nephrotic syndrome-patho.docx

7/27/2019 NEPHROTIC SYNDROME-PATHO.docx

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Pathophysiology

Predisposing factors: Precipitating factors:

Age: Blood vessels loose flexibility Gender: Most common in males, Race: Filipino dishes are high Alcohol drinking: When alcohol enters the blood

with age; baroreceptors are less cause of less levels of estrogen. in fats and cholesterol; pts diet stream, it interferes the transport of o2 & nutrients

sensitive with aging less levels of estrogen increases BP Is high in fats and cholesterol to the heart through aorta and smaller veins

Heredity: Both parents are Accumulation of fats in blood

hypertensive vessels

Obstruction of blood flow

in the circulatory system

Changes in arteriolar bed and increased

Systemic resistance

Increased after load

Decreased blood flow to organs

Renal hypofusion

Release of renin from Juxtaglomerular cells


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Angiotensin Angiotensin 2

Adrenal stimulation

Production of aldosterone Increased Na+ reabsorption

Increased H20 Reabsorption

Increased blood volume Increased blood pressure

HYPERTENSION

Diagnostics: Labs:

Excretory urography: ECG: Measures the Echocardiogram: CBC: Determine RBC, UA: May show BUN and creatinine

Reveals renal athrophy, electrical activity, Provides picture WBC, & platelet count microscopic of determine and monitor

indicating chronic rate, & rhythm of of the heart valves gross blood in the kidney function.

renal dse. Heart valve chambers & chambers urine & presence of

abnormal protein

levels.


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Surgical management: Nursing management: Medical management:

Surgical decompression Maintain prescribed meds, Losartan, anticoagulants Prolonged use of Losartan

Na+ control, proper diet

Breakdown of protein myoglobin

Damaged to kidney cells

If treated: If not treated:

Fair prognosis Infection

Renal scarring

Chronic glomerulo nephritis

Compensatory mechanism:

Antigen-antibody production

Fatigue Inflammatory & immune response

Deposition of antigen-antibody complex

Leukocytes infiltrate in the glomerulus


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Thickening of the glomerular filtration membrane

Fibrosis and loss of glomerular filtration membrane

Increased BUN Decreased GFR

Further destruction and deterioration of nephrons

Fatigue, increased BUN & creatinine Diminished renal reserve

Glomerular capillary HPN

Increased glomerular permeability/ filtration

Proteinuria


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Increased tubular protein Tubolointerstitial inflammation and fibrosis

reabsorption

Further loss of nephrons

Chronic kidney disease

Diagnostic: Labs:

X-ray, MRI CBC, UA,

UTZ, CT Scan Creatinine, MRI

Surgical management: Med management:

Nursing Management:

Kidney transplant

Maintain prescribed meds, Dialysis, electrolyte control,

Maintain fluid & electrolyte Fluid control

Balance, facilitate coping &

preventive measures

If treated: If not treated:

FAIR PROGNOSIS


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Increased destruction of blood cells\ Decreased Erythropoesis

Decreased Hemoglobin

Decreased RBC

Anemia

Renal Cardiovascular CNS

Renal failure Decreased creatinine Lack of oxygen in the heart Chest pain Confusion, Brain is deprived of

RBC, Hemoglobin CNS disturbance oxygen

Lack of oxygen delivered in the system

Severe anemia Tissue hypoxia Progress to coma

DEATH Coma

nephrotic syndrome-patho.docx

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