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Unit 4 > Lung Pathology > Flashcards

Flashcards in Lung Pathology Deck (41):
1

What is obstructive lung disease?

Airflow compromised: problem emptying the lung

2

What are the obstructive lung diseases?

COPD: asthma, chronic bronchitis/emphysema

3

What would pulmonary function tests show for obstructive lung disease?

Reduced FEV1(forced expiratory volume at 1 sec)/FVC (forced vital capacity)

4

What is restrictive lung disease?

Stiff, hard-to-expand lungs: problem filling the lung

5

What would pulmonary function tests show for restrictive lung disease?

Reduced TLC (total lung capacity),
Reduced DLCO (Diffusing lung capacity for carbon monoxide)

6

What are examples of restrictive lung disease?

UIP(usual interstitial pneumonia)

IPF (idiopathic pulmonary fibrosis)

7

What are the clinical features of pneumonia (infection of the lunch parenchyma)?

Fever and chills

Cough with yellow-green or rusty sputum

tachypnea

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

8

What are 2/3 categories of pneumonia that are more typically cased by bacterial infection?

lobar pneumonia (whole lob consolidation)

bronchopneumonia (bronchioles)

interstitial pneumonia is more likely viral

9

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

10

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)

11

what are the features of bronchopneumonia

pachy consolidation around bronchioles - multifocal and often bilateral

12

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)

13

homophilus influenzae commonly leads to seconday pneumonia in regard to exacerbation of what?

COPD

14

What is the most common cause of cystic fibrosis?

P aeruginosa

15

Legionella pneumophila causes community aquired pneumonia and pneumonia superimposed COPD. What is tramission source? How can you stain for this?

Water

Intracellular organisms - best stain is Silver

16

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

17

What is most common cause of atypical (interstitial pneumonia)?

Who does it affect?

What is the major complications?

mycoplasma pneumoniae

young adults - military, collage students

autoimmune hemolytic anemia - caused by IgM against I antigen on RBCs - "cold hemolytic anemia")

erythema multiforme

*doesn't gram stain b/c no cell wall

18

second most common cause of atypical pneumonia?

clamydia pneumonia

19

most common cause of atypical pneumonia in infants?

respiratory syncytial virus

20

post-transplant immunosupresive atypical pneumonia is caused by what?

cytomegalovirus

21

who can get pneumonia from influenza virus?

elderly, immunocompromised, pre-existing lung conditions ==> predisposes for Staph aureas or H influenzae pneumonia

22

what is cause of Q fever and pneumonia often in farmers of veternarians?

Coxiella burnetii

rickettsial organism deposited as spores on cattle by ticks - so no anthropod host needed for transmission

also survives high heat

23

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)

24

what causes tuberculosus?

inhilation of aerosolized mycobacterium tuberculosis

25

What happens after initial exposure to aerosolized M tuberculosis?

What are the pathological hallmarks?

primary TB

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

26

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

27

How does secondary TB present?

Fevers and night sweats

cough with hemoptysis

weight loss

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)

28

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)

29

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)

30

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

31

What happens to the air sacs in emphysema

destroyed (conversion of small balloons into a shopping bag

32

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

33

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)

34

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)

35

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)

36

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?

asthma

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

LATE PHASE
inflammation causes production of eosinophil major basic protein and sustained bronchoconstriction in late phase asthma which obstructes airway outflow

37

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

38

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)

39

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
-Necrotizing infection
-Allergic bronchopulmonary aspergillosis (see in CF patients and asthmatics)

40

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...

41

What are the clinical features of bronchiectasis?

Cough, dyspnea, foul smelling sputum

hypoxemia with cor pulmonale and secondary amyloidosis are complications