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
Q

renal cell carcinoma risk factors

A

older adult males
-smoking, hypertension/obesity, aqcuired polycystic disease from chronic dialysis, cadmium exposure and von hippel-lindau syndrome

26
Q

clinical renal cell carcinoma

A

hematuria, mass, pain, fever, polycythemia (tumor producing erythropoietin) and paraneoplastic syndromes

27
Q

pathology renal cell carcinoma

A

tumor invades renal vein from tubular epithelium, pale/clear forms common (large size prior to diagnosis)

28
Q

Wilms tumor/ nephroblastoma

A

one of the most common cancers in children

-abdominal mass, pain - increased frequency in inherited syndromes

29
Q

pathology wilms tumor

A

triphasic prolif cells with epi, stromal and blastemal components - busy looking
-appears like early nephron formation

30
Q

tx wilms tumors

A

surgery and chemo

  • very good prognosis
  • 92 - 95 % 5 year survival rate
31
Q

spread of acute pyelonephritis

A

-spread from urinary bladder, up the ureters and into the renal pelvis
ASCENDING
-can also spread hematongenously

32
Q

acute pyelonephritis etiology

A

urinary tract obstruciton, instrumentation, vesicoureteral reflux, pregnancy, gender (female) and age, diabetes and immune supression

33
Q

repeated bouts of pyelonephritis

A

lead to chronic pyelonephritis

-mononuclear inflammatory inflammation and irregular scarring

34
Q

large doses of analgesics may lead to..

A

interstitial drug induced nephritis with papillary necrosis

35
Q

clinical presentation of arterionephrosclerosis malignant form

A

rapid onset of renal failure, increased cranial pressure (naseau, vomiting and visual impairment and protenuria

36
Q

frequency of stones

A

by age 70, 11% of men and 6% of women will have had kidney stone

37
Q

renal cell carcinoma prognosis

A

stage dependent survival
stage 1 - 81%
stage 4 - 8%
tx: surgery ad radiation