Endocrinology Flashcards
What is diagnostic criteria for DM?
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)
Diagnostic Criteria for increased risk of DM aka prediabetes
FPG 100-125 = impaired fasting glucose
2h plasma glucose during OGTT of 140-199
When to test for DM?
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)
How does metformin work?
Decreases hepatic glucose production
- no weight gain no hypoglycemia
- contraindicated in patients w/ reduced kidney function*
SE of metformin
GI = diarrhea, cramping
Lactic acidosis
About sulfoylureas
Glyburide, glipizide
Increase insulin secretion (need insulin to work)
-SE = hypoglycemia, weight gain
About meglintides
Repaglinide, nateglinide
Increase insulin secretion
SE: hypoglycemia, weight gain
About thiazolidinediones
pioglitazone, rosiglitazone
Increase insulin sensitivity
-no hypoglycemia, increase HDL cholesterol
-SE: weight gain, edema, HF, bone fractures
About alpha gllucosidease inhibitors
acarbose, miglitol
Slow intestinal carbohydrate digestion/absorption
SE: GI= flatulence and diarrhea
What is GLP1
- 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
About GLP1 Agonists
Exenatide
mimics GLP-1
-injectable
SE: GI, risk of acute pancreatitis, C-cell hyperplasia/medullary tumors in animals
About DPP-IV inhibitors
Sitagliptin, vildagliptin
- no hypoglycemia, well tolerated
- SE: uritcaria, angioedema, possible risk of pancreatitis
Macrovascular & Microvascular Complications of DM
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
Acceptable glucose levels
70-130 before meals and after an overnight fast
<150 at 2hr after food
What comes from the anterior lobe of the pituitary
- GH
- PRL
- TSH
- LH
- FSH
- ACTH
What comes from the posterior lobe of the pituitary
- ADH (aka vasopressin)
- Oxytocin
Pituitary Adenoma -what to look for
Symptoms of hypo/hyper secretion or significant mass effect
-classic visual field deficiency is bitemporal hemianopsia
What causes acromeglay
pituitary adenoma most of the time
-if it occurs before epiphyseal plates close = pituitary giagantism
What labs do you order for acromegaly
- IGF-1 (insulin like growth factor)
- Oral glucose tolerance test confirms
- baseline GH is not a reliable test*
Tx of acromegaly
- Surgery
- if not surgical candidate = cabergoline( dopamine agonist), octreotide (somatostatin analog), pegvisomant
Central DI vs Nephrogenic DI
Central = posterior pituitary doesn't secrete ADH Nephrogenic = kidney doesn't respond to circulating ADH (renal dz or drugs like LITHIUM)
Presentation/ Diagnosis of DI
-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
Tx of DI
Central = desmopressin acetate Nephrogenic = thiazides or amiloride + salt restirction, NSAIDs
Dwarfism is assoc w/ which gene
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
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)
Drugs that can cause hyperthyroidism
Amiodarone
Symptomatic Tx of hyperthyroid
B-blockers
MMU and PTU
take effect w/in several weeks
-continue for 12-24 mo
**PTU in pregnancy and breasfeeding
(rare SE = agranulocytosis)
Radioactive Iodine for hyperthyroid
preferred to surgery especially in the elderly
***contraindicated in pregnancy
When to pick surgery over radioactive iodine
- pregos
- large goiters
- malignancy or suspicion of malignancy
Tx of opthalmopathy
IV methylprednisolone
Appearance of different thyroid states on radio iodine uptake
Graves = diffuse uptake
Toxic Mulitnodular Goiter = pockets
Toxic Adenoma = one spot
Subacute Thyroiditis
viral or postviral inflame process
**anterior localized neck pain w/ or w/o fver
1st line = NSAIDs; 2nd = steroids
What drugs can cause hypothyroidism?
Amoidarone, lithium
What antibodies are seen in hashimotos
Anti-microsomal/thyroid peroxidase antibodies TPOAb
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
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
Tx of thyroid cancer
Surgery
Primary hyperparathyroidism
80% = single parathyroid adenoma; usually >50y/o
Clinical presentation of hyperparathyroidism
bones, stones, abd groans, psychic moans w/ fatigue overtones
(may cause nephrogenic DI)
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)
EKG changes in hyperparathyroidism
prolonged PR interval, short QT, bradyarrhythimas, heart block, asystole
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
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)
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
Hypoparathyroidism
most common = iatrogenic i.e. surgical
Chvostek and Trousseau phenom
Chvostek = tap on facial nerve and can't stop twitching Trousseau = inflate cuff and cause carpal spasm
EKG in hypoparathyroidism
prolonged QT and T wave abnormalities
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)
Treatment of hypoparathyroid
Emergent = IV calcium gluconate and airway mgmnt
***Mg if needed
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
What aauses endogenous cushing syndrome
over secretion of glucocorticoids by the adrenal glands
-Divided into ACTH dependent and ACTH independent
ACTH dependent cushing syndrome =
most commonly caused by ACTH secreting pituitary adenoma (80% of the time) = cushing disease
ACTH independent cushing syndrome =
Adrenal adenoma, adrenal carcinoma, primary pgimented nodular adrenocortical disease
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
Electrolytes in cushing syndrome
Could be
- hyperglycemia
- glycosuria
- HYPOkalemia
Tx of cushing syndrome
Cushing Dz = transsphenoidal resection of pituitary adenoa
Ectopic ACTH syndrome = surgical excision of tumor
Exogenous = d/c steroid tx
Etiologies of adrenal insufficiency
1) primary = addisons
- adrenocortical disease (autoimmune = #1)
2) seondary = disorder of pituitary
3) tertiary = disorder of hypothalamus
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)
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)
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
Tx of adrenal insufficiency
Hydrocortisone = drug of choice
-fludrocortisone (not needed in secondary or tertiary)
Pheochromocytoma presentation
EPISODIC headache, sweating, tachycardia
Dx of pheo
plasma fractionated free metanephrines
24 hr urine catecholamines and metanephrines
CT or MRI of the abdomen and pelvis
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
what drugs can cause osteomalacia
- phenytoin, carbamazepine, valproate, barbituates
* *treat patients on phenytoin prophylactically
