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RC Test 3 > B4.057 Obstructive Lung Disease > Flashcards

B4.057 Obstructive Lung Disease Flashcards

1
Q

what are obstructive airway diseases

A

increased resistance to airflow due to partial or complete obstruction at any level
decreased maximal airflow rates during forced expiration (FEV1)

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2
Q

restrictive lung diseases

A

not airway disease
reduced expansion of lung parenchyma
decreased total lung capacity/volume
decreased compliance

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3
Q

emphysema

A 
abnormal permanent enlargement of the airspaces distal to the terminal bronchiole
destruction of walls without obvious fibrosis
small airway (bronchiole) fibrosis
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4
Q

epidemiology of emphysema

A

male predominance
smoking major cause
gradual development, symptoms seen at age 40+

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5
Q

when does emphysema manifest?

A

once 1/3 of the functioning lung parenchyma is impaired

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6
Q

2 primary emphysema types

A

centriacinar

panacinar

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7
Q

2 secondary emphysema types

A

distal acinar/paraseptal

irregular

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8
Q

centriacinar emphysema

A

central/proximal portions of acini (resp bronchioles) affected, but distal alveoli are spared
more common in upper lobes

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9
Q

most common type of emphysema

A

centriacinar

>95% of cases

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10
Q

panacinar emphysema

A

acini are uniformly enlarged from respiratory bronchiole to the alveoli
worst at bases of lungs

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11
Q

which type of emphysema is seen with alpha 1 antitrypsin deficiency

A

panacinar

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12
Q

distal acinar emphysema

A

distal acinus is predominantly involved
adjacent to pleura, along the septa
next to fibrosis, scarring, or atelectasis
worse in upper lungs

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13
Q

which type of emphysema predisposes to pneumothorax

A

distal acinar/ paraseptal

bullae near pleura is the issue

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14
Q

irregular emphysema

A

occurs in small foci

clinically insignificant

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15
Q

gross pathology of centriacinar vs panacinar emphysema

A

centriacinar has a mix of dilated and normal air spaces

panacinar is uniformly dilated

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16
Q

pathogenesis of emphysema

A

smoking/genetic predisposposition/ A1AT deficiency initiate cascade
lungs experience:
-oxidative stress, increased apoptosis and senescence
-inflammatory cells and release of inflammatory mediators
-protease/antiprotease imbalance
all result in alveolar wall destruction

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17
Q

what enzymes contribute to tissue damage in emphysema

A

proteases
neutrophil elastases
macrophage elastase
metalloproteinases

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18
Q

prevalence of A1AT def

A

1% of emphysema patients
100,000 americans
predisposed to liver disease

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19
Q

what finding might you see on histo of emphysema in addition to dilated air spaces

A

ruptured alveolar septae due to breakdown by proteases etc.

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20
Q

mechanism of emphysema

A

functional airflow obstruction
normally small airways are tethered open by the elastic recoil in the walls of surrounding alveoli
loss of elastic tissue in alveolar walls allows the resp bronchioles to collapse during expiration

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21
Q

chronic bronchitis definition

A

productive cough of unknown cause occurring for 3 or more months in at least 2 successive years
chronic irreversible obstruction of airflow

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22
Q

chronic bronchitis epidemiology

A

all people, all ages
longtime smokers, polluted urban areas
more common > 45
more common in men

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23
Q

pathogenesis of chronic bronchitis

A

initiating factor: exposure to noxious inhaled substances
mucus hypersecretion in airways (IL-13)
metaplasia/hypertrophy/remodeling of small airways
inflammation
infection (maintains disease process and causes acute exacerbations)

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24
Q

pathogenesis of chronic bronchitis in the context of smoking

A
  1. injures airway epithelium > chronic inflammation

2. impairs ciliary action of airway epithelium > mucus > infection

25
Q

histo findings in chronic bronchitis

A

goblet cell metaplasia of bronchial epithelium
increased size of mucus glands (thickness > 40% of bronchial wall)
mucus plugs
lymphocytes in bronchiolar wall

26
Q

anatomic compartment affected by chronic bronchitis

A

bronchus

27
Q

characteristics of a patient w predominant bronchitis

A 
40-45
mild dyspnea
copious sputum
rhonchi
common infections
repeated resp insufficiency
cor pulmonale common
increased airway resistance
normal elastic recoil
no weight loss
28
Q

CXR findings in chronic bronchitis

A

prominent vessels
large heart
cor pulmonale

29
Q

characteristics of a patient w predominant emphysema

A 
50-75
severe dyspnea
scant sputum
prominent weight loss
diminished breath sounds
occasional infections
terminal resp insufficiency/ cor pulmonale
normal airway resistance
low elastic recoil
30
Q

CXR findings in emphysema

A

hyperinflation, small heart

31
Q

complications of COPD

A

pulm hypertension leading to cor pulmonale (R heart failure)
pneumothorax with massive lung collapse (emph)
superimposed infections (bronch)

32
Q

asthma definition

A

chronic disorder of the conducting airways, usually caused by an immunological reaction
episodic bronchoconstriction due to increased airway sensitivity to a variety of stimuli
inflammation of bronchial walls
increased mucus secretion

33
Q

symptoms of asthma

A

recurrent episodes of wheezing, breathlessness, chest tightness, cough
particularly at night or in the early morning
usually reversible, either spontaneously or with treatment

34
Q

epidemiology of asthma

A

5% of pop
any age
most common in kids, decreases at puberty, increases with age
increasing incidence

35
Q

continuous asthma symptoms

A

status asthmaticus

can be fatal

36
Q

atopic asthma

A

evidence of allergen sensitization and immune activation

often with allergic rhinitis or eczema

37
Q

non atopic asthma

A

no evidence of allergen sensitization

38
Q

triggers of asthma

A 
seasonal
exercise
drugs
occupational
asthmatic bronchitis in smokers
39
Q

characterize atopic asthma

A 
most common type
begins in childhood
antigen is implicated
positive fam history
allergic rhinitis, urticarial, or eczema
40
Q

atopic asthma testing findings

A

IgE mediated type 1 hypersens
high serum levels of IgE
RAST detects presence of IgE for specific allergens
skin test wheal and flare reactions

41
Q

pathogenesis of atopic asthma

A

complex and multifactorial
TH2 and IgE response to environmental allergens in genetically predisposed individuals
fundamental abnormality is an exaggerated TH2 response to normally harmless environmental antigens

42
Q

susceptibility locus for asthma

A

chromosome 5q

encodes interleukins; IL-13

43
Q

environmental factors for asthma development

A

airborne pollutants
hygiene hypothesis
young children with aeroallergen sensitization and lower resp tract viral infections have a 10-30x risk of developing asthma

44
Q

drug induced asthma

A

several drugs can provoke

45
Q

aspirin induced asthma

A

+ recurrent rhinitis, nasal polyps
small doses of NSAIDs provoke asthmatic attacks and urticarial
inhibits COX pathway of AA metabolism > decrease PGE2
release inhibition of enzymes that generate pro inflamm mediators (LTB4,C4,D4,E4)

46
Q

histo findings with asthma

A

mucus plugs
curschmann spiral - coiled fragment of inspissated mucus
eosinophils
Charcot Leyden crystals from eosinophil breakdown

47
Q

airway remodeling seen in asthma

A

thickening of airway wall
sub BM fibrosis
increased vascularity and macrophages in lamina propria
increased size of submucosal glands and number of airway goblet cells
hypertrophy/hyperplasia of muscle

48
Q

what is bronchiectasis

A

destruction of airway muscle and elastic tissue, resulting in permanent dilation of bronchi and bronchioles
often due to chronic necrotizing infections

49
Q

clinical features of bronchiectasis

A

cough (copious, foul smelling, purulent sputum)
hemoptysis
recurrent acute infective exacerbations can lead to severe lung function impairment
dyspnea and wheezing

50
Q

primary causes of bronchiectasis

A 
idiopathic (30-53%)
postinfectious (29-42%)
congenital or hereditary
bronchial obstruction
other
51
Q

pathogenesis of bronchiectasis

A
  1. bronchial obstruction > normal clearing mechanisms are impaired > pooling of secretions distal to obstruction > secondary infection and inflammation
  2. severe infections > inflammation, necrosis, fibrosis, airway dilation
    both paths lead to destruction of bronchiole wall
52
Q

how does bronchiectasis arise in CF

A

inherited defect in ion transport impairs mucociliary action and creates airway obstruction by thick viscous secretions
predisposes to chronic bacterial infections > extensive airway damage > destruction of SM and elastic tissue

53
Q

result of bronchiectasis in CF

A

markedly dilated bronchi and fibrotic obliteration of smaller bronchioles

54
Q

what is primary ciliary dyskinesia

A

autosomal recessive syndrome
defect in ciliary motor protein (dynein)
ciliary function is necessary for proper rotation of organs during development and for bacterial clearance in the sinus and airways
poorly functioning cilia lead to retention of secretions and recurrent infections

55
Q

what is Kartagener’s Syndrome

A

50% of people w primary ciliary dyskinesia have it
situs inversus
bronchiectasis
sinusitis

56
Q

complications of bronchiectasis

A

cor pulmonale
amyloidosis
metastatic brain abscesses

57
Q

management of bronchiectasis

A

treatment of underlying cause
chest physical therapy to facilitate airway clearance
antibiotic therapy

58
Q

histo findings with bronchiectasis

A

necrotizing inflammation of bronchi and bronchioles
fibrosis
atelectasis and intraluminal secretions

RC Test 3 (22 decks)

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