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Urogenital Pathology > Tubules & Interstitium > Flashcards

Tubules & Interstitium Flashcards

1
Q

Listvpredisposing factirscto pyelonephritis

A
  1. Obstruction
  2. Vesico-ureteric reflux
  3. Bilhariziasis
  4. Instrumentation
  5. Female
  6. Pregnancy
  7. DM
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2
Q

Routes of infection by pyelonephritis are……

A

Ascending & bloodborne

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3
Q

Mention G&M features of pyelonephritis

A

G: pelvicalyceal system is acutely inflammed, renal parenchyma shows foci of suppuration which appear as yellow streaks radiating from renal papillae, to expand into abscesses in the cortex
M: pelvicalyceal system is acutely inflammed, renal parenchyma is infiltrated by neutrophils which collect in the interstitial tissue or within the tubular lumen to form abscesses

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4
Q

The more common cause of pyelonephritis is…….., describe its cause

A

Chronic reflux-assocaited pyelonephritis
Due to superimposition of UTI on congenital vesicourethral reflex & intrarenal reflux

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5
Q

Describe gross features of chronic pyelonephritis

A

Uni or bilateral, diffuse or in patches, uneven scarring involving pelvis, calyces or both leading to papillary blunting & marked calyceal deformities.

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6
Q

Describe microscopic features of chronic pyelonephritis

A
  1. Uneven interstitial fibrosis and an inflammatory infiltrate of lymphocytes, plasma cells may be neutrophils
  2. Dilation of tubules with atrophy of lining epithelium, many show PAS-+ve casts (thyroidization)
  3. Often neutrophils are seen in tubules
  4. Inflammation & fibrosis involve calyceal mucosa
  5. Arteriosclerosis due to HTN
  6. Glomerulosclerosis develops as 2ry process
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7
Q

Describe pathogenesis of drug induced interstitial nephritis

A

The drugs act as haptens that bind to some cytoplasmic & extracellular component of tubular cells thus become immunigenic & IgE- and cell-mediated immune reactions develop to them or their BMs. Mononuvlear infiltrate or granulomatous infiltrate suggest type IV hypersensitivity.

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8
Q

Describe micro feature of ADIIN

A
  1. Prominent eosinophilic & mononuclear interstitial infiltrate with tubular injury and eosinophilic casts
  2. Some cases may show non nectrotizing granulomas
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9
Q

Describe pathogenesis of analgesic nephropathy

A
  1. Renal papillary necrosis is the initial event, interstitial nephritis is 2ry
  2. Acetaminophen a phenacetin metabolite injures kidneys by covalent binding & oxidative damage
  3. Aspirin inhibits VD effect of PGs predispose papilae to ischemia
  4. Thus papillary damage is due to combination of direct toxic effects of phenacetin & ischemic injury
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10
Q

Describe G&M picture of analgesic nephropathy

A

G, necrotic papillae appear yellowish brown as a result of accumulation of breakdown products of phenacetin & other lipofuscin pigments, may show sloughed papillae in pelvis.
M, coagulative necrosis

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11
Q

List causes of ATN

A

Anoxic: mismatched blood transfusion, crush injuries, burns, shock
Toxic: poison (Hg-Cl, P, CCL4, insectiscides), drug (gentamycin & amphotericin)

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12
Q

Describe M picture of ATN

A
  1. Toxic ATN: is usually diffuse proxim. & pathchy distal., anoxic is patchy prox & distal
  2. ATN chct by necrosis of tubular epithelial in PCT, proteinaceous in DCT & interstitial edema.
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13
Q

Describe pathogenesis of benign nephrosclerosis

A
  1. Mainly result from endothelium dysfunction & platelet activation
  2. Medial & intimal thickening as a response to hemodynamic changes, aging, genetic defects or combination
  3. Hyalinization of arteriolar walls, caused by extravasation of PPs through injured endothelium & by inc deposition of BM
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14
Q

Describe G&M picture of benign nephrosclerosis

A

G, 1ry contracted kidney, outer surface is finely granulr & may show small cysts, cut surface shows irregular atrophy of cortex with loss of demarcation between cortex & medulla
M, hyaline arteriosclerosis, arterioles show thickening & hyalinization of their walls with luminal narrowing leading to diffuse ischemic atrophy of nephrons, large muscular arteries show intimal thickening with replication of internal elastic lamina along with fibrous thickening of media

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15
Q

Malignant HTN cut-off value is…..

A

Greater than 200/120

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16
Q

Describe pathogenesis of malignant nephrosclerosis

A

Injury results from long-standing HTN causes inc permeability of the vessels to fibrinogen, PPs, endothelial injury & platelet deposition, leads to appearance if fibrinoid necrosis of arterioles & small arteries. Mitogenic factors from platelets & plasma cause hyperplasia of vessels resulting in hyperplastic arteriosclerosis. Bec of luminal narrowing kidneys become markedly ischemic resulting in further inc BPP via RAAS

17
Q

Describe G&M picture of malignant nephrosclerosis

A

G, petechial hge on cortical surface (flea-bitten)
M, fibrinoid necrosis (necrotizing arteriolitis) hyperplastic arterioles (onion skin appearance), necrotizing glomerulitis.

18
Q

In malignant HTN, 90% of deaths are caused by……, while 10% are caused by……

A

Uremia
Cerebral Hge or HF

19
Q

Describe pathogenesis of urolithiasis

A
  1. Inc urinary components of stone constituents
  2. Changes in urine pH
  3. In avitaminosis A, desquamated metaplastic cells act as nidus
  4. Stasis
  5. Diminished factors inhibiting mineral deposition (pyrophosphate, mucopolysaccharide, diphosphnate, nephrocalcin)
20
Q

Comare urinary stones with respect type, colour, consistency, radio-opacity.

A

Oxalate: 1ry, black, hard/spinky , opaque
Urate: 1ry, yellow brown, smooth/hard, lucent
Triple phosphate: 2ry to alkaline urine due to infection, chalky white, friable & smooth, opaque

21
Q

List effects & complications of renal calculi

A
  1. Renal colic
  2. Hematuria esp oxalate
  3. Hydronephrosis & hydroureter: incomplete or intermittent obstruction
  4. Kidney atrophy is complete
  5. Squamous metaplasia due to irritation
  6. Stricture formation
  7. Malignant transformation into carcinoma of UB or pelvis
22
Q

List causes of:
1. Oxalate stones
2. Struvite
3. Uric acid

A
  1. Hypercalcemia & hypercalciuria, idiopathic hypercalciuria, hyperoxaluria, hyperuricosuria, UK metabolic defect
  2. Renal infection
  3. Hyperuricemia, hyperuricosuria, idiopathic
23
Q

Describe fate of hydronephrosis

A
  1. Unilateral hydronephrosis may remain silent
  2. Superimposed infection leads to pyonephrosis
  3. Bilateral leads to CRF
24
Q

Adult type PKD is inherited……., considered a type of……

A

AD
Ciliopathy

25
Q

Describe pathogenesis of ADPKD

A
  1. Normal cilia act as mechanosensors of fluid flow, the membrane protein responsible for this function is called polycystin
  2. Defective gene PKD1 & 2 are present on Ch16p which encodes polycysin-1
  3. Defective mechanosensing leads to Ca influx & dysregulation of cell proliferation lead to lateral outpouching that accumulate fluid at PCT or DCT
26
Q

Describe gross features of
1. ADPKD
2. ARPKD

A
  1. Kidneys are englarged weigh upto 4 kg, outer surface & cut-section show multiple cysts of variable size upto 3-4 cm, contain fluid may be clear, turbid, hemorrhagic
  2. Multiple cysts are seen in cortex & medulla and given the kidney sponge-like appearance. It usually presents at birth & young infants may die early from hepatic or renal failure.
27
Q

ADPKD symptomatises during…..& leads to CKD at……, it is associated with……

A

4th decade of life
Age fifty
Aneurysms of Circle if Willis

28
Q

Childhood PKD, ……is the abnormal protein

A

Fibrocystin

29
Q

list

A

Urogenital Pathology (9 decks)

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