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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
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)

Semester 3 (50 decks)

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