Urological Pathology

Question 1

Acute Pyelonephritis

Answer 1

Acute suppurative inflammation of the kidney caused by bacterial/viral infection. Usually due to an ascending infection from perineal organisms. Characterised by acute neutrophilic exudate within the tubules and interstitial inflammation.

Predisposing conditions: Urinary tract obstruction, urinary procedures (e.g. catheters), pregnancy, diabetes mellitus

Question 2

Three complications of acute pyelonephritis

Answer 2

Papillary necrosis: mainly seen in diabetics, and patients with obstruction

Pyonephrosis: total or almost complete obstrcution in the tract means pus is unable to drain and fills the renal pelvis and ureter.

Abscesses

Question 3

Chronic pyelonephritis

Answer 3

Chronic tubulointerstitial inflammation and renal scarring due to reflux or obstruction.

Reflux: vesicourethral refluc of urine into the kidney. Caused by abnormal insertion of the ureter into the bladder, plus multiple episodes of infection.

Obstructive: Reccurrent infections in addition to obstructions caused by stones, tumours or congential defects cause inflammation, scarring and parenchymal atrophy.

Question 4

Cause of renal stones

Answer 4

Most stones are composed of Ca2+ and PO4. Oxalate and urate also contribute to renal stone formation

May arise due to hypercalcaemia/hypercalcuria, infection, dehydration or hyperoxaluria.

• common causes of hypercalcaemia causing stones are hyperparathyroidism and sarcoidosis.

Question 5

Autosomal dominant polycystic kidney disease

Answer 5

Mutations alter the tubular epithelium growth and differentiation. Three genes identified (PKD 1-3)

Cysts appear when dilation in the nephron compress the parenchyma and impair renal function. May have cysts in the liver, pancreas and spleen, also predisposed to berry aneurysms.

Presents at age 30-40 with hypertension, haematuria, loin pain and large palpable kidneys.

Question 6

Autosomal recessive PKD

Answer 6

Presents in children with enalrged kidneys or still birth. Both kidneys are enlarged by pultiple dilated collecting ducts which form the systs. These replace the medulla and cortex and extend into the capsule.

Question 7

Proteinuria in renal disease

Answer 7

• Severe damage to the glomeruli cause loss of the filtration barrier and reduces the filtration surface, causing a substantial leakage of proteins.
• Tubulo-interstitial diseases cause ineffective reabsorption of small low Mw proteins in the filtrate
• Excessive quantities of protein in the blood which exceeds teh kidney’s capacity are filtered into the urine.

Question 8

Presentation of renal stones

Answer 8

Pain: renal colic due to passage of a stone along the ureter, or dull ache in the loins

haematuria

reccurent infection

obstruction.

Question 9

Renal cell carcinoma

Answer 9

Arises from epithelial cells in the kidney

Major risk factor is smoking. Obesity, radiation and acquired renal cystic disease also factors.

Present with haematuria as the tumour invades and bleeds into the collecting system, pain in the flanks and a palpable mass

Different microscopic appearances: clear cell carcinoma (due to VHL gene), papillary (associated with acquired cystic disease)

Question 10

Where do renal tumour metastasize to?

Answer 10

Blood

Lung

Bone

Liver

Brain

Question 11

Transitional cell carcinoma

Answer 11

Occurs in the renal pelvis, ureter, bladder and urethra which is lined by transitional epithelium. They project into the renal pelvis and present with haematuria or obstruction.

Smoking is the biggest risk factor

Question 12

Benign renal tumours

Answer 12

Oncocytoma: composed of large eosinophillic cells Similar to renal cell carcinoma

Angiomyolipoma: combination of abnormal blood vessels, smooth muscle and adipose tissue.

Question 13

Tumours of the bladder

Answer 13

Transitional cell carcinoma: 90% bladder cancer. Prsents as painless haematuria and urinary frequency. Most tumours are low grade papillary with no invasion of the lamina propria, some are flat. 20% are solid and invasive. Smoking and and aromatic amines are major risk factors.

Squamous cell carcinoma: arises from metaplastic squamous epithelium. Commonly occurs which chronic schistosomiasis.

Question 14

Benign prostatic hyperplasia

Answer 14

Common non-neoplastic enargemetn of the prostate gland, common after age 50. Glands and stroma of transition zone proliferate in response to DH-testosterone. Involves both lateral lobes. Alpha adrenergic receptors area activated which maintain smooth muscle tone around the urethra.

• Hyperplastic nodules compress and elongate the prostatic urethra, distorting its course.
• Peri-urethral zone enlargement affect sphincter mechanism
• Stomal oedema and periductal inflammation are common and may contribute to urinary obstruction.

Symptoms: frequency, urgency, incontinence, hesitancy, dribbling or intermittent stream.

Question 15

Complications of prostatic hyperplasia

Answer 15

Bilateral hydronephrosis

Bilateral hydroureter

Diverticulum

Muscular hypertrophy of the bladder

Compression of the urethra

Renal infection/failure/calculi

Question 16

Prostate cancer

Answer 16

Adenocarcinoma
Commonest cancer in men, increased risk if there is family history. Most tumours arise in the peripheral zone.

Spread can be direct stromal invasion into the prostatic capsule, urethra and bladder

Via lymphatics to sacral, iliac and para-aortic nodes

Via blood to bone in the pelvic, spine, lungs and liver.

Presentation: urinary symptoms - increased frequency, urinary retention. PR exam shows hard craggy prostate, Bone mets present with pain, pathological fractures or anaemia.

Question 17

Grading of prostatic tumours

Answer 17

Gleason score

Describes unusual glandular patterns. Grade 3 has irregular glands and grade 4 has fused glands.

Add scores of the two most prevalent patterns.

Question 18

Describe the pathology of diabetic nephropathy

Answer 18

DM causes damage to the vessels throughout the body. Severe atheroma in the renal artery may cause renal ischemic lesions and hypertension.

Glomerular disease: Capillary walls thicken. Mesangial matrix expands causing glomerulosclerosis, nodular expansion of the mesanium. In diabetics this causes proteinuria which increases as the disease progreses leading to nephrotic syndrome and renal failure.

Tubules: thickening of the basement membrane, tubular atrophy and intersitial fibrosis. Hyperglycaemia induces morphological changes and production of matrix proteins. Imbalance between synthesis and degradation means material accumulates in the matrix.

Renal papillary necrosis can occur if there is acute pyelonephritis and damage to the vasa recta.

Question 19

Glomerulonephritis

Answer 19

Diffuse proliferative glomerulonephritis: Acute lesion following a transient infection e.g. staphylococci, meningococci, pneuococci, BHstrep, viruses. Glomeruli are distended and there is an increase in cells due to proliferation and swelling of mesangium. All glomeruli involved. Interstital oedema and inflammatory infiltrate seen.

Focal proliferative glomerulonephritis: Some glomeruuli affected. Segemental necrosis is seen. Caused in several systemic diseases e.g. SLE, infective endocarditis, IgA disease.

Membrano-proliferative glomerulonephritis: Glomerular lesion with membrane thickening and proliferation. Capillary walls are thickened and a double layer of basement membrane is seen.