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Endocrinology Flashcards

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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
Graves Dz markers
-low TSH, high to normal T3 and T4 -HLA B8 and HLA DR3 -increased antithyroglobin and antithyroperoxidase (increased risk of other autoimmune dz)
26
Drugs that can cause hyperthyroidism
Amiodarone
27
Symptomatic Tx of hyperthyroid
B-blockers
28
MMU and PTU
take effect w/in several weeks -continue for 12-24 mo **PTU in pregnancy and breasfeeding (rare SE = agranulocytosis)
29
Radioactive Iodine for hyperthyroid
preferred to surgery especially in the elderly | ***contraindicated in pregnancy
30
When to pick surgery over radioactive iodine
- pregos - large goiters - malignancy or suspicion of malignancy
31
Tx of opthalmopathy
IV methylprednisolone
32
Appearance of different thyroid states on radio iodine uptake
Graves = diffuse uptake Toxic Mulitnodular Goiter = pockets Toxic Adenoma = one spot
33
Subacute Thyroiditis
viral or postviral inflame process **anterior localized neck pain w/ or w/o fver 1st line = NSAIDs; 2nd = steroids
34
What drugs can cause hypothyroidism?
Amoidarone, lithium
35
What antibodies are seen in hashimotos
Anti-microsomal/thyroid peroxidase antibodies TPOAb
36
How to work up a thyroid nodule
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
Thyroid Cancers (list names)
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
Tx of thyroid cancer
Surgery
39
Primary hyperparathyroidism
80% = single parathyroid adenoma; usually >50y/o
40
Clinical presentation of hyperparathyroidism
bones, stones, abd groans, psychic moans w/ fatigue overtones (may cause nephrogenic DI)
41
Dx of primary hyperthyroidism
-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
EKG changes in hyperparathyroidism
prolonged PR interval, short QT, bradyarrhythimas, heart block, asystole
43
Tx of primary hyperparathyroidism
Surgery (if experience symptoms or complications) Meds = intensive hydration, bisphosphonate AVOID = HCTZ diuretics, large dose vit A or D, and calcium containing products
44
Secondary hyperparathyroidism=
- 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
Tertiary Hyperparathyroidism
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
Hypoparathyroidism
most common = iatrogenic i.e. surgical
47
Chvostek and Trousseau phenom
``` Chvostek = tap on facial nerve and can't stop twitching Trousseau = inflate cuff and cause carpal spasm ```
48
EKG in hypoparathyroidism
prolonged QT and T wave abnormalities
49
Labs to check
- calcium (low) - PTH (low) - phosphate (elevated) - urinary calcium (low) - alk phos (normal) - serum magnesium (hypomagnesemia may exacerbate symp and decrease parathyroid function)
50
Treatment of hypoparathyroid
Emergent = IV calcium gluconate and airway mgmnt | ***Mg if needed
51
Cushing Syndrome Causes
Can be exogenous or endogenous * *exogenous is most common cause of cushing syndrome * *Cushing dz is most common cause of endogenous cushing syndrome
52
What aauses endogenous cushing syndrome
over secretion of glucocorticoids by the adrenal glands | -Divided into ACTH dependent and ACTH independent
53
ACTH dependent cushing syndrome =
most commonly caused by ACTH secreting pituitary adenoma (80% of the time) = cushing disease
54
ACTH independent cushing syndrome =
Adrenal adenoma, adrenal carcinoma, primary pgimented nodular adrenocortical disease
55
Work up of cushing sydnrome
``` 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
Electrolytes in cushing syndrome
Could be - hyperglycemia - glycosuria - HYPOkalemia
57
Tx of cushing syndrome
Cushing Dz = transsphenoidal resection of pituitary adenoa Ectopic ACTH syndrome = surgical excision of tumor Exogenous = d/c steroid tx
58
Etiologies of adrenal insufficiency
1) primary = addisons - adrenocortical disease (autoimmune = #1) 2) seondary = disorder of pituitary 3) tertiary = disorder of hypothalamus
59
Clinical presentation of adrenal insufficiency
- weakness, fatigue, anorexia, GI issues, hypoglycemia, hypotension, salt cravings * *hyperpigmentation/skin tanning only seen in primary/ADdisons dz (due to increased ACTH secretion)
60
Dx of adrenal insufficiency
- Early am serum cortisol (low) | - synthteic ACTH stim aka cosintropin stim test (if high = primary dz; if low = secondary or tertiary dz)
61
Labs in adrenal insufficiency
- hyponatremia - HYPERkalemia - hypoglycemia - hypercalcemia - serum DHEA are <1000 in all pts w/ Addisons - anti-adrenal antibodies are present in 50% of Addisons
62
Tx of adrenal insufficiency
Hydrocortisone = drug of choice | -fludrocortisone (not needed in secondary or tertiary)
63
Pheochromocytoma presentation
EPISODIC headache, sweating, tachycardia
64
Dx of pheo
plasma fractionated free metanephrines 24 hr urine catecholamines and metanephrines CT or MRI of the abdomen and pelvis
65
Tx of pheo
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
what drugs can cause osteomalacia
- phenytoin, carbamazepine, valproate, barbituates | * *treat patients on phenytoin prophylactically

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