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Module 3 Term 4 > Robbins Chapter 13: Lungs > Flashcards

Robbins Chapter 13: Lungs Flashcards

1
Q

Bronchial Tree

A

Bronchi–>bronchioles—>terminal bronchioles—> respiratory bronchioles—>alveoli duct—> alveolar sacs

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2
Q

Acinus

A

Respiratory bronchioles, alveolar ducts, alveolar sacs

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3
Q

ARDS

A

Rest failure occurring within 1 week of a known clinical insult w. bilateral opacities on chest imaging, not fully explained by effusions, atelectasis, CF, or fluid overload.it is a restrictive airway disease

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4
Q

ARDS symptoms

A

Integrity of alveolar-capillary membrane is compromised by endothelial and epithelial injury. There is respiratory insufficiency, cyanosis, severe arterial hypoxemia that is refractory to oxygen therapy.

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5
Q

Diffuse Alveolar Damage

A

histological manifestation of ARDS in the lungs.

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6
Q

Most frequent triggers of ARDS

A

pneumonia, sepsis, aspiration, trauma, pancreatitis, transfusion reactions

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7
Q

Acute Phase of ARDS

A

Capillary congestion, necrosis of alveolar epithelial cells, interstitial and intra-alveolar edema hemorrhage, collections of neutrophils in capillaries. Presence of hyaline membrane lining alveolar ducts

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8
Q

Organizing Stage of ARDS

A

Type II pneumocytes proliferate to regenerate alveolar lining.

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9
Q

Hyaline Membrane

A

fibrin rich edema and necrotic epithelial cells, intra-alveolar fibrosis. Line the alveolar ducts.

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10
Q

Poor Prognosis of ARDS

A

Advanced age, multi organ failure, bacteremia

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11
Q

Obstructive Airway Disease

A

Increase resistance to airflow caused by partial or complete obstruction at any level.

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12
Q

Restrictive Pulmonary Disease

A

Reduced expansion of lung parenchyma and decreased total lung capacity.

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13
Q

Types of obstructive disorders

A
  1. Emphysema
  2. Asthma
  3. Chronic Bronchitis
  4. Bronchiectasis
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14
Q

FEV1/FVC ratio in Obstructive disorders

A

FEV1/FVC ration is reduced. FEV1 is reduced and FVC is reduced or unchanged.

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15
Q

FEV1/FVC ration in Restrictive disorders

A

FEV1/FVC remains unchanged. FVC is reduced and FEV1 remains unchanged or is reduced proportionally.

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16
Q

Chronic Bronchitis initially affects..

A

the large airways

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17
Q

Emphysema affects..

A

the acinus.

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18
Q

COPD includes

A

chronic bronchitis and emphysema. It is irreversible

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19
Q

Emphysema

A

Permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls without significant fibrosis.

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20
Q

Lobule

A

A cluster of 3-5 acinus

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21
Q

4 major types of emphysema

A
  1. Centriacinar/Centrilobular
  2. Panacinar
  3. Distal Acinar
  4. Irregular

Only Centriacinar and panacinar cause significant airway obstruction.

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22
Q

Centriacinar/Centrilobular Emphysema

A

Respiratory bronchioles are affected and distal alveoli are spared. More severe in apical segments of upper lobes. More common in cigarette smokers.

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23
Q

Panacinar/Panlobular Emphysema

A

All of acinus is affected. More severe in lower lobes. Associated with alpha1-antitrypsin deficiency.

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24
Q

Distal Acinar/Paraseptal Emphysema

A

Distal part of acinus is abnormal. It occurs adjacent to areas of fibrosis & is more severe in upper half of lungs. More often present in young adults with spontaneous pneumothorax.

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25
Q

Irregular Emphysema

A

Irregular portions of acinus affected. Associated with scarring. Asymptomatic and maybe the most common form of emphysema.

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26
Q

Pathogenesis of Emphysema

A
  1. Inflammatory cells & mediators
  2. Protease-antiprotease imbalance
  3. Oxidative stress
  4. Airway infection
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27
Q

Inflammatory cells & mediators in Pathogenesis of Emphysema

A

Imflamm mediators increase (e.g. leukotriene B4, IL-8, TNF, etc) - they attract more inflammatory cells in circulation, amplify inflammatory process, & induce structural changes w. growth factors.

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28
Q

Inflammatory cells present in emphysema lesions

A

Neutrophils, Macrophages, CD4+, CD8+ T cells

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29
Q

Protease-Antiprotease Imbalance

A

Proteases released from inflammatory cells & epithelial cells that break down CT. In Pts that Deve,op emphysema there is a deficiency of anti-proteases.

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30
Q

Oxidative Stress

A

ROS are generated from cigarette smoke & released from activated inflammatory cells (macrophages & neutrophils). Cause tissue damage.

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31
Q

Airway infection in emphysema

A

Bacterial and/or viral infections can exacerbate emphysema

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32
Q

Alpha1-antitrypsin

A

Present in serum, tissue fluid, macrophages. Inhibitor of proteases (particularly elastase) secreted by neutrophils during inflammation.

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33
Q

Proteinase Inhibitor (Pi)

A

locus on chromosome 14 that encodes for Alpha1-antitrypsin.

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34
Q

Protease mediates damage of…

A

Extracellular matrix.

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35
Q

Small airways held open by…

A

elastic recoil of lung parenchyma. Loss of elastic tissue in walls of alveoli that surround respiratory bronchioles reduces radial traction and causes respiratory bronchioles to collapse during expiration.

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36
Q

In emphysema there is loss of..

A

alveoli and alveolar capillaries.

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37
Q

First symptom in Emphysema

A

Dyspnea

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38
Q

FEV1/FVC ratio in Emphysema

A

Reduced, FEV1 reduced, FVC normal or reduced.

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39
Q

Pink Puffers

A

Name for emphysema patients. Puffers due to dyspnea and hyperventilation, Pink because they are well oxygenated w. Hb.

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40
Q

Classic presentation of emphysema w. no bronchitic component

A

Pt is barrel chested & dyspneic, thin, prolonged expiration, sitting forward in a hunched over position.

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41
Q

Chronic Bronchitis Presentation

A

Dyspnea less prominent, hypoxia, cyanosis. Pts are obese

42
Q

Compensatory emphysema

A

Dilation of residual alveoli n response to loss of lung substance elsewhere

43
Q

Obstructive Overinflation

A

Expansion of lungs during air trapping

44
Q

Bullous Emphysema

A

Emphysema that produces large subpleural blebs (spaces >1 cm in diameter in the distended space). Blebs can rupture and lead to pneumothorax.

45
Q

Mediastinal/Interstitial Emphysema

A

Caused by entry of air into interstitial of lungs from where it can track to mediastinum & sometimes subcutaneous tissue.

46
Q

Chronic Bronchitis Diagnosis

A

It is diagnosed clinically: presence of persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.

47
Q

Early stages of Chronic Bronchitis

A

Cough raises mucoid sputum but airflow is not obstructed.

48
Q

Distinctive feature of chronic bronchitis

A

Hyper-secretion of mucus, beginning in the large airways. Environmental irritants induce hypertrophy of mucus glands in the trachea and bronchi as well as increase in mucin secreting goblet cells in epithelial surfaces of smaller bronchi and bronchioles.

49
Q

Causes of Chronic Bronchitis

A

Cigarette smoking (most common), air pollutants (e.g. sulfur dioxide, nitrogen dioxide). Irritants cause inflammation w. infiltration of macrophages, neutrophils, & lymphocytes. No eosinophils present.

50
Q

Airflow obstruction in Chronic bronchitis results from

A

1) small airway disease, induced my mucus plugging of bronchiolar lumen, inflammation, & bronchiolar wall fibrosis
2) coexistant emphysema

51
Q

Mucin gene

A

transcribed in bronchial epithelium which produces neutrophil elastase (increased as a consequence to cig smoke)

52
Q

Morphology of Chronic Bronchitis

A

Mucosal lining of large airways is hyperemic and swollen by edema fluid and is covered by a layer of mucinous or mucopurulent secretions.

53
Q

Diagnostic feature of chronic bronchitis

A

enlargement of mucus secreting glands.

54
Q

Chronic Bronchiolitis (Small airway disease)

A

Characterized by goblet cell metaplasia, mucus plugging, inflammation, and fibrosis

55
Q

Bronchiolitis obliterans

A

Complete obliteration of the lumen as a consequence of fibrosis. Can be seen in chronic bronchitis

56
Q

Clinical features of chronic bronchitis

A

Course is variable. sputum production persist indefinitely w.o ventilatory dysfunction while others develop COPD w. significant outflow obstruction marked by hypercapnia, hypoxemia, and cyanosis.

57
Q

Progressive Chronic Bronchitis

A

Development of pulmonary HTN, can lead to heart failure, recurrent infections, and ultimately respiratory failure.

58
Q

Asthma

A

Chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and early in the morning.

59
Q

Hallmarks of asthma

A

intermittent, reversible airway obstruction, chronic bronchial inflammation w. eosinophils, bronchial smooth muscle cell hypertrophy and hyperactivity, and increased mucus secretion.

60
Q

Cells involved in asthma inflammatory response

A

eosinophils, mast cells, macrophages, lymphocytes, neutrophils, and epithelial cells.

61
Q

Hygiene hypothesis

A

lack of exposure to infectious organisms in early childhood results in defects in immune tolerance & hyperactivity to immune stimuli later in life.

62
Q

Factors contributing to development of asthma

A

Genetic predisposition to type I hypersensitivity (atopy), acute and chronic airway inflammation, bronchial hyper responsiveness to stimuli.

63
Q

Subclasses of Asthma

A

Atopic and nontoxic

64
Q

Bronchospasm in asthma triggered by

A

Resp infections (esp viral), airborne irritants, cold air, stress, exercise.

65
Q

Patterns of inflammation in asthma

A

Eosinophilic (most common), neutrophilic, mixed inflammatory, and pouch-granulocytic.

66
Q

Atopic Asthma

A

Most common type of asthma and is an example of type I IgE-mediated hypersensitivity reaction. Usually begins in childhood. Associated w. excess Th2 cell activation. Cytokines produced by Th2 cells account for most of the features of atopic asthma.

67
Q

cytokines produced by TH2 cells

A

IL-4 IL-13 (stimulate IgE production) and IL-5 (activates eosinophils); IL-13 stimulates mucous production

68
Q

Mast cell derived mediators produce 2 waves of a reaction

A

Early (immediate) phase and late phase

69
Q

Early Phase reaction in Mast cell mediated asthma

A

dominated by bronchoconstriction, increased mucus production, and vasodilation.

70
Q

Bronchoconstriction mediated by

A

mediators released from mast cells such as histamine, prostaglandin D2, leukotriene LTC4, D4, and E4, and reflex neural pathways

71
Q

Late phase reaction in Mast Cell Mediated Asthma

A

Inflammatory in nature. Inflammation mediators stimulate epithelial cells to produce chemokines that promote recruitment of TH2 cells, eosinophils, leukocytes.

72
Q

Airway remodeling In asthma

A

Occurs with recurrent bouts of inflammation in bronchial wall. Hyperthrophy and/or hyperplasia of bronchial smooth muscle and mucus glands and increased vascularity, thickening of airway wall, sub-basement membrane fibrosis, goblet cell metaplasia.

73
Q

Onset of asthmatic attacks in atopic asthma can be preceded by

A

allergic rhinitis, urticaria, or eczema. Attacks may be triggered by allergens in dust, pollen, animal dander, food, or by infections.

74
Q

Diagnosis of Atopic Asthma

A

Serum radioallergosrobent tests (RASTs) that identify the presence of IgEs that recognize specific allergens.

75
Q

Wheal and Flare reaction

A

Skin test w. offending allergen, positive in atopic asthma

76
Q

Non-atopic asthma

A

No allergen sensitization, skin results negative. Rest infections due to viruses (e.g. rhinovirus, parainfluenza virus) & inhaled pollutants (e.g. sulfur dioxide, ozone, nitrogen dioxide) are common triggers. Thought that virus induced inflammation of resp mucosa lowers the threshold of sub epithelial vagal receptors to irritants.

77
Q

Drug induced asthma

A

caused by pharmacological agents, aspirin can cause asthma.

78
Q

Aspirin induced Asthma

A

recurrent rhinitis, nasal polyps, urticaria, and bronchospasm. can be due to decreased prostaglandin synthesis and increased leukotriene synthesis.

79
Q

Occupational asthma

A

can be triggered by fumes (epoxy, resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene), etc.

80
Q

Asthma Morphology

A

Overinflated lungs bc of air trapping, occlusion of bronchi and bronchioles by thick, tenacious mucous plus containing whorls of shed epithelium (Cruschmann spirals). Numerous eosinophils & Charcot-Leyden crystals (crystals made of eosinophil protein)

81
Q

Asthma Attack

A

dyspnea, wheezing due to bronchoconstriction and mucus plugging, which leads to trapping of air in distal airspaces & progressive hyperinflation of lungs. Can last from 1 to several hours and subside spontaneously or w. therapy.

82
Q

Status Asthmaticus

A

Severe asthma attack that does not respond to therapy and persists for days or weeks. Associated hypercapnia, acidosis, and hypoxia can be fatal.

83
Q

Asthma therapy

A

anti-inflammatory drugs (esp glucocorticoids) & bronchodilators/leukotriene inhibitors.

84
Q

Leukotrienes

A

potent bronchoconstrictors

85
Q

Eosinophils

A

Key inflammatory cells found in almost all subtypes of asthma, their products (major basic protein) are responsible for airway damage.

86
Q

Bronchiectasis

A

Permanent dilation of bronchi and bronchioles caused by destruction of smooth muscle and elastic tissue, typically results from chronic necrotizing infections. It is not a primary disorder as it occurs secondary to persistent infection/obstruction. Symptoms include cough and expectoration of purulent sputum. May complicate atopic asthma and chronic bronchitis.

87
Q

Conditions predisposing to bronchiectasis

A
  1. Bronchial obstruction
  2. Cystic Fibrosis: obstruction caused by viscid fluid & secondary infections.
  3. Immunodeficiency states (esp Ig deficiency) where there is recurrent bacterial infections.
  4. Primary ciliary dyskinesia
  5. Necrotizing/suppurative pneumonia
88
Q

Primary ciliary dyskinesia

A

Also called immotile cilia syndrome: Rare AR disorder associated w. bronchiectasis & sterility in male. impaired cilia impairs mucociliary clearance of airways—recurrent 2infections.

89
Q

2 process that contribute to bronchiectasis

A
  1. Infection

2. Obstruction

90
Q

Morphology of Bronchiectasis

A

It affects the lower lobes bilaterally usually, and air passages that are more vertical. When tumor or foreign body obstruction involvement may be localized to one segment of the lungs. Airways may be dilated to as much as 4 times their usual diameter & can be seen on gross examination almost to pleural surface.

91
Q

Clinical Features of Bronchiectasis

A

Severe, persistent cough associated w. expectoration of mucopurulent, sometimes fetid sputum. Other symptoms: dyspnea, rhino sinusitis, and hemoptysis. Symptoms are episodic, can lead to hypoxemia, hypercapnia, Pulmonary HTN, and for pulmonale.

92
Q

Chronic Interstitial Diseases (Restrictive/Infiltrative)

A

Bilateral, often patchy, pulmonary fibrosis affecting the walls of alveoli. There is reduced compliance (stiff lungs) that causes dyspnea. Bc of damage to alveolar epithelium & interstitial vasculature there is abnormal ventilation-perfusion ratio, leading to hypoxia. CXR shows small nodules, irregular lines, and ground glass shadows. May progress to resp failure, pulmonary HTN, & cor pulmonale. Results in diffuse scarring and gross destruction of lungs– “end stage” or “honey-comb” lung.

93
Q

Categories of Interstitial Lung Disease

A
  1. Fibrosing
  2. Granulomatous
  3. Eosinophilic
  4. Smoking-related
94
Q

Fibrosing Interstitial Diseases

A

Usual Interstitial Pneumonia/Idiopathic pulmonary fibrosis, Nonspecific interstitial pneumonia, cryptogenic organizing pneumonia, collagen vascular disease-associated, pneumoconiosis, therapy-associated (drugs, radiation)

95
Q

Granulomatous Interstitial Disease

A

Sarcoidosis + Hypersensitivity pneumonia

96
Q

Eosinophilic Interstitial Disease

A

Loeffler syndrome, drug allergy-related, idiopathic chronic eosinophilic pneumonia

97
Q

Smoking related interstitial disease

A

Desquamative interstitial pneumonia, respiratory bronchiolitis

98
Q

Idiopathic Pulmonary Fibrosis

A

pulmonary disorder of unknown etiology that is characterized by patchy progressive bilateral interstitial fibrosis. Also known as cryptogenic fibrosing alveolitis. Males affected more than female, occurs before age 50. Histological pattern is “usual interstitial pneumonia. Similar pathologic changes can be seen in asbestosis, collagen vascular disease, etc.

99
Q

Pathogenesis of IPF

A

Repeated injury & defective repair of alveolar epithelium often in genetically predisposed individual. Germ line mutations leading to loss of telomerase associated with increased risk. Fibroblastic/myofibroblastic proliferation– fibroblastic foci.

100
Q

MUC5B gene

A

gene in which genetic variant may alter mucin production (involved in IPF)

101
Q

Morphology of IPF

A

Cobblestone pleural surfaces of lungs due to retraction of scars along interlobular septa. Firm rubbery, white areas of fibrosis, occurs preferentially along lower lobes, sub pleural regions and interlobular septa. Patchy interstitial fibrosis, varying in intensity & worsens with time.

Module 3 Term 4 (3 decks)

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