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patho ch 3
| Term | Definition |
|---|---|
| Complement System (how is it activated, what does it do?) | proteins that destroy and remove microorganisms via opsonization and cell lysis - activates cascade of inflammatory mediators - triggered by presence of microorganisms |
| opsonization | making bacteria vulnerable to phagocytosis |
| Clotting | promote coagulation via clotting factor cascade and suppresses coagulation when clotting is complete - can also release inflammatory mediators |
| Kinin | STRONG vasoactive inflammatory mediators, will amplify inflammatory response |
| Steps of Cellular Response | 1. Chemotaxis 2. Cellular adhererence 3. Cellular migration |
| Chemotaxis | process of moving certain cells to injury site |
| Chemotactic factors | inflammatory mediators that attract specific cells |
| Diapedesis | process where cells can move thru endothelial junctions |
| Cellular Migration | 3rd step of cellular response where cells like leukocytes, erythrocytes and platelets migrate to injury site thru endothelial layer |
| Cardinal Signs | local manifestations of acute inflammation, such as erythema, edema, heat, pain and loss of function |
| Lymphadenitis Why does it occur | enlargement and inflammation of nearby lymph nodes filter/drain harmful substances at injury site |
| Pyrexia (what is it caused by) | Fever, inflammatory mediators acting on the hypothalamus |
| Leukocytosis | Elevated WBC count |
| ESR | erythrocyte sedimentation rate; tells you level of inflammation based on erythrocyte stacking/clumping due to fibrinogen activity |
| Fibrinogen | Clotting factor which can cause cell clumping thru fibrin |
| Treatment principles of acute inflammation | - decrease blood flow - reduce swelling - block inflammatory mediators (remember they can cascade) - decrease pain |
| RICE | Rest, Ice, Compression, Elevation used as treatment for inflammation such as in ankle sprain |
| Arachidonic acid | derived from plasma membrane of injured cells that can convert to prostaglandin (inflammatory mediator) causing inflammatory response |
| Prostaglandin (not too important) | Eicosanoids with hormone like effect regulating inflammation, blood flow and clotting |
| Prothrombin time | Time it takes to coagulate |
| Prothrombin | precursor protein that turns into thrombin that catalyzes fibrinogen to fibrin conversion |
| Glucocorticoids (MOA?) | - inhibit synthesis of chemical mediators (reduce redness, swelling, heat, pain) - suppress phagocyte infiltration and tissue damage from release of lytic enzymes - suppress lymphocyte proliferation - reduce immune component of inflammation |
| What are the plasma protein systems? | all are located in the blood plasma complement clotting kinin |
| Phases of tissue repair | Inflammatory phase Proliferative phase Remodeling phase |
| Inflammatory phase (what happens and with what?) | - 1st stage of tissue repair - Achieve hemostasis thru PLT release (thrombus formation), blood vessel constriction |
| Thrombus | Blood clot in blood vessel |
| Proliferative phase (what are main cells and what happens) | Stage 2 in tissue repair - PMN and macrophages remove necrotic tissue - provisional matrix is built and extracellular matrix is rebuilt (basement membrane/connective tissue) |
| Provisional Matrix | temporary extracellular matrix, basically like scaffold for cells during cellular migration |
| Extracellular matrix | Structural support for cells such as basement membrane and connective tissue |
| Remodeling Phase | 3rd stage of tissue repair - restore functional integrity - remodeling which is maturation of cells and degradation of provisional matrix |
| Adhesion Molecules | Provide stickiness to cells |
| Molecule receptors | attracts cells to form structural matrix |
| Proteinase enzymes | degrade dead tissue, inhibited by proteinase inhibitor |
| Growth factors | promotes regeneration of new cells/tissue |
| Matrix proteins | Structural proteins that rebuild extracellular matrix |
| Basement Membrane (what is its function) | noncellular, made of ECM proteins cellular structural support support re-epithelialization store growth factors restore neuromuscular function develop parenchyma |
| Parenchyma | functional tissue made up of cells with specific function ie neurons, myocardial cells and epithelial cells |
| What gets restored first, epithelium or basement membrane? | Basement membrane because it supports the epithelium |
| Connective Tissue | composed of collagen fibers, elastic fibers and glycoprotein for structural support, protein storage and transport |
| Fibroblasts (function and what activates it) | cells that reproduce and replace connective tissue layer, stimulated by macrophages |
| Elastin | protein contained in elastic fibers allowing stretching of tissue |
| Collagen | protein secreted by collagen fibers, excess = fibrosis/scarring |
| Glycoproteins (function) | regulate cell movement across matrix provide attachment site from cell to matrix makes cells function |
| Granulation tissue | connective tissue with extensive macrophage/fibroblasts and promotion of angiogenesis at site excess capillaries are lost after full healing |
| Angiogenesis | development of new blood vessels (especially capillaries) |
| What are the methods of restoring functional integrity | resolution regeneration replacement |
| Resolution | healing in response to mild injury/minimal cellular disruption, fast healing |
| Regeneration | 1. proliferation (growth/reproduction) 2. differentiation or diapedesis ONLY possible with cells that can divide |
| Differentiation | cells specialize after maturing |
| Replacement | scar tissue production when regeneration isnt possible |
| Partial regeneration (when does it happen) | occurs in extensive tissue damage, increased scarring/fibrous repair with partial regeneration |
| Permanent cells | cells that do not undergo mitosis (opposite of labile cells) |
| Labile Cells | Cells that constantly multiply and go thru mitosis (opposite of permanent cells) |
| Primary intention | all areas of wound is connected and closed, healing simultaneously faster healing and reduced risk of infection, reduced scarring |
| Secondary intention | Bigger wounds (craters like) that heals from bottom up greater risk for infection and scarring |
| Dehiscence | deficient scar formation where wound splits or bursts open often at suture line |
| Keloid developement | hypertrophic scar tissue |
| Adhesions | Fibrous connections between serous cavities and nearby tissues that reduce tissue movement of organs/loss of organ function |
| Main cells involved in chronic infection | monocytes, macrophages and lymphocytes |
| Difference between acute and chronic inflammation | acute = more heat and redness chronic = more pain and swelling |
| Complications of chronic inflammation | formulation of granulomas and scarring/fibrosis |
| granulomas | - nodular inflammatory lesions (macrophages), or basically clumps of macrophages - caused when immune mechanism/inflammatory response is insufficient - commonly seen in TB |
| Macrophages | mature monocytes that has moved from blood stream to site of injury stimulates fibroblast activity forms granulomas when it cannot phagocytize |
| Giant cells | phagocytes that can eat bigger particles than macrophages |
| Treatment for chronic inflammation | removing source of injury symptom management with drugs physical tx like RICE, diet and physical therapy |
| Ostia | tiny channels in nose for mucus drainage |
| Difference between acute sinusitis and chronic sinusitis | chronic may cause foul breath, sore throat, anorexia, hyposmia chronic sinusitis = disruption of mucociliary clearance acute sinusitis = to blockage of ostia and mucus outflow due to viral, allergens, etc |
| Sinusitis | blockage/obstruction of mucus in sinus due to primarily viral, and allergens |
| Complications of severe burn injuries | - fluid shifts causing impaired circulation, edema and dehydration - infection - overwhelming metabolic demand -> malnutrition - temperature regulation |
| Shock | inadequate perfusion (oxygenated blood flow) to tissue in the body |
| 3rd degree burns | capillaries and collagen are smoked, - can cause necrosis in the local area due to shock and hypovolemia due to fluid loss - eschar forms in the area (has to be removed) |
| hypovolemia | low fluid volume in blood vessels |
| Eschar | thick coagulated crust of dead tissue and exudate |
| Exudate | fluid leaking from wound |
| Clinical manifestations of 2nd dg burns | blistering, edema and serous exudate, blistering, redness, heat, pain |
| Clinical manifestations of 3rd dg burns | redness, eschar formation, edema and exudate |
| 3 lines of body defense against infection | 1. skin/mucous membranes 2. inflammatory response 3. immune response |
| what is the purpose of inflammatory response | promotes healing via inflammatory mechanism with goal to increase blood flow (vasodilation) and increased capillary permeability and WBC for phagocytosis |
| what is purpose of immune system | immune cells recognize and destroy harmful substances, last line of defense where if it fails disease can spread |
| vascular response | increased blood flow to site of injury (one of the main mechanism of inflammation) |
| chemical mediators of vascular response | nitrous oxide, histamines |
| acute inflammation | triggered by tissue injury, vascular response and cellular response is involved redness/warmth/swelling/pain occurs |
| cellular response | increase healing cells at site to prepare for tissue repair by alerting products of healing to migrate to injury site |
| PMN | polymorphonuclear neutrophils, involved in acute inflammation usually |
| steps of acute inflammation | injury -> vasodilation and increased blood flow (via histamine/Nitrous oxide) -> clotting factor recruitment -> WBC/neutrophil migration -> ingestion of pathogen/foreign material -> growth signals (ie. collagen etc) -> monocytes and macrophages |
| nonspecific markers of inflammation | fever, leukocytosis, elevated CRP/ESR |
| remodeling | maturation of cells and degradation of provisional matrix (remodeling phase of healing and tissue repair) |
| acute manifestations of sinusitis | facial pain in sinus region worsening w/ strain, fever, congestion/nasal discharge, postnasal drainage, cough, fatigue often caused by a prior URI |
| treatment for acute sinusitis | antibiotics, antihistamine, decongestants, nasal sprays surgical treatment for structural abnormalities like polyps |
| diagnostic criteria for chronic sinusitis | PE needs to have two of following 1. anterior/posterior mucopurulent drainage, facial pain/pressure/fullness, hyposmia, nasal obstruction 2. nasal polyps and/or purulent mucus/edema in middle meatus/ethmoid region CT scans |
| treatment for chronic sinusitis | glucocorticoids, antibiotics, nasal saline irrigation referral for ENT for possible surgical interventions |
| clinical manifestations of 1st dg burns | heat, swelling, pain, redness, loss of function |
| causes for chronic sinusitis (pathophysiology) | lasts 12+ weeks, multifactorial causes from environment (persistent infection/allergens) and possible genetic factors (metabolic abnormalities/immune deficiencies) |
| mucopurulent drainage | mixture of pus and mucus, looks very thick and possibly brown/gray/yellow/greenish color indicator of infection |
| rule of 9s | estimate areas of body affected (body is divided up to multiples of 9) babies have bigger heads proportionally |
| burns treatment | remove source of injury and cool/rinse skin wound dressing (changes Q1-2d or as per orders) airway, breathing, circulation fluid/nutrition management, antibiotics, analgesics hydrotherapy and skin grafts |
| what needs to be done with moderate/major burns | need to go to burn center |
Created by:
sleepingbear
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