REI/Office Flashcards

OCPs, STI, HRT, osteoporosis

1
Q

ddx of vulvar ulcers in young woman

A

Genital herpes, Folliculitis, Hidradenitis suppurativa, Trauma, Syphilis, Chancroid, Lymphogranuloma venerum, Granuloma inguinale

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2
Q

what is lupron used to treat?

A

precocious puberty
fibroids
prostate cancer in men
PCOS

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3
Q

When do you evaluate primary amenorrhea and what is on your DDX?

A

no secondary sex characteristics by 13
secondary sex characteristics, but no menses by age 15

Hypo-/normogonadotropic hypogonadism

  • constitutional delay
  • Kallman’s Syndrome
  • Prolactinoma
  • PCOS
  • CAH
  • stress, weight loss, anorexia
  • pituitary tumor

Hypergonadotropic hypogonadism
-ovarian failure

IF there is breast development,

  • Mullerian agenesis
  • AIS
  • imperforate hymen
  • vaginal septum
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4
Q

Primary amenorrhea. What is your evaluation?

A

hcg
TSH
prolactin
and check for breast develop.

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5
Q
Primary amenorrhea. 
hcg -negative
TSH-normal
prolactin-normal
Normal breast development.

What is on your differential? What is your next step?

A

AIS
Mullerian Agenesis

imperforate hymen, vaginal septum

pelvic exam, if normal

karyotype

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6
Q
Primary amenorrhea. 
hcg -negative
TSH-normal
prolactin-normal
NO
breast development.

What is on your differential? What is your next step?

A

Constitutional delay
Kallman’s
stress, weight loss, anorexia

PCOS
ovarian failure
pituitary tumor

Order FSH

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7
Q

How do you counsel a patient with Mullerian agenisis?

A
  • cause unknown
  • 15-40% have renal anomalies (horseshoe kidney, renal agenesis)
  • 10-15% have skeletal malformations
  • IVF with gestational carrier as the ovaries are normal
  • treatment goal is the creation of functional vagina to allow intercourse
  • McIndoe vaginoplasty-skin graft to form vagina
  • Vecchietti- abdominal or vaginal procedure where a spring loaded device is used to maintain tension on the vagina to stretch it and allow for intercourse.
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8
Q

How do you counsel a patient with AIS?

A
  • high testosterone, but absent receptor
  • 40% have no family history
  • Fertility is not possible
  • gonadectomy after puberty to decrease the risk of germ cell cancer
  • treatment goal is the creation of functional vagina to allow intercourse
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9
Q
Primary amenorrhea. 
hcg -negative
TSH-normal
prolactin-normal
NO
breast development.

FSH-high

What is on your differential? What is your next step?

A

hypergonadotropic hypogonadism

Turners
Swyer syndrome
Fragile X premutation
idiopathic premature ovarian failure
chemo/rads
ovarian surgery

Autoimmune disorders

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10
Q
Primary amenorrhea. 
hcg -negative
TSH-normal
prolactin-normal
NO
breast development.

FSH-low or normal

What is on your differential? What is your next step?

A
hypogonadotropic hypogonadism
irreversible causes
Hypothalamic tumor
kallman's-GnRH deficiency 
idiopathic

reversible
anorexia, exercise, stress

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11
Q

secondary amenorrhea.

What is on your differential and how do you evaluate?

A
hypothyroidism
hyperprolatinemia
pregnancy
ovarian failure
PCOS
anovulation
Brain tumor
functional hypothalamic amenorrhea

acquired end organ problem

  • cervical stenosis
  • ashermans

TSH, prolactin, estradiol, FSH, progestin challenge test

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12
Q

What is a progestin challenge test?

A
  • Give oral medroxyprogesterone acetate (Provera) 10 mg daily for 5-10 days or one intramuscular injection of 100-200 mg of progesterone in oil.
  • should see bleeding within 2 weeks after progestin is given

Withdrawal bleeding will usually be seen if the patient’s estradiol level has been over about 40 pg/ml.

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13
Q

Secondary amenorrhea.
TSH-normal
prolactin-normal

progestin challenge test- bleeding within 2 weeks.

DDX

A

This means that the patient is building a uterine lining and the problem is anovulation/PCOS.

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14
Q

Secondary amenorrhea.
TSH-normal
prolactin-normal

progestin challenge test- NO bleeding within 2 weeks.

DDX and next step

A

Order FSH

High FSH
Ovarian failure

Low or normal FSH

  • tumor
  • functional hypothalamic amenorrhea
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15
Q

Hypergonadotropic hypogonadism

Turner Syndrome
-work up

A
-cardiac echo-bicuspid aortic valve, coarctation of aorta
renal sonogram-renal anomalies
TFT-hypothyroidism
CBC-
Glucose screening-prone to diabetes
Lipid profile
celiac screen
hearing test
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16
Q

hypergonadotropic hypogonadism

Turner syndrome treatment

A

goal is to use exogenous hormones to mimic puberty.

Growth hormone when height is <5th%, usually age 2-5

Estrogen starting at age 13-14.
0.25-0.5mg daily, increase q 3-6 monhts until 2mg daily.
ADD progestin monthly after first bleed or after 12-24 months of estrogen

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17
Q

can turner’s patients get pregnant with their own eggs?

A

no, donor egg, with a gestational carrier (ideally)

relative contraindication to pregnancy

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18
Q

hypergonadotropic hypogonadism

What is swyer syndrome?

A

46 XY karyotype
Genetic condition where testes fail to differentiate, thus no testosterone or AMH production, thus no DHT production and thus no male external genitalia

10-15% have SRY gene mutations

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19
Q

hypergonadotropic hypogonadism

Swyer Syndrome counseling

A

gonadectomy at time of dx to avoid 20-30% risk of gonadoblastoma

  • mullerian structure present
  • no other medical problems
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20
Q

hypergonadotropic hypogonadism

Can patients w/Swyer Syndrome get pregnant?

A

yes, but need donor egg.

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21
Q

What kind of autoimmune disorders would cause hypergonadotropic hypogonadism?

How to dx?

A

autoimmune polyglandular syndrome type 1 and type 2

type 1-childhood onset caused by a mutation in regulator gene on chromosome 21

  • hypoparathy in 89%
  • adrenal insufficiency (60-80%)

type II is adult onset

  • adrenal insufficiency (100%)
  • thyroid (70%)

Dx: look for auto-antibiodies to 21 hydroxylase antibodies, anti-thyroid peroxidase and anti-thyroglobulin.

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22
Q

hypo/hypo
define anorexia

define bulimia

A

A-refusal to maintain normal body weight either through restricting or binging/purging

B-binging with a lack of self control with compensatory purging via vomiting, laxatives, fasting or exercise.
-2x weekly for 3 months

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23
Q

what is the female athlete triad?

A

disordered eating
amenorrhea
osteoporosis

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24
Q

If your patient is both hypothroid and hyperprolactemic, which do you treat first? why?

A

thyroid because low t3 and t4 will cause high TRH which will also cause high prolactinemia.

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25
Q

What is kallman syndrome?

A

hypogonadotropic hypogonadism
congenital GnRH deficiency caused by mutation in KAL gene
-X-linked

-anosmia because the KAL gene encodes the anosmia-1 neural adhesion molecule that promotes GnRH neuron migration

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26
Q

DDX for hyperprolactinemia

A
Physiologic increases in prolactin
Pregnancy
breastfeeding
stress
sexual intercourse
eating
exercise
REM sleep
menses

Pathologic causes

  • anything that decreases dopamine such as adenoma, hypothalamic stalk interruption bc that is where dopamine is transported, empty sella syndrome
  • hypothyroidism
  • reduced elimination of prolactin-renal failure, hepatic insufficiency, macroprolactinemia

Decreased excretion
-renal or hepatic dysfunction

neuro-chest wall injury

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27
Q

What medications cause hyperprolactinemia?

A

antipsychotics-haldol, risperidone, tricyclics, SSRI, chlorpromazine, thioridizine

prokinetics-metoclopromide

anti-HTN-alpha methyldopa, verapamil

morphine, ramitidine

buspirine

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28
Q

How does prolactin cause irregular menses and infertility?

A
  1. increased prolactin causes a decrease GnRH which causes a decrease in FSH/LH which causes a decrease in Estaradiol
  2. prolactin decrease androgen synthesis
  3. prolactin decreases aromatase activity
  4. prolactin causes early luteolysis
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29
Q

How high of a prolactin suggests adenoma?

A

200 ng/mL

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30
Q

Hyperprolactinemia workup

A
  1. repeat the level while fasting because a high-protein meal can elevate prolactin.
  2. check TSH, medications
  3. CMP to rule out real/hepatic dysfunction
  4. bHCG
  5. IGF-1 if concerned fro growth hormine excess
  6. brain MRI
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31
Q

macroadenoma workup

A

The question is which hormone is in overproduction?

  • TSH for thyrotrophic adenoma
  • FSH/LH for gonadotroph
  • IGF-1 for somatotropin-secreting hormone
  • 24hr urine free cortisol for corticotropin-secreting lesion

visual field testing

dopamine agonist

-q6months MRI

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32
Q

What are the treatment options for hyper PRL

A
  • do nothing
  • dopamine agonists
  • surgery
  • radiation
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33
Q

Name 2 dopamine agonists?

side effects?

A

bromocriptine 1.25mg PO at dinner or bedtime or give as vaginal suppository
-n/v, orthostatic hypotension, depression, nasal congestion

Cabergoline

  1. 25mg twice weekly or 0.5 weekly
    - rare n/v
    - well tolerated
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34
Q

When to operate on prolactinoma?

recurrence rate?
complications?

A

failed meds, has biparietal visual field defects, ademona size is unchanged despite normal prolactin level

microadenomas- <10%
macro->80%
complications-pit insufficiency, diabetes, CSF leak, meningitis, loss of vision, mortality

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35
Q

treatment for microprolactinoma

A

asymptomatic? rpt q 6-12 months
symptomatic-dopamine agonist, check PRL 1 months after starting, then 4-6 months, then yearly once stable.

follow with q2yr MRI

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36
Q

When to stop dopamine agonist?

A

2 years, asymptomatic, normal prolactin level, no tumor on MRI

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37
Q

Pregnancy, can they continue cabergoline or bromocriptine?

A

no, stop in 1st trimester

Only give meds for visual impairment

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38
Q

What is empty sella syndrome?

A

the subarachnoid space herniates down into the pituitary fossa which compresses the gland against the sella floor

80% occur in women
75% obese
40-50 yrs old
<1/3 are symptomatic

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39
Q

New patient infertility ddx

A

Ovarian

  • low egg count and/or quality
  • PCOS
  • endometriosis
  • primary ovarian insufficiency-turners, swyers, chemo/rad, ovarian surgery
  • hypogonadotropic hypogonadism-anorexia, stress, exercise, Kallman
  • hyper-PRL

Uterine/Cervical

  • polyp
  • fibroid
  • endometrial scarring

Fallopian tube
-PID

Male factor

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40
Q

define fertility, fecundibility, fecundity

A

fertility- abilty to achieve a clinicaly recognized pregnancy
fecundibility- ability to get pregnant in a single cycle
fecundity-ability to achieve a life birth

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41
Q

When to refer to REI for infertility?

A
  • oligomenorrhea
  • uterine, tubal disease, or peritoneal disease
  • stage III or IV endo
  • male factor
42
Q

infertility work up

A

Women

  • prenatal labs-CBC, Hep C, HIV, Type and screen
  • Ovarian reserve testing
  • TSH/Vit D
  • prolactin ONLY IF menstrual abnormality
  • US/Hysterosalpingogram
  • screen for CF, SMA, hemoglobinopathies

Men

  • Hep C, HIV, Type and screen
  • Semen analysis
43
Q

How to perform a clomiphene citrate challenge test?

A

Check FSH on cycle day 3, then give clomiphene 100mg PO on CD 5-9.
FSH should stay under 10, if it rises then E2 is not suppressing FSH and the pt may have diminished ovarian reserve

Check FSH/estradiol cycle day 2-4

  • Normal FSH <10 mIU/mL, High is >15
  • normal estradiol is 60-80pg/mL

YOU NEED BOTH FSH & E2, bc E2 suppresses FSH.

44
Q

How to diagnose diminished ovarian reserve?

what is it predictive of?

Next step if diagnoses?

A
  • AMH <1 on any cycle day
  • elevated FSH on clomiphene citrate challenge test
  • FSH >10 with normal estradiol on CD 2-3
  • antral follicle count <5-7 by sono
  • <4 ooctyes retrieved during IVF

predicts response to stimulation NOT ability to get pregnant

Consider testing for fragile X if unexplained diminished ovarian reserve.

45
Q

How to rule out anovulation?

A
  • monthly menses
  • LH surge on ovulation kit
  • day 21 progesterone >3 ng/mL
46
Q

DDX of male factor infertility

A

Pre-testicular

  • kallmann syndrome
  • idiopathic low GnRH–> low LH–>low T–> low sperm
  • steroids
  • pituitary mass
  • Hyper-PRL

Testicular

  • klinefelters, Y microdeletion
  • chemo/rads
  • trauma
  • varicocele

Post-testicular
-absent vas deferens, retrograde ejaculation, ED, ejaculatory duct or epididymal obstruction

47
Q

How to perform semen analysis?

What is a normal result?

Next step if abnormal

A

2-4 days abstinence

Volume-1.5ml
Concentration-15 mil/mL
Motility-40%
Morphology - AT LEAST 4%, 14% is excellent
-absent agglutination

-repeat semen analysis then refer to REI or urologist

48
Q

Minimal sperm counts for:

  • intercourse
  • IUI
  • IVF
  • ICSI
A

-Intercourse: >20mil
-IUI: >5 million total motile count
-IVF: 30k-100k per oocyte
-ICSI: 1 viable sperm per oocyte
intracytoplasmic sperm injection

49
Q

What factors make tubal reversal more successful?

A
  • Otherwise good fertility workup-must do semen analysis
  • method of tubal ligation-clips
  • isthmic is better than ampullary ligation (Isthmus, ampulla, infundibulum, fimbria)
  • tubal length greater than 4cm
  • 50-75% success
50
Q

When should you remove fibroids for fertility purposes?

A

ONLY if recurrent miscarriages, highly symptomatic or impinging on uterine cavity

51
Q

Ovulation induction w/clomiphene citrate

MOA

A

estrogen agonist/antagonist (SERM), binds to estrogen receptor on hypothalamus, which blocks estrogen’s negative feedback on hypothalamus. This creates a pseudo-hypoestrogenic state. Hypothalamus increases GnRH, which increases FSH, and thus follicle development.

52
Q

Ovulation induction w/clomid

administration and side effects

A
50mg daily on days 5-9
max 150-200mg
for 3 months if regular cycles
6 months if abnormal cycles
then refer to REI for IUI

hot flashes, headaches, visual changes
visual changes associated with increased risk of stroke.

53
Q

Ovulation induction w/letrozole

MOA

A

aromatase inhibitor leading to true hypoestrogenic state which increases GnRH, which increases FSH, stimulates follicle development.

54
Q

Ovulation induction w/letrozole

administration and side effects

A

2.5mg - 5mg PO x 5 days CD 3-7

hot flashes, headache, decreased bone mineral density, nausea, constipation

55
Q

PCOS which is better clomid vs letrozole

A

Letrozole is first line for induction

56
Q

When to do intracytoplasmic sperm injection?

A
  • male factor infertility
  • genetic conditions
  • few oocytes (cant take chances)
  • -frozen eggs
57
Q

When to do intracytoplasmic sperm injection?

A
  • male factor infertility
  • genetic conditions
  • few oocytes (cant take chances)
  • frozen eggs
  • failed traditional IVF
58
Q

recurrent pregnancy loss definition

A

2+ losses at <20wks

excluding molar, ectopic, biochemical pregnancies

59
Q

recurrent pregnancy loss ddx

A

Anatomic-fibroids, polyps, septumm adhesions
Genetics-autosomal trisomies due to aneuploid gametes, balanced translocations
Endocrine-hypothyroid, diabetes, PCOS,

Immunologic-lupus
Smoking, EtOH >2/day, caffeine (>300 mg/day)

Infectious-no strong evidence, perhaps BV and chlamydia
Thrombotic-only test if personal DVT hx of familial thrombophilia risk

60
Q

recurrent pregnancy loss workup

A
  • TVUS
  • saline sono
  • parental karyotypes
  • AMH, day 3 FSH/E2
  • prolactin
  • TSH (goal <2.5)
  • A1C <7%
  • anti-phospholipid work up ONLY if 3+ losses <10 wks
61
Q

Treatment for antiphospholipid syndrome

A

heparin 5k BID with ASA 81mg or lovenox 40mg daily with ASA 81mg

62
Q

When to test for antiphospholipic syndrome?

How to test for APS?

A

You need one clinical and one lab criteria:

  • hx of clots
  • 3+ losses <10 wks
  • PTD <34 wks due to PEC or placental insufficiency (IUGR).
  • test two 12 weeks apart
  • anti-cardiolipin
  • lupus anticoagulant
  • beta2 glycoprotein
63
Q

When to evaluate for precocious puberty?

A

<6 w/breast or pubic hair development
<8 w/both breast AND pubic hair development

64
Q

Precocious puberty

DDX

A

GnRH dependent- early activation of HPO axis

  • constitutional/idiopathic
  • CNS pathology

GnRH independent

  1. Ovarian tumors
  2. McCune allbright
  3. adrenal tumor/ CAH
  4. exogenous estrogen exposure
  5. hypothyroidism
65
Q

Precocious puberty workup

A

bone age via left wrist x-ray
GnRH stim test to differentiate between GnRH dependent vs independent causes

Give leuprolide 20 microgram subQ, check LH 30-40 minutes later, if >6 then HPO axis is activated and the cause is GnRH dependent

66
Q

Precocious puberty
workup

GnRH stim test with LH >6

next step?

A

MRI for CNS pathology looking for hamartoma

67
Q

indications for treatment of precious puberty

A
  1. sexual maturity progresses to next stage in 3-6
  2. growth velocity is >6cm/yr
  3. bone age advanced more than 1 year
  4. predicted adult height is less than target range or is gradually decreasing
68
Q

Treatment for GnRH dependent precocious puberty

what lab do you follow and how often?

A

GnRH agonist
check estradiol q3-6 months, goal <10 pg/mL

  • psychological counseling
  • treat the child like chronologic age.
69
Q

What is McCune Allbright Syndrome? and how is it diagnosed?

A

-continuous estrogen production because the G protein cannot turn off adenlyate cyclase

-clinically, but can test for GNAS mutation
Café-au-lait spots
Polyostotic fibrous dysplasia (PFD)
Precocious puberty
Hyperthyroidism
Growth hormone excess
Cushing syndrome
70
Q

Work up for premature adrenarche

treatment for isolated premature adrenarche

A
  1. x-ray for bone to differentiate precious puberty from isolated adrenarche.
  2. Exclude CAH by checking 17 OHP
  3. if isolated, serial exams/heigh checks
  4. consider imaging for adrenal mass
71
Q

work up for premature thelarche

A

none usually self-limited, but check for precious puberty

72
Q

work up premature menarche

A

consider McCune Allbright

check for other causes of vaginal bleeding in child-trauma, foreign body like tissue paper, infection, neoplasm

73
Q

How to diagnose PCOS

A

2 out of 3

  1. anovulation
  2. signs of hyperandrogenism (hair, acne, elevated testosterone, DHEAS)
  3. polycystic ovaries (12+ antral follicle or total volume >10cc
74
Q

PCOS workup

A

Are they ovulating?
-Check day 21 progestrone level to check for ovulation, >3 means ovulation

If anovulatory, rule out other causes of anovulation.

  • bhcg
  • TSH/PRL to rule out other causes of anovulation
  • CD 3 FSH/estradiol to get for hypo/hypo as the cause of anovulation

Rule out other causes of hyperandrogenism

  • testosterone
  • DHEAS if concerned for tumor
  • 17 OHP to rule of CAH
Check for metabolic syndrome 3/5
-fasting glucose >110
-waist >35in
-triglycerides >150
HDL <40
-BP >130/85

Check for endometrial hyperplasia-EMB

75
Q

Patient presents with excessive hair growth, acne, deepening of the voice

DDx

A
Elevated Androgens
PCOS
Exogenous androgens
Non-classical CAH
HAIR-AN syndrome
Androgen secreting ovarian and adrenal tumors
Cushing Syndrome
idiopathic
Menstrual irregularities
Thyroid dysfunction
hyperPRL
hypothalamic amenorrhea
primary ovarian insufficiency
obesity
76
Q

Hyperandrogenism work up

A
testosterone
DHEAS
SHBG
17 OHP to rule out CAH
TVS for ovarian tumor
ONLY get CT if concerned if concerned for adrenal malignancy
77
Q

What testosterone and DHEAS levels make you want to rule out tumors?

A

T> 200

DHEAS >700

78
Q

What organ does DHEAS come from?

A

adrenal gland

Dehydroepiandrosterone sulfate

79
Q

What organ does androstenedione come from?

A

50/50 ovary and adrenal cortex

80
Q

What is HAIR-AN syndrome?

A

Hyperandrogenism, insulin resistance, and acanthosis nigricans.

Ovarian Theca cell hyperplasia causing excess androgens

81
Q

You are testing for non-classical CAH. What lab do you order and how do you interpret the results?

A

17-OHP in the follicular phase early AM

<200 rules out non-CAH
>800 rules in non-CAH

in between 200 and 800–> repeat it, then perform ACTH stim test

82
Q

What is an ACTH stim test?

A

adrenocorticotropic hormone

give ACTH, if 17 OHP is greater than 1500, non-classical CAH is diagnosed

83
Q

Hyperandrogenism
elevated T and elevated DHEAS

CT showed adrenal mass,

Next Step?

A

rule of pheochromocytoma then perform FNA because most adrenal adenomas are malignant.

84
Q

Clinical features seen in cushing syndrome but not PCOS?

A

proximal muscle weakness, moon facies, easy bruising, buffalo hump, moon facies,

both can have hirsutism, HTN, central obesity

85
Q

If Hirsuitism patient has normal androgen levels and normal menstrual functions, which enzyme is likely the cause?

A

5-alpha reductase

86
Q

Treatment for hirsuitism

A

hair removal-plucking, wax, cream, electrolysis, laser

Medical OCPs, spirnolactone, eflornithine, finasteride, flutamide

87
Q

How do OCPs treat hirsuitism?

A

decrease LH and increase SHBG, decrease adrenal DHEAS, inhibits 5alpha reductase in the skin

60-80% of patients show improvement.
Can take 6 months.

88
Q

What is in sprintec?

A

Norgestimate 250mcg, ethinyl estradiol 35mcg

89
Q

spironolactone MOA, SE,

A

aldosterone antagonist

SE: dyspepsia, nausea, urinary frequency, fatigue, decreased libido, headache, sun sensitivity

USE WITH OCP-can cause feminization of male fetus

90
Q

eflornithine MOA, SE

A

inhibits ornithine decarboxylase which inhibits cell division and synthesis functions, which decreases hair growth

SE: skin sensitivity
apply cream BID and use with hair removal technique

91
Q

finasteride MOA, SE

A

5 alpha reductase inhibitor

least effective, few side effects

92
Q

flutamide MOA, SE

A

androgen receptor blocker used in prostate cancer

SE: dry skin, green urine with liver function abnormalities.

last line option

93
Q

What is the physiology of PCOS?

A

cycle of increased LH and insulin leading to high ovarian testosterone production. High T results in inhibition of follicular maturation resulting in many small follicles and anovulation.

94
Q

PCOS management if pregnancy is desired

vs pregnancy not desired

A

diet and exercise for everyone
-letrozole with or w/o metformin for ovulation induction

OCPs is first line

95
Q

Which type of male gonadal cells produce AMH?

A

serotli cells

96
Q

Which type of male gonadal cells produce testosterone?

A

leydig cells

97
Q

Describe the development of external male genitalia.

A

Leydig cells produce testosterone.
5a reductase converts T to DHT which leads to external genitalia and prostate.

SRY determine if gonads become ovaries or testes

98
Q

Which structures come from the wolffian ducts?

A

epididymus, vas deferens, seminal vesicle, ejaculatory duct

mesonephric

99
Q

Which structures come from the mullerian ducts?

A

fallopian tubes, uterus, cervix, and upper third of vagina

NOT Ovaries
paramesonephric duct

100
Q

What is the recommended daily allowance of calcium?

Vitamin D?

A

The RDA for calcium is 1,000 mg per day from ages 19 to 50 years and 1,200 mg per day in older women.

For vitamin D, the RDA is 600 international units per day to age 70 years and 800 international units thereafter.

101
Q

You get called for Ambiguous genitalia.

How do you evaluate this patient?

A

First get a hx and exam (drugs, maternal virilization, anybody in the family)

hyperpigmentation is suggestive of ACTH/adrenal origin.

17 OHP, karyotype, maternal u/s looking for luteoma

DDX
CAH- 17 OHP
aromatase deficiency
maternal tumor, drugs, luteoma