Flashcards in Lung Pathology Deck (41):
What is obstructive lung disease?
Airflow compromised: problem emptying the lung
What are the obstructive lung diseases?
COPD: asthma, chronic bronchitis/emphysema
What would pulmonary function tests show for obstructive lung disease?
Reduced FEV1(forced expiratory volume at 1 sec)/FVC (forced vital capacity)
What is restrictive lung disease?
Stiff, hard-to-expand lungs: problem filling the lung
What would pulmonary function tests show for restrictive lung disease?
Reduced TLC (total lung capacity),
Reduced DLCO (Diffusing lung capacity for carbon monoxide)
What are examples of restrictive lung disease?
UIP(usual interstitial pneumonia)
IPF (idiopathic pulmonary fibrosis)
What are the clinical features of pneumonia (infection of the lunch parenchyma)?
Fever and chills
Cough with yellow-green or rusty sputum
pleuritic chest pain (pain on inhalation due to stretching of pleura - bradykinin and PGE2 produced by inflammatory response activates innervation in pleura)
decreased breath sounds with dullness to percussion
elevated WBC count
What are 2/3 categories of pneumonia that are more typically cased by bacterial infection?
lobar pneumonia (whole lob consolidation)
interstitial pneumonia is more likely viral
Most common causes of lobar pneumonia?
Strep pneumoniae (95% community aquired in adults/eldery) and Klebsiella pneumoniae (aspiration of enteric fleura! - nursing homes and alcoholics)
air-sacs fill with neutrophils
what are the 4 phases of lobar pneumonia?
congestion -> edema
red hepatization (liver-like change) -> exudate formed in interstitum containing neutrophils and blood - ends up filling air sacss and giving lung spongy consistency
grey hepitization -> macrophages come in and clear up exudate
resolution - healing - lining of alveolar air sacs regenerates from stem cells (type II pneumocytes)
what are the features of bronchopneumonia
pachy consolidation around bronchioles - multifocal and often bilateral
what is the most common cause of secondary pneumonia (bacterial pneumonia superimposed on respiratory tract infection)?
Staph aureus secondary to primary infection that knocks out the cilliated respiratory epithelium that's needed for mucocilliary escalator-mediated clearance of pulmonary bacteria/debris
complicated by abses of empyema (puss in plural space)
homophilus influenzae commonly leads to seconday pneumonia in regard to exacerbation of what?
What is the most common cause of cystic fibrosis?
Legionella pneumophila causes community aquired pneumonia and pneumonia superimposed COPD. What is tramission source? How can you stain for this?
Intracellular organisms - best stain is Silver
which type of pneumonia is the one that will produce the least upper respiratory symptoms?
interstitial pneumonia (diffuse intersital inflammation- infiltration along the wall of the alveolar air sacs without major consolidation)
Air sacs are usually clear from infiltrates but walls are loaded with inflammatory cells
What is most common cause of atypical (interstitial pneumonia)?
Who does it affect?
What is the major complications?
young adults - military, collage students
autoimmune hemolytic anemia - caused by IgM against I antigen on RBCs - "cold hemolytic anemia")
*doesn't gram stain b/c no cell wall
second most common cause of atypical pneumonia?
most common cause of atypical pneumonia in infants?
respiratory syncytial virus
post-transplant immunosupresive atypical pneumonia is caused by what?
who can get pneumonia from influenza virus?
elderly, immunocompromised, pre-existing lung conditions ==> predisposes for Staph aureas or H influenzae pneumonia
what is cause of Q fever and pneumonia often in farmers of veternarians?
rickettsial organism deposited as spores on cattle by ticks - so no anthropod host needed for transmission
also survives high heat
What are most common organisms that cause aspiration pneumonia?
anaerobic bacteria - bacterioides, fusobacterium, peptococcus
classic presentation is lower right abcess (b/c carina is slightly deviated toward left causing left mainstem brinchus to branch at a more acute angle, causing more air to flow into right main stem bronchus, also right lung is bigger b/c cardiac compression on left)
what causes tuberculosus?
inhilation of aerosolized mycobacterium tuberculosis
What happens after initial exposure to aerosolized M tuberculosis?
What are the pathological hallmarks?
Focal caseating necrosis in the lower lobe of the lung and hilar lymph nodes
foci undero fibrosis and calcification to form the "Ghon complex" - classically in sub-plural region (close to visceral pleura) of lung
Generally asymptomatic! but leads to positive PPD
What leads to secondary TB?
reactivation of Ghon complex - can be due to AIDS or accomanies aging
usually secondary occurs at apex of lung (because oxygen tension is highest in apex)
forms cavitary foci or faceous necreosis ()
miliary pulmonary TB or tuberculous bronchopneumonea are also possible in secondary TB
How does secondary TB present?
Fevers and night sweats
cough with hemoptysis
biopsy reveals caseating granulomas; stain for acid fast bacilli will reveal red acid-fast baccili (differentiates from fungal causes of pneumonia with caseating necrosis e.g. criptococcocis, cocidiomycosis, histoplasmosis)
What are other organs affected by TB?
meninges - meningitis with caseating (necrotic tissue that retains its structure in cheese like matrix) granulomas at base of brain
cervical lymph nodes
kidney (sterile pyuria)
lumbar vertebrae (Pott disease)
what would the findings be for COPD on respiratory function tests?
decreased FVC, very decreased FEV1
decreased FEV1/FVC ration
increased TLC (due to air trapping)
What is the reed index? what is it in chronic bronchitis?
thickness of muscenous gland layer relative to the overall thickness of the brinhiole wall.
in chronic bronchitis reed index >50%
normal should be 40 or less
excess mucus produced can be coughed up or can move down and block airways resulting in airway trapping/obstruction
What happens to the air sacs in emphysema
destroyed (conversion of small balloons into a shopping bag
emphysemya causes aiway obstruction through what mechanisms?
loss of elastic recoil
collapse of the small airways due to loss of elastic recoil of alveoli due to destrion
in emphesema what is the mechanism for destruction of alveolar walls?
either excess production of proteases by alveolar macrophages that are release when macrophage destroys particulate matter or decreased production of anti-proteases (e.g. anti-tripsin) circulating in blood
smoking cases increase in proteases
alph1-anti-tripsin deficiency is secondary cause of emphysema (PiZ is mutated allele - PiM is normal allele)
what kind of lung disease is caused by smoking?
centriacinar emphysema (destruction of alveoli due to excess protease release from macrophages) affecting the upper lobes
alpha1 anti-tripsin deficiency is panacinar emphysema, in lower lobes
--- may also cause liver cerrhosis because non-functional alpha1anti-tripsin is produced and accumulates in endoplasmic recticulum hepatocytes (looks like pink PAS)
What differentiates emphysema from chronic bronchitis?
both can be caused by smoking both have dyspnea and cough
brinchitis has producting couph with mucus sputum
emphysema has minimal sputum, prolonged exhilation, weight loss (because of effort required to exhale extra TLC), and increased AP diameter of chest (barrel chest)
reversible collapsing of airways due to type 1 hypersensitiveity reaction leading to TH2 phenotype CD4+ T cells - (in genetically suseptible individuals) results in secretion if IL4,5,10 -- what is this?
TH2 release of IL4 allows plasma cell to class switch to IgE -->
IL5 calls in eosinophils
IL10 stimulates TH2 and inhibits TH1 helper Ts
EARLY PHASE: allergen cross-links surface IgE on mast cells which triggers histomine release from pre-formed granules
histomine causes vasodilation in arterioles and increased permeability in post-capillary venules.
mast cells also produce leukotrienes which initiate bronchoconstriction
LTC4 LTE4 LTT4 > cause contriction of
inflammation causes production of eosinophil major basic protein and sustained bronchoconstriction in late phase asthma which obstructes airway outflow
What are the clinical findings from asthma?
dyspnea and wheezing
productive cough containing Curshmann spirals admixed with aggrigated eosinophil major basic protein (Charcot-Leyden crystals)
severe unrelenting attack can result in status asthmaticus and death
What is bronchiectasis?
permanant dilation of bronchioles and bronchi which results in loss of airway tone and air trapping (blowing into straw vs blowing into large diameter pipe - velocity decreases and air doesn't get out)
What causes bronchiectasis?
What conditions is it associated with?
Necrotizing inflamation that damages airway walls
-cystic fibrosis (thick secretions, mucus plugging blocks tube and behind tube you get inflammation)
-Kartagener syndrome (impaired cillia)
-Tumor of forein body
-Allergic bronchopulmonary aspergillosis (see in CF patients and asthmatics)
What is kartagener syndrome?
dianin arm of cillia (ALL CILLIA) is damaged leading to impaired cilliary movement
sinusitis because respiratory epithelium is malfunctioning
brochiectasis because mucocilliary elivator doesnt work and backflow causes airway obstruction, inflammation behind obstruction and necrosis of brochiolar wall
infertiity because motility of sperm is impaired
sinus inversus - reversal or organs...