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Mapa Mental
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Zinab Keshk
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University M001 Mapa Mental sobre RENAL FAILURE, creado por Zinab Keshk el 09/04/2016.
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m001
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Creado por
Zinab Keshk
hace casi 9 años
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5081756
mind_map
2016-12-16T00:32:11Z
RENAL
FAILURE
RISK
FACTORS
ACUTE RENAL FAILURE (acute kidney
injury)
FUNCTION
PRODUCTION OF
EPO
EXCRETION
HOMEOSTASIS
ACID-BASE
BALANCE
EXCRETION
OF H+ IONS
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
GFR
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
RESTRICT
DIETARY
POTASSIUM
FIRST
STABILIZE
HEART USING
CALCIUM
GLUCONATE
IV INSULIN
TO 'MOP UP'
TO
ACCELERATE:
ADD IV
SALBUTAMOL
OR CALCIUM
RESONIUM p/o
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
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
VOLUME OVERLOAD
CAN PRESENT WITH EITHER:
TACHYCARDIA,
COLDNESS IN EXTREMITIES
POSTURAL HYPOTENSION
REDUCED SKIN TURGOR
OLIGURIA
CAUSED BY INCREASED FLUID INTAKE
WHICH DOES NOT ACCOUNT FOR POOR
RENAL FUNCTION
OEDEMA
ANKLE SWELLING
CONSIDER IV/ORAL DIURETICS
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
EXCRETION OF
ELECTROLYTES
>90 ML/MIN
CHRONIC RENAL FAILURE
SIGNS AND
SYMPTOMS
CRF EVENTUALLYAFFECTS MANY SYSTEMS IN THE
BODY
CNS
CONFUSION
SEIZURES
COMA
RENAL
POLYURIA
NOCTURIA
SODIUM & WATER RETENTION
HORMONAL
INFERTILITY
LOSS OF LIBIDO
AMENORRHOEA
IMPOTENCE
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
AETIOLOGY
STAGE 1
STAGE 2
STAGE 3
STAGE 4
STAGE 5
KIDNEY DAMAGE WITH NORMAL OF INCREASED
GFR
MILD DECREASE IN GFR WITH OTHER EVIDENCE OF
KIDNEY DISEASE
MODERATE REDUCTION IN GFR WITH OTHER
EVIDENCE OF KIDNEY DISEASE
SEVERE REDUCTION IN GFR
VERY SEVERE / END STAGE KIDNEY FAILURE
CAUSES
DIABETES
HYPERTENSION
POLYCYSTIC KIDNEY DISEASE
RENOVASCULAR
EFFECT ON
PHARMACOKINETICS
ABSORPTION
METABOLISM
DISTRIBUTION
ELIMINATION
NEPHROTOXICITY
DIARRHOEA
VOMITING
METABOLISM OF 25- TO
1,25-DIHYDROXYCHOLICALCIFEROL
INSULIN METABOLISH
FLUCTUATION IN DEGREE OF
HYDRATION
ASCITIES / OEDEMA
DEHYDRATION
SERUM PROTEIN
BINDING REDUCED
E.G. DIAZEPAM. MORPHINE, THYROXINE
MOST IMPORTANT
PARAMETER
GFR- NO. OF FUNCTIONING
NEPHRONS
DOSE ADJUSTMENTS
LOADING DOSES OF RENALLY EXCRETED DRUGS REQUIRED
ALTER DOSE / DOSING INTERVAL
BNF
AMINOGLYCOSIDES
AMPHOTERICIN
CICLOSPORIN
VANCOMYCIN
CAN BE
IMPAIRED
ANAEMIA
GIVE HORMONE
REPLACEMENT
POTASSIUM, HYDROGEN, SODIUM, PHOSPHATE, UREA
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5081756
mind_map
2016-12-16T00:32:11Z
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