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Semester 3 > Urinary Session 10 > Flashcards

Urinary Session 10 Flashcards

1
Q

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

A

Young pts e.g. Kidney dysplasia

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2
Q

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

A

Glomerulus

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3
Q

Which four compartments can be affected by cortex renal pathology?

A

Glomerular
Tubular (mainly PCT)
Intersticium
Vascular

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4
Q

What happens if the filter blocks in renal cortex pathology?

A

Decreased eGFR –> raised creatinine levels –> renal failure

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5
Q

What happens of the filter leaks in renal cortex pathology?

A

Proteinuria +/- haematuria

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6
Q

What damage tends to cause nephritic syndrome?

A

Endothelial

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7
Q

What is seen in nephritic syndrome?

A

Predominantly heamturia
Hypertension
Acute renal injury/failure

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8
Q

Describe the incidence of minimal change glomerulonephritis.

A

Seen in childhood/adolescence but incidence decreases with increasing age

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9
Q

What can minimal change glomerulonephritis cause?

A

Heavy proteinuria or nephrotic syndrome

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10
Q

Why is minimal change glomerulonephritis so called?

A

Change isn’t visible on histology, needs electron microscopy

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11
Q

Does minimal change glomerulonephritis respond to steroid Tx?

A

Yes but may recur if stopped

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12
Q

Does minimal change glomerulonephritis usually progress to renal failure?

A

No

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13
Q

What is the pathogensis of minimal change glomerulonephritis?

A

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

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14
Q

Doe immune complex deposition occur in minimal change glomerulonephritis?

A

No

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15
Q

How does DM cause nephrotic syndrome?

A

Microvascular dysfunction forms mesangial nodules

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16
Q

How does focal segmental glomerulosclerosis compare to minimal change glomerulonephritis?

A

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

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17
Q

How does focal segmental glomerulosclerosis lead to renal failure?

A

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

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18
Q

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

A

Sclerosised glomerulas

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19
Q

Does focal segmental glomerulosclerosis lead to nephrotic or nephritic syndrome?

A

Nephrotic

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20
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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21
Q

What is the ‘rule of thirds’ that membranous glomerulonephritis follows?

A

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

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22
Q

What is membranous glomerulonephritis associated with?

A

Lymphoma and other malignancies

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23
Q

What is the pathogenesis of membranous glomerulonephritis?

A

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

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24
Q

Where in the kidney does most renal pathology occur?

A

In the cortex

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25
Q

What is the commonest glomerulnephritis which presents at any age?

A

IgA nephropathy

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26
Q

What is the classical presentation of IgA nephropathy?

A

Visible/invisible haematuria +/- proteinuria

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27
Q

Why does IgA nephropathy have an association with mucosal infections?

A

These increase IgA proliferation so more is filtered in the glomerulus

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28
Q

How does the clinical course of IgA nephropathy vary?

A

Unknown mechanism from invisible haematuria to renal failure and dialysis

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29
Q

Is there an effective treatment for IgA nephropathy?

A

No

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30
Q

What is the pathogenesis of IgA nephropathy?

A

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

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31
Q

Give three hereditary nephropathies which lead to haematuria.

A

Thin GBM nephropathy
Benign familial nephropathy
Alpert syndrome

32
Q

Does benign familial nephropathy lead to renal failure?

A

No

33
Q

What is Alpert syndrome?

A

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

34
Q

What is Goodpasture syndrome?

A

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

35
Q

What is the pathogenesis of Goodpasture syndrome?

A

IgG autoantibody to collagen IV –> attacks BM in kidney

36
Q

How is Goodpasture syndrome treated?

A

Immunosuppression and plasmapheresis allow for some function retention if caught early

37
Q

What is vasculitis?

A

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

38
Q

What is the consequence if vasculitis is not caught early?

A

Rapidly progressive glomerulonephritis –> nephritic syndrome

39
Q

What is the pathogenesis of vasculitis?

A

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

40
Q

Describe the epidemiology of prostate cancer.

A

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

41
Q

What are the risk factors for prostate cancer?

A

Increasing age

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

42
Q

Why is mass screening for prostate cancer not offered?

A

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

43
Q

What can cause raised PSA levels?

A

BPH
Infection
Inflammation
Prostate cancer

44
Q

What is the usual presentation of prostate cancer?

A

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

45
Q

What is the unusual clinical presentation of prostate cancer?

A

Haematuria in some advanced cases

46
Q

How do pancreatic cancer bone metastases present on bone scan?

A

‘Hot spots’ as they are sclerotic

47
Q

What is the diagnostic pathway for pancreatic cancer?

A

DRE+PSA –> transrectal US guided biopsy of prostate

LUTS –> transurethral resection of prostate which occasionally picks up uncommon central tumours

48
Q

What are Tx decisions based on in pancreatic cancer?

A 
Pt age
DRE findings
PSA level
Gleason grade from biopsy
And nodal/visceral metastases on bone scan or MRI
49
Q

What is Gleason grading?

A

Low power microscopy used to examine architecture of biopsy

50
Q

What are the established Tx available for pancreatic cancer?

A

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

51
Q

What developmental Tx are available for prostate cancer?

A

High intensity focused US
Primary cryotherapy
High dose rate brachytherapy

52
Q

Give some examples of urological causes of haematuria.

A 
Advanced prostate cancer
Upper tract transitional cell carcinoma
Bladder cancer
BPH
Infection
Inflammation
Stones
Renal cell carcinoma
53
Q

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

A

Nephrological (glomerular)

54
Q

What is varicocele?

A

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

55
Q

Describe the epidemiology of bladder cancer.

A

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

56
Q

What are 90% of bladder cancers?

A

Transitional cell carcinomas

57
Q

What are the risk factors for bladder cancer?

A

Smoking
Occupational exposure
Schistosomiasis

58
Q

What type of bladder cell cancer does schistosomiasis lead to?

A

Squamous cell carcinoma

59
Q

What is the intitial definitive Tx for bladder cancer?

A

Transurethral resection and single chemotherapy dose directed at bladder

60
Q

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

A

75% superficial
5% in situ
20% muscle invasive

61
Q

What mortality is associated with muscle invasive bladder cancer?

A

50%

62
Q

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

A

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

63
Q

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

A

Renal cell carcinoma

64
Q

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

A

Increasing

65
Q

What are the risk factors for developing renal cell carcinoma?

A

Smoking
Obesity
Dialysis

66
Q

How does renal cell carcinoma spread?

A

Perinephric
Lymph nodes
IVC –> right atrium

67
Q

What treatment is currently available for localised renal cell carcinoma?

A

Surveillance +/- partial or radical nephrectomy

68
Q

What is removed in radical nephrectomy?

A

Kidney, adrenal, surrounding fat and upper ureter

69
Q

What treatment is currently available for metastatic renal cell carcinoma?

A

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

70
Q

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

A

Upper tract transitional cell carcinoma

71
Q

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

A

Smoking
Phenacetin abuse
Balkan’s nephropathy

72
Q

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

A

40%

73
Q

Where can upper tract transitional cell carcinomas be found?

A

Calyces

Upper ureter

74
Q

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

A

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

75
Q

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

A

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

Semester 3 (50 decks)

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