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This is a humorous medical meme showing an exaggerated, anatomically impossible scenario involving two urological/urinary procedures depicted simultaneously on a cross-section of the male pelvis. Here's what's shown:

What the diagram depicts

Left side: A doctor with their eye pressed to the eyepiece of a cystoscope - a long rigid instrument inserted through the penis (urethra) up toward the bladder. A shocked emoji is placed at the entry point.
Right side: A gloved hand performing a Digital Rectal Exam (DRE) - a finger inserted into the rectum to palpate the prostate gland. Another shocked emoji is placed at the point of contact.

The two real procedures being parodied

  1. Cystoscopy - a real procedure where a thin camera scope is passed through the urethra to examine the bladder and urethra (used to diagnose bladder cancer, stones, strictures, etc.)
  2. Digital Rectal Exam (DRE) - a real clinical exam where a physician inserts a gloved finger into the rectum to feel the prostate for enlargement, nodules, or abnormalities (used to screen for prostate cancer or BPH)

Why it's funny

Both procedures are real, both are genuinely invasive, and both are notoriously uncomfortable for patients. The meme exaggerates by showing them happening at the same time, with the doctor absurdly close to the patient - poking fun at the nature of these routine but awkward urological exams. The shocked emojis represent the "reaction" of the body at each entry point.

Hyperandronism in female

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hyperandrogenism female hirsutism virilization causes

A clinical photograph of a female patient's face and neck in a lateral profile view, demonstrating clinical signs of hyperandrogenism and virilization. The image reveals prominent hirsutism, characterized by coarse, dark hair growth in an androgen-dependent distribution, specifically involving the preauricular (sideburn) area, cheeks, and along the mandibular jawline. Accompanying these findings is an inflammatory acneiform eruption, presenting as erythematous papules and pustules clustered around the jaw and upper neck. This combination of acne and hirsutism is highly suggestive of an underlying hyperandrogenic state. The educational focus of this image is the recognition of physical manifestations of excessive androgen levels in female patients, which may be associated with conditions such as polycystic ovary syndrome (PCOS) or, in this clinical context, pregnancy-related luteoma.

A clinical photograph of a female patient's face and neck in a lateral profile view, demonstrating clinical signs of hyperandrogenism and virilization. The image reveals prominent hirsutism, characterized by coarse, dark hair growth in an androgen-dependent distribution, specifically involving the preauricular (sideburn) area, cheeks, and along the mandibular jawline. Accompanying these findings is an inflammatory acneiform eruption, presenting as erythematous papules and pustules clustered around the jaw and upper neck. This combination of acne and hirsutism is highly suggestive of an underlying hyperandrogenic state. The educational focus of this image is the recognition of physical manifestations of excessive androgen levels in female patients, which may be associated with conditions such as polycystic ovary syndrome (PCOS) or, in this clinical context, pregnancy-related luteoma.

This clinical photograph displays the lower face and neck of a female patient six months postpartum, illustrating symptoms of virilization. The primary visual finding is hirsutism, characterized by prominent, dark terminal hair growth along the cheeks, jawline, and chin. The skin in the perioral and mandibular regions shows subtle textural irregularities and evidence of acneic lesions, which are common dermatological manifestations of hyperandrogenism. This image serves as an educational example of the clinical presentation of androgen-secreting conditions during or after pregnancy, such as a pregnancy luteoma. The photograph documents the residual physical effects of severe hyperandrogenemia (elevated testosterone and androstenedione) as it gradually resolves following medical or surgical intervention.

This clinical photograph displays the lower face and neck of a female patient six months postpartum, illustrating symptoms of virilization. The primary visual finding is hirsutism, characterized by prominent, dark terminal hair growth along the cheeks, jawline, and chin. The skin in the perioral and mandibular regions shows subtle textural irregularities and evidence of acneic lesions, which are common dermatological manifestations of hyperandrogenism. This image serves as an educational example of the clinical presentation of androgen-secreting conditions during or after pregnancy, such as a pregnancy luteoma. The photograph documents the residual physical effects of severe hyperandrogenemia (elevated testosterone and androstenedione) as it gradually resolves following medical or surgical intervention.

This clinical photograph displays androgenized facial features in a 41-year-old female patient, illustrating the physical manifestations of hyperandrogenism and virilization. Key visible findings include hirsutism, characterized by coarse, dark terminal hair growth on the upper lip, chin, and jawline in a male-pattern distribution. The facial skin exhibits signs of thickening and a roughened texture. The jawline appears relatively prominent and squared, contributing to the overall masculinization of the facial phenotype. Such features in a female clinical context are often associated with systemic endocrine dysfunction, such as paraneoplastic syndromes secondary to hormone-secreting tumors (e.g., Krukenberg tumors or ovarian/adrenal malignancies). This image serves as an educational example of virilization symptoms used in the differential diagnosis of androgen-secreting pathologies in endocrinology and oncology.

This clinical photograph displays androgenized facial features in a 41-year-old female patient, illustrating the physical manifestations of hyperandrogenism and virilization. Key visible findings include hirsutism, characterized by coarse, dark terminal hair growth on the upper lip, chin, and jawline in a male-pattern distribution. The facial skin exhibits signs of thickening and a roughened texture. The jawline appears relatively prominent and squared, contributing to the overall masculinization of the facial phenotype. Such features in a female clinical context are often associated with systemic endocrine dysfunction, such as paraneoplastic syndromes secondary to hormone-secreting tumors (e.g., Krukenberg tumors or ovarian/adrenal malignancies). This image serves as an educational example of virilization symptoms used in the differential diagnosis of androgen-secreting pathologies in endocrinology and oncology.

This clinical comparison photograph illustrates the resolution of hirsutism in a 69-year-old female patient following the surgical removal of a Leydig Cell Tumor (LCT). Image (a) represents the pre-operative state, showing prominent male-pattern terminal hair growth on the upper lip (mustache area) and chin. The hair is dark, coarse, and relatively dense, characteristic of hyperandrogenism. Image (b) shows the post-operative result, demonstrating a significant reduction in terminal hair density and thickness in the same facial regions. The remaining hair is sparse and fine, indicating clinical improvement of virilization symptoms. The images serve as an educational example of the cutaneous manifestations of androgen-secreting ovarian tumors and the subsequent reversal of secondary sexual characteristics after hormonal normalization. Key educational concepts include the clinical signs of hyperandrogenemia in postmenopausal women and the diagnostic importance of recognizing sudden-onset hirsutism as a marker for underlying endocrine-active neoplasms like sex cord-stromal tumors.

This clinical comparison photograph illustrates the resolution of hirsutism in a 69-year-old female patient following the surgical removal of a Leydig Cell Tumor (LCT). Image (a) represents the pre-operative state, showing prominent male-pattern terminal hair growth on the upper lip (mustache area) and chin. The hair is dark, coarse, and relatively dense, characteristic of hyperandrogenism. Image (b) shows the post-operative result, demonstrating a significant reduction in terminal hair density and thickness in the same facial regions. The remaining hair is sparse and fine, indicating clinical improvement of virilization symptoms. The images serve as an educational example of the cutaneous manifestations of androgen-secreting ovarian tumors and the subsequent reversal of secondary sexual characteristics after hormonal normalization. Key educational concepts include the clinical signs of hyperandrogenemia in postmenopausal women and the diagnostic importance of recognizing sudden-onset hirsutism as a marker for underlying endocrine-active neoplasms like sex cord-stromal tumors.

Now let me read the main textbook sections on hyperandrogenism:
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hyperandrogenism women diagnosis management

Here is a comprehensive overview of Hyperandrogenism in Females:

Hyperandrogenism in Females

Hyperandrogenism (HA) is a state of excess androgen action in women, most commonly presenting as hirsutism, and less frequently as full virilization. - Berek & Novak's Gynecology, p. 1906

Androgens in Women - Normal Physiology

Androgens in women are produced equally by the ovaries and adrenal glands, under control of LH and ACTH respectively. The key androgens involved are:
  • Testosterone (principal circulating androgen)
  • Androstenedione
  • DHEA and DHEAS (adrenal markers)
Testosterone is converted peripherally to dihydrotestosterone (DHT) by 5α-reductase type 2 in the pilosebaceous unit (PSU) - DHT is the primary mediator of androgenic hair effects. Hyperinsulinemia and androgen excess both suppress hepatic SHBG production, increasing free (biologically active) testosterone. - Harrison's Internal Medicine 22E, p. 3182

Clinical Manifestations

1. Hirsutism

Excessive growth of terminal hair in a male distribution (midline, chin, upper lip, sideburns, chest, inner thighs, lower back). Hair is transformed from fine vellus to coarse, dark, pigmented terminal hair by androgens acting on the PSU.
Grading: The modified Ferriman-Gallwey scale scores 9 androgen-sensitive body sites (0-4 each). A score >8 is abnormal in most non-Hispanic white and African American women. Asian women may show acne/alopecia instead of hirsutism. - Harrison's Internal Medicine 22E, p. 3182

2. Acne

  • Jawline/lower face distribution
  • Severe or sudden onset acne in women should raise suspicion for HA

3. Androgenic Alopecia

  • Scalp hair thinning or male-pattern baldness (frontal-parietal)

4. Virilization (severe HA)

Indicates markedly elevated androgen levels (usually neoplastic cause):
  • Deepening of voice
  • Breast atrophy
  • Increased muscle bulk
  • Clitoromegaly
  • Increased libido
  • Acanthosis nigricans (sign of insulin resistance)

Clinical Photos of Hyperandrogenism

Below are clinical examples of hyperandrogenism in females:
Female patient with facial hirsutism (coarse dark hair along jawline and cheeks) and acne - features of hyperandrogenism
Facial hirsutism and acne along the jawline - classic signs of hyperandrogenism. Associated with PCOS or, in pregnancy, with a luteoma.
Postmenopausal female with prominent hirsutism from androgen-secreting Leydig cell tumor - before and after surgical removal
Before and after surgical removal of an androgen-secreting Leydig Cell Tumor - shows how virilizing tumors cause profound hirsutism that reverses post-operatively.

Causes (Etiology)

OVARIAN causes (most common)

CauseNotes
PCOS (most common overall)Accounts for ~70-80% of all HA cases
Functional ovarian hyperandrogenismExaggerated ovarian androgen response to LH
Hyperthecosis / Stromal hyperplasiaBenign theca/stroma proliferation; can cause virilization
Androgen-secreting ovarian neoplasmsSertoli-Leydig tumors, granulosa cell tumors, lipid cell tumors
Syndromes of extreme insulin resistanceInsulin stimulates ovarian androgen production

ADRENAL causes

CauseNotes
Congenital Adrenal Hyperplasia (CAH)21-hydroxylase deficiency in >90%; classic and non-classic forms
Cushing syndromeGlucocorticoid excess + adrenal androgen excess
Functional adrenal hyperandrogenismExcess adrenal androgen without clear enzyme defect
Adrenal neoplasms (adenoma/carcinoma)DHEAS >18.5 μmol/L (>7000 μg/L) suggests this
Premature adrenarcheEarly adrenal activation in childhood

OTHER causes

CauseNotes
HyperprolactinemiaProlactin can stimulate adrenal androgens
AcromegalyGH excess
ObesityIncreased peripheral conversion of androgens; reduces SHBG
DrugsAndrogens, anabolic steroids, valproic acid, cyclosporine, phenytoin, minoxidil, danazol
Idiopathic hirsutismNormal androgens, increased 5α-reductase activity
Pregnancy-relatedLuteoma, hyperreactio luteinalis
  • Harrison's Internal Medicine 22E, p. 946-980; Berek & Novak's Gynecology, p. 1909

Diagnostic Evaluation

Key red flags for tumor:
  • Rapid onset and rapid progression of hirsutism
  • Signs of virilization (clitoromegaly, voice deepening)
  • Total testosterone >12 nmol/L (>3.5 ng/mL) = likely androgen-secreting tumor
  • Total testosterone >7 nmol/L (>2 ng/mL) = suggestive of tumor (also seen in hyperthecosis)
  • DHEAS >18.5 μmol/L (>7000 μg/L) = suggests adrenal tumor
Hormonal workup:
  • Total testosterone (by LC/MS assay)
  • Free testosterone (calculated from total T + SHBG, or by LC/TMS)
  • DHEAS (adrenal androgen marker)
  • SHBG
  • FSH/LH (LH:FSH ratio >2 in PCOS)
  • Prolactin, TSH
  • 17-OHP (for CAH - elevated in 21-hydroxylase deficiency)
  • 24-hour urine cortisol or dexamethasone suppression test (if Cushing suspected)
Imaging:
  • Pelvic ultrasound (ovarian morphology, PCO appearance)
  • CT/MRI abdomen-pelvis (if adrenal or ovarian tumor suspected)

Diagnostic Algorithm

Algorithm for evaluation and treatment of hirsutism - showing branching based on hair growth pattern and testosterone levels, leading to diagnoses of PCOS, CAH, Cushing's, virilizing tumor, or idiopathic
Evaluation and Treatment of Hirsutism - Harrison's Internal Medicine 22E, p. 3183

PCOS - The Most Common Cause

Rotterdam Diagnostic Criteria (2 of 3 required):
  1. Clinical or biochemical hyperandrogenism
  2. Oligo/anovulation (menstrual irregularity, <8 cycles/year)
  3. Polycystic ovarian morphology on ultrasound (>12 follicles per ovary OR ovarian volume >10 mL)
Four phenotypes exist based on which 2-3 features are present. PCOS is also frequently associated with insulin resistance and hyperinsulinemia. - Berek & Novak's Gynecology, p. 1905

Treatment

Non-pharmacological

  • Weight loss (5-7% body weight over 6 months) reduces free testosterone and can restore ovulation in >75% of women with PCOS; reduces insulin resistance. - Berek & Novak's Gynecology, p. 1935

Pharmacological

CategoryAgentMechanism
Hormonal suppressionCombined oral contraceptives (COCs)Suppress LH → reduce ovarian androgens; increase SHBG; inhibit 5α-reductase in skin
MedroxyprogesteroneProgestational suppression
GnRH analoguesSuppress LH/FSH → reduce ovarian androgens
GlucocorticoidsSuppress ACTH → reduce adrenal androgens (in CAH)
AntiandrogensSpironolactoneAndrogen receptor blocker + weak inhibitor of steroidogenesis (most commonly used)
Cyproterone acetateAndrogen receptor blocker (not available in USA)
FlutamideAndrogen receptor blocker
5α-Reductase inhibitorsFinasterideBlocks testosterone → DHT conversion at PSU
Insulin sensitizersMetforminReduces insulin → reduces ovarian androgen stimulation; may restore ovulation
GLP-1 agonistsSemaglutide, liraglutideRecent evidence supports weight loss + hormonal improvement in PCOS with obesity (PMID 39178623)
Steroidogenic enzyme inhibitorsKetoconazoleInhibits androgen synthesis (rarely used due to hepatotoxicity)

Mechanical hair removal

  • Temporary: Shaving, waxing, threading, depilatory creams
  • Permanent: Laser hair removal, electrolysis
Note for patients desiring pregnancy: Antiandrogens are teratogenic (contraindicated); focus shifts to ovulation induction (clomiphene, letrozole, gonadotropins). COCs cannot be used in this group.

Summary Table

FeatureHirsutism only+ Oligomenorrhea+ VirilizationRapid onset
Most likelyIdiopathic / PCOSPCOSTumor / HyperthecosisAndrogen-secreting tumor
Key testFree testosteroneLH:FSH, pelvic USSTotal T, CT/MRITotal T >12 nmol/L → imaging

Recent evidence note: A 2025 meta-analysis (PMID 40806019) found intermittent fasting significantly improves anthropometric measures and hormonal profiles in women with PCOS. GLP-1 receptor agonists also show promising results for weight and androgen reduction in obese PCOS patients (PMID 39178623).
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