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PANCE > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is diagnostic criteria for DM?

A

1) A1c > or = 6.5%
2) Fasting glucose > or = 126mg/dl
3) 2hr glucose > or = 200 during oral glucose tolerance test
Classic symptoms and random glucose of > or = 200

confirm 1-3 w/ repeat testing
(remember DM is monitored w/ HgA1c and fructosamine which shows a smaller 1-2 week recent control)

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2
Q

Diagnostic Criteria for increased risk of DM aka prediabetes

A

FPG 100-125 = impaired fasting glucose

2h plasma glucose during OGTT of 140-199

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3
Q

When to test for DM?

A

All adults who are overweight >25kg/m and have one or more major risk factor (inactivity, 1st degree relative w/ DM, high risk race/ethnicity, HTN)
OR
at age 45 (if normal repeat q3 year; if pre diabetic check yearly)

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4
Q

How does metformin work?

A

Decreases hepatic glucose production

  • no weight gain no hypoglycemia
  • contraindicated in patients w/ reduced kidney function*
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5
Q

SE of metformin

A

GI = diarrhea, cramping

Lactic acidosis

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6
Q

About sulfoylureas

A

Glyburide, glipizide
Increase insulin secretion (need insulin to work)
-SE = hypoglycemia, weight gain

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7
Q

About meglintides

A

Repaglinide, nateglinide
Increase insulin secretion
SE: hypoglycemia, weight gain

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8
Q

About thiazolidinediones

A

pioglitazone, rosiglitazone
Increase insulin sensitivity
-no hypoglycemia, increase HDL cholesterol
-SE: weight gain, edema, HF, bone fractures

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9
Q

About alpha gllucosidease inhibitors

A

acarbose, miglitol
Slow intestinal carbohydrate digestion/absorption
SE: GI= flatulence and diarrhea

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10
Q

What is GLP1

A
  • produced from the proglucagon gene in intestinal L cells and is secreted in response to nutrients
  • given medically to stimulate insulin, inhibit inappropriate hyperglucagonemia, slows gastric emptying, decreases appetite, and improves satiety
  • DPP-IV is the enzyme that degrades this so we can also block this
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11
Q

About GLP1 Agonists

A

Exenatide
mimics GLP-1
-injectable
SE: GI, risk of acute pancreatitis, C-cell hyperplasia/medullary tumors in animals

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12
Q

About DPP-IV inhibitors

A

Sitagliptin, vildagliptin

  • no hypoglycemia, well tolerated
  • SE: uritcaria, angioedema, possible risk of pancreatitis
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13
Q

Macrovascular & Microvascular Complications of DM

A

MACRO

  • coronary heart disease
  • cerebrovascular disease
  • PVD

MICRO

  • retinopathy
  • nephropathy
  • neuropathy

should have daily aspirin, annual opt ham exam, annual serum albumin, and annual serum creatinine

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14
Q

Acceptable glucose levels

A

70-130 before meals and after an overnight fast

<150 at 2hr after food

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15
Q

What comes from the anterior lobe of the pituitary

A
  • GH
  • PRL
  • TSH
  • LH
  • FSH
  • ACTH
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16
Q

What comes from the posterior lobe of the pituitary

A
  • ADH (aka vasopressin)

- Oxytocin

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17
Q

Pituitary Adenoma -what to look for

A

Symptoms of hypo/hyper secretion or significant mass effect

-classic visual field deficiency is bitemporal hemianopsia

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18
Q

What causes acromeglay

A

pituitary adenoma most of the time

-if it occurs before epiphyseal plates close = pituitary giagantism

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19
Q

What labs do you order for acromegaly

A
  • IGF-1 (insulin like growth factor)
  • Oral glucose tolerance test confirms
  • baseline GH is not a reliable test*
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20
Q

Tx of acromegaly

A
  • Surgery

- if not surgical candidate = cabergoline( dopamine agonist), octreotide (somatostatin analog), pegvisomant

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21
Q

Central DI vs Nephrogenic DI

A 
Central = posterior pituitary doesn't secrete ADH
Nephrogenic = kidney doesn't respond to circulating ADH (renal dz or drugs like LITHIUM)
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22
Q

Presentation/ Diagnosis of DI

A

-polydipsia, polyuria, persistent thirst w/ dilute urine

  • high-normal plasma sodium concentration >142 (especially if urine osmlality is less than plasma osmolality)
  • 24 hr urine collection
  • Water deprivation test (will continue to have lots of clear pee)
  • DDAVP test (if central = decreased urine and increase osmolality but no significant effect in nephrogenic)
  • MRI of pituitary
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23
Q

Tx of DI

A 
Central = desmopressin acetate
Nephrogenic = thiazides or amiloride + salt restirction, NSAIDs
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24
Q

Dwarfism is assoc w/ which gene

A

All types are assoc w/ FGFR3 gene

  • most common = achondroplasia (delayed motor milestone & small size but otherwise normal development)
  • pituitary dwarfism = male infants w/ hypoglycemia and micropenis
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25
Q

Graves Dz markers

A

-low TSH, high to normal T3 and T4
-HLA B8 and HLA DR3
-increased antithyroglobin and antithyroperoxidase
(increased risk of other autoimmune dz)

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26
Q

Drugs that can cause hyperthyroidism

A

Amiodarone

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27
Q

Symptomatic Tx of hyperthyroid

A

B-blockers

28
Q

MMU and PTU

A

take effect w/in several weeks
-continue for 12-24 mo
**PTU in pregnancy and breasfeeding
(rare SE = agranulocytosis)

29
Q

Radioactive Iodine for hyperthyroid

A

preferred to surgery especially in the elderly

***contraindicated in pregnancy

30
Q

When to pick surgery over radioactive iodine

A
  • pregos
  • large goiters
  • malignancy or suspicion of malignancy
31
Q

Tx of opthalmopathy

A

IV methylprednisolone

32
Q

Appearance of different thyroid states on radio iodine uptake

A

Graves = diffuse uptake
Toxic Mulitnodular Goiter = pockets
Toxic Adenoma = one spot

33
Q

Subacute Thyroiditis

A

viral or postviral inflame process
**anterior localized neck pain w/ or w/o fver
1st line = NSAIDs; 2nd = steroids

34
Q

What drugs can cause hypothyroidism?

A

Amoidarone, lithium

35
Q

What antibodies are seen in hashimotos

A

Anti-microsomal/thyroid peroxidase antibodies TPOAb

36
Q

How to work up a thyroid nodule

A

1) TSH
2) US (everyone if known or suspected nodule)
3) Thyroid scintigraphy / Radionuclide scanning (if TSH is LOW) hot = benign; cold = consider malignancy
4) FNA biopsy

37
Q

Thyroid Cancers (list names)

A

1) Papillary = most common (80%) least aggressive
2) Follicular = 14%
3) Medullary = 3% = assoc w/ MEN = flussing, diarrhea, fatigue (increase calcitonin, increased CEA)
4) Anaplastic = least prevalent, extremely poor prognosis

38
Q

Tx of thyroid cancer

A

Surgery

39
Q

Primary hyperparathyroidism

A

80% = single parathyroid adenoma; usually >50y/o

40
Q

Clinical presentation of hyperparathyroidism

A

bones, stones, abd groans, psychic moans w/ fatigue overtones
(may cause nephrogenic DI)

41
Q

Dx of primary hyperthyroidism

A

-Hypercalcemia and elevated intact PTH levels
***must do 24h urinary collection for calcium and creatinine excretion before tx incase it is familiar hypercalcemia hypocalciuria
(remember that as calcium increases Phos decreases)

42
Q

EKG changes in hyperparathyroidism

A

prolonged PR interval, short QT, bradyarrhythimas, heart block, asystole

43
Q

Tx of primary hyperparathyroidism

A

Surgery (if experience symptoms or complications)
Meds = intensive hydration, bisphosphonate
AVOID = HCTZ diuretics, large dose vit A or D, and calcium containing products

44
Q

Secondary hyperparathyroidism=

A
  • Renal failure is the most common cause of secondary hyperparathyroidism
  • Others = vit D defiicency, inadequate intake, inadequate absorption (ex = secondary to GI disease causing malabsorption)
45
Q

Tertiary Hyperparathyroidism

A

because of prolonged hypocalcemia, usually secondary to chronic renal failure, that causes gland hyperplasia w/ resultant autonomous over secretion of PTH by the parathyroid glands

46
Q

Hypoparathyroidism

A

most common = iatrogenic i.e. surgical

47
Q

Chvostek and Trousseau phenom

A 
Chvostek = tap on facial nerve and can't stop twitching
Trousseau = inflate cuff and cause carpal spasm
48
Q

EKG in hypoparathyroidism

A

prolonged QT and T wave abnormalities

49
Q

Labs to check

A
  • calcium (low)
  • PTH (low)
  • phosphate (elevated)
  • urinary calcium (low)
  • alk phos (normal)
  • serum magnesium (hypomagnesemia may exacerbate symp and decrease parathyroid function)
50
Q

Treatment of hypoparathyroid

A

Emergent = IV calcium gluconate and airway mgmnt

***Mg if needed

51
Q

Cushing Syndrome Causes

A

Can be exogenous or endogenous

  • *exogenous is most common cause of cushing syndrome
  • *Cushing dz is most common cause of endogenous cushing syndrome
52
Q

What aauses endogenous cushing syndrome

A

over secretion of glucocorticoids by the adrenal glands

-Divided into ACTH dependent and ACTH independent

53
Q

ACTH dependent cushing syndrome =

A

most commonly caused by ACTH secreting pituitary adenoma (80% of the time) = cushing disease

54
Q

ACTH independent cushing syndrome =

A

Adrenal adenoma, adrenal carcinoma, primary pgimented nodular adrenocortical disease

55
Q

Work up of cushing sydnrome

A 
1) taking any steroids???
Then can be any of these 4 tests
1) 24h urinary free cortisone
2) overnight 1mg dexameth supp test
3) 48h 2mg/d dexamfhe supp test
4) late night salivary cortisol
Then
1) distinguish ACTH dependent from independent by checking plasma ACTH
56
Q

Electrolytes in cushing syndrome

A

Could be

  • hyperglycemia
  • glycosuria
  • HYPOkalemia
57
Q

Tx of cushing syndrome

A

Cushing Dz = transsphenoidal resection of pituitary adenoa
Ectopic ACTH syndrome = surgical excision of tumor
Exogenous = d/c steroid tx

58
Q

Etiologies of adrenal insufficiency

A

1) primary = addisons
- adrenocortical disease (autoimmune = #1)
2) seondary = disorder of pituitary
3) tertiary = disorder of hypothalamus

59
Q

Clinical presentation of adrenal insufficiency

A
  • weakness, fatigue, anorexia, GI issues, hypoglycemia, hypotension, salt cravings
  • *hyperpigmentation/skin tanning only seen in primary/ADdisons dz (due to increased ACTH secretion)
60
Q

Dx of adrenal insufficiency

A
  • Early am serum cortisol (low)

- synthteic ACTH stim aka cosintropin stim test (if high = primary dz; if low = secondary or tertiary dz)

61
Q

Labs in adrenal insufficiency

A
  • hyponatremia
  • HYPERkalemia
  • hypoglycemia
  • hypercalcemia
  • serum DHEA are <1000 in all pts w/ Addisons
  • anti-adrenal antibodies are present in 50% of Addisons
62
Q

Tx of adrenal insufficiency

A

Hydrocortisone = drug of choice

-fludrocortisone (not needed in secondary or tertiary)

63
Q

Pheochromocytoma presentation

A

EPISODIC headache, sweating, tachycardia

64
Q

Dx of pheo

A

plasma fractionated free metanephrines
24 hr urine catecholamines and metanephrines
CT or MRI of the abdomen and pelvis

65
Q

Tx of pheo

A

surgical resection = tx of choice

  • medical prep = control htn and vol expansion
  • pre-op use an alph adrenergic blockade first to control HTN followed by beta blockage to control tachycardia
66
Q

what drugs can cause osteomalacia

A
  • phenytoin, carbamazepine, valproate, barbituates

* *treat patients on phenytoin prophylactically

PANCE (18 decks)

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