26966104
Descripción
Fichas por Jenna Paterson, actualizado hace más de 1 año
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Creado por Jenna Paterson
hace alrededor de 4 años
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| Pregunta | Respuesta |
| Define AKI | Any of the following: ○ Increase in SCr by >=0.3mg/dl (>=26.5umol/l) within 48 hours; or ○ Increase in SCr by 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or ○ Urine volume <0.5ml/kg/h for 6 hours |
| What is a stage 1 AKI using the KDIGO classification system? | Serum creatinine 1.5-1.9x baseline OR >26.5umol/l OR urine output <0.5ml/kg for 6-12 hours |
| What is a stage 2 AKI using the KDIGO classification system? | Serum creatinine 2.0-2.9x baseline OR urine output <0.5ml/kg for >12 hours |
| What is a stage 3 AKI using the KDIGO classification system? | Serum creatinine >3x baseline OR serum creatinine > 353.6umol/l OR initiation of RRT OR urine output <0.3ml/kg for >12 hours OR anuria >12 hours. |
| What are pre-renal causes of AKI? | - Volume depletion (vomiting, diarrhoea, diuretics, burns, trauma, haemorrhage) - Cardiac pump failure (acute MI, cariogenic shock, arrhythmia) - Sepsis - Hepatorenal syndrome - Medications |
| What medications can cause an AKI? | ACEi/ARBs NSAIDs Antibiotics (trimethoprim, vancomycin, gentamicin) Immunosuppressants (cyclosporin, tacrolimus) Contrast |
| How does gentamicin cause an AKI? | ○ Can cause AKI if not monitored properly - trough levels must be measured appropriately. It is taken in to proximal cortical tubular cells for 28 days and can also affect blood supply to kidneys --> AKI. |
| How does trimethoprim cause an AKI? | Spironolactone effect - inhibits tubular secretion of creatinine and blocks distal potassium excretion - hence hyperkalaemia and high creatinine. |
| What comprises a glomerulonephritis screen, and in who would one be carried out? | If non visible haematuria and proteinuria: ANCA (screen for vasculitis) /ANA and compliment (screen for lupus and Sjogren's) /RF (not for RA, but for cryoglobulinemia)/urine protein:creatinine ratio |
| What are the principles of management of an AKI? | - Drug review - withhold all nephrotoxics if possible and beware of drugs which are renally excreted; may need dose reduction. - Ensure adequate volume status and perfusion pressure - Search for and treat infections early and appropriately - Optimise cardiac output and renal blood flow - may require inotropes - Search and treat acute complications (hyperkalaemia, acidosis, pulmonary oedema) ○ Initiate dialysis before uraemic complications emerge. |
| What are life-threatening complications of AKI? | - Hyperkalaemia - refractory to medical management (can't excrete, especiallly if oliguric) - Fluid overload - severe pulmonary oedema not responding to diuretics (can't excrete) - Severe uraemia - pericardial rub (pericarditis), uraemic encephalopathy - Severe acidosis - pH<7.1 (H+), HCO3 <10 with circulatory compromise |
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