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108 Cards in this Set
- Front
- Back
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monoclonal antibodies?
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OKT3, basiliximab, daclizumab
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polyclonal abs?
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RATG (thymoglobulin), ATG (ATGAM)
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OKT3:
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monoclonal ab, NOT used for induction
ADR: cytokine release syndrome (fever, chills, rigors, pruritis, changes in BP) use: APAP, diphenhydramine, steroids, indomethacin as premeds |
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cyclosporine:
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calcineurin inhibitor, potent immunosuppressive agent thought to inhibit IL-2
cyp3a4 substrate and inhibitor |
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nephrotoxic immunosuppressants:
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CSA, TAC
therefore NOT used at time of induction therapy vasoconstricts afferent arteriole |
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CYP 3A4 SUBSTRATES AND INHIBITORS:
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prednisone, CSA, TAC
substrate: sirolimus |
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monitoring parameters for CSA, TAC
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srcr, BUN, urine output, wt gain, edema, drug concentr.
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monitoring parameters for steroids
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sugar/glc, water retention, wt gain, BP
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what is 1st line therapy to avoid acute rejection
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use steroids with dose tapering
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MOA of steroids:
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block cytokine activation by binding to glucocorticoid response elements inhibiting IL-1,2,3,6, gamma interferon, tumor necrosis factor alpha
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ADRS of steroids:
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increase in appetite, insomnia, indigestion, mood changes, hyperlipidemia, glc alterations, wt gain, leukocytocytosis
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d-d inrxns of steroids:
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barbitutates, phenytoin, rifampin induce hepatic elim. of prednisone
prednisone decreases effectivness of vaccines and toxoids |
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what type of AB is sirolimus (rapamycin)
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macrolide ab inhibits t lymphocyte activation and proliferation
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adrs with sirolimus:
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hyperlipidemia, leukopenia, thrombocytopenia
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monitoring parameters with atg:
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lipid profile and myleosuppression (leukopenia, anemia, thrombocytopenia)
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what are the 4 types of ARF
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1. prerenal azotemia
2. functional ARF 3. acute intrinsic RF 4. postrenal obstruction |
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what is prerenal azotemia?
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decrease in renal profusion, presents with hypotensive, weakness, bleeding
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what is functional ARF:
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decrease in GFR without damage to kidney due to changes in glomerular afferent and efferent arteriole circumference, hemodynamic changes
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what is acute intrinsic RF:
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most worrisome, results from structural damage to kidney
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what is postrenal obstruction?
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obstruction of urine flow from kidney out of body, must involve both kidneys to cause ARF
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what types drugs cause functional ARF:
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cyclosporine, ACEIs, NSAIDS, hypercalcemia, hepatorenal syndrome
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what drugs cause intrinsic RF(acute tubular necrosis)?
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amphotericin B, aminoglycosides
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drugs that cause acute interstitial nephritis (intrinsic RF)?
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PCN, ciprofloxacin, sulfonamides
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drugs that cause postrenal rf?
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crystal deposition by oxalate, indinavir, sulfonamides, acyclovir
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prophylactic therapies in prevention of ARF
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hydration (sodium loading) normal saline, used to mitigate the nephrotoxicity of contrast dye, Amp B is to sodium load pt prior to giving nephrotoxin
hydration (dehydration is risk factor for ARF)- want to expand intravscular compartment and increase renal perfusion, solutions such as D5W distribute throughout the body which defies the purpose, initial rate of administration: 1-2 ml/kg/h calcium channel blockers: inhibit response of afferent arterioles of the kidney to vasoconstrictive agonists |
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have mannitol, loop diuretics, or dopamine shown to be effective in preventing nephrotoxicity?
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NONONONONONNNONNONO
NOOOOOOOOOOOOO |
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what prevents nephrotoxicity?
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hydration (sodium loading), theophylline, acetylcysteine (prior to contrast dye administration)
insulin (to maintain serum glc of 80-110 mg/dl) for critically ill pts |
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therapies that have proven benefit in preventing or treating ARF:
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diuretics: mannitol and furosemide
dopamine: dilate renal vasculature (evidence says NOT effective) |
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general clinical presentation of ARF:
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change in urinary habits
edema wt gain colored or foamy urine hypotension increase in serum creatinine urinalysis: casts, wbcs, rbcs renal ultrasound- check for renal obstruction |
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non-oliguric
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nmt 450 ml/day
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oliguric
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pt makes 50-450 ml/dy
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anuria
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urine output is < 50 ml/day
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ACEI does waht to efferent arteriole:
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dilates
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what is the most common type of community acquired renal failure?
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prerenal azotemia
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what drugs cause functional ARF
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csa, aceIs, NSAIDS
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what drugs cause acute interstitial nephritis
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PCN, CIPRO, sulfonamides
(acute intrisinic RF) |
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what drugs cause postrenal RF
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crystal deposition by oxalate, indinavir, sulfonamides, acyclovir
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what drugs cause acute tubular necrosis (acute intrinsic RF)
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amphotericin B, aminoglycosides
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what drugs are afferent arteriolar vasoconstrictors
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vasoconstrictor PG inhibitors:
NSAIDS, COX 2 inhibitors direct afferent arteriolar: vasoconstrictors, cyclosporine, amphortericin B, radiocontrast media, vasopressors |
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what drugs aer efferent arteriolar vasodilators:
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renin-angiotensin aldosterone: ACEIs, ARBs
direct efferent arteriolar vasodilators: diltiazem, verapamil (CCBs) |
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what are the indications for renal replacement therapy?
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A: acid base abnormalities: metabolic acidosis resulting from avvumulation of organic and inorganic acids
E: electrolyte imbalance: hypercalcemia, hypermagnesemia, hyperphosphatemia I: intoxications: salicylates, lithium, methanol, ethylene glycol, theophylline, phenobarbital O: fluid overload: post-op fluid gain U: uremia: high catabolism of ARF |
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what type of RRT for critically ill ICU pt?
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continuous veno-venous hemodialysis
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crcl equation:
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(140- pts age)ABW/ scr * 72
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complications associated with ckd:
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1. anemia
2. secondary hyperparathyroidism and hyperphosphatemia 3. altered fluid and electrolyte homeostasis 4. metabolic acidosis 5. malnutrition |
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corrected calcium equation
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measured total Ca plus (4- pts albumin)*0.8
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BP goals for ckd stages 1 to 4
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less than 130/80
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non HDL equation
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non HDL = TC - HDL
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what is the most common cause of resistance to erythropoietic therapy
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iron deficiency
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what is the mg of iron in polysaccharide iron?
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50 mg
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what is the mg of iron in ferrous gluconate
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36 mg
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what is the mg of iron in ferrous fumarate?
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100mg
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what is the mg of iron in ferrous sulfate
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65 mg
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calcium containing phosphate bidning agents decrease the absorption of which agents?
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iron, fluoroquinolones, zinc
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true or false: FOOD INCREASE THE ABSORPTION OF CINACALCET (SENSISPAR)
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true
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what is cinacalcet used for? moa?
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cinacalcet (sensipar): calcimimetic agent recently approved for tx of sHPT in ESKD pts and for tx of hypercalcemia in pts with parathyroid carcinomo acts on calcium sensing receptor on surface of chief cell of parathyroid
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true or false: FOOD INCREASE THE ABSORPTION OF CINACALCET (SENSISPAR)
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true
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what is cinacalcet used for? moa?
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cinacalcet (sensipar): calcimimetic agent recently approved for tx of sHPT in ESKD pts and for tx of hypercalcemia in pts with parathyroid carcinomo acts on calcium sensing receptor on surface of chief cell of parathyroid
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what are the treatment options for ckd at increased risk for uremic bleeding
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cryoprecipitate, desmopressin, estrogen
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monitoring parameters for anemia without iron deficiency
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Hb, Hct, T stat, ferritin, BP, blood loss, fatigue, weakness, SOB, angina, ADRs
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moa of sevelamer
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nonabsorbable hydrogel phosphate-binding agent which does no contain alluminum, calcium, magnesium
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what is sevelamer used for
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primary therapy in dialysis pts with severe vascular or soft tissue calcifications and used as 1st line phosphate binding agent in pts with stage 5 ckd
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what is unique about sevelamer
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lowers LDL and increases HDL
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aluminum hydroxide
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Amphojel
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Aluminum carbonate
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Basaljel
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magnesium hydroxide
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milk of magnesia
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rocaltrol
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calcitriol
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paricalcitol
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zemplar
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doxercalciferol
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hectorol
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cinacalet
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sensipar
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what vitamin d analog is associated with less hyperphosphatemia, suppresses the PTH fastest, and has an improved 3 yr survival rate among dialysis pts
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Paricalcitol (Zemplar)
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ADRs of erythropoietic growth factors
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HTN
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leading causees of CKD
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DM, HTN, glomerularnephritis
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which of the following drugs decreaes the absorption of iron
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ppis, h2 antagonists, antacids
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oral iron preparations decrease the absorption of
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fluoroquinolones
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hypophosph
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< 2 mg/dl
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hyperphosph
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> 4.5 mg/ml
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normal phos
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2.5-4.5 mg/ml
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pathophysiology of hypophosphatemia
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decreased GI absorption: phosphate binding (sucralfate, calcium carbonate-Tums, sevelamer)
increased urinary excretion: acetazolamide, osmotic diurectics, glucocorticoids, sodium bicarbonate) internal redistribution: anabolic steriods, glucagon, calcitonin, erythropoietin, insulin, dextrose |
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goals of therapy for hypophosph.
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add 12-15 mmol/L of phosphorus to IV hyperalimentation soluntions to prevent hypophor. in hospitalized pts
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mometasone
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Asmanex
powder qd, inhale quickly |
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budesimide
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Pulmicort
powder qd choice for pregnancy |
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fluticasone
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flovent
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beclomethasone
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Qvar
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flunisolide
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Aerobide
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triamcinolone
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Azmacort
INC |
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pirbuterol
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Maxair Autoinhaler
SABA |
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formoterol
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Foradil Aerolizer
LABA only used in COMBO with ICS, never monotherapy |
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Salmeterol
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Serevent Diskus
LABA only used in Combo with ICS, never monotherapy |
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montelukast
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Singular
leukotriene modifiers |
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zilcuton
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Zyflo
new ER bid 5 lipoxygenase inhibitor |
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Cromolyn
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Intal
mast cell stabilizer |
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nedocromil
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Tilade
mast cell stabilizer |
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ipratropium
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Atrovent
anticholinergic |
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theophylline
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Uniphyl
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omalizumab
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Xolair
immunomodulators last resort for pt over 12 |
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fluticasone/salmeterol
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Advair
Don't shake |
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budesonide/formoterol
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Symbicort
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green zone of peak flow meter
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89% of personal best
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yellow zone of peak flow meter
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50-80% of personal best need SABA
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red zone of peak flow meter
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<50% immediate need for SABA and MD --- ER
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LABA
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salmeterol (serevent discus)
formoterol (foradil aerolizer) black box warning increase asthma related death only used in combo with ICS, never mono-therapy not for acute exacerbation |
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ADRs of SABA
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tachycardia, muscle tremor, hyperglycemia, HA
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ADRs of ICS
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cough, dysphonia, oral thrush, osteoporosis, bruising
high doses: increased susceptibility to infection |
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4 components of asthma care:
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1 pt/doctor partnership
2 id and reduce exposure to risk factors 3 assess, tx, and monitor 4 manage exacerbations |
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mild exacerbation of asthma
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taking in sentences, increaes rr, walking, can lie down
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severe exacerbation of asthma
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hunched over
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uncontrolled asthma
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3 or more partly controlled symptoms in a week, an exacerbation in a week
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partly controlled:
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daytime sympt more 2x per week, any limitations in activity, any nocturnal symp, rescue relieft mroe than 2x per week, less than 80% predicted or personal best FEV or PEF, one or more exacerbations in a year
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