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2011-02-05 13:40:06

Chapter 31
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  1. ANP
    • Dilates the afferent arterial and constricts the efferent arterial
    • decreases renin secretion
    • inhibits the epithelial Na channel in the DCT
  2. In diabetic patients
    The high osmolarity caused by glucose concentration increases thirst
  3. Two affects of loop diuretics
    • increase the amount of solutes delivered to the distal tubules which decrease water lost
    • disrupt the counter current multiplier
  4. Thiazides
    • block the Na Cl co transporter in the distal tubules
    • Chlorothiazide
  5. Acetazolamide
    • carbonic anhydrase inhibitor
    • proximal tubule
    • blocks Na reabsorption through the Na H counter transport, No H to exchange
    • Cause a degree of acidosis
  6. Aldosterone inhibitors
    • spironolactone and eplerenone
    • inhibit the Na K pump in the collecting tubules
    • the Na then acts like an osmotic diuretic
    • K is sparring and aldosterone inhibitors also move K from intercellular to extralcellular
  7. Na channel blocker diuretics
    • amiloride and triampterene
    • inhibit Na absorption and K secretion in the collecting tubules
    • differ from aldosterone inhibitors by directly blocking the Na absorption on the luminal side
    • This decrease in intercellular Na stops the action of the basil membrane Na K pump
  8. Three main categories of acute renal failure
    • decreased blood supply. PreRenal condition. Hemorrhage, cardiac failure, low blood pressure
    • Intrarenal
    • Postrenal. obstruction of the urinary collecting system. Kidney stones of calcium, irate and cystine
  9. Main purpose of high blood flow to kidneys
    • provide enough plasma for the high rates of glomerular filtration needed for effective regulation of body fluid and solute concentration
    • Decreased blood flow is accompanied by decreases GFR and decreased output of salt and water
  10. Oliguria
    decreased urine production below the intake of salt and water
  11. Anuria
    total cessation of urine production
  12. Renal failure may be reversed
    • as long as blood flow does not fall below 20-25%
    • basil requirement of the renal tubule cells with no ATP pumps functioning
  13. Why can the kidney survive so long with diminished blood flow
    • when blood flow is reduced the GFR is reduced
    • The decrease in GFR reduces the amount of Na and Cl filtered and in turn reduces the amount that must be reabsorbed
    • This reduced reabsorption decreases the amount of oxygen needed for metabolism by the kidney
  14. Intra renal acute failure
    • conditions that injure the glomerular capillaries or other vessels
    • conditions that cause damage to the renal interstitial
    • conditions that damage the renal tubule epithelium
  15. Causes of prerenal failure
    • volume depletion; hemorrhage, diarrhea or vomiting, burns
    • cardiac failure; MI, valvular damage
    • vasodilation and hypotension; anaphylactic shock, anestesia, sepsis and infection
    • primary renal artery; stenosis or embolism
  16. causes of internal renal failure
    • small vessel and glomerular injury; vasculitis, cholesterol emboli, malignant hypertension,
    • Tubular epithelia injury (tubular necrosis); ischemia, heavy metal toxicity
    • renal interstitial injury; pyelonephritis, allergic nephritis
  17. Acute glomerulonephritis
    • type of intrarenal failure
    • usually caused by abnormal immune reaction
    • group A hemolytic beta streptococci
    • The immune complex gets trapped in the glomerulus
    • This tapping causes mesanchial cells to proliferate, many pores become blocked and the unblocked pores become excessively permeable
  18. Tubular necrosis
    • intrarenal failure
    • severe ischemia and poisons toxins and medication
  19. Tubular necrosis cased by ischemia
    • circulatory shock or other disturbances of blood flow
    • necrotic tubule cells slough off and plug the nephrons, the affected nephrons fail to excrete urine even after blood flow is returned if the plug is still there
    • The most common causes of ischemia are the prerenal causes associated with shock; hemorrhage, anesthetics, diureha, burnes ext
  20. Toxins that can cause acute renal failure
    • carbon tetrachloride
    • heavy metals; mercury and lead
    • insecticides
    • medications; tetracyclins
    • cancer drugs
    • cause cells to slough off and plug nephrons
    • If glomerular membrane is intact cells can regenerate in 10-20 days
  21. Blockage of urine excretion, post renal
    • if output from one kidney is blocked fluid volume will not change significantly
    • contralateral kidney will increase in size and urine production
    • chronic obstruction lasting more then several hours can lead to kidney failure
    • stones, bladder obstructions, urethra damage
  22. Physiology of acute renal failure
    • retention of water, waste products of metabolism, and electrolytes
    • can lead to edema and HTN
    • Retention of K is a large problem, develop hyperkalemia. Decreases the membrane potential which leads to a decreased AP
    • Also develop acidosis
  23. Chronic renal failure
    • results from the progressive and irreversible loss of large numbers of functioning nephrons
    • clinical symptoms occur when you lose around 70-75%
    • can occur from disorders in the blood vessels, glomeruli, tubules interstitial, lower urinary tract
    • end result is always the same, decrees in functional nephrons
  24. causes of chronic renal failure
    • metabolic disorders; DM, obesity, amyloidosis
    • HTN
    • Renal vascular disorders; atherosclerosis
    • Immune
    • Infection; pylonephritis, TB
    • primary tubular disorders; toxins
    • Urinary tract obstruction
    • Congenital; polycystic disease
  25. Adaptive change after loss of kidney mass
    • the functional kidney mass will hypertrophy and compensate for the loss of tissue
    • over a period of years the renal functional changes may lead to further injury of the remaining nephrons, mostly the glomeruli
    • There is a chronic increase in pressure and stretch of the small arterioles believed to cause sclerosis
    • This cycle of compensation and damage becomes vicous and leads to end stage disease
    • Only way to slow it down is to lower renal blood pressure, ACE inhibitrs
  26. Important risk factors for end stage renal disease
    • obesity
    • DM
    • HTN
  27. Vascular lesions that can lead to renal ischemia
    • atheroslerosis; large renal arteries with progressive sclerotic constriction. Usually affects one kidney more then the other
    • fibromuscular hyperplasia;
    • nephrosclerosis; sclerosis of small arterioles
  28. Benign nephrosclerosis
    • seen in 70% of people over age 60
    • occurs in small interlobular arteries and in afferent arterioles
    • begins with leakage of plasma through the endothelium, This causes fibrinoid deposits to develop in the medial layer followed by thickening of the vessel wall
  29. Glomeruloscerosis
    • sclerosis of the glomeruli
    • increqased frequency in DM and HTN
  30. Strptococcal infection glomerulinephtits
    • Strep infection is the leading cause of acute
    • chronic is lupus
  31. chronic glomerulonephritis
    • results from the accumulation of antibody-antigen complex in the glomerular membrane
    • causes inflammation, progressive thickening of membranes, eventual invasion of glomeruli by fibrous tissue
  32. Clinical conditions of the bladder that can lead to pylonephritis
    • pylonephritis; bacterial infection of the renal interstitial tissue
    • inability of the bladder to empty completely
    • obstruction in urinary outflow
  33. Cystitus
    inflammation of the bladder
  34. Vesicoureteral reflux
    urine is propelled up the ureters during matriculation
  35. Patients with pyelonephritis
    • infection usually affects the medulla more then cortex
    • can not concentrate urine ; loss of counter-current multiplier
  36. Creatinine filtration rate
    GFR x plasma concentration
  37. Isosthenuria
    inability of the kidney to concentrate urine
  38. Ability to concentrate urine with lose of nephrons
    • the rapid flow of fluid through the collecting ducts prevents water reapsoption
    • the rapid flow through the loop of henle and collecting ducts prevents counter current from operating properly
    • As more nephrons are destroyed the healthy ones compensate more by increasing there GFR and causing the above to loses in concentration
  39. Important clinical renal function test
    test the ability off the kidney to concentrate urine when water is restricted for 12 hours
  40. You can remove a kidney in renal hypertension
    if one kidney is ischemic and is the source of excess renin it can be removed
  41. Azotemia
    • increase in non protein nitrogen
    • urea, uric acid, creatinine
    • End produces of protein metabolism
    • measuring plasma concentrations gives a good indicator of renal disease
  42. Anemia in chronic renal failure
    decrease in erythropoietin secretion
  43. Osteomalacia in chronic renal failure
    • bones are partially degraded
    • serous damage to the kidney reduces the kidneys ability to generate the active form of vit D3
    • Also a rise in serum phosphate levels binds with calcium in the blood so ionized calcium falls stimulating parathyroid hormone release
    • secondary hyperparathyroidism causes a release of calcium from the bones
  44. Angiotension 2
    increases GFR but increases reabsorption more. Increase in Na reabsorption in the proximal tubules and a lower pressure in the vasa recta so less hydrostatic pressure leads to increased water absorption and increases plasma fluid and pressure
  45. Non hypertensive renal failure
    with loss of large numbers of nephrons but no release of renin from ischemia
  46. Normal plasma glucose but glucose in the urine
    renal glycosuria
  47. Aminoacidurea
    • failure to reabsorb amino acids
    • essential cystienurea; leads to kidney stones
    • simple glycineurea
  48. Rickets that is refractory to Vit D therapy
    • hypophosphatemia
    • renal inability to absorbe phosphate
    • so signs at first but after a while lose the ability to calcify bone
  49. Two types of diabetes insipidus
    • nephrogenic; inability of the kidneys to respond to ADH
    • nerogenic; inability of the hypothalamus to produce ADH
    • Person must drink large amounts of water
  50. Faconi's syndrome
    • increased urinary excretion of all amino acids, glucose, and phosphate
    • can also have failure to reabsorb bicarb
    • increased excretion of K and Ca
    • nephrogenic diabetes insipidus
  51. Causes of faconi's syndrome
    • heriditary defect in transport proteins
    • toxins or drugs
    • ischemic injury
  52. Rate of movement during dialysis depends on
    • solute concentration gradient; greatest transfer is at the beginning when gradient is the largest
    • rate of flow
    • surface area
    • permiability