PCOS & Hirsutism Flashcards
Define Hirsutism
Excess facial and body hair growth in a male pattern distribution in women, that is bothersome and not in keeping with ethnicity.
Define virilization?
An extreme form of hirsutism that may be associated with male pattern hair loss, deepening of the voice, increased muscle bulk and enlargement of the clitoris.
How is the severity of hirsuitism classified?
According to the Ferriman-Gallway scoring system, which looks at 9 areas that are affected by androgens - upper lip, chin, chest, arms, upper abdomen, lower abdomen, upper back, lower back and thighs - and assigns a score 0 (no hair) to 4 ( heavy hair growth.
A score of 8 or more indicates hirsutism and 15 or more indicates moderate to severe hirsutism.
What are the causes of hirsuitism?
There are 7 main causes:
95% of cases are caused by PCOS (72%) and Idiopathic (23%). Others include hyperandrogenic hirsuitism, CAH (1-10%), androgen secreting tumour, Cushing’s syndrome and Drugs.
Which drugs cause hirsuitism?
Danazol, anabolic steroids and sodium valproate (for epilepsy)
What are the causes features of hyperadrogenic hirsuitism? What are these patients at risk of?
Causes may be excess androgen production from adrenals or ovary.
They have anovulation, irregular menses, infertility.
- Elevated DHEA indicates adrenal origin.
- Elevated testosterone may be of adrenal/ovarian origin.
These patients are at risk of endometrial hyperplasia ďue to the elevated testosterone levels and
more testosterone being aromatized to oestrogen. Oestrogen has a (direct) proliferative effect on the endometrium.
What are the features of idiopathic hirsuitism? What is the cause?
These patients have normal serum androgen levels. They have regular menses.
Genetic/familial component - seen in women of Mediterranean and East Indian descent.
Cause:
They are thought to have increased skin sensitivity to androgens OR
Increased activity of 5alpha-reductase which converts testosterone to the more potent dihydrotestosterone (DHT).
Presentation of PCOS?
Hirsuitism, acne, central obesity, anovulation/oligomenorrhea/irregular menses, infertility, acanthus nigerans.
Presentation and evaluation for an androgen-secreting tumour? Incidence?
These patients have adrenal/ovarian tumours which results in very high levels of androgens (DHEA/ testosterone) and a SUDDEN onset of hair growth or progression, severe hirsuitism and signs of virilization.
- pelvic u/s for evaluation looking for an adrenal or ovarian tumour.
Incidence 0.2% of pts with hirsuitism.
CAH causes hirsuitism. What’s the incidence, risk factors, diagnosis?
Incidence: causes 1-10% of cases of hirsuitism .
Risk factors- genetics- higher risk os Ashkenazi jews, Latinos and Slavic ethnic groups.
Diagnosis: elevated serum 17-hydroporgesterone
During workup for hirsuitism, which pts require referral?
Patients with the following should be referred for further management;
1. CAH
2. Cushing’s syndrome
3. Androgen secreting tumour (Adrenal/ovarian tumour)
4. Hair growth worsens despite treatment
5. Ineffective treatment after 6-12mths
How do you counsel the patient with hirsuitism?
I would counsel this patient so that she can make an informed decision about which management option to pursue.
- So treatment choices depends on 1. her preference, 2. the extent to which the areas causing distress can be removed and 3. the availability of these options.
- she should be informed that a trial of 6mths is required before adjusting the dose or changing/add medication, because due to the life span of hair, 6mths is required to notice any effect.
Discuss the different treatment options:
No tx - for mild hirsuitism w/ no effect on QOL
Wt loss - for overweight pts. Decreases serum insulin, androgen production and conversion of androstenedione to testosterone. Wt loss increases SHBG which decreases free androgens.
Cosmetic - shaving/waxing/plucking/bleaching/electrolysis/laser.
Medical - COCs (1st line), cyproterone acetate (added to COC), gnrh analogies (induced medical oophorectomy), topical facial eflornithine, anti-androgens (spironolactone, fluoride, finasteride).
***advise that COCs containing levonorgestrel or norethisterone potentially exacerbate hirsuitism
What is the best marker of adrenal androgen production and why?
DHEAS
Bcuz DHEA (the predominant adrenal androgen) is also produced by the ovary (20%)
How is testosterone transported in blood?
1% unbound (metabolically active)
19% bound to albumin
80% bound to SHBG
T/F. Androgen receptors are only activated by DHEAS and testosterone.
False
Testosterone and DHT are the o lt andeigens that activate the receptors.
DHEA-S, DHEA and androstenedione are mostly bound to albumin and are converted to testosterone in peripheral tissues
