26. Hyperandgrogenism Flashcards

(59 cards)

1
Q

What is hyperandrogenism?

A

Increased androgen production or action.

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2
Q

What is hirsutism?

A

Growth of terminal hair in a male-pattern distribution that is socially undesirable.

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3
Q

What is virilization?

A

Development of male secondary sexual characteristics in a woman (e.g., hirsutism, deepened voice, clitoromegaly, defeminization).

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4
Q

What is acne vulgaris in the context of hyperandrogenism?

A

Hormonally influenced but not an endocrine disorder itself.

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5
Q

How does hair grow?

A

In cycles, not continuously.

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6
Q

What is the duration of the growth cycle in different body areas?

A

✅ Scalp: 5-7 years
✅ Face: 3-6 months

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7
Q

What are the three types of hair based on androgen response?

A

✅ Non-sexual hair: Independent of androgens.
✅ Ambosexual hair: Stimulated by low androgen levels (e.g., pubic hair at puberty).
✅ Sexual hair: Stimulated by high androgen levels, develops in male pattern (e.g., beard, upper pubic triangle).

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8
Q

What are the three types of hair?

A

✅ Lanugo: Fine, soft, silky prenatal hair coat.
✅ Vellus: Fine, usually non-pigmented, short.
✅ Terminal: Thick, dark, long.

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9
Q

What are the three phases of the hair cycle?

A

✅ Anagen (Active Growth): 85-95% of scalp hair, lasts about 3 years.
✅ Catagen (Regression): 1% of scalp hair, lasts about 2 weeks.
✅ Telogen (Resting): 5-15% of scalp hair, lasts about 3-4 months.

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10
Q

How many hair follicles are on the scalp?

A

About 100,000.

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11
Q

How many hairs are lost per day?

A

20-75 hairs/day.

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12
Q

How does the facial hair cycle differ from the scalp?

A

Facial hair: 4 months anagen vs 2 months telogen.

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13
Q

What makes up the pilosebaceous unit?

A

Hair follicle + sebaceous gland.

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14
Q

Why is the pilosebaceous unit important in androgen-related disorders?

A

✅ It is a sex steroid target with oestrogen + androgen receptors.
✅ It converts testosterone to 5α-DHT (the active androgen).

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15
Q

What are the three main androgens?

A

✅ Testosterone (primary active androgen).
✅ Dehydroepiandrosterone (DHEA) – a prehormone converted to testosterone.
✅ Androstenedione – another prehormone converted to testosterone.

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16
Q

What enzyme converts testosterone into its more potent form?

A

5α-reductase converts testosterone into dihydrotestosterone (DHT).

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17
Q

What modulates androgen effects in the blood?

A

Sex hormone-binding globulin (SHBG) acts as a buffer system in androgen regulation.

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18
Q

What is the role of Sex Hormone Binding Globulin (SHBG)?

A

SHBG binds androgens in circulation, modulating their effects and acting as a buffer system.

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19
Q

What is the most common ovarian cause of hyperandrogenism?

A

Polycystic ovarian syndrome (PCOS).

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20
Q

Which ovarian tumours can cause hyperandrogenism?

A

Androgen-producing tumours.

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21
Q

Which adrenal disorders can cause hyperandrogenism?

A

Congenital adrenal hyperplasia (CAH), adrenal adenomas, adrenal carcinomas, and Cushing’s syndrome.

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22
Q

What is pregnancy luteoma, and how does it cause hyperandrogenism?

A

A benign ovarian mass during pregnancy that produces excess androgens.

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23
Q

How does obesity contribute to hyperandrogenism?

A

Increases peripheral conversion of androgens and reduces SHBG, leading to more free androgens.

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24
Q

What endocrine disorders reduce SHBG, leading to more free androgens?

A

Hypothyroidism, hyperthyroidism, and hyperinsulinemia.

25
What is idiopathic hyperandrogenism?
Increased androgen sensitivity in target tissues without elevated androgen levels.
26
What medications can cause hyperandrogenism?
Testosterone, anabolic steroids, danazol.
27
What happens in cases of combined ovarian and adrenal pathology?
Both sources contribute to hyperandrogenism, leading to severe symptoms.
28
What key elements should be assessed in the history of a patient with hyperandrogenism?
Family history, previous investigations, and past treatments.
29
What aspects should be assessed during a physical examination for hyperandrogenism?
Signs of hirsutism, acne, virilization, obesity, and features of underlying endocrine disorders.
30
How is hirsutism documented?
Using scoring systems such as the Ferriman-Gallwey score.
31
How do FSH and LH levels help diagnose PCOS?
An inverted ratio (LH > FSH) is suggestive of PCOS.
32
What does a very elevated testosterone level suggest?
Androgen-producing tumour.
33
What does a mild elevation of testosterone suggest?
Ovarian source, such as PCOS.
34
Why is the free androgen index (FAI) more useful than total testosterone?
FAI indicates the bioavailable testosterone, which is a better measure of androgen activity.
35
How is FAI calculated?
FAI = (Total Testosterone × 100) / SHBG.
36
What does an elevated DHEAS level suggest?
Adrenal origin of hyperandrogenism (e.g., adrenal tumour or CAH).
37
What does an elevated 17α OH progesterone level suggest?
Congenital adrenal hyperplasia (CAH), possibly late-onset.
38
When should Cushing’s syndrome be investigated?
If adrenal androgens are elevated or if there is clinical suspicion (e.g., central obesity, moon face, striae).
39
What imaging is useful in diagnosing PCOS or ovarian tumours?
Ultrasound of the ovaries.
40
What should be presumed if all investigations are normal?
End-organ hypersensitivity (often diagnosed as idiopathic hyperandrogenism).
41
What is the general principle of treating hyperandrogenism?
Address the underlying cause and use targeted therapy to reduce androgen levels.
42
How do corticosteroids help in hyperandrogenism?
They suppress adrenal steroidogenesis (useful for adrenal causes like CAH).
43
How do combined oral contraceptives (COCs) help?
They suppress ovarian steroidogenesis and increase SHBG, which reduces free androgens.
44
What is cyproterone acetate, and how does it work?
It is an anti-androgen that binds to DHT receptors and reduces 5α reductase activity.
45
How does spironolactone help in hyperandrogenism?
It is an aldosterone antagonist with anti-androgen effects, binding to androgen receptors.
46
What are the benefits of drospirenone?
It is a spironolactone analogue with anti-mineralocorticoid, anti-androgen, and progestogenic properties.
47
What is the mechanism of action of finasteride?
It is a selective 5α reductase type II inhibitor, preventing the conversion of testosterone to DHT.
48
Why must GnRH agonists be combined with COCs?
To prevent bone loss while inhibiting ovarian steroidogenesis.
49
How does metformin help in hyperandrogenism?
It is an insulin-sensitizing agent, useful in women with PCOS and insulin resistance (IR).
50
What combination provides the best therapeutic result?
Anti-androgens combined with COCs, as they enhance SHBG levels and regulate the cycle.
51
Why is contraception essential when using anti-androgens?
Anti-androgens can be teratogenic and affect fetal development.
52
How does weight loss improve hyperandrogenism?
It increases SHBG and reduces insulin resistance.
53
Why is psychological support important?
Hirsutism and acne can cause distress and body image issues.
54
What is the role of cosmetic therapy?
Laser treatment is highly effective and should be continued alongside medical therapy.
55
How long does it take for acne to improve?
Approximately 6 weeks.
56
How long does it take for facial hair to show improvement?
Around 6 months for initial improvement
57
When should the dose be increased?
If there is no response after 6 months.
58
When should treatment be reviewed?
If there is no response after 18–24 months.
59
Which red flag symptoms require urgent investigation?
**- Testosterone > twice normal - Unilateral ovarian enlargement - Suspected Cushing’s syndrome - Virilization or rapid onset of symptoms - Failed therapy**