Endocrine-related things Flashcards
What is primary amenorrhea?
no menses by age 13 with no breast development
or no menses by age 15 WITH breast development
What are Tanner stages for breast development?
Stage 1: pre-pubertal
Stage 2: breast budding
Stage 3: breast + areola enlarging
Stage 4: areola elevates and form secondary mounts
Stage 5: adult presentation
How do you evaluate for primary amenorrhea?
History (medical problems-endocrine disorders, other signs of puberty, meds, prior chemotherapy leading to ovarian failure)
physical exam (weight to assess for low BMI, breast exam, pelvic exam assessing for tanner stages, evaluating for signs of Turners)
What is initial workup of primary amenorrhea?
pelvic US (assess for presence of uterus), b-hcg, TSH, prolactin, FSH, estradiol (will show streak gonads/low estrogen)
What are structural causes of primary amenorrhea?
Mullerian agensis, imperforate hymen, transverse vaginal septum
If you have breasts, you have ovaries! Except in androgen insensitivity
If FSH elevated, how would it change your differential for primary amenorrhea
Primary ovarian failure: think Fragile X or Turner syndrome. Get genetic testing, karyotype, exam (streak ovaries, widely spaced nipples, short stature).
What is SLE?
chronic multisystem inflammatory autoimmune disease.
- dsDNA is most specific, ANA not as specific.
- flare: decr complement and elevated dsDNA. RF for flare: active disease within 6 mo priorto pregnancy, active nephritis, discontinuation of hydroxychloroquine.
sx: fatigue, fever, arthralgia, myalgias, weight loss, rash.
Lupus nephritis: HTN, proteinuria. distinguish btw this and PEC w/ renal biopsy.
Recs: LDA, hydroxychloroquine, stop methotrexate and MMF prior to conception. If APS and no prior VTE, prophylactic anticoagulation. If APS + VTE, therapeutic!
What are adverse pregnancy outcomes w/ SLE?
PEC, FGR, neonatal lupus, incr risk pregnancy loss.
- anti-SSA and anti-SSB incr risk complete heart block (develops btw 18-22 weeks) - need weekly US to eval for hydros.
- delivery at 39wks.
What is galactorrhea?
What are causes?
What is workup?
milky discharge, bilateral unrelated to pregnancy or breastfeeding
- Prolactin is inhibited by dopamine and stimulated by TRH and nipple stim.
- causes: pregnancy/breastfeeding, excessive breast stimulation, meds, hyperprolactinemia.
- workup: med hx (antipsychotics, metoclopramide/reglan, SSRI, TCA, oral estrogen)
- breast exam
- prolactin (<25 nanograms/mL is normal), TSH, renal function, HCG (CKD can cause incr PRL)
- prolactin testing (early AM, fasting, no intercourse/nipple stim)
- visual field test
- MRI of pituitary fossa.
Treat if macroadenoma >1cm or hypogonadism/bothersome galactorrhea.
What is treatment of galactorrhea?
Dopamine agonists (bc inhibits prolactin)
- Cabergoline: long-acting/preferred. less severe SE. 0.25mg twice a week.
- Bromocriptine: SE=postural hypotension, N/HA. 2.5mg BID.
What are hormone units?
PAP= ng/mL
Progesterones (ng/ml)
Androgens (ng/ml)
Prolactin (ng/ml)
Estrogens pg/mL
FSH+LH, HCG mIU/ml - milli international units
TSH mIU/ml
What is hypothyroidism?
What are causes?
high TSH, low T4.
- sx: fatigue, cold intolerance, weight gain, constipation, dry skin, meals.
-exam: goiter, bradycardia.
- if Hashimoto’s (chronic autoimmune thyroiditis): elevated TPO Ab.
PRIMARY:
- autoimmune (Hashimoto’s) - most common. Has +TPO Ab but don’t need to order.
- infiltrative
- impaired thyroid synthesis (iodine deficiency, congenital)
- RAI ablation for prior hyperthyroid
- meds
SECONDARY (central) - inadequate thyroid stimulation by TSH (pituitary) or TRH (hypothalamus). TSH doesn’t increase as T4 falls so TSH can be normal/low or high.
- Tumors of pituitary or hypothalamus
- Radiation effect
- Sheehan’s hypopituitarism
- infiltative (sarcoid).
When do you use TPO Ab
indicated in patients with goiter, subclinical hypothyroid or PP thyroiditis to predict likelihood to progression to permanent overt hypothyroidism.
- If +TPO Ab but normal TFTs, has chronic autoimmune thyroiditis but NOT hypothyroidism. Check TSH yearly.
What is hyperthyroidism?
What is the workup and treatment?
Grave’s disease=most common disorder. Benign neoplasm=2nd most common.
-sx: anxiety, weakness, tremor, palpitations, heat intolerance, weight loss, perspiration, diarrhea, oligo/amenorrhea.
- exam: exophthalmos and pretrial myxedema, tachycardia, hyperreflexia, HTN.
Workup:
- measure TRAb (thyrotropin-R Ab)
- determine RAI uptake (determines toxic multi nodular goiter vs toxic adenoma 2/2 Grave’s) - AVOID IN PREGNANCY/BF
- thyroid US to measure blood low.
Tx: thioamides, RAI (requires thyroxine supplementation afterwards), or surgery. - start beta blocker.
What are the effects of inadequately treated hyperthyroidism in pregnancy?
Incr risk PEC, maternal heart failure and thyroid storm
Medically indicated PTD, LBW, miscarriage, stillbirth
What are effects of inadequately treated hypothyroidism in pregnancy?
Adverse perinatal: SAB, PEC, PTB, abruption, stillbirth
How do you diagnose and manage subclinical hyperthyroidism?
Low TSH, normal Free T4. not assoc w/ adverse prreg outcomes. Treatment not recommended bc no benefit.
Which pregnant patients to screen for thyroid disease?
Personal or fam hx
T1DM
Clinical suspicion
Don’t test asymptomatic woman w/ mildly enlarged thyroid (bc can have up to 30% enlargement of thyroid during pregnancy
If significant goiter, TFTs appropriate.
How do you diagnose thyroid disease during pregnancy?
TSH. If abnormally high or low, get free T4. IF suspected hyperthyroidism, total T3.
Pregnancy assoc w/ increasing T4 requirement 2/2 incr estrogen production. Dose of synthroid will increase in pregnancy.
- Pregnancy=30% increase in thyroid gland size (no change in FT4)
- TSH decreases in 1st tri (2/2 increasing HCG), stable in 2nd, rises in 3rd.
How do you manage thyroid disease?
If hypothyroidism: start levothyroxine 1-2microg/kg per day. Recheck TSH q4-6 weeks, titrate T4 replacement to TSH between low limit and 2.5.
Start approx 100 mcg qd.
If hyperthyroidism (low TSH, high T4), check TRAB. start antithyroid drug (Prophylthiouracil 100-600mg TID or methimazole 5-30mg BID). recheck free T4 and total T3 q4w and titrate to goal of high normal range.
What are the thionamides and mechanism of action?
Mechanism of action of PTU: decreases T4 to T3 conversion. Used for T3-predominant thyrotoxicosis. SE: rarely hepatotoxicity.
Methimazole in 1st tri assoc w/ rare embryopathy: esophageal atresia + aplasia cutis (skin defect).
Methimazole mechanism of action: thionamide antithyroid agent -inhibits thyroid peroxidase (reduces thyroid hormone synthesis).
What are side effects of thionamides (PTU and methimazole):
transient leukopenia up to 10%, doesn’t require cessation. Less than 1% have agranulocytosis (ANC < 100) - discontinue immediately!
What changes in thyroid function occur w/ hyperemesis and should thyroid function tests be performed?
HG causes high T4 2/2 hcg stimulating tSH-R. Don’t need treatment bc rarely symptomatic. Expectant mamagenet usually decreases serum T4.
How is thyroid storm and thyrotoxic heart failure diagnosed and treated in pregnancy?
Rare, acute, life threatening. Thyroid storm=hyeprmetabolic state 2/2 excess thyroid hormone. Clinical ddx w/ severe thyrotoxicosis + systemic decompensation.
Sx: F, tachycardiac, dysrhythmia, CNS dysfunction.
Decompensation preciptiated by PEC, anemia, sepsis.
IF suspected, TSH, free T4, total T3 but start treatment BEFORE results. Need to be in ICU
Treatment:
1. Drugs to inhibit thyroid release of T3/T4: PTU PO 1000mg load then 200mg PO q6. Iodine 1-2hrs post PTU (sodium iodide 500-100mg IV q8). IF allergy to iodine, give lithium carbonate.
2. Drugs to block peripheral conversion of T4 to T3: dexamethasone 2mg IV q6 x 24hr, hydrocortisone 100mg q8 for 24hr.
Control tachycardia w/ propranolol. But avoid if heart failure!
Treat underlying cause (infection, trauma). Fetal status will likely improve w/ maternal status is stabilized.
