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Renal > Week 4: Pathology of tubulointerstitial and Cystic renal diseases > Flashcards

Week 4: Pathology of tubulointerstitial and Cystic renal diseases Flashcards

1
Q

Define tubulointerstitial disease. Two principal causes?

A
  • Definition: group of disorders characterized by abnormalities of renal tubules and the interstitial. Can spare the glomueruli.
    1. inflammatory mediated injury
  • infectious
  • non infectious: interstitial nephritis
    2. Ischemic or toxic injury
  • acute tubular necrosis
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2
Q

Define pyelonephritis. Etiology? Pathogenesis?

A

-Definition: an acute suppurative bacterial infection of the kidney. Associated with UTIs.
ETIOLOGY
-bacterial infections caused by colonization of distal urethra and introits by coliform bacteria with adhesions on pili or upward spread by instruments
-most common: E.coli, other gram negative rods from fecal flora-Proteus, Klebsiella, Enterobacter, Strep faecalia, Pseudomonas aeruginosa
PATHOGENESIS
-most common mechanism: ascending infection from bladder
-promoted by obstruction, vesicoureteral reflux, or other reason for urinary stasis
-spread by blood less common

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3
Q

Predisposing conditions for pyelonephritis.

A
  • urinary tract obstruction
  • instrumentation, e.g. catheters
  • vesicoureteral reflex
  • pregnancy
  • females between 1-40, in males, incidence rises with age
  • diabetes mellitus-due to impaired leukocyte fxn, frequent micturition (fainting during or after urination), nephrogenic bladder
  • immunosuppression and immunodeficiency
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4
Q

Pathology of pyelonephritis

A
  • hallmark: patchy interstitial suppurative inflammation and focal tubular necrosis
  • gross: Large kidney, bulging cut surface, yellow streaks of pus, inflamed calyces and pelvis
  • micro: PMNs in interstitium and tubules with focal micro-abscesses
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5
Q

Clinical course of pyelonephritis.

A
  • acute onset of chills, fever, dysuria, frequent and urgency with costovertebral angle tenderness and pain
  • lab findings: pyruia, WBC casts, pathogenic organisms 10^3 to 10^5 organisms/mL
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6
Q

Complications of acute pyelonephritis

A
  • septicemia and gram negative shock
  • preterm labor
  • papillary necrosis: mainly with DM
  • pyonephrosis-pus fills in collecting systems of obstructed hydronephrotic kidney
  • perinephric abscess: extension of the inflammatory process outside the renal capsule
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7
Q

Define chronic pyelonephritis.

A
  • chronic tubulointerstitial inflammation and renal scarring with involvement of the calyces and pelvis
  • other factors involved in pathogenesis in addition to bacterial infection (e.g. reflux and obstruction)
  • chronic tubulointerstitial inflammation with scarring of the renal parenchyma and distortion of the renal calyces and pelvice
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8
Q

Etiology of chronic pyelonephritis

A
  1. chronic obstruction: acute renal infection and inflammation superimposed upon diffuse or localized obstructive lesions–>parenchymal atrophy and extensive scarring
  2. Reflux nephropathy: superimposition of urinary infection on congenital vesicoureteral reflex–>scarring
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9
Q

Pathology of chronic pyelonephritis

A
  • gross: irregular discrete corticomedullary scars (pitted), overlaying dilated blunted calyx (fibrosis and shrunken parenchyma)
  • micro: patchy atrophic tubules and hypertrophic surviving tubules, dilated with colloid casts (thyroidization), chronic interstitial inflammation, fibrosis
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10
Q

Clinical course of chronic pyelonephritis.

A
  • insidious course, not recognized until onset of renal failure with lassitude, headaches, weight loss, nausea, polyuria, nocturne. HTN and its complications
  • Lab findings: bacteriruia >10^5, low grade pyruria, proteinuria, elevated BUN and Cr (evidence of renal failure)
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11
Q

Define xanthogranulomatous pyelonephritis

A
  • distant variant of chronic pyelonephritis
  • foamy macrophages mixed with plasma cells, lymphocytes, neutrophils, giant cells
  • associated with stag horn calculus with superimposed proteus infection
  • yellow orange nodules mistaken for renal carcinoma
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12
Q

Causes of drug induced nephropathy (non infectious interstitial nephritis)

A
  • -delayed hypersensitivity reaction due to happen like effect. Onset ~2 weeks after exposure to drug
  • penicillins and rifampin
  • thiazides and cimetidine
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13
Q

Pathology of drug induced nephropathy

A
  • interstitial edema with lots of eosinophils and neutrophils.
  • may be granulomas (methicillin).
  • Tubular necrosis and regeneration are present and glomeruli are normal
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14
Q

Clinical course of drug induced nephropathy

A
  • 15 days after exposure, prevents with rash, fever, eosinophilia, hematuria, mild proteinuria
  • 50% have Cr elevation
  • acute renal failure may develop
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15
Q

Describe radiation nephritis.

A
  • 6-12 months after radiation

- micro: glomeruli hyalinization, severe interstitial fibrosis and tubular atrophy–>HTN, anemia, and proteinuria

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16
Q

Define acute tubular necrosis.

A
  • characterized by destruction of tubular epithelial cells and clinically by suppression of renal function
  • most common cause of acute renal failure
  • when urine falls below 400mL in 24 hrs
  • reversible
  • necrosis from ischemia or toxicity
17
Q

Pathogenesis of ischemic ATN

A
  • medulla is susceptible to ischemia because it receives small portion of blood fluid
  • ischemi–>vasoconstriction–>reduced GFR and oliguria
  • clinical complication after shock produced by severe bacterial infection, large burns, mismatched blood transfusion reaction, massive crushing injuries
18
Q

Pathology of ischemic ATN

A
  • focal tubular necrosis at multiple irregular points
  • rupture of BM sometimes
  • hyaline and granular casts of Tamm-Horsfall protein (glycoprotein normally secreted by TALH in normal urine)
  • pigment casts
  • glomeruli spared
19
Q

Etiology of nephrotoxic ATN

A
  • sensitive to toxic injury due to vast electrically charged surface for reabsorption, active transport for ions and organic acids, ability to concentrate urine
  • ethylene glycol
  • drugs: amphotericin B, gentamicin
  • metals
  • radiocontrast media
20
Q

Pathology of nephrotoxic ATN

A
  • more diffuse with toxic compared to segmental with ischemic
  • greatest injury usually in PT
21
Q

Pathology of ADPKD

A
  • gross: bilateral, large, polycystic kidneys
  • renal cysts vary in size
  • often contain colorless fluid/turbid hemorrhagic or gelatinous fluid
  • micro: variably sized cysts lined by simple epithelium with normally differentiated intervening parenchyma
22
Q

Etiology of ARPKD (autosomal recessive polycystic kidney disease or infantile polycystic kidney disease). Prognosis?

A
  • mutation on chromosome 6p (PKHD1). gene encodes fibrocystin, function unknown
  • failure to communicate between nephron and pelvicalyceal system
  • babies usually don’t survive long and older children have associated hepatic fibrosis
23
Q

Pathology of ARPKD

A
  • gross: bilaterally enlarged, multi cystic kidneys with normal contour. Uniform sized cysts
  • micro: cysts lined by uniform cuboidal cells, rare glomeruli but no normal parenchyma
24
Q

Describe medullary sponge kidney

A
  • congenital disorder with unknown pathogenesis
  • renal condition consisting of multiple cystic dilations of the medullary collecting ducts
  • usually asymptomatic unless presenting with secondary complication, usually in 40s-60s.
  • the dilations give sponge like appearance to renal medulla
25
Q

Describe uremic medullary cystic disease. Pathology?

A
  • usually originates in childhood but found in adolescents and adults
  • progressive renal failure and cyst formation in medullary and cortico-medullary regions of the kidney
  • gross: small contracted kidneys, granular surfaces, cysts are present near corticomedullary junction
  • micro: cotical tubular atrophy with interstitial fibrosis, cysts lined by flattened or cuboidal cells and border by inflammation or fibrosis
26
Q

Clinical features of uremic medullary cystic disease

A
  • polyuria, polydipsia -due to defect in concentration ability
  • sodium wasting
  • tubular acidosis also prominent
  • progression terminal renal failure in 5-10 years
  • assoc. with hepatic fibrosis, retinal dysplasia, hyperuricemia, and gouty arthritis
27
Q

Describe dialysis cystic disease. Etiology, pathology, clinical course

A
  • definition: cortical or medullary cysts occurring in patients with end-stage renal disease who have undergone prolonged dialysis
  • etiology: may be result of fibrosis than dialysis
  • gross: cysts containing clear fluid and some times calcium oxalate crystals
  • micrl: cysts lined by flattened epithelium, but foci of papillary hyperplasia of the tubular lumen are common
  • increased incidence of renal adenoma and renal cell carcinoma arising within the wall of cysts

Renal (30 decks)

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