Male genitourinary disorders Flashcards

1
Q

Review A & P (Porth, chpts 43 + 45)

* Esp review p. 1039 figure 43-4 and 43-5

A

d

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2
Q

Prostate

  • What is it?
  • where is it situated?
  • Shape?
  • Name of part of urethra it surrounds?
A
  • Is accessory organ in male urinary system
  • Secretory gland – produces prostatic fluid, which has various components that have different functions – helps to nurture sperm, helps to neurtralize pH of ejaculate + in women’s vagina
  • Anatomically: prostate is encapsulated; sits close to and inferior to the bladder and lies at the neck of the bladder;
  • Pear shaped organ….if core the pear have the urethra (NOT the ureter…which runs from kidney to the bladder) = the prostatic urethra; rest is the penile urethra (passes through penis)
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3
Q

Name structure other than prostate that is accessory gland that adds to ejaculate?

A

• Seminal vesicles also secretory: produce seminal fluid, which is also added to the ejaculate

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4
Q

Which structure is most important structure for neoplasia (both benign + malignant) in male GU system?

A

Prostate

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5
Q

Site of sperm production in testes?

Outline anatomy from there until ejaculate

A

Seminiferous tubules
–> becomes rete testes –> efferent tubules converge to form epididymus (site of final maturation of sperm) –> vas deferens –> sperm stored in ampulla of vas defens until ejaculated through urethra (can be fertile for up to 42 days)

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6
Q

How common is BPH in men?

A

• One of most common repro disorders in men…every single man beyond 50 or so will develop BPH!! Just severity is different

o >40 y ~20% have BPH
o >60 y ~50%
o >80 y ~90%

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7
Q

Where does the hypertrophy occur in BPH? Is it fast or gradual?

A
  • Gradual periurethral englargement (occurs around the urethra, central in the prostate)
  • Continual inc → will not stop unless you intervene
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8
Q

WHat tissues comprise the prostate? Which are growing and what kind of growth in BPH?

A

• P Comprised mostly of secretory cells (glandular tissue) but also have muscle tissue within the ducts – the muscle tissue is affected along with the exocrine tissues but is muscle so has HYPERTROPHY here, NOT hyperplasia

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9
Q

Etiology of BPH?

A

• Not all info is available – therefore et is unclear
• Ageing is the major risk factor –> Age related changes in adrogen levels??
o Altered T : E ?? (testosterone to estrogen ratio)
• Genetics, race, diet??
–> seen higher in African, lower in Japanese…possible genetic ties
–> role of these factors seem evident but unclear

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10
Q

What are androgens?

2 primary?

A

Male sex hormones

testosterone + DHT (Dihydrotestosterone)

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11
Q

WHy is the growth of the prostate (rather than atrophy) strange with increasing age?

A

Have to look at what supports the growth of the prostate…is reproductive, so supported by sex hormones. So if gland is increasing is size, would think that inc in sex hormones, but we know they decline with age…

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12
Q

What is DHT?

What role does E plan in relation to DHT?

A

T produced in testes, enters circulation + most enters accessory structures in repro tract (bit in other systems as well); 95% of T converts to DHT, which is the active form

Wiki: The enzyme 5α-reductase synthesizes DHT from testosterone in the prostate, testes, hair follicles, and adrenal glands

Estrogen responsible for facilitating action of DHT on the cells; sensitizes the prostatic cell for DHT binding + action, causing cells to carry out secretory fx and regulating proliferation of the cells

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13
Q

Patho of BPH?

A
  • Related to changes in T, DHT, and E
  • 5a reductase is enzyme responsible for T —–→ DHT
  • DHT supports prostate growth + fx
  • E sensitizes prostate to DHT
  • T declines with age → alters T:E ratio
  • Relative inc in E → sensitizes prostate to DHT → enlargement
  • Hyperplasia of periurethral tissue → compresses urethra
  • Also hypertrophy of smooth muscle (as these cells are also sensitized by E)
  • Impedes urine flow (Urine accumulates in bladder → attempt to urinate → partial voiding with residual volume)
  • Bladder wall thickens
  • Trabeculations + Diverticula form
  • Urine stasis
  • Ureters distend w urine = hydroureter (Backing up of urine as cannot exit bladder → fills ureters and then into kidneys…calices fill up)
  • Ureters loop downward & “fishhook”
  • Urine backs up in the kidney causing hydonephrosis
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14
Q

Why thickening of bladder wall in BPH?

Is this compensatory + helpful?

A

• Bladder has single layer of epithelial tissue (transitional tissue) → structural changes will occur to counter risk of rupture

which is compensatory but seems to worsen problem b/c can actually allow more and more urine to accumulate)

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15
Q

Why do Trabeculations + Diverticula form in the bladder in BPH?

Is this helpful?

A

Attempts to inc size of bladder to compensate for inc retention…

Folds in wall of bladder….further allows urine stasis in the bladder…not good!

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16
Q

Possible complications of urine stasis in BPH?

A

stones (calculi) + UTI

17
Q

Why does fishhooking occur in ureters?

A

D/t inc pressure in beginning of ureter causing structural change = “fish hook ureter” as ureter loops downward at point of attachment to bladder as it fills with urine (after hydroureter)

18
Q

What is hydronephrosis?

A

= the distension of the renal pelvis + the calyces

swelling of kidneys as fill with urine

19
Q

How does BPH lead to kidney failure?

A

• Accum of urine in kidneys, eventually causing presure of filtrate to be greater than in glomerulus, which prevents filtration…no more urine production + build up of nitrogenous wastes in the blood, ultimately resulting in kidney failure

20
Q
  • Fig 44-8 + 44-9 – show nodular appearance of prostate with BPH
  • 44-8 bottom shows cancer – develops peripherally
A

x

21
Q

Manifestations of BPH?

A

• Frequency (content urge to urinate…not uncommon to get up many times in night to urinate)
• Hesitancy – difficulty in starting urine stream
• Weak urine stream
• Terminal dribbling (droplets of urine passing after urine stream has stopped)
• Complete obstruction?
o Urine retention?

22
Q

Dx of BPH?

A

• Hx, mnfts, px
• Digital rectal exam
screening exam, routine in men >50yrs
• PSA – prostate specific antigen
• BUN, creatinine – want to see if kidney fx has been impacted
• Urinalysis – to assess for signs of renal calculi and infection – hematuria?

23
Q

How does DRE allow to differentiate between BPH and CA?

A

Palpation provides info differently for malignancy or BPH – with malignancy is peripheral, will feel defined lump

24
Q

PSA – prostate specific antigen
How does this test work?
What is PSAD and PSAV

A

component of prostatic fluid, enters circ so can measure in blood; NOT related to necrosis (not d/t cell death + release), this is normal constituent of blood; will measure PSA and the more you measure, the greater the quantity of secretion and therefore the greater enlargement of the prostate

o Shows enlargement, not definitive of whether is BPH or malignancy, etc.
o PSAD = density of the cells
o PSAV = velocity – speed at which the cells form
o Are controversies…test is routinely done but clear cut in terms of dx

25
Q

Tx of BPH?

A
  • Often no tx – may have some frequency, but generally able to manage by avoiding fluids 2-3hr before bedtime, alcohol, caffeine
  • Based on severity and complications
  • A adrenergic antagonists – objective is to act on muscles (in gland and urethra) to cause relaxation → dec obstruction → improves urination (This is symptomatic tx only)
  • 5a-reductase inhibitor (long term) → addressing part of underlying problem by dec DHT
  • If severe, combine both drugs
  • Sx is last resort – TURP or laser prostatectomy
26
Q

What is TURP?

A

o TURP = Transurethral Resection of the Prostate – go in through urethra, pass into the prostate

27
Q

Which is more common, prostate or testicular CA?
Death by this?
When does it typically occur?

A

Prostate

  • 3rd in CA deaths
  • Mostly after age of 65
28
Q

What is the etiology of prostate CA

A

Like all cancers, is genetic mutation!

29
Q

Risk factors for prostate CA?

A
  • Age
  • Diet
  • Ethnicity
  • Familial r/t both first and second degree relatives w P cancer
  • Androgens
30
Q

Patho of P CA

1) What kind of cancers are these?
2) Unicentric or multicentric in origin? Central or peripheral?

A

1) Adenocarcinomas - origin in glandular epithelial cells
2) Multicentric, peripheral site of origin
(meaning develops away from the urethra, close to the capsule)

31
Q

Whis prostatic CA often delayed in being diagnosed?

A

• No early manifestations (because away from urethra so not obstructing, etc)

32
Q

WHen do manifestations of prostate CA typically occur?
How does it progress?
Mets?

A

• Mnfts appear after invasion or mets – invasion into prostate; extension into adjoining structures
• Extension to bladder & seminal vesicle
• Mets to bone, liver & lungs – affects back, hips typically in bones (manifestations r/t this)
(See Fig 44-10, p. 1065)

33
Q

Manifestations of prostate CA?

A
  • Are various kinds…presentations vary
  • Prostatitis common – will present with inflm of prostatis as space-occupying lesion causes inflm. Important to be clear that prostatitis does NOT necessarily mean CA
  • Late hip and back pain (d/t bone mets)
34
Q

Dx of prostate CA?

A
  • Hx, Px
  • DRE → important screen (NOT diagnostic) for this, BPH + colorectal CA
  • PSA – exactly like in BPH
  • Biopsy – do transurethral sample…histology (extent, grading, etc) comes from this biopsy
  • US (usually with biopsy)
35
Q

Tx of prostate CA?

A
  • Stage, grade, and age based
  • Localized = low risk → active surveillanc
  • 1st line antiandrogens – this is manage the growth (not a cure), counteract androgens; estrogen is an example of this if used in high enough doses
  • Radical prostatectomy - will remove all of prostate, tumour, as well as the seminal vesicles
  • Radiation - chemo not shown to be very successful
36
Q

What does “active surveillance” mean for tx of prostate CA?

A

in some older men, low risk CA develops in prostate that doesn’t require treatment – is these individuals risk of that malignancy causing mets, death is quite low, intervention will cause more hassle…will monitor it instead (not an easy conversation with have the patient)