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263 Cards in this Set
- Front
- Back
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What is definiation of CKD
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Kidney damage or proteinuira for at least 3 months with or without decrease in GFR or
GFR <60 for >3months w. or without kidney damage |
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How many stages are there of chronic kidney disease
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0-5
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What is normal GFR
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120ml/min
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What is stage 0
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increase risk for CKD, GFR >90 ml/min +risk factors such HTN and Diabetes
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What is goal of stage 0
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screening and risk reduction
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What is Stage 1
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Pre-clinical CKD, GFR >90, but evidence of kindey damage
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What is goal of Stage 1
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reverse or stabilize Cardiovascualr risk reduction
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What is Stage 2 CKD
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Mild CKD, GFR 60-89 ml/min, and + evidence of kidney damage and adapting is occur
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What is goal of Stage 2
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Reverse or stabilize CVD risk reduction
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What is last stage of CKD reversal
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Stage 2--
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What is Stage 3 CKD
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Moderate CKD
GFR 30-59 |
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Does Stage 3 have too much damge to reverse
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YES
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What is goal of stage 3
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slow progession or stabilize, treat complications CVD risk reduction
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What is stage 4 CKD
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Severe CKD
GFR 15-29 |
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In Stage 4 progression to ESRD is within
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2-4 years
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What is goal of Stage 4
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slow progession, prepare for replacement, treat complications
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What is Stage 5 CKD
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Kidney failure GFR <15 ml/min
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Stage 5 is AKA ESRD, ESRD also is an adminstrative term for pts that
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have undergone transplation or are on dialysis
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What is goal of Stage 5
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RRT, treat complications
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Where is Uremia seen
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Stage 5 (build of nitougenous wastes + symptoms)
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Should you evaulate pts with diabetes or other higher risk populations YEARLY for CKD, using what
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Spot unrinary ablumin
mincoanalysis of urine |
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After an insult to kidney it leads to loss of nephrons, what happens
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adaptation, good nehprons increase in size and fuction
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After kidey adpats, solute balance is maintain though
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increase GFR of remaining nephrons
Increase in secretion Decrease in reabsorption |
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What is the negative consequnce of adaptation
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progression of kidney failure, other nehprons begin to wear out, and also die
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Progession of CKD is fueled by
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adaptation
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Loss of nehprons leads to
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Afferent Arteriole dialtion and efferent contsrition, leading to Increase GFR and Glomerular Pressure
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Increase in Glomerular pressure leads to
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capillary and endothelial and dysfuction, basement membrane thicking, and proteinuria
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What does proteinuria causes
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increase cytokines, and inflamation, causing glomerular and fibrotic scarring,
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Glomerular and tulointersitatla fibrotic scarring leads to
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damage adn slow loss of remaining nephrons
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What generally prevents proteinuria
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GBM (-) change glycosaminoglycans which are both CHARGE and SIZE exulusin
Epthelai cells (podocytes)(-) and charge exculsive |
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The GBM (glomerular basement membrane) is
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BOTH CHARGE and size exlusive, where epitherial cells are coated in (-) cahnge and only CHARGE exclusive
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Direct glomerular injury and HTN lead to damge to filtration barrier, which leads to
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proteinuria
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What are factors that Increase progression of kidney disease
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Backwards GODSHEMP
Genitics, Obesity, Dyslipidemia, Smoking Hyperglycemia, elveated BP, microalbumiura, presistants of iniation factor |
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Identification in easly stages of CKD is essentail, --and agressive managment of "progression factos" such as
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Weight Loos
Dyslipidema control Smoking cessiver Glycemia Control |
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It is important to control BP in CKD, and what is Goal
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YES goal in <130/80
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A goal of <125/75 only if
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>1g/day of proteinuria
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What is recommended treatment to optimize BP control in CKD
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ACE I or ARB are drug of choice
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You may need 2-3 drugs to get BP control , what is prefered inital combo
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ACE or ARB + thiazide diuretic
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The earilest clinical evidece for nephropathy is micoalbuminuria, which is
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LOW by abnormal amts of albumin in urine (30-299)
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Micoalbuminuria indicates the presence of
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increased glomerular capillary pressure
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Treatment of micoalbuminura can
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reverse or SLOW progession of CKD
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What is macroalbuminura
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>300 albumin/creatine
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Macroalbuminuria is assoicated with a
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progessive decline in GRP, increased BP, and high risk for kidney failure
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75% of diabetics with MACROabluminura will progress to
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ESRD in 20yrs
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Treatment of macroalbumuira can
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slow the progession to ESRD
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All pts with CKD or risk factor for CKD should be screened for
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albuminuria
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Diagnosis for albuminurai is only made after
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2 out of 3 + samples during a 3-6 month time period
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What are factors that can falsely increase albuminuria
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High protein meal
hematuria high blood pressure infection or dehydration |
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MAIN TREATMENT OF MICO or MACRO albuminuira with or WIHTOUT HIGH BP, should be treated with
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ACE or ARB to reduce abluminura b/c decrease Pressure in glomerulus
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What do ACE-I or ARB to
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Dialate efferent arteriole, which decrease GFR, adn Glomerular pressure, which decreases microalbuminuria
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A Decrease in GRF over the long term
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protext the kidney
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Improving glycemic control in both type 1 and type 2 daibetes cna
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decrease progession CKD
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Goals of glycmic A1c
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<7%
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Goals of pre-prandial glucose
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70-130
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Goals of post-prandial glucose
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<180
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Can protein restriction prevent CKD progession
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in pts with 3,4,5 CKD
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Correct of Dyslipidemia, smoking cessation and weight loss does what
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preventing progession of CKD
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What are complications of Stage 3-5 CKD
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VVEEGANN HIM PS
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The kidney metabolic fuction is metabolizing insulin, in CKD what happens to insulin
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decreased degration, leadsto increase insulin, and increased risk for hypoglycemia
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Hypoglycemic is even more common in diabetic pts on
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exogenous insulin
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CKD pts are always have hypothermia, or a body temp 1 degree lower, which means
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they have a fever at lower temperature
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A complication of Stage 3-5 Kidney disease is Na+ and H20 retnetion, what happens to FEna
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decrease
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Stage 3-5 CKD retains Na+ and H20, leading to
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HTN and edema
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Stage 3 GFR what happens in Na and H20
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decreased ability to dilute or concentrate urine
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Stage 4 GFR what happens in Na and H20
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decreased ability to adjust to change in Na and H20
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Managment of Na and H20 rentention in stage 3-4 CKD
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no salt added diet
cation with Na and H20 Treat edema with high doses LOOP diuretics + thiazides |
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Managment of Na H20 renetion in stage 5 CKD
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2-3 gram day restriction
1 Liter/day restriction High doses of loop diuretics + thiazies diuretics + dialysis |
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When does Hyperkalemia become a problem in CKD
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Stage 5
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Normal levles of K+ are maintained in stages 3 and 4 b/c of 2 mechansims
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increase DCT secretion of K+ in remaining healthy nehprons
increase K+ secretion into colon |
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What are things taht worsen hyperkalmia in CKDq
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metabolic acidosis, and constipation
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What drugs can worsen hyperkalemia
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Beta-blockers, Ace I, ARBS K+ sparing diuetics
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What is goal of K in CKD
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40-5.5
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What is magmenet of Hyperkalemia in CKD
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1. Treat underlying cause (meds, constipation)
2. Dietyary K+ restrciton 3. Med Therapy |
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What is chronic therapy treatment of hyperkalemia
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sodim polystrene sulonate (Exchanges Na for K could lead to edema)
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What is acute therapy for hyperkalmia
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1. Dialysis
2. IV Ca glucanote (arryhtmias) 3. insulin/glucose albuterol |
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What is mechanism of Acute Dialysis
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diffusion (removes K
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What is Acute/Fast mechansim for IV Calcium Gluconate
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Coutneracts K+ effect on heart (does not remove K
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How does actute/slow: Insulin + Glucose (Dextrose) work
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extraceulalr to intracellualr shift does not removed
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How does acute/slow Inhaled B-agonsits work
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Extraceullar to intracellular shift (does not remove)
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How does furosemide removed K
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urinary elimination
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What causes Metabolic acidosis in CKD pts
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impair renal amminonia production, decreases H+ excretion
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What does metabolic acidosis also contribute to
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hyperkalemia, renal bone disease, fatiuge, malnutrion and uremic sysmteims
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In CKD metabolic acidosis must first be evaluated for other causes (other than uremia)
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YES
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WHEN do you treat metabolic acidosis in pts with CKD
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when bicarb levels are <20meq/L AND symptoms are present
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Medication treatment for metaoblic acidosis
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Sodium Bicarb
Shol's Solution or Bicitra |
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What is Shohl's solution or bicitra
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Na citrate and critic acid--converted to bicarb
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Is drug therapy of metabolic acidosis needed once pt on dialysis
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NO--dialysis can correct
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Goal of HCO3 in CKD
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22-26
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What are complications of vitamins and minerals
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aluminum toxicity
hypermagnesemia decreased folic acid and other water soluble vitamin |
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What products should you avoid that have aluminum and magnesium
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maalox, mylanta
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Decrease folic and other water solbule is common on pts on dialsysi, need to replace with
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kidney pt specific vitamis
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When do complications of amemia begin in CKD
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develop GFP <60ml/min
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What stage does anemia begin in CKD
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signs and symptoms as early as stage 3
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How may pts with stage 5 CKD have anemia
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90%
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What should be check annual for anemia
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Hgb
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What are complications of anemia
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angina, HF, impaired sexual function, increased mortality, and increased hosptialization
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Symptoms of Anemia
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fatigue, SOB, cold intolerance, mental slugginshness, and chest pain
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The pathophysiology of anemia is mutifactorial, what is #1 cause of anemia
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decrease kidney production of EPO (erythropoietin
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EPO is produced in response to
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hypoxia
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90% of EPO is made in kidneys 10% in liver,what does it stimulates
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proliferation and differntiation of RBCs in bone marrow
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What are other causes of anemia besides decreased kidney production of EPO
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uremic toxins can inhibit
reduced RBXC life span iron deficiney folic and vit b12 or blood loss |
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When should Anemia WORK-UP begin
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when HgB fall <13.54 g/dl men
<12g/dl women |
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What is needs in Anemia work up
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rule out other causes, CBC, Iron studies
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What iron studies are needed
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ferritin and %transferrin saturation (TSAT%)
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What is Transferrin
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immediately available iron
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WHat is Ferritin
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stored iron
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Can you prevent or revese signs/symptoms and complications of anemia
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YES decrease left venticular hypertropy, and risk for CVD , imporve survial and quality of life
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When do you consider therapy for anemia
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HgB <11g/dL
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What are 3 steps for managment of Anemia
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1. Replete iron stores
2. Start chornic EPO replacement therapy 3. Prevent iron deficieny with maintenance therapt |
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What is an iron deficiency for PD-CKD or ND-CKD
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Ferrtin <100ng/ml or TSAT <20%
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What is iron deficieny for hemodialysis CKD
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Ferrtin <200ng/ml or TSAT <20%
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How do you replete iron stores if defiicent
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USE IV Iron Therapy to replete stores
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What are IV Iron Therapy available
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IV iron Dextran
IV Sodium ferric glconate in sucrose IV Iron Surcrose |
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Which IV iron therapy is not used as other due to side effects and NEED TO GIVE A TEST DOSE to prevent anaphylactsis
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IV IRON DEXTRAN
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What is goal of Iron stores if deficient
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HD-CKD Ferritin >200 and TSAT >20
PD-CKD and ND-CKD Ferrtin >100 and TSTAT >20 |
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What is 2nd step if HbG <11
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Administer EPO
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What types of EPO are available
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epoetin alfa
darbepoetin alfa |
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Epogen is recombinatnt human epoetin-alpha, what are routes available for use
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IV or SC
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Who is IV route used in and dosage in epoetin alpha
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Hemodialysis CKD pts dosed 3x a week with dialysis
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Who is SC route used in and dosage in epoetin-alpha
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PD-CKD or ND-CKD, dosed once or twice
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Can SC route of epoetin-alpha cause pain with injection
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YES
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Darbepoetin alpha has a unqiue molecular structure that allow for
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less frequent dosing, once a week to once a month
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Dosing for IV or SC darbepotein
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same (use IV for HD-CKD
use SC for ND-CKD or PD-CKD |
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Is there a conversion needed to switch pts from epoetin to darbepotein, and price
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YES conversion needed, darbepoetin much more expensive
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What is goal to maintain Hgb in CKD pts
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11-12 g/dL
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What HgB should I not exceed
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13 g/dL--pts do worse
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How long should one wait between dosage adjusts of EPO
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2 weeks
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Main side effect of EPO
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hypertension
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Is treatment once started for EPO--for LIFE
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YES
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What is step 3 of Anemia managment
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Prevent iron deficiency with maintenance iron therapy
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What is goal of preventing iron deficiency with maintaance iron therapy
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maximize effect of EPO
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What are dosage forms availalbe for giving a maintenace iron therapy
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Oral for ND-CKD or PD-CKD
IV for HD-CKD |
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What is oral therapy given for ND-CKD or PD-CKD
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elemental iron 200 in divided doses
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Iron therapy maybe ineffecitve alone to prevent the development of iron deficiency
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YES
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Maintaince IV is perferred for hemodialysis patients, example is
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Iron Sucrose IV once a week
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WHat is last CKD stage that maintains phosphate balance
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Stage 3 GFR <50
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When GFR is <50ml/min how is phophate balance maintained
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decrease phophate filtration, which stimualtes PTH secretion, and PCT reabsorption of phosphate, which maintain normal phosphate levels
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What happens when GFR <30ml/min
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decrease filration and Decreased PTH reabsorption of phospahte leads to HYPERPHOPHTATEMIA
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What are physiological actions of hyperphosphatemia
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decreases Vit D activation, decreases GI absopriton of Ca, and decrease serum Ca+ levels, in addtion increase stimulation of PTH secretion, leading to SECONDARY HYPERPARATHYROID
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What does Secondary hyperparathoridsm lead to
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incrase bone resoprtion, and leads to RENAL BONE DIASES (Osteisis Fibrosa Cystica)
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What is most common type of bone disease
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Ostetis fibrosa cystica
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What are other renal bone diseases
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osteomalacia (Vit D deficency)
Osteopenia/osteoprosis |
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What are symtoms of renal bone disease
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increase in fractures, bone pain, muscle weakness,
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Causes of Major complication of hyperphophatemia
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increae ca+ can lead to precipatation >55, l
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Complications of hyperphopahtemia
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extravascular calcification of joints, veesels, soft tissue other vital organs, and increased risk for CVD
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Treatment of hyperphosphatemia
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Dietary PO4 restriction
Phosphate Binders |
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Treatment of Secondary Hyperparathyroids
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1. treat hyperpohphatemia
2. treat vit D deficiency 3. give vit D 4. parathyroidectomy |
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What foods should one avoid that are high in phosphours
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milk, cheese eggs
beans ,choclate beer, carbonated beverage meats peanut butter, yogurt, ice cream |
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What foods should one avoid that are high in phosphours
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milk, cheese eggs
beans ,choclate beer, carbonated beverage meats peanut butter, yogurt, ice cream |
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When should dietary phsophate restriction begins
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Stage 3 or GFR <60
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How much should one reduce intake of phosphate
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60% of normal
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Dietary restirction alone is usually inadequate to control phosphate levels in what stage of CKD
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Stage 4
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Where do phosphate binds bind phosphate
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duodeum and jejunum
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IMPORTANT conseuling pts while taking phosphate binds
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NEED TO BE TAKEN WITH EACH MEACH< and ANY SNACKS that are high is phosphorus
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Are phosphate binds life-long treatmetn
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YES
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What is a first line therpay option for hyperphophatemia
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Caclium Carbonate
Calcium acetate |
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Caclium carbonate and Calcium acetate should not be used into pts with
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Serium Ca X PO4 products >55 mg/dL or high Ca or low PTH
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What are max doses fo Caclium carbonate and Caclium acetate daily
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1500 mg/day of elemental calcium or 2000mg day total for diet +binders
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What happens if one exceeds 1500mg day or elemental calcium or 2000mg total diet +binders
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increased risk for CVD
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What are side efffect of Caclium carbonate, or Caclium acetate
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constipation, nausea
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Caclium Carbonate is availabe as an TOC, has more elemental Ca, benfits of more expensive Rx Caclium actate
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less elemental Ca, better binder
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What is 1st line optino in patients with Serum Ca x PO4 product >55, high Ca or low PTH
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Sevelamer Hcl (Renagel) or Sevelamer Carbonate (Renvela)
Lanthanum Carbonate (Fosrenol) |
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What is MOA of Sevelmar HCL or Renagel or Sevelamer Carbonate (revela)
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Non-absorbable polymer does not contain Ca+ Mg+ or Al+
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What is benift of Sevelmar carbonate or Sevelamer HCL
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Carbonate possibly less SEs
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What is different about Lanthanum Carbonate or Fosrenol
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chewable-only tablet
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Can you take combinations of different phosphate binders
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Calcium Binder, Sevelmare, or Lanthanum
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What is the only short-term use Phosphate binder
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Aluminum hydroxide
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What is max useage of Aluminum hydroxide, and why
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30days, due to side effects eg. osteomalacia, anemia, fatal neurologic syndrome
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When should you consider use of Aluminum hydroxide
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when PO4 >7.0 mg/dL or correct calcium >11 or Ca X PO4 >65
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How do you treat vitamin D deficiency and secondary hyperparathroids in Stages 3-4 CKD
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can give unactivated form
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In Stages 3-4 CKD, 25-hydroxy vitamin D levels should be measure, how are treater if <30 ng/ml or >30
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<30 erogcalciferol
>30 cholecalciferol to maintain normal levels |
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How do you treat vitamin D deficiency and secondary hyperparathoridism in Stages 4-5
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use activated vitamin D
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What is benefit of actvivated Vitamin D3
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decrease PTH synthesis prevents or reverse hyperplasmis
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What is downside to useing activated vitamin D3
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increase calcium and phospahte absroption from gut and can lead to probelsm
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When do you NOT use activated Vitamin D
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if Ca or Phos are above target range
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What is active vitamin D
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calcitriol Vit D3
Analogs Vit D2 |
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What dosage forms are available for calcitriol
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Oral
IV |
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How is calcitriol dosed for oral/IV
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IV-- 3x week with dialysis
PO--TIW or QD |
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SEs of calcitriol (less with Analogs D2
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increase Ca and PO4
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What is benifit you using Vitamin D2 anaglos
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less likely to increase Ca and Phosphate levels
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What is MOA of Cinacalcet
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acts directly at calcium sensing rectpor on PTH to decrease PTH secretion
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What is indication for Cinacalcet
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secondary hyperparthroidusm in CKD pt on DIALYSSI
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Benefits of Cinacalcet
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does not increase Ca++ or PO4
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Can Cinacacet be used in addtion with vitamin D agents or in place
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YES
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Dosing of Cinacelcet
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once daily with meal
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SEs of Cinacalcet
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N/V, hypocalcemia, and drug interactions
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Another Complication of CKD is Uremic Bleeding causes of Uremic Bleeding
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decreased platelt aggregation/adhesiveness
alteration in platelt vessel wall interactions increased capillary friability |
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What are smtpoms of uremic bleeding
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ecchymosis, purpira, nose bleed, GI bleeds, and proglonged bled from venipunctue sites
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What are severe complication of uremic bleeds include hemorrhagic pericarditis, what should CKD pts avoid
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ASA, NSAIDS, 81mg OK
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What is treatment of uremic bleeding
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IV DDAVP, conjugated estrogens
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Another Complication of CKD is GI, symptoms inlcude
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nausea, vomiting, anoreix, diarrhea, gastric, abnormal mettallic taste, hiccups
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Treatment of Gastroparesis (slowing down of GI)
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erthromycin or metoclopramide to speed up motility
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Treatment of Gastricitis/esophagits
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H2 antagoinst of PPI
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Another complication is hypertension, what causes hypertension
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increased ECF, increased renin, increased sympatehtic activity, calcification of blood vessels, EPO use
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Treatment of Hypertension
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Dialysis
Na and H20 restrction drug therapy |
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What is goal BP pre-dialysis
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<140/90
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What is goal BP post dialysis
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<130/80
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Are we concerend about protecting kindey in Stage 5
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NO--instead heart
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Low serum albumin is
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#1 of increased mortaility
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What are absolutino contraindications of transplantation
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advanced forms (stroke CAD, caner , sevre pyshiactic illness, or persistant substance abuse
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What are lab levels for Scr and BUM for need for chronic dialysis
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Scr >12
BUN >100 |
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Signs and symptoms that indicate need for chonric dialysis
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intractable N/V
severe Hyperkalemia Uncontrolled fluid overload Pruitis, myoclonus |
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What are acess route of hemodialysis
|
ateriovenous fiust
areriovenous graft central venous catherter |
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And ateriovenous fistula anastamosis an antery and vein, requires
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1-2 to mature (to arterlize)
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An ateriovenous graft is an artifical conncention between artery and vein, takes
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2-3 weeks to mature
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Where is centeral venous cather place
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femoral subclavian or interal jugular vein (used more immediately
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The Dialysate soultion for hemodialysis contains purified water, and what electroyles
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NORMAL Na, Cl Glucose, decreased K Ca adn increased Bicarb
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What is contained in a dialysis prescription
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Blood flow rate
dialysis flow rate time ultrafiltarion rate (goal fluid loss type of dialyzer |
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Fluid removal on hemodialysis is AKA, and occurs as result of
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ultrafiltration occurs as result of hyrostatic pressure
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How are mtabolic wastes/solutes removed
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diffusion
convenction--wehre dsollved solutes are dragged acrosss the membrane with fluid via ultrafiltration |
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What are Hemodialysis SEs (intradialytic)
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hypotension (flip chair)
N/V muscle cramps |
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Other mahor problems of hemodialsysi
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acess-site infections/bacteremia, amylodosis, AV fistula/graft/catether thrombosis
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What are advantages of hemodialysis
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technique failure is low,
closer monting, higer solute clearance, better able to measure adeqaucy of dialysis |
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Disadvantages of heymodialysis
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3-4hrs x3, dialysis and acess complication, decline is residual renal fuction and encourage dependency
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Types of peritoneal dialysis
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continous ambulatory dialysis
automated perioneal dialysis (most common) |
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Perintoneal Dialysis Dialysate SOLUTION contains
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soultion containg dextrose or icodextrin
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What electroylytes are in perintoneal dialysis
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Normal Na Cl and Mg, decrase Calcium, NO K and lactate instead of Bicarb
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What is contained in a peritoneal dialysis prescription
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1. CAPD
2. APD 3. Number of exchanges per day 4. duration of dwells 5. volume of dialystate and ttype |
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How are metabolic waste/solutes removed in peritroneal dialysis
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removed by diffusion NO ultrafiltration
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How is fluid removed in Peritonal Dialysis
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removed by altering the osmotic pressure ---increase dextroxe conc removed more fluid
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What is continous ambulatroy peritoneal diaylsis
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instill 1-3L of sterile dialysiate into periotnal cavity, soluation dwells with the perioneal cavity for a specific time,
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After solutin dwells within the peritoneal cavity for a specifcied period of time, what happens
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fluid is drained and replaced with fresh solution
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How often in continous ambulatory done
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3 short exchanges during day, and one long exchange durgin ngith
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What is Automated Perionteal Dialysis
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patient hooked up at night to auotmoated cycle, multiple show dwells/exchange during the night
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What is wet vesion of APD
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daytime dwell of 12-14hrs
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What is dry vesion
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no daytime dwell--dry abdomen
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Complications of Peritonela Dialysis
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abosorption of glucose, lead to hypertridglycedmia, and weight gain/obesity
loss of albmin and other proteins, incrased insulin requires in pts with diabetes, and exit site infections |
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A common exit site infection is Peritonitis, are pts able to recognize
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YES--culture baf
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How is peritonits mangaged
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outpatient, given specic intraperional antibiotics
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What are advantages of Periotenal Dialysis
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< hemodynatic instability, less blood loss (better anemia)
preseve rediual renal fuction better clearnace of larger solutes |
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What are disadvantges of Perionteal Dialysis
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dialysis complication
acess compliacatoin technique failure is high burnout difficult to dermine adqeuacy of solute removal |
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What are absolute contrinindcations of peritoneal diysis
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other perioneal adhesions from pervious surgery
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What is Drug dosing important in Pts with severe chornic kidney disease (ESRD)
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take an average of 10-12 meds, and unnder go frequnet drug and dosage changes,
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Alteration not only renal elmination of drugs in pts with ESRD but also
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AMDE
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What are reasons absorption may be decreased in pts with ESRD
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drug interactions, gastricist, N/V, gastopathy, higher gastric pH
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Absorption also may increased in ESRD
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due to decreased first pass metabolism by liver, and decrease activity or p-glycoprotien
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What are alteration in distrubtion is pts with Severe CKD
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alterations in protein binding, and reduced tissue binding
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What causes alteration in protein binding of drug
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decreased albumin
uremic byproductes or drug metabolites compete for biding sites |
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Why does digoxin have reduced tissue binding (increase free conc of drug)
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competic with uremic byproducts and tissues, results in increase in serum conc
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The problems with alteration in binding, TOTAL conc is normal, however FREE drug conc is increased
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YES
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What is normal therapetic range of phenytoin
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10-20 mg/l
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Total phenytoin conc in the normal range can result in what b/c of alteration in albumin binding
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free conc can be in toxic range
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As renal functions worsens the therapetic range for phenytoin shifts
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DOWNWARD
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How is metabolism altered in CKD
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Decrease metabolism of drugs by renal cortex
Decreased liver clearance in CHRONIC renal failure |
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What happens in chronic renal failure
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Slowed phase I and II meatbolism, down regulation fo CYP450
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Is liver clearnace alter in acute renal failure
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NO
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B/c of Decrease renal metabolism and decrease liver clearance, what happens in codiein and morphine
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drugs are 10x are ptoent, excess therapeutic effect, and increase CNS depression
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What are PD alterations (examples
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NSAIDS, COX2 inhibitors
ACE inhibitor are ARBs |
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What are effects of ACE-i or ARB in PD alterations
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may increase Scr, IMPORTANT to continue as renal postive
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What happens in "STRESSED KIDNEY"
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hypoperfsion, hypovolemia and decreased blood flow
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How does "STRESSED KIDNEY compensate and role of NSAIDS
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increasing protaglsins, which increases blodd flow GFR and GCP--cause vasocontstrction decreases blood supply
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Must you determine type of kidney dysfuction for drug dosing
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YES--pre-renal ATN or CKD
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Should you always use more than one reference is drug dosing guids
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YES
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How do you adjustment load dos of drug
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Vd X Conc
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Is the adjustment of loading dose dependent on elmination
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NO--no change is needed
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WHen is there a change needed for loading dose
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if VD is altered due to kidnye dsyfurction as in digoxin
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What favors removal in hemodailysis
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Low MV
low PB Low VD high renal clearance water soluble |
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What type of hemodialysis favors removal
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high flux dialysis
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How are drugs typcially dosed on hemodialyssi
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Clcr <10,
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When should one adminstered medications on hemodialysis
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after hemodialysis if significantly removed
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Is Peritoneal Dialysis efficent at removing drugs
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NO
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How are drug dosed on repitoneal dialysis
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based on degree of residual renal fuction
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What is most efficent way at removing durgs
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CRRR Continous Renal replacement therapy
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