RENAL FAILURE

RENAL FAILURE

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

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	Erstellt von Zinab Keshk vor mehr als 8 Jahre