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path final > GENITOURINARY PATH > Flashcards

GENITOURINARY PATH Flashcards

1
Q

What are the Medullary cystic disease complex subtypes

A
  1. Medullary sponge kidney
  2. Nephronophthisis spectrum - Juvenile familial subtype (most common)
  3. Adult onset medullary cystic disease
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2
Q

Medullary spong kidney disease definition, clinical presentation, renal function, end result ?

A
  • Multiple cystic dilatation of the collecting ducts in the medulla of unknown cause
  • Occurs in adults as an incidental finding
  • Normal renal function
  • Most cases develop medullary nephrocalcinosis
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3
Q

Nephronophthisis Spectrum
- Definition
- Most common type
- Associations?

A

Definition: Cysts at the medulla and corticomedullary junction

Subtype:
- Juvenile familial subtype (most common type) - AR

Associations
- retinal malformation
- Joubert syndrome
- Meckel Gruber syndrome

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4
Q

Adult onset medullary cystic disease
- Inheritance

A
  • AD
  • Distinct from the nephronophthisis spectrum as it has separate genetics BUT similar morphology and progression to end stage renal disease in adult life.
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5
Q

Multicystic dysplastic kidney
- Inheritance
- Develops when ?
- Clinical presentation ?

A

Inheritance
- Sporadic

Develops
- in-utero

Clinical
- common cause of renal agenesis, following complete involution during childhood
- The affected kidney becomes nonfunctional. If bilateral renal failure results.

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6
Q

Multicystic dysplastic kidney associations ?

A

vesicoureteric reflux: most common and seen in up to 20%

pelviureteric junction obstruction

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7
Q

Acquired renal cystic disease
- epidemiology
- association

A

Epi
- Dialysis pt

Association
- RCC (12-18x increase)
- 7% dialysis will develop RCC over 10 years

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8
Q

Renal TB
- Definition
- Epidemiology
- Clinical
- RF

A

Def
- TB may involve the genitourinary tract with OR without lung involvement
- 2nd most common site after lungs

Epi
- Common globally, uncommon in australia

Clinical
- Asymptomatic
- May have cystitis or pyelonephritis
- May have frequency, nocturia, hematuria and pyruia

RF
- Low SES
- Smoking
- Low BMI

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9
Q

Renal TB
- Aetiology
- Pathophysio

A

Aetiology
- Usually Hematogeneously from pulmonary TB (but doesnt have to be)

Patho
- Colonizes the medulla*
- Infection contained by formation of granulomas with caseous necrosis
- In immune competent pts these remain stable or heal*
- however reactivation may occur if become immunocompromised (decades of latency)
- Caseous necrosis => Papillary Necrosis => SLough into calyces infecting and obstructing collecting system
- Ulcero-Cavernous lesions: when papillary lesions erode into the pelvicalyceal system => antegrade infection of lower tract

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10
Q

Morphology of Renal TB stages

A

Acute
- multiple cavities with yellow friable necrotic material involving the medulla
- Papillary necrosis

Late stage
- Cement of putty kidney with small contracted kidney

End stage
- Autonephrectomy with small calcified kidney
- Ureteral stricture common
- Bladder granuloma common - small bladder that can’t contract

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11
Q

Microscopic appearance of Renal TB

A

Chronic tubulointerstitial nephritis with caseating granulomas

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12
Q

Renal TB association

A

Amyloidosis

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13
Q

TCC
- definition
- epi

A

Definition
- Malignant tumour arising from the epithelium of the renal tract (urothelium/transitional epithelium).
In descending frequency occurs most commonly in bladder, pelvis, ureter and urethra.

Epidemiology
- Age range is 50-80.
- More common in males by 3:1

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14
Q

Classification (of epithelial bladder tumours - same as lung):

A

TCC Transitional cell (urothelial) carcinoma
- papillary
- carcinoma in situ / flat non-invasive

SCC
- Schistosomiasis
- due to chronic bladder irritation or infection from calculi
- often found later so higher mortality

Adenocarcinoma
- Rare, similar to GIT adenocarcinomas
- arise from urachal remnant
- Mortality same as SCC

SCC
- indistinguishable from SCC of the lung histologically - rare

Others
- Leiomyoma, embryonal sarcoma, lymphoma

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15
Q

TCC
- Clinical presentation ?
- RF ?

A

Clinical presentation
- Painless hematuria
- Hydronephrosis with flank pain if ureter obstructed
- Urinary retention if bladder outlet obsturcted

RF
- Smoking (highest risk)
- Aniline dyes, rubber and textiles
- Cancer treatment: Cyclophosphamide
- Radiation
- Chronic infection: Schistosomiasis

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16
Q

What are the 2 precursor lesions of TCC ?

A
  1. Non-invasive papillary lesions
    - Common with a range of atypia
  2. Carcinoma in situ (flat non-invasive)
    - Cytologically malignant cells present within a flat epithelium – the cells tend to be dyscohesive so shed easily in the urine
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17
Q

Morphology of TCC

A
  • usually T2 at diagnosis
  • Papillary, nodular, or flat infiltrating
  • Papillary low grade, can still invade but rarely fatal
  • CIS is commonly multifocal*
18
Q

Treatment for T1 and T2 cancer of TCC

A

T1: into lamina propria
- local endoscopic resection and intravesicle BCG

T2: into musuclaris propria (detrusor)
- Cystectomy and radiotherapy required

19
Q

Complications and prognosis of TCC

A
  • Recurrences common and often high grade
  • 98% 10 year survival in low grade even with recurrence
  • Late stage survival is poor
20
Q

Schistosomiasis pathophysio

A
  • Parasitic disease caused by immunologic reaction to schistosoma eggs trapped in tissue
  • Infected with the larval penetrating the skin, swimming in infected water
  • Chronic inflammatory response -> probably cycles of cell damage and repair
  • Initial bladder wall thickening. Chronic phase -> contracted calcified thick walled bladder
21
Q

Types of renal stones

A

Calcium
- Supersaturation of stone constituents exceed solubility of urine
- Hypercalciuria (most common), dehydration, hypercalcemia, sarcoidosis, hyperparathyroidism

Struvite (mag, ammonia, phosphate)
- Proteus or staph infection
- alkaline urine

Urate
- Hyperurecemia patients
- Gout, hematological malignancy, acidic urine
- Radiolucent
- Acidic urine

Cystine
- Genetic defects in reasorption of amino acids including cystine

22
Q

Adrenal adenoma Microscopy

A
  • Misoses absent or rare
  • Aldosterone Adrenal adenoma: Spironolactone bodies
  • <5cm
  • Solitary, Encapsulated Golden yellow (from lipids*)
23
Q

Adrenal carcinoma vs adenoma

A

Adrenal carcinoma
- More functional: usually virilising when functional (c.f. adenoma non-functional, asymptomatic 95%)
- Bi-modal and more common in kids than Adenoma
- Often large: 20cm (c.f. Adenoma <5cm)
- Smaller lesions may look like adenoma**

24
Q

Adrenal carcinoma RF

A
  • if seen in child must exclude Li-Fraumeni (TP53)
  • also associated with Beckwith-Wiedemann
25
Q

Prostate cancer generally what type ?

A

Acinar subtype*
Loss of the basal cell layer**

26
Q

Prostate cancer clinical presentation ?

A
  • Asymptomatic, usually detected by PSA / rectal exam
27
Q

Prostate cancer
- Aetiology

A
  • Androgen has a role (target of hormonal therapy)
  • Family history
  • High fat diet
  • BRCA2 mutation (20x)
28
Q

What causes BPH ?

A
  • Dihydrotesterone (DHT), an androgen derived from testosterone via 5-alpha-reductase is the major hormonal stimulus for hyperplasia
  • Located in stromal cells* -> spreads to epithelial cells later

Tx
- alpha-blockers
- 5-alpha-reductase inhibitors

29
Q

Wilms tumor clinical presentation

A
  • PAINLESS upper quadrant abdominal mass
  • Haematuria is seen in ~20% of cases
  • hypertension
  • von Willebrand disease is seen in
30
Q

HPV related SCC prognosis vs non-HPV related SCC

A
  • HPV related SCC has better prognosis
31
Q

How many % of nephroblastomatosis will turn into Wilms ?

A

30-40%

32
Q

Crossed fused renal ectopia which side more common ? Complications ?

A

Location
- Left-to-right (most common)

Complications
- Nephrolithiasis, infection, and hydronephrosis approaches ~50%

Associations
- ureteropelvic junction obstruction, vesicoureteral reflux, and renal multicystic dysplasia.
- Müllerian agenesis

33
Q

HIV nephropathy imaging ?

A
  • Rapidly enlarging bilateral echogenic kidneys
  • No hydronephrosis
  • Rapid renal failure
  • Striated kidneys on nephrogram
34
Q

Ureteritis cystica aetiology ?

A

Results from chronic urinary tract irritation due to stones and/or infection.
Organisms frequently involved include:
- Escherichia coli (most common)

Seen in diabetics with recurrent urinary tract infections.

35
Q

causes of Papillary necrosis ?

A

NSAIDS
Sickle cell disease
Acetominophen
Infection (TB)
Diabetes*

36
Q

Imaging of Papillary necrosis

A
  • Sloughed papillae appear as filling defects in the collecting system and ureters and may obstruct them and cause renal colic
  • “club-shaped” calices
37
Q

Causes of Medullary nephrocalcinosis

A
  • hyperparathyroidism
  • medullary sponge kidney
  • renal tubular acidosis (type 1)
  • hypervitaminosis D
  • milk-alkali syndrome
  • sarcoidosis
38
Q

Causes of Cortical nephrocalcinosis

A
  • Renal cortical necrosis (sepsis, ischemia)
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • Oxalosis
  • Vesicoureteral reflux (VUR)
39
Q

Causes of renal artery stenosis

A
  • FMD: mid to distal segment, string of pearls
  • Atherosclerosis: ostium
  • Takayasu arteritis: young woman with aortic involvement, ostium, long segment
  • NF-1: ostial and long segment
40
Q
A

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