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Pulmonary Week 2 > ICL 3.1: Pathology of Obstructive Lung Diseases > Flashcards

ICL 3.1: Pathology of Obstructive Lung Diseases Flashcards

1
Q

how many lobes do the lungs have?

A

right = 3

left = 2

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2
Q

describe the left and right bronchus?

A

right bronchus is slight shorter than the left

right bronchus arises a little proximally and at a steeper angle than the left

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3
Q

what type of cells are in the trachea/bronchi?

A

pseudostratified columnar, ciliated epithelial cells

there’s submuscoasl glands and cartilage too

bronchioles lack cartilage and submucosal glands; the smaller bronchioles are lined by conciliated clara cells

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4
Q

what is the conducting portion of the respiratory system?

A

conducting = trachea –> terminal bronchiole

respiratory = acinus

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5
Q

what is the acinus?

A

the terminal respiratory unit that consists of the respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli

a lobule consists of 3-5 terminal bronchioles with associated acini

in emphysema, this is what’s effected!

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6
Q

what is the structure of an alveolus?

A
  1. capillaries lined by endothelial cells
  2. in the alveolus itself, there’s type i and II pneumocytes

type I cover 95% of the alveolus and the function for gas exchange

type II are only 5% but they synthesize surfactant and they can divide and become type I pneumocytes if there’s injury

  1. alveolar macrophages = dust cells –> can become heart failure cells when they phagocytose hemocydrin
  2. supporting tissue rich in elastin
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7
Q

what are obstructive pulmonary diseases?

A

a group of diseases characterized by an increase in the resistance to airflow due to partial or complete obstruction at any level of the tracheobronchial tree

there’s a blockage of air going in and out!

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8
Q

what are the common features of obstructive pulmonary diseases?

A
  1. dyspnea
  2. chronic or recurrent obstruction to airflow within the lung
  3. limitation of maximal airflow rates during forced expiration (FEV1/FVC < 0.8)
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9
Q

which diseases are entailed when you’re talking about COPD?

A
  1. emphysema
  2. bronchitis

COPD is the 4th major cause of morbidity and mortally in the USA

asthma may also be a component of COPD but it’s only transient; emphysema and bronchitis are irreversible

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10
Q

what is the anatomic site, major pathologic changes, etiology and signs/symptoms of chronic bronchitis?

A

anatomic site = bronchus

pathologic changes = submucousal gland hyperplasia and hyper-secretion

etiology = tobacco smoke, air pollutants

symptoms = productive cough, sputum production

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11
Q

what is the anatomic site, major pathologic changes, etiology and signs/symptoms of bronchiectasis?

A

anatomic site = bronchus

pathologic changes = airway dilation and scarring

etiology = persistent or severe infections

symptoms = productive cough with purulent sputum, fever

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12
Q

what is the anatomic site, major pathologic changes, etiology and signs/symptoms of asthma?

A

anatomic site = bronchus

pathologic changes = smooth muscle hyperplasia, excess mucus, goblet cell hyperplasia, inflammation

etiology = immunological or undefined causes

symptoms = episodic wheezing, cough, dyspnea

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13
Q

what does wheezing vs crackles signify?

A

if you hear wheezing, think of bronchiole diseases

if you hear crackles/bubble sounds, think of alveolar problems

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14
Q

what is the anatomic site, major pathologic changes, etiology and signs/symptoms of emphysema?

A

anatomic site = acinus

pathologic changes = airspace enlargement, wall destruction*

etiology = tobacco smoke

symptoms = dyspnea

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15
Q

what is the anatomic site, major pathologic changes, etiology and signs/symptoms of small-airway disease/bronchiolitis?

A

anatomic site = bronchiole

pathologic changes = inflammatory scarring/obliteration

etiology = tobacco smoke, air pollutants, miscellaneous

symptoms = cough, dyspnea

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16
Q

what is asthma?

A

bronchial hyper-responsiveness triggered by allergens, infection, etc.

reversible obstruction that’s type I hypersensitivity mediated

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17
Q

54 year old male present with productive cough for 5 months and has been a smoker since 14. his cough is associated with SOB and a year ago he was treated for pneumonia even though cultures were negative. PE shows bilateral wheezes in the chest

diagnosis?

A

chronic bronchitis caused by chronic irritation from smoking

dyspnea + productive cough that lasts 5 months = chronic bronchitis

mucous caused superimposed pneumonia infection

wheezes = bronchiole disease

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18
Q

what is the required clinical criteria to diagnose chronic bronchitis?

A
  1. persistent cough with sputum production
  2. present for at least 3 months per year
  3. present for at least 2 consecutive years
  4. in the absence of any other identifiable cause
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19
Q

what is the pathogenesis of chronic bronchitis?

A

chronic irritation by inhaled substances (smoking)

microbiologic infections trigger acute exacerbation and maintain chronic bronchitis

most frequent in middle-aged male smokers

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20
Q

what are the morphologic changes in chronic bronchitis?

A
  1. mucous hypersecretion in large airways
  2. hypertrophy and hyperplasia of submucosal glands

this results in extra mucous produced in cough which is reported via the Reid index

  1. hyperplasia of goblet cells in bronchi and bronchioles
  2. variable degree of chronic inflammation and fibrosis – bronchiolitis obliterans
  3. squamous metaplasia and dysplasia
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21
Q

what is the Reid index?

A

thickness of submucous gland layer/thickness of the wall between epithelium and cartilage

normally the Reid index is 0.4 but with chronic bronchitis there’s an increase in the Reid index because there’s metaplasia of the submucosal goblet cells

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22
Q

what are the clinical features of chronic bronchitis?

A
  1. initial cough with productive sputum
  2. later dyspnea on exertion
  3. hypoxemia, mild cyanosis
  4. cor pulmonale with heart failure = JVD, peripheral edema, ascites, hepatomegaly
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23
Q

what is the hallmark name for patients with chronic bronchitis?

A

low pO2 = cyanosis = blue bloaters!

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24
Q

65 year old male with severe SOB for the last several months. smoker for 50 years. PE reveals a barrel chest. CXR reveals a flat diaphragm.

diagnosis?

A

emphysema

no mucous or cough, just SOB

flat diaphragm and barrel chest = lungs are over-inflated

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25
Q

what is the required morphologic criteria needed to diagnose emphysema?

A
  1. abnormal permanent airspace enlargement
  2. involvement distal to terminal bronchiole
  3. airspace wall destruction**
  4. lack of significant interstitial fibrosis
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26
Q

what is the incidence of emphysema?

A

more common and severe in males

clear association with cigarette smoking

generally does not become disabling until the 4th-7th decades but ventilatory deficits may make their first appearance decades earlier

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27
Q

how is emphysema classified?

A

it’s based on the anatomic distribution of the damage in the lobule

  1. centriacinar = proximal acinar is involved
  2. panacinar = the whole acinar is involved
  3. paraseptal = subpleural and upper half of the lungs is involved
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28
Q

which types of emphysema are the most common?

A

centrilobular accounts for > 95% of the cases

clinically significant airway obstruction is seen in both centriacinar and panacinar emphysema

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29
Q

what is centriacinar emphysema?

A

it starts in the respiratory bronchioles and destroys the central (proximal) parts of the acinus

both emphysematous and normal areas exist in the same acinus and lobule

predominately involves the upper lobes; especially apical segments

it’s more frequent in heavy smokers so it’s often seen in associated with chronic bronchitis

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30
Q

what is paniacinar emphysema?

A

associated with alpha-antitrypsin deficiency which normally inhibits proteases that break down elastin in the walls of the alveoli

more common in lower lobes and in the anterior margins of the lungs so it’s most severe in the lung bases –> it’s most common in the bases because that’s where there’s the most blood flow and the blood is what brings in all the inflammatory cells and neutrophils are sequestered in the lungs in the lower lobes and they release elastase!

it affects the ENTIRE acinus but there’s initial involvement of the peripheral alveoli and alveolar ducts

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31
Q

compare and contract centriacinar and panacinar emphysema

A

centiracinar
1. upper lobes

  1. cigarette smoking
  2. involves the central portion of the acinus

panacinar
1. lower lobes

  1. alpha antitrypsin deficiency
  2. involves the entire acinus
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32
Q

what is the pathogenesis of emphysema?

A

protease-antiprotenase theory

proteases are enzymes that digest proteins

alveolar wall destruction results from an imbalance of elastase, a protease, and alpha-antitrypsin, an antiprotenase

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33
Q

how does centriacinar emphysema happen?

A

smoke particles impact in small bronchi and bronchioles and form ROS that inactivate antiproteases while increasing inflammatory cytokines

then an influx of neutrophils and macrophages which leads to increased elastase

more common in the upper lobe because it’s less perfusion and there’s less α1-AT and smoke rises

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34
Q

how does panacinar emphysema happen?

A

α1-AT deficiency throughout acinus

neutrophils are normally sequestered in lungs, more in lower than upper lobe – neutrophils release elastase! so that’s why there’s more damage in the lower lobes with apnacinar emphysema

more common in the lower lobe – more perfusion

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35
Q

what are the clinical features of emphysema?

A

dyspnea is the initial symptom –> symptoms appear when at least 1/3 of the parenchyma is effected

not too much cough or sputum; you’ll only see it if there’s accompanying chronic bronchitis

when there’s severe emphysema, you’ll see marked inflation of the lungs, barrel chest, and flattened diaphragm

you’ll also see weight loss because of how hard it is to breath and enlargement of accessory muscles of respiration

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36
Q

what causes death in emphysema?

A
  1. respiratory acidosis and coma
  2. right sided heart failure
  3. massive lung collapse second to pneumothorax

some of the expanded alveoli can rupture and release air into the pleura

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37
Q

what is the hallmark name for people with emphysema? what are the hallmark signs of emphysema?

A

pink puffers

they have dyspnea because of the low pressure during expiration that will cause their lungs to collapse without elastin; so they pinch their nose and purse their lips and sit forward to try and increase the pressure in their lungs so that their bronchioles don’t collapse as much and this is where they get the name pink puffers!

they have to use accessory muscles of respiration to do this (so check for their enlargement) and they have prolonged, forced expiration so they lose a ton of weight because of how hard it is to breathe

oxygen saturation is maintained at near normal levels from over inflation of the lungs so they’re not cyanotic, they remain pink

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38
Q

36 year old female with jaundice and SOB for 6 months. her material aunt died at the age of 45 from hepatic failure.

diagnosis?

A

alpha1-antitrypsin deficiency

the alpha1 produced in the liver can’t leave the liver so it destroys hepatocytes and you get cirrhosis on top of the emphysema

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39
Q

what is alpha1-antitrypsin deficiency?

A

α1-AT is produced by liver and inhibits a variety of proteases (specifically elastase)

it accounts for 90% of antiprotease activity in the blood and without it, neutrophil elastase digests the human lung

production of alpha-AT depends on a pair of co-dominant alleles – Pi (protease inhibitor) gene on chromosome 14*.

think α1-AT deficiency when individual is diagnosed with emphysema at < 40 yrs of age

  • Normal phenotype Pi MM but alpha-antitrypsin deficiency has phenotype Pi ZZ
40
Q

20 year old male develops sudden onset left sided sharp chest pain

PE = hyper-resonance over left upper lobe

CXR = pneumothorax

diagnosis?

A

paraseptal emphysema

hyper resonance = lots of air in the pleural cavity

sharp pain = pleura

41
Q

what is paraseptal emphysema?

A

involves predominantly the distal portion of the acinus

usually more severe in upper half of lung

most prominent near the pleura, along the lobular connective tissue septa and at the margins of the lobules

**associated with spontaneous pneumothorax in young male adults

42
Q

40 year old female present with dyspnea for 2 years. CXR reveals flat diaphragm. routine lab tests reveal elevated AST and ALT?

diagnosis?

A

alpha1-antitrypsin deficiency

43
Q

what is overinflation?

A

enlargement of air spaces WITHOUT destruction so it’s NOT emphysema

44
Q

what is compensatory hyperinflation?

A

distension of airspace’s in the preserved lung after unilateral pneumonectomy or lobectomy

45
Q

what is obstructive overinflation?

A

patient breaths in but can’t get any of the air out

may be life threatening

usually occurs when there’s a tumor or we inhale a foreign body

46
Q

what is congenital overinflation?

A

congenital lobar overinflation in infants due to hypoplasia of bronchial cartilage

without cartilage in the bronchioles, you can’t exhale because the bronchioles are flacid and they’ll collapse during expiration and trap air

47
Q

5 year old with sudden onset severe dyspnea and paroxysmal cough with copious sputum. he was visiting his grandmother and played with her new puppy.

diagnosis?

A

asthma

48
Q

what is asthma?

A

chronic, relapsing inflammatory disorder characterized by tracheobronchial hyper-reactivity leading to paroxysmal, reversible airway narrowing (episodic bronchoconstriction)

two major components:
1. chronic airway inflammation

  1. hyperactive bronchial tree

relapsing = comes and goes

it’s reversible! so it doesn’t last

49
Q

who does asthma effect?

A

10% of kids

5% of adults

1/2 the cases develop i patients under 10 years old

there has been a significant increase in the incidence of asthma in the Western world in the past 3 decades

50
Q

what are the 2 types of asthma?

A
  1. extrinsic (immune)

2. intrinsic (non-immune)

51
Q

what is extrinsic asthma?

A

caused by exposure to extrinsic antigen

caused by type I IgE hypersensitive; usually begins in childhood

often there’s a family history of allergy or associated allergies like dust, pollen, food

cause by:
1. atopic (allergic) – most common

  1. occupational
  2. allergic bronchopulmonary aspergilliosis
52
Q

what is intrinsic asthma?

A

non-immune mechanism usually in adults

often there’s no family history of allergy or associated allergies

most common cause is respiratory tract infections like viruses

caused by:
1. drug induced (e.g. aspirin = AERD)

  1. pulmonary infections, especially viral
  2. inhaled irritants
  3. stress
  4. exercise
  5. cold
53
Q

30 year old male non-smoker present with sudden onset dyspnea following a flu like ilness

diagnosis?

A

intrinsic asthma

it is thought that virus-induced inflammation of respiratory mucosa lower the threshold of the subepithelial vagal receptors to irritants

54
Q

which substances in the body are bronchioconstrictors?

A
  1. leukotrienes, C4, D4, and E4
  2. acetylcholine
  3. histamine
  4. prostaglandins

these are all associated with asthma!

55
Q

what is the cyclooxyrgenase pathway?

A

prostaglandins –> prostacyclin –> vasodilation and increased vascular permeability

PGD2 causes vasodilation acting via the prostaglandin (DP) receptor on vascular smooth muscle, and myocontraction acting via the thromboxane (TP) receptor on bronchial smooth muscle

they play a role in the bronchospasm associated with asthma

56
Q

what does lipoxygenase do in the body?

A

produces leukotrienes like C4, D4, E4 which all cause bronchospasm and increased vascular permeability

they play a role in the bronchospasm associated with asthma

57
Q

what are the mediators involved with asthma?

A
  1. leukotrienes, C4, D4, and E4*
  2. acetylcholine
  3. histamine*
  4. prostaglandins
  5. platelet activating factor* which causes platelet aggregation and release of histamine and serotonin from their granules
  6. cytokines, IL1, TNF, IL6
  7. major basic protein of eosinophils which cause epithelial damage in the bronchus
58
Q

what is the genetic form of asthma?

A
  1. ADAM 33*
  2. IL4 receptor gene variants
  3. YKL-40*
  4. class II HLA alleles
59
Q

what is ADAM33?

A

ADAM33 belongs to a subfamily of metalloproteinases,mainly collagenases

ADAM33 is expressed on lung fibroblasts and bronchial smooth muscles

polymorphism accelerates proliferation of bronchial smooth muscle cells and fibroblasts which leads to narrowing of the bronchus

the above contributes to bronchial hyperactivity and subepithelial fibrosis that is associated with asthma

60
Q

how is IL4 associated with asthma?

A

IL4 receptor gene variant are associated with atopy and increased age and asthma

atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema)

61
Q

how is YKL-40 associated with asthma?

A

it’s a specific chitinases that is associated with asthma

it triggers TH2 inflammation

serum levels of YKL-40 correlates with the severity of asthma

62
Q

which drugs can induce asthma?

A

aspirin and NSAIDS inhibit COX pathway of arachidonic acid metabolism without effecting lipoxygenase pathway

this leads to decreased prostaglandin synthesis and increased production of leukotrienes = bronchoconstriction and increased permeability

urinary LTE4 levels are a marker of systemic cysLT production and are increased in AERS

63
Q

what is the triad of aspirin induced asthma?

A
  1. recurrent rhinitis/sinusitis
  2. nasal polyps
  3. asthma and often urticaria
64
Q

what are the microscopic features of asthma?

A
  1. mucous plugs in the lumen
  2. elevated eosinophil count*
  3. bronchial wall changes = airway remodeling!
    - thickened basement membrane
    - edema and inflammatory infiltrate of the bronchial wall, prominence of eosinophils and mast cells
    - hypertrophy of submucosal glands
    - hyperplasia of goblet cells in the mucosa
    - hypertrophy of smooth muscle
65
Q

what are the 2 histological hallmarks of asthma?

A
  1. charcot-leyden crystals

formed from eosinophil major basic protein – look like swords

  1. Curschmann spirals

strands of mucous to which epithelial cells may be attached/trapped

66
Q

what causes airway obstruction in asthma?

A
  1. primarily muscular contraction
  2. edema and inflammatory infiltrate

eosinophils and mast cells are the major components of the inflammatory infiltrate

eosinophils are destructive because of the major basic protein while mast cells release histamine

67
Q

what are the clinical features of asthma?

A

attacks that last several hours with wheezing, respiratory distress followed by prolonged cough and copious sputum

it’s a lot of recurrent attacks that are more disabling rather than lethal and the disease can disappear spontaneously

68
Q

what is status asthmatics?

A

incredibly severe bronchoconstriction associated with asthma that can last several days

they can die from ventilatory compromise

69
Q

what is bronchiectasis?

A

chronic necrotizing infection of the bronchi and bronchioles leading to irreversible dilation of these airways from destruction of the muscle and elastic tissue

usually associated with hereditary conditions or post infectious conditions

dilatation must be permanent

70
Q

25 year old male who had a common variable immunodeficiency diagnose when he has 10 years old presents with productive cough with foul smelling sputum for 6 months

CXR reveals prominent dilated bronchi

sputum grows psuedomonas aeruginosa

diagnosis?

A

bronchiectasis

low immunoglobulins and CD4 cells with immunocompromised people! makes them susceptible to bacteria

foul smelling is from pus in the bronchi

71
Q

which hereditary conditions are associated with bronchiectasis?

A
  1. cystic fibrosis
  2. immunodeficiency states
  3. Kartagener’s syndrome
72
Q

which conditions cause bronchiectasis?

A

any infection or objstruction that damages and permanently enlarges and thickens the bronchioles such as:

  1. hereditary conditions –> CF, immunodeficiency states, Kartagener’s
  2. posinfectious conditions –> necrotizing pneumonia
  3. bronchial obstruction
  4. post-transplant
73
Q

what is the pathogenesis of bronchiectasis?

A
  1. infection –> inflammation –> necrosis and fibrosis –> dilated airways
  2. obstruction –> normal clearing mechanisms impaired –> airway inflammation and pooling of bronchial secretions

obstruction and infection are important in the development of bronchiectasis

74
Q

what are the gross morphological changes associated with bronchiectasis?

A

generally effects the lower lobes bilaterally

most severe in the distal bronchi and bronchioles

airways may be dilated 4x normal size! they get so big that the bronchi can generally be followed to the pleural surface on gross examination

transected bronchi look like cysts filled with mucopurulent material/pus

75
Q

what are the microscopic changes associated with bronchiectasis?

A

ACTIVE DISEASE
1. acute chronic inflammatory exudate in walls of bronchi and bronchioles

  1. desquamation of the lining epithelium
  2. necrosis and ulceration of the wall
  3. squamous metaplasia*
  4. abscess formation*

CHRONIC DISEASE
1. fibrosis of the walls of the bronchi and bronchioles

  1. subtotal or total obliteration of bronchiolar lumen
76
Q

what are the clinical features of bronchiectasis?

A
  1. foul smelling sputum*
  2. hemoptysis
  3. paroxysmal cough worse in the morning from changing position draining pus into bronchi
  4. dyspnea and wheezing*
  5. pneumonia, lung abscess
  6. fever, weight loss, weakness
  7. cor pulmonale*, metastatic brain abscess, amyloidosis
77
Q

what is obstructive lung disease?

A

increased resistance to airflow due to partial or complete obstruction from trachea to respiratory bronchioles

78
Q

what is restrictive lung disease?

A

reduced expansion of lung parenchyma with decreased total lung capacity

79
Q

eosinophil basic protein

A

asthma

EBP damages epithelium

80
Q

elastase

A

emphysema

81
Q

PIZZ phenotype

A

emphysema

alpha1-antitrypsin deficiency phenotype

82
Q

ADAM 33

A

asthma

83
Q

YKL40

A

asthma

84
Q

charcot leyden cystals

A

asthma

made of major basic protein from eosinophils

85
Q

alveolar wall destruction

A

emphysema

86
Q

viral infections

A

extrinsic asthma

87
Q

goblet cell hyperplasia

A

asthma

88
Q

leukotriens

A

asthma

89
Q

foul smelling sputum

A

bronchiecstasis

90
Q

dilated bronchi with thick walls

A

bronchiecstasis

91
Q

emphysema + impaired liver function in 40 year old

A

alpha1-antitrypsin deficiency

92
Q

wheezing

A

bronchi

93
Q

crackles

A

alveoli

94
Q

thick bronchial basement membrane + eosinophilia

A

asthma

95
Q

mucus stands + trapped cells

A

Curschmann spirals

asthma

Pulmonary Week 2 (9 decks)

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