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Pathology pulmonlogy > Pulmonary pathology II: obstructive lung diseases > Flashcards

Pulmonary pathology II: obstructive lung diseases Flashcards

1
Q

Obstructive Lung Diseases

A 
-Airway obstruction due to bronchoconstriction, mucus 
plugging, or inflammation
*Asthma
*Chronic Bronchitis, emphysema (COPD)
*(Bronchiectasis)
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2
Q

obstructive is on

A

exhalation

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3
Q

physiological components

A
  • Decreased FEV1
  • increased total volume
  • increased residual volume
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4
Q

primary effect of obstructive diseases

A

-Primary effect on CO2 retention (decreased ventilation),

not oxygenation

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5
Q

asthma

A

-episodic, reversible, bronchoconstriction due to
increased responsiveness to stimuli
-unpredictable, disabling attacks of severe
dyspnea, coughing and wheezing
-sudden episodes of bronchospasm

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6
Q

status asthmaticus

A

state of unremitting attacksmay prove fatal

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7
Q

three components of asthma

A
  1. bronchoconstriction (acute phase)
  2. airway inflammation (late phase)
    - edema, infiltrates exacerbates luminal narrowing
  3. excess mucous with mucous plugging
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8
Q

what does a decrease FEV1 lead to?

A
  • hyperinflation of lungs
  • decreased expiratory flow more important than obstructive of inspiration
  • air can’t exchange if not exhaled.
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9
Q

asthma classification: extrinsic

A

(allergic, reagin-mediated, atopic)

  • Type 1 hypersensitivity to extrinsic allergen
  • subtypes: atopic, occupational
  • allergic bronchopulmonary aperigellosis (may not be IgE mediated)
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10
Q

asthma classification: intrinsic

A

nonimmune

  • exercise
  • stress
  • pulmonary infections (viruses)
  • inhaled irritants
  • cold
  • aspirin-induced
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11
Q

nonatopic (non-reaginic) asthma

A

most frequently triggered by respiratory tract infection
-viruses (rhinoviruses, parainfluenza virus)
-positive family history uncommon; normal IgE levels
-virus-induced inflammation lowers the threshold of
subepithelial vagal receptors to irritants
-irritants include sulfur dioxide, ozone, and nitrogen
dioxide

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12
Q

pulmonary function test altered by obstructive disease

A

FEV

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13
Q

types of asthma

A

nonatopic (non-reaginic) asthma

occupational asthma

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14
Q

inflammatory mediators/neurogenic signals/smooth muscle responses to irritants are

A
  • IgE mediated de-granulation of mast cells
  • direct mast cell damage or stimulation
  • cholinergic responses action on bronchial sm. muscle
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15
Q

two phases of pathogenesis of asthma

A
  • acute immediate response (minutes to hours)

- late-phase reaction

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16
Q

acute immediate response

A

-takes minutes to hours
-crosslinking of IgE on surface of mast cell
-mast cell degranulation and release of pre-formed
mediators
-mediators open mucosal epithelial junctions leading to
penetration of allergen

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17
Q

what is the respond to mediators for asthma?

A

bronchoconstriction, edema, mucus secretion, flushing, hypotension

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18
Q

what innervation plays a role in asthma?

A

vagal

-atropine can induce bronchoconstriction-> by increased cGMP

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19
Q

mast cell mediators

A
  • Histamine - Minutes to hours
  • Preformed; released from mast cell granules
  • Tissue responses
  • Leukotrienes - Hours
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20
Q

Preformed; released from mast cell granules

A

cross-linking of IgE

- increase in cGMP; increase in cAMP antagonizes degranulation
therapy: increase cAMP; also relaxes smooth muscle

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21
Q

Tissue responses in asthma

A

-smooth muscle contraction
-acute inflammation/edema and increased vascular
permeability
-mediated by H1 receptors

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22
Q

Leukotrienes from mast cells in asthma

A

-formed by release of arachidonic acid on mast
cell activation
-leukotrienes C, D, E – slow reacting substances of
anaphylaxis (SRS-A’s)
-tissue response - sustained smooth muscle contraction
-Leukotriene B - chemotaxis of neutrophils

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23
Q

last phase reaction in asthma

A

-mediated by leukocytes (neutrophils, eosinophils,
and lymphocytes)
-recruited by mast cell cytokines
-histamine from basophils; inflammatory injury
from neutrophils
-major basic protein of eosinophils causes
epithelial damage and airway constriction

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24
Q

morphology in asthma: Gross features

A

-lungs overdistended; hyperinflated; may be
areas of atelectasis
-occlusion of airways by thick, mucous plugs
*contain whorls of shed epithelium “Curschmann’s
spirals”
-eosinophils and Charcot-Leyden crystals (crystalloid
eosinophil membrane protein)

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25
Q

Microscopic features of asthma

A

-thickened basement membrane of bronchial
epithelium
-edema and inflammatory infiltrate in the
bronchial walls
-prominence of eosinophils (5-50% of cells)
-increase in size of submucosal glands +
hypertrophy of the bronchial wall muscle

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26
Q

clinical course of asthma

A

classic attack lasts up to several hours
-prolonged coughing to clear mucous secretions
-status asthmaticus - persists for days or weeks
-more discouraging and disabling than lethal
-progressive hyperinflation may produce
emphysema
-cor pulmonale and heart failure may eventually
develop

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27
Q

chronic bronchitis: patient usually present with

A

patient with persistent cough + sputum production for at least 3 mos. in a least 2 consecutive yrs.

28
Q

types if chronic bronchitis

A
  1. simple chronic bronchitis - productive cough but no
    evidence of airway obstruction
  2. Chronic asthmatic bronchitis - intermittent
    bronchospasm, wheezing - hyper-reactive airways
  3. obstructive chronic bronchitis (heavy smokers) -
    physiologic obstruction +emphysema
29
Q

two factors in chronic Bronchitis pathogenesis

A

1) chronic irritation by inhaled substances

2) microbiologic infections

30
Q

hypersecretion of mucus with mucus plugging happens with

A

secondary obstruction to air flow

secondary infection

31
Q

chronic damage to epithelium with metaplasia in chronic bronchitis

A
  • arge airways – squamous metaplasia

- small airways – goblet cell metaplasia

32
Q

what causes increase in mucus production in chronic bronchitis

A

-associated with hypertrophy of submucosal glands in

trachea and bronchi

33
Q

what are the accompanying alterations to small airways in chronic bronchitis

A

marked increase in goblet cells of small airways; mucus
plugging of the lumen
-inflammatory infiltration
-fibrosis of the bronchiolar wall
-mucosal secretion is under autonomic (vagal) control;
?hypersecretion caused by neurohormonal pathways (also
bronchoconstriction)

34
Q

what drugs for asthma are not helpful in late phase reaction

A

antihistamines and epinephrine do nothing to late phase reactions
-treat with steroids

35
Q

what is co-existent with bronchitis when accompanied with moderate-severe airflow obstruction?

A

emphysema

-dominant lesion

36
Q

role of infection is what in chronic bronchitis?

A

secondary
-not responsible for initiation of chronic bronchitis
-significant in maintaining bronchitis; acute
exacerbations
-cigarette smoke interferes with ciliary action
-also inhibits bronchial and alveolar leukocytes

37
Q

gross features in chronic bronchitis

A

-hyperemia, swelling, bogginess of mucous
membranes
-excessive mucinous to mucopurulent secretions
-heavy casts of secretions and pus

38
Q

morphology of large airways in chronic bronchitis

A

-enlargement of mucus-secreting glands of the trachea and
bronchi (Reid Index)
-ratio of the thickness of mucosal glands to the thickness of wall between the epithelium and the cartilage; normally < 0.4
-increased in proportion to severity and duration of the disease
-squamous metaplasia and dysplasia of large airways

39
Q

hallmark feature of chronic bronchitis

A

increased in size of submucosal glands + hypertrophy of bronchial wall muscle

40
Q

morphology of small airways in chronic bronchitis

A

-marked narrowing of bronchioles - goblet cell metaplasia,
mucous plugging, inflammation, and fibrosis
-most severe cases - bronchiolitis obliterans

41
Q

clinical features of chronic bronchitis

A

-persistent cough with production of copious
sputum
-eventual dyspnea on exertion develops
-hypercapnia, hypoxemia, and mild cyanosis
-long-standing disease leads to cor pulmonale
with cardiac failure
-acute intercurrent bacterial infections

42
Q

emphysema

A

-abnormal permanent enlargement of the airspaces distal to the terminal bronchiole
-enlargement due to destruction of walls without
obvious fibrosis (overinflation)

43
Q

what is involved with emphysema

A

-involves expansion of terminal bronchiole and
acini, including alveolar ducts
-clinical ventilatory deficits early, but not
symptomatic until late

44
Q

two main issues with emphysema

A
  • Decreased FEV1

- Destruction of terminal airways;formation of bullae

45
Q

what causes the decreased FEV1

A 
-collapse/obstruction of terminal airways on 
expiration
-decreased FEV1
-“pink puffers”
-can open airways OK, so well oxygenated
-symptoms occur only after extensive destruction of lung 
tissue
-barrel-chested with faint breath sounds
46
Q

Destruction of terminal airways, formation of bullae

A

Thin-walled coalescing of airspaces; not fibrotic

47
Q

Distinct types of emphysema

A

centriacinar (centrilobular) emphysema
panacinar (panlobular) emphysema
paraseptal (distal acinar) emphysema

48
Q

centriacinar (centrilobular) emphysema

A

-central or proximal parts of the acini formed by the respiratory bronchioles
-both emphysematous and normal airspaces exist
-more common and severe in upper lobes (apical
segments)
-inflammation in septa with deposit of black pigment
-associated with smoking and chronic bronchitis, coal
worker’s pneumoconiosis

49
Q

panacinar (panlobular) emphysema

A

acini are uniformly enlarged including respiratory
bronchiole and terminal blind alveoli
-prefix pan- refers to entire acinus, not entire lung
-occurs more commonly in lower zone and anterior
margins of lung
-most severe at bases
-associated with alpha1-antitrypsin deficiency

50
Q

paraseptal (distal acinar) emphysema

A

proximal portion of acinus is normal; distal portion dominantly involved
-more striking adjacent to the pleura, along tissue
septa, and margins of lobules
-adjacent to areas of fibrosis, scarring, or atelectasis
-more severe in upper half of lungs
-multiple, continuous, enlarged airspaces to > 2.0 cm
-?associated with spontaneous pneumothorax in young

51
Q

main theory behind emphysema pathogenesis

A

protease-antiprotease mechanism
-alveolar wall destruction results from imbalance of
proteases (elastase) and anti-proteases
-increased protease activity leads to break-down of
elastic components in the alveoli and airways
-results in loss of elastic recoil

52
Q

what does the lost of elastic recoil result in?

A

decreased spontaneous release of air from alveoli on
expiration
-terminal airways collapse under positive expiratory pressures due to decreased structural components

53
Q

alpha-1 anti-trypsin deficiency

A

homozygous patients with alpha1-antitrypsin
develop emphysema
-1-AT major inhibitor of proteases including elastase
-The most important therapeutic intervention in alpha1-
antitrypsin deficiency is cessation of smoking.

54
Q

pathogenesis behind A1ATD

A

-principle elastase from neutrophils
-neutrophils normally sequestered in lung (more in
lower zones)
-leads to elastase-mediated destruction of elastin

55
Q

smoking

A

Increased elastase activity
-smokers have greater numbers of neutrophils and macrophages in alveoli secondary to release of IL-8
from activated macrophages
-nicotine is chemotactic for neutrophils and cigarette
smoke activates the alternative complement pathway

56
Q

what does smoking induce?

A

-stimulates elastase from neutrophils and
macrophages (macrophage elastase is NOT inhibited
by alpha1-AT)
-oxidants in cigarette smoke and oxygen free radicals
inhibit alpha1-AT activity

57
Q

macroscopic features in centriacinar

A

not as voluminous; upper 2/3 affected

58
Q

macroscopic features of panacinar

A

voluminous lungs

59
Q

what are large apical blebs typical of?

A

-large apical blebs or bullae characteristic of irregular emphysema secondary to scarring

60
Q

microscopic morphology of emphysema

A

-abnormal fenestrations and destruction of septal
walls
-fusion of alveoli to form blebs or bullae
-respiratory bronchioles and vasculature deformed
and compressed by distortion of airspaces

61
Q

clinical manifestations in emphysema appear when

A

-do not appear until at least 1/3 of functioning parenchyma is
incapacitated

62
Q

clinical symptoms of emphysema

A
  • dyspnea progresses; may see cough or wheezing
  • weight loss may be severe
  • slowing of forced expiration
  • barrel-chested with prolonged expiratory effort
63
Q

senile emphysema

A

age-related alterations of the internal geometry of the lung (larger alveolar ducts and smaller alveoli)

64
Q

obstructive overinflation

A

trapping of air

65
Q

bullous emphysema

A

(>1 cm in distended state); often apical, associated with scarring; may give rise to pneumothorax

66
Q

interstitial emphysema

A

entrance of air into connective tissue stroma, mediastinum, or subcutaneous tissue

Pathology pulmonlogy (5 decks)

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