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11. Urinary > 9. Pathology of the Urinary System > Flashcards

9. Pathology of the Urinary System Flashcards

1
Q

What is the difference between primary and secondary disease of the urinary system?

A

Primary only affects the glomerulus, secondary is systemic disease that in turn has damaged the glomerulus.

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2
Q

What are the three sites of glomerular injury?

A

Subepithelial (within glomerular basement membrane), subendothelial, mesangial/paramesangial.

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3
Q

What is subepithelial glomerular injury?

A

Anything that affects podocytes/podocyte side of glomerular basement membrane.

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4
Q

What is subendothelial glomerular injury?

A

Damage inside the basement membrane.

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5
Q

What is mesangial/paramesangial glomerular injury?

A

Damage in supporting capillar loop.

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6
Q

What are the effects of pathology of the glomerulus on the filter?

A

It can block or it can leak.

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7
Q

What is the presentation of blocked filter?

A

Renal failure - hypertensive, haematuria.

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8
Q

What is the presentation of leaking filter?

A

Proteinuria (albumin), haematuria - separately or together depending on damage.

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9
Q

What is proteinuria?

A

The presence of excess serum proteins, <3.5g filtered every 24 hours, in urine.

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10
Q

What is proteinuria due to?

A

Podocyte damage, widening of fenestration slits causing protein to be leaked when it would normally not be filtered.

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11
Q

How do proteinuria and nephrotic syndrome compare in severity?

A

Proteinuria is less severe.

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12
Q

What is the quantitative definition of nephrotic syndrome?

A

Over 3.5g of protein filtered in 24hrs.

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13
Q

How does nephrotic syndrome cause oedema?

A

Lot of protein filtered, oncotic pressure is reduced so generalised oedema.

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14
Q

What are the common primary causes of proteinuria/nephrotic syndrome?

A

Minimal change glomerulonephritis, focal segmental glomerulosclerosis, membranous glomerulonephritis.

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15
Q

What are the common secondary causes of proteinuria/nephrotic syndrome?

A

Diabetes mellitus, amyloidosis.

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16
Q

When does minimal change glomerulonephritis present?

A

In childhood/ adolescence. Incidence reduces with age.

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17
Q

What does minimal change glomerulonephritis cause?

A

Heavy proteinuria or nephrotic syndrome.

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18
Q

How is minimal change glomerulonephritis treated?

A

It responds well to steroid but can recur once weaned off.

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19
Q

What gives minimal change glomerulonephritis its name?

A

Under a light microscope, the glomeruli look normal.

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20
Q

What is seen under electron microscopes with minimal change glomerulonephritis?

A

Damage to podocytes, widening fenestration slits allowing proteins to leak through.

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21
Q

What causes glomerulonephritis?

A

Cause unknown.

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22
Q

What is focal segmental glomerulosclerosis?

A

Focal = involving less than 50% of glomeruli on light microscopy. Segmental = involving part of the glomerular tuft. Glomerular sclerosis = scarring.

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23
Q

When does focal segmental glomerulosclerosis present?

A

In adulthood.

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24
Q

What causes focal segmental glomerulosclerosis?

A

A circulating factor, evidenced by the fact transplanted kidneys undergo same damage.

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25
Q

What can focal segmental glomerulosclerosis progress to?

A

Renal failure.

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26
Q

Are steroid effective in treating focal segmental glomerulosclerosis?

A

Not really, less responsive than minimal change glomerulonephritis.

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27
Q

What is the commonest cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis.

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28
Q

What causes membranous glomerulonephritis?

A

Immune complex deposits in the sub-epithelial space with some autoimmune basis. Some evidence for secondary causes, especially malignances.

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29
Q

What does the rule of thirds mean with membranous glomerulonephritis?

A

1/3 get better, 1/3 have stable proteinuria without symptoms, 1/3 progress to renal failure.

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30
Q

What is nephritic syndrome?

A

Renal failure due to blocking of filter.

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31
Q

What is the commonest glomerular nephropathy at any age?

A

IgA nephropathy.

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32
Q

What is IgA nephropathy?

A

Deposits of IgA antibody in the glomerulus. Presents with visible/ invisible haematuria and is linked mucosal infections.

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33
Q

What is the effective treatment for IgA nephropathy?

A

There is no effective treatment.

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34
Q

What are the two hereditary nephropathies?

A

Thin glomerular basement membrane nephropathy, and alport syndrome.

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35
Q

What is thin GBM nephropathy?

A

Nephropathy, benign familial nephropathy, isolated haematuria, thin GBM, benign course.

36
Q

What is Alport syndrome?

A

X linked, abnormal collagen IV, associated with deafness, progresses to renal failure.

37
Q

What are the renal complications of diabetes mellitus?

A

Progressive proteinuria, progressive renal failure, microvascular, mesangial sclerosis, basement membrane thickening.

38
Q

What is Goodpasture syndrome?

A

Very rapidly progressing glomerular nephritis.

39
Q

What causes Goodpasture syndrome?

A

Autoantibody to collagen IV in basement membranes. IgG deposition but no extracellular matrix deposit.

40
Q

How can Goodpasture syndrome be treated?

A

By immunosuppression and plasmaphoresis if caught early enough.

41
Q

What is vasculitis?

A

Inflammation of blood vessels.

42
Q

What are blood vessels in the glomerulus attacked by in vasculitis?

A

Anti-neutrophil cytoplasmic antibody.

43
Q

What forms immune complexes in the glomerulus (subepithelial deposits)?

A

Antigen abnormally recognised on podocytes, circulating IgG binds to it and this forms immune complex.

44
Q

How do mesangial deposits become present?

A

Immune complexes are deposited directly in the mesangium, no podocytes or basement membrane to act as a barrier.

45
Q

What is the most common cancer in men in the UK?

A

Prostate cancer.

46
Q

What is the second most common cause of death from cancer in men?

A

Prostate cancer.

47
Q

How does age affect the risk of prostate cancer?

A

Increasing age has increased risk, uncommon in men under 50 years old.

48
Q

How does family history affect the risk of prostate cancer?

A

Four times increased risk if one first degree relative has been diagnosed with it before 60 years old. Above 60 is probably age related rather than genetics.

49
Q

How does race affect the risk of prostate cancer?

A

Highest incidence in Afro-Caribbeans, then Caucasians, then Asians.

50
Q

What is the usual presentation of prostate cancer?

A

Mostly asymptomatic. Urinary symptoms from benign enlargement of prostate cause bladder over activity. Bone pain in advanced metastatic cancer.

51
Q

What is the unusual presentation of prostate cancer?

A

Haematuria in advanced prostate cancer.

52
Q

How is it decided if a biopsy of the prostate is required?

A

Digital rectal examination and serum PSA (prostate specific antigen).

53
Q

How is a biopsy of the prostate taken?

A

Under transrectal ultrasound guidance.

54
Q

How are lower urinary tract symptoms treated?

A

Transurethral resection of the prostate.

55
Q

What factors influence treatment decisions for prostate cancer?

A

Age, digital rectal examination (localised T1/2, locally advance T3, or advance T4), PSA level, biopsies (Gleason grade), MRI scan and bone scan (nodal/ visceral metastases).

56
Q

How are established prostate cancers treated?

A

Surveillance if cancer is low risk. Radical prostatectomy - open, laparoscopic or robotic. Radiotherapy - external beam or lose dose brachytherapy.

57
Q

How are development prostate cancers treated?

A

High intensity focussed ultrasound, primary cryotherapy - freeze prostate, brachytherapy - high dose.

58
Q

How are metastatic prostate cancers treated?

A

Hormones - surgical castration, medical castration. Palliation - single-dose radiotherapy, bisphosphonates, chemotherapy.

59
Q

How are locally advance prostate cancers treated?

A

Surveillance, hormones, hormones and radiotherapy.

60
Q

What are the two classes of haematuria?

A

Visible and non-visible.

61
Q

What is the chance of malignancy with visible haematuria?

A

20%.

62
Q

How is non-visible haematuria detected?

A

Via microscopy or urine dipstick.

63
Q

What are the urological causes of haematuria?

A

Cancer, nephrological, stones, infection, inflammation, benign prostatic hyperplasia.

64
Q

Which cancers can cause haematuria?

A

Renal cell carcinoma, upper track transition cell carcinoma, bladder cancer, advanced prostate cancer.

65
Q

What should history of haematuria include?

A

Smoking, occupation, painful/painless, other lower urinary tract symptoms, family history.

66
Q

What should examinations include in haematuria?

A

BP, abdominal mass, varicocele, leg swelling, assess prostate by DRE.

67
Q

What are the investigations for haematuria?

A

Urine culture and cytology, full blood count, ultrasound, and flexible cystoscopy.

68
Q

How common is bladder cancer in the UK?

A

7th most common cancer, but decreasing incidence.

69
Q

What is the male: female ratio for bladder cancer?

A

2.5:1.

70
Q

What is the most common type of bladder cancer?

A

Transitional cell carcinomas.

71
Q

What are the risk factors for bladder cancer?

A

Smoking - four times increased risk. Occupational exposure with 20 year latent period - rubber or plastics, handling of carbon, crude oil, and combustion, painteters, mechanics, printers, schistosomiasis.

72
Q

What are the stages of bladder cancer with their frequency?

A

75% are superficial Ta/T1.
5% are in situ Tis.
20% are muscular invasive.

73
Q

What are the treatment options for high risk non-muscle invasive transitional cell carcinoma?

A

Check cystoscopies. Intravesicular chemotherapy/immunotherapy.

74
Q

What is the treatment for low risk non-muscle invasive transitional cell carcinoma?

A

Check cystoscopies.

75
Q

What is the treatment for muscle invasive transitional cell carcinoma?

A

If potentially curative - radical cystectomy or radiotherapy, with or without chemotherapy.
If non curative - palliative chemotherapy/ radiotherapy.

76
Q

What is radical cystectomy?

A

Removal of the urinary bladder. A piece of ileum can be used to made a conduit from ureters to abdomen to collect urine in a bag or can reconstruct bladder with a piece of the small intestine.

77
Q

What is the epidemiology of renal cell carcinoma?

A

8th most common cancer in the UK, makes up 95% of all upper urinary tract tumours. Increasing incidence and mortality.

78
Q

What is the male: female ratio of renal cell carcinoma?

A

3:2.

79
Q

What proportion of renal cell carcinomas have metastases on presentation?

A

30%.

80
Q

What are the risk factors for renal cell carcinoma?

A

Smoking doubles risk, obesity, dialysis.

81
Q

Where do metastases of renal cell carcinomas go?

A

To lymph nodes, up renal vein and vena cava into the right atrium and into the subcapsular fat (perinephric spread).

82
Q

What is the treatment for established renal cell carcinomas?

A

Surveillance, radical nephrectomy (removal of kidney, adrenal, surround fat, upper ureter), or partial nephrectomy.

83
Q

What is the treatment for developmental renal cell carcinomas?

A

Ablation (removal of tumour from the surface of kidney via an erosive process).

84
Q

What is the palliative treatment for renal cell carcinomas?

A

Molecular therapies targeting angiogenesis, immunotherapy.

85
Q

What is the epidemiology of upper tract transitional cell carcinomas?

A

5% of all malignancies of the upper urinary tract. 5% from cancer spread from bladder up ureter, 40% spread to bladder.

86
Q

What are the investigations for upper tract transitional cell carcinomas?

A

Ultrasound - hydronephrosis = swelling of kidney due to backup of urine, CT urogram - filling defect and ureteric structure, retrograde pyelogram - inject contrast into ureter, ureteroscopy - biopsy and washings for cytology.

87
Q

What is the treatment of upper tract transitional cell carcinomas?

A

Nephro-uretectomy - removal of kidney, fat, ureter, and cuff of bladder.

11. Urinary (12 decks)

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