patho II test 3

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patho II test 3
2012-11-06 20:15:51

test 3 midterm
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  1. mortality rate of renal disease
  2. compare overll deaths from 2005-2009 to deaths from nephritis
    overall deaths were down by 11000 while nephrotic deaths were up by 5000
  3. what is another disease state that is raising in the rankings from 2005 to 2009 that could be associated with renal disease
  4. list and describe 4 congenital abnormalities affecting renal disease
    • agenesis -a lack or failure of development: bilateral, fatal
    • hypoplasia - condition of arrested development: unilateral more common than bilateral
    • ectopic - occuring in abnormal positins: usually at lower levels (pelvis). ureters may be linked, lead to UTI's
    • horseshoe - fusion at lower (most common) or upper: common state found in 1/500 to 1/100 autopsies (1/400 in children
  5. renal insufficiency
    renal fx ~25% of nl or GFR 25-30ml/min
  6. renal failure
    significant loss of renal fx
  7. ESRF
    les than 10% of renal fxn
  8. azotemia
    increase serum level of urea and/or creatinine
  9. uremia
    azotemia plus S&S of fatigue, anotexia, N/V, pruritus, neurologic changes due to toxic waste buildup, deficiencies, and electrolyte disorders
  10. acute kidney injury (AKI)
    • AKI term is replacing acure renal failure (ARF)
    • sudden decline in kidney fxn ans azotemia (meant to include broader range: injury from minimal to severe)
    • RIFLE criteria
  11. RIFLE criteria
    • Risk - increased creatinine x 1.5 or GFR decreased by >25%, UO <0.5ml/kg/hr x 6hr
    • Injury - increased Cr x 2 of GFR decreased by >50%, UO <0.5ml/kg/hr x 12hr
    • Failure - increased CR x 3 or GFR decreased by >75%, UO <0.3ml/kg/hr x 24 hr or anuria (abscence or defective excretion of urine)
    • Loss - Persistnet ARF = complete loss of kidney fxn > 4wks
    • ESKD - end stage kidney disease (>3months)
  12. give and explain 4 main anatomical sites of renal disease
    • glomeruli - damage often immunologic or inflammatory
    • tubules - ischemia, hypoxia, toxins
    • interstitium - toxins, drugs
    • blood vessels - vasculitis & atherosclerosis, often affects all renal structures
  13. pre-renal AKI - main cause and some examples
    • significant decrease in renal blood flow
    • renal ischemia, hypvolemia, hemorrhage, septic shock, massive pulmonary embolism, heart failure
  14. prognosis of pre-renal AKI
    with immediate, appropriate internention, pre-renal is reversible
  15. Intra-renal AKI - main cause and some examples
    • injury to nephrons
    • urine flow can drop below 400ml/day in 24 hres and to near zero soon after
    • ATN, GN
  16. prognosis of intra-renal AKI
    not immediately reversible, but with appropriate preventive and treatment measurs, may eventually be reversible
  17. Post-renal AKI - main cause and some examples
    • urinary excretion obstruction
    • stones, prostrate, post-catheterization-induced edema, tumors, neurogenic
  18. prognosis of post-renal AKI
    reversible if obstruction removed
  19. In what case was pre-renal injury happening and what was the tx
    • smoke inhalation and DIC
    • aggressive rehydration
  20. in what case was intra-renal injury happening and what was the risk
    • UTI
    • pyelonephritis
  21. in what cas was post-renal injury happening
    renal calculi/nephrolitiasis
  22. the kidney undergoes ischemic or nephrotoxic injury because of severe hypotension, aminoglycosides, or radiocontrast agents an producs granular and epithelial cell casts in urine
    acute tubular necrosis
  23. when does ATN most often occur
    post surgery (40-50% of cases)
  24. besides surgery what else is ATN associated with
    • severe sepsis
    • obstetric complications
    • severe trauma including burns
  25. are ATN and ARF interchangeable
    No, ARF failure can occur w/o ATN
  26. two general descriptions of ATN
    • post ischemic - hypotension, hypoperfusion, hypoxemia, reduced ATP, generation of ROS
    • nephrotoxic - can be produced by numerous anti-biotics, but the aminoglycosides (neomyocin, gentamicin, tobramycin) ar the major culprits
  27. three main etiologies of intrarenal acute renal injury/failure
    • acute glomerulonephritis
    • acute tunular necrosis
    • bilateral acute pyelonephritis
  28. inflammation of the glomerullus caused by numerous factors; infection, immunologic abnormalties, schemia, ree radical, drugs, toxins, vascular disorders, etc.
  29. The classification of glomerulonephritis can be described according to what five criteria
    • cause
    • pathologic lesions
    • disease progression (acute, rapidly progressive, chronic)
    • clinical presentation (nephrotic or nephritic syndrome, acute or chronic kidney syndrome)