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PP Ch 2
Pathophysiology Chapter 2
| Question | Answer |
|---|---|
| First Line of Defense | Non-specific, mechanical barrier - Unbroken skin and mucous membranes - Secretions such as tears & gastric juices w/ enzymes/chemicals to destroy potentially damaging material |
| Second Line of Defense | Non-specific - Phagocytosis (neuts & macrophages) - Inflammation |
| Third Line of Defense | Specific Defense - Immune System - Production of specific antibodies or cell-mediated immunity to recognize foreign Ags |
| Phagocytosis | Neutrophils & macrophages engulf & destroy bacteria, cell debris, or foreign matter |
| Inflammation | Normal response intended to limit effects of injury or a dangerous agent on the body |
| Arteriolar End (Normal Capillary Exchange) | Movement of fluid, electolytes, O2, & some nutrients out of capillary is based on hydrostatic pressure (blood pressure) |
| Venous End (Normal Capillary Exchange) | Hydrostatic pressure is decreased d/t the previous movement of fluid into the interstitial space, & osmotic pressure is relatively high b/c plasma ptns remain w/in the capillaries. |
| Lymphatic System (Normal Capillary Exchange) | Fluid that remains in tissues is picked up by the lymphatic system & returned to venous circulation. |
| Redness & Warmth (Inflammation) | Due to vasodilation, causes increased blood flow to damaged area |
| Swelling/edema (Inflammation) | Due to increased capillary permeability, causes shift of protein and fluid into the interstitial space |
| Pain (Inflammation) | Due to increased pressure of fluid on nerves and release of chemical mediators (PGs & kinins) - it's good . . . it alerts us to injury. |
| Fever/pyrexia (Inflammation) | Cytokines signal the hypothalamus to induce fever - common if inflammation is extensive - caused by pyrogens - high fever can indicate infection - fever can help impair growth & reproduction of pathogenic organism |
| Loss of Function (Inflammation) | May develop if cells lack nutrients. Due to edema interfering with movement. |
| Exudate | A collection of interstitial fluid formed in an inflammed area. Characteristics vary based on cause (Serous, Fibrinous, Purulent, Hemorrhagic) |
| Serous Exudate | Watery, consists primarily of fluid, some proteins, and WBCs |
| Fibrinous Exudate | Thick, sticky, high cell & fibrin content - increases risk of scar tissue - can't be wiped off like pus; it sticks to the wound. |
| Purulent Exudate | Indicates bacterial infection - thick, yellow-green, contains more WBCs, cell debris, and microorganisms; "pus" |
| Abscess | A localized pocket of purulent exudate in a solid tissue (i.e. brain) |
| Hemorrhagic Exudate | Occurs when blood vessels are damaged and bleeding into tissues occurs |
| Steps of Inflammation | 1. Injury 2. Cells release chemical mediators 3. Vasodilation 4. Increased capillary permeability 5. WBCs move to site of injury 6. Phagocytosis (removal of debris in preparation for healing) |
| Histamine | From Mast Cell granule - causes immediate vasodilation & increased capillary permeability to form exudate |
| Chemotactic Factors | From Mast Cell granules - ex. attract neutrophils to site |
| Platelet-Activating Factor (PAF) | From cell membranes of platelets - activate neutrophils and platelet aggregation |
| Cytokines | Ex. Interleukins & Lymphokines - from T-lymphocytes & macrophages - increase plasma proteins, ESR - induce fever, chemotaxis, leukocytosis |
| Leukotrienes | Synthesis from arachidonate in mast cells - later response: vasodilation & increased capillary permeability, chemotaxis |
| Prostaglandins (PGs) | Synthesis from arachidonate in mast cells - Vasodilation, increased capillary permeability, pain, fever, potentiate histamine effect |
| Kinins | Ex. bradykinin - from activation of plasma protein (kinogen) - Vasodilation & increased capillary permeability, pain, chemotaxis |
| Complement System | From activation of plasma protein cascade - Vasodilation & increased capillary permeability, chemotaxis, increased histamine release |
| Pyrogens | Fever-inducing substances released from WBCs &/or macrophages - reset the "thermostat" in the hypothalamus |
| Malaise | Feeling unwell |
| Anorexia | Loss of appetite |
| Systemic Effects of Inflammation | Mild fever (pyrexia), malaise, fatigue, HA, Anorexia |
| Chemotaxis | Chemicals draw WBCs to area |
| Diapedesis | Migration of WBC through capillary membrane |
| Potential Complications of Inflammation | Infection, Deep ulcers, Skeletal muscle spasm, Local complications |
| Infection (Potential Complications of Inflammation) | Microorganisms can more easily penetrate edematous tissues |
| Deep ulcers (Potential Complications of Inflammation) | Result of severe or prolonged inflammation |
| Skeletal Muscle Spasm (Potential Complications of Inflammation) | Protective response to pain |
| Local complications (Potential Complications of Inflammation) | Depend on site of inflammation but may include obstruction, loss of sensation, and decreased cell function |
| Chronic Inflammation (characteristics) | Less swelling & exudate, More WBCs & macrophages (immune cells) & fibroblasts (CT cells), continued tissue destruction, more scar tissue, granuloma (sometimes) |
| Granuloma | Small mass of cells with a necrotic center covered with CT. May develop around foreign objects or as part of infection, such as in TB. |
| Leukocytosis | Increased numbers of WBCs, especially neutrophils |
| Differential Count | Proportion of each type of WBC altered, depending on the cause |
| Plasma Proteins | Increased fibrinogen and prothrombin |
| C-Reactive Protein | A protein not normally in the blood, but appears with acute inflammation and necrosis within 24-48 hours |
| Increased ESR | Elevated plasma proteins increase the rate at which RBCs settle in a sample |
| Cell Enzymes | Released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation |
| Hypothalamus & Fever | 1. Release of pyrogens in circulation 2. Reset hypothalamic control -> high 3. Body responses increase temp (chills, vasoconstrict in skin, increase HR, et). 4. Body reaches new high temp |
| Treat to Lower Fever | 1. Reset hypothalamus to normal 2. Body increase heat loss (vasodilation, sweating, lethargy) 3. Body temp returns to normal |
| Aspirin (Acetylsalicylic Acid - ASA) | Decreases PG production -> decrease inflamm, pain, fever. Don't give to kids! Kids + viral infection + ASA = Reye's Syndrome(liver & brain damage) |
| Acetaminophen | Decrease fever & pain only - no effect on inflammation. |
| NSAIDs | Decrease PG production -> decrease inflamm, fever, pain. SE's: Allergy, delay clot, GI distress/stomach ulcers |
| Glucocorticoids | Derivitives of AC hormone - decreses cap perm, greater effectiveness of Epi & NE, decreases WBC & mast cell activity, reduced immune response. |
| Adverse Effects of Glucocorticoids | Atrophy of lymph tissue (increased infexn), Catabolic effects, Delayed healing, Delayed growth in kids, Aldosterone-like effect in kidney (retain Na & H2O) |
| 3 Types of Healing | Resolution, Regeneration, Replacement |
| Resolution | Minimal tissue damage (cells weren't destroyed), damaged cells recover & tissue returns to normal |
| Regeneration | Original cells killed but replaced by mitosis - only occurs in tissues with cells capable of undergoing mitosis |
| Replacement | Functional tissue replaced by scar (fibrous) tissue - occurs in cells with extensive damage or with cells incapable of mitosis (brain, sk. muscle, etc) -> loss of fxn. |
| Healing by First Intention | Wound edges are held together by a suture |
| Healing by Second Intention | Larger space between the wound edges |
| 3 Steps in Healing Process | 1. Injury & Inflammation 2. Granulation Tissue & Epithelial Tissue Growth 3. Scar (fibrous) Tissue Formation |
| Injury & Inflammation (Healing) | A clot seals wound edges (ptn fibers in clot contract to bring edges together); Immune cells remove foreign material & debris |
| Granulation Tissue | Highly vascular |
| Epithelial Tissue | Cells undergo mitosis & cover the wound surface |
| Scar (Fibrous)Tissue Formation | Fibroblasts produce collagen to reinforce scar |
| Complications of Scar Formation | LOF, Contractures/Obstructions, Adhesions, Hypertrophic Scar Tissue, Ulceration |
| Loss of Function (Complications of Scar Formation) | Result of loss of normal cells & specialized structures (hair follicles, nerves, receptors, etc) |
| Contractures/Obstructions (Complications of Scar Formation) | Scar tissue is non-elastic & can restrict ROM |
| Adhesions (Complications of Scar Formation) | Bands of scar tissue joining two surfaces that are normally separated (ex. abdominal surgery - scar tissue around organs) |
| Hypertrophic Scar Tissue (Complications of Scar Formation) | Overgrowth of fibrous tissue leads to hard ridges of scar tissue or keloid formation - mostly cosmetic but can be so sever that it blocks normal movement. |
| Ulceration (Complications of Scar Formation) | Blood supply may be impaired around scar - results in further tissue breakdown and ulcerations at a future time |
| Thermal Injury Burns | Flames, hot fluids |
| Non-Thermal Injury Burns | Chemicals, Radiation, Electric Shock |
| Acute Phase of Burn | Loss of first line of defense, inflammation can cause shock from massive movement of fluid from blood to tissues causing decrease BP - other organs don't get enough blood flow. High risk of infection. |
| Classification of Burns | Superficial Partial-Thickness (1st Degree); Deep Partial-Thickness (2nd Degree); Full-Thickness (3rd Degree) |
| Superficial Partial-Thickness (1st Degree) Burns | Involve the epidermis; little if any blister formation |
| Deep Partial-Thickness (2nd Degree) Burns | Involve the epidermis & part of the dermis; blister formation |
| Full-Thickness (3rd Degree) Burns | Destruction of all skin layers & often underlying tissues (hair follicles, etc) |
| Effects of Burn Injury (Both Local & Systemic) | Dehydration & edema, Shock, Respiratory problems, Pain, Infection, Increased metabolism |
| Dehydration & Edema (Effects of Burn Injury) | D/t evaporation of fluids &/or shifts of fluids from BVs to tissues |
| Shock (Effects of Burn Injury) | Inflamm leads to massive shift of water, ptns, & electrolytes into the tissues; loss of these substances from blood decreases circulation to other organs |
| Respiratory Problems (Effects of Burn Injury) | D/t inhalation of toxic or irritating fumes during burn; can decrease oxygenation of tissues &/or damage respiratory tract |
| Infection (Effects of Burn Injury) | Bacteria &/or fungi have greater access to tissues d/t loss of skin barrier |
| Increased metabolism (Effects of Burn Injury) | Needed for healing of damaged tissues; D/t loss of ptns in exudate at burn site |
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