02b: Prostate Flashcards Preview

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Flashcards in 02b: Prostate Deck (59)
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1
Q

Majority of blood to prostate comes from (X) artery off of (Y) artery.

A
X = inferior vesical
Y = internal pudendal
2
Q

Most common malignancy in males 15-35 years old:

A

Testicular cancer

3
Q

T/F: No major genetic factors for testicular cancer.

A

True

4
Q

Which aspect of history would put patient at risk for testicular cancer?

A

Undescended testis

5
Q

Diagnosis of testicular cancer via:

A

Hx, PE, and scrotal ultrasound

6
Q

Rx for testicular cancer:

A
  1. Surg excision of testicle (inguinal approach)

2. Chemo (super effective, even with metastasis)

7
Q

Which tumor markers can be followed to assess efficacy of Rx for testicular cancer?

A
  1. AFP
  2. bHCG
  3. LDH
8
Q

BPH treatment regimen:

A
  1. Alpha blockers (terazosin, doxazosin, tamsulosin, Alfuzosin)
  2. 5a-reductase inhibitors (Finasteride, Dutasteride)
9
Q

Function of alpha blocker Rx in BPH:

A

Relax smooth muscle at bladder neck

10
Q

Pt being treated for BPH: PSA will decrease by as much as (X)% due to (Y) meds.

A
X = 50
Y = 5a-reductase inhibitors
11
Q

T/F: BPH Rx regimen will not affect sexual function.

A

False - 5a-reductase inhibitors have potential sexual side effects (can be irreversible!)

12
Q

T/F: No major genetic factors for prostate cancer.

A

False - positive FHx and HPC1 gene are risk factors

13
Q

(High/low) (X) diet is risk factor for prostate cancer:

A

High

X = fat

14
Q

Why is PSA high in prostate cancer?

A

Cancer cells have destabilized basement membrane, so more leaks out

15
Q

“Med castration” for prostate cancer can include which hormonal treatments?

A
  1. GnRH agonist (Lupron)
  2. Estrogen
  3. Antiandrogens
16
Q

What’s the next step in Rx for patients with metastatic prostate cancer who have failed hormonal therapy?

A

Chemo (with goals to contain cancer and alleviate pain)

17
Q

Standard chemo Rx for prostate cancer includes (X). What’s the mechanism of action?

A

X = Abiraterone (in combo with prednisone)

Inhibits 17a hydroxylase (thus inhibiting androgen synthesis)

18
Q

Predominant blood supply to penis:

A

Internal pudendal a

19
Q

Which a predominantly responsible for blood supply to erectile tissue of penis?

A

Cavernosal a (runs through corpus cavernosa)

20
Q

T/F: Urethra runs through corpus cavernosa.

A

False - corpus spongiosum

21
Q

55 yo M smoker presents with complaints of erectile dysfunction. What do you suspect is the cause? What would you test for?

A

Arteriogenic (atherosclerotic);

DM, CAD, cholesterol, etc.
Check for distal pulses

22
Q

What are some endocrine diseases that cause erectile dysfunction?

A
  1. DM
  2. Thyroid disease
  3. Testosterone deficiency
23
Q

Basic workup for erectile dysfunction includes which labs?

A
  1. T, LH
  2. TSH
  3. Lipid/cholesterol panel
  4. HbA1c
  5. Prolactin
24
Q

Which PDE5 inhibitor would you recommend for patient with ED that is already paying for multiple meds?

A

Tadalafil (longest half-life, fewer doses; insurance won’t cover)

25
Q

Common side effects of viagra:

A

HA, flushing, dyspepsia; maybe transient/mild visual effects

26
Q

List the injectable meds for ED:

A

3 Ps:

  1. Papavarine (PDE inhibitor)
  2. Prostaglandin E1 (vasodilator)
  3. Phenoxybenzamine/phentolamine (alpha-R blockade)
27
Q

T/F: Penile prostheses are last-resort for erectile dysfunction.

A

True

28
Q

Priapism: (painless/painful) prolonged erection indicates arterial problem. Is this an emergency?

A

Painless

No; uncontrolled arterial flow

29
Q

Priapism: (painless/painful) prolonged erection indicates venous problem. Is this an emergency?

A

Painful

Yes, low-flow priapism (blood trapped in erection chambers); penis can become ischemic

30
Q

Rx options for priapism:

A

Oral meds (sympathomimetics), irrigation, shunts (extreme case)

31
Q

Condyloma on penis caused by:

A

HPV

32
Q

T/F: Circumcision essentially eliminates risk of penile cancer.

A

True

33
Q

RFs for penile cancer:

A
  1. Smoking
  2. Poor hygiene
  3. HPV infection/sex partners
34
Q

Sequence of spermatogenesis:

A

Spermatogonium, spermatocyte, spermatid, spermatozoan

35
Q

T/F: Exogenous testosterone decreases sperm production.

A

True

36
Q

Histo: endometrium in (X) phase has multiple simple, tubular glands in stroma with abundant mitotic activity.

A

X = proliferative

37
Q

Endometrium has (X) epithelium.

A

X = pseudostratified

38
Q

Day (X) of menstrual cycle begins change from proliferative to secretory endometrium.

A

X = 16

39
Q

Histo: endometrium in (X) phase has glands with prominent subnuclear vacuoles. There is (high/low) mitotic activity.

A

X = early secretory

No mitoses

40
Q

Day (X) of menstrual cycle: sub- and supra-nuclear vacuoles are seen with apical discharge.

A

X = 18

41
Q

Histo: endometrium in (X) phase has “saw-toothed” glands and (Y) in gland lumen.

A
X = late secretory
Y = secretions
42
Q

Max stromal edema in endometrium is seen on day (X) of menstrual cycle.

A

X = 22

43
Q

Predecidual changes in endometrium include:

A

Indistinct perviascular aggregates of cells with eosinophilic cytoplasm

44
Q

Stromal granulocytes in endometrium is classic for day (X) of menstrual cycle and represents preparation for:

A

X = 26

Menstruation (predecidual change; inflammatory cells enter stroma, ready to mop up debris from menstruation)

45
Q

Most common cause of dysfunctional uterine bleeding is:

A

Anovulatory breakdown (endometrium right around menopause loses ability to respond properly to hormones)

46
Q

Anovulation: excess (progesterone/estrogen) leading to disordered (X)

A

Estrogen, relative to progesterone

X = gland proliferation (super large grands with relative scarcity of stroma)

47
Q

Endometrial hyperplasia is related to abnormally high, prolonged level of (X). Which diseases/situations might cause this?

A

X = estrogen

  1. Menopause/persistent anovulation
  2. PCOD
  3. Granulosa cell tumors
  4. Estrogen replacement Rx
  5. Obesity
48
Q

Key histo characteristic that distinguishes high grade from low grade endometrial hyperplasia:

A

Presence of atypia

49
Q

20% of endometrial cancer is (X) type with (Y) cells. This type is (less/more) aggressive and (dependent/non-dependent) on estrogen.

A

X = non-endometrioid
Y = serous, clear
More
Non-dependent

50
Q

Endometrioid Adenocarcinoma grade depends on % of:

A

Solid growth pattern (non-squamous/non-morular);

G1 is up to 5%, G2 is 6-50%, G3 is over 50%

51
Q

Presence of plasma cell in endometrial stroma is pathognomonic for:

A

Chronic endometritis

52
Q

List some etiologies for chronic endometritis:

A
  1. Chronic PID
  2. Postpartm (retained gestational tissue)
  3. IUD
  4. TB or other infections (chlamydia)
53
Q

A(n) (X) cyst is also called a “chocolate cyst”.

A

X = endometriotic (filled with degenerated blood products)

54
Q

A mass of benign endometrial glands/stroma projecting into endometrial cavity.

A

Endometrial polyp

55
Q

Hydatidiform moles tend to occur in (older/younger) women.

A

Two ends of spectrum (below 20 and over 45)

56
Q

Which classic symptom would a woman with hydatidiform mole present with?

A

Bleeding in either late 1st T or early 2nd T

57
Q

T/F: Hx of hydatidiform mole puts woman at higher risk of having future incidence of moles.

A

True

58
Q

p57 staining will be positive in (complete/partial) hydatidiform mole.

A

Partial (imprinted gene is maternally expressed)

59
Q

T/F: Choriocarcinomas are highly malignant but also highly responsive to chemo.

A

True