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    Pathophysiology of Diabetes Mellitus Type 2

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    jnrue_aerith
    This document outlines the pathophysiology of type 2 diabetes mellitus. It begins with predisposing factors such as family history, obesity, and age. This leads to insulin resistance where beta cells in the pancreas become exhausted from trying to compensate. This causes a decrease in insulin production and secretion, preventing glucose from being absorbed by cells. The body begins to breakdown fat and protein instead, causing complications throughout the body like neuropathy, nephropathy, and retinopathy. If left untreated, this can progress to include ketoacidosis, coma and eventually death.

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    Pathophysiology of Diabetes Mellitus Type 2

    Uploaded by

    jnrue_aerith
    36K views7 pages
    This document outlines the pathophysiology of type 2 diabetes mellitus. It begins with predisposing factors such as family history, obesity, and age. This leads to insulin resistance where beta cells in the pancreas become exhausted from trying to compensate. This causes a decrease in insulin production and secretion, preventing glucose from being absorbed by cells. The body begins to breakdown fat and protein instead, causing complications throughout the body like neuropathy, nephropathy, and retinopathy. If left untreated, this can progress to include ketoacidosis, coma and eventually death.

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    Pathophysiology of Diabetes Mellitus Type 2

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    This document outlines the pathophysiology of type 2 diabetes mellitus. It begins with predisposing factors such as family history, obesity, and age. This leads to insulin resistance where beta cells in the pancreas become exhausted from trying to compensate. This causes a decrease in insulin production and secretion, preventing glucose from being absorbed by cells. The body begins to breakdown fat and protein instead, causing complications throughout the body like neuropathy, nephropathy, and retinopathy. If left untreated, this can progress to include ketoacidosis, coma and eventually death.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
    36K views7 pages

    Pathophysiology of Diabetes Mellitus Type 2

    Uploaded by

    jnrue_aerith
    This document outlines the pathophysiology of type 2 diabetes mellitus. It begins with predisposing factors such as family history, obesity, and age. This leads to insulin resistance where beta cells in the pancreas become exhausted from trying to compensate. This causes a decrease in insulin production and secretion, preventing glucose from being absorbed by cells. The body begins to breakdown fat and protein instead, causing complications throughout the body like neuropathy, nephropathy, and retinopathy. If left untreated, this can progress to include ketoacidosis, coma and eventually death.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOC, PDF, TXT or read online from Scribd
    Download as doc, pdf, or txt
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    The key takeaways are that diabetes mellitus type 2 is caused by a combination of genetic and lifestyle factors that can lead to insulin resistance and decreased insulin production by the pancreas over time. This dysregulation of blood sugar levels then causes various complications throughout the body if not managed properly.

    Some precipitating factors include frequent infections, high sugar diet, gestational diabetes, and sedentary lifestyle. Predisposing factors include family history, obesity, and older age. Genetics and excess body weight increase the risk.

    Long term high blood sugar can damage nerves (neuropathy), eyes (retinopathy potentially causing blindness), kidneys (nephropathy potentially causing kidney failure), and increase risk of cardiovascular disease like heart attacks and strokes. It can also impair wound healing.

    Ideal Pathophysiology of Diabetes Mellitus Type II

    Precipitating factors: Predisposing factors:


    1. frequent or chronic infections 1. family history of DM
    2. eating too much sweets 2. obesity
    3. development of glucose 3. Age above 40
    intolerance during drug
    Insulin resistance
    therapy
    4. delivery of over 9 lbs infants
    5. diet
    6. sedentary lifestyle Exhaustion of beta cells

     Insulin production/
    decrease secretion of
    insulin

    Degradation of proteins  Absorption of glucose by the cell  Breakdown of fat

    Cell starvation

    Stimulation of hunger mechanism via hypothalamus

    Hunger
    POLYPHAGIA

    FBS  140 mg/dL

    HYPERGLYCEMIA

    FBS  to 180 mg/dL

    Kidney filtration mechanism impaired


    Nerve Demyelinization Capillary basement
    membrane thickening
    GLYCOSURIA

     Acidity of urine
    NEUROPATHY
    Diffuse glomerular
    sclerosis
     Urethral flora
    Paresthesias &
    numbness NEPHROPATHY

    Impaired pain
    sensation UTI Vaginitis Renal failure

    NON-HEALING Delayed wound  Circulating POLYURIA & End-Stage Renal


    ULCERS healing blood volume ALBUMINURIA Disease

    Gangrene Hypovolemia

    HYPOTENSION &
    TACHYCARDIA
    F & E imbalance

     Number of solute relative to water

    Potassium ion retention Sodium ions lost

    Cardiac arrythmias Tissue dehydration

    DEATH POLYDIPSIA

    Increase viscosity of
    blood

    Capillary basement Thickening of blood Musculoskeletal effects


    membrane thickening vessel walls

    Abnormal retinal vascular Occlusion of plaque Impaired glucose absorption in


    permeability the muscle tissue

    Blood flow blocked


    Scarring Joint contractures

     Blood pressure Myocardial Diminished


    RETINOPATHY ischemia peripheral FATIGUE
    pulse
    HYPERTENSION
    Blurring of vision Myocardial
    infarction
    Stroke
    Blindness
    blindness Heart Failure
     Breakdown of fat  Fatty acids &  Fat content of the
    glycerol blood

    Weight Loss  ketone bodies in the Hyperlipidemia


    general circulation
     hydroxybutyric acid
     acetoacetic acid Formation of fatty
     acetone deposits on the
    walls of the blood
    vessels
    Convulsions Metabolic acidosis Acetone breath
    Atherosclerosis

    Nausea and vomiting Abdominal pain ↓ Cellular Potassium Body attempts to prevent Depressed central
    further decrease in pH nervous system
    Poor appetite Cardiac arrhythmias Kussmaul’s respirations

    Headache Coma
     Amino acid in the  Mobilization /
    general circulation degradation of proteins

    Hyperaminoacidemia

    Decreased urinary
    nitrogen

    Further sodium ion loss Potassium ion retention

    Dehydration Cardiac arrhythmias

    DEATH
    hunger

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