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  • ESRD Pathophysiology

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    The document discusses the pathophysiology of heart and kidney damage. It explains that reduced oxygen supply to heart cells can lead to contractility issues, increased heart rate, and ultimately myocardial infarction. In the kidneys, damage to glomeruli can cause inability to excrete waste, fluid retention, edema, and eventually end stage renal disease. Both conditions are exacerbated by modifiable risk factors like obesity, hypertension, and diabetes as well as non-modifiable factors like age, sex, and race.

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    122411065-ESRD-Pathophysiology

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    The document discusses the pathophysiology of heart and kidney damage. It explains that reduced oxygen supply to heart cells can lead to contractility issues, increased heart rate, and ultimately myocardial infarction. In the kidneys, damage to glomeruli can cause inability to excrete waste, fluid retention, edema, and eventually end stage renal disease. Both conditions are exacerbated by modifiable risk factors like obesity, hypertension, and diabetes as well as non-modifiable factors like age, sex, and race.

    Copyright:

    © All Rights Reserved
    Scarica in formato DOCX, PDF, TXT o leggi online su Scribd
    Segnala contenuti inappropriati
    80 visualizzazioni2 pagine

    ESRD Pathophysiology

    Caricato da

    nursing concept maps
    The document discusses the pathophysiology of heart and kidney damage. It explains that reduced oxygen supply to heart cells can lead to contractility issues, increased heart rate, and ultimately myocardial infarction. In the kidneys, damage to glomeruli can cause inability to excrete waste, fluid retention, edema, and eventually end stage renal disease. Both conditions are exacerbated by modifiable risk factors like obesity, hypertension, and diabetes as well as non-modifiable factors like age, sex, and race.

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    © All Rights Reserved
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    di 2

    PATHOPHYSIOLOGY

    HEART KIDNEY

    Myocardial O2 Kidney Function


    Supply
    Cellular hypoxia Damage to the Unable to
    Glomeruli Excrete
    Contractility Metabolic

    Hyperthtophy Fluid Retention


    Cardiac

    ESRD
    Baroreceptors and
    EDEMA
    Sympathtetic Receptors
    Stimulates
    DEATH Pulmonary
    Contractility Congestion

    HR

    Myocardial O2
    Demand
    MI
    PATHOPHYSIOLOGY

    MODIFIABLE FACTORS
    NON MODIFIABLE
    - Obesity FACTORS
    - Hypertension
    - Diabetes - Old Age
    - Sedentary - Male
    Lifestyle - Race
    - Heart Failure
    - Nephrotic
    Syndrome

    Decreased Blood Flow


    in the Renal Arteries

    Release of renin
    by
    juxtaglumerular

    Enters the
    Bloodstream
    Angiotensinogen in the liver
    to angiotensin I

    ACE converts angiotensin I


    to angiotensin II

    Vasoconstriction Release of
    Aldosterone
    Sodium Retention

    Increase Plasma

    BP

    Tissue
    Perfusion

    Oxygen Supply

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