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