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NUR 326 > men's reproductive > Flashcards

men's reproductive Flashcards

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
Q

prognosis of prostate cancer

A

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
Q

definition of erectile dysfunction

A

Inability to achieve or sustain an erection sufficient for satisfactory sexual intercourse

27
Q

another word of erectile dysfunction

A

impotence

28
Q

primary ED (rare)

A

Life-long inability to have a normal erection d/t Severe psychiatric problems & Early vascular trauma

29
Q

secondary ED (most common)

A

ED in someone with a history of normal erections

30
Q

organic causes of Secondary ED

A

Peripheral vascular disease: Arterial insufficiency, Excessive venous drainage, Sedentary lifestyle (risk factor)
Medications: Antidepressants, Antihypertensives
Endocrine problems
Trauma, Surgery (Radical prostatectomy)

31
Q

psychogenic causes of Secondary ED

A

Depression
Low desire
Performance anxiety
Strained relationship

32
Q

Physiology of a Normal Erection

A

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
Q

PNS =

A

parasympathetic nervous system

34
Q

cGMP =

A

cyclic guanosine monophosphate

35
Q

PDE-5 =

A

phosphodiesterase type 5

36
Q

sildenafil

A

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
Q

priapism

A

erection is painful or lasts more than 4hrs- medical emergency

NUR 326 (15 decks)

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