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CPR II Exam 2 > Chapter 15: The Lung - Congenital through Obstructive > Flashcards

Chapter 15: The Lung - Congenital through Obstructive Flashcards

1
Q

Except for the vocal cords, the entire respiratory tree is lined by what type of epithelium?

A

Pseudostratified, tall, columnar, ciliated epithelium

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2
Q

Bronchia mucosa contains population of neuroendocrine cells with neurosecretory granules containing which factors?

A
  • Serotonin
  • Calcitonin
  • Gastrin-releasing peptide (bombesin)
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3
Q

Numerous mucus-secreting goblet cells and submucosal glands are dispersed throughout the walls of which parts of the respiratory tree?

A
  • Trachea
  • Bronchi
  • NOT the bronchioles
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4
Q

What are 2 functions of the Type 2 pneumocytes of the alveolar epithelium?

A
  • Produce surfactant
  • Repair of alveolar epithelium by giving rise to type 1 pneumocytes
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5
Q

Pulmonary hypoplasia occurs in utero and what are 2 major causes?

A
  • Congenital diaphragmatic hernia
  • Oligohydramnios
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6
Q

Foregut cysts are most often located where in the lungs and which classification/type is most common?

Treatment?

A
  • Hilum or middle mediastinum
  • Bronchogenic = most common
  • Excision = curative!
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7
Q

Pulmonary sequestration refers to a discrete area of lung with what 2 features?

A
  1. Lacks any connection to the airway system
  2. Has abnormal blood supply arising from aorta or its branches
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8
Q

Congenital pulmonary adenomatoid malformations (CPAM/CCAM) are caused by what?

A

“Arrested development” of pulmonary tissue –> formation of intrapulmonary cystic masses WITH connection to tracheobronchial airways and pulmonary vasculature

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9
Q

Via which imaging modality can congenital pulmonary adenomatoid malformations be detected?

A

Fetal ultrasound

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10
Q

Congenital pulmonary adenomatoid malformations can be deadly due to what complications?

A
  • Hydrops or pulmonary hypoplasia
  • Can get infected later in life
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11
Q

Extralobar pulmonary sequestrations most commonly come to attention in infants how?

A
  • As mass lesions
  • Associated w/ other congenital anomalies
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12
Q

When do intralobal pulmonary sequestrations typically present and are often due to what?

A
  • Older children/adults
  • Due to recurrent localized infection or bronchiectasis
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13
Q

Atelectasis is a reversible disorder, except in cases caused by what?

A

Contraction atelectasis

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14
Q

What are the 3 main types of acquired atelectasis and what is each caused by?

A
  1. Resorption due to complete obstruction of airway (mucus plugs)
  2. Compression due to accumulation of material or air within pleural cavity (i.e., transudate/exudate/blood or pneumothorax)
  3. Contraction due to fibrosis or restrictive processes in pleura preventing full lung expansion
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15
Q

Which type of acquired atelectasis causes the mediastinum/trachea to shift toward the affected lung; which type causes a shift away?

A
  • Resorption —> mediastinum shifts toward affected lung
  • Compression –> mediastinum shifts away from affected lung
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16
Q

Which type of acquired atelectasia occurs in the setting of asbestosis?

A

Contraction atelectasis

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17
Q

Hemodynamic pulmonary edema is due to an increase in what; most commonly occuring in what setting?

A

↑ hydrostatic pressure –> left-sided CHF

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18
Q

What is the histological appearance of of the alveolar capillaries in hemodynamic pulmonary edema?

A

Engorged, and an intra-alveolar transudate appears as finely granular pale PINK material

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19
Q

Where does fluid accumulate initially in pulmonary edema due to hydrostatic pressure being greatest in these sites (dependent edema)?

A

Basal regions of the lower lobes

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20
Q

List 4 causes of decreased oncotic pressure, which cause “leaking out” and pulmonary edema?

A
  • Hypoalbuminemia
  • Nephrotic syndrome
  • Liver disease
  • Protein-losing enteropathies
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21
Q

List some of the etiologies which can cause direct injury to the alveolar wall leading to pulmonary edema?

A
  • Infections: bacterial pneumonia
  • Inhaled gases: high [O2] and smoke
  • Liquid aspiration: gastric contents; near drowing
  • Radiation
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22
Q

What are 2 causes of pulmonary edema of undetermined origin?

A
  • High altitude
  • Neurogenic (CNS trauma)
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23
Q

In long-standing pulmonary congestion (i.e., mitral stenosis), hemosiderin-laded macrophages are abundant, and what is the gross morphology of the lungs?

A

Soggy lungs become firm and brown (brown induration)

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24
Q

When the edema associated with pneumonia fails to stay localized and instead becomes diffuse alveolar edema what fatal condition may this lead to?

A

ARDS

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25
Q

Acute lung injury (aka noncardiogenic pulmonary edema) is characterized by the abrupt onset of significant _________ and __________ in the absence of __________.

A

Acute lung injury (aka noncardiogenic pulmonary edema) is characterized by the abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates in the absence of cardiac failure.

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26
Q

The histologic manifestation of both ALI and ARDS is what?

A

Diffuse alveolar damage (DAD)

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27
Q

What is an important early event in the pathogenesis of ALI/ARDS?

A

Endothelial activation

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28
Q

Following endothelial activation in ALI/ARDS there is adhesion and extravastion of which immune cells and what is the result?

A
  • Neutrophils
  • Degranulate and release proteases, ROS, and cytokines
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29
Q

Which factor is released inside of alveoli during ALI/ARDS that acts to sustain the ongoing pro-inflammatory response leading to more endothelial injury and local thrombosis?

A

Macrophage migration inhibitory factor (MIF)

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30
Q

The thickened protein-rich edema fluid + debris from dead alveolar cells accumulate in ALI/ARDS, and lead to the formation of what?

A

HYALINE membranes

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31
Q

If there is resolution of the injury in ARDS/ALI, what factors are released from macrophages which stimulate fibroblast growth and collagen deposition leading to fibrosis of alveolar walls?

A
  • TGF-β
  • PDGF
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32
Q

Following the fibroproliferative phase in ARDS, what 2 pathways may ensue and the result of each?

A
  • Resolution –> restoration of normal cellular structure and function
  • Fibrosis –> destruction and distortion of normal cellular structure –> IRREVERSIBLE
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33
Q

ALI/ARDS is more common and associated with a worse prognosis in whom?

A

Chronic smokers and alcoholics

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34
Q

During the acute stage of ALI/ARDS what is seen morphologically in the lungs?

A
  • Lungs are heavy, firm, red, and boggy
  • Exhibit congestion, interstitial and intra-alveolar edema, inflammation, fibrin deposition, and DAD
  • Alveolar walls become lined with waxy hyaline membranes
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35
Q

In the organizing stage of ALI/ARDS what are the type 2 pneumocytes doing and what begins to form?

A
  • Type 2 pneumocytes are proliferating
  • Granulation tissue forms in the alveolar walls and spaces
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36
Q

Fatal cases of ALI/ARDS often have superimposed?

A

Bronchopneumonia

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37
Q

What is seen on radiographic imaging of patient with ALI?

A

Diffuse bilateral infiltrates

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38
Q

Pt’s with ALI will have what sx’s?

A
  • Profound dyspnea and tachypnea
  • Followed by ↑ cyanosis and hypoxemia
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39
Q

Why may the hypoxemia associated with ALI/ARDS be refractory to O2 therapy; what acid-base disturbance may develop?

A

Due to ventilation perfusion mismatching and respiratory acidosis may develop

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40
Q

What is the cause of the ventilation perfusion mismatch and hypoxemia in ALI/ARDS?

A
  • Poorly aerated regions continue to be perfused
  • Perfusion = normal; but ventilation = decreased
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41
Q

ARDS is a diagnosis of exclusion using the criteria which can be remembered with mnemonic A.R.D.S.

A
  • Abnormal CXR (bilateral lung opacities)
  • Respiratory failure within 1 week of alveolar insult (ABRUPT)
  • Decreased PaO2/FiO2 ≤200 = hypoxia
  • Symptoms of respiratory failure are NOT due to HF/fluid overload
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42
Q

The causes of ARDS may be remembered with “SPARTAS.”

A
  • Sepsis
  • Pancreatitis/Pneumonia
  • Aspiration

- uRemia

  • Trauma
  • Amniotic fluid embolism
  • Shock
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43
Q

Neonatal respiratory distress syndrome is associated with what underlying risk factors?

A
  • Pre-term infant
  • Male gender
  • Maternal diabetes
  • Delivery by C-section
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44
Q

What is the characteristic finding on CXR of infants w/ neonatal respiratory distress syndrome?

A

“Ground-glass” picture

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45
Q

What plays a particularly important role in the synthesis of surfactant?

A

Glucocorticoids

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46
Q

Analysis of what in the amniotic fluid provides a good estimate of the level of surfactant in the alveolar lining?

A

Phospholipids

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47
Q

Oxygen is required in neonates affected by neonatal respiratory distress syndrome, but what are 2 complications which may arise?

A
  • Retrolental fibroplasia (aka retinopathy of prematurity)
  • Bronchopulmonary dysplasia
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48
Q

Infants that recover from RDS are also at increased risk for developing what 3 complications associated with preterm birth?

A
  • PDA
  • Intraventricular hemorrhage
  • Necrotizing enterocolitis
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49
Q

What is the term used to describe widespread ALI of unknown etiology associated with a rapidly progressive clinical course?

A

Acute interstitial pneumonia (aka idiopathic ALI-DAD)

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50
Q

What is the typical presentation of someone with Acute Interstitial Pneumonia?

A

Pt presents w/ ARF following an illness of <3 weeks duration that resembles a URI

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51
Q

When do most deaths associated with Acute Interstitial Pneumonia occur?

A

Within 1-2 months

52
Q

The radiographic and pathologic features of acute interstitial pneumonia are identical to what?

A

Organizing stage of ALI

53
Q

Which 2 obstructive lung diseases are grouped together and referred to as COPD?

A
  • Chronic bronchitis
  • Emphysema
54
Q

Asthma is distinguished from chronic bronchitis and emphysema by the presence of what feature?

A

Reversible bronchospasm

55
Q

Which obstructive lung disease is charactetrized by irreversible enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of the walls without fibrosis?

A

Emphysema

56
Q

Of the 4 major types of emphysema which 2 cause clinically significant airflow obstruction; which is most common?

A
  1. Centriacinar (centrilobular) = most common = Upper lungs
  2. Panacinar (panlobular) = Lower zones
57
Q

Where are lesions of centriacinar (centrilobular) emphysema most commonly seen and most severe?

A

Upper lobes, in the apical segments

58
Q

Centriacinar (centrilobular) emphysema occurs predominantly in whom and is often associated with what other lung disorder?

A

Heavy smokers, often in assoc. w/ chronic bronchitis (COPD)

59
Q

Panacinar (panlobular) emphysema occurs most commonly where in the lungs and is associated with what underlying abnormality?

A
  • Lower zone and anterior margins of lung, usually most severe at bases
  • Associated w/ α1-antitrypsin deficiency

*Image on right*

60
Q

Which type of emphysema most likely underlies many cases of spontaneous pneumothorax in young adults?

A

Distal acinar (paraseptal) emphysema

61
Q

What are some of the inflammatory mediators released by macrophages and resident epithelial cells which influence the development of emphysema?

A
  • Leukotriene B4
  • IL-8
  • TNF
62
Q

The pathogenesis of emphysema is related to an imbalance between which factors?

A

Proteases (i.e., elastase) and anti-proteases (α<strong>1</strong>-antitrypsin)

63
Q

Which gene related to protection from oxidatie stress may be mutated in emphysema and other smoking-related lung diseases?

A

NRF2

64
Q

α1-antitrypsin is encoded by which locus and on what chromosome?

A

Proteinase inhibitor (Pi) on chromosome 14

65
Q

Loss of elastic tissue in the walls of alveoli in emphysema causes respiratory bronchioles to do what during expiration?

A

Collapse —> functional airflow obstruction

66
Q

What are 3 inflammatory changes seen in the small airways of pt with emphysema and even young smokers that narrow the bronchiolar lumen and contribute to obstruction?

A
  • Goblet cell hyperplasia –> mucus plugging of lumen
  • Inflammatory infiltrate in bronchial walls w/ neutrophils, macrophages, B cells, and T cells
  • Thickening of the bronchiolar wall due to smooth m. hypertrophy and peribronchial fibrosis
67
Q

What is the characterisitc gross morphology seen in advanced emphysema?

A
  • Enlarged lungs which often overlap the heart
  • Large alveoli seen on cut surface of fixed lungs
68
Q

Microscopically, in emphysema, the large alveoli are separated by what and have fibrosis where?

A

Thin septa w/ only focal centriacinar fibrosis

69
Q

Which sx of emphysema typically appears first and what are some other associated sx’s that may be present?

A
  • Dyspnea that’s progressive
  • Cough or wheezing may be present, easily confused w/ asthma
  • Weight loss is common; may be severe enough as to suggest cancer
70
Q

What value and test is the key to diagnosis of emphysema?

A

Impaired expiratory airflow, best measured w/ spirometry

71
Q

Development of what associated w/ 2’ HTN is an indicator of poor prognosis in pt w/ emphysema?

A

Cor pulmonale and eventual CHF, related to 2’ pulmonary HTN

72
Q

How will a CXR of predominant bronchitis differ from predominant emphysema?

A
  • Bronchitis = prominent vessels; large heart
  • Emphysema = hyperinflation; small heart
73
Q

Obstructive overinflation is commonly caused by what; why is the form of emphysema significant?

A
  • Tumor or foreign object
  • Can be life-threatening emergency, due to affected portion distending and compressinf remaining lung
74
Q

What is a complication which may arise w/ Bullous Emphysema?

A

Rupture of bullae –> pneumothorax

75
Q

What is the primary or initiating factor in the pathogenesis of chronic bronchitis?

A

Exposure to noxious or irritating inhaled substances such as tobacco smoke and dust from grain, cotton, and silica

76
Q

What is the earliest feature seen in the pathogenesis of Chronic Bronchitis; over time there is a marked increase in what cell type?

A
  • Mucus hypersecretion
  • Assoc. w/ hypertrophy of the submucosal glands in trachea and bronchi
  • With time there is marked ↑ in goblet cells in small airways
77
Q

What is the role of infection in Chronic Bronchitis?

A
  • Significant in maintaining the pathologic state
  • Critical in producing acute exacerbation
78
Q

What are the characteristic gross morphological features of chronic bronchitis; enlargement of what?

A
  • Mild inflammation of airways (predominantly lymphocytes)
  • Enlargement of the mucus-secreting glands of the trachea and bronchi
79
Q

Althought the number of goblet cells increase slightly in Chronic Bronchitis what is the major change seen?

A

Size of mucous glands (hyperplasia)

80
Q

The increase in size of the mucous glands in chronic bronchitis can be assessed via what ratio?

A

Ratio of thickness of mucous gland layer to the thickness of the wall btw the epithelium and cartilage (Reid index)

81
Q

What morphological changes may the epithelium exhibit in Chronic Bronchitis and may lead to what complication?

A

Squamous metaplasia and dysplasia –> carcinoma

82
Q

In the most severe cases of Chronic Bronchitis, there may be obliteration of the lumen due to fibrosis and this is known as?

A

Bronchiolitis obliterans

83
Q

Long-standing severe chronic bronchitis commonly leads to what (cause of death)?

A

Cor pulmonale –> HF

84
Q

Early-onset allergic asthma is associated with inflammation due to what type of T cells and has good response to what tx?

A
  • TH2 helper T cell inflammation
  • Responds well to corticosteroids
85
Q

Respiratory infections due to what are common triggers of non-atopic asthma and may act in synergy with enviornmental allergens to cause atopic asthma?

A

Viruses (i.e., rhinovirus, parainfluenza, and respiratory syncytial virus)

86
Q

Non-atopic asthma attacks may be triggered by seemingly innocuous events, such as what?

A
  • Exposure to cold
  • Exercise
87
Q

Aspirin-sensitive asthma occurs most commonly in pt’s with what underlying disorders?

A

Recurrent rhinitis and nasal polyps

88
Q

Pt’s with aspirin-sensitive asthma suffer from what sx’s during an attack?

A
  • Asthmatic attacks

AND

  • Urticaria (aka hives)
89
Q

Describe how aspirin inhibiting cyclooxygenase plays a role in the pathogenesis of aspirin-sensitive asthma?

A

Leads to rapid ↓ in PGE2, which normally inhibit leukotrienes B4, C4, D4, and E4

90
Q

As asthma progresses and becomes more severe, there is ↑ local secretion of growth factors, which induce what 5 changes?

A
  • Mucus gland hypertrophy
  • Smooth m. proliferation
  • Angiogenesis
  • Fibrosis
  • Nerve proliferation
91
Q

A fundamental abnormality in the pathogenesis of asthma is an exaggerated response by which immune cells to normally harmless enviornmental allergens?

A

TH2 response

92
Q

What is the role of IL-4, IL-5, and IL-13 released from TH2 cells in asthmatic patients?

A
  • IL-4 stimulates class switching to IgE
  • IL-5 activates eosinophils
  • IL-13 stimulates mucus secretion and IgE production by B cells
93
Q

Other than TH2 cells what other type of T cell is seen in the late-phase reaction of asthma and what is it’s function?

A

TH17 produce IL-17 –> recruit neutrophils

94
Q

The bronchoconstriction characteristic of the early phase (immediate hypersensitivity) of asthma is triggered by what?

A

Direct stimulation of Vagal (parasympathetic)receptors by reflexes triggered via mediators produced bymast cells and other immune cells

95
Q

Which 2 types of mediators play a clear role in the bronchospasm, increased vascular permeability, and airway smooth muscle constriction seen in asthma?

A
  1. Leukotrienes C4, D4, E4
  2. ACh released from intrapulmonary parasympathetic nerves
96
Q

Which factors released from eosinophils in the late phase reaction of asthma cause damage to the epithelium?

A
  • Major basic protein
  • Esoinophil cationic protein
97
Q

Leukotrienes C4, D4, E4 are responsible for what 3 pathogenic processes in asthma?

A
  • Bronchoconstriction
  • Mucus secretion
  • ↑ vascular permeability
98
Q

There is an increased incidence of what 2 other allergic disorders in those with atopic asthma?

A
  • Allergic rhinitis
  • Eczema
99
Q

One susceptibility locus for asthma is located on what chromosome; near the gene cluster encoding what cytokines?

A
  • Chromosome 5q
  • IL-3, IL-4, IL-5, IL-9 and IL-13 + IL-4 receptor
100
Q

Polymorphisms in which interleukin gene have the strongest and most consistent associations w/ asthma or allergic disease?

A

IL13 gene

101
Q

Polymorphisms in which gene encoding a metalloproteinase, may be linked to ↑ proliferation of bronchial smooth m. cells and fibroblasts –> bronchial hyperreactivity and subepithelial fibrosis?

A

ADAM33

102
Q

Variants of which interleukin receptor gene is associated w/ atopy, elevated total serum IgE and asthma?

A

IL-4 receptor gene variants

103
Q

Increased serum levels and lung expression of which chitinase-like glycoprotein is correlated w/ disease severity, airway remodeling, and decreased pulmonary function in asthmatics?

A

YKL-40

104
Q

What is the most striking gross finding in pt’s dying of acute severe asthma (status asthmaticus)?

A

Occlusion of bronchi and bronchioles by thick, tenacious mucus plugs, which often contain shed epithelium

105
Q

The idea that microbial exposure during early development reduces the later incidence of allergic (and some autoimmune) diseases has been known as what?

A

Hygiene hypothesis

106
Q

What are 2 characteristic findings in the sputum or bronchoalveolar lavage specimens in a pt w/ severe asthma?

A
  • Curschmann spirals = Coiled mucus plus
  • Numerous eosinophils and Charcot-Leyden crystals composed of an eosinophil protein called galectin-10
107
Q

The characteristic histologic finding of “airway remodeling” in pt w/ asthma includes what 5 major changes?

A
  • Thickening of airway wall
  • Sub-basement membrane FIBROSIS
  • ↑ vascularity
  • ↑ in size of submucosal glands and # of goblet cells
  • Hypertrophy and hyperplasia of the bronchial wall muscle
108
Q

What are the 4 contributors to chronic irreversible airway obstruction in asthma?

A
  • Muscular bronchoconstriction
  • Acute edema
  • Mucus plugging
  • Airway remodeling
109
Q

What are the cardinal sx’s of asthma?

A
  • Chest tightness
  • Dyspnea
  • Wheezing
  • Cough (with or w/o sputum production)
110
Q

Chronic irreversible airway obstruction will show a decreased response to what?

A

Therapeutic agents –> Bronchodilators and/or Corticosteroids

111
Q

Disorder in which destruction of smooth muscle and elastic tissue by chronic necrotizing infections leads to permanent dilation of bronchi and bronchioles

A

Bronchiectasis

112
Q

List congenital or hereditary conditions which may lead to Bronchiectasis?

A
  • Cystic Fibrosis
  • Intralobar sequestration
  • Primary ciliary dyskinesia
  • Kartagener syndromes
113
Q

Many cases of Bronchiectasis lack any association with another disease process and therefore are what?

A

Idiopathic

114
Q

What are the 2 major conditions associated with Bronchiectasis and are often both necessary for its development?

A
  • Obstruction
  • Infection
115
Q

Which 3 organisms are the most common causes of lung infection in pt with CF?

A
  • Staphylococcus aureus
  • Haemophilus influenzae
  • Pseudomonas aeruginosa
116
Q

Which autoimmune disorders and other conditions are associated w/ developing Bronchiectasis?

A
  • Rheumatoid Arthritis
  • SLE
  • IBD
  • COPD
  • Post-transplantation
117
Q

In CF the primary defect in ion transport leads to defective what in the lungs?

A
  • Mucociliary action + airway obstruction by thick viscous secretions
  • Sets stage for chronic bacterial infections
118
Q

Primary ciliary dyskinesia is due to mutations in what?

A

Ciliary motor proteins (i.e., Dynein arm of microtubules)

119
Q

Half of the pt’s with primary ciliary dyskinesia have what syndrome and what is the triad of this syndrome?

A
  • Kartagener syndrome
  • Marked by situs inversus + bronchiectasis + sinusitis
120
Q

Males with Kartagener Syndrome tend to be what?

A

Infertile, as result of sperm dysmotility

121
Q

Allergic bronchopulmonary aspergillosis occurs in what 2 underlying conditions?

A
  • Asthma
  • Cystic Fibrosis
122
Q

Which stain can be used to demonstrate Aspergillus and what is seen?

A
  • Silver stain
  • Aggregates of fungal hyphae
123
Q

What are characteristic findings in the seurm of someone with Allergic Bronchopulmonary Aspergillosis?

A

High serum IgE and serum Abs to Aspergillus

124
Q

Bronchiectasis usually affects which lobes of the lung, particularly which air passages, and is most severe where?

A
  • Lower lobes bilaterally
  • Particularly air passages that are vertical
  • Most severe in the more distal bronchi and bronchioles
125
Q

Which lung disease will have dilated airways, sometimes up to 4x normal size?

A

Bronchiectasis

126
Q

What are the signs/sx’s of Bronchiectasis?

A
  • Severe, persistent cough w/ foul smelling, sometimes bloody sputum
  • Dyspnea and orthopnea in severe cases
  • Occasionaly hemoptysis, which can be massive!
127
Q

What are 3 potential complications of Bronchiectasis?

A
  • Cor pulmonale
  • Brain abscess
  • Amyloidosis

CPR II Exam 2 (23 decks)

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