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85 Cards in this Set

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Cryptorchidism
Undescended testes (hidden testicle). Can be anywhere, but usually felt in the inguinal canal. Increased risk of infertility (esp if bilateral). Unilateral 75%.
Changes = arrested germ cell development. hyalinization and eventual sclerosis of semniferous tubules. Leydig cells relatively spared...
Increased risk of testicular cancer.
Causes of testicular atrophy
Atherosclerotic narrowing of blood supply
Cryptorchidism
End stage orchitis
Irradiation
Malnutrition/ cachexia
Old age
Prolonged admin of female sex hormones
Inflammation of the balls? (orchitis)
What organisms in men <35 and which organisms in men >35?
Young males --> sexually transmitted eg gonorrhea and chlamydia.
Older males: e.coli and pseudomonas (enteric bacteria?)
Usually begin as a UTI, migrates up the ductus deferens to reach the epididymis.
Congestion and oedema, may progress to abscess formation/ may cause sterility.
What are the consequences of testicular torsion?
The twisting of the spermatic cord causes venous outflow obstruction and engorgement, --> sudden onset of testicular pain in an adolescent = emergency.
Oft associated with congenital syndrome; bell clapper abnormality (increased mobility of testis).
Testicular tumors...
males between 15 and 34yo. But can get them older.
95% are germ cell tumors (5% = stromal/ sex cord).
Half = seminoma's.
Seminoma
Account for half of all germ cell tumors. Peak age at dx is late 30's-40yo. Present as large palpable mass in the testis, pain in a fifth.
Sheets of large polyhedral cells, in a fibrous network. BULKY mass, but no haemorhage or necrosis. Produce bHCG but not AFP.
The affected testis is completely replaced in half of all cases.
Bacterial prostatitis
Usually result of retro-prostatic reflux of urine, contaminated with bacteria that cause UTIs (E.coli, g-ve rods, enterococci).
Px = fever, chills, dysuria.
Prostate is enlarged and boggy on DRE.
Sometimes follows catheteristation, cytoscopy or TURP.
(aseptic prostatitis is actually the most common- no hx of UTI)
Prostate cancer
Most common cancer of men.
Age related.
Half present with late-stage disease: urinary sx (nocturia, incomplete voiding), local pain, bone pain. No sx of early PC.
Arise in PERIPHERAL ZONE: late urinary obstruction, earlier palpation on DRE (firm and gritty).
How can anovulation be clinically divided into Oestrogen present or Oestrogen absent..
When given progesterone, those with estrogen will have withdrawal bleeding when P is removed (there is endometrial prolif?).
Those without estrogen present eg HPO axis disruptions, have no withdrawal bleeding. eg disease of the pituitary or the CNS.
Chronic anovulation with oestrogen present?
PCOS. increased LH to FSH.. The chronic stim of the theca cells causes androgen prod -> conversion to E --> increases in levels of both; -ve fb on HPO axis --> decreased LH; no ovulation. Large cystic anovulatory follicles.
Chronic anovulation with oestrogen absent?
Hypogonadotropic hypogonadism; decreased LH and FSH = decreased stimulation of the ovaries. Occurs with stress, physical exercise, dieting... changes to the hypothalamus. Also in chronic debilitating diseases such as malignancy, diabetes, IBD, ESRF.
Also with direct pituitary changes eg PRLoma.
What are some causes of regular but prolonged and excessive bleeding episodes:
submucous leimyomas, adenomyosis or endometrial polyps.
Primary dysmenorrhea- Cause?
Treatment?
(n.b secondary dysmen = underlying pelvic disease)
No cause other than excessive PG production by the secretory endometrium; stimulate powerful uterine contractions, that cut off blood supply temporarily --> ischemic pain that activates ANS pain fibres, lower back and lower abdominal cramping.
tx: OCP (decrease PG in menstrual fluid, inhibit ovulation and prod of PGs). Or NSAIDS.
What is anovulatory dysfunctional uterine bleeding (DUB) and who does it affect predominantly, and what sort of bleeding do they get.
Anovulatory: affects girls at menarche, and peri-menopausal women. There is no ovulation, so no progesterone. The unopposed E stimulates endometrial hyperplasia, that then sloughs off incompletely and irregularly (necrosed piecemeal), leading to irregular, prolonged and sometimes profuse bleeding.
Probably due to subtle hormonal imbalances.
What is ovulatory dub?
This accounts for the majority of dub (80%). Thought to be a result of luteal phase abnormalities, with decreased vascular tone of the blood vessels supplying the endometrium, resulting in increased blood loss when the spiral arteries spasm in P withdrawal. Bleeding is heavy, but of normal duration and regularity eg occurs at menses only.
What treatments can be used to manage DUB?
Basically, want to decrease the PGs or introduce prostaglandins to balance the E dominance of anovulation...
- NSAIDS (decrease PG)
- Tranexamic acid; inhibits local fibrinolysis
- Oral progestagins: halt endometrial growth and allow organised sloughing with their withdrawal.
- MIRENA; localised P, min's systemic effects.
- comb OCP; thins endometrium and makes menses regular.
- Androgens: antagonise estrogen --> endometrial atrophy and decreases menstrual blood loss by half.
tranexamic acid?
1st line non-hormonal in tx of DUB and also excessive uterine fibroid bleeding. Is derivative of lysine, so binds the lysine site on plasminogen and inhibits activation --> dont get fibrinolysis of clots; decreases bleeding.
What is the view of the orthodox jews on menstruation..
Dirty. Cannot touch a woman when she is menstruating, or for 7 days after and having had a ritual bath of immersion. Sex and all acts of intimacy are a SIN for both. Must sleep separately, cannot eat at the same table. Jewish woman experiencing recurretn intermenstrual bleeding faces serious dilemma with relationship.
Prenatal quad screen... for down's syndrome... what is it looking for?
Increased Inhibin A
Increased bHCG
Decresed Estradiol
Decreased AFP
What changes are associated with menopause (hormonally)?
Increasing FSH and LH, as decreased E production by under-active follicles...
Shortening of the length of the menstrual cycle (shortened follicular phase)
Decreased inhibin secretion... (related to FSH)
Propensity for anovulatory cycles --> increased E, decreased P, endometrial hyperplasia.
What are the health risks of peri-menopause? (mainly related to unopposed estrogen)
- Vaginal atrophy; infections, UTis
- breast cancer
- endometrial hyperplasia
- osteoporosis
- hyperlipidemia/ CVD
- gallbladder disease
How does low estrogen affect the vagina?
Decreased stimulate of glycogen liberation - decreased source for lactobacillus to convert to acid- pH rises --> less resistant to infection.
What are some options for oestrogenic HRT?
Oestriol: reduced changes to endometrium and breast = +ve.
Oestradiol: favorable effects on lipids (LDL etc)
Vaginal cream, pessaries, tablets, subcut pellets, injections.

Estrogen only; must be post-hysterectomy with no hx of endometriosis.
E+P therapy for all other women.
What are the options for the HRT regimen?
Can be sequential eg E and P for 14 days of each month, or continuous.
COntinuous may stimulate endometrium less than sequential regimens - less likely to cause hyperplasia.
What are the side effects for oestrogen, and what for progesterone..
oestrogen: nausea, headache, leg cramps, breast pain.

progesterone: PMS, pelvic bloating, weight gein, lipid changes, depression.
What are the risks of HRT?
Breast cancer: can't e on it for >5yrs.
Endometrial cancer.
Venous thrombo-embolism
Gall bladder disease.
What systemic skin conditions can also involve the vulva?
Psoriasis
Eczema
Allergic dermatitis
What conditions predispose to non-specific vulvitis?
diabetes, blood dyscrasias, uremia, malnutrition and avitaminosis.
What is a Bartholin's cyst
Obstruction of the bartholin duct, usually by preceding infection. Results in fluid accumulation. Can lead to Bartholin abscess; surgical excission or permanent opening (marsupialisation).
Fairly common, occur in all age groups.
(Bartholin gland- vaginal lubrication x2, similar to bulbourethral in the male).
Lichen sclerosis
(Chronic atrophic vulvitis)
Autoimmune condition causing atrophy and dryness + fibrosis and scarring of the vagina; pale gray, parchment like skin, with atrophy of epidermis and replacement of underlying dermis by dense fibrous tissue.
Most common after menopause; insidious and progressive.
Whats the deal with vulval intraepithelial neoplasm?
Uncommon malignant neoplasm: majority are SCC, and occur in women >60.
Association with HPV 16 and 18. Present as white or pigmented plaques on the vulva.
Extra-mammary Pagets?
Red, crusty, map-like area on the vulva. Does not metastasise but invades locally so prone to recurrance. May be accompanied by a palpable submucosal thickening or tumor.
What is the vaginal cancer that affects children?
Embryonal rhabdomyosarcoma- malignant embryonal rhabdomyoblasts, growas a rounded bulky masses that can fill and protured out of the vagina as a 'grape like mass'. cause death by peritoneal invasion.
Vaginal intra-epithelial neoplasia...
Uncommon. SCC. HPV.
Irregular spotting or frank vaginal discharge = only sx.
May present as late disease with rectal or urinary fistulae.
Difference between hypospadias and epispadias... which is more common.
Hypospadius: 1 in 300 live births.
Urethral opening on ventral surface, cf epispadius- dorsal surface.
Phimosis
Unable to completely retract the prepuce (foreskin) --> accumulation of secretions --> infection/ carcinoma.
Balanoposthitis
Infection of the glans penis and prepuce- unhygienic males with foreskin.
Tumors of the penis
Rare.
Condyloma acuminatum (HSV 6 + 11)
CIS, Invasive C.
Undescended testes.
1% of live male births. Mostly unilateral, 25% bilateral. Usually felt in the inguinal canal, but can be anywhere.
Isolated anomaly.
Complications- sterility if bilateral, and greater risk of testicular cancer.
What are the causes of testicular atrophy
Old age - narrowed atherosclerotic blood supply
Radiation
End stage orchitis
Hypopituitarism, or prolonged anti-prostate cancer tx (anti-androgens)
Generalised cachexia/ malnutrition
What must come to mind when a man presents with sudden onset testicular pain
Testicular torsion. Typically seen in adolecscence, when a bilateral anatomic defect (Bell Clapper abnormality) resulst in increased mobility of the testis.
If manually untwisted within 6 hours --> preserved testis.
What are the main barriers to infection in the female genital tract
1. Lactobacillus --> converts glycogen to acid when stimulated by E; in reproductive age females, the ACIDIC environment is number one barrier.
2. Cervix acts as physical barrier
3. Normal flora; compete with microbes for space and nutrients.
4. Mucous; has lysosymes etc
5. Ciliated cells in the uterus, continually flush out mucous and bacteria.
What are the factors that allow a microbe to colonise the female genital tract?
Attachment factors eg pilli/ fimbri
Trauma eg coital damage, warts.
Loss of Estrogen and lactobacillus (young, old)
What are the defence factors of the male genital tract?
Length of the urethra
Bactericidal properties of semen
Major defence = CONTINUAL FLUSHING.
What lab tests must be done when someone presents with acute abdomen?
FBC: leukocytosis (inflammatory, infective).
bHCG- may have ectopic preg/ premature abortion.
U + E: if in shock, monitor fluid replacement.
Lipase: >1000 --> pancreatitis.
Inflammatory markers: CRP, ESR
Urine dipstick:
- haematuria --> stone, infection, tumor
- Glucose + ketone --> DKA
- Protein, bilriubin: renal or liver disease.
LFTs: hepatobiliary
Blood gases: looking for CO2 decrease, as resp compensation for metabolic acidosis: seen in sepsis and intestinal ischemia (prolonged hypoxia --> lactic acidosis).
Serum Ca2+ - hypercalcemia can cause abdo pain (groans, stones, moans)
What would some signs on X-ray be that might indicate laparoscopy?
Fluid levels eg obstruction and dilation (with extra fluid production)
Contrast leak eg rupture
Gas in the peritoneum (pneumoperitoneum)
What physical signs might indicate urgent laparoscopy?
Worsening rigidity/ guarding
Progressive distension
Rectal bleeding
Severe localised tenderness (peritoneal involvement)
What is the blood supply of the penis?
Dorsal arteries: centrally placed, run in the interval/septa between the paired corpora cavernosa, on either side of the deep dorsal vein (drains all blood from the venous plexus). Supplies the fibrous tissue and the skin of the penis.
Deep arterie: pierce the crura and travel within the corpora cavernosa, supply the erectile tissue.
Artery of the bulb of the penis- posterior spongiosum + bulbourethral glands.
Where does llymph from the penis drain?
Mostly to the superficial inguinal lymph nodes.
What are some causes of male genital lesions, and say whether they're tender or non tender.
Ulcerative:
- HSV; blisters --> ulcer (tender)
- Syphilis- non-tender
- Chancroid (H.du-cry-u) - tender
- Malig eg SCC (non-tender)

Non-ulcerative:
- Warts
- Primary disease eg Psoriasis
- Balanitis eg due to Reiters, poor hygiene
Which bacteria are responsible for epididymitis?
Young man: chlamy and neisseria.
Older man: E.coli and pseudomonas.

= acute non-specific inflammation --> congestion, oedema, infiltration, macrophages.
What is granulomatous orchitis?
Rare cuase of unilateral testicular enlargement in middle aged men.
Distinguished from granuloma's in the spermatic tubules, and intertubular CT. Suspected auto-immune etiology.
What are the preferential sites of infection for Syphilis, Gonorrhea and Tubercuous, and what sort of infections do they produce.
Mumps?
Syphilis- affects testes first; produces gummas, or diffuse interstitial inflammation. Get obliterative endarteritis.
Gonorrhea- epididymitis; similar to non-specific infection. Reach epididymis by post urethra -> prostate -> seminal vesicles.
Tuberculosis: epididymis, spreads to testis. Caseating granulomatous inflammation.
Mumps- school age children, orchitis 1 week after parotid gland enlargement.
By age, decide what testicular tumor a patient is most likely to be affected by.
-infant- yolk sac tumor/ endodermal sinus tumor(most common in infants); Increased AFP. Malignant but good px .
20-30yo: Embryonal carcinoma; aggressive, smaller than seminoma, may contain foci of h+n. Produce AFP and HCG.
30s-40s: SEMINOMA. Most common (50%), bulky mass that replaces the entire testis in ~half. Devoid of h+n, may produce HCG (15%).
>65: Spermatocytic seminoma (uncommon- 1%). Slow growing, large, pale, gray.
Teratoma's: always benign?
More likely to be benign pre-pubertally. Generally malignant post-puberty.
Choriocarcinoma- only related to placenta?
no, in rare cases it can occur in the testis. It is a very aggressive tumor, with early metastasis to blood and lymph, and has poor response to chemo.
What is the clinical difference between seminoma's, and non seminomatous germinal cell tumors...
Seminoma's: localised to testes for a long time, local LN spread common.
NSGCTs: 60% of patients present with advanced disease.
Still typically present as PAINLESS ENLARGEMENT OF THE TESTES.
Describe the anatomy of the prostate
20g tubuloalveolar gland. Divided into 4 functional and anatomical zones: peripheral (ca), central, transitional (BPH), anterior fibromuscular stroma.

Tubuloalveolar- glands lined by 2 layers of cells; basal layer of low cuboidal epithelium, overlyed by layer of columnar secretory cells.
How does acute bacterial prostatitis occur, and how does it present?
Intra-prostatic refluex of urine, with infection by bacteria that normally cause UTIs: E.Coli, gram -ve rods, enterococci.
Sometimes follows catheterization, TURP or cytoscopy.
Presetn with dysuria + fever + chills.
Prostate is tender and boggy- a soft spongy enlarged gland (oedema, congestion, necrosis, abscess, suppuration).
What facilitates chronic bacterial prostatitis?
CBP; common in setting of recurrent UTI's cuased by the same organism, and difficult to treat due to poor prostate penetration by abx.
n.b chronic ABacterial prostatis actually most common- no hx of UTIs.
Prostate cancer
Adenocarcinoma, arising from the submucosal or main glands. 70% arise in peripheral zone, so no symptoms of early disease - 50% present with advanced disease (urinary obstruction, local or bone pain).
Gritty and firm when felt on DRE; metastasis by direct invasion eg to bladder, seminal vesicles, lymphatic spread to para-aortics, and haematogenous to bones.

histo: small and tightly spaced glands, lined by a single layer of low/ cuboidal ells. Nuclear atypia.
What are the four main stages/ requirements of male sexual function
Libido
Ability to achieve and maintain erection
Ejaculation
Detumescance (returns to flaccid state).
What are the four stages of the sexual response cycle
1. Excitement; heightened sexual awareness
2. Plateau phase; intensification, body responses.
3. Orgasmic phase: ejaculation, peak of sexual excitement.
4. Resolution: returns genitalia and body systems to pre-arousal state.
Components of sexual arousal and neural input onto erection?
Tactile stimulation - receptors in the penile skin and glans, converge to form dorsal nerve of penis --> S2-4 pudendal nerve DRG. Psychogenic stimuli is integrated into the limbic system.

Neural input: erection generating centre in the sacral segments of the spinal cord; tactile stimuli trigger increase SNS output --> vasodilation of penile arterioles.
Release of NO and vasoactive PG --> SMC relaxation.
(NO - activates guanylate cyclase -> GTP -> cGMP -> SMC relaxation.
Erection: mechanism (blood flow)
Relaxation of arteries and corpora smooth muscle results in increased blood flow into the lacunar network; engorge somewhat, and compress the trabecular smooth muscle against the tunica albuginea; causes passive closure of emissary veins --> increased inflow and decreased outflow - corpora become non-compressible cylinders from which blood does not escape.
PSNS- also promotes secretion of lubricating mucous from bulbouretrhal glands.
Point- Shoot- Score
Explain.
(Erection- Emission- Expulsion)
Point = erection: parasympathetic fibres (pelvic splanchnics) mediating the increased blood flow/ decreased outflow/ penile engorgement.

Shoot- sympathetic (T11-L2) = Emission (delivery of semen into posterior urethra); contraction of epididymis, ductus def, seminal vesicles and prostate; (internal vesical sphinctre tightly closed to prevent bladder backflow of semen).

Score: expulsion (S-NS- somatic impulses via pudendal nerve) --> rhythmic contraction of bulbospongiosis and ischiocavernous muscles --> forcible expulsion of semen through urethra.
Erectile dysfunction DSM IV criteria
1) persistent or recurrent inability to attain or maintain an adequate erection until completeion of sexual activity
2) disturbance causes considerable distress or interpersonal difficulties
3) Not explained by anyt other axis 1 disorder (eg libido, ejaculation, anorgasmia)
What are the three basic mechanisms of erectile dysfunction
1. Failure to intitiate (psychogenic, endocrine, neural)
2. Failure to fill (arteriogenic)
3. Failure to sustain volume (veno-occlusive dysfunction).

Multiple factors, and psychogenic factors frequently coexist.
Describe the most common causes of vasculogenic erectile dysfunction.
1. atherosclerosis; narrowed penile arteries - decreasd flwo, decreased rigidity.
2. Venous leaks: inadequate impedence of venous outflow.
3. Weakening of fibroelastic sheath of corpora; age associated, loss of complicanece, ineffective compression of tunical veins.
Treatment options for erectile dysfunction
Sildenafil (Viagra), taladafil, vardenafil: PDE5 inhibtiors, prolong activity of cGMP --> prolonged SMC relaxation and erection. 75% response rate, but ci'd in heart failure, cardiomyopathy or anti-anginal medications (hypotension).SEs: headache, flushing.

Androgen therapy: for prim/ second hypogonadism. ci'd in men with hormone sensitive ca eg prostate (measure PSA before and during).

Alprostadil (PGE); relaxes SMCs, can be given as indwelling semi-solid pellet (65% response rate), or intracavernosal injection (80% response, but invasive).

Cockring- block venous outflow.
Surgery- insertion of semi-rigid, inflatable penile prosthesis.
Requirements of female sexual response?
Oestrogens and androgens- work synergistically to enhance arousal.
Sensation must be intact (eg periph neuropath/ diabetes - problems)
SNS outflow tract must be intact (desire + orgasm) - (spinal cord injuries..)
Still requires vascular sufficiency (vaginal lubrication is a transudate of serum resulting from increased pelvic blood flow associated with arousal).
Peripheral PSNS activtiy - clitoral engorgement and vaginal secretion.
Pharmacological agents for female sexual dysfunction?
- sildenafil- no proven effect
- estrogen replacement- good for post-meno women; treats vaginal atrophy, increases lubrication and clit sensitivity.
- Clitoral vacuum device; increase cavernosal blood flow, engorgement, vaginal lubrication.
How does PCOS cause chronic anovulatory cycles?
Disturbance in androgens and oestrogen (mildly elevated) causes premature follicle atresia and persistant anovulation, instead forming large cystic spaces in the ovary.
This is classed as anovulation with estrogen present; thus endometrial growth occurs, and giving P and then withdrawing it will cause withdrawal bleeding.
Teratoma- where?
Typically ovaries, but can be anywhere in the midline.
Most common phenotype is cystic, with hair in it.
tx: puncture, drain, scrape.
What are some causes of anovulatory cycles with oestrogen absent...
1. Hypogonadotropic hypogonadism. Can be a result of pituitary or CNS disease... but usually, = excessive stress, exercise, dieting.
Other chronic debilitating diseases can disrupt the hypothalamix axis:
- end stage renal failure
- cancer
- IBD

Or/ lesions in the pituitary that interfere with gonadotrope secretion, or a prolactinoma that suppresses GnRH.
Ovulatory cycles: have deviations from this pattern that are predctable and regular, usually due to organic disease of the outtract. List 3.
1. regular but heavy nad prolonged bleeding... adenomyosis, subcut leiomyoma's, endometrial polyps (hormonally regulated..)
2. Regular menses but only spotting/ light bleeding (obstruction of outflow) --> intrauterine synechiae/ scarring of the cervix (Asherman's).
3. Intermenstrual bleeding --> cervical or endometrial polyps/ lesions.
What causes dysmennorhea?
Excessive production of PGE2 --> uterine contractions, that cut off blood supply --> ischemic activation of the ANS pain fibres. Give OCP to reduce menstrual PG production, or NSAIDs to limit production.
Metrorrhagia
Intermenstrual bleeding.
Menorrhagia
Prolonged or heavy cyclic menstruation (>8days) that interferes with daily living.
Abnormal uterine bleeding; who gets it? why?
10-30% of reproductive age women experience abnormaly uterine bleeding, with half of them being peri-menopausal.
Three quarters of these will have a primary functional abnormality of the HPO axis eg Dysfunctional Uterine Bleeding.

DUB: abnormally heavy or prolonged bleeding of uterine origin that is not due to pregnancy or recgonizable pelvic disease -->
Is ovulatory or anovulatory DUB more common?
Ovulatory: 80% .
Thought to be a distrrbance of luteal phase hormones/ abnormalities, that results in decreased vascular tone of the endometrial vessels, that results in increased rates of blood loss from vasodilation.
bleeding is heavy but regular.

cf. anovulatory: no ovultion = no progesterone --> unopposed E - endometrial proliferation/ hyperplasia --> sloughs incompletely and irregularly; bleeding becomes irregular, prolonged and sometimes profuse.
Most common at menarche and then again at peri-menopause.
What is the medical management options for DUB?
1. NSAIDS; suspected role of PG in DUB
2. Tranexamic acid; anti-fibrinolyitic, less clot dissolution --> less bleeding.
3. Oral progestins- halt endometrial growth and facilitate regular and organised sloughing; but get breast swelling, bloating, weight gain, acne.
4. Levornegestral-IUD (mirena); local Progesterone deliv means less systemic se's.
5. Combination OCP: thinner endometrium and regular menstrual bleeding.
6. Androgens: hypoestrogenic effect, induces endometrial artophy and halves menstrual output. But androgenic se's: wt gain, oily skin, acne.
What are the five changes to hormones during peri-menopausal period?
1. Shortening of length of cycle
2. rising fsh and lh
3. decreased inhibin
4. INcreased propensity for anovulation - increased E, decreased P
What are some health risks of perimenopause?
Think: estrogen up and down...
- vaginal atrophy --> uti's
- breast cancer
- osteoporosis
- gb disease
- cvd risk
- endometrial hyperplasia
Female presents with acute abdomen, tachycardia, low BP,pale .... last menstrual period was 6 weeks ago. Ddx?
- Ectopic pregnancy
- Tubal pregnancy with rupture --> haemosalpinx
-