Male Reproductive System Flashcards
cryptorchidism
undescended testes
cryptorchidism management
testicular US
referral to pediatric urologist for patient under 6 months old
diagnostic laproscopy
Hormonal therapy not effective
phimosis
foreskin cannot be retracted over
(normal in children 1-3 years old)
paraphimosis
retracted but cannot be forwarded
paraphimosis management
medical emergency
manual or surgical retraction to prevent necrosis
hypospadias
abnormal ventral placement of the urethral opening
hypospadias management
urgent surgical referral for repair
Peyronie Disease
Inelastic scar, or plaque, that shortens the tunica albuginea of the corpora cavernosa results in a curve of the penile shaft in erection
Peyronie Disease Pathophysiology
Trauma/flexion of the tunica albuginea results in tears [bleed and clots], subsequent fibrin deposition and perivascular inflammation and finally plaque like scarring
Peyronie Disease most common in _____ (age) due to ____
Most common in males 40 and 65 years of age, with loss of penile collagen
Peyronie Disease Management
referral to urology
Collagenase clostridium histolyticum (CCH) & steroid injections are probably most effective during the initial formation of Peyronie’s plaque, but success is limited with mature plaques.
Most common placing a suture on the opposite side of the graft to adjust curve OR
Nesbit procedure, involves excision of the plaque accompanied by “patch grafting”
Balanitis pathophysiology
Accumulation of glandular secretions (smegma), epithelial cells or mycobacterium smegmatis, candidiasis
diagnosis of balanitis
Subpreputial swab for C&S
Balanitis Management
hygiene
treat underlying cause:
Dermatitis—prescribe hydrocortisone 1% for up to 14 days.
Candidal balanitis—an anti-fungal “azole” cream until symptoms disappear or for up to 14 days. If there is uncomfortable inflammation, consider adding in hydrocortisone 1% cream for up to 14 days.
Bacterial balanitis—prescribe oral cloxacillin/cephalexin (clarithromycin if allergic) for 7 days.
If there is uncomfortable inflammation, consider adding in hydrocortisone 1% cream for up to 14 days.
Urethritis causes (2 types)
Neisseria gonorrhoeae develops 2 to 6 days after acquisition
Non-gonococcal urethritis (NGU) develop 1 to 5 weeks after acquisition
Treatment of urethritis
Gonococcal urethritis
Ceftriaxone 250 mg IM – single dose
PLUS EITHER
Doxycycline 100 mg PO bid for 7 days
OR Azithromycin 1 g PO in a single dose preferred compliance.
Non-gonococcal urethritis
Doxycycline 100 mg PO bid for 7 days
OR Azithromycin 1 g PO in a single dose preferred compliance
Epididymitis causes
Infectious
Rare causes: sterile acute
Behçet disease and Henoch Schönlein
Epididymitis Management
For epididymitis most likely caused by: STI chlamydial or gonococcal infections:
Ceftriaxone 250 mg IM in a single dose*
PLUS Doxycycline 100 mg PO bid for 10–14 days
OR Ciprofloxacin 500 mg PO in a single dose (ONLY with known sensitivity + ability to do test of cure)
OR Azithromycin 1 g PO – in Ontario due to resistance to Ciprofloxacin/quinolones
For epididymitis most likely caused by enteric organisms [e-coli and other gram negative bacilli]:
Ciprofloxacin 500 mg BID or 1 g (extended release daily) x 10 days
OR Levofloxacin 500 mg once daily x 10 days
Prostatitis pathophysiology
Prostatitis is generally NOT considered a sexually transmitted infection (STI)
Pathology of prostatitis is thought to be an alteration in the mechanical defenses of the urogential tracts: structural malformations, instrumentation of the tract can impact this.
Benign Prostatic Hyperplasia
BPH is a non-malignant prostate enlargement caused by excessive growth of epithelia (glandular) cells and smooth muscle cells. Overgrowth = obstruction of the urethra [aka s/s of BPH]
Function of prostate is
to produce fluids that contribute to ejaculation volume
BPH Management 2 major classes
1st line therapy:
5-α-reductase inhibitors
α1-adrenergic antagonists
5-α-reductase inhibitors
MOA
Dutasteride (Avodart), Finasteride (Proscar)
1st line for large prostates with mechanical obstruction
MOA = Reduce dihydrotestosterone production, which causes the prostate to shrink, which reduces mechanical obstruction of the urethra. May also delay BPH progression.
Benefits take months to develop.
α1-adrenergic antagonists selective
Silodosin [Rapaflo],
Tamsulosin [Flomax
α1-adrenergic antagonists nonselective
Alfuzosin, Terazosin
α1-adrenergic antagonists
MOA
1st line for smaller prostates with more dynamic obstruction s/s
MOA = Blockade of α1a receptors relaxes smooth muscle in the bladder neck, prostate capsule, and prostatic urethra, and thereby decreases dynamic obstruction of the urethra.
Benefits develop rapidly.
____ (Rx) can be used for both ED and BPH due to MOA = smooth muscle relaxation in bladder, prostate and urethra supports both conditions [see ED]
phospodiesterasie-5 inhibitor [PDE5 inhibitors]
s/e of α1-adrenergic antagonists
Hypotension, fainting, dizziness, somnolence, and nasal congestion (from blocking α1 receptors on blood vessels)
s/e of 5-α-reductase inhibitors
Decreased ejaculate volume and libido
Erectile Dysfunction pathophysiology
Sexual arousal [increased parasympathetic nerve impulse to the penis releasing local nitric oxide].
NO then activates guanylyl cyclase, enzyme that makes cyclic guanosine monophosphate (cGMP).
cGMP = arterial dilation and trabecular smooth muscle relaxation
Increase blood flow/pressure and trabecular relaxation = engorgement of sinusoidal spaces in the corpus cavernosum
This cases venous occlusion/reduced venous outflow = erection
Erection stops when cGMP is inhibited by Phosphodiesterase type 5 (PDE-5)
Relaxation of arterial and trabecular smooth muscle [pre-erection/flaccid states]
1st line therapy for Erectile Dysfunction
PDE-5 inhibitors
2nd line therapy for ED
Prostaglandin E1 Analogues &Vacuum erection devices [VED] [need referral to Urology]
Contraindications of PDE-5 Inhibitors
concurrent use of nitrates,
symptomatic hypotension
previous priapism
Scrotal/Testicular Masses and Swelling
(painful)
Epididymitis
Testicular Torsion (medical emergency)
Orchitis
Scrotal/Testicular Masses and Swelling
(non- painful)
Varicocele
Hydrocele
Spermatocele
Testicular cancer
RED FLAGS: TWIST SCORE
Testicular Workup for Ischemia and Suspected Torsion.
Hard testicle
Swelling
Nausea/vomiting
No scrotal reflex or Cremasteric reflex
High riding testicles
Prehn sign
Painful, usually unilateral, not relieved by scrotal support
orchitis
Acute inflammation of the testicles/scrotal sack often due to infection of the epididymis (see previous slides) or a systemic illness such as mumps & COVID 19
Varicocele
Dilation of a vein within the spermatic cord 90% on LEFT side
Red Flags: Varicocele
Older men is a late sign of a renal tumor
Hydrocele
Fluid in the tunica vaginalis and most common cause of scrotal swelling
Hydrocele diagnostic testing
transillumination and ultrasound
Hydrocele Treatment
Always a referral to urology,
self-limiting,
treat underlying cause,
may aspirate for comfort depending on size and not associated with infertility
Spermatocele
Diverticulum of the epididymis
Not associated with infertility
Testicular Cancer
Clinical Manifestations
Mass on right>left side with 1-2% being bilateral
Painless testicular enlargement or heaviness in scrotum, dull ache in abdomen
Hydrocele
Gynecomastia
Metastasis: cough, back pain, SOB, bloody sputum, supraclavicular nodes, dysphagia, CNS symptoms
Prostate Cancer
Red flag:
UTI or previous prostatitis without resolution/recurrence
Prostate Cancer Screening & Diagnosis
Initial screening should include DRE
Offer PSA screening to men with life expectancy > 10 years, starting at age 50 (45 if increased risk)
Penile Cancer Cause
mostly squamous cell carcinoma (glans or foreskin) the more lesions, the worse the prognosis
Penile Cancer Risk Factors
HPV, smoking, psoriasis tx with psoralen and UV light, uncircumcised, hx of phimosis and AIDS
PDE5-inhibitor pharmacology
Absorption is inhibited for sildenafil with high-fat meals
CYP3A4 inhibitors can significantly decrease metabolism of the PDE5 inhibitor. [e.g. Grapefruit juice avoided/elevate levels]
CYP3A4 inducers may decrease efficacy of the PDE5 inhibitor