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Pathology Term 5 > Week 2 - UT PROSTATE > Flashcards

Week 2 - UT PROSTATE Flashcards

UTI, Prostatitis & BPH, Prostate Cancer, Lithiasis, Renal Cysts & Tumours

1
Q

What is the commonest causative pathogen for clinical UTIs?

A

E. coli (90%)

  • uropathogenic strains (UPEC)
  • P fimbriae or pili –> bind to tubular epithalial cells (urothelium)
  • colonize colon –> spread to urinary tract
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2
Q

What is the reccurence rate for UTIs?

A

40%

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3
Q

What is the commonest route of entry for UTI causing pathogens?

A

urethra**

-less common is via blood supply (systemic spread)

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4
Q

Why are UTIs more common in females?

A

ANATOMY:

  • short urethra
  • closer proximity to colon
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5
Q

What features predispose a patient to UTIs?

A
  • females (anatomy)
  • sexual activity
  • UT abnormalities/obstructions –> stones, tumours, etc
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6
Q

What are the clinical features of UTIs?

A
  • dysuria
  • low grade fever
  • frequency + urgency of urination
  • *flank pain + high grade fever –> pyelonephritis
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7
Q

What are the complications of UTIs?

A
  • E. coli septicemia
  • endotoxins –> DIC
  • prostatitis
  • prostatic abscess
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8
Q

What stream do you use when obtaining a urine specimen for a possible UTI?

A

Midstream clean catch urine specimen

**MSSU –> midstream samples of urine

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9
Q

What are the diagnostic measures for UTIs: E.coli?

A
  • blood –> leukocytosis (neutrophilia)
  • MSSU
  • dipstick –> leukocyte esterase (neutrophils) + nitrite POSITIVE
  • urine –> pyuria, neutrophils, bacteria (+RBCs after centrifugation)
  • MacConkey agar
  • microscopy gram stain
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10
Q

What agar is used for UTIs, what colour does E. coli show as and why?

A 
MacConkey agar
-selective, indicator media
-24hrs, 37degrees, aerobic
-PINK colony** --> lactose fermented by bacteria --> acid released --> pH indicator causes PINK colour of E. coli
N.B. --> Beta-hemolytic on blood agar
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11
Q

What type of bacteria is E. coli?

A

gram negative bacilli; lactose fermenting

-Entero.. + Klebsiella also ferment lactose

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12
Q

How doe we confirm presence of E. coli (i.e. to differentiate from other lactose fermenting bacterium such as entero.. and klebsiella)?

A

Further tests to confirm:

  • E. coli = urease NEGATIVE
  • unlike Klebsiella and Proteus (urease positive)
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13
Q

What are the functions of the prostate?

A
  • delivery of semen
  • protection and nutrition of sperm
  • acid phosphatase
  • prostate specific antigen (PSA)
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14
Q

Which prostate zones are typically involved in BPH vs. cancer?

A 
transitional zone --> BPH
peripheral zone (posteriorly) --> cancer
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15
Q

What is the normal prostate histology?

A
  1. fibromuscular stroma
  2. double layered epithelium glands (basal layer - flat + columnar epithelium - secretory)
  3. secretions (corpora amylaceae –> protein aggregates - major component of seminal fluid)
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16
Q

What are the clinical features of prostatitis?

A
  • inflammation
  • edema
  • rectal pain
  • obstruction/dysuria
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17
Q

What are the different types of prostatitis?

A
  1. acute suppurative prostatitis (5%)
    - E. coli; rarely Staph or N. gonnorrhoeae
  2. chronic non bacterial/chronic pelvic pain syndrome (90%** - commonest)
    - chronic inflamm, symptoms, no pathogens
  3. asymptomatic inflammatory prostatitis
    - only WBCs, no symptoms, no pathogens
  4. granulomatous prostatitis
    - BPH, infarction, post TURP, idiopathic, TB, allergic (eosinophilic)
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18
Q

How is prostatitis diagnosed?

A
  • fluid examination after prostatic massage

- needle aspiration study of prostatic tissue

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19
Q

What is the microscopy of prostatitis?

A
  • oedema

- plenty of inflammatory cells between glands

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20
Q

What does prostatic cancer feel like on DRE?

A

-hard irregular stony swelling

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21
Q

What is the cause of BPH?

A
  • non-neoplastic

- androgen induced hyperplasia**

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22
Q

What is testosterone converted to in BPH?

A

testosterone –> DHT –> hyperplasia
-DHT = dihydrotestosterone –> stimulates growth factor release via action on nuclear androgen receptors –> stimulates cell division

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23
Q

What enzyme converts testosterone to DHT?

A

5-alpha reductase type II

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24
Q

What is the morphology of BPH?

A
  • nodular hyperplasia of glands + stroma (like in breast, thyroid, etc)
  • stromal and gland hyperplasia
  • hyperplastic cystic glands, secretions, double epithelial layer maintained*
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25
Q

True or False?

BPH is a precursor to carcinoma

A

FALSE

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26
Q

What common drug is used to treat BPH?

A

Finasteride

-5-alpha reductase inhibitor

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27
Q

True of False?

There is maintenance of the double layered epithelium in prostatic cancer

A

FALSE

-single layer

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28
Q

What are the gross features of BPH?

A
  • grey white
  • nodular hyperplasia
  • periurethral transitional zone
  • bulges into bladder (BALL VALVE - median lobe of prostate) –> Sx.
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29
Q

What are the complications of BPH?

A
  • *enlarged prostate –> median lobe - ball valve**
  • urinary obstruction
  • urine retention –> inflammation, infections, urolithiasis (stones)
  • hypertrophy of wall
  • mucosal trabeculations
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30
Q

What is TURP?

A

Trans Urethral Resection of the Prostate

-for diagnosis + treatment of BPH (Dx. by microscopy of prostatic tissue)

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31
Q

What is the most common male cancer?

A

prostate cancer

  • adenocarcinoma, elderly (>50yrs)
  • but deaths due to prostate cancer in second to lung
  • many are small/clinically insignificant
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32
Q

Why is prostate cancer known as incidental cancer?

A

if tested, seen in many elderly dying of OTHER causes

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33
Q

What is the only population screening test available for prostate cancer?

A

PSA

  • controversial
  • now discouraged
  • lack of specificity
  • % of free PSA compared to bound total PSA is lower in pts. with prostatic cancer
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34
Q

What are the gross features of prostate cancer?

A
  1. irregular, stony hard

2. peripheral zone/posterior

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35
Q

What is the etiology of prostatic cancer?

A
  • ?androgens (castration decreases swelling + tumour growth –> therefore androgen dependent tumour)
  • genes (ETS, PTEN) - tumour suppressor
  • ?environment/diet
  • NOT BPH!
36
Q

What is PSA and its normal serum range?

A

Prostate Specific Antigen

  • proteolytic enzyme
  • liquifies semen
  • NOT cancer specific
  • normal serum PSA <4.0ng/L
  • increased in prostate damage/malignancy
37
Q

What is the pathogenesis of prostatic cancer?

A

dysplasia –> PIN (prostatic intraepithelial neoplasia - insitu) –> CANCER

38
Q

What are the microscopic features of prostatic cancer?

A
  1. pleomorphic irregular cells (clusters)
  2. single layer glands (no basal layer)
  3. no secretions (non-functioning glands)
39
Q

What is the scoring method used to stage prostatic cancer?

A

Gleason Scoring

  • biopsy microscopy study
  • 2 prominent areas
  • add the values (2–>10 - max)
  • e.g. 3+4=7
  • limitations –> depends on accuracy of the biopsy
40
Q

Outline staging of prostatic cancer?

A
  1. localised to one part of prostate (90%)
  2. spread to multiple parts of prostate
  3. cancer is touching the prostate capsule
  4. spread beyond the capsule (i.e. LNs) (10%)
41
Q

What is the commonest type of stone in uro/nephrolithiasis?

A

Calcium stones (80%)

  • oxalate/phosphate/urate salts
  • alkaline urine
  • stone first, obstruction later
  • small, spike + cause haemorrhage
42
Q

What are the etiologies for calcium stone lithiasis?

A
  • Hypercalciuria (familial 54%); increased gut absorption –> COMMONEST**
  • rarely: defective tubular reabsorption of calcium (renal hypercalciuria)
  • UTI = common risk factor
  • hyperparathyroidism (rare <10%)
43
Q

What is the second common type of stones?

A

Struvite stones (15%)

  • magnesium ammonium phosphate (triple phosphate)
  • staghorn stone
  • “obstruction first, stone later”*
44
Q

What is the typical cause of struvite stones?

A
  • chronic UTI with gram neg. rods (split urea)
  • pH > 7
  • urea splitting Proteus, Klebsiella, etc. (NOT E. coli)
45
Q

What are the 2 least common types of stones and their causes?

A

Uric acid stones (6%)

  • pH <5.5
  • high protein (meats), malignancy, gout** (25%)
Cystine stones (2%)
-genetic --> failure of reabsorption
46
Q

Which stone typically produces urinary colic?

A

Calcium oxalate

  • unilateral, small 1-3mm stones
  • passage causing paroxysmal intense colicky pain in the loin, radiation to anterior (renal or ureteral “colic”) - “writhing in pain” + hematuria (NO casts)
47
Q

What are the clinical symptoms of urinary colic?

A

BASED ON LEVEL OF OBSTRUCTION

  1. pelvis/ureteropelvic junction
    - deep flank pain, no radiation
    - due to stretching of renal capsule
  2. ureter
    - acute, severe colicky pain in the flank radiating to testes/vulva
    - nausea/vomiting
    i. upper ureter (DDx cholecystitis)
    ii. middle ureter (DDx appendicitis)
    iii. distal ureter (DDx pelvic inflamm. disease)
  3. ureterovesical junction
    - irritative voiding/dysuria
    - pain in tip of penis/vulva
48
Q

What is the gross feature of struvite/staghorn/triple phosphate stones?

A

Large stone molds to pelvis and calyceal system

-obstruction –> urine retention –> infection –> stone formation

49
Q

What are the complications of staghorn stones?

A
  • chronic irritation –> squamous metaplasia/carcinoma (rare)
  • ureteral stricture, infection, sepsis
  • obstruction –> hydronephrosis* –> CRF
  • secondary inf. (pyelonephritis, abscess)
50
Q

What is hydronephrosis?

A
  • dilatation of renal pelvis + calyces with atrophy of parenchyma
  • secondary to obstruction
  • congenital –> ureteric atresia, kinks, torsion, etc
  • acquired –> CALCULI, TUMOURS, inflammation stricture, foreign body, neurogenic, pregnancy
51
Q

What does bilateral hydronephrosis suggest?

A

obstruction at or below the bladder

52
Q

What is hydroureter and how can it cause polyuria?

A
  • dilatation of ureter

- bilateral partial hydroureter –> polyuria due to defective tubular function

53
Q

Why is unilateral complete/partial hydronephrosis commonly asymptomatic?

A

one of the kidneys is still functioning normally

54
Q

What are the complications of hydronephrosis?

A
  • infection, lithiasis (triple phosphate)
  • atrophy
  • CRF
55
Q

How do cysts form in the kidneys?

A
  • cysts form due to misconnection in the nephrons

- genetic/acquired

56
Q

What is the commonest type of kidney cysts?

A

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

N.B. simple cysts also common yet do not produce clinically significant Sx.

57
Q

What type of genetic cysts can form in infants?

A

Infantile Polycystic Kidney Disease (ARPKD) –> (autosomal recessive)

58
Q

What type of cysts are acquired cysts?

A
  • simple cysts**

- dialysis associated cysts

59
Q

What age does ADPKD typically develop?

A

~40yrs

  • partial lack of tubular development
  • bilateral, large, cystic kidneys (size of a footy)
60
Q

What are the clinical features of ADPKD?

A
  • flank pain
  • mass
  • hematuria
  • recurrent UTIs
  • minor trauma –> HEMATURIA
  • CRF ~50yrs - common cause of dialysis
61
Q

What is the commonest mutation present in ADPKD?

A
  • PKD-1 gene (polycystin) on chromosome 16 (85%)

- PKD-2 in 15%; PKD-3 rare

62
Q

What other associations are there with ADPKD?

A
  • liver, splenic, pancreatic cysts (30%)
  • cerebral berry aneurysms (20%)
  • diverticulosis coli
63
Q

What is ARPKD?

A
  • infantile PKD
  • autosomal recessive
  • PKHD1 –> rare (1:30,000)
  • complete disorganisation
  • small cysts (SPONGE kidney)
  • normal size –> renal failure
  • associated with liver cysts
  • perinatal, infantile + juvenile forms
64
Q

What are the size parameters for benign and malignant renal tumours?

A 
<3cm = benign
>3cm = malignant
65
Q

What are the 2 types of benign renal tumours?

A
  • adenoma

- angiomyolipoma (rare)

66
Q

What are the malignant renal tumours, and specify which is common in both adults and children?

A
  1. renal cell carcinoma** - common (adults)
  2. Wilm’s/Nephroblastoma * - common (childhood)
  3. transitional cell carcinoma (of renal pelvis - common in urinary bladder, however)
67
Q

What is renal cell carcinoma AKA?

A

clear cell carcinoma

68
Q

What age and gender does renal cell carcinoma typically affect?

A

~60yrs

males 3:1

69
Q

What are the 2 types of renal cell carcinoma?

A
  1. familial
    - less common (10%)
    - VHL gene (Von Hippel-Lindau) –> familial carcinoma synd. –> early age, bilateral, multiple
  2. sporadic
    - single, more common
    - risk factors: tobacoo**, obesity
    - clear cells, well demarcated, grows into renal vein
70
Q

What is the characteristic finding of sporadic renal cell carcinoma?

A

grows/extends into renal vein

71
Q

What are the gross features of renal cell carcinoma?

A
  1. yellow, fat-like, well demarcated
  2. necrosis; haemorrhage
  3. renal vein extension (cancer cells are well-cohesive)
72
Q

What is the classic triad of clinical features in RCC? and what is the commonest symptom?

A
  1. hematuria
  2. flank pain
  3. mass* (<10%)

**hematuria (50%) = most common Sx.

73
Q

True or False?

RCC is well known for paraneoplastic syndromes

A

TRUE

-it secretes hormones

74
Q

What paraneoplastic syndromes are possible in RCC?

A
  • PTH –> hypercalcemia
  • EPO –> polycythemia
  • HTN, amyloidosis, leucocytosis + eosinophilia
75
Q

What is the 5yr survival rate for RCC?

A

~40%

76
Q

What is the microscopy of RCC?

A
  • clear cells –> looks like lipoma BUT nucleus is in centre and is round NOT pushed to periphery
  • uniform
  • NO pleomorphism
  • papillary –> in familial
77
Q

What age is typically affected in Wilm’s tumour - nephroblastoma?

A

2-5yrs

-98% <10yrs

78
Q

What are the Sx. of Wilm’s tumour?

A

asymptomatic, HTN or hematuria

79
Q

What is the difference between sporadic and familial cases of Wilm’s tumour?

A

sporadic (80%) –> unilateral
familial (10%) –> bilateral
-WT1 gene mutation

80
Q

What are the gross and microscopic features of Wilm’s tumour?

A

Gross:
-large, bulky, haemorrhagic, soft/grey

Micro:
-dark, blue embryonic blast cells forming primitive tubules + glomeruli

81
Q

What structures are comprised of urothelium?

A

“transitional epithelium”

  • renal pelvis
  • ureters
  • bladder
  • parts of urethra
82
Q

Which site is the most common for transitional cell neoplasms?

A

urinary bladder –> papillary growth

83
Q

What are the characteristic features of transitional cell neoplasms?

A
  • painless hematuria

- malignant cells in urine (c.f. RCC where there are none)

84
Q

What are the risk factors for transitional cell neoplasms?

A
  • beta-naphthylamine
  • smoking
  • chronic cystitis
  • schistosomiasis –> squamous cell carcinomas commonest
85
Q

What are the 2 structural types of transitional cell neoplasms?

A
  1. papillary carcinoma –> invasive papillary carcinoma** COMMONEST (low grade)
  2. flat non-invasive carcinoma (CIS) –> flat invasive/infiltrative carcinoma (high grade)
86
Q

What is the microscopic feature of transitional cell neoplasms?

A
  • pleomorphic cells forming papillary structures

- infiltration + haemorrhage

87
Q

Common type of stone seen in hydronephrosis is?

A

struvite stone

  • hydronephrosis is due to chronic obstruction
  • obstruction THEN stone in triple phosphate stones

Pathology Term 5 (6 decks)

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