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RENAL FAILURE
The loss of kidney function
Sudden interruption of kidney function toregulate fluid and electrolyte balance andremove toxic products from the body
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Diuretics
Are used to lower blood volume because of hypertension, congestive
heart failure, or edema
Increase volume of urine by increasing proportion of glomerular
filtrate that is excreted Loop diuretics are most powerful; inhibit AT salt in thick ascending
limb of LH
Thiazide diuretics inhibit NaCl reabsorption in 1st part of DCT
Carbonic anhydrase inhibitors prevent H20 reabsorption in PCT whenHC0s
- is reabsorbed
Osmotic diuretics increase osmotic pressure of filtrate
17-78
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Diuretics and Their
Mechanisms of Action
1. Osmotic Diuretics Decrease Water Reabsorption by
Increasing Osmotic Pressure of Tubular Fluid
2. Loop Diuretics Decrease Active Sodium-Chloride-
Potassium Reabsorption in the Thick Ascending Loop ofHenle
3. Thiazide Diuretics Inhibit Sodium- Chloride
Reabsorption in the Early Distal Tubule
4. Carbonic Anhydrase Inhibitors Block Sodium-Bicarbonate Reabsorption in the Proximal Tubules
5. Competitive Inhibitors of Aldosterone Decrease Sodium
Reabsorption from and Potassium Secretion into the
Cortical Collecting Tubule
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CLINICAL FINDINGSOLIGURICPHASE
Hypernatremia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
Hypermagnesemia
Metabolic acidosis
DIURETIC PHASEHyponatremia
Hypokalemia
Hypovolemia
CONVALESCENT PHASENormal Urine Volume
Increase in LOC
BUN stable and normal
May develop CRF
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Acute Renal Failure
Prerenal
Intrarenal
Postrenal
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Phases of Acute Renal Failure
1. Oliguric phase
2. Diuretic phase
3. Recovery or convalescence
Four phases of acute renal failure
(Brunner and Suddarth)
1. Initiation phase
2. Oliguric phase
3. Diuretic phase
4. Convalescence or recovery phase
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PRERENAL CAUSES INTRARENALCAUSESPOSTRENAL CAUSES
Calculi
BPH
Tumors
Strictures
Blood clots
TraumaAnatomic malformation
Hypotension Acute tubular necrosis (ATN)
Diabetes mellitusCardiogenic shock
Acute vasoconstriction Malignant hypertension
Hemorrhage Acute glomerulonephritis
TumorsBurns
Septicemia Blood transfusion reactions
CHFNephrotoxins
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NURSING CAREMonitor fluid and electrolyte balance.
Monitor alteration in fluid volume.
Promote optimal nutritional status
Prevent complications from impaired mobility
Prevent fever and infection
Support client/S.O. & reduce/relieve anxiety
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Diagnostics
a. Increased BUN and serum creatinine level.
b. Decreased urinary creatinine clearance.
c. Elevated blood sugar and triglycerides.
d. Increased scrum potassium.
e. Anemia (decreased hemoglobin andhematocrit).
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Acute renal failure -PATHOPHYSIOLOGY
Prerenal CAUSE:
Factors interfering with perfusion andresulting in diminished blood flow and
glomerular filtrate, ischemia, and oliguria;include CHF, cardiogenic shock, acutevasoconstriction, hemorrhage, burns,septicemia, hypotension, anaphylaxis
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CLINICAL FINDINGSSTAGE 1Diminished Renal
Reserve
STAGE 2Renal Insufficiency
STAGE 3End Stage
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Hemorrhage
Shock
Burns Hypovolemia
Renal vascular
obstruction-(A/V)thrombosis
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Renal insufficiency
a. GFR is 25 percent of normal.
b. BUN and serum creatinine increased
(azotemia).
c. Fatigue and weakness, mild anemia.
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Chronic Renal Failure
Dermatologic dry skin, pruritus, uremicfrost
CNS seizures, altered LOC,
anorexia, fatigueCVS Acute MI, edema,
hypertension, pericarditis
Pulmo Uremic lungs
Hema Anemia
Musculoskeletal loss of strength, footdrop, osteodystrophy
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Chronic Renal Failure
PATHOPHYSIOLOGY
STAGE 1= reduced renal reserve, 40-75% lossof nephron function
STAGE 2= renal insufficiency, 75-90% loss ofnephron function
STAGE 3= end-stage renal disease, more than90% loss. DIALYSIS IS THE TREATMENT!
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Renal/Intrarenal(kidney tissue pathology)
Acute tubular necrosis
Nephrotoxins
Aminoglycosides orNSAIDs
Heavy metals
-(carbon tetrachloride, arsenic,lead, mercury
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Prerenal disease
Inadequate
filtration
Nephrosclerosis
Heart Failure Vasodilatation Hypovolemia
Systemic Hypotension
Atherosclerois
Renal artery
stenosis
Renal Ischemia
Prerenal Disease
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CLINICAL FINDINGSNausea and vomiting Uremic frost
Decreased urinary output DyspneaHypotension (early)Azotemia
Hypertension (later) LethargyConvulsions Memory impairment
Pericardial friction rub CHF
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Accumulation
of solute
Systemic Hormonal
Changes in blood
Inc. excretion of
Solute per nephron
Glomerulosclerosis
Extrarenal organ
Damage; uremic
Syndrome;toxic
Effects on renal cells
Tubular cell damage
& interstitial fibrosis
Tubular
hyperthrophy
High intraglomerular
Pressure and inc. filtrationof macromolecules
Glomerular hypertrophy
and inc. SNGFRLoss of Neprhons
Maintenance of internalEnvironment up to limits
of Nephron adaptation
And hyperthrophy
Pathophysiology of CRF
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Chronic Renal Failure
Predisposing factors:
DM= worldwide leading cause
Recurrent infectionsExacerbations of nephritis
urinary tract obstruction
hypertension
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It occurs in stages, is irreversible, and results
in uremia or end-stage renal disease CRF
affects all of the major body systems and
requires dialysis or kidney transplant tomaintain life
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The result is azotemia to UREMIA
The nephrons left intact are subjected to an
increased work load, resulting in hypertrophy
and inability to concentrate urine.
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Chronic Renal Failure
CRF is a progressive, irreversible reduction inrenal function such that the kidneys are nolonger able to maintain the body
environment. Gradual, Progressive irreversible destruction
of the kidneys causing severe renaldysfunction.
The GFR gradually decreases as the nephronsare destroyed.
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Prerenal(renal ischemia)
Serious cardiovascular
disorders
Peripheral vasodilation
Severe
vasoconstriction
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Kidney function
The Nephron producesurine to eliminate waste
Impaired urine productionand azotemia
Secretes Erythropoietin toincrease RBC
ANEMIA
Metabolism of Vitamin D Calcium and Phosphateimbalances
Produces bicarbonate and
secretes acids
Metabolic ACIDOSIS
Excretes excessPOTASSIUM
HYPERKALEMIA