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Clin Med- P > Endocrine Extra + Meds > Flashcards

Endocrine Extra + Meds Flashcards

1
Q

what is cushing’s syndrome?

A

symptoms and signs due to cortisol excess

  • think of this as 4 main causes either due to exogenous or endogenous source of hormones
    1) . exogenous: long term high dose glucocorticoid therapy (MC)
    2) . endogenous: cushing’s disease, ectopic ACTH producing tumor, adrenal tumor
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2
Q

difference between cushing’s disease and syndrome

A

cushing’s disease can be a cause of cushing syndrome, disease is a pituitary gland tumor/hyperplasia that overproduces ACTH

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3
Q

CP of cushing’s syndrome

A

truncal/central obesity, moon facies, buffalo hump, supraclavicular fat pad, thin extremities, thin skin, striae, acanthosis nigricans, hirsutism, oily skin

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4
Q

what are the 3 screening tests often used for cushing’s syndrome?

A

1) . 24 hr free urinary cortisol (usually increased)
2) . nighttime salivary cortisol (increased)
3) . low dose (1 mg) overnight Dexamethasone suppression test (no suppression of cortisol level)
* any one of these with the results are suggestive of cushing’s

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5
Q

how do you differentiate between cushing’s disease and other causes of cushing’s syndrome based on testing?

A

cushing’s disease: cortisol suppression with high dose (8 mg) Dexamethasone test

  • *plus increased ATCH
  • both ectopic ACTH tumor and adrenal adenoma (dec ACTH) will NOT have cortisol suppression with high dose test
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6
Q

what are the classic Cushing syndrome labs?

A

hyperglycemia, hypokalemia, leukocytosis

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7
Q

how do you workup potential cushing syndrome causes after initial testing?

A

ACTH pituitary adenoma/hyperplasia = pituitary MRI
adrenal tumor = abdominal CT
ectopic ACTH producing tumor = chest imaging

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8
Q

how to treat causes of cushing’s syndrome?

A

1) . stop exogenous steroid use (WITH TAPER)
2) . cushing disease: transphenoidal resection
3) . adrenal tumor: tumor excision
4) . ectopic tumor: resect if possible

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9
Q

what is adrenocortical insufficiency?

A

adrenal gland does not produce enough hormones (cortisol, aldosterone or both) either in a chronic or acute situation (acute = addisonian crisis)

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10
Q

difference between primary and secondary chronic adrenocortical insufficiency

A

primary = Addison Disease, adrenal gland destruction (lack of cortisol and aldosterone)
*caused by AUTOIMMUNE (MC in US), infection (MC in developing), vascular, meds, trauma
secondary = pituitary failure of ACTH secretion (lack of cortisol ONLY)
*caused by history of exogenous corticosteroid use (MC)

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11
Q

sxs of chronic adrenocortical insufficiency

A

lack of cortisol = weakness, myalgias, fatigue, n/v, abd pain, anorexia/weight loss, ha, sweating, salt craving, hypotension
+ Primary (aldosterone loss) = hyperpigmentation, orthostatic hypotension

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12
Q

what baseline labs do you get in chronic adrenocortical insufficiency?

A

1) . 8am ACTH
* Primary = elevated, decreased in secondary

Hypoglycemia (addison’s also has HYPOnatremia and HYPERkalemia)

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13
Q

what is the screening test for chronic adrenocortical insufficiency?

A

high dose ACTH (cosyntropin) stimulation test (after administering ACTH, serum cortisol should rise)
* absence of cortisol rise at all or still under 18 means adrenal insufficiency

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14
Q

how do you treat chronic adrenocortical insufficiency

A

Glucocorticoid replacement: dexamethasone

Minerocorticoid replacement too in Addison’s: Fludrocortisone

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15
Q

what is important for patient education in a patient with chronic adrenal insufficiency?

A

cortisol is a stress hormone and people with this must be treated with IV glucocorticoids and isotonic fluids pre and post procedures
*normal daily dosing must be tripled during illness, surgery or high fever

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16
Q

what is adrenal crisis? what are common causes of this?

A

acute adrenocortical insufficiency
sudden worsening of sxs in a person with dx/un-dx chronic adrenal insufficiency due to a precipitated stressful event
*MC cause: abrupt stop of glucocorticoids
-others: undx addison pt subjected to stress, pt with addison who didn’t increase meds during illness, bilateral adrenal infarction

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17
Q

what additional sxs do you get with adrenal crisis?

A

SHOCK- hypotension, hypovolemia

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18
Q

how to tx adrenal crisis

A

isotonic fluids (normal saline or D5NS) + IV hydrocortisone (if known addison pt) OR IV Dexamethasone

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19
Q

what is hyperaldosteronism and what are the two main causes?

A

-too much aldosterone (acts on principal cells to retain Na and water)
Primary (doesn’t depend on renin): idiopathic or bilateral adrenal hyperplasia most common, Conn syndrome (adrenal tumor in zona glomerulosa)
Secondary (due to increased renin): renal artery stenosis (MC), hypoperfusion to renal arteries (CHF, hypovolemia, nephrotic syndrome)

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20
Q

CP of hyperaldosteronism

A

USUALLY AS

but if sxs: HTN (HA, facial flushing) + HYPOkalemia (prox muscle weakness, polyuria, hypomag) + metabolic alkalosis

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21
Q

primary hyperaldosteronism is a cause of what?

A

secondary hypertension

*suspect pts who develop HTN at extremes of age (under 30 or over 60), not controlled on multiple BP meds

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22
Q

screening tests for primary vs secondary hyperaldosteronism

A

primary: aldosterone to renin ratio 20:1 (WAY higher aldosterone than renin)
Secondary: high renin levels

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23
Q

how to confirm primary hyperaldosteronism

A

1) . oral sodium loading test = get high aldosterone level in urine
2) . saline infusion test = no suppression of aldosterone levels (usually response is decrease)
3) . venous blood sample draining from adrenal = high aldosterone

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24
Q

tx of bilateral hyperplasia or conn syndrome (primary hyperaldosteronism)

A

BH: spironolactone, ACEI, or CCB + correct electrolyte probs

Conn syndrome: surgical excision + spironolactone

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25
Q

what are the five criteria of metabolic syndrome

A

1) . LOW HDL (under 40 M and under 50 W)
2) . HIGH fasting TGs ( at least 150)
3) . HIGH BP (at least 135 systolic or at least 85 diastolic)
4) . HIGH fasting BG (at least 100)
5) . increased abdominal obesity (waist circumference > 40in M and 35 in W)
* need at least 3 of the 5

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26
Q

what is the key component of metabolic syndrome?

A

insulin resistance

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27
Q

what is the most common type of pituitary adenoma?

A

prolactinoma

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28
Q

what hormone inhibits prolactin release?

A

dopamine

29
Q

CP for prolactinoma in women and men

A

W: hypogonadism (oligomenorrhea, amenorrhea, infertility), galactorrhea (rare)
M: hypogonadism (erectile dysfunction, decreased libido, infertility)
*both could cause bitemporal hemianopsia if pressing on optic chiasm

30
Q

how diagnose prolactinoma?

A

endocrine studies: increased prolactin, decreased LH/FSH

  • also check for endocrine probs with other pituitary hormones (TSH, GH, ACTH)
  • MRI to look for pituitary tumor
31
Q

how to tx prolactinoma?

A
  • dopamine agonists 1st line for sxs pts: bromocriptine, cabergoline
  • may watch and wait if asxs
  • transsphenoidial resection for those refractory to medical management
32
Q

what is HTN, LDL, and A1c goals for a diabetic pt? what are the drugs we might use to tx over this goal?

A

HTN goal = under 140 systolic and under 90 diastolic
*use ACEI or ARB if BP is over OR microalbuminemia present
LDL < 100, A1c <7% (depends on pt)

33
Q

what are the 4 types of diabetic neuropathy + MC?

A

1) . symmetric polyneuropathy (MC) = progressive sensory loss of distal extremities in “stocking-glove” distribution, usually LE first + may lead to foot ulcer formation
2) . autonomic: orthostatic hypotension, gastroparesis (occurs after many years)
3) . cranial mononeuropathy: often affects EOM (CN III: diplopia & ptosis with pupil sparing)
4) . peripheral mononeuropathy: carpal tunnel syndrome (median nerve), ulnar neuropathy

34
Q

Tx of diabetic neuropathy

A

OPTIMAL GLUCOSE CONTROL = FIRST

  • pregabalin and duloxetine FDA approved
  • can also use amitriptyline or gabapentin
35
Q

PP and CP of diabetic gastroparesis

A

PP: decreased GI motility and gastric emptying due to impaired neural control of gastric function
CP: N/V, EARLY SATIETY, upper abd pain, bloating + hx of longtime DM

36
Q

how to diagnose and tx diabetic gastroparesis

A

dx: EGD usually done first to rule out other causes, nuclear gastric emptying scintigraphy shows delayed gastric emptying with NO obstruction
tx: 1st line is improved glycemic control and diet modifications, metoclopramide or erythromycin increase GI motility

37
Q

what is the most common cause of end stage renal disease?

A

DM

38
Q

what is diabetic nephropathy? how to diagnose this? what is seen on histology?

A

progressive kidney destruction leading to microalbuminuria (1st sign)

dx: urine dipstick positive for proteinuria (between 30-300), 24 hr urine protein
* histology = Kimmelstiel-wilson lesion (pink hyaline material around glomerular capillaries from protein leakage)

39
Q

how to tx and screen for microalbuminemia?

A

tx: ACEI or ARB (reduces protein leakage and slows progression of damage)
*also low sodium diet and strict glucose control
screen annually for microalbuminuria, BUN, and Cr

40
Q

what is the somogyi vs dawn phenomenon? how to tx each

A

1) . somogyi: nightly HYPOglycemia followed by rebound hyperglycemia (3 am LOW - sOmogyi)
- reduce nightly NPH, move PM NPH dose earlier, give a bedtime snack
2) . dawn: rise in serum glucose between 2-8am
- bedtime injection of NPH, increase NPH dose, avoid carb snack late at night

41
Q

what level is considered hypoglycemia? how to tx mild-mod and severe types

A 
<70 (sweating, tremors, palps, tachy, pale/clammy skin, HA, confused, blurred vision, nausea)
mild-mod tx = fasta cting carb, juice, hard candies + recheck
severe tx (under 40 usually) = IV bolus D50 or IV glucagon
42
Q

C peptide is elevated with what?

A

ENDOGENOUS insulin production (body’s insulin)

43
Q

8 classes of DM 2 medications

A

1) . biguanides
2) . sulfonylureas
3) . meglitinides
4) . thiazolidinediones (TZDs)
5) . alpha-glucosidase inhibitors
6) . GLP-1 agonists
7) . DPP4 inhibitors
8) . SGLT2-inhibitors

44
Q

what is the process of managing type 2 DM?

A

1) . Initial management: diet, exercise, lifestyle changes
2) . if unable to control glucose with lifestyle changes then initiate oral medications (Metformin usually initial therapy)
3) . maximize metformin before adding new medication
4) . add insulin if glucose control still not good after multiple oral meds (also consider HA1c)

45
Q

MOA of metformin

A

decreases hepatic glucose metabolism and increases peripheral glucose utilization

46
Q

metformin has no effect on what?

A

pancreatic beta cells = no risk of hypoglycemia

47
Q

4 benefits to metformin

A

NO hypoglycemia, weight loss, decreased triglycerides, decreased CV risk

48
Q

3 AtDRs of metformin and two contraindications

A

ADRs: GI complaints (MC), vitamin b12 deficiency (dec b12 absorption), lactic acidosis in pts predisposed to hypoperfusion
Contraindications: Severe renal or hepatic impairment

49
Q

can you give iodinated IV contrast to a patient on metformin?

A

NO- must hold metformin 24 hrs prior to IV contrast and resumed 48 hrs after with creatinine monitoring

50
Q

what are the sulfonylurea medications?

A 
2nd gen (MC used) = "ides"
*Glipizide, glyburide, glimepiride
1st gen less commonly used due to ADRs = tolbutamide, chlorpropamide
51
Q

MOA of sulfonylurea and therefore biggest ADR

A

stimulates beta cell insulin release (non glucose dependent) = risk of HYPOGLYCEMIA

52
Q

indication for sulfonylurea medications

A

in addition to metformin or initial therapy in pts with contraindications to metformin

53
Q

5 ADRs of sulfonylurea meds

A

HYPOGLYCEMIA, weight gain, GI upset, dermatitis, disulfuram rxn (chlorpropamide only)

54
Q

what are the two meglitinide meds and their MOA

A

“glinides” = repaglinide, nateglinide

stimulates beta cell insulin release (more glucose dependent, postprandial) = LESS HYPOglycemia than sulfonylureas

55
Q

2 ADRs for meglitinide meds and what is special about repaglinide

A

Hypoglycemia (less than sulfas tho) and weight gain

*R = safer to use in pts with chronic renal dz

56
Q

meglitinide indications for use

A

in combination with metformin or initial therapy in pts with contraindications to metformin

57
Q

2 TZD meds and MOA

A 
"glitazones" = Pioglitazone, Rosiglitazone
MOA = increases insulin sensitivity at peripheral receptor sites, muscle and adipose (no effect on beta cells)
58
Q

2 big ADRs of TZD meds

A

1) . CARDIO- peripheral edema, fluid retention, CHF
2) . Monitor LFTs (hepatotoxicity)
* NO pts with heart failure, active liver dz, bladder ca hx

59
Q

two alpha-g meds and MOA

A

acarbose, miglitol

MOA = delays intestinal glucose absorption

60
Q

big ADR for alpha-g meds

A

GI = flatulence, diarrhea, hepatitis

61
Q

3 meds for GLP1 agonists and MOA

A

LIRAGLUTIDE*, exenatide, dulaglutide

MOA = increases insulin secretion (glucose dependent) and delays gastric emptying

62
Q

indications for Liraglutide and other GLP1 agonists

A

weight loss and reduction of CV events

63
Q

ADRs and contraindications for GLP1 agonists

A

ADRs: hypoglycemia (less than sulfas bc glucose dependent), GI, Pancreatitis
Contras: hx of pancreatitis or gastroparesis, medullary thyroid cancer

64
Q

2 DPP4 inhibitor meds and MOA

A 
"gliptins" = sitagliptin, linagliptin
MOA = increases GLP1 levels (increased insulin release, decreased glucagon, dec hepatic glucose production)
65
Q

ADRs for DPP4 inhibitors

A

acute pancreatitis, renal failure, GI

*not associated with hypoglycemia unless combined with insulin secretagogues

66
Q

3 SLGT-2 inhibitor meds and MOA

A 
"flozin" = empagliflozin, canagliflozin, dapagliflozin
MOA = inhibits sodium-glucose transport leading to increased urinary glucose excretion
67
Q

3 good things about SLGT-2 inhibitors

A

1) . improves CV outcomes and decreases HF risk (esp E)
2) . reduces BP
3) . weight reduction

68
Q

2 main ADRs of SLGT-2 inhibitors

A

transient N/V, UTIs/yeast infections

Clin Med- P (124 decks)

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