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287 Cards in this Set
- Front
- Back
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Edema is a clinically dectable increase in
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interstital volume
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How much weight is gain before edema is clinally evident
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10 lbs
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Disease state most commonly assoicated with genealized edema
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Moderate to Severe CKD
Nephortic Syndrome HF Liver cirrhosis |
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What are 2 models of edema
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overflow model
underfilling model |
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What is overflow model of edema
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primary defrect in renal sodium excretion leading to ECF expasion
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What is underfilling models
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decreased effective ciculating volume, and hypoperfusion of the kideys stimulates Na+ and H20 retnetion
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What are types of Edema
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Perphieral edema
Pulomary Edema Anasarca Ascites |
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What are types of peripheral edema
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pedal, pretibial or presacral
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How is peripheral edema semiquantitavely evaulated as
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1+ to 4+ pitting
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What is anasarca
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total body edema
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What is Ascites
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pertinoneal fluid, which can store up to 10-20 L
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What is the only form of edema that is dangerous or life threatenting
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pulomary edema
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What are main principals of edema magements
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1. Treat underling cause
2. Dietary Na+ restriction 3. Loops, THiazides, Spironolactone |
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What are the drugs of choice for edema managment
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Loop diuretics
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What ClCr ar Loops direucts effect at
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<30 ml/min
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What are use of Thiazie diuretics since mainly BP managment
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mild edema, adjuctive therapy
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Are Thiazide effect at Clcr <30 ml/min alone
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NOT
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What is Spironolactone drug of choice for
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ascites
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25% of CO goes to kindeys, and 20% of plasma is
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flitered by kidenys GFR (125 ml/min)
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How much urine is made in day
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1.5 -2.0 L--all rest is reabsorbed
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How does diuretics reach stie of action through tbular lumen
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actively secreted into the urine by PCT (thought organic acids or base pump)
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What drugs are NOT secreted into PCT
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spironolactone and eplerenone
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Where do spironolactone and eplereone enter
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distal tubular cells via plasma
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Are dirureics higly protein bound
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YES
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Oral Furosemide is what % bioavail
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50%
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What is oral bioavail of bumetanide, and torsemdie
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80-100%
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How often can furosemide be dose (lasix)
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every 6 hours
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How often can torsemide be dosed
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bid
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How often are thiazide dosed
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qd
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Spironolatones has a short half-life, however why is it dosed qd
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its active metabolite has much longer half-lfie
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What is the noram maxim fractional excretion of sodium that u can block
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20%
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What the maxium fractional % of sodium you can block in Loop diuretcs
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2%--no better effect by increasing dose
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What is diuretic resistance
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decreased pharacolical respone or decreased diuresis to a given dose of a diuretic
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What are causes of diuretic resistance
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pharmacokinetic resistance
pharmacodynamic resistance |
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What is a pharmacokinetic resistancew
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factors that dcrease the amount of drug getting to the stie of action
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What is a pharmacodynamic resistance
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factors that decrease the response at site of action,
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What are PK factors that DECREASE concetrion of drug at SITE of action
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Decrease or slow absoprtion
Decrease Serum albumin Decrease Renal Blood FLow Increase Oranic acids competing for tubular secretion site Proteinuria |
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Decrease of slowed absroption can lead to decrease PEAK conc at stie of action issue in pts with
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HF
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A decreased serium albumin does what
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decreased diuretic deliver to kidney (albumin is taxi)
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A decreased serum albumin can be seen in pts with
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Nephrotic syndrome and Chonric Liver disease
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Decrease Renal blood flow decreases diuretic deliver to the kidney, a possible issue in pts with
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CKD or HF
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Increased organic acids competing for the tublar sevretion stie can be seen in pts with
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CKD
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What does proteinuria lead to
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increase binding of the diuretic to the prein the the urine
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Proteinuria can be seen in pts with
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Nephrotic syndrome
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PD issues leading to duretic resistance does what
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decrease response at site action (ONLY DESCRIBED WITH LOOP DIURETICS)
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What are types of decreased response at site of action
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Braking
Rebound Na retention Altered conc-response 2 Na+ reabsorption |
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What is braking
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decrease in response to a loop diuretic during acute dosing
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Braking "phenomenon of overdosing" is a short-term physiological response to
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prevent excessive Na+ and fluid loss
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Braking can occur
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in anyone receive a loop diretuc
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How do you manage braking
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avoid over agressive diuresis and intravascular volume loss--REMOVE FLUIDS slowly
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Where is rebound sodium retention seen
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Lopp diruetics with shorter half-lives (fursoemide and bumetanide
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When does rebound sodium retnetion occur
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after the diuretic conc falls below the threshold (at the end of the dosing interval)
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Rebound Sodium retention can occur at any time in pts who
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do NOT adhere to a sodium restricted diet
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Mangement of Rebound Soium Retention
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give short activing diuretics 2-3 times a day and maintain Na+ restriction
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What is altered conc response
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do not the get the same even though you have the same or greateer diruetic conc at site of action
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Altered concentration response can be seen in pateitns with
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HF, Nephrotic Syneomes and Liver cirrhosis
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What may altered concentration resone be due to
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increased Na retention at other tubular stie
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Management of Altered concentration response
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give most effective dose or maximal effect dose 2-3 times a day
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What is secondary sodium reabsorption
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chonric adpative process that can occur in anyone receive loop dieuretics long term
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What happens in secondary Sodium reabsoprtion
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reabsroption occur at a second spot--distal tubule
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What is management of secondary sodium reabsoprtion
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combination therapy
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Altered concetnration response does not happen in what disease state
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CKD
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What is managment of decreased delivery to site of action
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give HIGER DOSES of diretics
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What is managment of alter concetnration response
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give most effective or max dose bid-tid
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What is managment of revound Na+ retention
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matian sodium restirction and give most effect or max dose bid tid
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What is mangment of secondary na+ reabsorption
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combination therapy
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Where is peripheral edema usually managed
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outpatient
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How do peripheral edema usually managed
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Diertary Na+ restritionct
Check hidden source of Na )med Check for meds that cause of edema |
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What are medications that can cause edema
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NSAIDS, dihdropyridine, Ca+ Channel blockers, thiazolidedoine, and estronges
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What is FIRST thing you do to manage Peripheral Edema
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Start with low dose oral loop such as lasix 20-40 qd or bid
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What is GOAL of perihperal dema
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SLOWLY reduce edema
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Should you titrate dose and internal based on response--
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YES
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Where is acute magfement of SEVERE edema managed
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hopstial
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How do you manage acute SEVERE EDEMA
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Check for hidden shouce of Na
Check for meds that cause edema acess compliance with medcation and Na+ restriction |
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What is FIRST thing you do to manage Severe edema (med wise)
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IV bolus dosing initally or IV infuciton
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How do you deterine the loop diuretic dose in SEVERE edema
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depends on previous hisotry, and disease state
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How do you manage Severe edema, if not adequate response
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double the inital dose untril response--or until maximal effective dose for disease state is reach
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What is considered an anqeuate reponse to loop iduretic
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>500ml urine in 2 hrs
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Once you find the mosdt effective dose (or max reached, what should you do
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give is as often as needed typicall bid to tid
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If loop alone is inadeuates whawt should you do
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combination of loop + thizide or K+sparing diuretic
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If giving a combination loop IV, when should thiazie be administered
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0.5 to 1 PRIOR to loop
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What is managment of Ascites (Liver Cirrhois drug of choice)
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spironolactone--drug of choice for hyperaldosteronism
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What is dosing of spironolactone for ascites
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50-100 mg qd with food up to 400 mg/day
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What is fastest you can tirate spironolactone
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no faster than 3-5 days
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If inital dose of spironolactone is inadueates, or pt has peripheral edema use
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combination therapy with loop
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What is ideal ratio for spironolactone/fursemide
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100 spironolactone/40mg day fursosemide
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What is usual startign dose of oral fursemide for managemtn of Acites
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40 mg
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What is maximal effective dose of fursosemide
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80mg at one time
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Can you adminstered the loop dirutetic more often to improve response
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YES
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What is goal fluid loos of ascites WITHOUT edema
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500ml/day (0.5 kg/day)
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What is goal fluid loss of ascites with edema
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1000mg/day 1.0 kg/day
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What are adverse effect of diuresis
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hypovolemia,
azotemia electrolytice abnormalies acid base disordres otottocity |
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What is azotemia
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increase Scr and increase BUM
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Ototoxicty for fursoemide should be <
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<4mg/min
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What are minotoring things that should be done for diuretics
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Daily weight
Input and Output Electrolytes Vital Signs Kidney function |
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What are 3 main funtions of kidney
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1. Endocrine function
2. Metabolic function 3. Excretory function |
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What is endrocrine function of kidney
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secretion of renin and erythropoetin
production/met of prostalandsin and kinins |
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What is Metabolic function of kidney
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activat of Vitamin D, gluconeisgenis, metabolism of instulin, sterioud, and drugs
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Does kidney have CYP P450 activity
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YES
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What is excretory function (elimination of kidney
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filtration +secretion-absorption
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GFR is passive diffusion, and is single best index of
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functioning renal mass
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Does GFR decrease after age 40
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yes 0.75 ml/min per year
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Elimination of drugs corelates best with
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GFR
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Are secretion and reabsorption hard to measure
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YES
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What is Purpose of Assesment
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1. Determine Kidney dysfution
2. Severity 3. Follow progression 4.Adjust meds and anticipate complication |
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What are types of actue renal failure
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1. Pre-renal
2. Acutre Intrinsic 3. Pot renal |
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What is pre-renal acute renal failure
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Hypovolemia, decreased blood to kidney, so kidneys reabsorb na and H20
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What is Acute instric
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inside the kidney (acute tubular necrossi, intersistal nephritis, GN
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What is pot renal
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after the kidney (obstruction_--such as kidney stone
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What are number 1 and 2 cause of CKD
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HTN and diabetes
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What info is needs for Clinical Assent
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Pt history
Physical exam Lab vaules |
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What Tests are needed for clinical assesment
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1. lab values
2. urinalysis 3. Urine chemistires 4. Imaging/Biospy 5. Estimation GFR |
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What lab values are important
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Serum Creatinine
BUN |
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What is Creatinine
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breakdown product in muscle
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Sercum creatinine levles are dependent on its
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production and elmination
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Production of Creatinine is dependent on
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muscle mass, age, race genrer boddy mass,
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How is Creatinie elminated
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primarily by filtaretion though glomerulus, secreted, NOT reabsobed
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Is how much creatinie secreted dependent of Kidney function
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YES
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What is normal range of Scr
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0.4-1.2 mg/dl
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Should Scr be used alone to determine degree of kidney function
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NO
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Creatinien is frequently used to
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estimate GFR
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How are amino acids broke down
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amonia and urea
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What happens to urea
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under filration and proimal tubule reabsoprtion
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What is normal BUN
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5-20
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What are factors that increase BUN
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Kidney dysfuction
High protein diet hypercatabolism hypovolemia GI bleeding Steriods |
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What are factors the decrease BUN
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starvation and advanced liver disease
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What is normal BUN/Scr Ratio
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10-15:1
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What does a ratio >20 indicated
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possible pre-renal disease (decreased ciculating volume)
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Why is a ratio >20 indicative of pre-renal disease
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decreased cirualting volumes means increase water/Na and urea reabsorption
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What can inhibit expected rise in ratio
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Liver disease or decreased protien intake
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How is urinalyisis preformed
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dpstick method
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What is normal pH of urine
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4.5-7.8
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What does an increase pH indicate
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presence of urea spliting bacteria
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Should there normally be protein in urine
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NO--indictaed possible glomerular damage
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Typically values in Urinialsis are zero
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YES
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What is normal excretion of protein/albumin
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protein 150mg/day
albumin 30 mg/day |
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Persistent elevated proteinuria or albuminura is
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an important marker of kidney damge
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Micoalbuminura is an
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early indcator of subclincial kideny damage
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All pts with CKD and those with risk factor should be tested for microabumuira using
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an albumin specifc test
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The standard dipstick what does a negative value indicate
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<150 mg/day of protein.albumin
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The standard dipstck what does Trace value indicate
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150-300 mg/day
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The standard dipstick what does 1+ to 4+ indicate
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300mg to 15 mg day
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What does a negative value on albumin specifc test mean
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<30 mg
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What does a 20 to 100mg/L value indicate on a albumin specific test mean
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30-300 mg/day of ablumin
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The standard urine dipstick and albumin specifc dipstick are what type of measurement
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semi-quntitative
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What is a qunatative measurement
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Spot Urine Sample
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When is the Spot urine same take
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1st morning speciema after waking
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On Sport Urine sample what is Normal Albuminura
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<30
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One Spot Urine sample what is Microalbuminura
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30-299
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On Spot Urine sample what is macroalbuminuria
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>300
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How many protein/albumin tests are needed with 3-6 month time period to diagnosis persitsten micoalbuminuria or macoalbuminura
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2 out of 3 + rests
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What are factos that can falsely increase protein ablumin in urine
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high protein diet
high blood pressure hematuria dehydration infection vigourous exercise |
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What does urine sediment measure
|
cells and castsPr
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Pre-renal dysfuciton cells and casts present
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CELLS-NONE
CASTS--NONE or HYALINE |
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Interstital Nephritis cells and casts
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CELLS--WBCs, Eosinophils
CASTS-WBC granular |
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Glomerulonephritis cells and casts
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CELLS--RBCs and WBCw
Casts--RBC |
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Cells and Casts of Acutre tubular necrosis
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Cells-varies
Casts-Muddy brown or tubular |
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What are urine chemistries of urine taken
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Urine Na+ conc
Urine osmolality |
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What do Urine Sodium concetration determine
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Pre-renal
ATN |
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What do Urine osmolality measure
|
ATN, IN
Pre-renal |
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A Urine Sodium Concentration for pre-renal is
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LOW <20 meq/L--due to secondary retnetion of sodium
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A urine Sodium Concetration for ATN
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HIGH >40 meq/L--due to tubular injury
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A Urine Osmolality for ATN or IN is
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LOW<350-450 (dilute) due to loss of conc ability
|
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Urine osmolality for pre-renal is
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HIGH >500 (concentrated urine)
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What is Noram Fractional Exretion of Sodium
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1%
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What is Pre-renal fractional exretion of Sodium
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<1%
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What is ATN Fractional exretion of sodium
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>2%
|
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What can affect results of Fractional excretion of Sodium
|
diuretics and dopamine
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What is normal fractional excretion of Urea Nitrogen
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50-65%
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What is fractional exretion of urea in PRE-RENAL
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<35%
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What is raction excretion of urea in ATN
|
N/A
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Do Diuretics and dopamine affect results of fractional exretion of urea
|
NO
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What is normal uruine output
|
500-2000ml
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What is Nocturia
|
decreased ability to conc urine
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What is non-oliguria
|
>500ml/day
|
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What is oliguria
|
<500 ml/day
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What is anuira
|
<50ml/day--obstrution of shock no kidney fuction
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What is gold standard for measurement of GFR
|
Creatinine
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|
|
The precent of tubular secretion of Cr increases with
|
decreasing kidney fxn
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|
Clearance of creatinie from the body tends to
|
overestmie true GFR
|
|
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Overestmieation increases with
|
decreasing kidney fuction
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What are equations for Clcr/GFR in adults with STABLE kidney function (Scr not rapidly changing)
|
Cockcroft-Galt
MDRD |
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What are ClCr/GFR equations for adults with UNSTABLE kidney function
|
Chiou, and Jelliffe
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|
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What are ClCr/GFR equations for children <12 YOA
|
Schwarts, and Counahan-Barratt
|
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Who should you use to calculate Cockcroft-Gault equation
|
use in adults with stable kidney function (Scr not rapidly chaning)
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|
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What is equation of choice for adjusting drug doses
|
Cockcroft-Gault equation
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Limitations of Cockroft-Gault equation
|
Stable Kindey fuction
Not adequately studied in women, elderyl obses Not accurate in pts with liver diase |
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What are some controversial/higly debatd issue with Cockroft-Gault
|
rounding vs no
Body wt. who are obses, short or amputations |
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What is equation of choice for stagings CKD
|
MDRD
|
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MDRD better estimes true GFR, and other benefits
|
no weight or height
|
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MRRD limiation
|
only accurate in Stable kindey fxn, not studietn in pts with normal kidney fucntion, diabtes, obesity elderly or drug dosing
|
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Are MRDR and Cockroft Gault accurate in pts with liver disease
|
nO
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Should MDRD be used for drug dosing
|
nO
|
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What are limitation of all estimation equations
|
all use serium cretinine and do not consider urien output
|
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What can increase Scr
|
high protein diet, exerxise, muscle mass
|
|
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What can lower Scr
|
paralysis, steriods, cirrhosis
|
|
|
What drugs can competitvely inhbiit proximal tubular secretion fo creatinine, which increases its level
|
cimetidien, and trimethoprim
|
|
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What is ClCr/GFR with 0 urine output
|
ZERO
|
|
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What is definiation of unstable kidney fuction
|
INcrease Scr >50% 24hrs
previous CKD (scr >2) increase 1mg in 24 hrs |
|
|
Chious Jellife, Baerter are used in pts with changing kidney fuciton
|
YES
|
|
|
Cockcroft-Gault or MDRD overstime actual kindey fuction during intal
|
stage of ARF
|
|
|
Cockcroft-Gault or MDRD can UNDERestime actual kidney function during
|
recovery stage of ARF
|
|
|
What is Azotemia
|
abnormallevels of nitrogen containing compounds (urea, creatinien)
|
|
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What is Uremia
|
nitrogenous wastes + symptoms
|
|
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Up to 23% of critically ill pts will have kidney probelsm
|
YES
|
|
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90% of individuals who suvive ARF, recover enough renal fuction to live normal lives
|
YES
|
|
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What are some risk factors for acture renal failure
|
DART BPM
Dehydration Acute infection Rabdo Trauma Blood vessel thombosis Pharmacologic Male |
|
|
What is definiation of ARF
|
decreased GFR over hours to days (<2-4 weeks)
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What is CKD
|
presence of proteinurai for at least 3 months with GFR <90 ml/min
|
|
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Diagnosis of ARF is based on
|
RIFLE
risk, injurt, failure, loss and end stage |
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What are 2 components of RIFLE
|
GFR and UO
|
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What are types of ARF
|
Pre-renal (decreased renal perfusion
Intrinsic Postrenal |
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What controls afferent arteriole tone
|
Vasodilators (Prostglandins
|
|
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What controls effeernt areriole
|
vasocontrtions (angiotensin II and NE
|
|
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What is furnctional renal failure
|
decline in GFR and hydrostatic pressure, resulting in decrased blood flow to kidney
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Why does GFR DECLINE secondary to reduced hydrostatic pressure
|
decrease blood flow to kideny from Afferent arteriole vasoconstricts
Efferent arteriole dilates |
|
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What causes functional ARF
|
Reduced effective blood volume such as CHF, cirrhosis, pulmonary HTN, and HYpoalbuminermia
or Renovasuclar disease Drugs |
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What drugs can causes fuctional renal failure
|
NSAIDS COX02
ACE-I ARBs Immunosuppresent |
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How do NSAIDS and Cox-2 inhibitors cuase Functional ARF (Ibuprofen, Celecoxbi)
|
Decrease renal prostaglanids, resulting in vasocontsrtion of AFFERENT arteriole
|
|
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How do ACE inhbitor cause Fucntion ARF
|
decrease angiotension II and dialtion of efferent arteriole
|
|
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How do ARB causes Functional ARF (losartan, irbesartan)
|
decrease angiotension effects--vasodiation of effertn
|
|
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How do immunosuppressant (cyclosprotien tacrolimus) cause fuctional ARF
|
renal vascocontsrtion
|
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Functional renal failure is alteration in afferent/efferent arteriole tone--no stuructral damge, and overlaps with
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causes of prerenal dysfuction
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What is pre-renal ARF
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hypoperfusion of renal parenchyma
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What are causes of PRerenal ARF
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Low effective blood volume
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What are causes of Low effective blood voluem for prerenal ARF
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Hypotension
Hemmorrhage Hypoalbuminerai dehydration diruetic therapy |
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How does pre-renal compensate
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Sympathetic nervous systme
Renini angiotension-aldosterone ADH |
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Activation of SYmpathetic nervous system, Renin-andiogsin-aldosterone, and ADH does what
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Thirst, increase fluid intake Na and water retention, and Afferent arterioe DIALTION and efferent CONSTRICTION
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Instrinsic ARF is damage to kidney itself, such as
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renal vasculate
glomeruli tubule intersitum |
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What is Renal Vascualr damage
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Renal artery thromobisis
Renal vasculitis Hypertensive emergy HUS (hemolytic uremia syndrome) TTP (thrombotic throbycytopenic purpura |
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Glomerular Damage is rare, causes include
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Systemic Lupus erythematosus
Poststeococall GN Antiglomerular Basement mebrane disease |
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What causes 85% of intrinsic ARF
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ATN (actue tubular necrosis)
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What is main causes of ATN
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Ischemia
Toxins |
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What can cause IScemia in ATN
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hypotension or vasoconstrtion (extension or prerenal)
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What can cause TOxins in ATN
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Contrast dyes, heavy metals,, and aminoglycsides
Endogenosu (myoglobin, hemoglobin uric acid) |
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The tubules have high oxygen demand, so ischemia or toxins do what
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cause tubular cells to die and slough off into the tubular lumen, and increase tublar pressure with decreases GFR
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Tubular injury results in loss of the kidney's ability to
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concentrate urine
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If ischemia and toxins removed before necrosis occurs,how long is recovery
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203 week maintenace phase, followed by 2-3 weeks recovery phase
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What drugs cause ATN
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Chemotherapy
Aminoglycosides Antifungals Radiocontrast Media |
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What do Chemotherapy drugs to ATN (cisplain, carboplatin, ifosamide
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direct tubular toxicity
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What do aminoglgycoside antinbotics cause (gentamicin, tobramycin, and amikacin)
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direct tubular toxicity
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What do antifungals cause (Amphotericin B)
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direct tubular toxicity and vasoconstriction
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What do Radiocontrast media (diatrizoate, Iohexol) cause
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direct tubular toxicity and vasoconstriction
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What causes Acute Interstial nephristis
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Immunologic response to Infections (viral ,bacterial)
Drugs (causes inflammtion and edemda |
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What drugs cause Acute IN
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Pencillin, Ciro, and Sulfa, (like having a allergic reaction in kidney
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What is Postrenal ARF
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Bladder obsturction
Uretheral Renal Pevlis/tubulues |
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What causes a bladder outlet obsturction
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prostate hyperthrophy or cancer
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What causes uretheral post renal ARF
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Kidney stones, blood clots
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What causes Renal pelvis or tbulues obsturction
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Kidney stones or Drugs
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What drugs causes Posternal ARF
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ATM A HIT C
Acylovir Topiramate Methorexate Anticholingeric HMG COA Indinair Trimethoprim/Sulfa |
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Signs and symptoms of ARF
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Decreased UO
Urine Discolation Pain Uniation Severe abd pain |
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Are Scr vaules behind GFR values
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YES
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An aburpt decline or increase in urine output over the last 4 hours suggests
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change in renal fuction
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How do you treat ARF
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Prevent ARF
minimize futher renal damage provide suppotive measure until kidney function returns |
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How do you prevent ARF
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Daily filud intake 2 Liter Day
to avoid dehydration Identify medications that put ppts at risk |
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General treatment to Pre-renal
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Hemodyanmic support
Volume replacement |
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General treatemnt to Instital damge
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Removal of agent
Immunosupprive therapy |
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General treatmetn to Post renal
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remove obstruction
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Only treatment of ARF is supportive therapy--renal function recovery does nto begin until
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all insults are remvoed
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What are frequent complication of ARF--electrolytes wise
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Hypernatermia
Hyperkalemia |
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How do you manage hypernatermia
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no more than 3g/day
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How do you manage hyperkalemia (big risk b/c 90% eliminated renally)
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reduced K+ intake
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Serum K+ >6 is life threating treating with
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Insulin + Dextrose
Kayexalate |
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Are Diuretics useful in ARF
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NO--
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What may direutics be useful for in ARF
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Volume overload in early ARF
Oliguric ATN in ICU pts |
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What diuretic should you avoid in ARF
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K sparring
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Diuretic resisatnce is common in ARF, how can it be overcome
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continous infusions and combing classes (loops + thiazides)
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Dopamine affinty is dictated by dose (D1 is most important), what is Renal Dose Dopamine
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1-5mcg/kg/min
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What does Dopamine do
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Increases urine output--but does not help anyhting else
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What are indications for Renal Replacement therapy (Dialysis)
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AEIOU
Acid-base abnorm Electrolye imbalance Intoxication Fluid Overload Uremia |
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What are type of RRT
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Intermittent hemodislyssi (4hr)
Continous Renal Replacement |
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What is recovery time for Pre-renal and need for RRT is it reversible
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recovery time 48hrs
Rare for RRT Usually reversible |
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What is recovery tiem for Fuctional ARF, and need for RRT, and reversible
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recovery hrs-days
Rare for RRT Ususally reversible |
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What is recovery time for ATN, Need for RRT, and Reversible
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Revcovery 7-21 days
Need for RRT (oliguic 85%) non-oliguic 30-40% reversible 60% |
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What is recovery tiem for post-renal, need for RRT, and reversible
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recvoery 48hrs
Need for RRT rare Reversbile |
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Contrast Dyes are used for CT scans, and can cause
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CIN contrast induced nephropathy
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What are 2 ways that cause CIN
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1. Direct toxicity (decrease antioxidant, and increases free radicals)
2. Ischemia (vasoconstrtion) |
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How should a contrast agent be choosen
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one with lower osmolar, and iodine content
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What are some risk factors for CIN
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Pre-existing renal
Dehydration Heart failure High volume of contrast Hyper or Hypotensin |
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Contrast toxicity can occur within minutes, so interventions need to start prior, include
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Fluids
NAC Sodium Bicard |
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What is benefit of fluids
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dilute contrast media
prevent vasoconstriction avoid tubular obstruction |
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What is fluid chose
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1. Oral intake and
2. NS (NaCl) |
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What is benefit of NAC
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antioxidant
free radical scanvenger |
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NAC should be given with
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IV hydration
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THe hypothesis is that the contrast injury is from free radicals generated in an acid envirotion, what is benfit of Sodium Bicarb
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increase medullary pH, and slows radical production
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Does Fenoldopam help prevention CIN
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NO
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Maintaining a blood glucose between 80-110 reduced
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CIN
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