CRR 6/Kern

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julieaburch
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104486
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CRR 6/Kern
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2011-10-05 13:28:38
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CRR Kern
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CRR 6/ Kern
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  1. How is 90% of potassium secreted?
    • Renally
    • (10% GI)
  2. Where is essentially all filtered potassium reabsorbed?
    Early-to-mid distal tubule
  3. Most of the potassium that appears in the final urine is derived from secretion by what two areas?
    • Late Distal Tubule
    • Early Collecting Duct
  4. What is the effect of aldosterone on sodium, potassium, and volume levels?
    • Hypernatremia
    • Hypokalemia
    • Volume Overload
  5. Hypokalemia is classified as a plasma K level of what?
    < 3.5 mEq/L
  6. Does Hypokalemia cause acidosis or alkalosis?
    Alkalosis -- potassium moving out of the cell causes H to move in
  7. What is by far the most common cause of Hypokalemia?
    Diuretics
  8. What two tubular dysfunction syndromes are associated with Hypokalemia?
    Bartter's and Gitelman's Syndromes
  9. A urine potassium level of < 20 mEq/L indicates what?
    Hypokalemia due to diarrhea -- likely a result of using laxatives
  10. A urine potassium level of > 20 mEq/L (but still hypokalemic) indicates what?
    A hypokalemia due to urinary loss: hyperaldosteronism or diuretics, alkalosis (vomiting), tubular dysfunction syndromes (Bartter's and Gitelman's Syndromes), or Hypomagnesemia
  11. How is Hypokalemia due to Hyperaldosteronism differentiated from the other causes of Hypokalemia?
    Urine Potassium > 20 mEq/L and High BP
  12. How is redistribution Hypokalemia treated? Potassium depletion Hypokalemia?
    • Redistribution Hypokalemia: usually does not need potassium replacement
    • Potassium Depletion Hypokalemia: usually develops slowly and can be treated orally
  13. What do we need to monitor when administering IV Potassium? How do we administer it (type/rate)?
    • Cardiac Rhythm (don't want to mimic lethal injection)
    • Dilute Potassium (< 80 mEq/L)
    • Infuse Slowly (< 40 mEq/Hr)
  14. What test should be done on a patient diagnosed with hypokalemia due to hyperaldosteronism?
    MRI of adrenal gland to look for adrenal adenoma
  15. Hyperkalemia is classified as a plasma K of what?
    > 5.5 mEq/L
  16. Does Hyperkalemia cause acidosis or alkalosis?
    Acidosis
  17. What is the biggest cause of Hyperkalemia?
    Renal Failure
  18. What type of Kalemia are the following things associated with?

    Hemolyzed blood specimen
    Prolonged use of tourniquet
    Leukocytosis
    Thrombocytosis
    Pseudohyperkalemia
  19. What is major difference is seen between Acute and Chronic Hyperkalemia (other than time)?
    Acute has an abnormal EKG; chronic has normal EKG
  20. What is the treatment method for Acute Hyperkalemia?
    • Medical Emergency
    • Reverse Cardiac Toxicity
    • Shift Potassium into Cells -- Insulin; Sodium Bicarb
    • Increase Elimination -- Kayexalate (Na/K exchange agent); Dialysis
    • Stop Further Intake
  21. What is the treatment method for Chronic Hyperkalemia?
    • Low Potassium Diet
    • Avoid Drugs Causing Hyperkalemia
    • Increase Urinary Potassium Excretion -- Diuretics; Exogenous Mineralocorticoid (fludrocortisone)
  22. Identify the pathology below:
    • Tubular Atrophy, as seen in Hypertensive Nephrosclerosis
    • Shows small tubules with marked thickening of the tubular basement membranes -- a characteristic feature of tubular atrophy
  23. What are two common renal consequences of hypertension?
    • Tubular Atrophy
    • Interstitial Fibrosis
  24. Identify the pathology below:
    • Glomerulosclerosis
    • There is collagen deposition in Bowman's space, surrounding the collapsed glomerular capillary tuft (the glomerular capillary basement membranes stain darker red). This is another common feature of hypertensive renal disease
  25. What are the two main causes of renal artery stenosis?
    • Atherosclerosis
    • Fibromuscular dysplasia
  26. What can cause "renovascular hypertension" due to renin production by the ischemic kidney? This causes ischemic atrophy of the kidney. The renin production by the ischemic kidney induces hypertension. If it is unilateral, the contralateral kidney suffers hypertensive renal damage
    Renal Artery Stenosis
  27. Fibromuscular dysplasia is relatively rare. There are several different variants of fibromuscular dysplasia of the renal arteries. What is the most common?
    Medial Fibroplasia with Aneurysms
  28. Angiogram of fibromuscular dysplasia in renal artery stenosis shows irregular narrowing and dilation of the renal arteries. What does this resemble?
    "Beads on a string" or a string of sausages
  29. Identify the pathology below:
    • Renal Artery Stenosis: Medial Fibroplasia with Aneurysms
    • Note the variable thickness of the wall of the artery; normally the wall should be more or less the same thickness all around. In this case the wall is thickened on the top, thinned (possibly aneurysmal) on the lower left
  30. Renal artery stenosis has a progressive course if untreated. What is the treatment, if detected early? If detected late?
    • Early: angioplasty, stent replacement
    • Late: blockade of the renin-angiotensin system with drugs
  31. What is the gross appearance of the kidneys with malignant hypertension?
    Kidney appears swollen; there are petechial hemorrhages on the surface
  32. What are the following histological changes seen in?
    "Mucoid intimal change" in arteries and arterioles
    "Fibrinoid necrosis" in arteries, arterioles, and glomeruli
    Thrombotic lesions in arteries, arterioles, and glomeruli
    Ischemic changes
    Malignant Hypertension
  33. Identify the pathology below:
    • Mucoid Intimal Change in Malignant Hypertension
    • Marked swelling of the intima; it appears pale and edematous
  34. Identify the pathology below:
    • "Fibrinoid Necrosis" as seen in Malignant Hypertension
    • The "fibrinoid necrosis" of blood vessels refers to the accumulation of brightly eosinophilic material (probably plasma proteins) within vessel walls; it resembles aggregated fibrin.
  35. Identify the pathology below:
    • Arteriolar Thrombosis as seen in Malignant Hypertension
    • Trichrome stain shows deposition of fibrin (red) in afferent arteriole to glomerulus, representing thrombosis of the arteriole. The glomerulus looks collapsed and ischemic
  36. Identify the pathology below:
    • Malignant Hypertension
    • EM picture of glomerular capillary showing accumulation of material between the GBM and the endothelial cell lining; this is characteristically seen in malignant hypertension and the thrombotic microangiopathies such as TTP and HUS.
  37. Identify the pathology below:
    • Malignant Hypertension
    • Note the marked thickening of the wall of the two arteries, with multilayered appearance (so called "onion skinning"). There is widening of the interstitium by fibrosis, with many small, atrophic renal tubules. The glomerulus looks collapsed and poorly perfused
  38. In which causes of vasculitis is renal involvement common?
    • Polyarteritis nodosa (classic): medium sized arteries affected
    • Wegener's granulomatosis: small vessels
    • Microscopic polyangiitis: small vessel
    • Henoch-Schonlein Purpura (HSP): small vessels
    • Cryoglobulinemia: small vessels
  39. What are the following manifestations of?
    Necrotizing arteritis -- "fibrinoid necrosis" in vessel walls
    Infarction of tissue supplied by vessel
    Some types -- necrotizing glomerulitis (pauci-immune crescentic GN)
    Vasculitis
  40. Identify the vasculitis:
    Predominantly affects medium-sized vessels -- tends to involve the main renal artery or teh larger branches within the kidney.
    Usually not associated with necrotizing glomerulonephritis
    Glomeruli may suffer ischemic damage
    Multi-system disorder -- kidneys, GI, heart, PNS, musculoskeletal system, gonads, etc
    Renal involvement -- 65-100% (renal failure, proteinuria, hematuria)
    M:F ratio about 2:1
    Peak age: fifth and sixth decades
    Labs: anemia, leukocytosis, thrombocytosis, eosinophilia, high erythrocyte sedimentation rate, circulating immune complexes (30-90%)
    Hepatitis B virus surface antigen present in ~30%
    Classic Polyarteritis Nodosa (PAN)
  41. Hepatitis B surface antigen (HBsAg) is present in about 30% of cases of what?
    Classic Polyarteritis Nodosa (PAN)
  42. Identify the pathology below:
    • Classic Polyarteritis Nodosa (PAN)
    • Note the larger artery with fibrinoid necrosis of the wall
  43. What is a rare type of vasculitis that involves eosinophilia, asthma, and granulomas?
    Churg-Strauss Syndrome
  44. What is a common type of vasculitis that often involves skin, and is associated with "leukocytoclastic vasculitis"?
    Hypersensitivity Vasculitis
  45. What are the two types of renal involvement associated with small vessel vasculitis? What is the main etiology?
    • Necrosis of arteries and/or arterioles
    • Necrotizing (often crescentic) Glomerulonephritis -- "pauci-immune" (no immune complexes present)
    • Etiology: anti-neutrophil cytoplasmic antibodies (ANCAs)
  46. What does small vessel vasculitis in the kidney usually present as?
    Necrotizing/Cresentic Glomerulonephritis (clinically as rapidly progressive glomerulonephritis [RPGN])
  47. Identify the pathology below:
    • Small Vessel Vasculitis
    • Fibrinoid necrosis involving a small artery in the kidney
  48. Identify the pathology below:
    • Small Vessel Vasculitis
    • Necrotizing glomerulonephritis, with leakage of fibrin into Bowman's space. Often associated with RPGN
  49. What type of ANCA is associated with Wegener's Granulomatosis?
    PR3-ANCA (aka C-ANCA): cytoplasmic; anti-proteinase 3
  50. What type of ANCA is associated with microscopic polyangiitis?
    MPO-ANCA (aka P-ANCA): perinuclear; anti-myeloperoxidase
  51. What is defined as arterial occlusion leading to ischemic necrosis of the kidney? Causes include atherosclerosis/thrombosis, and thromboemboli.
    Renal Infarction
  52. What type of appearance does an acute infarct cause to the gross kidney? A long-standing infarction?
    • Pale
    • Yellow to tan
  53. Identify the pathology below:
    • Renal Infarct
    • This is acute ischemic or coagulative necrosis in the kidney. The cell bodies remain, but become eosinophilic; the nuclei are lost. If the persons survives, the area will likely be replaced by fibrosis (scar)
  54. What shape do scars from infarcts tend to be? What shape is caused by chronic pyelonephritis?
    • V-shaped -- tip of V points toward infarcted artery
    • Broad, U-shaped scars
  55. What are the laboratory features related to cholesterol embolism?
    • Eosinophilia
    • Proteinuria
    • Hypocomplementemia
    • May develop acute renal failure
  56. Identify the pathology below:
    • Cholesterol Embolization
    • the slit-like spaces in the center of the artery are the cholesterol crystals (actually, it's their slit-like empty space)
  57. What are the clinical features associated with Renal Cortical Necrosis? What is the most common etiology?
    • Acute renal failure with oliguria and anuria
    • Placental abruption
  58. Identify the pathology below:
    • Renal Cortical Necrosis: Acute Stage
    • This shows the characteristic features of ischemic necrosis: loss of cell nuclei, cell bodies are preserved but become eosinophilic. Both the glomerulus and tubules are affected
  59. Identify the pathology below:
    • Renal Cortical Necrosis: Chronic Stage
    • Notice that the outer surface is extensively fibrotic, with numerous sclerotic glomeruli; the inner portion is a bit better preserved
  60. How does Ischemic Nephropathy present in the following areas: glomeruli, tubules, interstitium, and vessels?
    • Glomeruli: ischemic features (glomerulosclerosis)
    • Tubules: severe atrophy
    • Interstitium: fibrosis
    • Vessels: arteriosclerosis
  61. Identify the pathology below:
    • Ischemic Nephropathy
    • Indentation of the surface overlying a scar. The V probably points to the artery that was involved

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