Chapter 9_2 flashcards

Question 1

Acute Inflammation: Characteristics & Key Processes

Answer 1

Characterized by vasodilation, increased capillary permeability, and WBC migration to the site of injury. [Text, cite: 1, 48]

Question 2

Acute Inflammation: Vascular Phase Details

Answer 2

Begins with transient vasoconstriction, followed by prolonged vasodilation and increased permeability mediated by histamine and bradykinin. Capillary pores open, allowing fluid (exudate/transudate), WBCs, and platelets to the site, causing redness, warmth, swelling. [Text, cite: 1, 14, 48, 61]

Question 3

Acute Inflammation: Cellular Phase Details

Answer 3

Chemotaxis (chemical signals attract WBCs/platelets). Leukocytosis (increased WBC release). Margination (WBCs line up along endothelium). Adhesion (via selectins/integrins). Diapedesis/Transmigration (WBCs squeeze through capillary pores into tissues). [Text]

Question 4

WBC Predominance in Acute Inflammation Over Time

Answer 4

First 6-24 hours: Neutrophils predominate. Next 24-48 hours: Monocytes arrive and differentiate into macrophages, which become predominant in persistent inflammation. Exceptions: Viral infections (lymphocytes), Allergic reactions (eosinophils), Pseudomonas infections (neutrophils for several days). [Text]

Question 5

Inflammatory Mediators: Histamine

Answer 5

Released from mast cells, basophils, platelets. Causes arteriolar vasodilation, large artery vasoconstriction, and increased permeability of venules. [Text, Table 9-1, cite: 2, 49, 14, 61]

Question 6

Inflammatory Mediators: Prostaglandins (PGs)

Answer 6

Released from WBCs/cell membranes via phospholipase action on phospholipids yielding arachidonic acid, then conversion by COX-1 or COX-2 enzymes. PG1 (COX-1) for gastric mucus, renal perfusion, platelet aggregation. PG2 (COX-2) for inflammation, pain, fever, swelling. [Text, Fig 9-7, Table 9-1, cite: 2, 49]

Question 7

Inflammatory Mediators: Leukotrienes

Answer 7

Synthesized from arachidonic acid via lipoxygenase pathway in WBCs/mast cells. Provoke bronchiole inflammation in asthma, bronchospasm, and increased vascular permeability. [Text, Fig 9-7, Table 9-1, cite: 2, 49]

Question 8

Inflammatory Mediators from WBCs (General Role from Study Guide)

Answer 8

TNF-alpha, interleukins, and leukotrienes are released by WBCs. [cite: 2, 49] These promote the inflammatory response, fever, and immune cell recruitment. [Text, cite: 2, 49]

Question 9

Inflammatory Mediators: Cytokines (TNF-alpha, ILs)

Answer 9

Produced by macrophages and other WBCs. Modulate inflammation (amplify/deactivate), cause localized and systemic effects (fever, appetite loss, lethargy, cachexia via TNF-alpha; ILs stimulate platelet production, cause fatigue/anemia). [Text, Table 9-1, cite: 2, 49]

Question 10

Acute Phase Proteins: Source, Examples & Functions

Answer 10

Released by the liver, stimulated by cytokines. Examples: C-reactive protein (CRP - marks foreign material, activates complement), fibrinogen (forms rouleaux for ESR), serum amyloid A (prolonged secretion -> amyloidosis), hepcidin (diminishes iron storage). [Text]

Question 11

Chronic Inflammation: Definition & Cellular Hallmark

Answer 11

Inflammatory reaction persisting for weeks to months without resolution or healing. Characterized by the predominance of monocytes, lymphocytes, and macrophages. [Text]

Question 12

Chronic Inflammation: Etiologies

Answer 12

Persistent infections (e.g., Mycobacterium tuberculosis [TB]), hypersensitivity disorders (autoimmune diseases like RA, SLE), prolonged exposure to toxic agents (e.g., coal dust leading to anthracosis), atherosclerosis, some cancers. [Text]

Question 13

Chronic Inflammation: Mechanism of Tissue Damage

Answer 13

Constant secretion of destructive macrophage products (free radicals, proteases, cytokines, angiogenesis growth factors, fibroblast activators) causes repeated tissue damage, delayed healing, and replacement of injured cells with connective tissue. [Text]

Question 14

Granuloma Formation: Process & Example

Answer 14

Characteristic of chronic inflammation. Macrophages aggregate and transform into epithelial-like (epithelioid) cells, surrounded by lymphocytes, fibroblasts, and connective tissue. Epithelioid cells may fuse into giant cells. Example: Tubercle in TB, where macrophages surround M. tuberculosis. [Text]

Question 15

Diagnosis of Tuberculosis (TB)

Answer 15

Diagnosed through: Chest X-ray (detects tubercles/granulomas)[cite: 3, 50], Sputum culture (to identify Mycobacterium tuberculosis)[cite: 3, 50], and TB skin test (e.g., Mantoux; suggests exposure but does not confirm active disease)[cite: 3, 50]. [Text]

Question 16

Laboratory Tests Indicating Active Inflammation

Answer 16

Elevated C-reactive protein (CRP), Erythrocyte Sedimentation Rate (ESR), and fibrinogen levels in the bloodstream. [Text]

Question 17

Phases of Wound Healing: 1. Hemostasis

Answer 17

Shortly after injury: Exposed collagen surfaces attract platelets -> aggregation. Platelets secrete inflammatory mediators (serotonin, histamine, platelet-derived growth factor). Vasoactive amines (epinephrine) cause short-term vasoconstriction, limiting blood loss. Clot formation begins. [Text, cite: 4, 51]

Question 18

Phases of Wound Healing: 2. Inflammation

Answer 18

Follows hemostasis. Characterized by vasodilation, increased vascular permeability, and chemotaxis. WBCs (neutrophils first, then macrophages) arrive to clean the wound. Cardinal signs: warmth, redness, swelling, pain are present. [Text, cite: 4, 51]

Question 19

Wound Appearance 2 Days Post-Op & Indicated Phase

Answer 19

Wounds that are pink, dry, and slightly warm 2 days post-op are likely in the inflammatory phase of healing. [cite: 6, 53]

Question 20

Phases of Wound Healing: 3. Proliferation, Granulation, Angiogenesis, Epithelialization

Answer 20

Fibroblasts (key cells) synthesize collagen and form granulation tissue (foundation of scar). Vascular endothelial cells create new blood vessels (angiogenesis), stimulated by VEGF, PDGF, FGF, TGF-beta, IL-1. Epithelial cells migrate and proliferate to form a new surface (epithelialization). [Text, cite: 5, 52]

Question 21

Phases of Wound Healing: 4. Wound Contraction and Remodeling

Answer 21

Remodeling begins ~3 weeks after injury. Scar tissue is structurally refined and reshaped by fibroblasts and myofibroblasts. Wound contraction (especially in secondary intention) occurs due to myofibroblasts pulling wound edges together. Collagen is reorganized. Tensile strength builds to 70-80% of original after 3 months. [Text, cite: 5, 52]

Question 22

Nutrition for Wound Healing: Proteins

Answer 22

Essential for cellular regeneration and synthesis of connective tissue. [cite: 7, 54] A state of positive nitrogen balance (intake > excretion) is required for wound repair. [Text]

Question 23

Nutrition for Wound Healing: Vitamin A

Answer 23

Supports epithelialization and fortifies epithelial mucous membranes. [Text, Table 9-3, cite: 7, 54]

Question 24

Nutrition for Wound Healing: Vitamin C

Answer 24

Required for collagen synthesis and strength. [Text, Table 9-3, cite: 7, 54]

Question 25

Nutrition for Wound Healing: Fats

Answer 25

Essential components of cell membranes that are synthesized during the healing process. [Text, cite: 8, 55]

Question 26

Nutrition for Wound Healing: Role of Supplements

Answer 26

Supplements are generally unnecessary if dietary intake of essential nutrients (proteins, vitamins, fats, minerals) is sufficient. [Text, cite: 8, 55]

Question 27

Complication: Wound Dehiscence

Answer 27

Opening of a wound’s suture line (previously closed wound edges open and rupture). [Text, cite: 9, 56] Risk factors include obesity, vomiting, coughing, increased abdominal pressure, and tension on sutures. [Text, cite: 9, 56]

Question 28

Complication: Fistula

Answer 28

An abnormal connection between two epithelium-lined organs or vessels that normally do not connect (e.g., tracheoesophageal fistula). [Text, cite: 10, 57]

Question 29

Complication: Wound Evisceration

Answer 29

Opening of a wound with extrusion (protrusion) of internal tissues and organs. [Text, cite: 10, 57] Requires immediate wound protection with sterile, saline-moistened dressings and prompt surgical evaluation. [Text]

Question 30

Complication: Stricture

Answer 30

An abnormal narrowing or closure of a tubular body passage from the formation of scar tissue (e.g., esophageal stricture). [Text, cite: 11, 58]

Question 31

Complication: Contracture

Answer 31

An inflexible shrinkage of wound tissue that pulls the edges toward the center of the wound. [Text, cite: 11, 58] Often occurs in burn wounds and can limit mobility when across a joint surface. [Text]

Question 32

Complication: Keloid Formation

Answer 32

Hyperplasia of scar tissue; an excessive accumulation of epithelium and collagen forming a hypertrophic scar. Etiology unknown; more common in persons of African descent. [Text]

Question 33

Complication: Adhesions

Answer 33

Abnormal bands of internal scar tissue that can form after invasive surgical procedures. Can limit mobility (if in joint) or cause pain/obstruction (if around organs). [Text]

Question 34

Pediatric Concern: Aspirin and Salicylate NSAIDs

Answer 34

Avoided in children and adolescents, especially with viral infections, due to the risk of Reye’s syndrome (life-threatening disorder: mitochondrial failure -> liver failure & encephalopathy). [Text, cite: 12, 59]

Question 35

Pediatric Concern: Antibiotics

Answer 35

Antibiotics are appropriate for treating confirmed bacterial infections in children. [cite: 13, 60]

Question 36

Vascular Phase of Inflammation: Trigger & Outcomes

Answer 36

Triggered by inflammatory mediators like histamine. [cite: 14, 61] Leads to: Vasodilation, Increased capillary permeability, and WBC migration to the site of injury. [cite: 14, 61]

Question 37

Nonpharmacological Treatments for Inflammation: Cold Therapy (Cryotherapy)

Answer 37

Application of cold to decrease tissue temperature. Physiological effects: Reduced pain, blood flow, edema, inflammation, muscle spasm, and metabolic demand. Recommended for acute injury/trauma. [Text]

Question 38

Nonpharmacological Treatments for Inflammation: Heat Therapy

Answer 38

Application of heat to tissue. Physiological effects: Pain relief, increased blood flow, enhanced tissue metabolism, decreased muscle spasm, increased elasticity of connective tissue. Often recommended for chronic inflammation. [Text]

Question 39

Pharmacological Treatment: Corticosteroids (e.g., Dexamethasone, Prednisone)

Answer 39

Mechanism: Inhibit the enzyme phospholipase, which breaks down cell membrane phospholipids into arachidonic acid, thus diminishing inflammation at an initial step. Most potent anti-inflammatory agents. For short-term use due to adverse effects (Table 9-2). [Text]

Question 40

Pharmacological Treatment: NSAIDs (e.g., Ibuprofen, Aspirin)

Answer 40

Mechanism: Block both cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) pathways, preventing production of prostaglandin 1 (PG1) and prostaglandin 2 (PG2). Side effects (gastric irritation, renal dysfunction, decreased clotting) often due to PG1 inhibition. [Text]

Question 41

Pharmacological Treatment: COX-2 Inhibitors (e.g., Celecoxib)

Answer 41

Mechanism: Selectively block the COX-2 pathway, thus primarily inhibiting prostaglandin 2 (PG2) which causes pain, edema, and muscle spasm, while intending to spare COX-1 effects. [Text]

Question 42

Pharmacological Treatment: Monoclonal Antibodies (Biological Agents)

Answer 42

Laboratory-synthesized antibodies targeting specific inflammatory mediators. TNF inhibitors (e.g., adalimumab, infliximab) and Interleukin inhibitors (e.g., anakinra, secukinumab) are used for various inflammatory disorders like RA and IBD. [Text]

Question 43

Primary Intention Wound Healing: Process & Outcome

Answer 43

Edges of wound are cleanly demarcated, easily brought together, no missing tissue (e.g., surgical wound). Simple, rapid healing with minimal scarring. Re-epithelialization is predominant. [Text]

Question 44

Secondary Intention Wound Healing: Process & Outcome

Answer 44

Extensive tissue loss. More intense and longer inflammation. Abundant granulation and fibrous tissue necessary. Wound contraction by myofibroblasts closes tissue gap. Substantial scar formation and thinning of epidermis. High susceptibility to infection/complications. [Text]

Question 45

Tertiary Intention Wound Healing: Process & Outcome

Answer 45

Wound is missing a large amount of deep tissue and is contaminated. Cleaned and left open for 4-5 days before closure (may require packing/drainage). Granulomas may form around foreign materials. Prominent scarring; commonly requires a skin graft. [Text]

Question 46

Eschar: Definition & Appearance

Answer 46

Dead tissue that sheds or falls off from healthy skin. Common in burn wounds and pressure injuries. Typically tan, brown, or black, often with a crusty top layer. [Text]

Question 47

Débridement: Purpose

Answer 47

The removal of necrotic tissue from a wound to promote and enable re-epithelialization and new growth of healthy tissue. [Text]