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Pulmo Flashcards

1
Q

Unit of respiration

A

Bronchioles (w/o cartilage and submuco)-> terminal bronchiole -> acinus -> respi bronchiole -> alveolar duct -> alveolar sac -> alveoli

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2
Q

Permit passage of bacteria, exudates, air between alveoli

A

Pores of Kohn

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3
Q

Loss of lung volume by inadequate expansion of air spaces

A

Atelectasis

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4
Q

When obstruction prevents air from reaching distal airway
Air present becomes aborbed and alveolar collapse follows
Usually by mucus

A

Resorption atelectasis

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5
Q

Passive, relaxation
Accumulation of fluid, blood or air within pleura mechanically collapsing adjacent lung
Pleural effusion
Pneumothorax

A

Compression pneumothorax

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6
Q

Cicatrization

Local or generalized fibrotic changes in lung or pleura hamper expansion and inc elastic recoil during expiration

A

Contraction atelectasis

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7
Q

Bilateral (endothelial and epithelial) damage

A

Acute lung injury

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8
Q

ALI caused by (3)

A

1 acute onset dyspnea
2 dec arterial oxygen pressure (hypoxemia)
3 bilateral pulmo infiltrates on chest

In absence of L heart failure (non cardiogenic pulmonary edema)

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9
Q

Clinical syndrome by diffuse alveolar capillary and epithelial damage
Rapid life-threatening respiratory insufficiency, cyanosis, severe arterial hypoxemia refractory to oxygen therapy -> multiple organ failure

A

Acute Respiratory Distress Syndrome

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10
Q

ARDS histo pathognomonic

A

Diffuse alveolar damage (DAD)

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11
Q

ARDS is caused by imbalance of

A

pro inflammatory and anti inflammatory mediators

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12
Q

Cells with important role in ARDS

Called by

A

Neutrophils

IL-8

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13
Q

Mediators involved in ARDS

A 
IL-8
IL-1
Macrophage
Neutrophil
TNF B, PDGF

Balanced by IL-10 (anti inflam)

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14
Q

Vascular leakiness and loss of surfactant render the unit unable to expand but the degree of injury and severity is determined by

A

Balance between destructive and protective factors

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15
Q

Dark red, firm, airless and heavy
Capillary congestion, necrosis of epithelial cell, interstitial and intra-alveolar edema and hemorrhage
Neutrophil in capillary

A

Acute phase of ards

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16
Q

Most characteristic finding

Fibrin-rich edema fluid admixed with remnants of necrotic epithelial cell

A

Hyaline membrane

Similar to rds in newborn

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17
Q

Vigorous proliferative type II pneumocyte to regenerate alveolar lining
Organization of fibrin exudate with intra-alveolar fibrosis
Thickening of septa by proliferation of interstitial cell and collagen dep

A

Organizing stage of ARDS

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18
Q

85% of patients with ALI or ARDS develop within

A

3 days after injury

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19
Q

Syndrome of progressive respiratory insufficiency by diffuse alveolar damage in setting of sepsis, severe trauma or diffuse pulmonary infection

A

ARDS

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20
Q

Alveolar edema, epithelial necrosis, accum of neutrophil, hyaline membrane lining alveoli

A

ARDS

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21
Q

Diffuse obstructive disorders

A

Emphysema
Chronic bronchitis
Bronchiectasis
Asthma

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22
Q

In obstructive lung disease,

FVC
FEV1
FEV/FVC Ratio

A

FVC normal or slightly decreased
FEV1 SIGNIFICANTLY decreased
Ratio DECREASED

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23
Q

In diffuse restrictive disease,

FVC
FEV
FEV/FVC ratio

A

FVC decreased
FEV normal or dec proportionately
FEV/FVC ratio: Near Normal

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24
Q

Restrictive diseases causes by (2)

A

1 chest wall disorder in a normal lung (obesity, pleural problem, GBS)
2 acute or chronic ILD (pneumoconiosis, intersitial fibrosis, sarcoidosis)

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25
Q

Abnormal permanent enlargement of air spaces with destruction of walls distal to terminal bronchioles and without fibrosis

A

Emphysema

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26
Q

Site: Bronchus
Mucuous gland hypertrophy and hyperplasia with hypersecretion
Tobacco smoke, air pollutant
Cough and sputum production

A

Chronic bronchitis

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27
Q

Site: Bronchus
Airway dilation and scarring
Persistent and severe infection
Cough, purulent sputum and fever

A

Bronchiectasis

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28
Q

Site: Bronchus
Smooth muscle hypertrophy, hyperplasia, excessive mucus and inflammation
Immunologic and undefined cause
Episodic wheezing, cough, dyspnea

A

Asthma

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29
Q

Site: Acinus
Air space enlargement, wall destruction
Tobacco smoke
Dyspnea

A

Emphysema

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30
Q

Site: bronchiole
Inflammatory scarring, partial obliteration of bronchiole
Tobacco smoke, air pollutant
Cough, dyspnea

A

Small airway disease

Bronchiolitis

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31
Q

Small airway disease
Alveolar wall destruction
Overinflation

A

Emphysema

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32
Q

Small airway disease
Productive cough
Airway inflammation

A

Chronic bronchitis

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33
Q

Reversible obstruction

Bronchial hyperresponsiveness by allergen, infection

A

Asthma

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34
Q

Cluster of 3-5 acinu

A

Lobule

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35
Q

4 major types of emphysema

A

Centriacinar
Panacinar
Distal acinar
Irregular

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36
Q

Central or proximal acini formed by respiratory bronchioles affected with sparing of distal alveoli

A

Centriacinar

Centrilobular

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37
Q

Centriacinar lesions are located in

A

upper lobes

apical

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38
Q

Centriacinar emphysema occurs bec of

A

Smoking in people without alpha1 antitrypsin deficiency

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39
Q

acini uniformly enlarged from bronchiole to terminal blind alveoli
alpha1 antitrypsin deficiency

A

Panacinar

Panlobular emphysema

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40
Q

Pancinar emphysema tends to occur

A

On lower lung zones and in alpha 1 antitrypsin deficiency

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41
Q

Distal emphysema proximal portion of acinus normal but distal is primarily involved
More striking adjacent to pleura along lobular CT septa at margin of lobule and adjacent to areas of fibrosis, scarring and atelectasis

A

Distal acinar

Paraseptal

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42
Q

Distal acinar paraseptal emphysema is more common in

A

upper half of lungs

43
Q 
Multiple contiguous large spaces ranging in diameter from less than 0.5 to more than 2 cm 
Cystic structure with progressive enlargement becoming bullae
Cause unknown (spontaneous pneumothorax)
A

Distal acinar paraseptal emphysema

44
Q

acinus irregularly involved
invariably associated with scarring from healed inflammatory disease
Most common form

A

Irregular emphysema

45
Q

Atelectasis pathogenesis

A

Toxic exposure (tobacco and pollutants)
Inflammation with neutrophil, mac, IL8 and oxidant
Epithelial injury and proteolysis of ECM, elastin degradation

46
Q

80% of patients with congenital alpha 1 antitrypsin def develops

A

panacinar emphysema

47
Q

Gene polymorphism influence susceptibility to development of COPD resulting to inadequate repair of elastin injury

48
Q

Results from insufficient wound repair, loss of epithelial, endothelial and mesenchymal cell

49
Q

Pathogenic role in emphysema

A

MMP 9 and 12

50
Q

Pale voluminous lung obscuring heart at autopsy

A

Panacinar emphysema

51
Q

Deep pink less voluminous with upper 2/3 affected
Destruction of alveolar walls without fibrosis with enlarged spaces
Dec alveolar capillaries
Loss of elastic tissue
Bronchiolar inflamm and submucosal fibrosis

A

Centriacinar emphysema

52
Q

Barrel chested
Dyspneic
Prolonged expiration
Sitting forward hunched position
Severe air space enlargement and low diffusing capacity
Pink puffer bec of dyspnea and adequate oxygenation

A

Emphysema without bronchitic component

Pink puffer

53
Q

Pronounced chronic bronchitis
History of recurrent infection with purulent sputum
Less prominent dyspnea with diminished drive
Retains CO2, hypoxic and cyanotic
Obese
Blue bloater
CHF/Cor pulmonale

A

Blue bloaters

54
Q

Arises from pulmonary vascular spasm inducing hypoxia and loss of pulmo capillary surface from alveolar destruction

A

Secondary pulmonary hypertension

55
Q

Compensatory dilation of alveoli in resp to loss of lung substance elsewhere
Surgical removal of lobe

A

Compensatory emphysema

56
Q

Lung expansion bec of air trapping
Subtotal obstruction by tumor or foreign object
Life threatening

A

Obstructive overinflation

57
Q

Large subpleural bleb or bullae >1cm diameter

Subpleural and may rupture leading to pneumothorax

A

Bullous emphysema

58
Q

Air entry into CT of lung, mediastinum and subcu tissue
Inc intraalveolar pressure (vomiting or whooping cough), partial obstruction of bronchiole on respirator, fractured rib
Swelling of head and neck with chest crepitation

A

Mediastinal interstitial emphysema

59
Q

Persistence of productive cough for at least 3 consecutive months in at least 2 consecutive years

Smokers and cigarette dwellers aged 40-65y M

A

Chronic bronchitis

60
Q

Distinctive feature of chronic brochitis

Single most important cause

A

Hypersecretion of mucus in large airway

Smoking

61
Q

Cigarette and pollutants induce

A

hypertrophy of mucous glands in trachea and main bronchi

Marked inc in mucin-secreting globlet cell with infiltration of CD8 lympho, mac and neutro without eo

62
Q

Morphologic basis of airflow limitation in chronic bronchitis

A

1 peripheral, small airway disease (goblet cell metaplasia with mucus plug, inflamm and wall fibrosis)
2 coexistent emphysema

63
Q

Mucus secretion is mediated by

A

IL 13 from T cell

64
Q

Tobacco exposure induces

A

transcription of mucin gene MUC5AC and neutrophil elastase

65
Q

Coexistent secondary role in maintaining inflamm and exacerbating symptom

A

Microbial infection

66
Q

Hyperemic swollen airway

Mucinous secretion with enlargement of glands

A

Chronic bronchitis

67
Q

Ratio of thickness of submucosal gland layer to that of bronchial wall

N =

A

Reid index

0.4

68
Q

Goblet cell metaplasia, mucous plugging, inflammation, fibrosis
Complete obliteration of lumen due to fibrosis

A

Chronic bronchiolitis

69
Q

Intermittent reversible airway obstruction
Chronic bronchial inflamm with eosinophil
Bronchial smooth muscle cell hypertrophy and hyperactivity
Inc mucus secretion

70
Q

Hygiene hypothesis

A

Eradication of infection alter immune homeostasis and promote allergic and harmful immune response

71
Q

Evidence of allergen sensitization in a patient with allergic rhinitis, emphysema

72
Q

Bronchospasm is triggered by

A 
Respiratory infection - viral
Irritants 
Cold air
Stress 
Exercise
73
Q

Etiologic factors of asthma

A

1 genetic predisposition to Type I hypersensitivity (atopy)
2 acute and chronic airway inflammation
3 bronchial hyperresponsiveness

74
Q

Critical role in the pathogenesis of asthma

A

TH2 helper t cell

75
Q

Excessive TH2 reaction against environmental agents

Cytokines produced

A

Classic atopic form

IL4
IL5
IL13

76
Q

stimulates IgE production

77
Q

Activates eosinophil

78
Q

Stimulated mucus production and promotes IgE by B cell

79
Q

Bronchoconstriction
Inc mucus production
Variable vasodilation

A

Early immediate reaction

80
Q

Inflammation
Activation of eosinophil, neutro and T cell
Chemokine production that recruit more TH2 and eo

A

Late phase reaction

81
Q

Chemoattractant and activator of eo

82
Q

Structural changes from repeated inflammation

Hypertrophy of smooth muscle and mucus gland
Inc vascularity and
Subepithelial collagen deposition

A

airway remodelling

83
Q

Susceptibility loci of asthma

A

Long arm of ch 5q (IgE, mast cell and eo)

ch 20q ADAM 33 (proliferation of bronchial smooth ms and fibroblast) - airway remodelling

84
Q

High serum YKL 40 correlates

A

with severity of asthma

85
Q

Most common type of asthma
Positive family history of atopy
By various environmental trigger

A

Atopic asthma

86
Q

Atopic asthma is an example of

A

Type I IgE mediated hypersensitivity reaction

87
Q

No evidence of allergen sensitization
Negative skin test result
Triggered by respiratory infection due to viruses and inhaled air pollutants

A

Non-atopic form

88
Q

Virus induced inflamm of respiratory mucosa lowers

A

threshold of subepithelial vagal receptor to irritant

89
Q

Drug that provokes asthma

A

Aspirin

Recurrent rhinitis and nasal polyp, urticaria and bronchospasm

90
Q

Stimulated by fumes (epoxy resin, plastic), organic and chemical dust and gases

A

Occupational asthma

91
Q

Occlusion of bronchi and bronchiole by thick tenacious mucous plug

92
Q

Whorls of shed epithelium

A

Curschmann spirals

93
Q

Crystalloid made up of eosinophil protein

A

Charcot-Leyden crystal

94
Q

Severe dyspnea, wheezing
Difficulty in expiration with difficulty to get air in and out leading to progressive hyperinflation with distal air trapping

95
Q

Severe paroxysm not responding to therapy and persisting for days and weeks

A

Status asthmaticus

96
Q

Key inflammatory cell in all subtypes of asthma

Produce MBP

A

Eosinophil

97
Q

Airway remodelling

A

Subbasement membrane thickening

Hypertrophy of bronchial gland and smooth muscle

98
Q

Permanent dilation of bronchi and bronchiole by destruction of ms and elastic tissue assoc with necrotizing infection

Secondary persisting to infection or obstruction

Cough, expectoration of copious amounts aof purulent sputum

A

Bronchiectasis

99
Q

Tumors, foreign body, mucus impaction

Localized to obstructed lung segment

A

Bronchial obstruction

100
Q

Widespread severe bronchiectasis from obstruction by secretion of viscid mucus

A

Cystic fibrosis

101
Q

Rare autosomal recessive associated with bronchiectasis and sterility in males
Structural abnormalities of cilia impair mucociliary clearance leading to persistent infection and reduces mobility of spermatozoa

A

Kartegener syndrome

102
Q

Pathogenesis of bronchiectasis

A

1 obstruction

2 chronic persistent infection

103
Q

Bronchiectasia affects the

A

lower lobes bilaterally particularly air passages that are vertical
Most severe at distal bronchi and bronchiole

104
Q

Intense acute inflammatory exudate within walls of bronchi and bronchioles, desquamation and ulceration

Peribronchiolar fibrosis in chronic case

A

Bronchiectasis

Pathology (24 decks)

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