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Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Benign renal tumours?

A

Angiomyolipoma

Oncocytoma

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2
Q

Malignant renal tumours?

A

Clear Cell RCC (75%)
Papillary RCC (15%)
Chromophobe RCC (5%)
Collecting Duct RCC (<1%) v aggressive

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3
Q

What is the most common benign renal tumour?

A

Angiomyolipoma

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4
Q

Why may angiomyolipomas get removed even though they are benign?

A

Because there is a risk of severe haemorrhage when they are large

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5
Q

What should be considered if there are bilateral angiomyolipomas?

A

Tuberous Sclerosis

Genes TSC1 and TSC2

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6
Q

Features of oncocytoma?

A

1/3 cases have central scar

microscopically solid nests of eosinophilic cells

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7
Q

Bilateral or multifocal oncocytoma should make you consider?

A

Birt-Hogg-Dube syndrome

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8
Q

What accounts for 90% of primary renal malignancies?

A

RCC (90%)

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9
Q

Risk factors for RCCs?

A 
smoking
obesity
HTN
acquired cystic kidney disease (from dialysis)
genetic factors
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10
Q

Classic presentation of RCCs?

A 
Classic triad (flank pain, mass, haematuria) - only 10%
Incidental CT finding- 50%
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11
Q

What occurs in 30% of patients with RCC?

A

Paraneoplastic Syndromes

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12
Q

Treatment of RCC?

A

If localised- partial or radical nephrectomy

If mets- surgical metastasectomy (if low volume), cytoreductive nephrectomy (? benefit)

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13
Q

How many patients who undergo ‘curative’ resection for RCC still develop mets?

A

30-40%

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14
Q

Inheritance pattern of Von Hippel Lindau Disease?

A

Autosomal Dominant

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15
Q

What carcinomas are associated with Von Hippel Lindau disease?

A

Clear cell RCC and clear cell cysts
Retinal/ cerebellar hemangioblastomas
Pheochromocytoma

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16
Q

What type of transformation is associated with a very bad prognosis?

A

Sarcomatoid transformation

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17
Q

What is the name given to a nephroblastoma?

A

Wilm’s tumour

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18
Q

When does Wilm’s tumour occur?

A

In childhood

98% in under 10s

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19
Q

Genes associated with Wilm’s tumour?

A

WT1 and WT2 on chromosome 11

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20
Q

How are Wilm’s tumours detected?

A

Often as a palpable mass

Can be very large in size

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21
Q

Prognosis of Wilm’s tumour?

A

Good- over 90% long term survival

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22
Q

Benign tumours of the urinary tract?

A

Urothelial papillomas
Inverted urothelial papilloma
leiomyoma

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23
Q

Malignant tumours of the urinary tract?

A

Urothelial carcinoma (>90%)
SCC
Adenocarcinoma

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24
Q

Epidemiology of bladder cancer?

A

Risk increases with age
50s-80s
M>W

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25
Q

Causes of haematuria?

A 
Cancer (RCC, upper urothelial carcinoma, bladder cancer, advanced prostate cancer)
Stones
Infection
Inflammation
BPH (large)
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26
Q

Risk factors for bladder cancer?

A 
smoking
occupation
pelvic radiotherapy
immunosuppression with cyclophosphamide
stones
Schistosoma haematobium infection 
genetics (rarely)
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27
Q

Clinical features of bladder cancer?

A 
haematuria (gross or microscopic)
painful micturition
urgency
frequency
weight loss, bone pain, pelvic mass
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28
Q

Diagnosis of bladder cancer?

A

USS, CT, MRI

Histology Gold Standard

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29
Q

Urothelial Carcinoma in Situ Features?

A

high grade flat urothelial lesion
reddening or granularity of mucosa
diagnosed by urine cytology as cells are readily shed

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30
Q

Risk of urothelial carcinoma in situ progression?

A

High risk

50% become invasive carcinoma within 5 years

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31
Q

Treatment of urothelial carcinoma in situ?

A

Intravesical BCG

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32
Q

Treatment of urothelial carcinoma?

A

high grade superficial tumours- intravesical BCG
detrusor muscles invasive tumours- radical cystectomy or external beam radiotherapy
high risk of recurrence

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33
Q

Secondary malignant tumours of the bladder usually come from?

A

Prostate
Rectum
Cervix

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34
Q

What percentage of malignant bladder tumours are secondary?

A

15%

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35
Q

Acute pyelonephritis causative organisms?

A 
E coli
proteus
Klebsiella
Enterobacter
Pseudomonas
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36
Q

Clinical features of acute pyelonephritis?

A

loin pain, fever, rigors, malaise

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37
Q

Predisposing factors for acute pyelonephritis?

A

urinary tract obstruction, DM, VUR, pregnancy, instrumentation

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38
Q

2 paths for pyelonephritis?

A

Lower urinary tract (ascending)

Haematogenous (endocarditis)

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39
Q

Characteristics of chronic pyelonephritis?

A

interstitial inflammation and scarring

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40
Q

Causes of chronic pyelonephritis?

A 
Chronic obstructive (unilateral or bilateral)
Reflux associated
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41
Q

What is hydronephrosis?

A

dilatation of the renal pelvis and calyces
atrophy of the renal parenchyma
caused by obstruction to urine outflow

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42
Q

Causes of obstruction that causes hydronephrosis?

A

Congenital

Acquired (foreign body, tumour, BPH, inflammation)

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43
Q

When does bilateral hydronephrosis occur?

A

Only when obstruction occurs below the level of the ureters (e.g., BPH)

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44
Q

What occurs if hydronephrosis is left untreated?

A

irreversible damage and ESRF

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45
Q

Renal failure definition?

A

renal dysfunction resulting in elevated blood urea and creatinine and reduction in GFR with metabolic and endocrine disturbances

46
Q

Types of renal failure?

A

Acute (AKI)

Chronic (CKD)

47
Q

Causes of renal failure?

A

Pre-renal - circulatory failure
Renal - Glomerular (GN, DM, amyloid), Tubular (ATN, tubulointerstitial nephritis), vascular (HTN, vasculitis)
Post-renal- obstruction

48
Q

Acute Renal Failure Onset?

A

develops over days/weeks

potentially reversible

49
Q

Acute Renal Failure Clinical Features?

A

oliguria, fluid retention, symptoms of uraemia, arrhythmias, metabolic acidosis, bleeding tendency, retention of drugs, lower response to infection, lower wound healing

50
Q

Metabolic disturbances of AKI?

A 
Inc. urea
Inc. creatinine
Inc. H+
Inc. K+
Inc. PO4
Inc. Na and water retention
51
Q

What is acute tubular necrosis (ATN)?

A

often referred to as acute tubular injury

occurs in 3 main contexts: ischaemia, following nephrotoxic agents, damage from pigments

52
Q

3 phases of ATN?

A

initiating, maintenance, recovery

53
Q

Macroscopic appearance of ATN?

A

cortical pallor and swelling, medullary congestion

54
Q

Microscopic features of ATN?

A 
loss of brush border of proximal tubular epithelial cells
epithelial flattening
granular casts
tubular mitoses
interstitial oedema

minimal interstitial inflammation

55
Q

CRF timeline?

A

Over months/years

Irreversible

56
Q

Main causes of CKD?

A

chronic GN, chronic pyelonephritis, DM, polycystic kidney disease, HTN, drugs, hereditary

57
Q

Histological feature of CKD?

A

interstitial fibrosis
tubular atrophy
global glomerulosclerosis

58
Q

Presentation of CKD?

A

Picked up incidentally
Follow up of known illnesses
Symptoms of uraemia

59
Q

What causes renal osteodystrophy?

A

CRF -> phosphate retention and hypocalcaemia

  • > secondary hyperparathyroidism
  • > inc. osteoclast activity and bone resorption
60
Q

Electrolyte change in CKD?

A

Dec. Ca, Inc. PO4, Inc. PTH

61
Q

Characteristics of nephritic syndrome?

A 
RBCs and red cell casts in urine
renal dysfunction
oliguria
oedema
HTN
62
Q

Characteristics of nephrotic syndrome?

A

proteinuria (3.5g/24hrs)
hypo-albuminemia
oedema
hyperlipidaemia

63
Q

Glomerular changes in renal disease?

A

Hypercellularity
Thickening of GBM
Crescent formation

64
Q

Who is Minimal Change Disease common in?

A

Children

65
Q

Clinical features of Minimal Change Disease?

A 
selective proteinuria (nephrotic levels)
normal BP and renal function
no RBCs
66
Q

Pathophysiology of Minimal Change Disease?

A

direct injury to podocytes due to abnormal cytokine response

67
Q

Treatment of Minimal Change Disease?

A

90% respond to steroids

68
Q

Detection of Minimal Change Disease?

A

Light microscopy- normal glomeruli
Immunofluorescence- negative
Electron microscopy- extensive food process effacement

69
Q

Clinical features of Focal Segmental Glomerulosclerosis (FSGS)?

A

usually nephrotic levels of proteinuria (>3.5mg/24 hours)

70
Q

Treatment of FSGS?

A

no cure
doesn’t usually respond to steroids
recurs even post-transplant

71
Q

Detection of FSGS?

A

Light microscopy- FSGS
IF- negative
EM- extensive foot process effacement

72
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

73
Q

What is the pattern of progression in membranous glomerulonephritis?

A

1/3 remit
1/3 continue
1/3 progress to renal failure

74
Q

Detection of membranous glomerulonephritis?

A

LM- thickening of glomerular capillary walls, silver stain- BM ‘spikes’
IF- IgG and complement, granular along capillaries
EM- subepithelial immune-complex deposits

75
Q

When does post-infectious glomerulonephritis occur?

A

4 weeks after Group A streptococcus infection classically

76
Q

Presentation of post-infectious glomerulonephritis?

A

Majority are nephritic presentation

5-10% with nephrotic range proteinuria

77
Q

Prognosis of post-infectious glomerulonephritis?

A

in children good- 95% full recovery

in adults more variable

78
Q

Bad prognostic factors in post-infectious glomerulonephritis?

A

nephrotic presentation

crescents

79
Q

Detection of post-infectious glomerulonephritis?

A

LM- diffuse global proliferative GN with neutrophils ++
IF- granular capillary walls and lesser mesangial IgG and C3
EM- scattered subepithelial ‘hump shaped’ deposits +/- mesangial deposits

80
Q

What is the clinical presentation of crescentic GN?

A

Rapidly progressive GN

81
Q

Microscopy of Crescentic GN?

A

proliferation of extra capillary and inflammatory cells

82
Q

Causes of RPGN?

A

Pauci-immune GN
Anti-GBM disease (Goodpasture syndrome)
Immune-complex mediated

83
Q

What is Pauci-immune vasculitis?

A

systemic disorder

characterised by inflammation of blood vessels

84
Q

What is Pauci-immune GN usually associated with?

A

Anti-neutrophil circulating antibodies (ANCA)

85
Q

How does Pauci-immune GN usually present?

A

Usually nephritic

treatable if caught early

86
Q

What is anti-GBM disease/ Goodpasture syndrome?

A

production of auto-antibodies against alpha 3 chain of type IV collagen which if found in glomerular BM and in the lung

87
Q

What are the 2 major features of Goodpasture syndrome?

A

haemoptysis

acute renal failure (rapidly progressive esp. in young males)

88
Q

Treatment of anti-GBM/ GP syndrome?

A

plasmapheresis and immunosuppression

89
Q

Detection of anti-GBM GN?

A

LM- segmental necrotising GN with crescents
IF- global linear IgG along capillary walls
EM- nothing

90
Q

What is membranoproliferative GN?

A

combined nephritic/nephrotic presentation often with hypocomplementemia and progressive renal failure

91
Q

How many types of membranoproliferative GN are there?

A

2
Type I
Type II- dense deposit disease

92
Q

What percentage of membranoproliferative GN progress to ESRF?

A

40%

93
Q

Detection of membranoproliferative GN?

A

LM- diffuse global endocapillary hypercellularity with thickening of capillary walls
IF- IgG and IgM complement, granular capillary wall and mesangium
EM- subendothelial and mesangial complexes with reduplication of the GBM

94
Q

What disease is related to IgA nephropathy?

A

Henoch-Scholein purpura (HSP)

95
Q

Detection of IgA nephropathy?

A

LM- variable, usually mesangial hypercellularity
IF- mesangial IgA deposition
EM- mesangial immune deposits

96
Q

Detection of diabetic nephropathy?

A

LM- mesangial expansion, capillary wall thickening and arteriolar hyalinosis
IF- none
EM- diffuse BM thickening +/- foot process effacement

97
Q

Renal amyloidosis typically presents as?

A

Nephrotic range proteinuria

98
Q

In children, who are UTIs most common in?

A

Uncircumcised boys

99
Q

2 paths of UTIs?

A

ascent of bacteria (more common)

haematogenous (S. aureus)

100
Q

When are asymptomatic UTIs significant?

A

During pregnancy

101
Q

In what patients would a suprapubic aspirate be most appropriate?

A

Neonates

102
Q

2 media for bacterial cultures?

A

MacConkey’s medium

CLED medium

103
Q

Organisms in UTI?

A 
E Coli (95%)
Staph saprophyticus (2%) (sexually active young women)
Enterobacter
Pseudomonas aeruginosa
Streptococci
Enterococci
104
Q

Resistant organisms?

A

MRSA
ESBL
CPE
VRE

105
Q

Prevention of re-infection?

A

Good hygiene
fluids
frequent micturition
*******Not prophylaxis with antibiotics- only promotes resistant strains

106
Q

Causes of relapsing UTIs?

A

Stones
Anatomical Abnormalities
No cause (most cases)

107
Q

Risk factors for UTIs?

A

Mechanical factors
Host factors
Bacteria factors

108
Q

Mechanical risk factors for UTIs?

A 
females
obstruction
catheter
VUR
pregnancy
sexual activity
DM
neurological
109
Q

Host factors for UTIs?

A

host antibacterial mechanisms impaired

110
Q

Bacteria factors for UTIs?

A

Fimbriae
Haemolysins
Urease

111
Q

Why should early morning urine samples be collected?

A

Tuberculosis

Pathology (13 decks)

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