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131 Cards in this Set
- Front
- Back
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What is pneumonia basically?
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any infection of the parenchyma of the lung
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What is the relationship to the size of the microbe to the distance it travels?
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inversely proportional
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what clears small microbes?
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humoral & cellular immunity
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What are some impairments to host defense?
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loss of cough reflex
injury to mucocillary sys interference w mp pulmonary edema accumulation of secretions CF |
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What are some things that cause you to lose your cough relfex?
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anesthesia
coma neuromuscular disorders drugs ie alcohol |
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What are some things that injure the mucociliary sys?
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smoking
viral infections genetics intubation |
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How does haemophilus evade the host defense?
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toxin paralyzes cilia
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How does bordetella evade the host defense?
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toxin paralyzes the cilia
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How does psuedomonas evade the host defense?
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ciliostatic
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How does mycoplasma evade the host defense?
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ciliostatic
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How does infulenza evade the host defenses?
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hemagglutinin
neuroaminidase |
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How does mycobacterium TB evade the host defesne?
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escapes phagocytic killing
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What are 2 patterns onf community aquired pnuemonia?
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Lobar
Lobular |
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What are some sx of community aquired pneumonia?
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fever, chills, productive cough, hemoptysis, chest pain, tachypnea, SOB, fatigue, headache, loss of appetite, confusion
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CAP lobar pneumonia
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entire lobe
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CAP lobular pneumonia
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aka bronchopneumonia
patchy areas around bronchiole |
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What are the 4 stages of CAP lobar pneuomia?
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congestion
red hepatization grey hepatization resolution |
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What is involved in congestion in CAP lobar pneumonia?
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vascular engorgement - capillary leak
neutrophil migration intra-alveolar fluid |
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What is involved in red hepatiziation in CAP lobar pneumonia?
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confluent exudate with RBCs
red, firm, airless lung liver like consistency |
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What is invovled in grey hepatization in CAP lobar pneumonia?
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fibrinosupparative exudate
disinigration of red cells |
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What is involved in resolution of CAP lobar pneumonia?
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enzymatic degredation
resorption expetoration MP ingestion fibroblastic organization |
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What is plueritis?
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fibrinous reaction to underlying inflammation
may resolve or form fibrinous plaques |
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What are some complications of CAP pneumonia?
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abscess, epmyenma, organization, bacteremic dissemination
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What is empyema?
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spread into the pleural space
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What are some organisms that commonly cause CAP?
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strep pneumoniea
haemophilus infulenza Moraxella caterrhalis staph aureus klebsiella pneumonia psuedomonas aeruginosa legionella |
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Strep Pneumonia
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most common cause of CAP
grm + diplococcus endongenous flora in 20% = false + sputum samples |
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Haemphilus influenza
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common CAP in elderly & young
grm - coccobacillus Type B encapsulated form! |
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What bacteria is the most common bacterial cause of acute exacerbation COPD?
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haemophilus influenza
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Moraxella caterrhalis
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grm - diplococcus
2nd cause of COPD exacerbation associated w sinitis & otis media |
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Staph aureus
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IV drug abusers
high incidence of complications nosocmial |
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Klibsiella pneumonia
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most common gram - bacterial pneumonia
***alcoholics viscid capsular polysaccharide causes thick gel sputum |
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Pseudomonas Aeruginosa
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usually not CAP
CF pts nosocomial infection |
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Legionella pneuomphilia causes what 2 illnesses
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Legionarie's disease
Pontiac Fever |
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Legionella pneumophilia
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gram - rod
water immunosuppressed pts high mortality potentially |
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What is an atypical pneumonia?
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varied clinical course
URI or chest colds cough may be absent numerous extrapulmonary sx |
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Why is it atypical?
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moderate to no sputum
no physical findings of chest consolidation moderate to no elevation WBC lack alveolar exudate |
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What organisms cause atypical pneumonia?
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mycoplasma pneumonia
viruses (influenza, adeno) chlamydia pneumonia coxiella burnetti (Q fever) |
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Mycoplasm pneumonia organism
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smallest
no cell wall no seasonal variation |
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mycoplasma pneumonia disease
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indidious, trachobronchitis
early sputum w no orgs peribronchial inflam w occasional organizing pneumonia extrapulm manifestations common |
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What are some extrpulmonary manifestations of mycoplasm pneumoniae?
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rashes 10-20%
anemia (hemolytic) cold agglutinins |
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What 2 viruses cause pneumonia?
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influenza
RSV |
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What are the characteristics of the influenza virus?
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enveloped ssRNA
hemagglutinin- attatchment Neuraminidase |
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What is antigenic drift in influenza?
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minor changes in hemagglutinin & neuraminidase
causes epidemics |
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What is antigenic shift in influenza?
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recombination events giving new antigenic structure
causes pandemics |
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What is the big name for RSV?
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Respiratory Syncytial Virus
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When are where do you get RSV?
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worldwide in winter & early spring in temperate climates
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Who does RSV affect?
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children & infants
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What percent of the target patients get RSV?
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100% of children within 1 yr of age
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What do you see on a CXR in RSV?
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hyperinflation
intertitial findings (patchy infiltrates) flattening of the diaphram |
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RSV is the most common cause of?
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tracheobronchitis & pneumonia in children & infants
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What 2 protiens does RSV have?
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G - attatchment
F - cell fusion |
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What is the pathogenesis of RSV?
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virions invadee respiratory epithelial cells resulting in cell death
dead cells & mucus result in obstruction "giant cell" pneumonia w mixed inflammatory infiltrate |
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Epidemiology of Chlamydia pneuomoniae?
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children & elderly w afibrile, mild pneumonia
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Psittocosis
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from birds
aerosol |
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Symptoms of psittacosis?
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high fever, arthralgias, non-productive cough
may be fatal, slow recovery meningoencephalitis, hepatitis, & rash |
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What is nosocomila pneumonia?
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hospital aquired
serious often life-threatening due to underlying disease, immunosupprssion, invasion |
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What are some organisms that cause nosocomila pneumonia?
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grm - rods (e.coli & pseudomonas)
staph aureus |
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What is a lung abscess?
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local suppurative process within the lung, characterized by necrosis of lung tissue
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What are some mechanism of lung abscess formation?
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aspiration
antecedent bacterial infection septic embolism direct traumatic penetration hematogenous spread |
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What organisms cause lung abscesses?
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mixed & anerobic
strep bacterodies staph Klebsiella **nocardia & actinomyces (O2) |
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What are clinical presentations of lung abscess?
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cough - copious foul smelling sputum
fever weight loss chest pain clubbing digits |
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Gross findings in lung abscess?
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cavitary lesion filled w suppurative material composed of neutrophils & necrotic debris
more common in the right lung gangrene of the lung chronic cases -> fibrosis |
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Aspiration pneumonia is found in what pts?
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markedly debilitated (stroke)
repeated vomiting intubated pts |
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what do you see grossly with aspiration pneumonia?
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necrotization with abscess formation
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Mycobacterium tuberulosis organism characteristics
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slender aerobic rods
mycolic acid cell wall acid fast airborne - highly infectious |
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What is the most common ID cause of death in the world?
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TB
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How long does it take for the PPD test to become +?
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2-4 wks later
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What is a downside to the PPD?
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doesnt differentiate btwn infection & disease
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What is the clinical presentation of primary TB
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previously unexposed
asympotmatic |
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Where on the lung do you find primary TB?
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posterior upper lobe
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What is the gross findings of primary TB?
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nodule on posterior upper lobe with central caseous necrosis
granulomatous inflammation with necrosis |
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What is the course of primary TB?
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goes to lymphatics & disseminates to hilar LN w caseous necrosis - may heal or become fibrotic & calcify
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What is a reason you can have TB disease but a - PPD
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so immunosuppressed cant mount a hypersensitivity rxn
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What is Ranke complex?
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calcified ghon complex
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What is progressive TB?
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dec cell mediated immunity
children, elderly, immunsupp. resembles acute bac pneumon. |
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Where do you see progressive TB?
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lower, middle lobe with consolidation w necrosis & cavitations
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What are some of the findings with progressive TB?
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hilar adenopathy
pleural effusion possible dissemination |
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What happens in secondary TB?
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previously sensitized host
weakened immunity - reactivation or reinfection |
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What are the sx of secondary TB?
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fever - low grade
night sweats fatigue anorexia weight loss productive cough hemoptysis |
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What do you see with secondary TB?
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hilar adenopathy, bacteremia less common
apical lessions - coalesce & expand central caseous necrosis w peripheral fibrosis |
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What is found in the granulomatous inflammation & necrosis of secondary TB?
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epitheliod cells
multinucleated giant cells lymphocytes macrophages bacteria in necrotic material |
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Lesions of secondary TB can erode?
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bronchus - evacuation of caseous material
blood vessels - hemoptysis |
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Millary TB
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ressembles millet seeds
enters systemic circulation numerous grey-white lesions in affected organs |
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What are some presenting manifestations of isolated organ TB?
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meninges
kidneys adrenal bones fallopian tubes |
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Lymphadenitis?
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most frequent form of extrapulmonary TB
cervial LN most common |
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What is the gold standard for diagnosing TB?
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sputum culture
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What are 3 types of fungal pneumonia?
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histoplasmosis
coccidioidomycosis blastomycosis |
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Histoplasmosis
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dimorphic fungus
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What are the 2 phase of histoplamosis?
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Mycelial (spore)
yeast |
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What form of histoplasmosis is infectious?
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mycelial spore form from the enviornment 25 degrees C
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What form of histoplasmosis is not infcetious?
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yeast in host - 37 degrees C
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Where do you get histoplasmosis?
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soil & birds (inhaled)
ohio & Mississippi river valley *no person to person spread |
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Let's talk about the yeast form of Histoplasmosis
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uninucleate
spherical to oval narrow-based budding similar pathogenesis to TB |
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Primary pulmonary histoplasmosis sx
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asymptomatic usually
fever, chills, myalgia, non-productive cough usually self-limiting |
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What is the pathogeneis of histoplasmosis?
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taken up by alveolar MP enter LN and disseminate - granulomatous inflam w central necrosis
lesions may heal or become fibrotic, calcified or cavitate |
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Chronic histoplasmosis is similar to
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secondary TB
low grade fever, night sweats, fatigue granulomatous lesions in lung apicies w central necrosis |
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Progressive disseminated histoplasmosis
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immunocomprimised
primarily extrapulmonary fever, chills, productive cough, dyspnea, hemoptysis, malaise, headache, wt loss, diarrhea, anemia, purpura, lymphadenopathy, hepatospelnomegaly |
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What is the pathogenesis of progressive disseminated histo?
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in MP & free in tissue
no inflammation no granulomas high mortality needs aggressive Tx |
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What are the 2 phases of coccidioides?
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arthroconidia
spherules |
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What form of coccidioides is infectious?
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arthroconidia in environment
no human to human spread |
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What form of coccidioides is not infectious?
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spherules
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where do you get coccidioides?
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SW US, nothern, central mexico
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What does arthroconidia do?
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block fusion of phagosom & lysosome in MP
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What are sx in coccidioides?
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asymptomatic
lung lesions - rashes |
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What are some characteristics of coccidiodies?
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thick walled non-budding spherules
spherule contains endospores |
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What is the pathological findings in coccidoides?
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lesions w acute infla w surrounding granulomas & central necrosis
org found in central necrosis dissemination is rare |
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what are the 2 phases of blastomycosis?
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mycelial form - envir - infect
yeast in host no human to human spread |
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Where do you find blastomycosis?
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mississippi, ohio, missouri river valleys
great lakes - WI! canada Europe, Africa, Middle East, India |
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What does blastomycosis look like?
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round yeast - bigger
thick, double contoured wall broad base buds multiple nuclei |
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acute blastomycosis infection
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sudden onset
fever, chills, productive cough, arthralgias, myalgias more common to have an acute |
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Chronic blastomycosis
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more common than acute infect.
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disseminated blasto
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immunocompromised
skin, bone |
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Findings in blastomycosis
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MP cant ingest yeast-neutrophils
granulomas may calcify, fibrose |
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acute lesions
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suppurative, neutrophilic
more organisms |
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chronic blasto lesions
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granulomas surrounding neutorphilic inflammation
less organsims |
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disseminated blastomycosis infections
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numerous organisms with little or no inflammation
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Bacteria that cuase infection in immunocomprised?
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pseudomonas
mycobacteria legionella listeria |
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viruses that cause infection in immunocomprimised?
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CVM
Herpes |
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Fungus that causes infection in immunocoprimised?
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pneumocysits carinii
aspergillosis candidiasis cryptococcus neoformans |
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CMV
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dsDNA in herpes family
can remain latent in WBC |
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Sx of CMV in different groups
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asymptomatic in normal ppl
interuterine w cong. defects systemic in suppressed (pneumonia, hepatitis, colitis, tetinitis) |
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Sx of CMV overall
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fever, leukopenia, thrombocytopenia, non-productive cough, SOB
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Nonspecific pathological findings in CMV?
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interstitial mononuclear infiltrate
focal necrosis hyaline membranes exudate |
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Characteristic cytopathic features of CMV
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endothelial cells!
enlarged cells large intranuclear basophilic inclusions w halos (owl eyes) smaller basophilic inclusions in the cytoplasm |
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Pneumocystis carinii
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ubiquitous fungus
cyst & trophozoite stages airborne high degree of seropositivity in pop |
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Pneumocystis carinii in children
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subclinical infection in 65-100% of kids
becomes latent/opertunistic |
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what is pneumocystis carnii often copathogens with?
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CMV
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what is the clinical course of pneumocystis carinii?
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indolent, non-productive cough, dyspnea, fever, hypoxia, crackles
can progress rapidly to respiratory failure |
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What does pneumocystis look like?
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round oval cysts (flying saucer)
grooves, dark staining foci |
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What does pneumocystis stick to and how?
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type I pneumocytes via fibronectin
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what is the pathology of pneumocystis?
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intraalveolar proteinaceous exudate with bubble -> orgs
min interstitial pneumonitis interstitial fibrosis & chronic inflam type 2 pneumocytes hyperplasia |
