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Questions and Answers
What is the primary function of neutrophils in the inflammatory process?
What is the primary function of neutrophils in the inflammatory process?
Which of the following cells is responsible for synthesizing collagen during the proliferative phase of wound healing?
Which of the following cells is responsible for synthesizing collagen during the proliferative phase of wound healing?
Which of the following is a common complication of the proliferative phase of wound healing?
Which of the following is a common complication of the proliferative phase of wound healing?
What is the primary function of macrophages during wound healing?
What is the primary function of macrophages during wound healing?
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What type of cells are responsible for antibody-mediated immunity?
What type of cells are responsible for antibody-mediated immunity?
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What is the primary function of T helper cells?
What is the primary function of T helper cells?
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What type of cells are responsible for cell-mediated immunity?
What type of cells are responsible for cell-mediated immunity?
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What is a "left shift" in a differential white blood cell count?
What is a "left shift" in a differential white blood cell count?
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Which of the following is NOT a factor that can impair wound healing?
Which of the following is NOT a factor that can impair wound healing?
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Which of the following is an example of a labile cell?
Which of the following is an example of a labile cell?
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Which of the following is an example of a permanent cell?
Which of the following is an example of a permanent cell?
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What is the main difference between primary and secondary intention wound healing?
What is the main difference between primary and secondary intention wound healing?
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What is the role of angiogenesis in wound healing?
What is the role of angiogenesis in wound healing?
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Which of the following is a characteristic of chronic inflammation?
Which of the following is a characteristic of chronic inflammation?
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Why would corticosteroids impair wound healing?
Why would corticosteroids impair wound healing?
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What is a common risk factor that can lead to wound dehiscence?
What is a common risk factor that can lead to wound dehiscence?
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Which type of wound is characterized by the tearing of tissue that may require suturing?
Which type of wound is characterized by the tearing of tissue that may require suturing?
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What is a significant characteristic of a Stage IV pressure ulcer?
What is a significant characteristic of a Stage IV pressure ulcer?
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What should be avoided in the treatment of clean wounds?
What should be avoided in the treatment of clean wounds?
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Where are venous stasis ulcers commonly located?
Where are venous stasis ulcers commonly located?
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What is the appearance of arterial ulcers?
What is the appearance of arterial ulcers?
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Which method should NOT be used for debriding heel eschar?
Which method should NOT be used for debriding heel eschar?
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What is the most important factor in the healing of arterial ulcers?
What is the most important factor in the healing of arterial ulcers?
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What is a recommended practice for preventing pressure ulcers in bedfast patients?
What is a recommended practice for preventing pressure ulcers in bedfast patients?
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What indicates an initial presentation of a pressure ulcer?
What indicates an initial presentation of a pressure ulcer?
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What is the primary purpose of inflammation during tissue repair?
What is the primary purpose of inflammation during tissue repair?
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Which of the following is NOT a cardinal sign of inflammation?
Which of the following is NOT a cardinal sign of inflammation?
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During the vascular phase of acute inflammation, which of the following occurs?
During the vascular phase of acute inflammation, which of the following occurs?
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What role do neutrophils play during the cellular phase of acute inflammation?
What role do neutrophils play during the cellular phase of acute inflammation?
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Which chemical mediator is responsible for inducing smooth muscle contraction of bronchioles?
Which chemical mediator is responsible for inducing smooth muscle contraction of bronchioles?
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What is the function of the complement system in inflammation?
What is the function of the complement system in inflammation?
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Which type of white blood cell becomes macrophages during the inflammatory response?
Which type of white blood cell becomes macrophages during the inflammatory response?
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Which signaling molecules are primarily released by activated macrophages to promote inflammation?
Which signaling molecules are primarily released by activated macrophages to promote inflammation?
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What is the typical lifespan of neutrophils during an inflammatory response?
What is the typical lifespan of neutrophils during an inflammatory response?
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Which of the following mediators causes vasodilation during the acute phase of inflammation?
Which of the following mediators causes vasodilation during the acute phase of inflammation?
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What effect do leukotrienes have in the inflammatory response?
What effect do leukotrienes have in the inflammatory response?
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Which type of immunity involves physical and chemical barriers including skin and mucosa?
Which type of immunity involves physical and chemical barriers including skin and mucosa?
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What initiates the acute phase response characterized by fever and increased neutrophil release?
What initiates the acute phase response characterized by fever and increased neutrophil release?
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Which of the following is an effect of bradykinin in the inflammatory process?
Which of the following is an effect of bradykinin in the inflammatory process?
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Flashcards
Role of Inflammation
Role of Inflammation
Physiological response to tissue injury, infection, or foreign bodies.
Acute Inflammation
Acute Inflammation
Quick, short-term response to injury marked by redness, swelling, heat, pain, and loss of function.
Chronic Inflammation
Chronic Inflammation
Long-term inflammation that can damage tissues and organs, often due to persistent irritants.
Cardinal Signs of Inflammation
Cardinal Signs of Inflammation
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Vascular Phase of Inflammation
Vascular Phase of Inflammation
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Cellular Phase of Inflammation
Cellular Phase of Inflammation
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Neutrophils
Neutrophils
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Macrophages
Macrophages
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Bradykinin
Bradykinin
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Histamine
Histamine
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Cytokines
Cytokines
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Arachidonic Acid Metabolites
Arachidonic Acid Metabolites
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Complement System
Complement System
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Phagocytosis
Phagocytosis
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Granuloma
Granuloma
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Abscess
Abscess
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Normal WBC Count
Normal WBC Count
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Eosinophils
Eosinophils
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Bacterial infection response
Bacterial infection response
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Phase I of Wound Healing
Phase I of Wound Healing
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Phase II of Wound Healing
Phase II of Wound Healing
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Phase III of Wound Healing
Phase III of Wound Healing
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Keloid
Keloid
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Factors for Effective Healing
Factors for Effective Healing
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Impaired Wound Healing Causes
Impaired Wound Healing Causes
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Types of Wounds
Types of Wounds
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Wound Dehiscence
Wound Dehiscence
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Evisceration
Evisceration
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Pressure Ulcers
Pressure Ulcers
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Stage I Pressure Ulcer
Stage I Pressure Ulcer
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Stage IV Pressure Ulcer
Stage IV Pressure Ulcer
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Arterial Ulcers
Arterial Ulcers
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Venous Stasis Ulcers
Venous Stasis Ulcers
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Debridement
Debridement
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Prevention of Pressure Ulcers
Prevention of Pressure Ulcers
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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!