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    Hypovolemic Shock Pathophysiology

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    KAYCEE
    The document summarizes the pathophysiology of hypovolemic shock secondary to massive upper gastrointestinal bleeding from ruptured esophageal varices. It describes how chronic hepatitis C infection can lead to liver cirrhosis, portal hypertension, and eventual variceal rupture/bleeding through a series of interconnected steps over many years, ultimately resulting in hypovolemic shock from blood and fluid loss.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    Hypovolemic Shock Pathophysiology

    Uploaded by

    KAYCEE
    45 views8 pages
    The document summarizes the pathophysiology of hypovolemic shock secondary to massive upper gastrointestinal bleeding from ruptured esophageal varices. It describes how chronic hepatitis C infection can lead to liver cirrhosis, portal hypertension, and eventual variceal rupture/bleeding through a series of interconnected steps over many years, ultimately resulting in hypovolemic shock from blood and fluid loss.

    Original Title

    HYPOVOLEMIC SHOCK PATHOPHYSIOLOGY

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    The document summarizes the pathophysiology of hypovolemic shock secondary to massive upper gastrointestinal bleeding from ruptured esophageal varices. It describes how chronic hepatitis C infection can lead to liver cirrhosis, portal hypertension, and eventual variceal rupture/bleeding through a series of interconnected steps over many years, ultimately resulting in hypovolemic shock from blood and fluid loss.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    45 views8 pages

    Hypovolemic Shock Pathophysiology

    Uploaded by

    KAYCEE
    The document summarizes the pathophysiology of hypovolemic shock secondary to massive upper gastrointestinal bleeding from ruptured esophageal varices. It describes how chronic hepatitis C infection can lead to liver cirrhosis, portal hypertension, and eventual variceal rupture/bleeding through a series of interconnected steps over many years, ultimately resulting in hypovolemic shock from blood and fluid loss.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 8

    Pathophysiology of Hypovolemic Shock1 Secondary to Massive Upper

    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary


    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection
    Predisposing Factors: Precipitating Factors:
    -Age: 54y/o -Compromised Immune System
    -Gender: Female -Poor Diet
    -Family History -Socioeconomic Status
    -Alcoholic Drinker for 35 years -Occupation
    -Smoker for 17 years -Contact with Infected blood
    (Sharing of needles: Tattoo)

    Excessive Alcohol Ingestion Introduction of Hepatitis C


    virus

    Increased liver synthesis of


    triglycerides and fatty acids, Attacks Liver
    reduction in oxidation of fatty
    acids, and decreased release
    of lipoprotein

    Fat accumulation in the


    parenchymal cells of the liver
    and distention of cytoplasm
    with fats

    Liver Steatosis/Fatty Liver

    Hepatocyte damage

    Inflammation of the liver


    (Hepatitis)

    Alteration in Blood and Stimulates liver to produce Induction of Immune response


    Lymph flow collagen
    Antigen-antibody complexes
    Liver parenchyma destruction Collagen builds up quickly
    Activation of complement
    Fibrosis/Scarring system

    LIVER CIRRHOSIS A
    2
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection
    A

    Immune complex formation in


    circulation

    Immune complex deposition in


    vascular

    Vasculitis ( Inflammation of
    Blood vessels)

    Impairs blood supply

    Ischemia in the liver

    Virus is not killed

    Viral antigen persists in the


    liver

    Viral Infection

    CHRONIC HEPATITIS C
    3
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection

    LIVER CIRRHOSIS

    Vascular Compression Increase Arterial Loading

    Increase resistance of blood Increase flow through hepatic


    flow to the liver artery

    Decrease blood flow to the Increase blood volume in


    hepatic vein sinusoid and vein

    Portal Congestion Congestion

    PORTAL HYPERTENSION

    Faulty protein synthesis


    Increase pressure in capillary Hepatic Shunting
    bed
    Hypoalbuminemia
    Diversion of blood to
    Increase capillary collateral channel
    Decrease colloidal
    osmotic pressure
    Fluid shift to extravascular
    Blood bypasses to the liver
    compartment

    Increase portal flow


    Ascites

    C
    4
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection
    C

    Esophageal Varices

    Protrusion in esophageal
    lumen

    Erosion

    Rupture

    Bleeding Hematemesis and Melena

    MASSIVE UPPER
    GASTROINTESTINAL
    BLEEDING

    Blood loss

    Intravascular volume

    Decrease cardiac output

    Antidiuretic hormone, Shift of interstitial Catecholamine


    aldosterone secretion fluid

    Increased volume Increased heart rate, Increased systemic


    force of contraction vascular resistance

    Increased cardiac output


    5
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection
    Increased cardiac output

    Continued volume loss Decreased systemic Decreased Pulmonary


    pressure pressure

    Decreased cardiac output

    Decreased tissue
    perfusion

    Impaired cellular
    metabolism

    HYPOVOLEMIC
    SHOCK
    6
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection

    B Macrophages surround them and


    wall them off in tiny, hard capsules

    Impaired Detoxification Activity


    Hypersensitivity to the organism

    Toxin exaggeration
    Hypersensitivity to the organism
    Increase susceptibility to infection
    D Inside the giant cells, caseous
    Inhalation of droplet infected with necrosis occurs (granular cheesy
    Mycobacterium Tuberculosis appearance)

    Proliferation of T-lymphocytes in
    Trapped in the upper airways
    the surrounding of the central core
    of the caseous necrosis causing
    Activated primary defenses some lesions
    (mucus-secreting goblet cell and
    cilia)
    Fibrosis and Calcification happens

    If untreated, bacteria reaches and


    deposits itself in lung periphery As the lesion ages, it then results to
    (Lower part of the upper lobe or granuloma formation (tubercle)
    Upper part of the lower lobe:
    alveoli)
    Collagenous scar tissue
    encapsulates tubercle to separate
    Bacteria is quickly surrounded by
    organism from the body
    polymorphonuclear leukocytes and
    engulfed by alveolar macrophages
    Progresses to grow and multiply
    Mycobacterium organisms are
    carried off by the lymphatics to the
    hilar lymph nodes (Ghon Complex) Cell Mediated immunity

    Macrophages (epithelial cells)


    PULMONARY TUBERCULOSIS
    engulfs the bacteria
    7
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection

    Aspiration of Bacteria in Lower


    Respiratory Tract

    Failure of first line of Defense

    Bacterial invasion into the lungs


    and proceed into the Lower
    Respiratory tract

    Pneumonia (HAP)

    Triggered Inflammatory response

    Inflammatory Response Lymphocytes produce cytokines

    Release of Chemical Mediators Increase WBC

    Vasodilation and Increase Release of Killer T-cells,


    capillary permeability Macrophages, Phagocytes, and
    Antibodies
    Fluid shifting and Edema
    Migration to Alveoli

    Killer T-cells, Macrophages,


    Phagocytes, and Antibodies take
    effect to pathogens

    Purulent exudate formation

    Filling of WBC in alveoli and


    normally air containing space
    8
    Pathophysiology of Hypovolemic Shock Secondary to Massive Upper
    Gastrointestinal Bleeding Secondary to Ruptured Esophageal Varices Secondary
    to Portal Hypertension Secondary to Liver Cirrhosis Secondary to Chronic
    Hepatitis C Infection
    Filling of WBC in alveoli and
    normally air containing space

    Exudate or Fluid accumulation Continuous exudates or Fluid


    in Alveoli accumulation

    Multiplication of growth of the Alveolar damage


    organism
    Alveolar Collapse
    Fluid filled alveoli/Lobar
    compartment
    Atelectasis (Segmental
    Atelectasis)
    Rupture of Inflammed
    endothelial cells

    Excess fluid accumulation in


    space pericardial

    Pleural Effusion

    LEGEND:
    PRECIPITATING FACTORS PREDISPOSING FACTORS

    DISEASE PROCESS SIGNS AND SYMPTOMS

    DISEASE CONTINUATION

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