Male Reproductive Flashcards
Testicular cancer risk factors
Family history
Caucasian
Cryptorchidism
HIV
Cryptorchidism
One or both testes fail to descend from the abdomen to the scrotum
If note corrected by 12 or never corrected 2-6x more likely to develop testicular cancer
Seminomas (germ cell tumor—testicular cancer)
Arise from immature germ cells
Slow-growing
Non-aggressive
Easily cured with radiation
Nonseminomas (germ cell tumor—testicular cancer)
Arise from mature germ cells
More aggressive
Usually treated with surgery
Testicular cancer early symptoms
Enlargement of testicle
Painless mass
If discomfort present: ache in groin, scrotal heaviness
High survival rate if detected early
Testicular cancer late symptoms
Frank pain with rapid growth
Hemorrhage
Symptoms based on metastasis: cough, hemoptysis, leg swelling, back pain, dizziness
Treated with chemo
Prostate
Gland surround the urethra
Produces seminal fluids that contribute to ejaculate volume
4-20 g
BPH
Prostate can be 50-80g
Nonmalignant enlargement of prostate
Overgrowth of epithelial, smooth muscle, or stromal cells
Prostate—overgrowth of epithelial cells
Causes MECHANICAL obstruction of urethra
Treat with finasteride, dutasteride
Prostate—overgrowth of smooth muscle cells
Causes DYNAMIC obstruction of urethra
Treat with tamsulosin
BPH risk factors
Age
Family history
Race/ethnicity (highest in African Americans; lowest in Japanese)
BPH etiology theories
Hormone imbalance
DHT accumulation
BPH theory—hormone imbalance
Testosterone decreases with age but estrogen levels don’t creating a hormonal imbalance
BPH theory—DHT accumulation
5-alpha-reductase converts testosterone to DHT
High levels of DHT accumulate growth factors which cause acne, hair on chest (not scalp), growth of prostate cells
BPH symptoms
Urinary frequency Urinary urgency Delay in initiation Reduction in form—weak urine stream Increased urination time Dribbling Inability to completely empty bladder UTI
BPH complications
Obstructive nephropathy
Bladder stones
UTI
Kidney issues
BPH treatment by stage
Mild: watchful waiting
Moderate: pharm
Severe: surgery, microwave options
finasteride
5-alpha-reductase inhibitor
finasteride indication
Mechanical obstruction of urethra—increased epithelial cells in prostate
finasteride MOA
Inhibits 5-alpha-reductive from converting testosterone to DHT
By blocking conversion of testosterone to DHT finasteride decreases epithelial tissue in the prostate which prevents mechanical obstruction
DHT
More potent form of testosterone
Principal hormone responsible for stimulating prostate growth
Prostate size and finasteride
finasteride works best in very enlarged prostates with much epithelial tissue; will not work well with smaller prostates
Overall blood testosterone and finasteride
finasteride reduces DHT in blood but does NOT decrease overall circulating testosterone
When will patients see results with finasteride?
6-12 months
finasteride SE
Impotence
Decreased libido
Gynecomastia
Increased hair growth
PSA and finasteride
finasteride decreases PSA levels
Must measure PSA levels prior to/6months after starting
If PSA not decreasing may need evaluation for prostate cancer
finasteride miscellaneous
Used to treat male-pattern baldness
Teratogenic—pregnant woman should not handle
Men on finasteride cannot donate blood
dutasteride
5-alpha reductase inhibitor
dutasteride indication
Mechanical obstruction of urethra (like finasteride)
dutasteride MOA
Blocks conversion of testosterone to DHT, thereby decreasing epithelial tissue in prostate
dutasteride SE
Impotence
Decreased libido
Increased hair growth
Gynecomastia
tamsulosin class
Alpha-1-adrenergic antagonist
tamsulosin MOA
Rapidly relaxes smooth muscle cells in the bladder, prostate, and urethra
Selective for alpha receptors in the prostate (no systemic effect)
tamsulosin indication
Dynamic obstruction of urethra (smooth muscle overgrowth)
tamsulosin and PSA
tamsulosin does NOT reduce PSA levels
When will patient see results with tamsulosin?
Immediately
BPH combination therapy
Jalyn (dutasteride + tamsulosin)
Prostate cancer
Most common male cancer in US
Prostate cancer risk factors
Age >50 Family history High fat diet Altering sex hormone production Race (greatest in Blacks, lowest in Asians/Natives)
Prostate cancer early symptoms
Asymptomatic
Prostate cancer late symptoms
BPH type presentation
Metastasis (bone pain if metastasis to bone; cough/hemoptysis if metastasis to lungs)
Prostate cancer treatment
No medications
Surgery, chemo, or radiation
PSA vs. DRE
PSA can detect cancer 5-15 years before DRE
If high risk for prostate cancer may need PSA but if low risk DRE will suffice
Erectile dysfunction
Impotence
Primary ED
Rare
Life-long inability to have an erection due to psychiatric issues, early vascular trauma
Secondary ED
Most common
ED in someone with a history of normal erections
Organic causes of secondary ED
PVD (arterial insufficiency, excessive venous drainage, sedentary lifestyle)
Medications (antidepressants, BP meds)
Endocrine issues
Trauma, surgery (radical prostastectomy )
Psychogenic causes of secondary ED
Depression
Low desire
Performance anxiety
Strained relationship
Erection physiology
Sexual arousal-increased PNS/increased NO release-cGMP activation-arterial/smooth muscle relaxation-increased inflow/reduced outflow-erection
PDE-5
Removes cGMP needed for erection
sildenafil class
PDE-5 inhibitor
sildenafil MOA
Inhibits PDE-5 which increases/preserves cGMP
Only enhances the normal response to sexual stimuli
Does not cause erection immediately
no effect on erection quality/men w/o ED
sildenafil indications
ED
Pulmonary/arterial HTN
BPH
sildenafil timing
Can take up to 4 hours before sexual activity
Onset 30-60 min
sildenafil SE
Headache
Flushing
Dyspepsia
Hypotension
sildenafil and safety
Contraindicated if history of CVD
Don’t take with nitrates due to significant hypotension
Call 911 if chest pain/MI symptoms during sex
Sudden loss of vision/hearing
Don’t take more than once a day
Priapism is a medical emergency
Priapism
Painful erection
Erection > 4hr
Medical emergency
