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129 Cards in this Set

  • Front
  • Back
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.