Renal & Urologic

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Renal & Urologic
2013-03-26 15:21:02

BC Boston College CRNA NU 672 Pathophysiology
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  1. Why is the right kidney lower than the left?
    It is lower because of the liver.
  2. How much of the cardiac output do the kidneys receive?
  3. What is the normal distribution of blood flow between the cortex and the medulla?
    • Cortex 90%
    • Medulla 10% (in shock, the blood shifts to the medulla
  4. How many nephrons does each kidney have?
    1 million!
  5. What does the glomerular filtrate?
    • Water
    • Glucose
    • Electrolytes
    • Creatinine
  6. What should NOT be in GFR and why?
    Proteins, WBC, RBCs - they are too big! (That's what she said.)
  7. Why is the GFR important and how much does it filter every minute?
    The GFR provides a gauge of renal function it makes about 125 mL/min!
  8. What are the three processes of the nephron?
    • 1) Glomerular filtration - glomerulus gets filtrates from the blood (ultrafiltration)
    • 2) Tubular reabsorption - put filtrates back in blood
    • 3) Tubular secretion - excrete metabolites
  9. What is the normal urine output?
    1 mL/min
  10. What is the normal specific gravity?
    How does it reflect kidney function?
    • 1.010 - 1.025
    • This reflects the ability of the kidneys to dilute or concentrate the urine.
  11. In which conditions do you expect a high specific gravity?

    Do you have too much ADH or too little?
    SIADH - too much ADH.
  12. In which conditions do you expect a low specific gravity?

    Do you have too much or too little ADH?
    Diabetes insipidus - too little ADH.
  13. Why do creatinine levels reflect the GFR?
    Creatinine is a product of creatine metabolism in the muscles that is freely filtered in the glomeruli. It's not reabsorbed from the tubules into the blood, and it's only minimally secreted into the tubules from the blood.

    Muscles don't change very much, so the levels should be relatively stable.

  14. What does this graph show?
    By the time you see a creatinine of 2.0, the kidney is functioning is down to 50-60%.

    If you wait until you see a change in levels, it's already too late.
  15. What is BUN and is it a good biomarker for kidney function?
    Blood urea nitrogen is less specific for renal insufficiency than creatinine. It is related to protein metabolism and is made in the liver.

    It may be falsely elevated if you had an upper GI bleed, the nitrogenous waste of the RBCs would contribute.
  16. What is the normal BUN:Cr ratio?
  17. What are the two main functions of the kidney?
    Elimination and Endocrine!

    Elimination: Regulate fluid, electrolyte, & acid-base balanceEliminate metabolic wastes (urea, uric acid, creatinine) and drugs and their metabolites

    Endocrine: activate vitamin D, secrete erythropoietin, participate in BP control via RAA, regulate osmolality of ECF ADH
  18. Why are kidneys so susceptible to damage?
    High BP, polycystic kidney disease, DM, infection, autoimmune diseases... its function is to concentrate everything and it encounters lots of harmful metabolites.
  19. What are the various types of renal failure?
    • Prerenal
    • Intrinsic
    • Postrenal
  20. Which type of renal failure is the most common?
  21. What causes prerenal azotemia?
    It is caused by impaired renal blood flow leading to ischemia in the nephrons.
  22. What is the most common form of intrinsic renal failure?
    ATN (acute tubular necrosis)
  23. What are the pathophysiologic processes related to renal failure?
    • Fluid volume excess
    • Electrolyte and acid-base abnormalities
    • Accumulated nitrogenous wastes
    • Hormonal inadequacies
  24. What is the onset on acute renal failure?
    Hours to days, about half the nephrons not functions. Clears up in a few weeks (<3months) or it can become chronic.
  25. What is the onset of chronic kidney disease?
    Months to years, 90-95% of the nephrons are irreversibly damaged.
  26. What are the mechanisms by which intrinsic renal failure occurs?
    ATN, interstitial nephritis, nephrotoxic drugs (aminoglycosides, IV contrast) --> Actual tissue damage to the kidney caused by inflammatory or immunologic processes or from prolonged hypoperfusion
  27. How does ATN happen?
    Destruction of tubular epithelial cells; cells slough off, causes direct obstruction of tubule, increases pressure, backleak, afferent arteriolar vasoconstriction, decreased GFR.

    Filtrates will go into interstitial space --> kidney injury

  28. How does postrenal failure occur?
    Obstruction of the urine outflow anywhere from the calyces to the urethral meatus

    (BPH, renal calculi, bladder/urethral cancer, urethral stricture)
  29. What are the 3 phases of ATN?
    • Onset: precipitating event through tubular injury; hours to days; BUN/Cr gradually increase
    • Maintenance Phase: Decr in GFR, oliguria, continual increases in BUN/Cr/K/lytes, metabolic acidosis --> HTN
    • Recovery Phase: gradual incr in UOP and fall in Cr
  30. What is chronic kidney disease?
    It is either kidney damage or a GFR less than 60 mL/min.

    The stages of CKD depend on GFR.
  31. What is uremia?
    Urine in blood.
  32. What is ESRD?
    • A GFR < 15 mL/min
    • Need dialysis or transplant
  33. What is the pathophysiology of CKD?
  34. What happens to children who get CKD?
    • Growth impairment
    • Development delay
    • Delay in sexual maturation
    • Bone abnormalities
    • Psychosocial problems
  35. How do kids < 5 y/o get CKD?
    Congenital malformations such as renal dysplasia or obstructive uropathy.
  36. How do kids > 5 y/o get CKD?
    Acquired diseases (glomerulonephritis), inherited disorders
  37. What is nephrotic syndrome?
    An increase in glomerular permeability and a loss of plasma proteins in the urine
  38. What are the characteristics of nephrotic syndrome?
    • proteinuria (>3.5 g/day)
    • hypoalbuminemia (<3 g/day)
    • hyperlipidemia (cholesterol > 300 mg/dL) - liver tries to catch up and you end up in seeing more lipids
    • generalized edema (mostly in face)
  39. If you see a patient with protein in their blood, low serum albumin, increased cholesterol, and generalized edema, what do you suspect?
    nephrotic syndrome

  40. What is the pathogenesis for glomerulonephritis?
    Glomerular injury occurs from antigen-antibody complexes because they get trapped.

    • Inflammatory damage
    • Leukocytes, fibrin, lysosomal enzymes
    • Damage to membrane permeability
  41. What is the difference between acute and chronic glomerulonephritis?
    Acute: Group A streptococcal, 7-10 days throat/skin infection, symptoms 10-21 days (hematuria, proteinuria, decr GFR, edema, HTN, oliguria)

    Chronic: Progressive course leading to CRF (DM, HTN, incr cholesterol, tubular dilation and atrophy)
  42. Why does smoking cause damage to the kidneys?
    Toxins and vasoconstriction
  43. What is the treatment of CKD?
    • Conservative management (prevent or slow the rate of nephron destruction, treat UTIs, antihypertensive therapy, stop smoking)
    • Dialysis or transplant
  44. How does dialysis generally work?
    There are two compartments and the solutes move via diffusion (urea & potassium move out, water follows them by osmosis, and bicarb moves back in). There is a semipermeable membrane and the RBC/plasma do not cross.
  45. What is a concerning complication of hemodialysis?
    Disequilibrium syndrome - mental status change caused by cerebral edema, rapid changes in solute concentration, it's easier to clear BUN than Cr.
  46. What are the advantages and disadvantages to hemodialysis?
    Advantages: more efficient clearance, short time needed for treatment

    Disadvantages: disequilibrium syndrome, muscle cramps, hemorrhage, air embolus, hemodynamic changes
  47. What are the advantages and disadvantages to peritoneal dialysis?
    Advantages: easy access (peritoneal membrane is highly vascular and semipermeable), few hemodynamic complications

    Disadvantages: protein loss, peritonitis, hyperglycemia, respiratory distress, bowel perforation
  48. What are the goal of dialysis?
    Remove byproducts of metabolism, remove volume, regulate electrolyte levels
  49. What are two neurogenic bladder disorders?

    How do they differ from each other?
    • Spastic bladder dysfunction: impaired ability to store urine
    • Flaccid bladder dysfunction: impaired ability to empty the bladder
  50. What is vesicoureteral reflux?
    It is the abnormal movement of urine into the bladder or ureter