Renal Flashcards
How do you classify aki
Stage 1 : 1.5- 1.9 x baseline
Less < 0.5 ml/kg hour for 6-12 hour
Stage 2: 2-2.9 baseline
<0.5 ml/kg over 12 hr
Stage 3: > 3 baseline
<0.3 mls/kg over 24hrs
What is the classification system for CKD
G1-5 based on gfr
A1-3 based on acr
What is the definition of contrast induced nephropathy
Development of Aki within 48 hours of a contrast load
Creat > 44 or 25% rise
Mechanism of contrast induced nephropathy
Nephrotoxicity from reactive oxygen species
Contrast induced diuresis
Highly viscous urine
Risk factors contrast induced nephropathy
> 75
Renal impairment
Nephrotoxic drugs
IV rather oral contrast
How can you prevent contrast induced nephropathy
Avoid contrast Use low osmolality or non ionic Stop nephrotoxics Pre hydration saline 1ml/kg Mac 600mg bd for 2/7 IV na bicarbonate
Mechanism of action of cvvhf
Convection
Movement of solute and water down hydrostatic pressure gradient
Mechanism of action of cvvhd
Diffusion
Countercurrent flow of blood and diasylate with diffusion of solutes down a concentration gradient
How do you prescribe rrt
Dose of effluent ; 25-35mls/kg Pre post replacement : 30:70 Fluid balance target Anticoagulant Flow rate - Trieste up to 250mls/ hr
How big is myoglobin
16,000 da
Pathophysiology of cerebral salt wasting
Tropically occurs following SAH and characterised by renal loss of sodium due to increased ANP and BNP causing increased renal perfusion pressure
Criteria for cerebral salt wasting diagnosis (blood and urine)
Hyponatraemia
High urine and serum osmolality
Urinary sodium >40
Hypovolaemia
Criteria for diagnosis of siadh on blood and urine
Hyponatraemia Low serum osmolality High urine osmolality High urinary sodium Euvolaemic or hyper
Causes of nephrogenic Diabetes insipidus
Lithium Amphotericin B Demeclocycline Amyloid Pkd Sickle cell Bartter syndrome Inherited
Cause of cranial diabetes insipidus
TBI Brain tumour Phenytoin ethanol Idiopathic tB encephalitis Sarcoidosis Leukaemia Thyroidits Genetic
Pathophysiology cranial DI
Lack of ADh or vasopressin
Secreted in the post pituitary under hormonal control from hypothalamus
Vasopressin increases water permeability in the dct leading to water reabsorption and salt exertion via aquporins, urea removal in collectin duct snd increase na absorption in loop henle
Peripheral vasoconstriction
Diagnosis of cranial di on fluid deprevation test
No water for up to 18hours
Urine osmolality < 300
Then give desmopressin
> 800 (50% increase)
Diagnosis of nephrogenic di on water deprivation test
No water for up to 18hours
Urine osmolality < 300
Then give desmopressin
< 500 (<50% increase)
Pathophysiology of nephrogenic di
Improper response of the kidney transplant to adh
- damage to loop henle or collecting ducts
Treatment of nephrogenic di
Consume enough fluid to equal the amount produced
Treat any reversible causes
Amiloride/ hydrochorothiazide
Pathophysiology of DKA
Absolute or relative insulin deficiency which when combined with high glucagon, cortisol and catecholamines stimulates lipolysis abs ketogenesis leading to a metabolic acidosis
Hyperglycaemia results from increase hepatic gluconeogenesis and glycolysis
Characteristic changes in dka
Osmotic diuresis due to hyperglycaemia
Vomiting
Reduced oral intake
Causes dka
Surgery
Infection
Mi
Non compliance
Diagnostic criteria dka
Glucose > 11
Ketonuria > 3 or 2+
Bicarbonate <15 or ph <7.3
