Inflammation and Tissue Repair Quiz
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Questions and Answers

What is the primary function of neutrophils in the inflammatory process?

  • Stimulate B-cell proliferation and antibody production
  • Release vasoactive substances, such as heparin and histamine
  • Phagocytosis of bacteria and debris in acute injury or infection (correct)
  • Kill parasitic helminths (worms)
  • Which of the following cells is responsible for synthesizing collagen during the proliferative phase of wound healing?

  • Macrophages
  • Fibroblasts (correct)
  • Neutrophils
  • Lymphocytes
  • Which of the following is a common complication of the proliferative phase of wound healing?

  • Keloid formation
  • Hemorrhage
  • Infection
  • Hypergranulation (correct)
  • What is the primary function of macrophages during wound healing?

    <p>Phagocytosis of bacteria and debris (C)</p> Signup and view all the answers

    What type of cells are responsible for antibody-mediated immunity?

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

    What is the primary function of T helper cells?

    <p>Stimulate B-cell proliferation and antibody production (B)</p> Signup and view all the answers

    What type of cells are responsible for cell-mediated immunity?

    <p>T cells (D)</p> Signup and view all the answers

    What is a "left shift" in a differential white blood cell count?

    <p>An increase in the number of neutrophils, including immature neutrophils (C)</p> Signup and view all the answers

    Which of the following is NOT a factor that can impair wound healing?

    <p>Adequate nutrition (D)</p> Signup and view all the answers

    Which of the following is an example of a labile cell?

    <p>Mucosal lining cells (B)</p> Signup and view all the answers

    Which of the following is an example of a permanent cell?

    <p>Myocardial cells (C), Nerve cells (D)</p> Signup and view all the answers

    What is the main difference between primary and secondary intention wound healing?

    <p>The depth of the wound (D)</p> Signup and view all the answers

    What is the role of angiogenesis in wound healing?

    <p>Formation of new blood vessels (A)</p> Signup and view all the answers

    Which of the following is a characteristic of chronic inflammation?

    <p>Presence of fibroblasts (C)</p> Signup and view all the answers

    Why would corticosteroids impair wound healing?

    <p>They inhibit the inflammatory response (B)</p> Signup and view all the answers

    What is a common risk factor that can lead to wound dehiscence?

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

    Which type of wound is characterized by the tearing of tissue that may require suturing?

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

    What is a significant characteristic of a Stage IV pressure ulcer?

    <p>Extensive destruction of fascia, muscle, bone, tendon (D)</p> Signup and view all the answers

    What should be avoided in the treatment of clean wounds?

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

    Where are venous stasis ulcers commonly located?

    <p>Malleolus and tibial area (D)</p> Signup and view all the answers

    What is the appearance of arterial ulcers?

    <p>Necrotic with minimal drainage (A)</p> Signup and view all the answers

    Which method should NOT be used for debriding heel eschar?

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

    What is the most important factor in the healing of arterial ulcers?

    <p>Improving perfusion (A)</p> Signup and view all the answers

    What is a recommended practice for preventing pressure ulcers in bedfast patients?

    <p>Reposition every 2 hours (C)</p> Signup and view all the answers

    What indicates an initial presentation of a pressure ulcer?

    <p>Non-blanching erythema (A)</p> Signup and view all the answers

    What is the primary purpose of inflammation during tissue repair?

    <p>To remove microorganisms and necrotic tissue (B)</p> Signup and view all the answers

    Which of the following is NOT a cardinal sign of inflammation?

    <p>Improved function (C)</p> Signup and view all the answers

    During the vascular phase of acute inflammation, which of the following occurs?

    <p>Increased vascular permeability (D)</p> Signup and view all the answers

    What role do neutrophils play during the cellular phase of acute inflammation?

    <p>They migrate to the area of injury and perform phagocytosis (B)</p> Signup and view all the answers

    Which chemical mediator is responsible for inducing smooth muscle contraction of bronchioles?

    <p>Bradykinin (A)</p> Signup and view all the answers

    What is the function of the complement system in inflammation?

    <p>Coat microorganisms to facilitate phagocytosis (A)</p> Signup and view all the answers

    Which type of white blood cell becomes macrophages during the inflammatory response?

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

    Which signaling molecules are primarily released by activated macrophages to promote inflammation?

    <p>IL-1 and TNF-α (B)</p> Signup and view all the answers

    What is the typical lifespan of neutrophils during an inflammatory response?

    <p>10 hours (B)</p> Signup and view all the answers

    Which of the following mediators causes vasodilation during the acute phase of inflammation?

    <p>Histamine (A)</p> Signup and view all the answers

    What effect do leukotrienes have in the inflammatory response?

    <p>Enhance bronchoconstriction and microvascular permeability (C)</p> Signup and view all the answers

    Which type of immunity involves physical and chemical barriers including skin and mucosa?

    <p>Innate Immunity (A)</p> Signup and view all the answers

    What initiates the acute phase response characterized by fever and increased neutrophil release?

    <p>IL-1 and TNF-α (C)</p> Signup and view all the answers

    Which of the following is an effect of bradykinin in the inflammatory process?

    <p>Increases pain sensitivity (D)</p> Signup and view all the answers

    Flashcards

    Role of Inflammation

    Physiological response to tissue injury, infection, or foreign bodies.

    Acute Inflammation

    Quick, short-term response to injury marked by redness, swelling, heat, pain, and loss of function.

    Chronic Inflammation

    Long-term inflammation that can damage tissues and organs, often due to persistent irritants.

    Cardinal Signs of Inflammation

    Redness, swelling, heat, pain, and loss of function are key indicators of inflammation.

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    Vascular Phase of Inflammation

    Phase involving vasodilation and increased capillary permeability, leading to heat and swelling.

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    Cellular Phase of Inflammation

    Involves migration of neutrophils and platelets to the injury site, leading to phagocytosis.

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    Neutrophils

    White blood cells that migrate to injury sites for phagocytosis, typically within 6-12 hours.

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    Macrophages

    Derived from monocytes, these cells ingest pathogens and secrete inflammatory mediators for several days.

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    Bradykinin

    Chemical mediator that increases vascular permeability and pain sensitivity, activates from plasma proteins.

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    Histamine

    Released by mast cells to induce transient vasodilation during acute inflammation.

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    Cytokines

    Signaling proteins that promote or inhibit inflammation, released by immune cells.

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    Arachidonic Acid Metabolites

    Mediators like prostaglandins that induce vasodilation and bronchoconstriction during inflammation.

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    Complement System

    Group of plasma proteins that aids in opsonization, recruitment of inflammatory cells, and cell lysis.

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    Phagocytosis

    Process by which cells like neutrophils and macrophages ingest and destroy pathogens.

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    Granuloma

    A structure formed when macrophages surround and 'wall off' foreign proteins.

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    Abscess

    A localized collection of pus requiring incision and drainage, formed by fibroblasts walling off infection.

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    Normal WBC Count

    The standard range of white blood cells in the blood, which is 5,000-11,000 per ml3.

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    Eosinophils

    WBCs (1-6%) that increase during allergic reactions and infections by parasites, killing parasitic worms.

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    Bacterial infection response

    Characterized by an increase in neutrophils, which may include immature neutrophils ('bands').

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    Phase I of Wound Healing

    Hemostasis; the primary goal is to stop blood loss during injury.

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    Phase II of Wound Healing

    Inflammatory Phase; cleans debris, with neutrophils and macrophages arriving.

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    Phase III of Wound Healing

    Proliferative Phase; focuses on building new tissue through granulation and epithelization.

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    Keloid

    Abnormal scar tissue that grows excessively and is more common in African-Americans.

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    Factors for Effective Healing

    Include removal of necrotic tissue, infection control, adequate nutrition, and oxygen delivery.

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    Impaired Wound Healing Causes

    Include factors like malnutrition, vascular disease, diabetes, smoking, and some medications.

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    Types of Wounds

    Categories of wounds including surgical and traumatic.

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    Wound Dehiscence

    Separation of a surgical wound often accompanied by a sensation of 'giving way.'

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    Evisceration

    Protrusion of organs through an open surgical wound, considered a surgical emergency.

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    Pressure Ulcers

    Skin breakdown caused by unrelieved pressure, also known as bed sores.

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    Stage I Pressure Ulcer

    Skin intact but with tissue damage; non-blanching erythema.

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    Stage IV Pressure Ulcer

    Extensive damage involving muscle, bone, or tendons.

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    Arterial Ulcers

    Ulcers caused by atherosclerosis, appearing necrotic with minimal drainage, usually in distal extremities.

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    Venous Stasis Ulcers

    Ulcers resulting from chronic venous insufficiency, often jagged and weeping.

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    Debridement

    Removal of non-viable tissue to promote healing.

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    Prevention of Pressure Ulcers

    Includes repositioning, using pressure-reducing devices, and assessing skin.

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    Study Notes

    Inflammation, Tissue Repair & Wound Healing

    • Inflammation is a physiological response to tissue injury, infection, or foreign bodies.
    • It's mediated by inflammatory chemicals and aims to remove microorganisms, necrotic tissue, and initiate tissue repair.
    • Cardinal signs of inflammation include redness, swelling, heat, pain, and loss of function.

    Types of Immunity

    • Innate Immunity:
      • Includes physical and chemical barriers like skin, mucosa, and substances like mucus, cilia, and skin secretions.
      • Has an inflammatory response—non-specific but important
      • Contains natural killer cells (a type of lymphocyte)
    • Adaptive Immunity: A separate system

    Acute Inflammation

    • Vascular Phase:

      • Vasodilation at the site of injury increases blood flow, causing heat and redness.
      • Increased capillary permeability leads to fluid leakage into interstitial spaces, causing swelling and pain.
      • Proteins in the exudate pull in further fluid.
    • Cellular Phase:

      • Activated platelets release inflammatory mediators.
      • Neutrophils migrate to the injury site, typically within 6-12 hours.
      • They engage in phagocytosis (ingest and destroy) pathogens.
      • Monocytes transform into macrophages
      • Macrophages secrete inflammatory mediators, continue phagocytosis, and have a longer lifespan than neutrophils.

    Key Inflammatory Mediators

    • Arachidonic Acid Metabolites (e.g., prostaglandins, leukotrienes): Synthesized by neutrophils and macrophages
      • Prostaglandins and leukotrienes can increase inflammation, making asthma worse.
    • Bradykinin: Activated from plasma proteins, increases vascular permeability, induces smooth muscle contraction (bronchoconstriction), and increases pain sensitivity.
    • Histamine: Released by mast cells, causes transient vasodilation and increased capillary permeability.
    • Complement: Plasma proteins activated by antibodies or pathogen surfaces.
      • Opsonization: Coating pathogens to enhance phagocytosis.
      • Cell lysis: Destruction of cells.

    Chemical Mediators (Cytokines)

    • Cytokines are signaling molecules.
    • IL-1 and TNF-α are released from activated macrophages.
    • They stimulate neutrophils to adhere to endothelial cells and stimulate phagocytosis.
    • They contribute to the acute phase response, which includes fever, release of neutrophils, hypotension, tachycardia, anorexia, malaise, and cortisol release.
    • They stimulate increased inflammatory protein synthesis in the liver.

    Chronic Inflammation

    • Chronic inflammation arises from unresolved injuries, infections, or foreign bodies.
    • Macrophages, lymphocytes, and fibroblasts become predominant.
    • Fibroblasts increase scarring and deformity risk.

    Examples of Chronic Inflammation

    • Granuloma: Macrophages "wall off" foreign proteins (e.g., latent tuberculosis).
    • Abscess: Fibroblasts wall off infection sites. Antibiotics usually don't penetrate abscesses; I&D (incision and drainage) is often necessary.

    Inflammation & Disease

    • Uncontrolled or inappropriate inflammation can damage tissues and contribute to various diseases, such as rheumatoid arthritis, sepsis, and inflammatory bowel disease.

    White Blood Cell (WBC) Count Differential

    • Normal WBC count: 5,000-11,000/mL³.
    • Neutrophils: 40-70% of WBCs; primary responders to acute injury or infections; short lifespan
    • Eosinophils: 1-6% of WBCs; involved in allergic reactions and infections involving intestinal parasites; release inflammatory chemicals
    • Basophils: 0-2% of WBCs; release vasoactive substances (heparin, histamine) during inflammation
    • Monocytes/Macrophages: 5% of WBCs; immature macrophages; circulate in blood; phagocytose pathogens and debris, involved in repairing injured tissue. Lymphocytes: Major immune cells involved in cell-mediated and antibody-mediated immunity.

    Tissue Regeneration

    • Tissue regeneration varies.
    • Labile cells (e.g., mucosal linings, bone marrow) continuously divide and are quickly replaced.
    • Stable cells (e.g., parenchymal cells in liver and kidney) stop dividing when no longer needed but can regenerate if necessary.
    • Permanent cells (e.g., nerve cells, myocardial cells) cannot regenerate.

    Wound Healing Process

    • Phase I (Hemostasis): Stop blood loss.
    • Phase II (Inflammatory): Clean debris. Neutrophils and macrophages arrive at the injury site to phagocytose bacteria and debris.
    • Phase III (Proliferative): Build new tissue. Fibroblasts synthesize collagen and induce angiogenesis to form new blood vessels.
    • Phase IV (Remodeling): Strengthen the new tissue. Collagen reorganizes to strengthen the scar through scar remodeling for 2 years.

    Wound Healing Types

    • Primary intention: Wound edges are approximated; heals via surface epithelialization.
    • Secondary intention: Wound edges are not approximated, and healing is bottom-up by granulation tissue.

    Things Needed for Effective Wound Healing

    • Removal of necrotic tissue.
    • Control of infection.
    • Adequate nutrition.
    • Adequate oxygen delivery: this can impact a healing wound if oxygen cannot reach it from the blood supply.
    • Maintain a moist wound environment.

    Causes of Impaired Wound Healing

    • Malnutrition (protein, carbohydrate, vitamins—A, C, and zinc).
    • Vascular disease (decreased oxygen release, microvascular disease, impaired leukocyte function).
    • Diabetes.
    • Hypoxia.
    • Smoking.
    • Medications (corticosteroids, chemo).

    Types of Wounds

    • Surgical wounds
    • Traumatic wounds (Lacerations, abrasions, contusions, punctures)
    • Pressure ulcers
    • Burns
    • Arterial ulcers
    • Venous stasis ulcers

    Wound Dehiscence/Evisceration

    • Dehiscence: Separation of a surgical wound.
    • Evisceration: Protrusion of organs through an open surgical wound.

    Pressure Ulcers

    • Skin breakdown caused by un-relieved pressure over bony prominences.
    • Caused by poor nutrition, incontinence, and moisture.
    • Factors reducing tissue resistance include: duration of pressure, friction, shear, aging, diabetes, moisture, and vascular disease.
    • Risk factors for ulcers include: paralysis/immobility, orthopedic surgery, confusion/sedation, impaired sensation, heart failure, arterial disease, COPD, diabetes, malignancy, and elderly patient status.

    Pressure Ulcer Assessment

    • Staging (I–IV)
    • Size (length, width, depth)
    • Wound bed (granulation, slough, eschar, necrotic tissue)
    • Drainage
    • Peri-wound skin
    • Undermining
    • Tunneling

    Pressure Ulcer Treatment

    • Maintain moist wound bed and avoid maceration.
    • Remove non-viable tissue.
    • Treat infection.
    • Avoid cytotoxic solutions.
    • Relieve pressure and improve nutrition.

    Debridement

    • Removal of necrotic tissue (e.g., heel eschar with mechanical, autolytic, or enzymatic methods)
    • Necessary for sepsis or advancing cellulitis. Generally, avoid debriding heel eschars, however, other instances of the wound being infected may require debridement.

    Arterial Ulcers

    • Etiology: atherosclerosis, tissue hypoxia, trauma.
    • Location: distal extremities.
    • Appearance: necrotic, minimal drainage.
    • Prevention/Assessment/Treatment: improve perfusion, protect from injury, assess wound circulation, ankle-brachial index, keep wound clean, hyperbaric therapy, revascularization.

    Venous Stasis Ulcers

    • Etiology: chronic venous insufficiency, edema.
    • Location: medial malleolus, tibial.
    • Appearance: jagged, weeping.
    • Prevention/Assessment/Treatment: control edema, protect from injury, assess wound circulation, ankle-brachial index, keep wound clean (debride as needed), hyperbaric therapy, compression.

    Critical Thinking/Review Questions

    • Why do corticosteroids impair wound healing?
    • What factor is most important to heal an arterial ulcer? A venous stasis ulcer?
    • Which chemical mediator is involved in generating a febrile response to an infection?
    • Which white blood cell is the primary responder to bacterial infection?
    • Which tissue type is best able to be regenerated?
    • Which wound type heals by secondary intention?
    • Which condition is likely to cause chronic inflammation?
    • What stage is this pressure ulcer?

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    Description

    Test your knowledge on inflammation, tissue repair, and wound healing. This quiz covers the physiological responses to injury, types of immunity, and the phases of acute inflammation. Dive into the mechanisms that protect and heal the body!

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