NR 283 Week 2 Pre-Class Answers: Fall 2021 (solved)
Unit 2 Pre-Class Answers (Chapters 5, 6, 7, &20) Chapter 5: Inflammation and Healing 1. List and describe each of the 3 body defense mechanisms: a. 1st line – mechanical barriers: Physical [skin, mucus membranes] & Chemical [lysosome-saliva/tears, skin’s acidic pH & fatty acid content, lactic acid & high salt concentrations in sweat] b. 2nd line – nonspecific mechanisms: Phagocytosis, Inflammation, Fever, Antimicrobial Proteins [Interferon & Complement] c. 3rd line – specific defense: Immune Response, Cell-mediated and/or Humoral Response; B and T cell; lymphocytes undergo selective process that specializes them for reacting to only 1 specific antigen or immunogen 2. What is the definition of inflammation? Body’s nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, & sometimes loss of function; intended to localize and remove an injurious agent. 3. What are possible causes of inflammation? Direct physical damage [cuts, sprains, caustic chemicals-acids/alkali, ischemia/infarction, allergic reactions, extremes of hot/cold, foreign body-splinters/glass, and infection. 4. Why is inflammation helpful to the body? It begins the process of healing, diluting toxic materials with ↑ of fluid to area, allows for clotting, antibodies arrive to fight any invading microbes, fibrin mesh started-begins wound closure ↓ microbe entry access, ↑ permeability brings more nutrients to heal faster. 5. Which cells phagocytize bacteria and microbes? 2 listed Neutrophils phagocytize bacteria; Macrophages leave bloodstream & phagocytize microbes. 6. Overall, what is the role of chemical mediators in inflammation? Damaged Mast cells and platelets release chemical mediators [histamine, serotonin, prostaglandins, & leukotrienes] into interstitial fluid & blood. They aid in triggering the inflammation, prolonging, and can intensify the effects of other chemicals w/in response; some effects can be reduced by antihistamines and anti-inflammatory drugs. a. What are cytokines specific role? Cytokines are communicators in tissue fluids, they send messages to lymphocytes and macrophages, immune system, or hypothalamus to induce fever. Unit 2 Pre-Class Answers b. How do anti-inflammatory drugs work to reduce inflammation? Non-Steroidal AntiInflammatory Drugs (NSAIDs)- ↓ production of prostaglandins & ↓ swelling in musculoskeletal system. Steroidal & Corticosteroids-synthetic chemicals related to natural glucocorticoids [Hydrocortisone], hormones produced by adrenal cortex gland. Short term treatment but negative effects that impact health care. Aspirin [ASA] ↓ prostaglandin synthesis at site of inflammation = ↓ inflammatory response. Anti-inflammatory drugs ↓ platelet adhesion, blood clotting, ↓ pain (analgesic effect) & ↓ fever (antipyretic effect). 7. Why does vasoconstriction happen immediately, but then vasodilation occurs? Blood is stopped from excreting out of the body if wound present, thanks to nerve reflexes at the site of the injury. Vasodilation then occurs once the rapid release of chemical mediators is identified, causing local vasodilation, this allows for more blood flow in &/to the area effected (hyperemia). ↑ Permeability of capillary membrane so plasma proteins & fluids can move into interstitial space. ↑ fluids dilute toxic materials if present. Globulins act as antibodies & fibrinogen forms fibrin mesh around wound in attempt to localize it. Blood clotting = ↑ fibrin mesh (wall off affected area). 8. What are the cardinal signs of local inflammation & what causes each one? Rubor / Erythema [redness]; Calor [warmth]; Tumor [swelling / edema]; Dolor [pain] Redness/warmth d/t ↑ blood flow into damaged area; Swelling/edema d/t shift of protein & fluid into interstitial space; Dolor [pain] d/t ↑ pressure of fluid on nerves, esp. enclosed areas, & local irritation of nerves d/t chemical mediators (bradykinins); Loss of function if ↓ nutrients to cells OR swelling mechanically interferes w/function (restricted joint movement). 9. Describe the different types of exudate and common examples: a. Serous {watery}-mainly fluid w/small amt of protein & WBC’s i. allergic reactions ii. burns b. Fibrinous Thick & Sticky; high cell & fibrin content i. ↑ risk for scar tissue formation in area if this exudate present c. Purulent Thick/yellow-green; contains lg # WBC’s, cell debris, & microorganisms i. Indicates bacterial infection w/ exudate called “PUS” Unit 2 Pre-Class Answers d. Abscess localized picket of purulent exudate or pus in solid tissue i. Can be around a tooth or in the brain e. Hemorrhage contains RBC’s; present if blood vessels have been damaged i. Septicemia d/t Pasteurella (Mannheimia) haemolytica -respiratory inf 10. What are the systemic signs of inflammation? Mild fever; malaise (unwell feeling); fatigue; headache; anorexia (loss of appetite) a. What causes a fever? Present if inflammation is extensive; WBC’s &/or macrophages release pyrogens (fever-producing substances-Interleukin-1); pyrogens circulate in bld & hypothalamus triggered to reset at higher temp. MACROPHAGES ARE MONOCYTES[WBC] THAT LEFT BLOOD STREAM b. Why are fevers beneficial? Impairs growth & reproduction of pathogen; impedes iron release (bacterial nutrient); ↑ metabolism & stimulates immune responses c. Where is the thermostat in the brain? Hypothalamus d. Why do we shiver, cover up, and become pale when we have a fever? Heat production mechanisms (shivering) are activated to ↑ cell metabolism; Pallor & cooler temp d/t vasoconstriction ↓ loss of heat (involuntary); Covering up or curling up into ball = conserve heat (voluntary). Mechanisms continue until temp returns baseline 11. Why would we do a complete blood count and include differential? CBC for specific enzymes present during severe inflammation and necrosis [↑WBC ↑CRP (serum C-reactive protein) ↑Erythrocyte sedimentation rate (ESR), ↑ immature neutrophils “shift to the left”] Differential count (proportion of each type of WBC) indicates VIRAL from BACTERIAL. Blood smear exam (included in CBC) abnormal cells; Inflammation etiology = brief exposure (damaging agent) values norm w/in 48hrs. 12. What 6 lab levels will increase when there is inflammation in the body? a. Leukocytosis ↑WBC specifically Neutrophils b. Differential count ↑ w/specific WBC depending on etiology (Eosino, neutron, etc) c. Plasma Proteins ↑ Fibrinogen & Prothrombin d. C-Reactive Protein (CRP) normally= 0; Valued = acute inflammation &/or necrosis [w/in 24-48 hours] e. Erythrocyte Sedimentation Rate (ESR) ↑ plasma proteins ↑ rate that RBC’s settle in sample Unit 2 Pre-Class Answers f. Cell enzymes ↑ d/t released from necrotic cells & enter tissue fluids & blood; can indicate location of inflammation [ALT-liver & ; CK-MB - ; ALT – liver] 13. Describe the potential complications of acute inflammation: a. Local complications: depends on inflammation site; joint (movement) lungs(O ) ₂ b. Infection: develops in inflamed tissue d/t microorganisms easily penetrating skin/mucosa (if damaged &/or FB) and blood supply impaired c. Skeletal muscle spasms: may be initiated by inflammation d/t musculoskeletal inj 14. What is a granuloma and why does it happen during chronic inflammation? Granuloma = small mass of cells w/necrotic center & covered w/connective tissue; appears during chronic inflammation d/t ↑ collagen w/ ↑ tissue destruction & ↑ fibrous scar tissue forming 15. Describe potential complications of chronic inflammation: Deep ulcers can occur d/t cell necrosis & lack of cell regeneration = erosion of tissue. Leads to perforation (erosion through cell wall) of viscera or extensive scar tissue development 16. What is the RICE approach and how does each step reduce inflammation? Rest; Ice; Compression; Elevation 17. When and how is cold therapy useful in inflammation? Early stages of acute injury -ICEcauses local vasoconstriction = ↓ edema ↓ pain; 20 minutes on / 20 minutes off 18. When and how is heat therapy useful in inflammation? Long-term therapy; can incorporate mild exercise (if chronic condition) w/heat = ↑ circulation ↓ excess fluid ↓pain causing chemical mediators ↓ waste metabolites 19. Briefly describe the three types of healing: a. Resolution: Minimal tissue damage; damaged cells recover & tissue returns to normal w/in short period of time (sunburn) b. Regeneration: Damaged tissue cells capable of mitosis. No replication then damaged tissue replaced w/ identical tissue from proliferation of nearby cells. Limited if organization of complex tissue is altered (fibrous tissue liver-distortion) c. Replacement: Connective tissue (scar or fibrous tissue formation) occurs when extensive damage or cells unable to perform mitosis; Wound filled in (packed) & covered by some form of tissue (allograft or autograft) d. Healing by 1st intention: wound is clean, no foreign materials &/or necrotic tissue, & edges are held close together w/minimal gap (surgical incision)
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nr 283 week 2 pre class answers fall 2021
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nr 283 week 2 pre class answers
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unit 2 pre class answers chapters 5
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6
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7
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amp20
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chapter 5 inflammation and healing
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list and describe each of the 3 body
