Renal Flashcards
(111 cards)
1
Q
Benign renal tumours?
A
Angiomyolipoma
Oncocytoma
2
Q
Malignant renal tumours?
A
Clear Cell RCC (75%)
Papillary RCC (15%)
Chromophobe RCC (5%)
Collecting Duct RCC (<1%) v aggressive
3
Q
What is the most common benign renal tumour?
A
Angiomyolipoma
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
5
Q
What should be considered if there are bilateral angiomyolipomas?
A
Tuberous Sclerosis
Genes TSC1 and TSC2
6
Q
Features of oncocytoma?
A
1/3 cases have central scar
microscopically solid nests of eosinophilic cells
7
Q
Bilateral or multifocal oncocytoma should make you consider?
A
Birt-Hogg-Dube syndrome
8
Q
What accounts for 90% of primary renal malignancies?
A
RCC (90%)
9
Q
Risk factors for RCCs?
A
smoking obesity HTN acquired cystic kidney disease (from dialysis) genetic factors
10
Q
Classic presentation of RCCs?
A
Classic triad (flank pain, mass, haematuria) - only 10% Incidental CT finding- 50%
11
Q
What occurs in 30% of patients with RCC?
A
Paraneoplastic Syndromes
12
Q
Treatment of RCC?
A
If localised- partial or radical nephrectomy
If mets- surgical metastasectomy (if low volume), cytoreductive nephrectomy (? benefit)
13
Q
How many patients who undergo ‘curative’ resection for RCC still develop mets?
A
30-40%
14
Q
Inheritance pattern of Von Hippel Lindau Disease?
A
Autosomal Dominant
15
Q
What carcinomas are associated with Von Hippel Lindau disease?
A
Clear cell RCC and clear cell cysts
Retinal/ cerebellar hemangioblastomas
Pheochromocytoma
16
Q
What type of transformation is associated with a very bad prognosis?
A
Sarcomatoid transformation
17
Q
What is the name given to a nephroblastoma?
A
Wilm’s tumour
18
Q
When does Wilm’s tumour occur?
A
In childhood
98% in under 10s
19
Q
Genes associated with Wilm’s tumour?
A
WT1 and WT2 on chromosome 11
20
Q
How are Wilm’s tumours detected?
A
Often as a palpable mass
Can be very large in size
21
Q
Prognosis of Wilm’s tumour?
A
Good- over 90% long term survival
22
Q
Benign tumours of the urinary tract?
A
Urothelial papillomas
Inverted urothelial papilloma
leiomyoma
23
Q
Malignant tumours of the urinary tract?
A
Urothelial carcinoma (>90%)
SCC
Adenocarcinoma
24
Q
Epidemiology of bladder cancer?
A
Risk increases with age
50s-80s
M>W
25
Causes of haematuria?
```
Cancer (RCC, upper urothelial carcinoma, bladder cancer, advanced prostate cancer)
Stones
Infection
Inflammation
BPH (large)
```
26
Risk factors for bladder cancer?
```
smoking
occupation
pelvic radiotherapy
immunosuppression with cyclophosphamide
stones
Schistosoma haematobium infection
genetics (rarely)
```
27
Clinical features of bladder cancer?
```
haematuria (gross or microscopic)
painful micturition
urgency
frequency
weight loss, bone pain, pelvic mass
```
28
Diagnosis of bladder cancer?
USS, CT, MRI
| Histology Gold Standard
29
Urothelial Carcinoma in Situ Features?
high grade flat urothelial lesion
reddening or granularity of mucosa
diagnosed by urine cytology as cells are readily shed
30
Risk of urothelial carcinoma in situ progression?
High risk
| 50% become invasive carcinoma within 5 years
31
Treatment of urothelial carcinoma in situ?
Intravesical BCG
32
Treatment of urothelial carcinoma?
high grade superficial tumours- intravesical BCG
detrusor muscles invasive tumours- radical cystectomy or external beam radiotherapy
high risk of recurrence
33
Secondary malignant tumours of the bladder usually come from?
Prostate
Rectum
Cervix
34
What percentage of malignant bladder tumours are secondary?
15%
35
Acute pyelonephritis causative organisms?
```
E coli
proteus
Klebsiella
Enterobacter
Pseudomonas
```
36
Clinical features of acute pyelonephritis?
loin pain, fever, rigors, malaise
37
Predisposing factors for acute pyelonephritis?
urinary tract obstruction, DM, VUR, pregnancy, instrumentation
38
2 paths for pyelonephritis?
Lower urinary tract (ascending)
| Haematogenous (endocarditis)
39
Characteristics of chronic pyelonephritis?
interstitial inflammation and scarring
40
Causes of chronic pyelonephritis?
```
Chronic obstructive (unilateral or bilateral)
Reflux associated
```
41
What is hydronephrosis?
dilatation of the renal pelvis and calyces
atrophy of the renal parenchyma
caused by obstruction to urine outflow
42
Causes of obstruction that causes hydronephrosis?
Congenital
| Acquired (foreign body, tumour, BPH, inflammation)
43
When does bilateral hydronephrosis occur?
Only when obstruction occurs below the level of the ureters (e.g., BPH)
44
What occurs if hydronephrosis is left untreated?
irreversible damage and ESRF
45
Renal failure definition?
renal dysfunction resulting in elevated blood urea and creatinine and reduction in GFR with metabolic and endocrine disturbances
46
Types of renal failure?
Acute (AKI)
| Chronic (CKD)
47
Causes of renal failure?
Pre-renal - circulatory failure
Renal - Glomerular (GN, DM, amyloid), Tubular (ATN, tubulointerstitial nephritis), vascular (HTN, vasculitis)
Post-renal- obstruction
48
Acute Renal Failure Onset?
develops over days/weeks
| potentially reversible
49
Acute Renal Failure Clinical Features?
oliguria, fluid retention, symptoms of uraemia, arrhythmias, metabolic acidosis, bleeding tendency, retention of drugs, lower response to infection, lower wound healing
50
Metabolic disturbances of AKI?
```
Inc. urea
Inc. creatinine
Inc. H+
Inc. K+
Inc. PO4
Inc. Na and water retention
```
51
What is acute tubular necrosis (ATN)?
often referred to as acute tubular injury
| occurs in 3 main contexts: ischaemia, following nephrotoxic agents, damage from pigments
52
3 phases of ATN?
initiating, maintenance, recovery
53
Macroscopic appearance of ATN?
cortical pallor and swelling, medullary congestion
54
Microscopic features of ATN?
```
loss of brush border of proximal tubular epithelial cells
epithelial flattening
granular casts
tubular mitoses
interstitial oedema
```
**minimal interstitial inflammation**
55
CRF timeline?
Over months/years
| Irreversible
56
Main causes of CKD?
chronic GN, chronic pyelonephritis, DM, polycystic kidney disease, HTN, drugs, hereditary
57
Histological feature of CKD?
interstitial fibrosis
tubular atrophy
global glomerulosclerosis
58
Presentation of CKD?
Picked up incidentally
Follow up of known illnesses
Symptoms of uraemia
59
What causes renal osteodystrophy?
CRF -> phosphate retention and hypocalcaemia
- > secondary hyperparathyroidism
- >inc. osteoclast activity and bone resorption
60
Electrolyte change in CKD?
Dec. Ca, Inc. PO4, Inc. PTH
61
Characteristics of nephritic syndrome?
```
RBCs and red cell casts in urine
renal dysfunction
oliguria
oedema
HTN
```
62
Characteristics of nephrotic syndrome?
proteinuria (3.5g/24hrs)
hypo-albuminemia
oedema
hyperlipidaemia
63
Glomerular changes in renal disease?
Hypercellularity
Thickening of GBM
Crescent formation
64
Who is Minimal Change Disease common in?
Children
65
Clinical features of Minimal Change Disease?
```
selective proteinuria (nephrotic levels)
normal BP and renal function
no RBCs
```
66
Pathophysiology of Minimal Change Disease?
direct injury to podocytes due to abnormal cytokine response
67
Treatment of Minimal Change Disease?
90% respond to steroids
68
Detection of Minimal Change Disease?
Light microscopy- normal glomeruli
Immunofluorescence- negative
Electron microscopy- extensive food process effacement
69
Clinical features of Focal Segmental Glomerulosclerosis (FSGS)?
usually nephrotic levels of proteinuria (>3.5mg/24 hours)
70
Treatment of FSGS?
no cure
doesn't usually respond to steroids
recurs even post-transplant
71
Detection of FSGS?
Light microscopy- FSGS
IF- negative
EM- extensive foot process effacement
72
What is the commonest cause of nephrotic syndrome in adults?
Membranous glomerulonephritis
73
What is the pattern of progression in membranous glomerulonephritis?
1/3 remit
1/3 continue
1/3 progress to renal failure
74
Detection of membranous glomerulonephritis?
LM- thickening of glomerular capillary walls, silver stain- BM 'spikes'
IF- IgG and complement, granular along capillaries
EM- subepithelial immune-complex deposits
75
When does post-infectious glomerulonephritis occur?
4 weeks after Group A streptococcus infection classically
76
Presentation of post-infectious glomerulonephritis?
Majority are nephritic presentation
| 5-10% with nephrotic range proteinuria
77
Prognosis of post-infectious glomerulonephritis?
in children good- 95% full recovery
| in adults more variable
78
Bad prognostic factors in post-infectious glomerulonephritis?
nephrotic presentation
| crescents
79
Detection of post-infectious glomerulonephritis?
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
What is the clinical presentation of crescentic GN?
Rapidly progressive GN
81
Microscopy of Crescentic GN?
proliferation of extra capillary and inflammatory cells
82
Causes of RPGN?
Pauci-immune GN
Anti-GBM disease (Goodpasture syndrome)
Immune-complex mediated
83
What is Pauci-immune vasculitis?
systemic disorder
| characterised by inflammation of blood vessels
84
What is Pauci-immune GN usually associated with?
Anti-neutrophil circulating antibodies (ANCA)
85
How does Pauci-immune GN usually present?
Usually nephritic
| treatable if caught early
86
What is anti-GBM disease/ Goodpasture syndrome?
production of auto-antibodies against alpha 3 chain of type IV collagen which if found in glomerular BM and in the lung
87
What are the 2 major features of Goodpasture syndrome?
haemoptysis
| acute renal failure (rapidly progressive esp. in young males)
88
Treatment of anti-GBM/ GP syndrome?
plasmapheresis and immunosuppression
89
Detection of anti-GBM GN?
LM- segmental necrotising GN with crescents
IF- global linear IgG along capillary walls
EM- nothing
90
What is membranoproliferative GN?
combined nephritic/nephrotic presentation often with hypocomplementemia and progressive renal failure
91
How many types of membranoproliferative GN are there?
2
Type I
Type II- dense deposit disease
92
What percentage of membranoproliferative GN progress to ESRF?
40%
93
Detection of membranoproliferative GN?
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
What disease is related to IgA nephropathy?
Henoch-Scholein purpura (HSP)
95
Detection of IgA nephropathy?
LM- variable, usually mesangial hypercellularity
IF- mesangial IgA deposition
EM- mesangial immune deposits
96
Detection of diabetic nephropathy?
LM- mesangial expansion, capillary wall thickening and arteriolar hyalinosis
IF- none
EM- diffuse BM thickening +/- foot process effacement
97
Renal amyloidosis typically presents as?
Nephrotic range proteinuria
98
In children, who are UTIs most common in?
Uncircumcised boys
99
2 paths of UTIs?
ascent of bacteria (more common)
| haematogenous (S. aureus)
100
When are asymptomatic UTIs significant?
During pregnancy
101
In what patients would a suprapubic aspirate be most appropriate?
Neonates
102
2 media for bacterial cultures?
MacConkey's medium
| CLED medium
103
Organisms in UTI?
```
E Coli (95%)
Staph saprophyticus (2%) (sexually active young women)
Enterobacter
Pseudomonas aeruginosa
Streptococci
Enterococci
```
104
Resistant organisms?
MRSA
ESBL
CPE
VRE
105
Prevention of re-infection?
Good hygiene
fluids
frequent micturition
*********Not prophylaxis with antibiotics- only promotes resistant strains
106
Causes of relapsing UTIs?
Stones
Anatomical Abnormalities
No cause (most cases)
107
Risk factors for UTIs?
Mechanical factors
Host factors
Bacteria factors
108
Mechanical risk factors for UTIs?
```
females
obstruction
catheter
VUR
pregnancy
sexual activity
DM
neurological
```
109
Host factors for UTIs?
host antibacterial mechanisms impaired
110
Bacteria factors for UTIs?
Fimbriae
Haemolysins
Urease
111
Why should early morning urine samples be collected?
Tuberculosis
