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STEP2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Carpo-pedal spasms, muscle cramps, paresthesias, chronic alcoholism

A

Hypomagnesium induced hypocalcemia

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2
Q

how do you treat hypomagnesium induced hypocalcemia?

A
  1. administer Magnesium sulfate

2. replenish calcium

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3
Q

Furosemide has what effect on glucose levels?

A

> hyperglycemia

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4
Q

a LOW TSH with a LOW T4 ==

A

hypothyroidism secondary to pituitary failure

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5
Q

what is the normal 6 year range of puberty in boys vs girls?

A 
boys = 9-14
girls = 8-13
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6
Q

RET gene mutation is mnemonic for what endocrine cancer?

A

RET gene mutation = MEN2A malignancies (medullary thyroid cancer)

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7
Q

What is the first step of management if MEN2A is on your differential?

A

MEASURE urine metanephrine concentrations :

MEN2A is associated with parathyroidism, medullary thyroid cancer, & pheochromocytomas

BEFORE surgical removal of thyroid and parathyroid you MUST r/o pheochromocytoma to prevent Intraoperative catecholamine release from a pheochromocytomaresulting in hemodynamic instability during the surgery

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8
Q

People who receive bilateral adrenalectomy for refractory Cushing syndrome are at risk for what new syndrome?

A

Nelson syndrome= removing the adrenals makes the pituitary gland angry/enlarged!!> pituitary adenoma!!

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9
Q

which aldosterone receptor antagonist is the 1st line tx for hyper-aldosteronism caused by bilateral adrenal hyperplasia?

A

Eplerenone

Eplerenone EXCUSIVELY binds to mineralcorticoid recptors for antagonism; unlike Spirinolactone which binds to MCs & androgen receptors

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10
Q

why is medical tx with Eplerenone preferred over surgical bilateral adrenalectomy for hyper-aldosteronism?

A

removing adrenals&raquo_space; lifelong use of exogenous mineralocorticoids, cortisol> risk of adrenal insufficiency

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11
Q

You need to MASTER hypercortisolism:

what is the 3 step protocol to evaluating the source/cause?

A
  1. measure 24 cortisol
  2. measure ACTH
    • if LOW= NEGATIVE FB= ACTH independent hypercortisolism = adrenal hyperplasia
      OR exogenous steroids)
    • if HIGH = ACTH dependent hypercortisolism = something in body (pit or
      carcinoid/SCLC) is over producing ACTH > over production of cortisol
  3. if ACTH is high, measure cortisol after high dexa admin
    • suppression = pituitary adenoma
    • no suppression = carcinoid or SCLC
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12
Q

causes of low ACTH/ independent hypercortisolism

A
  1. adrenal hyperplasia

2. exogenous steroids

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13
Q

causes of high ACTH/ ACTH dependent hypercortisolism?

A
  1. pituitary adenoma
  2. SCLC
  3. Carcinoid
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14
Q

which causes of ACTH dependent hypercortisolism&raquo_space; suppression with HIGH DEXA?

A

pituitary adenoma

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15
Q

cause of Cushing disease=

A

diseases come from organs (pituitary adenoma, SCLC, carcinoid)

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16
Q

the cause of metabolic acidosis is dx with analysis of the serum (serum anion gap and serum osmol gap).

So,

how is metabolic ALKALOSIS dx?

A

looking at the URINE chloride concentration

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17
Q

how does a low urine chloride metabolic alkalosis respond to fluid resuscitation?

A

it will correct with fluids.

18
Q

what are causes of a low urine chloride metabolic alkalosis?

A

hypvolemia

CF

19
Q

how does a high urine chloride metabolic alkalosis respond to fluid resuscitation?

A

it will not correct with fluids

20
Q

what are causes of a high urine chloride metabolic alkalosis?

A
  • Hypokalemia (intracellular shift of H+) ✓
  • hyperaldosteronism => hypokalemia ✓
  • Conn syndrome = hyperaldo = hypokalemia ✓
  • High alkali load (e.g., due to antacid use, alkalization therapy w/ potassium citrate for uric acid stones) ✓
  • Loop or thiazide diuretics ✓
  • Hypercapnia/Hypoventilation (inc CO2= inc H+> triggers renal compensation via inc Bicarb) ✓
    Severe magnesium deficiency
Other (less common causes):
- Bartter syndrome (same as LOOPs). ✓
- Gitelman syndrome (same as Thiazides= inc Bicarb) ✓
Cushing syndrome 
Liddle syndrome (hyperaldosteronism) ✓
Licorice ingestion [18]
21
Q

what is the only cell line that is ELEVATED in hypercortisolism?

A

Leukocytosis!!!!!!!!!!!!!!!!!!

hypercortisolism= apoptosis in monocytes, lymphocytes, and eosinophils, causing an absolute decrease in the number of these types of leukocytes.

However, excess cortisol levels also inhibit neutrophil apoptosis and promote neutrophil migration out of the endothelial lining of vessels (demargination), which leads to neutrophilic leukocytosis and a blood leukocyte count that is overall increased.

22
Q

Corticotropin stimulation test is used to evaluate for….

A

adrenal insufficiency; you give ACTH to see if the adrenals respond to it

23
Q

what is the whipple TRIAD?

what does it signify?

A

episodic hypoglycemia that is both documented and relieved with rest/glucose admin

insulinoma

it was just a Whipple Insult

24
Q

what test is done to dx Insulinoma?

what values are monitored during this test?

what values confirm dx?

A

a 72 hour fasting test

monitors for serum glucose, C-peptide, & pro-insulin

dx: a low serum glucose with an elevated C-peptide & pro-insulin

(C-peptide and proinsulin are measures of the endogenous production of insulin and are decreased in natural hypoglycemia; hypoglycemia with elevated C-peptide and proinsulin levels should raise concern for insulinoma.)

25
Q

what does Transsphenoidal hypophysectomy treat?

A

Acromegaly vis pituitary adenoma

*resectable surgery it tx of CHOICE compared to medication (dopamine agonists/somatostatin analogs) *

26
Q

explain the symptoms in limited verses diffuse systemic scleroderma (SSc)

A

limited SSc = CREST syndrome = Calcinosis cutis, Raynauds, Esophageal dysmotility, Sclerodactyly, Telangiectasias

diffuse SSc= Myocardial fibrosis, Pulm fibrosis/Interstitial lung disease, Pulmonary HTN, Renal HTN

27
Q

what are the Clx findings of a pt with hyperosmolar hyperglycemic state?

what is always the onset of these findings? pathophys of why?

A

Clx: progressive confusion/lethargy, increased urination, dry MM & skin in T2DM pt (may be undiagnosed)

Onset: infection (PNA or cellulitis), stress, or surgery/trauma
- BC physiologic STRESS> INC in blood sugar > HHS when pt cant release insulin

28
Q

in a Hyperosmolar Hyperglycemic pt, do you manage infection first or check finger stick blood glucose first ?

A

in HHS, ALWAYS manage blood sugar first!

29
Q

what disease causes RTA 2?

A

fanconi

30
Q

what is the CAUSE of 2ndary Hyperparathyoidism?

A

CKD & a lack of 1,25(OH)D3

  • cirrhosis
  • CKD
  • rickets/osteomalacia
  • vit D deficiency
31
Q

what is the pathophys of 2ndary Hyperparathyoidism via CKD?

A
  • a dying kidney no longer converts inactive 25(OH) Vit D3 to active 1,25(OH) Vit D3»» NO 1,25(OH) Vit D3 to drive GI absorption of Ca = Hypocalcemia

Hyperphosphatemia bc body can’t excrete it bc RF

32
Q

What level of thyroglobulin confirms a dx of EXOGENOUS thyrotoxicosis?

A

a LOW thyroglobulin level.
- thyroglobulin is the natural precursor of T3/T4 hormone.
- in EXOGENOUS thyrotoxicosis, youre consuming synthetic T3/T4 (herbal weight loss supplements/L-thyroxine consumption)
> body NFB on TSH = low/no thyroglobulin = no endogenous T3/T4

33
Q

Most common etiology of PRIMARY hyperparathyroidism

A 
#1 = parathyroid adenoma 
2= parathyroid hyperplasia (MEN1)
3= cancer
4= lithium (blocks CaSR from sensing calcium levels> CaSR tells PTH to inc in order to make more Ca)
34
Q

Most common etiology of SECONDARY hyperparathyroidism

A
  • CKD
  • Vit D deficiency (liver cirrhosis or reduced exposure to sunlight)
  • Cholestasis (VitD is fat soluble & needs proper bile flow to be reabsorbed)
35
Q

firstline tx for primary hyperparathyroidism?

what do you do if 1st line fails to decrease calcium?

A

1 parathyroidectomy!! will decrease Ca

If surgery fails, add Cinacalcet (will inc the CaSRs sensitivity to calcium> NFB to dec PTH)

36
Q

firstline tx for secondary hyperparathyroidism?

A
  • Sevelamer (phosphate binder) === Prioritize the Hyperphosphatemia
  • Sevalamer the Phosphate pussycat*
  • Vit D supplement w/ ergocalciferol
37
Q

what are the Clx symp od congenital hypothyroidism?

A 
hypotonia
prolonged newborn jaundice (>cretinism)
macroglossia
umbilical hernia 
BIG head
38
Q

what chromosome is altered in Beckwith-Wiedemann syndrome?

what are the dx labs

A

chromosome 11p

labs: high insulin (enlarged pancreas), > LOW glucose

39
Q

why do children with BWS receive abdominal US & AFP screenings every 3 months until they are 8yo & 4yo respectively?

A

BWS = inc risk of ABD TUMORS:

  • Wilms tumor
  • hepatoblastoma
  • neuroblastoma
  • adrenal tumors
40
Q

what thyroid state (hyper/hypo)» gynecomastia?

A

HYPERthyroidism == gynecomastia

- TSH low w/ T3/T4 high

41
Q

what H2-receptor antagonist causes gynecomastia?

A

Cimetidine

42
Q

Pubertal gynecomastia in boys physiology

what is the management?

A

The boys body is experiencing a greater increase in Estrogen compared to Testosterone> uni/bilateral gynecomastia

Management: observation/reassurance (E:T hormone levels balance out by 17-18 yo)

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