Patho 3

  1. What factors contribute to acute pyelonephritis? (p.12-13)
    • manifestation of UTI - bacteria; cystitis, prostatitis, urethritis
    • organisms - E. coli; Proteus klebsiella; enterobacter; pseudomonas
    • result of manipulation of urinary tract - catheterization; cystoscopy
    • routes - bloodstream, lower urinary tract
  2. What parts are involved in acute pyelonephritis?
    kidney and renal pelvis
  3. Clinical manifestations of acute pyelonephritis?
    (p.13)
    • pain @ costovertebral angle
    • signs of systemic infection - fever, chills, malaise
    • UA = pyuria, bacturia
  4. Azotemia
    • any substantial rise in plasma concentration of non-protein nitrogenous compounds
    • = urea and creatinine
  5. Prerenal ARF
    • result of decreased blood flow
    • - inadequate perfusion
    • - decreased glomerular filtration in presence of otherwise normal renal function
    • - no parenchymal damage
    • cause is outside kidney
  6. Causes of ARF
    • Outside kidney
    • Systemic hypotension or hypovolemia
    • - decreased cardiac output (CHF)
    • - burns, trauma (hemorrhage)
    • - dehydration
    • - bacterial sepsis
    • - bilateral renal stenosis
    • - any situation resulting in shock, thus renal hypoperfusion
  7. Is prerenal ARF reversible?
    • Yes.
    • If renal blood flow quickly restored and cardiac output normal
  8. Prolonged hypoperfusion in prerenal ARF can lead to...
    • Acute tubular necrosis
    • prolonged hypoperfusion --> severe damage to renal tubules --> ischemic acute tubular necrosis
  9. Causes of postrenal ARF
    • beyond kidneys
    • - obstruction of urethra or bladder neck
    • - ureter obstruction
    • = bilateral if 2 kidneys
    • = unilateral if 1 kidney
  10. Examples of causes of postrenal ARF
    • benign prostatic hypertrophy (BPH)
    • blood clots
    • tumors
    • renal calculi
    • foley catheter obstruction
    • urethral strictures
  11. Intrarenal ARF
    • Result of any lesion in any part of the kidney
    • - glomeruli - progressive glomerulonephritis
    • - blood vessels - malignant hypertension
    • - DIC
    • - HUS
    • - tubules and interstitium - acute tubular necrosis, allergic acute interstitial nephritis
  12. Major cause of intrarenal ARF
    • ATN - acute tubular necrosis
    • - ischemic
    • - nephrotoxic
  13. Differentiate between prerenal and intrarenal ARF in terms of parenchymal damage.
    • prerenal - NO parenchymal damage
    • intrarenal - + parenchymal damage
  14. How will urine labs differ between prerenal and intrarenal ARF?
    (urine sodium concentration, BUN/creatinine ratio, etc.)
    Image Upload 1
  15. ATN
    Acute Tubular Necrosis
    • Acute injury of renal tubules
    • Result in acute suppression of renal function:
    • - decreased GFR
    • - oliguria = UOP < 400mL/day
    • - anuria
    • - increased BUN and serum creatinine levels (azotemia)
  16. Ischemic ATN
    • Segmental necrosis with rupture of basement membrane
    • Injury to renal tubules
    • Response to shock or dehydration
    • = decreased renal blood flow
    • = decreased GFR
    • Impaired Na+, Cl-, and fluid reabsorption
    • Little urine produced
    • = not concentrated (isotonic)
    • = increased Na+ concentration (>40 mEq/L)
    • Ischemia >60 minutes not likely reversible
  17. Nephrotoxic ATN
    • No rupture of basement membrane - quicker repair process
    • Causes:
    • = poisons
    • = metals - mercury, organic solvents
    • = drugs - cephalosporins, gentamicin, tobramycin, constrast
    • Reversible if treated quickly
  18. In ARF, oliguric phase is represented by approximately how much UOP?
    (p.16)
    • < 400 mL/24 hours
    • (< 0.5 mL/kg/hr)
Author
cgordon05
ID
16849
Card Set
Patho 3
Description
pyelonephritis and renal failure
Updated