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Renal System > Patho > Flashcards

Patho Flashcards

1
Q

What are 5 causes of Chronic renal failure?

A

1) Diabetic nephropathy
2) Glomerulonephritis
3) Hypertension
4) Interstitial nephritis
5) Chronic urinary outflow tract obstruction
6) Pyelonephritis
7) Polycystic kidney disease
8) Other congenital kidney diseases / malformations
9) Tumours
10) Unknown

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2
Q

What are 6 systemic manifestations/complicates of end stage renal disease?

A

1) Fluid and electrolytes
– Dehydration and fluid overload
– Anaemia
– Hyperkalaemia
– Metabolic acidosis

2) Calcium, phosphate and bone
– Hyperphosphataemia
– Hypocalcaemia (but later may have hypercalcaemia)
– Secondary hyperparathyroidism
– Renal osteodystrophy

3) Haematologic
– Anaemia
– Bleeding diathesis

4) Cardiopulmonary
– Hypertension
– Heart failure
– Cardiomyopathy
– Pulmonary oedema
– Uraemic pericarditis

5) Gastrointestinal
– Nausea and vomiting
– Bleeding
– Oesophagitis, gastritis, colitis

6) Neuromuscular
– Myopathy
– Peripheral neuropathy
– Encephalopathy

7) Skin
– Dermatitis
– Pruritus (itch)
– Sallow colour

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3
Q

What are 3 treatment options for chronic renal failure?

A

1) Haemodialysis
– Involves removal of solutes across a semi-permeable membrane within a dialysis
machine, from blood circulated through an extra-corporeal circuit

2) Peritoneal dialysis
– Involves removal of solutes across the peritoneal membrane into peritoneal dialysate
fluid.

3) Renal transplant
- need to be on immunosuppressive therapy for life

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4
Q

In chronic renal failure, both kidneys are (small, contracted/large and hypertrophic). The histological features include: (3).

A

Small and contracted kidneys (bilateral)

1) Widespread glomerulosclerosis
2) Tubular atrophy
3) Interstitial fibrosis

  • Urine volume may be normal(ish) initially, or may even have polyuria as tubules cannot concentrate glomerular filtrate.
  • Terminal oliguria when no functioning nephrons left.
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5
Q

In acute renal failure, there is:
i) Oliguria/anuria: ____________________

ii) Azotaemia: ________________________

A

Oligo/Anuria: marked ↓ in/absence of urine production

Azotaemia: Progressive/rapid ↑serum creatinine

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6
Q

What are 3 pre-renal causes of ARF?

A
  1. Hypotension
  2. Haemorrhage
  3. Severe dehydration
  4. Shock
  5. Heart disease
  6. Liver failure
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7
Q

What are 3 renal causes of ARF?

A
  1. Glomerulonephritis
  2. Acute tubular necrosis (due to drugs, toxins, pigment, etc)
  3. Acute interstitial nephritis
  4. Haemolytic uraemic syndrome
  5. Vasculitis
  6. Severe infections (eg. pyelonephritis, bilateral)
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8
Q

What are 2 post-renal causes of ARF?

A

1) Acute urinary tract outlet obstruction (eg. due to blood clots, stones, tumour, etc)

2) Acute atonia, hypotonia of the bladder to the nerve damage (neurogenic bladder)

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9
Q

What are 4 Ix for renal failure?

A

1) Blood tests:
- urea, creatinine, electrolytes

2) Urine tests:
- Protein, Hb, Myoglobin, RBC, WBC

3) Imaging:
- IVU, US KUB, CT urogram, CT/MRI, etc.

4) Kidney biopsy

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10
Q

What are 3 examples of renal disease?

A

1) Glomerular disease
2) Tubulo-interstitial disease
3) Vascular disease

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11
Q

What are 5 clinical presentations of glomerular disease?

A

1) Nephrotic syndrome
2) Nephritic syndrome
3) Microscopic hematuria
4) Proteinuria
5) ARF
6) CRF

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12
Q

What is nephrotic syndrome?

A

A leaky glomerular filter

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13
Q

What are 5 clinical manifestations of nephrotic syndrome?

A

1) Heavy proteinuria
2) Hypoalbuminemia
3) Anasarca
- generalised edema due to ↓serum oncotic P
4) Lipiduria
5) Hyperlipidemia (bi-product of hepatic albumin synthesis)
6) Polyuria with frothy urine (due to large amounts of protein in urine)

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14
Q

What are 2 complications of nephrotic syndrome?

A

1) Infection
2) Thromboembolism (loss of anticoagulants)

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15
Q

Why is the age of the px important in the differential diagnosis of nephrotic syndrome?

A

Causes of nephrotic syndrome in children and adults often differ

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16
Q

Px with nephrotic syndrome may be classified as steroid-sensitive or steroid-resistant. Childhood nephrotic syndrome is almost always _________________.

A

Childhood almost always steroid-sensitive

only if the child does not respond to treatment, will a renal biopsy be performed.

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17
Q

What is nephritic syndrome?

A

Glomeruli are damaged - some are unable to filter; others leaky

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18
Q

What are 5 clinical manifestations of nephritic syndrome?

A

1) Oliguria
2) Azotaemia
3) Oedema (usually not as prominent as in nephrotics)
4) Hypertension ← fluid retention
5) Gross hematuria
6) Proteinuria - mild to moderate, sometimes in nephrotic range

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19
Q

What are 3 complications of nephritic syndrome?

A

1) Hypertensive encephalopathy
- seizures
- strokes

2) Fluid overload
- CHF
- acute pulmonary edema

3) Acute kidney impairment
- uraemia
- HyperK+, HyperPO4
- HypoCa2+

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20
Q

What is glomerulonephritis?

A

“Inflammation of the glomeruli”
- diseases characterized by increased glomerular cellularity caused by proliferation of indigenous cells and/or leucocyte infiltration.

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21
Q

What are 3 antibody-mediated mechanisms for glomerular injury?

A

1) In situ formation of immune complexes
- against native antigen eg. Anti-GBM disease (Goodpasture’s Disease).
- against planted antigen that localises in glomerulus eg. HBV.

2) Circulating immune complexes
- antigen in excess of antibody leads to circulating immune complexes that get lodged in the glomeruli eg. Lupus nephritis.

3) Antineutrophil Cytoplasmic Antibodies (ANCA)
- antibodies bind to the neutrophils in glomeruli
→ release toxic granules and substances in the glomeruli
→ glomerular damage.

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22
Q

What are 2 Ix for mechanisms of glomerular injury?

A

1) IF
- Allows determination of what types of antibody and complement involved

2) EM
- Allows more precise localisation of immune complexes
– Allows identification of ultrastructural pathology eg. GBM abnormalities

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23
Q

What are 3 microscopy methods used in a renal biopsy?

A

1) LM: formalin
2) IF: Fresh
3) EM: Glutaraldehyde

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24
Q

What are 4 causes of nephrotic syndrome?

A

Common:
1. Minimal change disease
2. Idiopathic focal segmental glomerulosclerosis (FSGS)
3. Membranous glomerulonephritis.

Uncommon:
1. Membranoproliferative glomerulonephritis.
2. IgA nephropathy

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25
Q

True or false:
Minimal Change Disease is the most common cause of childhood nephrotic syndrome. It has a very good prognosis as it is curable with steroids.

A

True

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26
Q

What is the etiology and pathogenesis of Minimal Change Disease?

A

Unknown

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27
Q

In Minimal Change Disease:
Proteinuria: (±)
LM: __________
IF: ________________
EM:_______________

A

In Minimal Change Disease:
Proteinuria: Selective
LM: no abnormality
IF: no deposits
EM: fusion of foot processes and occasionally detachment from basement membrane

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28
Q

Focal Segmental Glomerulosclerosis causes (nephritic/nephrotic) syndrome and is steroid (sensistive/resistant).

A

FSG:
Nephrotic
Steroid Resistant

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29
Q

What is the etiology and pathogenesis of Focal Segmental Glomerulosclerosis?

A

Idiopathic and 2° causes
- podocyte injury w loss of podocytes

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30
Q

In Focal Segmental Glomerulosclerosis:
Proteinuria: (±)
LM: __________
IF: ________________
EM:_______________

A

In Focal Segmental Glomerulosclerosis:
Proteinuria: +
LM: segmental sclerosis of glomeruli
IF: sclerotic lesions stain w IgM and C3
EM: loss of podocytes

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31
Q

True or false: Focal segmental glomerulosclerosis, though steroid resistant, can be treated and often do not progress to chronic renal failure.

A

False, many progress to chronic renal failure

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32
Q

What is the most common cause of nephrotic syndrome in children?

A

MCD

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33
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous Glomerulopathy

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34
Q

In Membranous glomerulopathy:
Proteinuria: (±)
LM: __________
IF: ________________

A

In Membranous glomerulopathy:
Proteinuria: +
LM: basement membrane thickening
IF: IgG and C3 on the epi-membranous side of basement membrane (“spikes” or “string of pearl appearance”).

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35
Q

What are 3 causes of nephritic syndrome?

A

Usually glomerulonephritis:
1. IgA nephropathy
2. Post-infectious glomerulonephritis
3. Lupus nephritis
4. Membranoproliferative glomerulonephritis

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36
Q

What is the most common cause of glomerulonephritis?

A

IgA nephropathy

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37
Q

What are 2 microscopic features of IgA nephropathy?

A

1) Microscopic proteinuria w hematuria

2) Mesangial proliferation with mesangial deposits of immune complexes containing IgA

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38
Q

What is post-infectious glomerulonephritis?

A

Glomerulonephritis follows infection by nephritogenic strains of streptococci, classically streptococcal pharyngitis.

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39
Q

In Post-infectious Glomerulonephritis:
(Nephrotic/Nephritic)
LM: __________
IF: ________________
EM: ________________

A

In Post-infectious Glomerulonephritis:
Nephritic
LM: diffuse proliferative changes
IF: Granular IgG and C3
EM: sub-epithelial humps of large electron-dense deposits

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40
Q

What is Lupus Nephritis?

A

2° SLE
- any clinical/histological pattern
- aggressive forms a/w proliferative changes, present w nephritic syndrome and may have crescents
- membranous variant present w nephrotic syndrome

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41
Q

What is seen on an IF of lupus nephritis?

A

“Full house” pattern
IgG, IgA, IgM, C1q, C3

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42
Q

In Membranoproliferative Glomerulonephritis:
(Nephrotic/nephritic)
LM: ______________
a/w: ________________

A

In Membranoproliferative Glomerulonephritis:
BOTH Nephrotic/nephritic
LM: proliferative changes involving mesangium + thickening of basement membrane
a/w: ↓serum C3

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43
Q

In which condition is Crescentic glomerulonephritis seen?

A

1) Post-infectious glomerulonephritis (most commonly rapidly progressive)

2) Goodpasture’s

3) Other RPGN (eg. ANCA related)

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44
Q

Rapidly Progressive Glomerulonephritis requires _________________, otherwise all progress to ______________.

A

Requires immunosuppressive treatment, otherwise all progress to renal failure

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45
Q

How is RPGN classified?

A

IF staining pattern:
1) IF+
- immune complex proliferative GN, but if linear pattern, due to anti-GBM disease.

2) IF- (pauci-immune)
- due to systemic vasculitis. (ANCA-related)

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46
Q

What is Goodpasture’s syndrome?

A

Anti-glomerular basement membrane disease
- antigen is part of D-chain of Type IV collagen

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47
Q

What organs are most commonly affected in Goodpasture’s syndrome?

A

Kidney and Lungs (both have basement membrane with similar type 4 collagen)

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48
Q

In Goodpasture’s syndrome:
LM: ________________
IF: _________________

A

In Goodpasture’s syndrome:
LM: Crescentic glomerulonephritis
IF: linear immunofluoresence for IgG

49
Q

What is amyloidosis?

A

Extracellular accumulation of fibrillary proteins which show positive staining with the Congo red stain, with apple green birefringence under polarised light examination.

In the kidney, usually occurs in patients with either:
– Plasma cell dyscrasia (AL amyloid)
– Chronic inflammatory diseases or neoplasms (AA amyloid)

50
Q

What is the most likely diagnosis for a renal biopsy that shows:
1) Amorphous material in glomerulus, arteriole and interstitium

2) Congo Red positive

3) Apple green birefringence under polarised light

A

Amyloidosis

51
Q

True or false:
Acute mild hypertension can commonly cause hypertensive nephrosclerosis.

A

False.
Only common in px with long standing, poorly controlled HTN

52
Q

In hypertensive nephrosclerosis,
Proteinuria: (±)
Arterioles show _____________
Arteries show ______________

A

In hypertensive nephrosclerosis,
Proteinuria: low grade till 2° FSGS
Arterioles show hyalinosis ± muscular thickening
Arteries show arteriosclerosis

53
Q

What are 2 histological findings in a renal biopsy of a px with malignant hypertension?

A

1) Fibrinoid necrosis of arterioles and glomeruli

2) Mucoid intimal thickening of arteries

54
Q

What is the commonest cause of ESRD in SG?

A

Diabetic nephropathy

55
Q

What is the pathogenesis of diabetic nephropathy

A

Hyperglycemia leads to the non-enzymatic glycosylation of collagen and other glomerular matrix and GBM proteins. Also occurs in blood vessels in the kidney.

56
Q

What are 7 histological findings in diabetic nephropathy?

A

Glomeruli:
1) GBM thickening (EM)
2) Mesangial widening (↑matrix and cells → Kimmelstiel-Wilson nodules)
3) Hyalinosis lesions (protein insudation)
4) Microaneurysms of glomerular capillary loops.
5) Eventually, glomerular sclerosis.

Tubules:
6) Thickened tubular basement membranes
7) Tubular atrophy

Interstitium
8) Interstitial fibrosis

Vessels:
9) Arteriolar hyalinosis
10) Arteriosclerosis

57
Q

Diabetic nephropathy predisposes a patient to ___________

A

Pyelonephritis

58
Q

What are 4 congenital malformations of the kidney?

A

Size/number:
1) Renal Agenesis
- bilateral → die
- unilateral → opp. kidney hypertrophy (compensate)

2) Renal hypoplasia
- small, ↓lobules and calyces
- oligomeganephronia (hypertrophic glomeruli)
- Primitive glomeruli and tubules in dense fibrous or fatty interstitium

Position/shape:
3) Displacement of kidneys
- within pelvis → kinking of ureters →obstruction + UTI

4) Horseshoe kidney
- fusion of lower/upper poles
- complication → renal calculi

59
Q

What are 3 types of cystic kidney diseases?

A

1) Cystic renal dysplasia
2) Polycystic kidney disease (AD/AR)
3) Medullary cystic disease
4) Acquired cystic disease
5) Localised/simple renal cysts
6) Misc.

60
Q

What is the pathogenesis of cystic renal dysplasia?

A

abnormal metanephric differentiation, with persistence of primitive / abnormal structures.

61
Q

Cystic renal dysplasia is often:
(uni/bilateral)
a/w___________

A

Both uni and bilateral
a/w other abnormalities (eg. ureteric atresia, agenesis)

62
Q

What is the gross finding of cystic renal dysplasia?

A

Enlarges, irregular kidneys that are multicystic

63
Q

What are 3 microscopic features of cystic renal dysplasia?

A

1) Lobar disorganisation

2) Multiple cysts lined by flattened epithelium

3) Presence of primitive / immature structures:
- Islands of undifferentiated mesenchymal cells.
- Islands of cartilage tissue.
- Primitive ductal structures.

64
Q

In polycystic kidney disease,
AD affects (adults/children)
AR affects (adults/children)

A

AD: Adults
AR: Children

65
Q

AD Polycystic kidney disease usually ends in ___________ due to mutations in ______________ genes.

A

Ends in renal failure due to loss of parenchyma over time with multiple cysts (in mid to late adulthood)

Due to mutations in PKD1 and 2 (code for Polycystin-1 and 2 proteins)

66
Q

What is 1 primary and 3 secondary causes of urolithiasis?

A

Primary:
- Supersaturation of urine w crystalline material (most commonly calcium salts)

Secondary:
1) UTI
- Crystalline material encrust on a necrotic focus

2) Indwelling catheter or foreign body in the bladder

3) Vitamin A deficiency producing squamous metaplasia of upper urinary tract mucosa.

4) Low urinary pH predisposes to formation of uric acid stones

67
Q

What are 3 types of renal calculi?

A

1) #1 Calcium (eg. calcium oxalate)

2) Triple stones (15%)
(Magnesium ammonium phosphate)
- follow infections

3) Urate stones (5-10%)
- px w gout and leukemia

4) Cysteine stones (1-2%)
- a/w genetic defect in renal transport/amino acids

68
Q

What is the pathogenesis of “Triple stones” (Magnesium ammonium phosphate)?

A

A/w infections bt urea splitting bacteria (eg. PROTEUS)

Urea converted to ammonia → alkaline urine → precipitation of Magnesium ammonium phosphate salts → massive stones (staghorn calculi)

69
Q

What type of calculi are staghorn calculi?

A

Magnesium ammonium phosphate stones (usually due to proteus infection)

70
Q

What is the most common cause of calcium oxalate stones?

A

Idiopathic

  • also a/w hypercalcaemia due to hyperparathyroidism, diffuse bone disease, vitamin D intoxication, sarcoidosis, milk-alkali syndrome, renal tubular acidosis of Cushing’s syndrome
71
Q

What are 2 mechanisms/ pathogenesis of idiopathic hypercalciuria?

A

1) Absorptive hypercalciuria: hyperabsorption of calcium from the intestine, with prompt increased renal output without hypercalcaemia.

2) Renal hypercalciuria due to intrinsic impairment in renal tubular reabsorption of calcium

72
Q

What are 4 sequelae/effect of renal calculi?

A

1) Urinary stasis → necrosis or renal failure (depending where)
2) Ulceration
3) Bleeding
4) Infection
5) Pain
6) Fistula formation

73
Q

What are 4 disorders of the renal tubules/interstitium?

A

1) Acute tubular necrosis
2) Acute interstitial nephritis
3) Acute pyelonephritis
4) Chronic pyelonephritis
5) Xanthogranulomatous pyelonephritis
6) Tuberculosis
7) Sarcoidosis
8) Neoplastic infiltrates (leukemias, myeloma, etc.)

74
Q

What is the most common cause of ARF?

A

Acute tubular necrosis

75
Q

Acute tubular necrosis is (reversible/irreversible) in most cases and (not) associated with necrosis of glomeruli or adjacent renal cortical tissue.

A

Acute tubular necrosis is reversible in most cases if the cause is corrected, as the damaged / dead tubular epithelial cells can be replaced by regenerating residual viable cells.

And NOT a/w necrosis of glomeruli or adjacent renal cortical tissue (unlike zonal infarction of the kidney or renal cortical necrosis).

76
Q

What are the 3 phases of acute tubular necrosis?

A
  1. Oliguric phase:
    Renal failure, oliguria
  2. Polyuric phase:
    Polyuria, tubular cells regenerating
  3. Recovery phase:
    Renal function recovering
77
Q

What are 6 causes of acute tubular necrosis?

A

Ischaemic causes: (hypotension/hypovolemia and reduced renal perfusion)
1) Shock
2) Hemorrhage
3) Major surgery
4) Severe burns
5) Dehydration

Toxic causes:
1) Endogenous products
2) Drugs
3) Heavy metals
4) Organic solvents
5) Others (eg. venom)

78
Q

What are 2 histological features of acute tubular necrosis?

A

1) The tubular epithelial cells show varying degrees of:
– Swelling
– Vacuolation
– Flattening
– Sloughing
– Loss of PAS-positive brush border
– Necrosis

2) There may also be tubular dilation and interstitial oedema

79
Q

What are 3 causes of acute interstitial nephritis?

A

1) #1 Drugs
2) Toxins
3) Metabolites
4) Autoimmune
5) Non-renal infections
6) Idiopathic

80
Q

In px with acute interstitial nephritis,
px present with ___________
urinalysis show ______________

A

Acute interstitial nephritis:
present with variable degrees of renal impairment and often ARF
Urinalysis show RBC, WBC, eosinophils, mild proteinuria

81
Q

What is the pathogenesis of drug-induced acute interstitial nephritis?

A

Usually allergic or T-cell mediated HS rxn to antibiotics, diuretics, NSAIDs

82
Q

What are 3 common presentations of drug-induced acute interstitial nephritis?

A

1) Fever
2) Rash
3) Hematuria
4) Proteinuria
5) Eosinophilia
6) Renal impairment/failure

83
Q

What is acute pyelonephritis?

A

Infection of the kidney
(usually due to bacterial infection)

84
Q

What are 2 ways bacteria can reach and infect the kidney, causing acute pyelonephritis?

A

1) Ascending/Retrograde spread from bladder
- more common
- predisposing factors:
a) Lower UT obstruction
b) Vesicoureteric reflux
c) DM
d) pregnancy

2) Hematogenous spread
- less common

85
Q

What are 4 clinical features of acute pyelonephritis?

A

1) Chills, fever
2) Flank tenderness and pain
3) Dysuria
4) Frequency of micturition
5) Often >100,000 / ml bacteria in urine
6) Pyuria (may have pus casts)

86
Q

What are 3 complications of acute pyelonephritis?

A

1) ARF
2) Septicemia
3) Pyonephrosis
4) Perinephric abscess

87
Q

What are 2 causes of chronic pyelonephritis?

A

1) Vesico-ureteric reflux
- Reflux of urine from bladder, up the ureter, to the kidney

– Predisposes to recurrent kidney inflammation and progressive scarring (usually more prominent at the renal poles)

– Usually begins in childhood

2) Obstruction
- Predisposes to recurrent kidney infection and progressive scarring

88
Q

What are 2 gross and 2 histological findings in chronic pyelonephritis?

A

Gross:
1) Cortical depression
2) “flea-bitten” appearance

Micro:
1) Thyroidisation
2) Tubular atrophy
3) Pericapsular fibrosis

89
Q

Xanthogranulomatous pyelonephritis mimics _________.

A

Renal cell carcinoma

90
Q

What is the most common causative organism of xanthogranulomatous pyelonephritis?

A

Proteus

91
Q

Xanthogranulomatous pyelonephritis:

Gross features (1)
Microscopic (2)

A

Gross: Enlarged kidney, replaced by yellow nodules with firm, grayish white tissue.

Micro: Foam cells, giant cells, lymphocytes, plasma cells

92
Q

What is hydronephrosis?

A

Dilatation of renal pelvis and calyces with progressive enlargement of the kidney with parenchymal atrophy due to obstruction of urine outflow

93
Q

What are 2 gross and 3 microscopic features of hydronephrosis?

A

Gross:
1) Enlarged kidney
2) Renal cortex thinned and atrophic

Micro:
1) Dilated tubules and bowman’s spaces
2) Flattened tubular epithelium
3) Tubular atrophy w fibrosis
4) Disappearance of glomeruli

94
Q

What is pyonephrosis?

A

Infected hydronephrosis with frank pus in the dilated calyces and pelvis.

95
Q

What is pyoureter?

A

Hydroureter infected and contains pus.

96
Q

What are 4 causes of obstruction in the urinary system?

A

Congenital Anomalies:
1) Urethral valves/strictures
2) Bladder neck obstruction
3) Uretero-pelvic junction narrowing or obstruction

Acquired Obstruction:
4) Benign prostatic hypertrophy
5) Calculi
6) Tumours – carcinoma of prostate, bladder tumours, carcinoma of cervix or uterus
7) Inflammation of prostate, ureter, urethra
8) Sloughed papillae or blood clots

Functional disorder:
9) Neurogenic (spinal cord damage)
10) Functional obstruction along urinary tract.

97
Q

What are 3 malignant tumours of the kidney?

A

1) Renal cell carcinoma (85%)
2) Urothelial carcinoma
3) Nephroblastoma (Wilms tumour) in children

98
Q

What is a benign tumour of the kidney?

A

Angiomyolipoma

99
Q

Where do renal cell carcinomas arise from?

A

Tubular epithelium

100
Q

Clear cell RCC may be sporadic (most common) or a/w _______________________

A

von Hippel Lindau (VHL) syndrome (Associated with chromosome 3p deletions and mutations of the VHL gene).

101
Q

What are 2 clinical features of Renal Cell Carcinoma?

A

1) Painless haematuria.
2) Mass in flank.
3) Fever due to necrosis.

102
Q

What are 2 types of renal cell carcinoma?

A

1) Clear cell RCC.
2) Papillary RCC.
3) Chromophobe RCC

103
Q

What are 3 gross features of clear cell RCC?

A

1) Solitary, unilateral, with a circumscribed appearance.
2) Yellowish cut surfaces with foci of necrosis and haemorrhage.
3) Invasion of renal vein not uncommon.
4) Tendency to metastasize widely; metastasis may be late.

104
Q

What are 2 microscopic features of clear cell RCC?

A

1) Polygonal cells with clear cytoplasm.
2) Delicate branching vasculature.
3) Invasion of renal vein and its branches may be seen.

105
Q

True or false:
Urothelial carcinoma may be non-invasive or invasive and only involves areas lined by urothelium. It may be multifocal and grossly and microscopically identical to urothelial carcinoma of bladder.

A

True
May be non-invasive papillary urothelial carcinoma or invasive urothelial carcinoma.

Involves the areas of the kidney lined by urothelium i.e. pelvi-calyceal system.

May be multifocal, and also associated with urothelial carcinoma of the ureter and bladder.

Grossly and microscopically identical to urothelial carcinoma of the bladder.

106
Q

What is Wilms tumour?

A

Nephroblastoma
Paediatric tumor usually diagnosed between ages of 2 and 5 years.

  • a/w congenital malformations – WAGR syndrome, Denys-Drash Syndrome and Beckwith-Wiedemann syndrome.
107
Q

What are 2 clinical feature of Wilms tumour?

A

1) Large abdominal mass.
2) Fever due to necrosis and hemorrhage

108
Q

What is the treatment of choice for Wilms tumour?

A

Combination nephrectomy and chemotherapy
- good prognosis even for tumors that have spread beyond the kidney

109
Q

What is a gross features of Wilms tumour?

A

Well circumscribed grayish white, soft mass.
- Begins in renal cortex and replaces entire kidney

110
Q

What are 3 microscopic features of Wilms tumour?

A

1) Sheets of small blue cells (blastemal component)
2) Abortive tubular and glomeruloid structures (epithelial component)
3) Spindle-shaped cells (stromal component).
4) Heterologous elements such as striated/smooth muscle and cartilage may be found

111
Q

Where do Wilms tumours usually spread to?

A

1) Lungs
2) Liver
3) Brain
4) Lymph nodes
- both hematogenous and lymphatic spread

112
Q

What is the most common mesenchymal tumour of the kidney?

A

Angiomyolipoma

113
Q

What is a angiomyolipoma?

A

Benign mesenchymal tumour composed of a combination of adipose cells, myoid spindle cells and blood vessels, in varying proportions.

114
Q

Can angiomyolipoma be accurately diagnosed on CT?

A

Yes, because of its fat content

115
Q

What is the gross appearance of angiomyolipoma?

A

Unencapsulated.
Variegated cut surfaces, with yellow (fatty) areas

116
Q

What is a microscopic finding of angiomyolipoma?

A

Mixture of myoid spindle and epithelioid cells, adipocytes and blood vessels, often thick-walled.

The myoid cells show immunostaining for HMB-45.

117
Q

What are 2 risk factors for bladder carcinomas?

A

Non-occupational:
1) Cigarette smoke
2) Schistosomiasis
3) Cyclophosphamide
4) Phenacetin

Occupational
1) 2-Napthylamine
2) 4-aminobiphenyl
3) Benzidine

118
Q

What are 3 malignant tumours affecting the bladder?

A

1) Papillary urothelial carcinoma (non-invasive)
2) Invasive urothelial carcinoma
3) Squamous cell carcinoma
4) Adenocarcinoma
5) Other types are rare

119
Q

What are 2 benign tumours of the bladder?

A

1) Papilloma
2) Inverted papilloma
3) Nephrogenic adenoma

Renal System (8 decks)

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