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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

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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