ENDOCRINOLOGY Flashcards
(39 cards)
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
Male hypogonodism
Kallmans
Klinefelters
Kallmans
ANOSMIA with hypogonadism
problem originates in hypothalamus
low GnRH, FSH, LH
Klinefelters (XXY)
TALL MEN
LH & FSH are super high but LH/FSH receptors on testicles are insensitive so no testosterone produced
treatment: give testosterone
effect of OCPs on levothyroxine dose for hypothyroid
estrogen causes increase in thyroid-binfing globulin which leads to a decrease in free T4. in pts with primary hypothyroidism on thyroid supplementation, thyroid stimulating hormone levels should be checked 12 weeks after starting OCPs. the dosage of leveothyroxine may need to be increased
- drugs that increase TBG & decrease free T4–may require higher dose of thyroxine replacement
- drugs that encrease TBG & increase free T4–may require lower dose of thyroxine replacement
- estrogen, tamoxifen, raloxifene, methadone, heroin
2. androgens, danazol, anabolic steroids, glucocorticoids
initial work up for adrenal mass
serum electrolytes, dexamethasone suppression testing, 24-hour catecholamine, metanephrine, vanillylmandelic acid and 17-ketosteroid measurement
Anion Gap formula
MUDPILES
AG=Na- (Cl- + HCO3-) Methanol Uremia DKA Propylene glycol INH/Iron Lactic acidosis Ethylene glycol Salicylates
Diabetes
-diagnosis
- AIC>6.5%
- fasting glu>126
- glu >200, on glu tolerance test
- random glu>200 in symptomatic patient
Delayed Puberty
when do you diagnose a boy?
- if no testicular enlargement by 14 yo or is testicles are 2.5cm or less. will need Xray bone to see bone age
Subclinical hypothyroidism
- increased TSH, normal T4
- TSH>10 start levothyroxine
- TSH <10 & +anti-TPO or symptoms or pregnancy then start levothyroxine
Gestational Diabetes
- target blood glucose levels
- treatment
- targets:
fasting <95
1hr postpran < 140
2hr postprand <120 - treatment
1st-line: dietary modifications
2nd line: insulin, metformin, glyburide
avoid neonatal macrosomia, shoulder dystocia, hypoglycemia
