men's reproductive Flashcards

(37 cards)

1
Q

risk factors of testicular cancer

A

Family history
Caucasian
Cryptorchidism
HIV infection

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2
Q

Germ Cell Tumors: Seminomas

A

Arise from immature germ cells
Slow growing, nonaggressive
Easily cured with radiation

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3
Q

Germ Cell Tumors: Nonseminomas

A

Arise from mature germ cells
More aggressive
Usually treated with surgery

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4
Q

Early CM of testicular cancer

A

Enlargement of testicle
Painless mass noted
If discomfort present: Ache in groin, Sensation of heaviness

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5
Q

Late CM of testicular cancer

A

Possible frank pain
Manifestations based on metastatic spread: Cough, Hemoptysis, Swelling of lower extremities, Back pain, Dizziness

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6
Q

BPH: Definition & Risk Factors

A

Nonmalignant enlargement of prostate: ↑ epithelial cells, ↑ smooth muscle cells, Stromal cells.

RF: Age, Family history, Race/Ethnicity
LUTS: Lower urinary tract symptoms

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7
Q

BPH Etiology

A
  1. Hormone Imbalance: Testosterone and estrogen (estradiol)
  2. DHT Accumulation
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8
Q

What is DHT

A

Testosterone + 5 alpha-reductase = DHT

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9
Q

Why is DHT important in development of BPH?

A

Acts on skin: acne
Acts on hair follicles: hair on chest BUT off scalp
Stimulates growth of prostate cells

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10
Q

BPH: Clinical Manifestations

A

Frequency and urgency
Delay in initiation
Reduction in force
Increased urination time
Dribbling

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11
Q

BPH: Complications

A

Obstruction
UTI
Renal problems

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12
Q

treatment of BPH

A

Mild symptoms = watchful waiting
Moderate symptoms = drug therapy: 5-alpha reductase inhibitors, Alpha1-adrenergic antagonists
Severe symptoms = invasive options

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13
Q

Finasteride

A

class: 5-alpha-reductase inhibitors
Indication: Mechanical obstruction of urethra
MOA: Blocks conversion of testosterone to DHT; Decreases epithelial tissue in prostate
SE: Impotence, Decreased libido (5-10%), Gynecomastia
Side note: Decreases prostate specific antigen (PSA) levels, Used for male-pattern baldness.
Caution in Handling

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14
Q

Will finasteride work in someone with a smaller prostate?

A

not really, works best on very enlarged prostates

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15
Q

When will the patient see results for finasteride?

A

6-12 months & have to take this for the rest of their lives.

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16
Q

Dutasteride

A

class: 5-alpha-reductase inhibitors
Indication: Mechanical obstruction of urethra
MOA:Blocks conversion of testosterone to DHT; Decreases epithelial tissue in prostate
Adverse Effects: Similar to finasteride

17
Q

Tamsulosin

A

class: Alpha1-Adrenergic Antagonists
MOA: Relaxes smooth muscle cells, Selective for alpha receptors in the prostate
Indication: Dynamic obstruction of urethra
Adverse effects: Well tolerated
Abnormal ejaculation

18
Q

When will the patient see the results of tamsulosin?

A

works quickly and is taken for life.

19
Q

which race has the highest and lowest rate of prostate cancer?

A

African-American men = highest
Asians and Native American men = lowest

20
Q

what age do incidence increase rapidly for prostate cancer?

A

Incidence increases rapidly after 50.
> 80% of all cases in men > 65 yo.

21
Q

risk factors for prostate cancer

A

Age
Familial tendency
High fat diet

22
Q

CM for prostate cancer

A

Early: asymptomatic
Later: BPH type presentation, Metastasis: Bone, Lungs
Prognosis: Stage dependent, Early diagnosis

23
Q

what are the benefits of using PSA?

A

Small survival benefit with PSA screening in randomized trials.
Use of the PSA test was associated with a 50% drop in prostate cancer deaths in the U.S.

24
Q

what are the harms of using PSA?

A

Would take 48 diagnoses of prostate cancer to prevent 1 death.
Only 1 in 3 men with a positive PSA will have prostate cancer.
Many unnecessary biopsies.
Side effects of unnecessary treatment include erectile dysfunction, urinary incontinence, bowel problems.

25
prognosis of prostate cancer
Low, intermediate, and high-grade CA. Severity depends on a couple things: Gleason score (higher = worse), Tumor volume: PSA Level (higher and rapid rise = worse), Number of “cores” positive (more = worse)
26
definition of erectile dysfunction
Inability to achieve or sustain an erection sufficient for satisfactory sexual intercourse
27
another word of erectile dysfunction
impotence
28
primary ED (rare)
Life-long inability to have a normal erection d/t Severe psychiatric problems & Early vascular trauma
29
secondary ED (most common)
ED in someone with a history of normal erections
30
organic causes of Secondary ED
Peripheral vascular disease: Arterial insufficiency, Excessive venous drainage, Sedentary lifestyle (risk factor) Medications: Antidepressants, Antihypertensives Endocrine problems Trauma, Surgery (Radical prostatectomy)
31
psychogenic causes of Secondary ED
Depression Low desire Performance anxiety Strained relationship
32
Physiology of a Normal Erection
Sexual arousal increased PNS and nitric oxide release Activation of cGMP Relaxation of arteries and smooth muscles Increased inflow and reduced outflow Engorgement and erection
33
PNS =
parasympathetic nervous system
34
cGMP =
cyclic guanosine monophosphate
35
PDE-5 =
phosphodiesterase type 5
36
sildenafil
class: PDE-5 inhibitor MOA: Inhibits PDE5, Increases and preserves cGMP levels, Only enhances the normal response to sexual stimuli Indications: Relief of ED, Pulmonary arterial hypertension, BPH Timing of drug: up to 4hrs before sexual activity (onset 30-60 minutes) SE: HA, flushing, dyspepsia Caution: Preexisting CV disease, if on nitrate Rx, Hypotension If you have chest pain or other signs of a heart attack during sex, stop and call 911 Sudden loss of vision in one or both eyes, sudden loss of hearing. no more than once per day
37
priapism
erection is painful or lasts more than 4hrs- medical emergency