralization

52
Q

Vitamin D deficiency cause: drugs:

A

anti-convulsants: phenytoin, CARBAMAZEPINE,

isoniazid, rifampin