By the end of this lecture, fourth
year student should be able
" Define hirsuti sr
- Difforentiate it from
hypertrichosis.
- Describe the nomal physlology of
hair growth.
Learning -Explain the etiology and
pathopbysiolgy of hirautium.
Outcomes
"Recognize the clinical evaluation
and diagnosis of hirsut sn.
Discuss the manaqement strateqies,
including lifentyle, medical, and
procedural Lnterventions.
"Identify tha ethical considerations
in trea tmont.
Hirsutism is
defined as
presence of
Coarse hair
in females
in a male
like
pattern.
A£fects 5-15$ of
WOmen, often
causing digtresu
"Affeats 5-15% of women.
(Pakistan 2)
" Extremely distressing
especially in young women
Introduct "Paychosocial and emotional
ion impact.
" Usually associated with
underlying endocrine
disorders.
"Can be an isolated condition.
Phases of Hair Growth:
Physiolog
Y of Hair " Anagen: active growth phase
Growth "Catagen: Transition phase
" Telogen: Resting and shedding
(1/2) phase.
Types of Hair:
Physiolog "Lanugo: fine hair on foetuses
y of Hair Vellus: fine, non-pigmented
Growth hair
" Terninal: coarse,
(2/2) hair
pigmented
Key Androgens:
" Testosterone
"Dihydrotestosterone (DHT) (via
Hormonal 5a-reductase)
Regulatio "Androstenedione
" Dehydroepíandrosterone (DHEA)
n of Hair
Growth Androgen-sensitive areas:
-Face, ahest, lower abdomen,
upper thighs and back
Androgen Excess (most common)
"PCOS
" Androgen-secreting tunors
(ovary/adrenal)
" Non-classíc congenital adrenal
hyperplasia (CAH)
"Cushing syndrome
Aetiology Non-Androgenic Causes
"Medications (e.g- minoxidil,
phenytoin, coticosteroids)
" Idiopathic hirsutí sm
"Genetic/Familial
prediposltion
yndrome.
netabol1c obesity, cealatance,
Insulin
ASsoaaion:
ultraaound. (PCOs)
GVaries
ar Polycystlc Syndrome
hyperandrogenism.
1ínical/biochemical " Ovary C
"Oligolanovuatian.
diagnozia: for three
Polycysti
of aut
TWo (2004): Criteria Rotterdam
cauSe cOnOn Most
Ovarian Tunors:
Arrhenoblastamas, Leydig,
hilar cell tumors.
Androgen Adrenal Tumozs: Adenomas,
Secreting carcinomas.
Tumours
C1inical clues: Rapid
onset, virilization (deep
voice, clitoromegaly),
Cushingoid features.
History:
" Onset, progression, family
history
"Menstrual irregularities,
aone, voice changes.
Clinical " Medications
Evaluatio
Physical Examination:
n
" Perriman-Gallwey Score (9
areaS, SCore >6 is
signí ficant) .
"Signs of virilization,
Cushing's features, thyroid
abnormalities.
Hormonal tests:
"Testosterone (total & free)
" DAEA-S (adrenal source)
"17-hydroxyprogesterone (CAH
sCreening)
Investigat "LH/ESH ratio (PCOs indicator)
ions:
Inaging:
"Pelvic ultrasound (PCOs,
ovarian tumours)
CT/MRI (Adrenal tumours)
Management
ILESTYCE COSNETIC DIAPAcoIOGICAL EROCEDUnAT
PGDIFZCATIO TREATEITS TREATHT IeLEZEICNs
Lifestyle Modifications
01 02 03
Weight loss! Reduces FLrat-1ine
5-10 insulin theraDy LD
reduction resistance Ovewe1ght
Lmproves and androgen PCO patientt.
hirsutiam by production.
40-550.
Cosmetic
and
Physical
Therapies
Caratic:
" Blsaching, waxing,
depilatory crsams.
Physicli
Laser thezapy (30%
halr reduction
after 3-4
3easíon).
" Electrolysis
(persanent but
timn-consuning)
Pharnacologic Management
Androgen Suppression:
Combined Oral Contraceptives (COCs)
(Oestrogen increases SHBG, reducing free
testosterone).
" Anti-androgens: Spironolactone,
Cyproterone acetate, Flutamide.
"5 alpha reductase inhibitors: Finasteride
"Insulin Sensitizers: Metformin (PCOs) .
Special Considerations:
DaSteride
Spironolacton Risk of
Pregnancy: e: monitor metabolism
Teratogenic, for effects
needs
contraception hypezkalaemia (monitor
lípíds/
gtucuset
Ethical Considerations:
Off-labe l drug use (for examp le. ,
finasterlde).
Ensuring effective contraception when
USing teratogenic medications
Addressing psychosocial impact (body
Image, depress lon)
KeyTakeaways
1 Multifsceted 2 Pers onaized
Concition Approach
Hinsumit acomples TNate shoud be tored
COnctio hsaias Caes to indvpsterSnee
ndarogmet opnons and prlrcs
3 Long-Term Managernent
Hiusm chs equir ongong menagemet ecdng intye
chenget, ctherapes, and haronalteatrent
