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
2
Q
What is the reccurence rate for UTIs?
A
40%
3
Q
What is the commonest route of entry for UTI causing pathogens?
A
urethra**
-less common is via blood supply (systemic spread)
4
Q
Why are UTIs more common in females?
A
ANATOMY:
- short urethra
- closer proximity to colon
5
Q
What features predispose a patient to UTIs?
A
- females (anatomy)
- sexual activity
- UT abnormalities/obstructions –> stones, tumours, etc
6
Q
What are the clinical features of UTIs?
A
- dysuria
- low grade fever
- frequency + urgency of urination
- *flank pain + high grade fever –> pyelonephritis
7
Q
What are the complications of UTIs?
A
- E. coli septicemia
- endotoxins –> DIC
- prostatitis
- prostatic abscess
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
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
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
11
Q
What type of bacteria is E. coli?
A
gram negative bacilli; lactose fermenting
-Entero.. + Klebsiella also ferment lactose
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)
13
Q
What are the functions of the prostate?
A
- delivery of semen
- protection and nutrition of sperm
- acid phosphatase
- prostate specific antigen (PSA)
14
Q
Which prostate zones are typically involved in BPH vs. cancer?
A
transitional zone --> BPH peripheral zone (posteriorly) --> cancer
15
Q
What is the normal prostate histology?
A
- fibromuscular stroma
- double layered epithelium glands (basal layer - flat + columnar epithelium - secretory)
- secretions (corpora amylaceae –> protein aggregates - major component of seminal fluid)
16
Q
What are the clinical features of prostatitis?
A
- inflammation
- edema
- rectal pain
- obstruction/dysuria
17
Q
What are the different types of prostatitis?
A
- acute suppurative prostatitis (5%)
- E. coli; rarely Staph or N. gonnorrhoeae - chronic non bacterial/chronic pelvic pain syndrome (90%** - commonest)
- chronic inflamm, symptoms, no pathogens - asymptomatic inflammatory prostatitis
- only WBCs, no symptoms, no pathogens - granulomatous prostatitis
- BPH, infarction, post TURP, idiopathic, TB, allergic (eosinophilic)
18
Q
How is prostatitis diagnosed?
A
- fluid examination after prostatic massage
- needle aspiration study of prostatic tissue
19
Q
What is the microscopy of prostatitis?
A
- oedema
- plenty of inflammatory cells between glands
20
Q
What does prostatic cancer feel like on DRE?
A
-hard irregular stony swelling
21
Q
What is the cause of BPH?
A
- non-neoplastic
- androgen induced hyperplasia**
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
23
Q
What enzyme converts testosterone to DHT?
A
5-alpha reductase type II
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*
25
True or False?
| BPH is a precursor to carcinoma
FALSE
26
What common drug is used to treat BPH?
Finasteride
| -5-alpha reductase inhibitor
27
True of False?
| There is maintenance of the double layered epithelium in prostatic cancer
FALSE
| -single layer
28
What are the gross features of BPH?
- grey white
- nodular hyperplasia
- periurethral transitional zone
- bulges into bladder (BALL VALVE - median lobe of prostate) --> Sx.
29
What are the complications of BPH?
* *enlarged prostate --> median lobe - ball valve**
- urinary obstruction
- urine retention --> inflammation, infections, urolithiasis (stones)
- hypertrophy of wall
- mucosal trabeculations
30
What is TURP?
Trans Urethral Resection of the Prostate
| -for diagnosis + treatment of BPH (Dx. by microscopy of prostatic tissue)
31
What is the most common male cancer?
prostate cancer
- adenocarcinoma, elderly (>50yrs)
- but deaths due to prostate cancer in second to lung
- many are small/clinically insignificant
32
Why is prostate cancer known as incidental cancer?
if tested, seen in many elderly dying of OTHER causes
33
What is the only population screening test available for prostate cancer?
PSA
- controversial
- now discouraged
- lack of specificity
- % of free PSA compared to bound total PSA is lower in pts. with prostatic cancer
34
What are the gross features of prostate cancer?
1. irregular, stony hard
| 2. peripheral zone/posterior
35
What is the etiology of prostatic cancer?
- ?androgens (castration decreases swelling + tumour growth --> therefore androgen dependent tumour)
- genes (ETS, PTEN) - tumour suppressor
- ?environment/diet
- NOT BPH!
36
What is PSA and its normal serum range?
Prostate Specific Antigen
- proteolytic enzyme
- liquifies semen
- NOT cancer specific
- normal serum PSA <4.0ng/L
- increased in prostate damage/malignancy
37
What is the pathogenesis of prostatic cancer?
dysplasia --> PIN (prostatic intraepithelial neoplasia - insitu) --> CANCER
38
What are the microscopic features of prostatic cancer?
1. pleomorphic irregular cells (clusters)
2. single layer glands (no basal layer)
3. no secretions (non-functioning glands)
39
What is the scoring method used to stage prostatic cancer?
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
Outline staging of prostatic cancer?
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
What is the commonest type of stone in uro/nephrolithiasis?
Calcium stones (80%)
- oxalate/phosphate/urate salts
- alkaline urine
- stone first, obstruction later
- small, spike + cause haemorrhage
42
What are the etiologies for calcium stone lithiasis?
- Hypercalciuria (familial 54%); increased gut absorption --> COMMONEST**
- rarely: defective tubular reabsorption of calcium (renal hypercalciuria)
- UTI = common risk factor
- hyperparathyroidism (rare <10%)
43
What is the second common type of stones?
Struvite stones (15%)
- magnesium ammonium phosphate (triple phosphate)
- staghorn stone
- "obstruction first, stone later"*
44
What is the typical cause of struvite stones?
- chronic UTI with gram neg. rods (split urea)
- pH > 7
- urea splitting Proteus, Klebsiella, etc. (NOT E. coli)
45
What are the 2 least common types of stones and their causes?
Uric acid stones (6%)
- pH <5.5
- high protein (meats), malignancy, gout** (25%)
```
Cystine stones (2%)
-genetic --> failure of reabsorption
```
46
Which stone typically produces urinary colic?
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
What are the clinical symptoms of urinary colic?
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
What is the gross feature of struvite/staghorn/triple phosphate stones?
Large stone molds to pelvis and calyceal system
| -obstruction --> urine retention --> infection --> stone formation
49
What are the complications of staghorn stones?
- chronic irritation --> squamous metaplasia/carcinoma (rare)
- ureteral stricture, infection, sepsis
- obstruction --> hydronephrosis* --> CRF
- secondary inf. (pyelonephritis, abscess)
50
What is hydronephrosis?
- 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
What does bilateral hydronephrosis suggest?
obstruction at or below the bladder
52
What is hydroureter and how can it cause polyuria?
- dilatation of ureter
| - bilateral partial hydroureter --> polyuria due to defective tubular function
53
Why is unilateral complete/partial hydronephrosis commonly asymptomatic?
one of the kidneys is still functioning normally
54
What are the complications of hydronephrosis?
- infection, lithiasis (triple phosphate)
- atrophy
- CRF
55
How do cysts form in the kidneys?
- cysts form due to misconnection in the nephrons
| - genetic/acquired
56
What is the commonest type of kidney cysts?
Autosomal Dominant Polycystic Kidney Disease (ADPKD)
N.B. simple cysts also common yet do not produce clinically significant Sx.
57
What type of genetic cysts can form in infants?
Infantile Polycystic Kidney Disease (ARPKD) --> (autosomal recessive)
58
What type of cysts are acquired cysts?
- simple cysts**
| - dialysis associated cysts
59
What age does ADPKD typically develop?
~40yrs
- partial lack of tubular development
- bilateral, large, cystic kidneys (size of a footy)
60
What are the clinical features of ADPKD?
- flank pain
- mass
- hematuria
- recurrent UTIs
- **minor trauma --> HEMATURIA**
- CRF ~50yrs - common cause of dialysis
61
What is the commonest mutation present in ADPKD?
- PKD-1 gene (polycystin) on chromosome 16 (85%)
| - PKD-2 in 15%; PKD-3 rare
62
What other associations are there with ADPKD?
- liver, splenic, pancreatic cysts (30%)
- cerebral berry aneurysms (20%)
- diverticulosis coli
63
What is ARPKD?
- 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
What are the size parameters for benign and malignant renal tumours?
```
<3cm = benign
>3cm = malignant
```
65
What are the 2 types of benign renal tumours?
- adenoma
| - angiomyolipoma (rare)
66
What are the malignant renal tumours, and specify which is common in both adults and children?
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
What is renal cell carcinoma AKA?
clear cell carcinoma
68
What age and gender does renal cell carcinoma typically affect?
~60yrs
| males 3:1
69
What are the 2 types of renal cell carcinoma?
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
What is the characteristic finding of sporadic renal cell carcinoma?
grows/extends into renal vein
71
What are the gross features of renal cell carcinoma?
1. yellow, fat-like, well demarcated
2. necrosis; haemorrhage
3. renal vein extension (cancer cells are well-cohesive)
72
What is the classic triad of clinical features in RCC? and what is the commonest symptom?
1. hematuria
2. flank pain
3. mass* (<10%)
**hematuria (50%) = most common Sx.
73
True or False?
| RCC is well known for paraneoplastic syndromes
TRUE
| -it secretes hormones
74
What paraneoplastic syndromes are possible in RCC?
- PTH --> hypercalcemia
- EPO --> polycythemia
- HTN, amyloidosis, leucocytosis + eosinophilia
75
What is the 5yr survival rate for RCC?
~40%
76
What is the microscopy of RCC?
- clear cells --> looks like lipoma BUT nucleus is in centre and is round NOT pushed to periphery
- uniform
- NO pleomorphism
- papillary --> in familial
77
What age is typically affected in Wilm's tumour - nephroblastoma?
2-5yrs
| -98% <10yrs
78
What are the Sx. of Wilm's tumour?
asymptomatic, HTN or hematuria
79
What is the difference between sporadic and familial cases of Wilm's tumour?
sporadic (80%) --> unilateral
familial (10%) --> bilateral
-WT1 gene mutation
80
What are the gross and microscopic features of Wilm's tumour?
Gross:
-large, bulky, haemorrhagic, soft/grey
Micro:
-dark, blue embryonic blast cells forming primitive tubules + glomeruli
81
What structures are comprised of urothelium?
"transitional epithelium"
- renal pelvis
- ureters
- bladder
- parts of urethra
82
Which site is the most common for transitional cell neoplasms?
urinary bladder --> papillary growth
83
What are the characteristic features of transitional cell neoplasms?
- painless hematuria
| - malignant cells in urine (c.f. RCC where there are none)
84
What are the risk factors for transitional cell neoplasms?
- beta-naphthylamine
- smoking
- chronic cystitis
- schistosomiasis --> squamous cell carcinomas commonest
85
What are the 2 structural types of transitional cell neoplasms?
1. papillary carcinoma --> invasive papillary carcinoma** COMMONEST (low grade)
2. flat non-invasive carcinoma (CIS) --> flat invasive/infiltrative carcinoma (high grade)
86
What is the microscopic feature of transitional cell neoplasms?
- pleomorphic cells forming papillary structures
| - infiltration + haemorrhage
87
Common type of stone seen in hydronephrosis is?
struvite stone
- hydronephrosis is due to chronic obstruction
- obstruction THEN stone in triple phosphate stones
Pathology Term 5
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