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Pathophysiology Predisposing factors: Age: Blood vessels loose flexibility with age; baroreceptors are less sensitive with

aging Gender: Most common in males, cause of less levels of estrogen. less levels of estrogen increases BP Precipitating factors: Race: Filipino dishes are high in fats and cholesterol; pts diet Is high in fats and cholesterol Alcohol drinking: When alcohol enters the blood stream, it interferes the transport of o2 & nutrients to the heart through aorta and smaller veins

Heredity: Both parents are hypertensive

Accumulation of fats in blood 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

Angiotensin

Angiotensin 2

Adrenal stimulation

Production of aldosterone

Increased Na+ reabsorption

Increased H20 Reabsorption

Increased blood volume

Increased blood pressure

HYPERTENSION

Diagnostics: Excretory urography: Reveals renal athrophy, indicating chronic renal dse. ECG: Measures the electrical activity, rate, & rhythm of Heart valve chambers Echocardiogram: Provides picture of the heart valves & chambers

Labs: CBC: Determine RBC, WBC, & platelet count UA: May show microscopic of gross blood in the urine & presence of abnormal protein levels. BUN and creatinine determine and monitor kidney function.

Surgical management:

Nursing management:

Medical management:

Surgical decompression

Maintain prescribed meds, Na+ control, proper diet

Losartan, anticoagulants

Prolonged use of Losartan

Breakdown of protein myoglobin

Damaged to kidney cells If treated: Fair prognosis If not treated: 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

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

Increased tubular protein reabsorption

Tubolointerstitial inflammation and fibrosis

Further loss of nephrons

Chronic kidney disease

Diagnostic: X-ray, MRI UTZ, CT Scan

Labs: CBC, UA, Creatinine, MRI

Surgical management: Nursing Management: Kidney transplant Maintain prescribed meds, Maintain fluid & electrolyte Balance, facilitate coping & preventive measures

Med management:

Dialysis, electrolyte control, Fluid control

If treated:

If not treated:

FAIR PROGNOSIS

Increased destruction of blood cells\

Decreased Erythropoesis

Decreased Hemoglobin

Decreased RBC

Anemia

Renal

Cardiovascular

CNS

Renal failure

Decreased creatinine RBC, Hemoglobin

Lack of oxygen in the heart

Chest pain

Confusion, CNS disturbance

Brain is deprived of oxygen

Lack of oxygen delivered in the system

Severe anemia

Tissue hypoxia

Progress to coma

DEATH

Coma

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