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129 Cards in this Set
- Front
- Back
atherosclerosis
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multifocal chronic vascular disease of intima-lg.arteries
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athero char.
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inflammatory lipid plaques
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clinical athero indicators
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lumen stenosis, complicated plaque, vessel weakening
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causes
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genetics, environment
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athero can lead to
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aneurism, rupture, ischemic heart disease, cerebral, peripheral vascular disease
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plaque area between necrosis, lumen
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fibrous cap
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foam cells
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macrophages, sm. musc. cells w/cholesterol
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cell types, plaque
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monocytes, tcells, foamcells, lymphocytes, sm.musc
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plays role, athero plaque growth
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neovascularization - many in plaques, can rupture
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5 complications atheroplaque
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ulceration, hemorrhage, thrombosis, calcification, rupture
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location calcification athero
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plaque, areas of necrosis, in and on collagen
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mural thrombosis cause
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disrupted flow around plaque dmgs lumen, thrombi embolize
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plaque hemorrhage cause
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fibrous cap tears, proteolytic enzymes
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multifactorial process athero
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dynamic process - genetics, local, systemic factors
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purpose thrombosis
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rapid response, prevent blood loss
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common type thrombus, lung
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saddle embolus, sudden death
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clotting cascade main events
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prothrombin, thrombin, fibrinogen, fibrin
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after tissue dmg, 4 events
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vasoconstriction, platelet adhere/activate, coagulation, hemostatic plug
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3 causes anti-thrombosis
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anticoagulants, antiplatelet, fibrinolytics
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fibrinolytics
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attracted to, break down fibrin
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localized vasoconstriction causes
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neurogenic or humoral (hormones or cytokines)
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platelet adhesion factors
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vonWillebrand, collagen, platelet-platelet, endothelium-platelet
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primary hemostasis steps
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adhesion, shape change, granule release, recruitment platelets to plug, aggregation
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2ndary hemostasis events
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tissue factor release, phospholipids expressed, (activates coag. factors) thrombin activation, fibrin polymerization
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prob.with pharma. platelet deactivation
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too many interconn. chem. paths for pharma.solution
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main causes thrombus formation
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endothelial dmg, abnormal flow(stasis or turbulence), platelet activity enhancement, reduced anticoag.factors, ALL INTERCONNECTED
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4 potential outcomes, thrombus
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growth or lysis, embolization, organization
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consequence of embolization
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block vessel, infarct
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embolism
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any material moving through circ. which obstructs lumen
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thrombus in circulation
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thromboembolism
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atherosclerotic plaque in circulation
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atheroembolism
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most comm. cause of myocardial infarct
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athero decr. coronary blood supp.
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myocardial infarct cause
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coronary arts can’t supp. o2, so tissue, myocardium can’t function
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gradual coronary artery narrowing
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angina pectoris
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gradual coronary art. narrowing leads to
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sudden coronary art. occlusion - myocard. infarct
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infarct - inner 3rd myocardium, why
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inner third blood supp. tenuous
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name infarct inner 3rd myocardium
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sub-endocardial infarct
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2 causes infarct
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arterial or venous occlusion
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myocardial infarct, healing first half day
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ischemic injury, necrosis, hemorrhage
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myocardial infarct 2,3,4 stages healing
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inflammation, granulation tissue - neovasculature, scar
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complications - ischemic heart disease
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angina, death, ventricular aneurism, cong.heart failure, thrombi, thromboemboli, valve incomp., valve dilatation
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3 rupture locations - ischemia
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free wall, intervent. septae, papillary musc.
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3 causes heart valve stenosis
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commissures fuse, leaflets fibrose, calcification
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6 causes valve regurgitation
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annulus dilates, cusps retract, length of cords shortens or lengthens, cusps perforate
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cause of valve prolapse
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abnormal increase in matrix, tissue weakens
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pop.susceptible to infective endocarditis
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patients with heart valve replacements
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essential feature - infective endocarditis
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BACTEREMIA - bacteria in blood
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symptoms infectious endocarditis
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cardiac valves infected, grow vegetations, heart probs
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contents infectious end. vegetations
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clot elements, platelets, fungus, bacteria organisms, gran. tissue
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infective endocarditis - valve usually involved
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mitral
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bacteremia cause of infectious end., result of
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invasive op., dental procedure, catheterization, infection, etc.
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infective end. pathogenesis
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valve disease, endocard. dmg, thrombus, infection
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percent inf.endocard. effect normal vs abnorm. valves
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70 percent abnorm (prolapse etc) 30 percent normal
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predisposing conditions to inf. endocard - valve disease
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drugs, alcohol, liver disease, cirrhosis, Cancer
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infective endocard complications
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fever, malaise, valve dmg., infarcts, emboli, septic shock, nephritits
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diff. btwn. venous/arterial thrombus
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arterial: lines of zon, alternating layers, venous - gelatinous
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def, cause obst. lung dis
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airflow obst, physical or loss of elasticity
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Obst. lung dis. characteristics
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reduced FEV (forced exp.vol at 1sec, forced vital capac)
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3 comm obst. lung diseases
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asthma, bronchitis, emphysema
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asthma therapy
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treat inflammation - pharma bronchodilation
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define asthma
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epidsodic reversible bronchospasm
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bronchospasm def
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exaggerated constriction response to stimuli
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extrinsic asthma
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entry phase half hour - hour, late phase 4-8hrs. later
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extrinsic asthma early phase
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mast cells, mediators bronchoconstrict, vasodilate, incr. mucin prod.
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bronchoconstriction - why
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antigens dep in lungs, parasympathetic stimulation
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extrinsic asthma late phase
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LEUKOCYTE RECRUITMENT - EOSINOPHILS -
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chars of late phase extrinsic asthma
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proteins released - toxic to epithelial walls, sustain inflamm response
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def. intrinsic asthma
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irritants normally causing transient bronchoconstriction instead cause sustained.
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sever bronchiole asthma
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status asthmaticus - lungs overinflated, bronchi obstructed with mucin
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asthma pathology summary
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edema, hyperemia, inflam. infiltrate, esp.eosinophils, incr. mucosal glands, epithelial necrosis, thickening sm. musc.
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leading cause of death in Canada
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COPD
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define COPD
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2 overlapping diseases - bronchitis, emphysema
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COPD - symptoms
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dyspnea, cough, wheezing
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2 types COPD
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pink puffers, blue bloaters
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pink puffer desc.
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more emphysematous than bronchitic - have adequate o2 - lean forward and hyperventilate
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blue bloater desc.
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obese, freq. pulmonary infections, lower dyspnea and resp. drive, Low o2, High CO2
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blue bloaters die of
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edema, cyanosis, develop heart failure
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Puffers vs. bloaters
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puffers more emphysematous, bloaters more bronchitic
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emphysema
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PERMANENT dilation of airspace DISTAL to erminal bronchioles, destruction of alveolar walls
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% adults with emphysema at autopsy
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50%
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3 types emphysema
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centro, pan, and distal acinar
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most common type of emphysema
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centroacinar - 95 percent of cases
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centroacinar def.
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bronchioles effected, distal structures spared. Alveoli only effected in extreme cases
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pan acinar def and cause
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effects ENTIRE LOBULE, caused by GENETIC alpha1 deficiency
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May be present in DISTAL acinar
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Bulla’s - LARGE spaces in lungs
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cell types attracted to alveoli by smoke
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neutrophils, macrophages
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tissue damage in alveoli - smoke
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neutorphils, macroph rel. proteases, direct damage from smoke: free radicals
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chronic bronchitis def
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persistent cough 3 months, two years running
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cause chronic bronchitis
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smoking
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chronic bronchitis char
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HYPERSECRETION MUCOUS, maintained by infection
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contributing factors - lung disease in smokers
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direct epithelial injury, inflam cell action - incr. susc. to infection
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define bronchiectasis
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permanent dilation of bronchial wall
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functional char. restrictive lung disease
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lung volume compliance diffusion capacity REDUCED, flow maintained
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functional char obstructive lung disease
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REDUCED FLOW
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two types of restrictive lung disorders
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extrinsic or intrinsic
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extrinsic restrictive lung disorder
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chest wall problems
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intrinsic restrictive lung disorder
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lung itself
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acute resp. distress syndrome def
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high mortality rate (1/3). dmg to alveolar epithelium and capillaries by pulmonary aspiration, sepsis, trauma.
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acute resp. dist. syndrome main char
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imbal. btwn. pro and anti-inflam cytokine mediators
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most common disease of lung vessels
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pulmonary thromboembolism
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pulm thromboembol occurs where
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pulm arterial tree, usually from deep veins of legs
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pulm. thromboemb. risk factors
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immobility, trauma, surgery, childbirth
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4 clinical consequences pulm thromboemboli
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heart failure/death, fibrinolysis, pulm. hypertension, pulm infarct
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end stage many pulm. disorders
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pulm. hypertension, dyspnea, systemic edema, Rside heart failure
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3 main pulmonary defense mechanisms - combat pneumonia
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cough reflex, mucociliary apparatus, immune reactions - alveolar macrophages
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agents effecting disease mechanism
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anasthesia (cough reflex gone), smoking
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most comm. community cause pneumonia, target pop.
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streptococcus. COPD, reduced immune syst,spenectomy and blood disorder patients
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3 other causes comm. acquired pneumonia
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hemophilous flu (kids) staphlococcus viral resp.tract inf.
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two main organisms atypical comm. acquired pneumonia
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mycoplasma pneumoniae, chlamidia
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aspiration pneumonia def
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aspiration of oral/gastric contents
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aspiration pneumonia due to
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vomitting while unconscious
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aspiration pneumonia causes
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bacterial and chemical damage to lungs
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aspiration pneumonia sign. to dentists
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anaerobic oral bacterial aspiration during dental procedures
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aspiration of oral bacteria during dentistry can cause
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lung abscess
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4 main risk groups TB
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urban poor, HIV+, elderly, aboriginals
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TB causative organism
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mycobacterium tuberculosis
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TB transmission mode
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airborne
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percent people develop TB disease
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15 percent, usually immunosupressed - otherwise, no disease
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TB pathology
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arrest. pulm. macrophages, proliferate, cause caseous necrosis
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orig site TB infection and nodes
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Ghon focus - ghon complex with nodes
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spread of TB in individual
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bacteremia and seeding
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delayed hypersens. reaction in TB
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nodes react, mediators released, granuloma form, mycobacteria killed via nitrous oxide
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consequence of TB infection
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never fully eliminated, causes scarring
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Term: TB disease growing from primary infection
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progressive primary tuberculosis
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Term: reaction TB
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in lung apex, where high vol. O2 (mycobacterium aerophilic)- rapid walling off of infectious focus
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cavitation
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virulent strains of TB cause necrosis, cavities form, virus spreads via cavities to airways and blood
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cavitation spread
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coughing
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miliary TB
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through lungs and body via seeding - millet
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TB presentation in HIV+patients
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progressive pneumonia, skin tests remain negative - NO CD4’s to combat disease.
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