Session 9

Question 1

Describe focal glomerular pathology.

Answer 1

Pathology involving less than 50% of the glomeruli on light microscopy.

Question 2

Describe diffuse glomerular pathology.

Answer 2

Pathology involving more than 50% of glomeruli on light microscopy.

Question 3

Describe segmental glomerular pathology.

Answer 3

Pathology involving part of the glomerular tuft.

Question 4

Describe global glomerular pathology.

Answer 4

Pathology involving the entire glomerular tuft.

Question 5

Describe membranous glomerular pathology.

Answer 5

Thickening of the glomerular capillary wall.

Question 6

Describe proliferative glomerular pathology.

Answer 6

Increased numbers of cels in the glomerulus which may be proliferating glomerular cells or infiltrating circulating inflammatory cells.

Question 7

Describe crescent glomerular pathology.

Answer 7

Accumulation of cells in the Bowman’s space.

Question 8

Describe glomerulosclerosis.

Answer 8

Segmental or global capillary collapse causing little or no filtration.

Question 9

Describe glomerulonephritis.

Answer 9

Any condition associated with inflammation in the glomerular tuft.

Question 10

Describe nephrotic syndrome.

Answer 10

Blockage of the glomerulus causing reduced eGFR, leading to AKI.

Question 11

Describe nephritic syndrome.

Answer 11

Significant loss of protein in urine causing reduced blood oncotic pressure so oedema forms.

Question 12

Damage to what is the most likely cause of proteinuria/nephrotic syndrome?

Answer 12

Podocytes or the subepithelium.

Question 13

What are the common causes of proteinuria/nephrotic syndrome?

Answer 13

Minimal change glomerulonephritis; focal segmental glomerulosclerosis; membranous glomerulonephritis; diabetes mellitus.

Question 14

Describe minimal change glomerulonephritis.

Answer 14

Commonly presents in children; doesnt progress to renal failure; responds to steroid treatment but may recur; causes heavy proteinuria/nephrotic syndrome; little histological change.

Question 15

Describe focal segmental glomerulosclerosis.

Answer 15

Less responsive to steroid treatment than minimal change glomerulonephritis; most commonly found in adults; caused by circulating factors damaging podocytes; fibrotic tissue replaces podocytes; leads to renal failure.

Question 16

Describe membranous glomerulonephritis.

Answer 16

Most common cause of glomerular pathology; caused by immune complex deposits; usually autoimmune; may be secondary to other pathologies; capillary loops thicken and GBM looks spiky histologically; rule of 3rds (3rd improve, 3rd stay same, 3rd deteriorate to renal failure).

Question 17

How can diabetes mellitus cause glomerular pathology?

Answer 17

Causes leaky capillaries which leads to proteinuria; microvascular complications can reduce eGFR and cause renal failure; mesangial sclerosis causes nodules to form; basement membrane thickens which can cause renal failure.

Question 18

What glomerular pathologies commonly cause haematuria?

Answer 18

IgA nephropathy is most common; hereditary nephropathies (Alport); thin glomerular basement membrane.

Question 19

Describe Alport syndrome in relation to the kidneys.

Answer 19

X-linked condition causing abnormal collagen IV formation, leads to GBM not forming properly (appears split and laminated histologically), leads to renal failure.

Question 20

What are the common causes of nephritic syndrome?

Answer 20

Goodpasture syndrome, vasculitis.

Question 21

Describe Goodpasture syndrome in relation to the kidneys.

Answer 21

Anti-GBM disease: autoantibody to collagen IV is found in the basement membranes and causes acute onset of severe nephritic syndrome due to blocked filtration.

Question 22

How can Goodpasture syndrome be treated?

Answer 22

Immunosuppression and plasmapheresis.

Question 23

How is intraglomerular mesangial damage usually caused?

Answer 23

By immune complex deposition as immune complexes can easily enter the mesangium due to the lack of BM, usually IgA-containing immune complexes are deposited.

Question 24

What is vasculitis?

Answer 24

Inflammation of vessels due to a group of systemic disorders.

Question 25

What are the risk factors for prostate cancer?

Answer 25

Being male, increasing age, family history of CaP, BRCA2 gene mutation, race (black>white>asian).

Question 26

Is prostate cancer routinely screened for, why?

Answer 26

No, most older men have CaP so screening would cause overdiagnosis and overtreatment which would reduce the quality of life of the unnecessarily diagnosed patients. Prostate may also be enlarged or PSA raised due to other causes.

Question 27

How does prostate cancer usually present?

Answer 27

Normally asymptomatic but may have urinary symptoms (bladder overactivity, prostate pressing on urethra or bladder causing symptoms); bone pain if boney mets; haematuria in very advanced CaP.

Question 28

What is the diagnostic pathway for CaP?

Answer 28

DRE detects enlarged prostate or serum PSA levels are increased; transurethral ultrasound-guided biopsy of the prostate is taken; if +ve for CaP then TURP is performed.

Question 29

How is prostate cancer graded?

Answer 29

Using the Gleason scoring criteria.

Question 30

How is localised CaP treated?

Answer 30

Surveillance of the Ca; may be offered robotic radical prostatectomy or radiotherapy early on; if advanced local CaP then may be offered hormones and radiotherapy.

Question 31

How is metastatic CaP treated?

Answer 31

Hormones +/- chemotherapy (LHRH agonists); pallation as single dose radiotherapy, chemo or bisphosphonates; removing prostate wont remove Ca or improve quality of life.

Question 32

What differential diagnoses can be given from haematuria?

Answer 32

Cancers (RCC, UT TCC, bladder Ca, advanced prostate Ca); stones; infection; inflammation; benign prostatic hyperplasia; nephrological pathology.

Question 33

What investigations would be performed on a patient presenting with haematuria?

Answer 33

FBC, U&E, USS bladder, flexible cystoscopy, urine cultures and sensitivity, cytology of urine.

Question 34

What are the risk factors of bladder Ca?

Answer 34

Smoking, occupation (rubber or plastic manufacture, handling of carbon, crude oil, combustion, smelting, painters, mechanics, printers, hairdressers), schistomiasis.

Question 35

How is bladder cancer treated initially?

Answer 35

TURBT to remove the tumour.

Question 36

How is bladder Ca treated if initial treatment fails?

Answer 36

Cystoscopies are checked; intravesical chemo for low risk non muscle-invasive TCC; intravesical immunotherapy for high risk non muscle-invasive TCC; neoadjuvant chemo with radical cystectomy or radiotherapy for curative muscle-invasive TCC; neoadjuvant chemotherapy and palliative chemo or radiotherapy for non-curative muscle-invasive TCC.

Question 37

What are the risk factors for RCC?

Answer 37

Smoking, obesity, dialysis.

Question 38

How can RCC spread?

Answer 38

Perinephric to fat around the kidneys; via the lymph system; via the IVC to the right atrium of the heart.

Question 39

How is localised RCC treated?

Answer 39

Surveillance to see the rate of growth of RCC as small tumours are unlikely to metastasise; radical nephrectomy; partial nephrectomy.

Question 40

How is metastatic RCC treated?

Answer 40

Palliative: molecular therapy to target angiogenesis (tyrosine kinase inhibitors). Resistant to chemo and radiotherapy.

Question 41

Where does UTTCC usually spread to?

Answer 41

The bladder.

Question 42

What are the risk factors for UTTCC?

Answer 42

Smoking, phenacetin abuse, Balkan’s nephropathy.

Question 43

How is UTTCC investigated?

Answer 43

USS for hydronephrosis; CT urogram for filling defect or ureteric strictures; retrograde pyelogram; ureteroscopy for biopsy and cytology washings.

Question 44

How are UTTCCs treated?

Answer 44

Nephro-ureterectomy as standard.