renal disease II Flashcards

1
Q

Acute Pyelonephritis

A

AKA: tubulointerstitial nephritis
suppurative inflammation in the renal pelvis, tubules and interstitium caused by bacterial infection
-neutrophil infiltration, clustering in the tubular lumens
-sudden onset of pain at the costovertebral angle

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2
Q

Drug induced interstitial nephritis

A

caused by AB, NSAIDS and duiretics

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3
Q

pathogenesis of drug induced interstitial nephritis

A

hypersensitive, drug binds to tubular or interstitial cells and act as a hapten with an immunogenic response (eosinophils and PMNs)
-glomeruli NOT involved

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4
Q

clinical drug induced intersitial nephritis

A
rapid onset  ( 2 to 40 days)
 fever, eosinophilia, renal dysfunciton with HEMATURIA but no real protenuria
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5
Q

pathologic findings of drug induced interstitial nephrtis

A

interstitial mononuclear cell infiltration and edema, eosinophils, non-nectroitizing granulomas, dilation of tubules, necrosis of epithelium

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6
Q

drug induced interstitial nephritis prognosis

A

generally good, full recovery (6 - 8 weeks) with removal of the drug and corticosteroids

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7
Q

Acute tubular necrosis

A

clinical and path condition where renal funciton declines rapidly with evidence of tubular epithelial damage/necrosis from ischemia (shock) or toxin
-acute kidney injury - oliguria (1/4-1/2 normal pee), electroylte imbalance and decreased GFR

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8
Q

what causes acute tubular necrosis

A

severe trauma, ischemia, septicemia, toxins

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9
Q

features of acute tubular necrosis

A

dilation of tubules, edema, necrosis of tubular epithelium

  • focal pathology with ischemic injury
  • diffuse injury from a toxin
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10
Q

tx of acute tub necrosis

A

supporative care, dialysis
prognosis is the absence of preexisting kidney disease fully recover, harder when other kindey disease present
-regeneration of tubular epithelium in a few weeks

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11
Q

Arterionephrosclerosis

A

thickening and sclerosis of renal arteries associated with benign hypertension
apolipoprotein L1 gene deficiency - malignant form

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12
Q

pathology of arterionephrosclerosis

A
  • grossly small kidney / atrophic (granular), thin cortex
  • hylaine arteriosclerosis and fivroelastic hyperplasia in mm. arteries (benign form)
  • hyperplasia artherioslcerosis (malignant form)
  • tubular atrophy and fibrosis
  • global sclerosis of glomeruli
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13
Q

contributing factors arterionephrosclerosis

A
  • malignant hypertension (200/120) assoc with the malignant hyperplastic arteriosclerosis form
  • diabetes
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14
Q

clinical arterionephrosclerosis

A

cranial pressure, proteinuria, ischemia leading to acute kidney injury

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15
Q

thrombotic microangiopathies

A

TTp (thrombotic thrombosytopenia purpura) and hemolytic uremic syndrome (HUS)
-widespread microthrombi in capillaries with RBC damage (schistocytes)

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16
Q

HUS

A

endothelial cell injury leads to comsumption of platelets and activation

  • mainly from shiga toxin of e. coli
  • often occurs in children
17
Q

TTP

A

acquired or inherited defect of ADAMTS (plasma protease) - degrades vWF, activates platelets

18
Q

difference in HUS and TTP

A

HUS predominately kidney, TTP can affect other organs (widespread)

19
Q

Urolithiasis

A

aka renal stones

  • result in urinary tract obstruciton, ulceration and urothelial bleeding
  • small stones to ureters and produce flank pain (serious)
  • large stones remain in the pelvis and may be manifested by hematuria and superimposed infection
20
Q

pathology urolithiasis

A

stones are unilarteral 80% of the time within calyces and pelvis (maybe bladder)

21
Q

staghorn calculi

A

large stones will form a cast of the pelvis and calyceal system

22
Q

types of stones

A

calcium (increased pee calcium), magnesium ammonium phosphate (infection with proteus or staph pre-disposes and alkaline pee)and uric acid (gout, leukemia or acidic urine)

23
Q

Hydronephrosis

A

dilation of renal pelvis/calyces with parenchymal atrophy becasue of obstruction

24
Q

causes of hydronephrosis

A

renal stones, UTI, enlarged prostate, neoplasms, meurogenic bladder, pregnancy

25
renal cell carcinoma risk factors
older adult males -smoking, hypertension/obesity, aqcuired polycystic disease from chronic dialysis, cadmium exposure and von hippel-lindau syndrome
26
clinical renal cell carcinoma
hematuria, mass, pain, fever, polycythemia (tumor producing erythropoietin) and paraneoplastic syndromes
27
pathology renal cell carcinoma
tumor invades renal vein from tubular epithelium, pale/clear forms common (large size prior to diagnosis)
28
Wilms tumor/ nephroblastoma
one of the most common cancers in children | -abdominal mass, pain - increased frequency in inherited syndromes
29
pathology wilms tumor
triphasic prolif cells with epi, stromal and blastemal components - busy looking -appears like early nephron formation
30
tx wilms tumors
surgery and chemo - very good prognosis - 92 - 95 % 5 year survival rate
31
spread of acute pyelonephritis
-spread from urinary bladder, up the ureters and into the renal pelvis ASCENDING -can also spread hematongenously
32
acute pyelonephritis etiology
urinary tract obstruciton, instrumentation, vesicoureteral reflux, pregnancy, gender (female) and age, diabetes and immune supression
33
repeated bouts of pyelonephritis
lead to chronic pyelonephritis | -mononuclear inflammatory inflammation and irregular scarring
34
large doses of analgesics may lead to..
interstitial drug induced nephritis with papillary necrosis
35
clinical presentation of arterionephrosclerosis malignant form
rapid onset of renal failure, increased cranial pressure (naseau, vomiting and visual impairment and protenuria
36
frequency of stones
by age 70, 11% of men and 6% of women will have had kidney stone
37
renal cell carcinoma prognosis
stage dependent survival stage 1 - 81% stage 4 - 8% tx: surgery ad radiation