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5081756
RENAL FAILURE
Descripción
University M001 Mapa Mental sobre RENAL FAILURE, creado por Zinab Keshk el 09/04/2016.
Sin etiquetas
m001
university
Mapa Mental por
Zinab Keshk
, actualizado hace más de 1 año
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Menos
Creado por
Zinab Keshk
hace más de 8 años
7
0
0
Resumen del Recurso
RENAL FAILURE
RISK FACTORS
MEDICINES
NSAIDS
RISK FACTORS: HYPOVOLAEMIA, ELDERLY, ACEI, ARBs, PRE-EXISTING RENAL INSUFFICIENCY
INHIBIT COX ENZYMES AND THUS PG PRODUCTION
RENAL PGs MEDIATE DILATATION OF AFFERENT ARTERIOLE
THEREFORE, AFFERENT VASOCONSTRICTION OCUURS
POOR RENAL PERFUSION
LOW GFR
ACE I
RISK FACTORS, ELDERLY, RENAL IMPAIRMENT
INHIBIT ACE WHICH CONVERTS AT1 TO AT2
AT2 MEDIATES VASOCONSTRICTION OF EFFERENT ARTERIOLE
THEREFORE, EFFERENT VASODILATION OCCURS
POOR RENAL FILTRATION
LOW GFR
RISK OF HYPERKALAEMIA DUE TO POOR EXCRETION PERFORMANCE
ACIDOSIS AGGRAVATES HYPERKALAEMIA
MAY CAUSE CARDIAC ARRHYTHMIAS
FIRST STABILIZE HEART USING CALCIUM GLUCONATE
IV INSULIN TO 'MOP UP'
TO ACCELERATE: ADD IV SALBUTAMOL
OR CALCIUM RESONIUM p/o
RESTRICT DIETARY POTASSIUM
ACIDOSIS
USUALLY 40-60 MMOL OF H+ EXCRETED RENALLY
RENAL IMPAIRMENT HINDERS THIS
H+ RETENTION
TREAT WITH SODIUM BICARBONATE
PRODUCES CO2 + H2O
TAKE CAUTION WHEN TREATING BOTH ACIDOSIS AND HYPERKALAEMIA
ADMINISTERING CALCIUM GLUCONATE & SODIUM BICORBONATE CAN CAUSE INSOLUBLE PRECIPITATE
NOT TO BE ADMINISTERED AT THE SAME TIME
CALCIUM MALABSORPTION
VITAMIN D METABOLISM BEGINS IN THE LIVER AND IS COMPLETED IN THE KIDNEY
POOR RENAL FUNCTION MEANS THAT INSUFFICIENT VITAMIN D IS BEING FULLY METABOLISED
THEREFORE LESS ACTIVE 125 DIHYDROXYCOLICALCIFEROL IS BEING PRODUCED
LESS CALCIUM ABSORBED IN THE BODY
GIVE ORAL CALCIUM
AVOID EFFERVESCENT TABLETS
SOME HAVE HIGH LOAD IN SODIUM OR POTASSIUM
SODIUM
HYPERNATRAEMIA
CAUSED BY: SODIUM OVERLOAD, HYPOTONIC FLUID LOSS OR REDUCED WATER INTAKE
HYPONATRAEMIA
CAUSED BY: DILUTION OR WATER OVERLOAD
HYPERPHOSPHATAEMIA
PHOSPHATE EXCRETED VIA KIDNEY
POOR KIDNEY EXCRETION
LESS PHOSPHATE EXCRETION
ELEVATED SERUM PHOSPHATE
GIVE PHOSPHATE BINDING SALTS (ALUDROX / TITRALAC)
UREA
NAUSEA, VOMITING, ANOREXIA
ACCUMULATION OF TOXIC PRODUCTS FROM PROTEIN CATABOLISM
LIMIT PROTEIN INTAKE
ACUTE RENAL FAILURE (acute kidney injury)
WHAT IS IT?
ABRUPT & REVERSIBLE DECLINE IN GFR
RESULTS IN INCREASE IN BLOOD UREA NITROGEN (BUN), CREATININE AND OTHER WASTE PRODUCTS THAT ARE USUALLY TO BE EXCRETED RENALLY
IT IS A SYNDROME, NOT A SINGLE DISEASE STATE
CAUSED BY NECROSIS RESULTING FROM ISCHAEMIA, NEPHROTOXIN EXPOSURE, MICROVASCULAR NEPHROPATHY (DM)
AETIOLOGY
STAGE 1: PRERENAL
MOST COMMON FORM OF AKI
CAUSED BY: HYPOVOLAEMIA, DECREASED CARDIAC OUTPUT, SYSTEMIC DILATATION (CAUSED BY ANAPHYLAXIS) AFFERENT ARTERIOLAR CONSTRICTION, EFFERENT ARTERIOLAR DILATITION
STAGE 2: INTRARENAL
ACUTE TUBULAR NECROSIS IN THE KIDNEY RESULTING FROM ISCHAEMIA OR DIRECT TOXIC ACTION
SEPSIS, MYOGLOBIN FROM RHABDOMYOLYSIS, RENAL TRANSPLANTATION, NEPHROTOXINS (E.G. AMINOGLYCOSIDES)
STAGE 3: POSTRENAL
INJURY AT THE BLADDER STAGE
CAUSED BY OBSTRUCTION OF UT, BLOOD CLOTS, URINARY STONES
SYMPTOMS
VOLUME DEPLETION
TACHYCARDIA,
COLDNESS IN EXTREMITIES
POSTURAL HYPOTENSION
REDUCED SKIN TURGOR
OLIGURIA
VOLUME OVERLOAD
CAUSED BY INCREASED FLUID INTAKE WHICH DOES NOT ACCOUNT FOR POOR RENAL FUNCTION
OEDEMA
ANKLE SWELLING
CONSIDER IV/ORAL DIURETICS
CAN PRESENT WITH EITHER:
MANAGEMENT
1. IDENTIFY PATIENTS AT RISK
2. PROLONG LIFE
3. RAPID DIAGNOSIS
THE FASTER, THE DIAGNOSIS, THE MORE POSITIVE THE PROGNOSIS
4. WITHDRAW/AVOID NEPHROTOXIC DRUGS
5. CORRECT FLUID AND ELECTROLYTE BALANCE
6. ESTABLISH AND MAINTAIN ADEQUATE DIURESIS
LOOP DIURETICS
AID HYPERKALAEMIA TREATMENT & MANAGEMENT OF FLUID OVERLOAD
FUNCTION
PRODUCTION OF EPO
CAN BE IMPAIRED
ANAEMIA
GIVE HORMONE REPLACEMENT
EXCRETION
HOMEOSTASIS
ACID-BASE BALANCE
EXCRETION OF H+ IONS
EXCRETION OF ELECTROLYTES
BLOOD PRESSURE
HORMONE SECRETION
PLASMA VOLUME
VITAMIN D METABOLISM
MONITORING FUNCTION
CREATININE
BY PRODUCT OF MUSCLE METABOLISM
FILTERED VIA THE KIDNEYS
NO TUBULAR REABSORPTION
UREA
PROTEIN & AA CATABOLISM
NH3 PRODUCTION
EXCRETED VIA KIDNEYS
ELECTROLYTES
POTASSIUM, HYDROGEN, SODIUM, PHOSPHATE, UREA
GFR
>90 ML/MIN
CHRONIC RENAL FAILURE
SIGNS AND SYMPTOMS
CRF EVENTUALLYAFFECTS MANY SYSTEMS IN THE BODY
CNS
CONFUSION
SEIZURES
COMA
BONE
OSTEOMALACIA
PAIN
OSTEOSCLEROSIS
HYPERPARATHYROIDISM
BLOOD
ANAEMIA
PLATELET ABNORMALITIES
CVS
HYPERTENSION
HEART FAILURE
PERICARDITIS
VASCULAR DISEASE
PERIPHERAL OEDEMA
GI TRACT
NAUSEA
VOMITING
WEIGHT LOSS
PERIPHERAL NEUROPATHY
RENAL
POLYURIA
NOCTURIA
SODIUM & WATER RETENTION
NEPHROTOXICITY
AMINOGLYCOSIDES
AMPHOTERICIN
CICLOSPORIN
VANCOMYCIN
HORMONAL
INFERTILITY
LOSS OF LIBIDO
AMENORRHOEA
IMPOTENCE
CAUSES
DIABETES
HYPERTENSION
POLYCYSTIC KIDNEY DISEASE
RENOVASCULAR
AETIOLOGY
STAGE 1
KIDNEY DAMAGE WITH NORMAL OF INCREASED GFR
STAGE 2
MILD DECREASE IN GFR WITH OTHER EVIDENCE OF KIDNEY DISEASE
STAGE 3
MODERATE REDUCTION IN GFR WITH OTHER EVIDENCE OF KIDNEY DISEASE
STAGE 4
SEVERE REDUCTION IN GFR
STAGE 5
VERY SEVERE / END STAGE KIDNEY FAILURE
EFFECT ON PHARMACOKINETICS
ABSORPTION
DIARRHOEA
VOMITING
METABOLISM
METABOLISM OF 25- TO 1,25-DIHYDROXYCHOLICALCIFEROL
INSULIN METABOLISH
DISTRIBUTION
FLUCTUATION IN DEGREE OF HYDRATION
ASCITIES / OEDEMA
DEHYDRATION
SERUM PROTEIN BINDING REDUCED
E.G. DIAZEPAM. MORPHINE, THYROXINE
ELIMINATION
MOST IMPORTANT PARAMETER
GFR- NO. OF FUNCTIONING NEPHRONS
DOSE ADJUSTMENTS
LOADING DOSES OF RENALLY EXCRETED DRUGS REQUIRED
ALTER DOSE / DOSING INTERVAL
BNF
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