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    Ôm M Ôm M M Ômmm MM MMM MM MM C MMMMMMCM "M MM MMM M

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    This document summarizes the pathophysiology of chronic kidney disease due to long-standing hypertension in a 53-year-old female teacher with a high salt diet and low water intake. Prolonged high blood pressure can damage the kidneys over many years by reducing blood flow and causing scarring of the glomeruli and tubules. As kidney function declines below 50%, the remaining nephrons must work harder to compensate, leading to further damage in a continuous cycle. When function declines below 10-15%, end-stage renal disease develops, characterized by build-up of waste, fluid overload, and complications like anemia and bone disease that require dialysis or transplant for survival.

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    Ôm M Ôm M M Ômmm MM MMM MM MM C MMMMMMCM "M MM MMM M

    Uploaded by

    mayxzine
    175 views3 pages
    This document summarizes the pathophysiology of chronic kidney disease due to long-standing hypertension in a 53-year-old female teacher with a high salt diet and low water intake. Prolonged high blood pressure can damage the kidneys over many years by reducing blood flow and causing scarring of the glomeruli and tubules. As kidney function declines below 50%, the remaining nephrons must work harder to compensate, leading to further damage in a continuous cycle. When function declines below 10-15%, end-stage renal disease develops, characterized by build-up of waste, fluid overload, and complications like anemia and bone disease that require dialysis or transplant for survival.

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    PATHOPYSIOLOGY-ernan

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    This document summarizes the pathophysiology of chronic kidney disease due to long-standing hypertension in a 53-year-old female teacher with a high salt diet and low water intake. Prolonged high blood pressure can damage the kidneys over many years by reducing blood flow and causing scarring of the glomeruli and tubules. As kidney function declines below 50%, the remaining nephrons must work harder to compensate, leading to further damage in a continuous cycle. When function declines below 10-15%, end-stage renal disease develops, characterized by build-up of waste, fluid overload, and complications like anemia and bone disease that require dialysis or transplant for survival.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd
    Flag for inappropriate content
    Download as docx, pdf, or txt
    175 views3 pages

    Ôm M Ôm M M Ômmm MM MMM MM MM C MMMMMMCM "M MM MMM M

    Uploaded by

    mayxzine
    This document summarizes the pathophysiology of chronic kidney disease due to long-standing hypertension in a 53-year-old female teacher with a high salt diet and low water intake. Prolonged high blood pressure can damage the kidneys over many years by reducing blood flow and causing scarring of the glomeruli and tubules. As kidney function declines below 50%, the remaining nephrons must work harder to compensate, leading to further damage in a continuous cycle. When function declines below 10-15%, end-stage renal disease develops, characterized by build-up of waste, fluid overload, and complications like anemia and bone disease that require dialysis or transplant for survival.

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    Download as DOCX, PDF, TXT or read online from Scribd
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    Download as docx, pdf, or txt
    of 3

    PATHOPYSIOLOGY

    Risk Factor:

    Hypertension

    y y y
    y

    Prolonged

    BP

    Age:53 Gender: female Occupation: teacher Diet: high salt intake and low intake of water

    Nephrolithiasis

    UTI

    Stones obstruct the urine in the kidney Enlargement of the kidney Urinary stasis

    Change in the intimal lining of the blood vessel

    Decreased renal blood flow Decreased renal reserved Damage to nephrons

    Hardening of the blood vessels Accumulation of fibrin in the vessel Intravascular clotting

    Bacteria starts to grow Infection and impaired kidney function

    50% damage

    More than 75% damage

    Kidney damage

    Renal insufficiency

    As nephron are destroyed, the remaining nephrons undergo changes to compensate lost ones

    Remaining nephrons must filter more solute particles from the blood

    Hypertrophy of the remaining nephrons

    Nephrons cannot tolerate the work

    Further damage of nephrons

    80-90% damage

    Renal failure

    Impaired kidney function and uremia

    Continuous decline in renal function

    >90% kidney damage

    y y y y

    Reduction in renal capillaries Scarring of glomeruli Atrophy & fibrosis of tubules Decreased kidney mass

    End stage renal disease (ESRD)

    Sodium and water retention

    Build up of waste(BUN,Creati nine) in the blood

    Decreased production of erythropoietin

    H+ retention

    hyperphospatemia

    Decreased Vit. D

    Calcium level Urine output Excess fluid goes to the extremities Build up of waste in the skin Decreased production of WBC by the bone marrow Nausea & vomiting

    hypocalcemia

    Oliguria

    Peripheral edema

    pruritus

    purpura

    Anemia

    RBC that carry O2 in the muscles and tissues Fatigue weakness

    Stimulate parathyroid gland

    Release of PTH

    SOB,DOB

    Increased absorption of calcium in the intestine, and increased calcium resoroption from the bone osteodystrophy

    Knee pain

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