Inflammation and Healing
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Questions and Answers

Which of the following is the primary function of inflammation in the context of immunity?

  • To activate adaptive immunity by presenting antigens.
  • To directly destroy pathogens through phagocytosis.
  • To wall off and confine pathogens, stimulate immune response, and promote healing. (correct)
  • To produce antibodies that neutralize foreign substances.

    • What is the role of neutrophils in the inflammatory response?

  • Releasing histamine to increase vascular permeability.
  • Secreting anti-inflammatory cytokines to resolve inflammation.
  • Producing antibodies to target specific pathogens.
  • Phagocytosis and release of destructive free radicals (correct)

    • Which of the following best describes exudate, formed during inflammation?

  • A fluid accumulation that causes swelling, potentially containing proteins and cells. (correct)
  • A thick, fibrous mesh that walls off the infected area preventing further spread.
  • An accumulation of scar tissue that impairs tissue function.
  • A collection of dead cells and cellular debris that inhibits immune cell migration.

    • How do basophils and mast cells contribute to the inflammatory response?

    <p>By degranulating and releasing histamine, increasing vascular permeability. (C)</p> Signup and view all the answers

    What is the collective role of plasma proteins, such as complement and kinins, in the inflammatory process?

    <p>To mediate chemotaxis, vasodilation, vascular permeability, and clotting. (B)</p> Signup and view all the answers

    Which cytokine is primarily associated with promoting inflammation?

    <p>Interleukin-1 (IL-1) (A)</p> Signup and view all the answers

    What is the function of the clotting cascade during inflammation?

    <p>To form a fibrinous mesh that prevents infection spread and stop bleeding. (A)</p> Signup and view all the answers

    Which of the following systemic manifestations is/are associated with inflammation?

    <p>Increased circulating leukocytes and fever. (B)</p> Signup and view all the answers

    What differentiates acute inflammation from chronic inflammation regarding duration and tissue changes?

    <p>Acute inflammation is self-limiting and typically resolves within 2 weeks, while chronic inflammation can lead to scar tissue or deformity. (C)</p> Signup and view all the answers

    The increased synthesis of plasma proteins during systemic inflammation is stimulated by which cytokine?

    <p>Tumor necrosis factor (TNF) (D)</p> Signup and view all the answers

    Which intervention is generally contraindicated during the acute inflammatory phase if an infectious process is suspected?

    <p>Heat application (D)</p> Signup and view all the answers

    What is the primary difference between healing by primary intention and healing by secondary intention?

    <p>Secondary intention involves greater tissue loss compared to primary intention. (B)</p> Signup and view all the answers

    A patient is taking systemic corticosteroids. Which of the following is a potential complication related to wound healing?

    <p>Impaired epithelialization (C)</p> Signup and view all the answers

    Which of the following is a systemic manifestation of inflammation?

    <p>Fever (B)</p> Signup and view all the answers

    What is the primary function of interleukins and tumor necrosis factor alpha (TNF-$ abla$) in the inflammatory response?

    <p>Mediate inflammatory responses. (B)</p> Signup and view all the answers

    Which of the following is the MOST direct objective of the inflammatory process?

    <p>To limit the extent of tissue damage and prevent further infection while initiating healing. (D)</p> Signup and view all the answers

    Which of the following represents a potential risk associated with the administration of systemic corticosteroids during the healing process?

    <p>Impaired epithelialization, potentially delaying wound closure. (A)</p> Signup and view all the answers

    In the context of wound healing, what is the PRIMARY distinction between 'healing by primary intention' and 'healing by secondary intention'?

    <p>Primary intention is characterized by minimal tissue loss and close apposition of wound edges, whereas secondary intention involves substantial tissue loss requiring granulation. (B)</p> Signup and view all the answers

    Following an injury, a patient develops a localized inflammatory response. Which of the following treatment strategies should generally be AVOIDED if an infectious process is suspected?

    <p>Application of heat to promote increased blood flow. (D)</p> Signup and view all the answers

    Which of the following is the MOST accurate description of 'dehiscence' in the context of dysfunctional wound healing?

    <p>The breakdown or rupture of a previously closed wound, increasing the risk of infection. (A)</p> Signup and view all the answers

    During inflammation, which cellular event directly leads to increased vascular permeability?

    <p>Degranulation of basophils and mast cells releasing histamine. (A)</p> Signup and view all the answers

    Which characteristic is most indicative of chronic inflammation compared to acute inflammation?

    <p>Development of scar tissue and potential deformity. (D)</p> Signup and view all the answers

    What is the primary function of the fibrinous mesh formed during the coagulation cascade at an inflamed site?

    <p>To prevent the spread of infection and stop bleeding. (D)</p> Signup and view all the answers

    Which of the following exudates is typically associated with the earliest stages of inflammation?

    <p>Serous exudate (D)</p> Signup and view all the answers

    What is the primary role of complement proteins during the inflammatory response?

    <p>Chemotaxis and target cell lysis. (B)</p> Signup and view all the answers

    Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF) contribute differently to systemic inflammation. What is a specific function attributed more directly to TNF compared to IL-1?

    <p>Induction of fever as an endogenous pyrogen. (C)</p> Signup and view all the answers

    A patient presents with elevated levels of C-reactive protein (CRP), TNF-alpha, IL-1, and IL-6. What is the most direct physiological consequence of these elevated markers?

    <p>Increased inflammation. (A)</p> Signup and view all the answers

    During mast cell degranulation, what is the combined effect of leukotrienes, prostaglandins, and platelet-activating factor?

    <p>Increased vascular permeability, vasodilation and chemotaxis. (C)</p> Signup and view all the answers

    How does the release of proteolytic enzymes from basophils and mast cells directly contribute to the inflammatory response?

    <p>By degrading the extracellular matrix, facilitating leukocyte migration. (D)</p> Signup and view all the answers

    If a patient exhibits lethargy, fever and muscle catabolism, which cascade of events connects muscle catabolism to increased inflammation markers?

    <p>Muscle catabolism leads to increased plasma proteins -&gt; increasing C-reactive protein and ESR (A)</p> Signup and view all the answers

    Flashcards

    Inflammatory Process

    The body's response mechanism to limit damage and infection.

    Phases of Wound Healing

    Stages include Coagulation, Inflammatory, Proliferation, Remodeling, and Maturation.

    Primary Intention Healing

    Healing with minimal tissue loss, leads to straightforward recovery.

    Secondary Intention Healing

    Healing that occurs with significant tissue loss and results in an open wound.

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    Dysfunction During Healing

    Problems like scarring, impaired epithelialization, and wound disruption that can hinder recovery.

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    Innate Immunity

    The first line of defense against pathogens, involving barriers like skin and mucous membranes.

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    Adaptive Immunity

    The third line of defense that is specific and acquired over time through exposure to pathogens.

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    Inflammation

    A response that confines pathogens, stimulates immune response, and promotes healing.

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    Neutrophils

    A type of white blood cell that engages in phagocytosis and releases free radicals to kill pathogens.

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    Cytokines

    Signaling proteins secreted by immune cells to communicate and regulate the immune response.

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    Exudates

    Fluids that accumulate in inflamed tissues, indicating the severity of inflammation.

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    Cardinal Signs of Inflammation

    The four observable signs: redness, swelling, heat, and pain.

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    PLASMA PROTEINS

    Proteins in the plasma involved in clotting and inflammation, such as complement and kinins.

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    Basophils & Mast Cells

    White blood cells that release histamine to increase vascular permeability during inflammation.

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    Acute vs Chronic Inflammation

    Acute is short-term and localized, while chronic is long-term with possible scar tissue.

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    Treatment Implications

    Various methods to manage inflammation and promote healing.

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    End Result of Inflammation

    Can lead to either regeneration (original structure) or repair (scar tissue).

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    Inflammatory Cytokines

    Interleukin-1, Interleukin-6, and Tumor Necrosis Factor Alpha are key cytokines in inflammation.

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    Inflammation Purpose

    To wall off pathogens, stimulate immune response, and promote healing.

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    Neutrophils Function

    Engage in phagocytosis and release free radicals to destroy pathogens.

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    Macrophages Role

    Phagocytose pathogens and release cytokines to recruit other immune cells.

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    Histamine Release

    Increases vascular permeability and causes dilation of blood vessels during inflammation.

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    Cytokine Types

    Signaling molecules like IL-1 (proinflammatory) and IL-10 (anti-inflammatory) that regulate immune responses.

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    Complement System

    Group of plasma proteins that enhance immune responses through chemotaxis and cell lysis.

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    Vascular Changes in Inflammation

    Includes increased permeability, vasodilation, and emigration of leukocytes.

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    Goals of Inflammation

    Contain injury, eliminate pathogens, and initiate repair.

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    Study Notes

    Inflammation and Healing

    • Inflammation is the body's 2nd line of defense against pathogens.
    • Innate immunity is the 1st line of defense.
    • Adaptive/acquired immunity is the 3rd line of defense.
    • Inflammation works by walling off pathogens to minimize damage.
    • It also stimulates the immune response, and promotes healing.
    • Leukocytes (WBCs) are key players in inflammation.
    • Neutrophils: phagocytosis, release free radicals, cause purulent exudate.
    • Macrophages: phagocytosis, release cytokines.
    • Eosinophils: degranulate.
    • Basophils & mast cells: degranulate, release histamine, increasing vascular permeability, dilate blood vessels, release chemotactic factors, proteolytic enzymes, heparin, leukotrienes, prostaglandins, and platelet-activating factor.

    Phagocytosis

    • A critical process in inflammation.
    • Involves the engulfing of pathogens by phagocytes.
    • Stages: recognition and attachment, engulfment and phagosome formation, fusion with lysosomes, phagolysosome formation, and destruction and digestion.

    Basophils & Mast Cells

    • Degranulate to release histamine, increasing vascular permeability and dilating blood vessels.
    • Crucial for chemotaxis, attracting other immune cells to the site of infection.
    • Release other important substances like proteolytic enzymes, heparin, leukotrienes, prostaglandins, and platelet-activating factor.

    Inflammation at the Tissue Level

    • Vascular permeability increases, causing a swelling or edema.
    • Blood vessels dilate.
    • Leukocytes (WBCs) migrate into the tissue.
    • This is a response to damage.
    • Inflammation includes vasodilation, and increased permeability.

    Plasma Proteins in Inflammation

    • Complement proteins: chemotaxis (movement of cells), target cell lysis, vasodilation, clotting cascade.
    • Kinins: vasodilation.
    • Clotting factors: form fibrinous mesh, preventing infection spread, and stopping bleeding.
    • All these increase vascular permeability and cause pain.

    Cytokines in Inflammation

    • Interleukins (e.g., IL-1, IL-6, IL-10): some pro-inflammatory, others anti-inflammatory.
    • Interferon (IFN): protects against viral infections. Interferons bind to uninfected cells to produce antiviral proteins, blocking viral nucleic acid synthesis.
    • Tumor necrosis factor (TNF): endogenous pyrogen, increasing plasma protein synthesis.
    • These have crucial roles in regulating the inflammatory response.

    Three Events of Inflammation

    • Injury leads to endothelial cells binding of neutrophils and macrophages.
    • Vasoactive chemicals are released.
    • Chemokines are released.
    • Vasodilation occurs.
    • Neutrophils and macrophages enter tissue, and initiate phagocytosis.

    Acute vs. Chronic Inflammation

    • Acute: localized, self-limiting, discrete events, less than 2 weeks.
    • Chronic: more diffuse, scarring, and deformity, longer than 2 weeks.

    Four Cardinal Signs of Inflammation

    • Pain, heat, redness and swelling, are caused via tissue damage, release of vasoactive mediators, vasodilation, and increased permeability.

    Localized Clinical Manifestations of Inflammation

    • Redness, swelling, heat, pain, loss of function, and exudative fluids.
    • All associated with inflammation.

    Exudates

    • Classified as different types: hemorrhagic, purulent, fibrinous, serous.
    • Hemorrhagic (a lot of blood).
    • Purulent (pus).
    • Fibrinous (fibrous material).
    • Serous (clear fluid).

    Systemic Clinical Manifestations

    • Fever, circulating leukocytes, lethargy, muscle catabolism (an increase in plasma proteins), C-reactive protein (helps determine the severity of inflammation), TNF a, IL-1, IL-6, erythrocyte sedimentation rate (ESR).

    Goals of Inflammation

    • Limit the inflammatory process.
    • Prevent and limit infection.
    • Initiate adaptive immune response.
    • Initiate healing (can result in regeneration or repair (scar tissue)).

    Treatment Implications in Inflammation

    • Intervene or not (treatment depends on the situation).
    • Antihistamines.
    • Systemic corticosteroids/glucocorticoids.
    • Fever reducers.
    • Elevation of the extremity, heat (heat is often used in conjunction with other modalities to treat the inflammatory process). Infectious processes (often treated with antibiotics or antifungals).
    • I & D (incision and drainage).

    End Result of Inflammation

    • Regeneration (return to original structure/function) or Repair (scar tissue).

    Healing

    • Primary Intention: minimal tissue loss.
    • Secondary Intention: significant tissue loss, open wound.

    Wound Healing

    • Phases of healing: coagulation, inflammatory, proliferation, remodeling, maturation.

    Dysfunction During Healing

    • Scarring, keloid, impaired epithelialization, corticosteroid use, or hypoxemia, nutritional deficiencies, wound disruption, or dehiscence (increases risk of infection).

    The Mature White Blood Cell

    • Neutrophil

    Systemic Manifestations of Inflammation

    • Fever, increased circulating leukocytes, lethargy, muscle catabolism, increased plasma protein levels, increased C-reactive protein (inflammation marker), increased erythrocyte sedimentation rate (ESR).

    Cytokines

    • Interleukin-1, Interleukin-6, and Tumor necrosis factor Alpha (TNF-α): pro-inflammatory cytokines secreted by Macrophages.

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