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Renal Disorders
Treatment of Renal Disorders
| Question | Answer |
|---|---|
| Definition of acute renal failure | Rapid decline or cessation of kidney function. |
| Risks for developing acute renal failure | Trauma Surgery DM HTN CV Disease Hypotensive Episodes MODS Crush Injuries Allergic Reactions |
| Prerenal causes of acute renal failure | Decreased blood flow to the kidneys: Decreased intravascular volume Redistributed volume Decreased CO Renal Artery Stenosis or thrombosis |
| Intrarenal causes of acute renal failure | Direct damage to kidneys: Ischemia Nephrotoxic drugs Myoglobin, rhabdomyolysis glomerulonephritis |
| Postrenal causes of acute renal failures | Obstruction of urine flow mechanical obstruction functional obstruction |
| Pathophysiology of acute renal failure | Decreased renal blood flow -> ischemia -> RAA mechanism -> vasoconstriction |
| Name the 3 phases of acute renal failure | 1) Oliguric phase 2) Diuretic phase 3) Convalescent phase |
| Ion exchange resin | Kayexalate: - Removes K+ from blood and increases sodium. (Short-term measure) |
| Phosphate Binders | Amphojel: Removes phosphate through the stool. |
| Drug given to increase renal perfusion | low dose dopamine. |
| Purpose of giving hypertonic glucose with insulin? | shift K+ into cells |
| Nursing diagnoses with acute renal failure | Fluid volume excess Risk for injury Altered tissue perfusion: Renal High risk for infection Altered nutrition |
| Creatinine | Released at a constant rate and filtered by glomerulus but not reabsorbed -Not produced at a constant rate - Altered by muscle mass, gender, age, diet, drugs, diseases |
| Urea | By product of protein metabolism and used to estimate uremic solute retention and elimination -Not produced at a constant rate (altered by illness, burns, trauma, sepsis, meds, and diet) - Increased by steroids - Increased by protein catabolism |
| Biomarkers of AKI | NGAL KIM-1 |
| NGAL | Neutrophil Gelatinin-Associated Lipocalin - Elevated with epithelial injury of pulmonary disease, asthma, acute bacterial infections, - More accurate marker of kidney fx in post ischemic or nephrotoxic kidneys |
| Elevated blood levels of NGAL occur ___hrs after injury | 2-6 hours |
| KIM-1 | Kidney Injury Molecule-1 -Significantly elevated after ischemic or nephrotoxic AKI |
| What is KIM-1 used for? | Used to differentiate ischemic and nephrotoxic injury from chronic renal dx and UTI |
| Oliguria | Less than 200-500cc in 24hrs |
| How is AKI prevented in rhabdomyolysis | MASSIVE fluid intervention |
| Normal intraabdominal pressure | Below 5-7 mmHg to 12 mmHg |
| CIN | Contrast Induced Nephropathy |
| Risk factors for CIN | DM Dehydration Nephrotoxic drugs Cardiac failure hemodynamic instability |
| Treatment for CIN | Volume expansion (Crystalloids) Dialysis N-acetylcysteine |
| Nephrotoxins | Radiologic Contrast Media Aminoglycosides Amphotericin B Vancomycin |
| Management of AKI with aminoglycosides | Decrease dosage as prevention and stop when AKI identified. |
| Risk factors for Aminoglycosides AKI | Elderly Dehydration |
| Indication for amphotericin B | Treatment of fungal infection |
| Risks with amphotericin B | cumulative doses |
| Treatment of amphotericin B toxicity | Give over 24 hours and Sodium load |
| Management of vancomycin toxicity | Assessment and monitoring of peak and trough levels of the medication |
Created by:
keelerd
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