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Endocrine-related things Flashcards

1
Q

What is primary amenorrhea?

A

no menses by age 13 with no breast development
or no menses by age 15 WITH breast development

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2
Q

What are Tanner stages for breast development?

A

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

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3
Q

How do you evaluate for primary amenorrhea?

A

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)

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4
Q

What is initial workup of primary amenorrhea?

A

pelvic US (assess for presence of uterus), b-hcg, TSH, prolactin, FSH, estradiol (will show streak gonads/low estrogen)

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5
Q

What are structural causes of primary amenorrhea?

A

Mullerian agensis, imperforate hymen, transverse vaginal septum
If you have breasts, you have ovaries! Except in androgen insensitivity

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6
Q

If FSH elevated, how would it change your differential for primary amenorrhea

A

Primary ovarian failure: think Fragile X or Turner syndrome. Get genetic testing, karyotype, exam (streak ovaries, widely spaced nipples, short stature).

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7
Q

What is SLE?

A

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!

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8
Q

What are adverse pregnancy outcomes w/ SLE?

A

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.
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9
Q

What is galactorrhea?

A

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.

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10
Q

What is treatment of galactorrhea?

A

Dopamine agonists (bc inhibits prolactin)

  1. Cabergoline: long-acting/preferred. less severe SE. 0.25mg twice a week.
  2. Bromocriptine: SE=postural hypotension, N/HA. 2.5mg BID.
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11
Q

What are hormone units?

A

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

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12
Q

What is hypothyroidism?

A

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).

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13
Q

When do you use TPO Ab

A

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.

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14
Q

What is hyperthyroidism?

A

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 blocke.

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15
Q

What are the effects of inadequately treated hyperthyroidism in pregnancy?

A

Incr risk PEC, maternal heart failure and thyroid storm
Medically indicated PTD, LBW, miscarriage, stillbirth

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16
Q

What are effects of inadequately treated hypothyroidism in pregnancy?

A

Adverse perinatal: SAB, PEC, PTB, abruption, stillbirth

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17
Q

How do you diagnose and manage subclinical hyperthyroidism?

A

Low TSH, normal Free T4. not assoc w/ adverse prreg outcomes. Treatment not recommended bc no benefit.

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18
Q

Which pregnant patients to screen for thyroid disease?

A

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.

19
Q

How do you diagnose thyroid disease during pregnancy?

A

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.
20
Q

How do you manage thyroid disease?

A

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 adn total T3 q4w and titrate to goal of high normal range.

21
Q

What are the thionamides and mechanism of action?

A

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).

22
Q

What are side effects of thionamides (PTU and methimazole):

A

transient leukopenia up to 10%, doesn’t require cessation. Less than 1% have agranulocytosis - discontinue immediately!

23
Q

What changes in thyroid function occur w/ hyperemesis and should thyroid function tests be performed?

A

HG causes high T4 2/2 hcg stimulating tSH-R. Don’t need treatment bc rarely symptomatic. Expectant mamagenet usually decreases serum T4.

24
Q

How is thyroid storm and thyrotoxic heart failure diagnosed and treated in pregnancy?

A

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.

25
Q

How is thyroid nodule/thyroid cancer assessed during pregnancy?

Signs of malignancy on thyroid US?

A

H&P, TSH, neck US. 90% of solitary nodules are benign.

Hypoechoic pattern, irregular margins, microcalcifications.
If US suspicions, fine-needle aspiration. CANNOT do radioidone scanning. If had RAI prior to 12wks, no incr risk bc fetal thyroid gland doesn’t develop prior to 12wks.

What is management of thyroid cancer in pregnancy?
Consult MFM, endocrinology and surg onc. Thyroidectomy before 3rd tri but often delay until PP. If not aggressive, postpone.

26
Q

How is postpartum thyroiditis diagnosed and treated?

A

Thyroid dysfunction with 12 mo of delivery (hypo or hyper): transient autoimmune thyroiditis found in 5-10% of women after childbirth
2 stages:
1st=thyrotoxicosis (excessive release of thyroid hormone), abrupt onset, small painless goiter. Hyeprthyroid sx (palpitations, fatigue, irritability, weight loss, heat intolerance).
2nd=overt hypothyroid: sx.

Treatment: thioamides often ineffective but B-blocker helpful. Most will resolve spontaneously. ⅓ develop permanent overt hypothyroidism.

27
Q

What is the differential diagnosis of galactorrhea?

A

Pregnancy
Stress
Recent cessation of breastfeeding
Hypothyroidism (thyrotropin releasing factor similar to prolactin releasing hormone. TRF elevated in hypothyroidism so stimulates prolactin).
Meds (OCPs, antipsychotics, ritalin)
CENTRAL
- pituitary tumor releasing prolactin
- hypothalamic tumors
- Nonpituitary tumor

28
Q

What is differential diagnosis of hirsutism?

A

idiopathic or familial responsible for 50% cases
second most common cause is PCOS

Differential diagnosis:
- familial, PCOS, CAH, androgen secreting tumor, drugs, hypothyroidism, severely elevated pRL, Cushing’s.

29
Q

What is the workup for hirsutism?

A

Total testosterone (androgen secreting ovarian tumor), 17-OHP (r/o non-classical CAH), DHEAS (adrenal tumor), TSH, prolactin, 24hr urine free cortisol (Cushing’s disease), HCG

  • if DHEAS >700, suspect adrenal tumor. Get CT of adrenal and endocrine consultation.

If labs normal, regular cycles but hirsutism present, suspect familial and offer multimodal tx.

If suspect PCOS: total testosterone, SHBG.

30
Q

What is treatment of hirsutism?

A
  • weight loss: increases SHBG, decreases free testoeterone
    -OCPs: incr SHB decrease ovarian androgen production
  • Anti-androgens (can cause feminization of male fetus)
    —spironolactone: decr androgen production - potassium sparing diuretic. SE=diuresis effect.
    –finasteride: 5-alpha reductase inhibitor: decr testosterone conversion to DHT
    – flutamide: androgen-R agonist
    –topical eflornithine: irreversibly inhibits ornithine decarboxylase in the skin
31
Q

What is metabolic syndrome

A
  • BP <130/85
  • waist circumference >35
  • elevated fasting glucose >100
  • HDL < 50
  • triglycerides >150
32
Q

What is secondary amenorrhea and what are causes?

A

no menses for > 3 months if normal menses or > 6 months if irregular menses.

  • pregnancy
  • hypothalamic dysfunction or functional hypothalamic amenorrhea (eating disorders, exercise, stress)
  • hyperprolactinema
  • thyroid disorders
  • hypopituitarism (Sheehan’s syndrome)
  • Sherman’s syndrome
    -POI
  • anovulation w/ hyperandrogenism (PCOS, adrenal gland tumor, ovarian tumor)
  • non-classical CAH
  • Cushing’s
  • Meds (psychotropics, demo, mirena IUD)
33
Q

What is the workup and treatment for secondary amenorrhea?

A

Labs: HCG, TSH, PRL, FSH, LH, estradiol

  • If labs normal and hx surgery: trial of E/P. If no bleeding, do HSG/hysteroscopy for washerman’s
  • If hyperandrogenism present (hirsutism, acne, balding): add testosterone, DHEA-S, 17-OHP, 24hr urine free cortisol (Cushing’s)
  • if PCOS: lipid panel, GTT, a1c.

Treatment: underlying cause, dopamine agonist, weight gain, stress reduction, surgery for Sherman’s.
- Hormone therapy if hypoestrogenic and not wanting to conceive
- ovulation induction if pt wants to conceive

34
Q

What is differential for child w/ breast and axillary hair development?

A

Idiopathic precocious puberty
hypothyroid
CNS neoplasm
Ovarian neoplasm
Adrenal neoplasm
McCune Albright syndrome
Exogenous steroid ingestion

35
Q

What is the normal sequence of pubertal milestones in females?

A

Thelarche (age 11)
Adrenarche
growth spurt
Menarche (13)

36
Q

What is workup for suspected precocious puberty?

A

FSH - elevated
LH - elevated
TSH - nl
PRL - nl
testosterone
Estrogen
Xray (wrist) for bone age - advanced
US abdomen + pelvic - normal
MRI brain - normal

37
Q

What is treatment for precocious puberty?

A

GnRH agonists to suppress gonadotropin secretion
- goal is arrest puberty and stop premature fusion of epiphyses (to avoid compromising final height)

38
Q

What are causes of hyperprolactinemia?

A

pregnancy/prolactinoma/PCOS
Renal failure
OCP
Liver disease, lung disease
Adenoma, acromegaly
Chest wall disease
Infiltrative disease of pituitary
Thyroid disease
Nursing, nipple stim
Sex, stress, sleep surgery

Pharmacologic causes: antipsychotics (SSRI), anticonvulsants (valproate, lithium), anti-HTN (labetalol, methyldopa), antihistamines (ranitidine), opiates, OCP, metoclopramide.

39
Q

Difference between micro and macroadenoma?

A

Micro < 10mm. management=expectant. Yearly prolactin, MRI q2yr
Macro <10mm, bromocriptine, mRI q6 and 12 months then yearly

40
Q

How do you manage hyperprolactinemia in pregnancy?

A

Discontinue meds after conception. Monthly visual field exam w/ neuro testing. Restart therapy if sx or severe hA. Can breastfeed on meds.

41
Q

What is androgen insensitivity syndrome?

A

X-linked recessive. 46 XY

  • Testes make testosterone and AMH. Androgen receptor not sensitive so no internal or external genitalia.
    Puberty: high estrogen 2/2 peripheral conversion from testosterone causes feminization (BREASTS) bc no androgen action to oppose it.
    Phenotypic female w/ primary amenorrhea, absent uterus, has testes (inguinal hernia) no pubic/axillary hair, high testosterone.

incr risk testicular cancer: bilateral gonadectomy post-puberty to prevent. then need estrogen therapy to maintain secondary sex characteristics.

Differs from Mullerian dysgenesis: mullerian dysgenesis have normal axillary/pubic hair, short vagina, normal testerosterone, 46 XX

42
Q

What is Mullerian dysgenesis?

A

46 XX, normal breast/external genitalia/pubic/axillary hair. Absent vagina without cervix, usually rudimentary uterus at best. ddx: MRI/US when primary amenorrheic

Non-surgical approach=1st line (vaginal dilators).surgical approach: create neovagina using skin graft.

Key words: MRKH, scoliosis, renal anomalies

43
Q

What is gonadal dysgenesis?

A

Perrault syndrome: 46 XX – gonadal dysgenesis and sensorineural deafness. No puberty or breasts but have uterus 2/2 absence of AMH.
Swyer syndrome (SRY mutation): 46 XY; gonadal dysgenesis. No puberty or breasts but have uterus 2/2 absence of AMH. appears female, streak ovaries

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