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Medicine Boards > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

lymphocytic hypophysitis

A

most cases occur during or after pregnancy

causes hypopit and possibly symptoms of a mass lesion

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2
Q

Explain lab findings for Hypopit (GH, FSH/LH, TSH, ACTH, Prolactin)

A

GH = depressed IGF-1, diminished response to insulin tolerance test

FSH/LH = depressed FSH, LH, estradiol, testosterone

TSH = depressed free T4 and TSH

ACTH = low cortisol and depressed ACTH, positive cortisol response to ACTH, (depressed response of 11-deoxycortisol and cortisol to metyrapone)

Prolactin = may be elevated due to loss of tonic inhibition

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3
Q

Treatment of acute pituitary apopexy

A

Glucocorticoids! until acute adrenal insufficiency has been ruled out. May also need urgent neurosurgical decompression,

T4 replacement is indicated only AFTER hypoadrenalism is ruled out or treated

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4
Q

In what cases can pituitary gland be diffusely enlarged? (not tumor)

A
  1. untreated primary hypothyroidism

2. normal pregnancy

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5
Q

If suspected cushings disease, what would you order?

A

24-hr urine cortisol excretion + dexamethasone suppression test
or
late night salivary cortisol level (elevated)
serum ACTH level (elevated or inappropriately ‘normal’)

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6
Q

Name 2 lab tests you should always order after diagnosis of hyperprolactinemia?

A
  1. pregnancy test

2. TSH – bc hypothyroidism can cause hyperprolactinemia

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7
Q

Indications for surgery for pituitary adenomas

A
  • Secreting GH, ACTH, or TSH
  • adenomas with mass effect
  • visual field defects
  • hypopituitarism
  • prolactinomas unresponsive to dopamine agonists
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8
Q

How to diagnose DI?

How to differentiate between central and nephrogenic?

A
  1. Urine Osm <200 + inability to concentrate urine during water deprivation test
  2. Desmopressin challenge test – if positive (urine concentrates) = central DI –> order MRI pituitary. if negative (urine does not concentrate) = nephrogenic DI –> order kidney US
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9
Q

Treatment of Chronic central DI? Nephrogenic DI? acute DI after neurosurgery or head trauma?

A
  1. PO or IN desmopressin
  2. thiazide diuretic and salt restriction
  3. if unable to PO –> D5/0.45NS, add desmopressin if UOP high or hypernatremia
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10
Q

What lab tests do you order with asymptomatic empty sella?

A

Cortisol, TSH, free (or total) T4. If all normal - do nothing. Frequently seen in multiparous women.

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11
Q

name 3 forms of destructive thyroiditis. what is MOA of possibly thyrotoxicosis?

A
  1. Subacute (de Quervain), silent (painless), postpartum thyroiditis
  2. thyroid damage releasing preformed thyroid hormone into circulation
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12
Q

What are you concerned about in a patient who has sore throat or fever and taking methimazole or PTU?

A

presumed agranulocytosis until proven otherwise

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13
Q

Most important lab to check 1 week after pituitary surgery despite lack of symptoms?

A

Sodium
SIADH common 3-7 days post op
Initially may have DI (polyuria high-normal Na, dilute urine) followed by SIADH then again DI
Central DI may be temporary or permanent

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14
Q

What is one important screen to perform for diabetic female looking to get pregnant?

A

Dilated eye exam – b/c diabetic retinopathy gets worse with pregnancy. Monitor every trimester, and closely for 1 yr post partum.

Rapid improvement in glycemic control in the setting of retinpathy is associated with temporary worsening of retinopathy, and in pregnancy - goals are tight glycemic control.

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15
Q

How to treat glucocorticoid induced osteoporosis? What makes you moderate vs severe risk?

A

Oral bisphosphonates are 1st line in adult men/women with moderate to high fracture risk regardless of age.

In <40yo
High risk - previous osteoporotic fracture
Moderate - hip or spine BMD Z score < -3, or rapid bone loss (>10% at hip or spine over 1 yr) and continuing steroids at >7.5mg/day for >6months

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16
Q

what is Denosumab?

A

Monoclonal antibody against the receptor activator of nuclear factor κB ligand (RANKL), reduces bone resorption by inhibiting the development of osteoclasts.

Twice yearly injections, no endpoint or drug holiday like bisphosphonates

It circulates in the blood for up to 9 months after SQ injection, but once cleared from the circulation, bone resorption transiently but dramatically increases, resulting in an abrupt decline in bone mineral density and, in some cases, vertebral fractures.

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17
Q

When would you order calcitonin in setting of thyroid nodules?

A

in patients with hypercalcemia or a family history of thyroid cancer or MEN2

18
Q

Indication for FNAB

A

thyroid nodules >1cm with normal TSH level and suspicious sonographic features

OR

thyroid nodules <1cm with risk factors of thyroid cancer or suspicious ultrasound characteristics

19
Q

Name 3 ways to diagnose hypercortisolism (cushings syndrome)

A

1mg overnight dexamethasone suppression (fail to suppress cortisol <3mg/dL)

24hr urine cortisol (elevated) - twice

late night salivary cortisol (elevated) - twice

20
Q

How to differentiate between ACTH depending or independent cushings syndrome? How about pituitary vs. ectopic source of ACTH production?

A
  1. check ACTH level
    - – if <5, independent, get abd CT.
    - – if >20, dependent, get pituitary MRI/CT
  2. 8mg dexamethasone suppression. Used when you don’t find anything on MRI pituitary but ACTH is high.
    - — If pituitary ACTH source - should suppress cortisol by 50%
    - — If cortisol production is NOT suppressed –> ectopic tumor get CT c/a (SCLC, bronchial carcinoid, pheo, medullary thyroid cancer). If it IS suppressed – get intrapetrosal sinus sampling for ACTH to confirm pituitary source.
21
Q

Pheochromocytoma is associated with these 3 conditions

A
  1. MEN2
  2. von Hippel-Lindae disease
  3. neurofibromatosis type 1
22
Q

what are the 2 main causes & what labs diagnose primary hyperaldosteronism?

A
  1. aldosterone producing adrenal adenoma (40%) or bilateral adrenal hyperplasia
      • aldosterone-renin activity ratio of >20 with plasma aldosterone of >15 (normal <5)
      • confirm by giving high salt load (IV or PO) and having nonsuppressible elevated plasma aldosterone
    • ** testing cannot be done if pt is on spironolactone or eplerenone
23
Q

Secondary ammenorrhea with low estradiol + low/inapprop normal FSH and LH

Diagnosis ?
Possible causes?

A
  1. HYPOgonadotrophic hypogonadism
  2. hypothyroidism, hyperprolactinemia, hypothalamic (stress, weight loss, exercise), pituitary (tumor, sheehan syndrome)

“secondary”

24
Q

Secondary ammenorrhea with low estradiol + high FSH and LH.

Diagnosis?
Possible causes?

A
  1. HYPERgonadotropic hypogonadism
  2. premature ovarian insufficiency (autoimmune), chemotherapy, pelvic radiation

“Primary”

25
Q

How does hypothyroidism cause secondary ammenorrhea?

A

Causes secondary increase in prolactin levels (high TSH, high prolactin)

26
Q

Labs of primary testicular failure vs. secondary male hypogonadism

A

both have low testosterone 8am x 2

  1. primary – elevated FSH and LH
  2. secondary – now or normal FSH and LH
27
Q

causes of primary testicular failure

A 
Klinefelter syndrome (karyotype) 
atropy 2/2 mumps orchitis 
autoimmune destruction 
previous chemotherapy or pelvic irradiation 
hemochromatosis
28
Q

causes of secondary testicular failure

A

sleep apnea
hyperprolactinemia
hypothalamic or pituitary disorders (hemochromatosis, pituitary/hypothalamic tumor)
use of opiates, anabolic steroids, or glucocorticoids ***

29
Q

How does estrogen vs. testosterone affect thyroid hormone (thyroxine T4)?

A

Estrogen: (tamoxifien, raloxifene, OCP, pregnancy)
- increase thyroxine-binding globulin –> DECREASES free thyroxine (metabolicallya ctive) –> need to increase synthroid dose

Testosterone: (androgens, anabolic steroids)
- decrease thyroxine-binding globulin –> INCREASES free thyroxine (metabolically active) –> need to reduce synthroid dose

30
Q

Which oral anitglycemic agents help with weight loss?

A

GLP-1 mimetics (exenatide, liraglutide)

SGLT2 inhibitors (dapgliflozin, empagliflozin, canagliflozin)

pramlintide (amylinomimetic)

31
Q

Diagnostic criteria for HHNK

A

plasma osm >320 mOsm/KgH2O
glucose <600mg/dL
(no or low ketones)
(normal pH and bicarb)

32
Q

Diagnostic criteria for DKA

A

BG>/=250
pH= 7.3
Bicarb = 15 with anion gap
+ketones

33
Q

In DKA, replace potassium when level is ____

and add glucose to infusion when BG is ____

A
  1. <5.5

2. <250

34
Q

When and how do you screen pregnant women for gestational diabetes?

A

at 24-28 wks gestation

75gram 2hr OGTT

35
Q

In pregnancy what at glucose goals, premeal/1hr post prandial/2hr post prandial?

A

<95 / <140 / <120

36
Q

What antihypertensive agents can be used in pregnancy?

A

beta blockers (except atenolol)
methyldopa
CCB
hydralazine

37
Q

What is Whipples triad? significance? evaluation?

A

neuroglycopenic symptoms + hypoglycemia =55 + resolution of symptoms with glucose ingestion

if met - evaluate for hypoglycemia (in patients without diabetes). Can be postprandial or fasting.

postprandial – within 5hrs of last meal, commonly seen in gastric bypass or gastrectomy, meals consistent of simple carbs are usually the cause –> use mixed meal testing to diagnose

fasting – always screen for surreptitious use of oral agent esp sulfonylurea or insulin (urien screen for sulfonylurea and meglitinide). then can check for insulinoma, substrate deficiency, etc

38
Q

what two main classes of oral DM meds cause hypoglycemia?

A

Sulfonylureas (glipizide, glimepiride, etc)

Meglitinides (repaglinide, nateglinide)

39
Q

how to diagnose insulinoma?

A

72hr fast
If BG <45 + serum insulin >5-6 + elevated C-peptide
get abdominal CT

40
Q

Does iron deficiency anemia effect A1c measurement?

A

Yes – can erroneously increase the hemoglobin A1c level due to an increase in the proportion of older erythrocytes. Treat with iron then recheck

41
Q

How do you treat Type 2 amiodarone-induced thyrotoxicosis (destructive thyroiditis) ? whats the time frame of onset?

A

Step 1 is actually starting Prednisone (before you even dc amio) b/c half-life is around 40 days

moderate- to high-dose prednisone that can be gradually tapered over 1 to 3 months.

Affects 5% of patients taking amiodarone and can occur at any time during or up to 9 months after treatment.

42
Q

What is type 1 vs type 2 thyrotoxicosis?

A

Type 1 (hyperthyroidism) amiodarone-induced thyrotoxicosis occurs in patients with underlying multinodular goiter or latent Graves disease and is associated with increased vascularity on color flow Doppler ultrasonography.

Type 2 (destructive thyroiditis) usually affects those without thyroid disease and is not associated with increased vascularity on color flow Doppler.

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