42. Problems of the Male Reproductive System Flashcards
Label A-F.
a) bladder
b) prostate (middle lobe)
c) prostate (isthmus)(anterior lobe)
d) EUS
e) seminal gland
f) prostate (inferoposterior lobe)
Label A-F.
a) bladder
b) peritoneum
c) levator ani
d) membranous urethra
e) prostatic urethra
f) obturator internus
Describe the structure and function of the prostate.
Describe the 3 glandular regions of the prostate and indicate where BPH and prostatic cancers are most likely to occur.
Sits under bladder. 20g and continues to grow throughout life. Base closely related to neck of bladder, apex in contact with the fascia on superior aspect of urethral sphincter. Muscular anterior surface, comprised of lobes: median, anterior, posterior and lateral. Bladderpasses down through prostate. Function: secretes alkaline liquid that helps neutralise acidic environment in the vagina and also has anticoagulant properties to stop seminal fluid from getting too thick so sperm can’t swim.
Peripheral zone: 70%, surrounds urethra, outer ring of tissue, more distal. Origin of 70-80% of prostatic cancers.
Central zone: 25%, surrounds ejaculatory ducts.
Transition zone: 5%, surrounds proximal urethra, under prostate, site of benign prostatic hyperplasia or hypertrophy (b/c its SM helping to propel seminal fluid and get hyperplasia of epithelial cells). And 10-20% of prostate cancers.
What cells does BPH affect, and in what zone?
What should you feel in a digital rectal exam if the prostate is normal, BPH or cancer?
What is the aetiology of BPH?
Epithelial and stromal cells mainly in transitional zone.
Normal: smooth, rouded, 1 index finger should fit across/walnut. BPH: smooth but significantly bigger. Cancer: adenocarcinoma in glandular tissue of peripheral zone - feels nodular and hard.
Age-related enlargement caused by increased cell proliferation and decreased apoptosis. Linked to testicular androgens: testosterone exposure (more exposure = more enlargement). Normally increases in size through life unless castrated before puberty. Other factors: oestrogen (testosterone can be converted to oestradiol - stimulate growth?), prostatic stromal and epithelial tissue interactions, NTs from gland.
Urethra narrowed -> blocks outflow of urine from bladder.
Decsribe on a cellular level how BPH occurs.
In stoma cell testosterone mainly converted to oestradiol -> binds to oestrogen receptor -> stromal cell proliferation. Testerone can also bind directly to androgen receptor in luminal epithelium, or in the basal epithelium be converted to DHT and then bind to androgen receptor, which antagonises apoptosis. In contrast, oestrogen leads to apoptosis of epithelial cells (oestradiol causes apoptosis when it binds to ER-beta receptors). In BPH, due to testosterone exposure, get increased proliferation of stromal cells (fibroblasts and SM). B/c trying to push fluid from bladder through, get hypertrophy.
As men age, aromatase and 5-alpha reductase increase in activity and convert androgen hormones into estrogen and DHT, respectively, leading to a decrease in testosterone but raised levels of DHT and estrogen.
List some signs and symptoms of BPH.
How common is BPH?
How is BPH diagnosed?
SHITE (slow stream, hesitancy, intermittent flow, terminal dribbling, emptying incomplete), FUN (frequency, urgency, nocturia). Blood in urine/semen, pain/burning during urination. Can cause backflow and stagnation of ureters all the way back to kidney.
All men over 40: 50% develop histological hyperplasia, 50% of these will have LUTS, some will develop enlarged prostate and others BOO (bladder outlet obstruction).
History, digital rectal exam, ultrasound (+ biopsy, USS can check volume, width, height, length), blood test for PSA: increases with age but in BPH never more than 10ng/ml, but for cancer in glandular tissue massive increase to 300-400ng/ml. Normal 50-59 ys: 0-3ng/ml, >70yrs: 0-5ng/ml.
How is BPH treated with medications?
Wait and see b/c not everyone develops serious symptoms. 2 types of pharmacotherapy, can be combined:
α-1 adrenergic blockers: blocks sympathetic activation to SM, relaxes SM in bladder neck and prostate (stromal section of TZ where lots of SM has been proliferating) improving urine flow rate.
5-α-reductase inhibitors: 2 isoforms (Type 1 and 2 - T2 predominant prostatic reductase). Stops conversion of testosterone to DHT = slows action of testosterone on cells. T1 = ubiquitous), dutasteride, finasteride. Testosterone also linked to male pattern baldness so drugs help with hair regrowth.
How is BPH treated surgically?
What are some symptoms of prostate cancer?
TURP (transurethral resection of the prostate - remove central core) for failed voiding trials, recurrent gross hematuria, UTI, renal insufficiency 20 to obstruction. Open prostatectomy for v. large prostates >75g or concomitant bladder stone, inner core shelled out leaving PZ, but can damage nerves to penis. Laser ablation. Transurethral microwave. High energy ultrasound therapy.
Similar to BPH, PSA, if raised, tends to be much higher than in BPH. Growth of glandular part of prostate can press on urethra too - gives intermittant flow etc.
Distinguish between direct and indirect inguinal hernias.
What kind of inguinal hernias are men and women more likely to have?
Direct: 15%, old age, doesn’t enter deep inguinal ring or extend beyond the superficial inguinal ring, neck medial to inferior epigastric artery. deep inguinal ring test -ve. Loops of intestine herniate out through abdominal body wall where there’s a weak spot.
Indirect: 85%, young, enters deep inguinal ring and reaches scrotum (labium majus), neck lateral to inferior epigastric artery, deep inguinal ring test +ve. Loop of intestine able to pass through inguinal ring into scrotum, follows same path as testes.
Women: hernia coming under inguinal ligament; men: above inguinal ligament. ~25% men will have inguinal hernias in life, 2% of females.
Label A-G. What is the yellow triangle and how is it related to hernias?
a) inferior epigastric artery
b) deep inguinal ring
c) rectus abdominus muscle
d) superficial inguinal ring
e) inguinal ligament
f) exernal iliac vessels
g) ductus deferens
Traingle: Hesselbach’s triangle - direct inguinal hernias leave abdomen through this triangle. (Hernia medial to epigastric vessels).
What is this condition and how is it treated?
Direct inguinal hernial. Tx: truss if reducable (can push hernia back with finger), otherwise surgery.
57-year-old man with intraoperative laparoscopic view of hernia - is it direct or indirect?
- Open arrows = inferior epigastric artery*
- Solid arrows = inguinal ligament*
- D = hernia defect*
- Curved arrow = deep inguinal ring*
- Arrow heads = medial boundary*
Direct - medial to epigastric vessels.
What is this conditon? What causes it?
Indirect inguinal hernia. Failure of inguinal canal to close properly after passage of testes in utero. 60% to R b/c R testes takes longer to get into scrotum. Loops of intestine can go through processus vaginalis if not closed, go through deep and inguinal ring. Always need surgery, done laproscopically.
What is erectile dysfunction and the main causes?
How many arteries are in corpus cavernosum?
Describe how the penile vascular anatomy behaves when the penis goes from flaccid to erect.
Spectum: complete inability to have an erection, inconsistent ability to achieve erection, ability to have short-term erections. Increases with age, affects 1/10 men. Most due to vascular disease or diabetes mellitus.
2 - one in R and one in L.
Flaccid: blood into corpus cavernosal arteries. SM in walls of BV. Erection: Inflow increaesed b/c SM relaxes and increases lacuna space and compresses and stretches the veins (subtunicular venular plexus) so blood can’t get out. Penile BP increases and can go above systolic which blocks arteries in penis and keeps blood in corpus cavernosum.
Describe the nervous/molecular pathway causing erection.
What happens to cGMP?
What are some treatments for erectile dysfunction?
Non-adrenergic non-cholinergic parasympathetic nerve from sacral outflow carries AP -> releases NO which diffuses across synapse and into SM in wall of artery -> attaches to souble Guanylyl Cyclase (2nd messenger) which is activated to produce cGMP -> causese relaxation of SM -> erection.
Noradrenaline works on same receptors in SM of urethra but from sympathetic neuron and result is contraction.
cGMP: broken down by phosphodiesterase type 5 enzyme to GMP.
Sildenafil (viagra) a PDE-5 inhibitor which keeps SM BV relaxed in penis to enhance blood flow. Also vardenafil (levitra) and tadalafil (cialis). Need to be sexually stimulated.
When is a penile prosthesis needed?
What is Peyronie’s disease? How is it treated?
What is a variocele, what side is it usually on and why?
Nerve and spinal cord injuries - replace corpus cavernosum with 2 rods, bladder fluid filled and a pump to pump fluid into tubes and mimic erection.
Bent penis - scar tissue forms in shaft, causes bending/deformity, painful erections and difficulties with sexual intercourse. Tx: non surgical = stretching exercises, para-aminobenzoate, topical verapamil, surgical = remove scar tissue. [Pic].
Varicose veins of the scrotum (pampiniform venous plexus). V common 10-15%, always in L testis, usually harmless but can cause infertility in 35-40%, 2o rise in temperature. R vein drains to inferior vena cava and L drains to renal vein at a right angle -> increase in hydrostatic pressure of the L spermatic vein which is transferred to venous plexus of spermatic tone, causing its dilation.
What condition is this?
Variocele.
