Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
214 Cards in this Set
- Front
- Back
|
size of thyroid nodules that need FNA
|
>1cm
|
|
|
best initial test for male hypogonadism
|
8am total testosterone
|
|
|
most useful test to determine whether obese patients have type 1 or type 2 DM
|
measure pancreatic autoantibodies (islet cell antibodies or glutamic acid decarboxylase antibodies)
|
|
|
ADA recommends - when to screen for DM?
|
>/=45 or asymptomatic but increased risk for diabetes
|
|
|
when to screen for gestational DM
|
24-28 weeks
|
|
|
oral glucose testing for gestational DM
|
75g glucose load, check glu at 1 and 2 hours after 0 - 180 and 153 are cutoffs
|
|
|
goals of getational DM treatment
|
fasting and premeal glucose <95; 1 hour PP <130-140
|
|
|
falsely low A1C (3)
|
hemolytic anemia, hemoglobinopathies, recent blood transfusions
|
|
|
How often should one check A1C?
|
q3mos if uncontrolled, q6mos if stable
|
|
|
initial insulin dose in type 1 DM
|
0.5 units/kg/d (more sensitive)
|
|
|
initial insulin dose in type 2 DM
|
1-1.5 units/kg/d
|
|
|
total bolus of rapid acting insulin per amount of CHO consumed
|
1 unit for every 10-15 grams of carbohydrate + correction factor
|
|
|
correction factor for bolus preprandial insulin based on preprandial glucose levels (type 1 DM)
|
1 unit for every 40-50mg/dL above 100
|
|
|
correction factor for bolus preprandial insulin based on preprandial glucose levels (type 2 DM)
|
1 unit for every 25mg/dL above 100
|
|
|
premeal glucose target
|
80-130 mg/dL
|
|
|
plasma glucose goals in critically ill hospitalized patients
|
140-180 mg/dL
|
|
|
plasma glucose goals in noncritically ill hospitalized patients (as per ADA recommendations)
|
90-140 fasting and premeal; <180 postprandial
|
|
|
most common causes of DKA
|
new onset type 1 DM, missed dose / inappropriate dose (+/- serious illness or infection), MI
|
|
|
when to switch to D51/2NS 150-250 ml/h in DKA/HHS
|
when sugars drop to 200 in DKA and 300 in HHS
|
|
|
treatment for hypoglycemic unawareness (<70 but no symptoms)
|
decrease insulin, increase PO intake; keep glucose 150-200 at all times for several weeks to reset response to hypoglycemia
|
|
|
mainstay of treatment for advanced diabetic retinopathy
|
laser photocoagulation
|
|
|
when to screen for retinopathy: type 1 DM
|
at 5 years of diagnosis, annually
|
|
|
when to screen for retinopathy: type 2 DM
|
at diagnosis, annually
|
|
|
when to screen for retinopathy: pregnant women with DM
|
first trimester, every trimester
|
|
|
when to screen for retinopathy: diabetic women planning to conceive
|
during preconception planning, every trimester
|
|
|
when to test for microalbuminuria?
|
at diagnosis in type 2 and at year 5 of diagnosis in type 1
|
|
|
recently diagnosed or well-controlled diabetes, develops acute proximal leg pain or weakness and weight loss
|
diabetic amyotrophy
|
|
|
differentials for hypoglycemia (3)
|
hepatic glycogen stores depleted (starvation, sepsis, hepatic dysfunction), ETOH suppression of hepatic glucose production; cortisol deficient
|
|
|
diffirentials for fasting hypoglycemia in non-DM person
|
insulinoma, injection of insulin, ingestion of SU or meglitinide
|
|
|
how to differentiate insulinoma from insulin injection
|
both with low glucose, high insulin and negative urine or blood metabolites of SU or meglitinides but C peptide increased in insulinoma
|
|
|
how to differentiate insulin injection from SU/meglitinide use
|
both with lowglucose, high insulin but C peptide increased in SU/meglitinide ingestion and urine/plasma metabolites (+)
|
|
|
Whipple's triad
|
hypogly symptoms, low blood glucose (in lab), resolution after glucose ingestion
|
|
|
labs to order when Whipple's triad is observed (6)
|
72 hour fast, measure glucose, proinsulin, insulin, C-peptide, B-OHbutyrate, SU levels
|
|
|
treatment of postprandial hypoglycemia
|
small, frequent meals
|
|
|
two major hormones of the posterior pituitary
|
ADH, oxytocin
|
|
|
symptoms of hypothalamic dysfunction
|
excessive eating, hypersexuality, somnolence, profound hypothermia, central DI
|
|
|
type of adrenal insufficiency that presents with hyperpigmentation, hyperK
|
primary adrenal insufficiency
|
|
|
megestrol acetate relationship to adrenal insufficiency
|
has some glucocorticoid activity, can suppress ACTH secretion, (so, monitor for hypocortisolism once drug is discontinued)
|
|
|
differential diagnosis of polyuria
|
central DI, primary polydipsia, meds (phenothiazines causing dry mouth), hypothalamic lesions (sarcoidosis), osmotic diuresis, uncontrolled, DM, post-obstructive diuresis, hypercalcemia
|
|
|
sodium levels and diabetes insipidus
|
DI unlikely if <136; DI likely if >high normal or elevated; if normal, do water deprivation test
|
|
|
When is the water deprivation test finished?
|
nomal findings - Uosm >600 (appropriate); or if DI diagnosed - Uosm fails to concentrate for 2 hours; Posm >295, serum Na >145, patient lost >5% body weight
|
|
|
After water deprivation test, you give desmopression, what do you expect?
|
in central DI, Uosm increases by 50%; in nephrogenic DI, UOsm doesn't change
|
|
|
treatment of central DI
|
desmopressin via nasal spray (also SQ or IV forms)
|
|
|
size of microadenomas vs macroadenomas
|
micro is <10mm, macro is 10mm or greater
|
|
|
most common pituitary tumor
|
nonfunctioning adenoma
|
|
|
most common functional pituitary tumor
|
prolactinoma
|
|
|
surgery is first line therapy for macroadenomas and hypersecretory pituitary tumors except
|
prolactinoma (medical therapy with dopamine agonist is preferred)
|
|
|
name 4 physiologic causes of hyperprolactinoma
|
pregnancy, nipple stimulation, exercise and food intake
|
|
|
not all patients with hyperprolactinemias have prolactinomas - for example (3)
|
hypothyroid, liver disease, kidney failure with crea <2
|
|
|
medications that can increase prolactin secretion (6)
|
haldol, risperidone, other antidopaminergic drugs; opiates, metoclopramide and domperidone, verapamil
|
|
|
SSx of hyperprolactinemia
|
ED, decreased libido, amenorrhea, oligomenorrhea, galactorrhea,hirsutism, headaches, osteopenia
|
|
|
oral dopamine agonists available in US
|
bromocriptine and cabergoline
|
|
|
compare bromocriptine and cabergoline
|
bromocriptine given daily, cabergoline once or twice weekly; cabergoline more expensive but more tumor shrinkage and normalization of prolactin levels; better tolerated too
|
|
|
can dopamine agonists be withdrawn in prolactinomas?
|
yes, if prolactin level normal x 2 years and no visible tumor is seen on MRI
|
|
|
When is surgery be considered over medical treatment in prolactinomas?
|
in cystic prolactinomas
|
|
|
management of prolactinoma in pregnancy
|
prolactin levels not useful; pit gland triples in size during pregnancy; stop drug after conception, reinstitute after nursing is completed; unless with vision compromise restart BROMOCRIPTINE, or transsphenoidal SURGERY; or DELIVERY should be considered
|
|
|
How is acromegaly diagnosed?
|
elevated IGF1 level (random) - not GH levels; oral GLUCOSE TOLERANCE TEST with nadir GH <1 ng/mL excludes disease
|
|
|
primary therapy for acromegaly
|
transsphenoidal RESECTION; SOMATOSTATIN analogues or RADIATION therapy for residual disease
|
|
|
somatostatin analogues
|
octreotide and lanreotide, monthly injections
|
|
|
adverse effects of somatostatin analogues
|
diarrhea, abdominal bloating, increased risk of cholelithiasis
|
|
|
second line / third line medical therapy for acromegaly
|
cabergoline, GH receptor antagonist pegvisomant
|
|
|
safety monitoring of pegvisomant
|
serial LFTs (transaminitis) and MRI (tumor growth)
|
|
|
treatment of TSH-secreting pituitary adenoma
|
resection, for residual disease - somatostatin analogue or adjuvant radiation therapy
|
|
|
major thyroid antibodies (3)
|
antiTPO, antiTG, anti TSH receptor antibodies
|
|
|
the anti-TSH-receptor antibodies (2)
|
thyroid-stimulating immunoglobulins and thyrotropin-binding inhibitory immunoglobulins
|
|
|
autoantibodies in Hashimoto's / autoimmune hypothyroidism
|
antiTPO
|
|
|
autoantibodies in Grave's / autoimmune hyperthyroidism
|
TSI or TBII antibodies
|
|
|
serial measurements of antithyroid antibodies are not recommended except
|
women who wish to become pregnant whose antiTPO is positive and TSH is normal - high risk of infertility, preterm delivery and miscarriage so serial measurements are appropriate
|
|
|
condition/s where thyroglobulin levels are increased
|
hyperthyroidism and destructive thyroiditis
|
|
|
condition/s where TG levels are decreased
|
factitious thyrotoxicosis
|
|
|
tumor marker in patients with history of medullary thyroid cancer
|
calcitonin
|
|
|
when is measurement of calcitonin levels indicated?
|
fam history of med thyroid cancer, features of MEN2, biopsy results suggestive of med thyroid cancer
|
|
|
high RAIU
|
thyrotoxicosis (enjdogenous production of thyroid hormones)
|
|
|
low RAIU
|
thyroiditis or exposure to exogenous thyroid hormones
|
|
|
preferred treatment of hyperthyroidism for patients with Grave's ophthalmopathy
|
thyroidectomy
|
|
|
pathophysiology of TMNG and toxic adenoma
|
mutation in TSH receptor gene leads to autonomy of function and secretion of T4 and T3 from the nodules affected
|
|
|
treatment of TMNG
|
RAI or surgery depending on size and symptoms
|
|
|
treatment of choice for toxic adenoma
|
radioactive iodine ablation
|
|
|
types of destructive thyroiditis
|
subacute (De Quervain), silent, postpartum thyroiditis
|
|
|
lab findings in subacute thyroiditis
|
inc ESR CRP, inc FT4 T3, low TSH
|
|
|
time course of subacute thyroiditis
|
4-6 weeks hyperthyroid state, then short euthyroid state, then 6 weeks hypothyroid state then back to euthyroid
|
|
|
treatment of thyrotoxic phase of subacute thyroiditis
|
no antithyroid meds, may give beta blockers, NSAIDs, corticosteroids if unresponsive to NSAIDs and markedly elevated FT4 or T3 levels
|
|
|
causes of drug induced thyrotoxicosis
|
amiodarone, IFN alpha, IL2, lithium; iodine loads (contrast, pvidone-iodine)
|
|
|
two forms of amiodarone-induced thyrotoxicosis
|
type 1 (iodine-induced) and type 2 (destructive thyroiditis)
|
|
|
treatment of amiodarone-induced thyrotoxicosis
|
type 1 - give antithyroid agents; type 2 give corticosteroids; if unresponsive, thyroidectomy
|
|
|
lab findings in subclinical hyperthyroidism
|
low TSH with normal T3 T4
|
|
|
lab shows subclinical hyperthyroidism - next step
|
repeat in 3-6 months; treat if TSH <0.1 esp if 65 and older, have heart disease, postmenopausal or symptomatic; RAI preferred
|
|
|
most frequent cause of hypothyroidism
|
Hashimoto thyroiditis, ffd by iatrogenic
|
|
|
drugs that can cause hypothyroidism
|
amiodarone, lithium, IFN alpha, IL2
|
|
|
manifestations of hypothyroidism (5)
|
weight gain, cold intolerance, constipation, menorrhagia, depression, fatigue, reduced endurance, weight gain, impaired concentration and short term memory, dry skin, edema, mood changes, psychomotor retardation, ms cramps, myalgia, reduced fertility
|
|
|
PE findings in hypothyroidism (6)
|
reduced basal temp, bradycardia, diastolic HTN, delayed recovery phase of DTR, dry and cold skin, brittle hair, enlarged thyroid, pallor, hoarseness,
|
|
|
How should levothyroxine be taken?
|
1 hour before or 2-3 hours after food intake or calcium- or iron-containing supplements
|
|
|
target TSH level in hypothyroid
|
0.5-4.3 microunits/mL; higher range may be appropriate for elderly 80 above
|
|
|
When is treatment indicated in subclinical hypothyroidism?
|
if TSH >10 microunits / mL or if markedly symptomatic, have goiter, are pregnant, or planning to; or (+) antiTPO
|
|
|
TSH goal in patients desirous of becoming pregnant but have subclinical hypothyroidism
|
0.5-2.5 microunits/mL
|
|
|
structural disorders of the thyroid gland
|
nodules, goiters, cancers
|
|
|
factors associated with increased thyroid cancer risk (6)
|
age <20 or >60; male, previous head or neck irradiation, fam history (esp medullary) cancer, rapid growth, hoarseness
|
|
|
PE findings associated with thyroid cancer (4)
|
hard palpable nodules, local cervical LAD, fixation to adjacent tissue, VC paralysis
|
|
|
work-up of nodule
|
first test is TSH, if low, check FT4 T3 and radionuclide scan; if normal or high US then FNA
|
|
|
US characteristics of cancerous thyroid nodules
|
microcalcif, increased nodular vascularity, hypoechogenicity, irregular border, taller than wide in sagittal view
|
|
|
US chars of benign thyroid nodules
|
hyperechogenicity, (+) halo, comet tail, inc periph nodule vascularity, pure cyst
|
|
|
Which thyroid nodules need to be biopsied?
|
solid and hypoechoic >1cm or mixed cystic >2cm; smaller nodules >0.5 cm if with other risk factors
|
|
|
Bethesda classification on FNA biopsy results
|
benign, malignant, nondiagnostic, suspicious, follicular neoplasm and follicular lesion of undetermined significance (last 3 imply increased risk of malignancy)
|
|
|
how should benign nodules be monitored?
|
US q 6-18 months; if stablefor at least 18 months may extend to longer intervals
|
|
|
NOTE cancer risk is the same for solitary nodule
|
or with multiple nodules.
|
|
|
biopsy findings in medullary thyroid cancer
|
plasmacytoid, spindle, round or polygonal cells on biopsy
|
|
|
other tests to include in patients diagnosed with medullary thyroid cancer
|
RET proto-oncogene sequencing and measurment of plasma mtanephrine and normetanephrine levels
|
|
|
staging of papillary cancer
|
in less than 45 y/o - stage I any size, cervical LN involvement but without distant spread; stage 2 is distant spread; in >45 y/o; stage 1 <2cm; stage 2 is >2cm but <4cm; stage 3 is >4cm stage IV has invaded nearby neck structures or superior med LN or distant spread
|
|
|
TSH goals in thyroid cancer according to Am Thyroid Assn Guidelines
|
if persistent disease, <0.1; if disease free but HR, 0.1-0.5; if disease free and low risk 0.3-2.0 microunits/mL
|
|
|
lab findings in sick euthyroid syndrome
|
low T3, low FT4, TSH variable (low, high or normal); reverse T3 high
|
|
|
When does thyroid function tests return to normal after illness?
|
8 weeks
|
|
|
TSH goals in pregnancy and preconception
|
planning 0.1-2.5; first trimester 0.1-2.5; second and third trimesters 0.1-3.0
|
|
|
what happens to dose requirements of levothyroxine in pregnancy?
|
increase
|
|
|
treatment for thyroid storm
|
antithyroid drugs, iodine solution, high-dose steroids, BB, lithium (rarely)
|
|
|
two most common findings of myxedema coma
|
AMS and hypothermia
|
|
|
lab findings in cortisol deficiency
|
low sodium, normal potassium, high BUN, low sugars, low anemia, leukopenia, increased eos and lymphos; serum cortisol <5, response to cosyntropin <18
|
|
|
lab findings in aldosterone deficiency
|
low Na, high K, low aldos, high renin
|
|
|
lab findings in adrenal androgen deficiency
|
low serum DHEA and DHEAs levels
|
|
|
standard drug for mineralocorticoid replacement
|
fludrocortisone 0.05 to 0.1 mg/day
|
|
|
how to interpret random serum cortisol in critically ill
|
if >15 (normal albumin) or >12 (alb <2.5), AI unlikely
|
|
|
features of Cushing syndrome
|
prox ms weakness, mult ecchymoses, prominent supraclav fat pads, violaceous striae, hypoK, unexplained osteoporosis, new-onset HTN, DM
|
|
|
most common cause of Cushing syndrome
|
exogenous steroids
|
|
|
three approaches to evaluate hypercortisolism
|
24 hour urine free cortisol excretion, loss of feedback of cortisol with dexa suppression testing, loss of diurnal variation with late night salivary cortisol measurement
|
|
|
gold standard for diagnosing Cushing
|
24 hour urine free cortisol excretion; 3-fold or 4-fold increase over normal values is diagnostic
|
|
|
if 24 hour urine free cortisol excretion non diagnostic, next step?
|
overnight dexa supp test: 1mg dexa @ 11pm, check 9am serum cortisol - <2ug/dL normal; if >5 ug/dL suggests Cushing
|
|
|
what is the "standard" low-dose dexa suppressiontest?
|
dexa 0.5mg is given q6h x 48 hours to suppress serum cortisol levels
|
|
|
almost all adrenal tumors that are functional, >6cm or have unfavorable imaging chars should be removed except
|
aldosterone-secreting tumors which can be treated medically
|
|
|
these adrenal incidentalomas can be followed
|
<4cm, nonfunctional, with favorable imaging characteristics
|
|
|
what are pheochromocytomas
|
tumors composed of chromaffin cells that secrete biogenic amines (NE, E, dopamine) and their metabolites
|
|
|
triad that highly suggests pheochromocytoma
|
severe headache, diaphoresis, palpitations
|
|
|
biogenic amine that is usually secreted by pheochromocytomas
|
most common is NE which causes HTN, but some secrete only epinephrine, which causes hypotension
|
|
|
genetic disorders associated with pheochromocytomas
|
MEN2, Von Hippel Landau, NF1
|
|
|
why measure metanephrines in pheochromocytoma?
|
NE and E are metabolized intra-tumorally, so measurement of metabolites is more appropriate
|
|
|
first lab test to order in pheochromocytoma
|
urine and plasma metanephrines (if disordant, urine metanephrines is more specific and more reliable; if suspicion is high, plasma metanephrines is more sensitive and is preferred)
|
|
|
when to suspect pheochromocytoma (7)
|
cyclic spells of the triad; familial predisposition, previous vasopressor response to anges or angio, adrenal incidentaloma, HTN <20y/o, drug-resistant HTN, unexplained CMP or AFib
|
|
|
most effective treatment for pheochromocytomas
|
lap adrenalectomy
|
|
|
preoperative treatment of pheochromocytoma
|
previously, phenoxybenzamine started 10mg OD or BID titrated up to max of 80, some use short-acting prazosin, doxazosin or terazosin; beta blockers when alpha blockade achieved, calcium channel if third agent needed
|
|
|
intraoperative treatment of HTN in pheochromoctyoma
|
nitroprusside
|
|
|
excessive autonomous aldosterone production by zona glomerulosa, independent of the RAS
|
primary hyperaldosteronism
|
|
|
causes of primary hyperaldosteronism
|
adrenal adenoma, bilateral adrenal hyperplasia, unilater hyperplasia or adrenal carcinoma
|
|
|
primary manifestations of primary hyperaldosteronism
|
HTN, hypoK, metabolic alkalosis
|
|
|
evaluation of primary hyperaldosteronism
|
check midmorning aldosterone and renin level; aldosterone exceeds 15, renin low or undetectable; ratio >30 has 90% sensi and speci; ratio of 20-30 is suggestive
|
|
|
what meds should be discontinued before checking aldosterone and renin levels in primary hyperaldosteronism
|
spironolactone and eplerenone
|
|
|
how to confirm primary hyperaldosteronism once plasma renin-aldosterone ratio suggests the diagnosis?
|
salt-loading test - given sodium PO or IV; aldosterone levels are supposed to go down (<5) but remain >10 in the disease; (or measure 24h urine aldosterone secretions on 3rd day of salt loading - <12 in normal)
|
|
|
treatment of choice for primary hyperaldosteronism caused by bilateral adrenal hyperplasia
|
spironolactone or eplerenone; may add amiloride, low dose thiazide diuretic
|
|
|
side effects of spironolactone
|
gynecomastia, mastodynia, impotence, decreased libido in men, menstrual irregularities in women
|
|
|
treatment of adrenocortical cancer
|
surgical removal, adjuvant with mitotane
|
|
|
MOA of mitotane
|
adrenal cytotoxic drug; alters steroid peripheral metabolism, directly suppresses the adrenal cortex and alters cortisone metabolism leading to hypocortisolism (Lysodren)
|
|
|
what is Inhibin B?
|
protein product of ovarian granulosa cells and testicular Sertoli cells that inhibits FSH secretion
|
|
|
testicular cells are stimulated by? produces what?
|
Leydig by LH, produces testosterone; Sertoli by FSH and testosterone, responsible for spermatogenesis
|
|
|
*the most accurate measure of a patient's androgen status
|
morning total testosterone levels (except when SHBG is increased - elderly, or decreased - obese; where a free testosterone level is better)
|
|
|
most common congenital cause of hypogonadism
|
Klinefelter syndrome or XXY karyotype
|
|
|
acquired causes of primary hypogonadism (5)
|
pelvic irradiation, chemo, mumps orchitis, trauma, torsion
|
|
|
What is primary hypogonadism? testosterone, FSH LH levels?
|
testicular failure; low testosterone with high FSH LH
|
|
|
What is secondary hypogonadism? testosterone, FSH LH levels?
|
hypothalamic or pituitary defect - low testosterone with low or inappropriately normal LH and FSH levels
|
|
|
*congenital secondary hypogonadism
|
Kallman syndrome or idiopathic hypogonadotropic hypogonadism with anosmia
|
|
|
acquired causes of congenital hypogonadism
|
hyperprolactinoma, pit adenomas or other sellar masses, chronic opiate use, corticosteroids, infiltrative diseases s.a. hemochromatosis
|
|
|
symptoms of hypogonadism (7)
|
decreased testicular size, erectile dysfunction, absence of morning erections, decreased muscle strwength, gynecomastia, low libido, fatigue
|
|
|
How to work up hypogonadism?
|
check morning total testosterone; if >350 Dx excluded, if <200 confirmed, if 200-350 (equivocal) check free testosterone; if hypogonadism confirmed, check LH and FSH
|
|
|
other work-up of hypogonadism after total, free testosterone, LH and FSH levels
|
karyotype (if Klinefelter suspected), serum prolactin (if hyperprolactinemia suspected), iron saturation (transferrin and ferritin) (if hemochromatosis suspected); MRI pit gland to rule out masses
|
|
|
adverse effects of testosterone replacement
|
increased Hct, worsened sleep apnea, BPH, dyslipidemia, increased risk of prostate cancer, long term adverse cardiovascular effects
|
|
|
labs to check on patients on testosterone replacement
|
Hct and PSA levels
|
|
|
PE findings in anabolic steroid abuse
|
excessive muscular bulk, acne, gynecomastia, decreased testicular volume; low sperm counts in lab; hypogonadism and infertility, low HDL, hepatotoxicity, erythrocytosis, psych disorders
|
|
|
single best test to assess male fertility
|
semen analysis, repeat if first results abnormal, if abnormal twice, refer to endo or uro
|
|
|
causes of gynecomastia
|
meds (spironolactone, cimetidine, calcium blockesr, ACEi), liver disase, kidney disease, male hypogonadism, testicular cancer, hyperthyroidism, adrenal tumors, HCG secreting tumors, androgen insensitivity syndrome
|
|
|
differentiate gynecomastia from lipomastia
|
gynecomastia is subareolar glandular tissue whereas lipomastia is accumulation of fat in the breast
|
|
|
lab evaluation of gynecomastia
|
total testosterone, estradiol, HCG, LH, TSH
|
|
|
gynecomastia + increased HCG, next step?
|
testicular US, if negative, chest and abdominal US
|
|
|
gynecomastia + increased estradiol, next step?
|
testicular US, if negative, adrenal CT or MRI, if negative likely idiopathic or elevated peripheral aromatase activity
|
|
|
gynecomastia + increased LH and testosterone levels, next step?
|
if all evaluation unremarkable then likely diagnosis is androgen insensitivity syndrome
|
|
|
FGE LTA
|
FSH granulosa cells, LH theca cells androstenedione
|
|
|
define primary amenorrhea
|
lack of menses by age 16 + normal body hair pattern and normal breast development
|
|
|
define secondary amenorrhea
|
absence of menstrual cycle for 3 cycles of 6 months in previously menstruating woman
|
|
|
Asherman syndrome
|
one cause of secondary amenorrhea - repeated D&C causes endometrial scarring
|
|
|
causes of secondary amenorrhea
|
rule out pregnancy (most common), consdier Asherman; then 40% will be due to ovarian causes, most commonly PCOS; other causes include hypothalamic amenorrhea, hyperprolactinemia, thyroid disease, primary ovarian insufficiency
|
|
|
risk factors for functional hypothalamic amenorrhea
|
low body weight and fat percentage, rapid and substantial weight loss, eating disorders, excessive exercise, severe emotinal stress, severe nutritional deficiencies, chronic or acute illness
|
|
|
lab evaluation for amenorrhea
|
serum HCG (pregnancy), prolactin (hyperprolactinemia), FSH (primary amenorrhea), TSH (thyroid disorders); pelvic US, pit MRI
|
|
|
initial lab test for amenorrhea is abnormal, next step?
|
progesterone challenge test to assess estrogen sufficiency
|
|
|
interpret progesterone challenge test
|
withdrawal bleeding within 1 week with if estrogen sufficient - consider PCOS; no withdrawal bleeding if estrogen-deficient, consider hypothalamic amenorrhea or pit adenoma
|
|
|
lab evaluation of hirsutism
|
DHEAS level, TSH, prolactin, toatl testosterone, follicular phase 17 OHprogesterone (thyroid disease, hyperprolactinemia, ovarian / adrenal tumors, late-onset CAH)
|
|
|
hirsutism + total testosterone >200
|
pelvic US and adrenal CT to exclude ovarian or adrenal neoplasm
|
|
|
hirsutism + plasma DHEAS >700
|
adrenal CT to exclude adrenal cortisol-secreting and/or androgen secreting neoplasm
|
|
|
most common cause of hirsutism
|
PCOS
|
|
|
Rotterdam criteria for PCOS
|
anovulation, hyperandrogenism (clinical or biochemical), polycystic ovaries on US
|
|
|
clinical manifestations of PCOS
|
menstrual irregularity, infertility, insulin resistance, hyperandrogenism
|
|
|
treatment of PCOS
|
depends on which symptoms is most bothersome; contraceptives (mens irreg); clomiphene or metformin (infertility); diet, exercise, metformin (insulin resistance); OCP, spironolactone (hyperandrogenism
|
|
|
dfeine female infertility
|
cant conceive in 1 year with regular unprotected sex; (if >35 y/o, then 6 months)
|
|
|
normal calcium levels
|
9-10.5
|
|
|
relationship of PTH and calcium
|
inverse
|
|
|
differentials for hypercalcemia
|
primary hyperparathyroidism in MEN 1 and 2; sarcoidosis, malignancy
|
|
|
PTH-hormone-mediated hypercalcemia
|
primary (adenoma, hyperplasia, carcinoma) tertiary, familial hypercalciuric hypercalcemia, lithium therapy-associated
|
|
|
nonPTH-mediated hypercalcemia
|
malignancy, granulomatous disease (sarcoid, TB), endocrinopathies (hyperthyroid, AI) drugs (thiazide, calcium supp, vit D or A), immobilization
|
|
|
causes of factitious hypercalcemia
|
(due to increased plasma proteins that bind calcium) HIV, chronic hepatitis, multiple myeloma - check ionized, will be normal
|
|
|
how does lithium cause hypercalcemia?
|
changes set point for calcium-sensing receptor (or CSR) in parathyroid cell membrane
|
|
|
four conditions to think of in PTH vs calcium levels graph
|
vit D deficiency, hypoparathyroidism, primary hyperPTH and hypercalcemia or malignancy
|
|
|
treatment for primary hyperparthyroidism
|
surgery is most effective; bisphosphonates and cinacalcet (calcimimetic agent)
|
|
|
most common cause of PTH-independent hypercalcemia, most frequent cause of acute hypercalcemia in hospitalized patient
|
malignancy
|
|
|
tumors that cause humoral hypercalcemia of malignancy
|
squamous cell carcinomas (lung)
|
|
|
treatment of acute hypercalcemia
|
fluids, furosemide (evidence lacking), IV bisphosphonates (zoledronate more efficaceous and longer duration), calcitonin SQ for rapid correction
|
|
|
treatment for hypercalcemia from increased intestinal calcium absorption (Vit D intox / granulomatous disease)
|
glucocorticoids
|
|
|
Trousseau sign
|
carpopedal spasm induced by prolonged BP cuff application
|
|
|
what is hungry bone syndrome?
|
protracted hypocalcemia with deposition of calcium into unmineralized bone matrix (after parathyroidectomy)
|
|
|
causes of hypocalcemia
|
VIt D def, Vit D resistance, hypoPTH, PTH resistance, hypomagnesemia, extravascular deposition (pancreatitis, hungy-bone syn, rhabdo, tumor lysis), sepsis, acute resp alkalosis
|
|
|
treatment of hypocalcemia
|
slow IV calcium infusion until symptoms relieved; correct Mg and Vit D. oral Ca as IV is tapered
|
|
|
FDA approved antiresorptive agent (classes)
|
bisphosphonates, SERM, calcitonin
|
|
|
FDA-approved antiresorptive agents for prevention of osteoporosis in women
|
alendronate, risedronate, ibandronate, zoledronate, estrogen, raloxifene
|
|
|
MOA of bisphosphonates
|
bind to bone matrix, decrease osteoclast activity, slows bone resorption
|
|
|
bisphosphonate given annually, given every 3 months
|
zoledranate, ibandronate
|
|
|
MOA of denosumab
|
antiresorptive agent, humanized monoclonal Ab against receptor activator of nuclear factor kB RANK ligand, which is a key signal in activating bone resorption, leading to decreased osteoclastogenesis
|
|
|
MOA of teriparatide
|
recombinant human PTH
|
|
|
why give recombinant PTH in osteoporosis?
|
chronic elevation of PTH results in bone loss but transient spikes have anabolic effects on bone
|
|
|
black box warning for teriparatide
|
risk of osteosarcoma; so give for only 2 years and C/I in hyperparthyroid, Paget, elevated Alk Phoas, bone malig or h/o radiation therapty
|
|
|
optimal Vit D level
|
20-30
|
|
|
treatment of Vit D deficiency (25OHD <20)
|
8 weeks of ergocalciferol 50,000 every week ffd by repeat serum 25OHD level
|
