ENDOCRINOLOGY Flashcards
Diabetes
diagnosis
1 of the following: 2 fasting glucose >126 or 1 random glucose >200 with symptoms or abnormal glucose tolerance test HbA1c> 6.5%
Type 2 Diabetes medications
- Metformin
- Sulfonylureas
- Dipeptidyl Peptidase (DPP-IV) inhibitors
- Thiazolidinediones
- Alpha-glucosidase inhibitors
- insulin secretagogues
- SGLT inhibitors
- GLP analogs
1.metformin
mech: blocks gluconeogenesis
adv: no hypoglycemia, no weight gain
contraind: renal insufficiency, contrast of contrast agents
AE: lactic acidosis
- glyburide, glimepiride,glipizide
mech: causes increased release of insulin from pancreas
disadv: hypoglycemia, SIADH
d/c glyburide in renal failure b/c metabolized extensively by kidneys - stigliptin, linagliptin, saxagliptin, alogliptin
mech: increases insulin release, blocks glucagon
add as 2nd agent to metformin
AE: nasopharyngitis - rosiglitazone, prioglitazone
mech: increasing peripheral insulin sensitivity
disadv: worsen CHF, fluid retention, weight gain - acarbose, miglitol
mech: block absorption of glucose at intestinal lining
disadv: diarrhea, abdominal pain, bloating, flatulence - neteglinide, repaglinide
mech: short acting, increase insulin from pancreas
disadv: hypoglycemia - dapagiflozin, canagliflozin, empagliflozin
disadv: causes UTIs, hypotension - exenatide, liraglutide, dulaglutide
mech: increase insulin, decrease glucagon
adv: promotes weight loss
AE: pancreatitis
Insulin
long-acting
short-acting
long acting (steady state) + short-acting insulin (mealtime)
long-acting
- glargine (lantus): qd
- detemir
- NPH: bid
short-acting (mealtime, last about 2 hrs)
aspart, lispro, glulisine
regular insulin last about 6 hours
DKA 1. presentation 2. diag lab findings 3. treatment
DKA more common in type 1 diabetes
1. presentation
hypervent’n-compen. for metabolic acidosis (low bicarb) fruity breath-acetone
confusion-hyperosmolar state
- diag
intial test: serum bicarb & anion gap. low serum bicarb implies elevated anion gap = marker for severe DKA
lab findings:
- hyperglycemia >250
- hyperkalemia (without insulin K builds up outside the cell. will quickly translate to hypokalemia as DKA is treated. MUST SUPPLEMENT WITH K)
- decreased serum bicarb
- elevated anion gap
- low pH, low CO2 as respiratory compensation
- high levels: acetone, acetoacetate, beta hydroxybutyrate
- very high glucose artificially drops Na levels
treatment:
- labs (chemistry, abgs, acetone level) and fluids
- high glucose + low bicarb = insulin
- K
Acute, Severe Hypercalcemia
- possible causes
- presentation
- treatment
- most common primary PTH
others: PTHrP, too much vita, granulomatous dx, Tb, Histoplasmosis, Berrylliosis, thiazides (increase Ca reabsorption) - confused, constipated, short QT syndrome, renal insuff, ATN, kidney stone, polyuria & polydipsia (nephrogenic diabetes insipidus)
3.
- hydration with NA
- bisphosphonate (pamidronate, xolendronate)-inhibits osteoclasts. take 1 week to kick in
- furosemide ONLY AFTER HYDRATION. loops increase Ca excretion
- Calcitonin
- steroid if granulomatous disease
Hypocalcemia
- possible causes
- presentation
- treatment
- surgical removal of parathyroid glands, low Mg (MG helps release PTH from gland), low vit D, fat malabsorption (bind Ca in gut), PTH resistance, acute hyperphosphatemia (phosphate binds Ca)
- seizures, neural twitching (trousseau & chvostek signs), arrhythmias-long QT
- treatment: replace CA. replace vit D if deficiency or hypoparathyroidism
Cushings (hypercortisolism) 1. diagnostic tests -these test don't tell you about cause 2. indicators of source ACTH low, ACTH high 3. next step
- 1mg overnight dexamethasone suppression test, if + (doesn’t suppress) confirm with 24 hr cortisol, late night salivary cortisol (normal = low)
2.ACTH low = origin is adrenal. CT/MRI adrenals
ACTH high = origin is pituitary or ectopic production - high dose dexamethasone suppression test . no suppression then ectopic or ca. CT chest
Addison's Disease 1. presentation 2. diagnosis labs tests 3.treatment
- fatigue, anorexia, weakness, hypotension, hyper pigmented skin, thin, weight loss
- labs: hyponatermia, hyperkalemia, hyperchloremic metabolic acidosis -cant excrete H+ or K+ because no ALD
tests: CT adrenals & cosyntropin (synthetic ACTH) stim test (measures cortisol before & after admin of cosyntropin. if adrenal insufficiency won’t get rise in cortisol - steroid replacement
acute: fluids and hydrocortisone
stable (nonhypotensive): prednisone
fludrocortisone used if renin high or still hypotensive after prednisone
Hyperaldosteronism
presentation
test
treatment
presents with HTN, metabolic alkalosis, hypokalemia (low K can lead to motor weakness and nephrogenic diabetes insipidus –>polyuria, polydipsia with normal glu)
tests:
low renin , HTN, high ALD despite salt loading with NS
CT adrenals
treatment:
adenoma –>surgery
hyperplasia–> spironolactone
Pheochromocytoma (MEN II)
presentation
tests (best initial, most accurate)
treatment
presentation: headache, palpitation, tremor, anxiety, flushing, episodic HTN
tests
best first test: high plasma & urinary catecholamines, plasma-free or urine metanephrine levels
most accurate: CT/MRI adrenals
MIBG to detect metastatic dx
treatment
- PHENOXYBENZAIME FOR ALPHA BLOCKADE FIRST TO AVOID HYPERTENSIVE CRISIS INTRAOPERATIVELY
- propranolol AFTER phenoxybenzamine
- surgical/laparoscopic resection
Congenital Adrenal hyperplasia 1. general characteristics 2. 3 kinds 21 hydroxylase deficiency 11 hydroxylase deficiency 17 hyroxylase deficiency
- all forms of CAH: high ACTH, low ALD, low cortisol, treatable with prednisone (inhibits pituitary)
21 hydroxylase deficiency (most common):
hirsutism from high adrenal androgens & hypotension
virilization
diag by high 17 hydroxyprogesterone levels
ambiguous genitalia in girls
salt wasting, low Na, high K
give glucocorticoids and mineralocorticoids, high Na diet
11 hydroxylase deficiency: hirsutism from high adrenal androgens & HTN virilization ambiguous genitalia in girls fluid and Na retention, HTN
17 hyroxylase deficiency
fluid and Na retention, HTN
low adrenal androgen levels
all pts phenotypically female
note: in CAH, HTN is caused by increased 11-deoxycorticosterone, which acts like mineralocorticoid. Because 11 and 17 hydroxyls deficiency involve increased 11-deoxycorticosterone, there is hypertension.
When do you investigate prolactinoma?
test? treatment?
- pregnancy has been excluded
- metoclopramide, phenothiazines, tricyclics excluded
- prolactin very high >200
- hypothyroidism excluded since high thyrotropin-releasing hormone stimulates prolactin
- nipple stimulatin, chest wall irritation, stress, exercise excluded
test: MRI brain
treatment:
#1 DA agonist: bromocriptine or cabergoline (less AEs)
if failed medical therapy then surgery
Acromegaly
presents
diagnosis
present:
bigger feet, head, fingers, nose, jaw, sweat glands (intense sweating)
problems with joints
amenorrhea (GH co-secreted with prolactin)
cardiomegaly % HTN
colonic polyps
diabetes (treatment resistant, GH acts as anti-insulin)
diag:
1st: IGF levels
most accurate: glucose to suppress GH (if suppressed acromegaly r’d/o)
MRI will show lesion but need know function of tumor before visualization
treatment:
surgical resection with transphenoidal removal
octreotide/lanreotide (suppresses GH release)
carbegoline can suppress GH release
pegvisomant =GH receptor antagonist
Primary Amenorrhea
primary -genetic defect
Turners Syndrome (XO) short stature, webbed neck, wide spaced nipples, scant pubic/axillary hair.
Mullerian agenesis
Testicularization feminization
genetically male, but looks/feels/acts like woman
no testosterone receptors = no penis/prostate/scrotum
Secondary Amenorrhea
PCOS:
hairy & infertile & obese
treat with metformin
virilization with spironolactone
others:
Premature ovarian insuffiency, pregnancy, exercise, extreme weight loss, hyperprolactinemia
