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  • Cva Patho

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    kriska_ortiz
    190 Ansichten2 Seiten
    This document summarizes the pathophysiology of diabetes mellitus. It lists modifiable factors like smoking, alcohol consumption, hypertension, and sedentary lifestyle as well as non-modifiable factors like age over 40 and male sex that can increase risk. The key pathophysiological processes described are the destruction of pancreatic alpha and beta cells leading to failure to produce insulin and excess glucagon production, resulting in increased blood glucose levels, glycoprotein deposits, and wasting of lean mass. Complications involve damage to small blood vessels, nerves, kidneys, and increased risk of infection and cerebrovascular accidents.

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    CVA PATHO

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    This document summarizes the pathophysiology of diabetes mellitus. It lists modifiable factors like smoking, alcohol consumption, hypertension, and sedentary lifestyle as well as non-modifiable factors like age over 40 and male sex that can increase risk. The key pathophysiological processes described are the destruction of pancreatic alpha and beta cells leading to failure to produce insulin and excess glucagon production, resulting in increased blood glucose levels, glycoprotein deposits, and wasting of lean mass. Complications involve damage to small blood vessels, nerves, kidneys, and increased risk of infection and cerebrovascular accidents.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Als DOC, PDF, TXT herunterladen oder online auf Scribd lesen
    Markieren Sie unangemessene Inhalte
    190 Ansichten2 Seiten

    Cva Patho

    Hochgeladen von

    kriska_ortiz
    This document summarizes the pathophysiology of diabetes mellitus. It lists modifiable factors like smoking, alcohol consumption, hypertension, and sedentary lifestyle as well as non-modifiable factors like age over 40 and male sex that can increase risk. The key pathophysiological processes described are the destruction of pancreatic alpha and beta cells leading to failure to produce insulin and excess glucagon production, resulting in increased blood glucose levels, glycoprotein deposits, and wasting of lean mass. Complications involve damage to small blood vessels, nerves, kidneys, and increased risk of infection and cerebrovascular accidents.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Als DOC, PDF, TXT herunterladen oder online auf Scribd lesen
    Markieren Sie unangemessene Inhalte
    von 2

    PATHOPHYSIOLOGY

    MODIFIABLE FACTORS: NON-MODIFIABLE FACTORS:

    Smoking, Alcohol Consumption, Age(40years old), Sex (Male)


    Hypertension II and Sedentary
    Lifestyle

    Weight Loss

    Destruction of Alpha and Beta cells of the pancreas Increase Acidosis


    Polydipsia, Ketones
    Polyuria and
    Polyphagia
    Failure to produce insulin Production of excess glucagon

    Increase Increase serum glucose levels Production of glucose from protein and
    osmolarity due to
    Glycoprotein cell wall deposits fat stores
    glucose Fatigue
    Wasting of lean masses
    Impaired immune Small Accelerated
    Wt. Loss
    function vessels Atherosclerosis
    disease
    Hypertension

    Symmetrical Numbness Diabetic Thrombus


    loss of and tingling Nephropathy CEREBROVASCULAR
    Emboli ACCIDENT
    protective in the
    sensation extremities Renal
    Affectation Hemiparesis
    Decrease Tissue
    Infection
    Perfusion (brain)
    Decrease production Hemisensory loss
    Lab result: of erythropoeitin
    WBC Cerebral hypoxia
    27.31 Syncope / Vertigo
    3
    Decrease RBC
    5 -10x10 /µL production in the bone
    4/15/2011 Cerebral ischemia
    marrow

    Short term ischemia


    Anemia
    (<10 -15 minutes)

    Temporary Deficits

    No Permanent Damage
    MID CEREBRAL ARTERY ANTERIOR CEREBRAL POSTERIOR CEREBRAL VERTEBROBASILAR
    ARTERY ARTERY ARTERY

    Apraxia Ataxia Hemisensory loss Hemiparesis (Left Dysphagia Dysarthia


    left upper upper extremities)
    extremities Hemiplegia (Left
    lower extremities)

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