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Flashcards in Urinary Session 10 Deck (75):
1

In which population is pathology in the medulla more commonly seen?

Young pts e.g. Kidney dysplasia

2

Pathology in which compartment of the cortex starves the nephron of blood?

Glomerulus

3

Which four compartments can be affected by cortex renal pathology?

Glomerular
Tubular (mainly PCT)
Intersticium
Vascular

4

What happens if the filter blocks in renal cortex pathology?

Decreased eGFR --> raised creatinine levels --> renal failure

5

What happens of the filter leaks in renal cortex pathology?

Proteinuria +/- haematuria

6

What damage tends to cause nephritic syndrome?

Endothelial

7

What is seen in nephritic syndrome?

Predominantly heamturia
Hypertension
Acute renal injury/failure

8

Describe the incidence of minimal change glomerulonephritis.

Seen in childhood/adolescence but incidence decreases with increasing age

9

What can minimal change glomerulonephritis cause?

Heavy proteinuria or nephrotic syndrome

10

Why is minimal change glomerulonephritis so called?

Change isn't visible on histology, needs electron microscopy

11

Does minimal change glomerulonephritis respond to steroid Tx?

Yes but may recur if stopped

12

Does minimal change glomerulonephritis usually progress to renal failure?

No

13

What is the pathogensis of minimal change glomerulonephritis?

Unknown circulating factor --> podocytes effaced and loss of filter slit diaphragms

14

Doe immune complex deposition occur in minimal change glomerulonephritis?

No

15

How does DM cause nephrotic syndrome?

Microvascular dysfunction forms mesangial nodules

16

How does focal segmental glomerulosclerosis compare to minimal change glomerulonephritis?

Adult condition with increasing incidence with increasing age
Less responsive to steroids
Visible change on histology
Leads to renal failure

17

How does focal segmental glomerulosclerosis lead to renal failure?

Unknown circulating factor --> podocytes effaced --> glomerulus scars --> renal failure

18

What pathological change is visible on histological examination of focal segmental glomerulosclerosis?

Sclerosised glomerulas

19

Does focal segmental glomerulosclerosis lead to nephrotic or nephritic syndrome?

Nephrotic

20

What is the commonest cause of nephrotic syndrome in adults?

Membranous glomerulonephritis

21

What is the 'rule of thirds' that membranous glomerulonephritis follows?

1/3 pts remit
1/3 pts don't deteriorate
1/3 pts deteriorate and need dialysis/transplant

22

What is membranous glomerulonephritis associated with?

Lymphoma and other malignancies

23

What is the pathogenesis of membranous glomerulonephritis?

Antigen and antibody (IgG) --> immune complex --> deposited subepithelial in membrane --> damage to podocytes due to body response to phospholipase A2 receptor

24

Where in the kidney does most renal pathology occur?

In the cortex

25

What is the commonest glomerulnephritis which presents at any age?

IgA nephropathy

26

What is the classical presentation of IgA nephropathy?

Visible/invisible haematuria +/- proteinuria

27

Why does IgA nephropathy have an association with mucosal infections?

These increase IgA proliferation so more is filtered in the glomerulus

28

How does the clinical course of IgA nephropathy vary?

Unknown mechanism from invisible haematuria to renal failure and dialysis

29

Is there an effective treatment for IgA nephropathy?

No

30

What is the pathogenesis of IgA nephropathy?

Increased IgA --> mesangial damage as not protected by glomerular BM --> mesangial proliferation

31

Give three hereditary nephropathies which lead to haematuria.

Thin GBM nephropathy
Benign familial nephropathy
Alpert syndrome

32

Does benign familial nephropathy lead to renal failure?

No

33

What is Alpert syndrome?

X-linked disease causing abnormal collagen IV --> deafness and thin, abnormal GBM --> renal failure in neonates

34

What is Goodpasture syndrome?

Relatively uncommon but clinically important cause of rapidly progressive glomerulonephritis causing acute and severe nephritic syndrome and pulmonary haemorrhage in smokers

35

What is the pathogenesis of Goodpasture syndrome?

IgG autoantibody to collagen IV --> attacks BM in kidney

36

How is Goodpasture syndrome treated?

Immunosuppression and plasmapheresis allow for some function retention if caught early

37

What is vasculitis?

Group of systemic disorders which does not involve immune complexes/antibody deposition which can lead to nephritic syndrome

38

What is the consequence if vasculitis is not caught early?

Rapidly progressive glomerulonephritis --> nephritic syndrome

39

What is the pathogenesis of vasculitis?

ANCA + neutrophils --> abnormal cytoplasmic activation of neutrophils --> attack endothelium --> thrombosis and necrosis --> crescent glomeruli --> renal failure

40

Describe the epidemiology of prostate cancer.

Most common cancer in men
More common in developed countries
Most pts asymptomatic with localised disease and more likely to die from CVD

41

What are the risk factors for prostate cancer?

Increasing age
FHx: 4x increase if 1st degree relative diagnosed white>Asian

42

Why is mass screening for prostate cancer not offered?

Low specificity of PSA test --> over-diagnosis, over-treatment and possible reduction in QoL due to Tx

43

What can cause raised PSA levels?

BPH
Infection
Inflammation
Prostate cancer

44

What is the usual presentation of prostate cancer?

Asymptomatic
Urinary symptoms +/- bladder inactivity
Bone pain due to metastases

45

What is the unusual clinical presentation of prostate cancer?

Haematuria in some advanced cases

46

How do pancreatic cancer bone metastases present on bone scan?

'Hot spots' as they are sclerotic

47

What is the diagnostic pathway for pancreatic cancer?

DRE+PSA --> transrectal US guided biopsy of prostate
LUTS --> transurethral resection of prostate which occasionally picks up uncommon central tumours

48

What are Tx decisions based on in pancreatic cancer?

Pt age
DRE findings
PSA level
Gleason grade from biopsy
And nodal/visceral metastases on bone scan or MRI

49

What is Gleason grading?

Low power microscopy used to examine architecture of biopsy

50

What are the established Tx available for pancreatic cancer?

Surveillance
Open/laparoscopic/robotic prostatectomy
External/low dose ratebrachytherapy (intrinsic radioactive iodine implant)
LHRH antagonists
Palliation - single dose radiotherapy, chemotherapy, bisphosphonates

51

What developmental Tx are available for prostate cancer?

High intensity focused US
Primary cryotherapy
High dose rate brachytherapy

52

Give some examples of urological causes of haematuria.

Advanced prostate cancer
Upper tract transitional cell carcinoma
Bladder cancer
BPH
Infection
Inflammation
Stones
Renal cell carcinoma

53

Is a nephrology cal or urological cause of haematuria more common in younger pts?

Nephrological (glomerular)

54

What is varicocele?

Variscose veins in scrotum which are usually prominent on the left but if prominent on the right suggest kidney tumour

55

Describe the epidemiology of bladder cancer.

4th commonest cancer in men, 11th in women who present later

56

What are 90% of bladder cancers?

Transitional cell carcinomas

57

What are the risk factors for bladder cancer?

Smoking
Occupational exposure
Schistosomiasis

58

What type of bladder cell cancer does schistosomiasis lead to?

Squamous cell carcinoma

59

What is the intitial definitive Tx for bladder cancer?

Transurethral resection and single chemotherapy dose directed at bladder

60

Describe the distribution of staging in pts presenting with bladder cancer.

75% superficial
5% in situ
20% muscle invasive

61

What mortality is associated with muscle invasive bladder cancer?

50%

62

What further Tx can be used in bladder cancer following initial resection?

Non muscle invasive: intravesical immunotherapy
Muscle invasive: neoadjuvant chemo and radical cystectomy with reconstruction if pt can self catheterise
Or radiotherapy

63

What is the 8th commonest cancer in the UK causing 95% of all upper urinary tract tumours?

Renal cell carcinoma

64

How is the incidence and mortality in renal cell carcinoma changing?

Increasing

65

What are the risk factors for developing renal cell carcinoma?

Smoking
Obesity
Dialysis

66

How does renal cell carcinoma spread?

Perinephric
Lymph nodes
IVC --> right atrium

67

What treatment is currently available for localised renal cell carcinoma?

Surveillance +/- partial or radical nephrectomy

68

What is removed in radical nephrectomy?

Kidney, adrenal, surrounding fat and upper ureter

69

What treatment is currently available for metastatic renal cell carcinoma?

Molecular therapies targeting angiogenesis (tyronase/tyrosine kinase inhibitors)
Palliative Tx

70

What causes the 5% of all upper tract carcinomas not due to renal cell carcinoma?

Upper tract transitional cell carcinoma

71

What are risk factors for developing upper tract transitional cell carcinoma?

Smoking
Phenacetin abuse
Balkan's nephropathy

72

What proportion of pts with upper tract transitional cell carcinoma will develop metastases due to spread in the urine down to the bladder?

40%

73

Where can upper tract transitional cell carcinomas be found?

Calyces
Upper ureter

74

What initial investigations are performed to identify upper tract transitional cell carcinoma?

US for hydronephrosis
CT urogram for filling defect/ureteric stricture
Retrograde pyelogram
Ureteroscopy for biopsy and cytology washings

75

What treatment is currently available for upper tract transitional cell carcinoma?

Nephro-urectomy (kidney, fat, ureter and bladder cuff)