Renal Lecture 3 (Part 2) PV3

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  1. How long does it take for chronic renal failure to develop?
  2. In most pt w/chronic renal failure, regardless of the cause, there is a decrease in GFR to less than ___ml/min an eventually needing dialysis.
  3. What are the most common (top 3) causes of chronic renal failure?
    • DM
    • HTN
    • Polycystic kidney disease.
  4. How are ACE-I helpful in chronic renal failure?
    ACE-I may actually be protective, can slow progression of glomerular sclerosing in diabetics and others w/nephropathy.
  5. Describe the classifications of chronic renal disease
    • Stage 1:  Kidney damage with normal or ↑
    • GFR; GFR > 90
    • Stage 2:  Kidney damage with mild ↓ GFR; GFR 60-80
    • Stage 3:  Moderately ↓ GFR; GFR 30-59
    • Stage 4:  Severely  ↓ GFR; GFR 15-29
    • Stage 5:  Kidney failure; GFR < 15 or dialysis
  6. Describe the 3 stages of chronic renal failure adaption.
    • Stage 1: ↓ GFR → ↑ BUN & Cr
    • Stage 2: Potassium levels maintained until GFR ↓ to 10% of normal
    • Stage 3: ECF volume regulation
  7. In chronic renal failure, the Pt can be relatively asymptomatic until function is less than ___% of normal.
    10%; Key is relatively asymptomatic
  8. In chronic renal failure, the BUN/Cr don’t increase in direct relationship to GFR, there is certain amount of renal reserve. Only after more than __% decrease in GFR there is a significant increase in BUN and creatinine
  9. In chronic renal failure, : K+ are maintained until GFR drops to about 10% of normal. Pretty significant drop until K becomes a problem. Why is this?
    • The remaining nephrons are working overtime to secrete excess K+.
    • Also aldosterone secretion will increase, greater loss of K+ by GI tract
    • Those w/haven’t quite dropped to this level (10% of normal), may be slippery slope so if they got overwhelmed by K+
  10. What are the metabolic manifestation of CRF?
    • Hyperkalemia
    • Metabolic acidosis
    • Hyperphosphatemia
    • Hypocalcemia
    • Hypermagnesemia
    • Increased uric acid
    • Decreased albumin
  11. What are the most common electrolyte disturbances in CRF?
    • hyperkalemia
    • hyperphosphatemia
    • hypocalcemia
    • hypermagnesiumia
  12. Why do we see decreased serum albumin in CRF?
    • Albumin now going out in urine d/t loss of integrity of epithelial cells.
    • Negative charge keeps albumin in IV space, but as kidney cells die off, loose integrity and now can leave.
    • And sometimes d/t protein restrictions some pt in renal failure are on.
  13. Why do we see metabolic acidosis in CRF?
    kidney can no longer excreted the non volatile acids.
  14. Most lethal of these metabolic complications in CRF?
  15. We generally maintain ability to get rid of K pretty well for a few reasons. When would you see hyperkalemia?
    Cr clearance of less than 5-10 but in case of tissue trauma or exogenously administered K+.
  16. If K level greater than ___ or EKG changes are present, immediate tx should be initiated
  17. What is the 1st tx for hyperkalemia?
    Ca+ gluconate. 10-20ml of 10% solution. That will have an immediate onset but duration is short
  18. After Ca+ gluconate, what is the next step in tx of hyperkalemia?
    the K+ should get shifted into intracellular space (by glucose and insulin). 10 u of regular insulin and 15ml of D50W.
  19. Besides Ca+ gluconate and insulin/glucose, what else can we do to treat hyperkalemia?
    50-100 mEq of bicarb will also be useful in that situation.

    Bicarb helpful bc pt probably corrects metabolic acidosis as well
  20. For hyperkalemia, how long does the bicarb and glucose/insulin tx last?
    Bicarb has short DOA but glucose & insulin should last 4-6hr.
  21. What are the cardiovascular complications of CRF?
    • Fluid overload
    • CHF
    • HTN
    • LVH
    • Uremic pericarditis
    • Tamponade
  22. What drives the fluid overload, CHF and HTN in chronic renal failure?
    • Na/Water retention driving these.
    • As well as abnormalities in RAAS system
  23. So remember we said that we have enough functioning nephrons we don’t generally have s/s develop until 40% of functioning nephrons remain, a lot of compensatory mechanisms. What may be a common sign of the compensatory mechanism failing?
    Polyuria, nocturia. Failure of countercurrent mechanism fails to concentrate the urine
  24. What are the hematologic manifestations of CRF?
    • Anemia
    • Impaired WBC & platelet function
    • Uremic bleeding
  25. What is the common HB and Hct in CRF?
    Typically the hemoglobin concentration is in range of 6-8g/dL x3, get typical Hct in pt w/CRF
  26. When do the hematologic manifestations of CRF occur?
    Occurs when creatinine clearance is less than 30ml/min.
  27. Why do we see anemia in CRF?
    And the anemia is d/t decreased erythropoietin production along w/decreased RBC production overall and decreased RBC survival
  28. What happens because there is less HgB in CRF?
    • less oxygen carrying capacity, increase in 2,3 DPG shifts O2 dissociation curve to the right so increased O2 delivery.
    • And pt acidotic as well, also shifts cure to right helping with oxygen delivery
  29. Chronic anemia in CRF is usually well tolerated unless.....
    • Chronic anemia is usually well tolerated unless pt has CAD on top of this.
    • In general CRF patients often show a lot of fatigue and exercise intolerance
  30. What can happen to coagulation in chronic renal failure?
    • The platelets are also not really working properly, decreased platelet aggregation, defective Von Willibrand’s factor so bleeding can result.
    • DDAVP may be helpful, may increase circulating levels of factor 8 (VW factor).
  31. Why don't we give transfusions in CRF patients who have anemia?
    • Transfusions not done for many reasons. Don’t really help and may result in HLA antigen sensitization making future transplant difficult
    • However erythropoietin therapy may help w/anemia.
  32. What pulmonary manifestations of CRF?
    • Increased minute ventilation (compensation for metabolic acidosis)
    • Interstitial edema
    • Pulmonary edema (dt volume overload)I
    • ncreased A-a gradient, hypoxemia
    • & pleural effusions
  33. What are the endocrine manifestations in CRF?
    • Insulin resistance (abnormal glucose tolerance)
    • 2° hyperparathyroidism (predisposed to fx)
    • High triglyceride levels, have an abnormal lipid metabolism and that can be responsible for increased rate of artherosclerosis
    • Hormones eliminated by kidney will be at higher levels (Insulin, glucagon, growth hormone)
  34. What are the neurological manifestations of CRF?
    • Peripheral neuropathy
    • Autonomic neuropathy
    • Seizures
    • Lethargy
    • Can manifest from irritability to somnolence, impaired thinking.
    • And all of this is result of uremic encephalopathy.
  35. What are the GI manifestations of CRF?
    • Anorexia
    • N & V
    • Gastroparesis & dynamic ileus because of the autonomic neuropathy
  36. In CRF, gastric acid is secreted in increased amounts causes ulcer and GI bleeding in _-_% of patients.
  37. What parts of ESRD does dialysis help?
    It helps most of the medical complications of ESRD, hypervolemia, metabolic acidosis, metabolic disturbance, muscle weakness, HTN
  38. For hemodialysis, where is the native arteriovenous fistulas made from?
    Native arteriovenous fistulas (cephalic vein to radial artery) preferred
  39. Which is preferred, the native AV fistula or synthetic?
  40. What is good about the synthetic fistula for HD?
    Synthetic grafts need less time to endothelialize
  41. How long does the native fistula need to mature before it can be used?
    Native needs to mature for 6-8weeks before it can be used.
  42. What is important for us to know about the fistula?!?!
    • And if they have one inserted we know where the surgeon plans to create it (don’t start IV there).
  43. What is the advantage of the native graft over the synthetic graft for an AV fistula?
    patency and rate of thrombosis is better w/a native graft
  44. What is good and bad about PD vs HD for CRF?
    • Peritoneal cavity is the semipermeable membrane
    • Less efficient than HD (takes longer) but you can do it at home
    • Peritonitis is a risk
  45. In terms of the patient who is on dialysis (HD or PD) what do we need to know??
    • Goal is to have pt about 2.5kg above their dry weight when going into OR.
    • Caution w/fluids and expect these patients will be very labile
  46. Name an osmotic diuretic, it's MOA and it's tubular site of action.
    • Mannitol
    • Inhibit water reabsorption by ↑ing tubular osmolarity
    • PCT (mostly)
  47. Name an loop diuretic, it's MOA and it's tubular site of action
    • Furosemide
    • Inhibit Na-K-Cl co-transport
    • Thick asc. L of H Luminal membrane
  48. Name an thiazide diuretic, it's MOA and it's tubular site of action
    • HCTZ
    • Inhibit Na-Cl co-transport
    • Early distal tubule Luminal membrane
  49. Name an carbonic anhydrase inhibitor diuretic, it's MOA and it's tubular site of action
    • Acetazolamide
    • Inhibit H secretion & HCO3 reabs. ↓ing Na reabs.
    • PCT
  50. Name an aldosterone antagonist diuretic, it's MOA and it's tubular site of action
    • Spironolactone
    • Inhibit aldosterone, ↓ Na reabs. & K secretion
    • Collecting tubules
  51. Name an Na channel blocker diuretic, it's MOA and it's tubular site of action
    • Triamterene
    • Block Na entry into channels, ↓ Na reabs. & K secretion
    • Collecting tubules
  52. What is a bit different about carbonic anhydrase?
    • These drugs inhibit this enzyme, which is important for reabsorption of bicarb in the proximal tubule
    • End up acting as weak diuretics bc they interfere w/Na reabsorption.
  53. Why do we use carbonic anhydrase in the boring eye room?
    used to tx increased intraocular pressure because they inhibit enzyme carbonic anhydrase and cilliary processes and decrease production of aqueous humor
  54. How much carbonic anhydrase would we give in boring eye room for increased intraocular pressure?
    Intraoperatively, surgeon feels the intraocular pressure is up , they will ask us to give 250-500mg of IV Diamox intraop.
  55. Glomerulonephritis causes what % of ESRD?
    • 10-15% of ESRD (responsible for a reasonable percentage of ESRD)
    • so it’s following diabetes and HTN as most common causes.
  56. What do we typically see in glomerulonephritis?
    Inflammation, hematuria, RBC casts
  57. What are the RBC casts from?
    • The tubules are really small, what happens is because there is hematuria, look under microscope there will be these tiny little casts that form—they take shape of tubule—and have nothing but red cells in them.
    • They plug the tubules and takes on the shape of the tubules.
    • What they see when they examine the sediment on the UA.
  58. What else could case RBC casts? (besides hematuria of Glomerulonephritis)
    • Hematuria from other causes (like trauma, malignancy, *KIDNEY STONES*, UTI).
    • Also think of bladder tumor.
    • So differential in a way, kidney stone will cause a lot of pain where as a bladder tumor won’t. (kidney stone is common cause of hematuria
  59. What is the primary cause of glomerulonephritis?
    Primary – inflammatory disease of kidneys may be IgA mediated or post-stretococcal
  60. What are secondary causes of glomerulonephritis?
    Secondary – associated with DM, HTN, SLE
  61. What 5 syndromes are associated w/glomerulonephritis?
    • Asymptomatic hematuria
    • Acute glomerulonephritis
    • Rapidly progressing glomerulonephritis
    • Chronic glomerulonephritis
    • Nephrotic syndrome
  62. Name the types of Tubulointerstitial
    • Acute Interstitial Nephritis
    • Pyelonephritis
    • Chronic Tubulointerstitial Nephropathy
  63. What is acute interstitial nephritis?
    Inflammation of interstitium around tubules
  64. What will we see in acute interstitial nephritis?
    • Renal insufficiency, sterile pyuria, WBC casts
    • Hematuria & proteinuria (not as likely like in glomerulonephritis)
    • Rash, fever, eosinophilia
  65. What are the causes of acute interstitial nephritis?
    Cause – drugs (antibiotics, NSAIDs), infectious processes, autoimmune processes
  66. What is pyelonephritis?
    • Acute inflammation 2° bacterial infection
    • Can be particularly nasty in elderly or immunocompromised patients
    • Sepsis can result.
  67. Chronic Tubulointerstitial Nephropathy is a common cause of CRF. What would we see?
    Pyuria, mild proteinuria, minimal to no hematuria, hyperkalemia, metabolic acidosis, polyuria
  68. What is the cause of Chronic Tubulointerstitial Nephropathy
    Chronic NSAIDs or tylenol
  69. List the disorders of tubular function
    • Bartter’s syndrome
    • Gitelman’s syndrome
    • Liddle’s syndrome
    • Pseudohypoaldosteronism type I
    • Fanconi’s syndrome
    • Renal tubular acidosis (group of disorders)
  70. Are disorders of tubular dysfunction largely inherited?
  71. Bartter’s syndrome: what did Sue say about it.
    • Autosomal recessive
    • 2 forms: Neonatal & “Classic form” (onset age 2-3 years)
    • (it's a disorder of tubular function)
  72. Is it Gitelman’s syndrome recessive or dominant?
    • Autosomal recessive
    • (it's a disorder of tubular function)
  73. Is Liddle’s syndrome recessive or dominant?
    • Autosomal dominant
    • (it's a disorder of tubular function)
  74. What is Pseudohypoaldosteronism type I? Is it recessive or dominant?
    • Autosomal dominant
    • Resistance to aldosterone with sodium loss
    • (it's a disorder of tubular function)
  75. What is Fanconi’s syndrome caused by? Is it dominant or recessive?
    • Autosomal recessive
    • Acquired in heavy metal poisoning & exposure to certain drugs including chemotherapeutics
    • (it's a disorder of tubular function)
  76. What is Renal tubular acidosis (group of disorders)???
    Altered sodium and chloride transport resulting in hyperchloremic metabolic acidosis
  77. A type of renal cystic disease is Polycystic kidney disease, is it recessive or dominant?
    • BOTH! (autosomal recessive or dominant)
    • Recessive: 1/20000 live births
    • Dominant: 1/800 live births (more common)
  78. How often dose ESRD develop in Polycystic kidney disease?
    ERSD develops in 50% of cases
  79. Name some systemic diseases w/renal involvemen
    • Hypertension
    • Diabetes mellitus
    • Sickle cell disease
    • Vascular diseases of the kidney (if there is vascular disease systemically then they’ll be vascular disease in the kidney and that can lead to renal failure)
  80. What treatment may be necessary in polycystic kidney disease?
    Nephrectomy may actually be necessary because of pain or infection for these patients.
  81. Trauma can cause Rhabdomyolysis. Wha tis this and what does it have to do w/RF?
    • Release of damaged skeletal muscle contents
    • Myoglobin is responsible for renal injur (same kind that HB can cause from incompatible blood transfusion)
  82. What is Abdominal compartment syndrome? What does this cause?
    • ↑ Intra-abdominal pressure causes organ dysfunction
    • Hypotension
    • Respiratory compromise
    • Mesenteric (liver & kidney) ischemia
    • Renal failure
  83. When would abdominal compartment syndrome occur?
    That usually results if the pt is multiple trauma, lots of IVF, and now sequestration of that fluid.
  84. What changes in U/O would we see w/abdominal compartment syndrome? (Each pressure will cause....)
    • Oliguria when intra-abdominal pressure is > 15 mm Hg
    • Anuria if > 30 mm Hg
  85. What is the usual treatment for abdominal compartment syndrome?
  86. What is the key for anesthesia and the kidney?
    Key here is really preserving renal blood flow and perfusion pressure to the kidney, suppressing vasoconstrictor, salt retaining stress responses from surgical stimulation, post-op pain, and of course avoiding nephrotoxic agents
  87. What types of Nephrotoxicity are we concerned about w/anesthetic agents
    • Fluoride induced (Enflurane & Methoxyflurane)
    • Vinyl halide induced (Sevoflurane- Compound A)
  88. What are the effects of surgery itself on renal function?
    • Blood volume losses (volume and O2 carrying capacity is lost)
    • Risk of trauma to GU system organs (esp GYN)
  89. Fentanyl, MSO2, Demerol we dose according to GFR. Describe this dosing.
    • If GFR is greater than 50ml/min we can give 100% of the normal dose.
    • If it’s 10-50ml/min we want to go down to 75% of the normal dose.
    • If it’s less than 10, we want to give 50% of the normal dose
  90. What three pain medications do we not change the dosing according to GFR?
    For Alfentanil, Remifentanil, and Sufentanil, we can give 100% of the dose for any GFR
  91. For our pre-anesthesia assessment, what are we concerned about for our patient w/renal disease?
    • Normal renal function or not. If not, if RF, then look at whether they are on HD.
    • How impaired is their renal function?
    • If not on dialysis, use lab values to  their renal function.
    • Are they making urine?
    • Is renal function stable, getting worse, or getting better?
    • If on dialysis, assess volume status. Need to know when they were last dialyzed.
    • Depending on situation, basic monitoring or ECHO may help w/volume assessment also.
  92. What labs would we check in pre-anesthesia assessment?
    • Beside renal function, most impt is their potassium.
    • Any elective surgery should be postponed in K is above 5.5.
    • Acid base balance might be nice to check, but not always necessary.
  93. What should we keep in mind in general when giving medications to someone in RF?
    think in terms of fact they will general volume of distribution is big, decreased clearance, decreased protein, so less protein binding and more free drug.
  94. What should we keep in mind regarding pre-op mediations?
    • And uremia will disrupt the BBB. So they will be more sensitive to sedatives.
    • So if we’re sedating pt pre-op, be cautious.
    • May want to give an H2 blocker because of their acidity.
  95. For induction drugs: what should we keep in mind for our patient in RF?
    • Succinylcholine: caution w/K+ but at same time, they have autonomic neuropathy, they have a lot of stomach acid. So make a thoughtful choice depending on pt situation. Careful to take all these things into consideration.
    • Cisatracurium: best choice of NDMR but think in terms of onset. Can load up by giving more and get quicker onset but how long will surgery be?
  96. What about IVF administration in the patient in RF?
    • Don’t want K+ containing IVF so often NS is used.
    • If not on dialysis give 3-5ml/kg/hr.
    • If on dialysis, then only replace insensible water losses.
    • Some people will say to replace it w/D5W, if urine then replace u/o w/0.45% NaCl
  97. In RF patient, Replace Blood w/usual 3:1 if blood loss is less __% of total blood volume if more than ___% of blood volume  more like 1:1. of blood to prevent overload
    10%; 10%
  98. How can anemia effect our volatile anesthetics?
    • Anemia can decrease the blood gas solubility of volatiles.
    • If solubility decreased then more rapid onset of volatiles.
  99. What two pain medications (on the last slide) should we avoid in a kidney transplant?
    • Ketorolac
    • Morphine
  100. What are our pre-op concerns for the patient undergoing a kidney transplant?
    • Full set of labs: chem, coags, CXR, EKG.
    • And co-morbidities like PFT may be indicated.
    • Need to know status of dialysis and if not performed 6-8hr prior to surgery, check K+ and assess volume status in pre-op area.
    • Pt have increased risk of atherosclerosis so need to determine CV risk, DM or HTN, or demonstrated atherosclerosis.
    • Maybe if that’s the case need further CV workup pre-op.
  101. How long is a kidney transplant surgery? What is the blood loss?
    • Procedure is short, less than about 3hr
    • Usual minimal blood loss
  102. Do they take out the damaged non functional kidney when doing a kidney transplant?
    • And usually for the recipient, the donor kidney is put in non-anatomic position.
    • Don’t take out diseased kidney to put in the donor kidney.
  103. Describe how the arteries and veins are attached in a kidney transplant
    • Renal artery of the donor anastomosed to the external iliac artery of the recipient and the venous anastomosed is the same.
    • The renal vein of the donor kidney is anastomosed to the external iliac vein of the recipient
  104. What is the preferred agent for induction w/a kidney transplant?
    There isn't one, just be careful w/dosing!
  105. You'll see urine output right away with a kidney transplant. What things might we give to increase u/o and improve funciton of the graft?
    Often have us give Mannitol, loop diuretics,+/- dopamine, maybe phenolapine to increase u/o and improve function of the graft.
  106. To prevent rejection in a kidney transplant, what might we give?
    Steroids (methylprednisolone)
  107. Immediate urine production is seen in over __% of living donor pt and __-__% of cadaver transplants
    90%; 40-70%
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Renal Lecture 3 (Part 2) PV3
2013-11-19 02:47:06

11/18/13, renal lecture 3 part 2
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