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    Add as Friendacute renal failure

    by: shaheem

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    1 : ACCUTE RENAL FAILURE SHAHEEM.T. K DEPT :PHARMACY PRACTICE THE ERODE COLLEGE OF PHARMACY 1
    2 : Background Common in Hospitalized patients Associated with high Morbidity and Mortality Often Multifactorial Identifiable risk factors. 2
    3 : KIDNEY Is the main organ which help excretion Play important role in filtering body waste Maintain electrolytic balance 3
    4 : Acute Renal Failure DEFENITION It manifests as an marked decline the GF rate occurring a period of days or week. This results an accumulation of toxins & nitrogenous waste products. The patient having rapid decline of renal function is known as acute or chronic renal failure 4
    5 : Sudden decrease in function (hours-days) Often multifactorial Pre-renal and intrinsic renal causes 70% oliguric UOP < 400 ml Non-oliguric (up to 65%) Associated with high mortality and morbidity 5
    6 : EPIDOMIOLOGY Common case in general population Common in hospitalized case ARF develop in 2% to 25% patient in icu 6
    7 : ETIOLOGY PRE RENAL AZOTEMIA Resulting from decreased renal perfusion rate high BUN/creat ratio, normal urinary sediment Treat by correction of predisposing factors 7
    8 : 2. ACUTE INTRINSIC RENAL FAILURE Due to structural damage to the kidney POST RENAL OBSTRUCTION Obstruction of renal flow from kidneyout of the body 8
    9 : CLASSIFICATION Pre-renal (functional) Renal (structural) Post-renal (obstruction) 9
    10 : PRE RENAL CAUSES Intravascular volume depletion Hemorrhage Sodium depletion Redistribution of ECF “Third space” accumulation Edematous disorders Drugs 10
    11 : PATHO PHYSIOLGY ARF progress in three steps 1.Initiating phase Time between the renal insult &the point at which extra renal factors no longer reverse the damage caused by the obstruction or other cause of damage 11
    12 : A. Urine out put: Oliguric ( less than 400 ml) Anuria (less than 100 ml) 12
    13 : B. NITROGENOUS WASTE PRODUCT ACCUMULATION Azotemia S cr & sulphate , phosphate , organic acid level climb rapidly Serum sodium concentration falls below normal Hyper kalemia occurs due to accumulation of organic acids 13
    14 : II.MAINTANANCE PHASE Begin with urine out put rise above 500 ml / day Azotemia & associated laboratories finding may be persist until urine out put reaches 1000-2000ml/day The maintenance phase carry a risk of fluid and electrolytic abnormality 14
    15 : 3.RECOVERY PHASE Renal function gradually retain to normal most recovered renal function appeared in the first two week 15
    16 : CLINICAL PRESENTATION OF ARF SYMPTOMS Change in urinary habit ,weight gain, flank pain SIGHNS Edema, urine may colored or foamy Vital signs may indicate orthostatic hypotension in volume depleted patients 16
    17 : CLINICAL EVALUATION PHYSICAL FINDINGS Urine out put 20-500ml/day Uremia Metabolic acidosis Hypo natremia 17
    18 : DIAGNOSTIC TEST URINALYSIS Examination of sediment RBC casts or dysmorphic RBCs Acute glomerulonephritis Small vessel vasculitis Identification protein,glucose,ketones 18
    19 : Microscopic view Red Blood Cell Cast 19
    20 : Dysmorphic Red Blood Cells 20
    21 : Red Blood Cells 21
    22 : Urinary Sediment WBC Cells and WBC Casts Acute interstitial nephritis Acute pyelonephritis 22
    23 : White Blood Cells 23
    24 : Urinary Sediment RTE cells, RTE cell casts, pigmented granular (“muddy brown”) casts Acute tubular necrosis 24
    25 : Renal Tubular Epithelial Cell Cast 25
    26 : Pigmented Granular Casts 26
    27 : BLOOD CHEMISTRY BUN (8 - 20mg/dl) S cr (0.6 -1.4mg%) Increased HB level due to dehydration Abnormal serum electrolyte values K level above 5meq/L (3.5-5.8) Ca level below 4 meq/L (4-6 ) 27
    28 : RADIOGRAPHY FINDINGS Ultra sound may detect upper UT obstruction UT calculi Enlarged kidney may suggest ATN Radio nuclide scan Computed tomography Renal biopsy 28
    29 : TREATMENT OBJECTIVES Correct reversible cause of ARF Preventing or minimizing further renal damage or complication Treat underlying infection Correct and maintaining proper fluid &electrolytic balance Treat body chemistry alteration especially Hyperkalemia& metabolic acidosis 29
    30 : Contn…. Dis continuing nephro toxin drugs Improve urine out Treat systemic manifestation of ARF 30
    31 : MANAGMENT 1. fluid management: fluid intake should match fluid lose fluid overload should be avoided to minimize hyper tension & CHF If the kidney do not respond to fluid replacement therapy ,other measures taken have include 31
    32 : LOOP DIURETICS MANNITOL DOPAMINE ADENOSINE ANTAGONISTS 32
    33 : Frusemide 100mg IV;if no response within 1 hour; give 240mg IV; if urine output follows,give 5-50mg/h continuous infusion or 500-1500mg/day in dived doses to maintain urinary output Increase renal blood flow via their vasodilating effect Monitor urine output and serum electrolytes infuse less than 4mg/min to avoid ototoxicity 33
    34 : Torasemide May given to patient allergic to furosimide Is a sulfonamide, Loop-type diuretic Oral or I.V dosage of torasemide is 10-20mg daily given in a single dose.If the diuretic response is inadequate, dosage can be titrated upward doubling the daily dose until the desired response is attained. Max.Dose:single dose should not exceed 200mg. 34
    35 : Metalazone Combination therapy with a loop diuretic and a diuretic from different pharmacologic class and with a different mechanism of action can be effective in overcoming diuretic resistance Amiloride,Triamterene,Spironolactone-synergistic effect Metalazone-Effective diuresis at GFR less than 20ml/min 35
    36 : Dopamine 1-5 microgram/kg/min IV-increase the renal blood flow (vasodilator effect) Monitor urine output,blood pressure,IV site for extravasations 36
    37 : PRECUATIONS Serum electrolyte levels should be monitored Asses B.P GI rexns include abdominal pain, diarrhea & nausea Blood glucose level should be monitored in diabetic patient receiving loop diuretic because these agents cause hyperglycemia & impaired glucose tolerance 37
    38 : cont…. Patients who r allergic to sulphonamides may be hyper sensitive to the bumetanide & furosamide Furosamide may cause agranulocytosis 38
    39 : Significant interactions 1.aminoglycoside antibiotics may potentiate oto toxicities when administered with loop dirutics 2.NSAIDS: may hamper the diuretic response to furosamide and bumetinide Synergic activity with other anti hypertensive agents 39
    40 : Mannitol(20%) 12.5-25mg IV over 3-5min An osmotic diuretic, may reduce tubular cell damage by acting as an impermeable solute that reduces cell swelling. Monitor electrolytes 40
    41 : Precautions and monitoring effects Mannitol is contra indicated in patient with anuria , pulmonary edema or congestion, severe dehydration Electrolyte imbalance ,headache ,blurred vision, nausea , vomiting Urine output ,serum and urine Na,K should be monitored 41

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