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Respiratory Medicine Exam I > Obstructive & Restrictive Lung Disease, Vascular Disease, Pleura > Flashcards

Obstructive & Restrictive Lung Disease, Vascular Disease, Pleura Flashcards

1
Q

3 types of acquired atelectasis

A

Resorption
Compression
Contraction

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2
Q

Atelectasis characterized by aiway obstruction with gradual resorption of air reducing lung expansion

A

Resporption

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3
Q

Atelectasis characterized by fibrotic or other innate restrictive process in the pleura or peripheral lung restricting lung expansion

A

Contraction atelectasis

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4
Q

Atelectasis characterized by accumulated material in pleural cavityy, squeezing the lung parenchyma

A

Compression atelectasis

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5
Q

Interstitial fluid in alveolar spaces shows up as pink proteinaceous material on histological slides of lung parenchyma, what condition is this indicative of?

A

Pulmonary edema

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6
Q

What are some hemodynamic causes of pulmonary edema?

A

“Pushing out” — Left sided heart failure (MCC), volume overload, pulmonary vein obstruction

“Leaking out” — hypoalbuminemia, nephrotic syndrome, liver dz

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7
Q

Pulmonary edema may also occur due to injury to alveolar wall. What might cause this type of injury?

A

Bacterial pneumonia
Sepsis
Smoke inhalation
Aspiration

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8
Q

What are 2 important causes of pulmonary edema of which the mechanism is unknown?

A

Neurogenic (brain injury)

High altitude

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9
Q

2 diseases on the ARDS spectrum

A

Acute lung injury (ALI) — acute onset, hypoxemia, bilateral infiltrates, no evidence of cardiac failure

Acute respiratory distress syndrome (ARDS) — worsening hypoxemia

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10
Q

Condition that is diagnosed based on presence of histologic manifestations of ARDS

A

Diffuse Alveolar Damage (DAD)

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11
Q

2 pathogenic mechanisms for infection with ARDS

A

Either due to inhalation or because something has entered bloodstream (sepsis, bacteremia, etc.) - so it can come from airway or circulation!

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12
Q

Physiologic measurement used to characterized degree of hypoxia in ARDS

A

PaO2/FiO2 ratio

If <300 it can be characterized as ALI, if it is <200 it can be characterized as ARDS [so ALI is basically mild form of ARDS]

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13
Q

4 characteristics necessary for diagnosis of ARDS

A

Abrupt onset of symptoms

Hypoxemia (PaO2/FiO2 <200)

Bilateral infiltrates

Non-cardiac in nature

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14
Q

Pathogenic mechanism of ARDS

A

Acute lung injury —> endothelial activation —> adhesion/extravasation of neutrophils —> accumulation of intraalveolar fluid, formation of hyaline membranes —> resolution of injury

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15
Q

Diffuse alveolar damage (DAD) is characterized by ______ membranes composed of edema + fibrin + cell debris.

What are 2 other characteristics associated with diffuse alveolar damage?

A

Hyaline

Decreased surfactant —> stiff lungs

Decreased aeration —> ventilation-perfusion mismatch (RBCs not getting close enough to airways due to hyaline!)

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16
Q

4 Stages of progression of ARDS

A
  1. Exudative (edema, hyaline membranes, neutrophils)
  2. Proliferative (fibroblast proliferation, organizing pneumonia, early fibrosis)
  3. Fibrotic (extensive fibrosis, loss of normal alveolar architecture)
  4. Either RESOLUTION or FIBROSIS —
    Resolution: restoration of normal cell structure/function
    Fibrosis: destruction/distortion of normal cell structure

NOTE fibrosis is IRREVERSIBLE

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17
Q

Compare/contrast acute interstitial pnuemonia different from ARDS/DAD?

A

AIP has same clinical presentation as ARDS

AIP has same histology as ARDS/DAD

Difference is that AIP cannot be attributed to a specific etiology (AIP often presents in middle aged women, usually preceded by a viral illness)

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18
Q

MCC of COPD/Chronic bronchitis

A

Smoking

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19
Q

Obstructive pulmonary disease characterized by alveolar wall destruction and overinflation

A

Emphysema

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20
Q

Obstructive pulmonary disease characterized by productive cough and airway inflammation

A

Chronic bronchitis

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21
Q

Reversible obstructive pulmonary disease characterized by bronchial hyperresponsiveness triggered by allergens, infection, etc.

A

Asthma

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22
Q

Diagnostic criteria for chronic bronchitis

A

Persistent cough with sputum production for 3 months out of 2 consecutive years

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23
Q

Predominant pathophysiologic mechanism in chronic bronchitis

A

Mucous gland hyperplasia —> damage to airway epithelium

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24
Q

3 primary complications of chronic bronchitis

A

Squamous metaplasia —> dysplasia —> carcinoma

Bronchiectasis

Death from respiratory infection

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25
Q

Clinical presentation of emphysema on CXR and PFTs

A

CXR: Enlarged lungs, flattened diaphragm, and increased AP diameter

PFTs: FEV1/FVC reduced

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26
Q

Characteristic patient presentation of chronic bronchitis

A

“Blue bloaters”

Overweight and cyanotic

Elevated hemoglobin

Peripheral edema

Rhonchi and wheezing

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27
Q

Characteristic patient presentation of emphysema

A

“Pink puffers”

Older and thin

Severe dyspnea

Quiet chest

X-ray: hyperinflation with flattened diaphragms

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28
Q

Pathogenic mechanism of alpha-1 antitrypsin deficiency

A

Deficiency in alpha 1 antitrypsin (trapped in liver, causes liver damage) leaves neutrophil elastase uninhibited, which causes lung damage

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29
Q

What type of emphysema is present in alpha1 antitrypsin deficiency?

A

Predominantly basilar panacinar emphysema

[differentiate from COPD which is centrilobular, centriacinar, or proximal acinar]

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30
Q

Genetic mechanism of alpha 1 antitrypsin deficiency

A

Deficiency encoded by Pi (proteinase inhibitor) gene on Chr14; Z allele is associated with decreased circulating enzyme

Homozygous PiZZ individuals have markedly decreased a1-AT, with a majority developing panacinar emphysema

[Serum testing for a1-AT is the primary means of dx]

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31
Q

4 primary complications of emphysema

A

Respiratory failure

Coronary artery disease

Right heart failure (cor pulmonale)

Pneumothorax with lung collapse

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32
Q

3 components of asthma

A

Recurrent airway obstruction with a reversible component

Airway hyperresponsiveness

Airway inflammation

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33
Q

What are the 2 types of asthma?

A

Atopic (extrinsic) — 2/3 of all pts

Non-atopic (intrinsic) — 1/3 of all pts

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34
Q

Describe atopic asthma in terms of demographics and diagnostic features

A

Atopic asthma represents 2/3 of all asthma patients; may affect any age but typically presents in childhood

There is usually family hx of asthma

Characterized by elevated IgE levels (type I hypersensitivity) — eosinophils, mast cells, lymphocytes

Triggers may include a variety of allergens

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35
Q

Describe non-atopic asthma in terms of demographics and diagnostic features

A

Non-atopic asthma represents 1/3 of all asthma pts, often older pts

Typically normal IgE levels — T lymphocytes and neutrophils

Triggers may include cold, exercise, infection

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36
Q

Immune mechanism of atopic asthma using pollen as example

A

Pollen Ag recognized by dendritic cell, which signals to Th2 CD4+ cell

Th2 cell overreacts (hyperreactive phenomenon characteristic of asthma), and tells B cell lineage to form IgE antibodies at high levels

Mast cells attracted by IgE, eosinophils recruited and the next time the immune system recognizes pollen, mediators react very strongly producing asthmatic symptoms

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37
Q

What mediators are responsible for the symptoms seen in asthma?

A

Bronchoconstriction is d/t Leukotrienes C4-D4-E4, histamine, prostaglandin D2, ACh

Mucus secretion and increased vascular permeability d/t leukotriens C4-D4-E4

Recruitment of inflammatory cells due to interleukins

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38
Q

What are the consequences if asthma goes uncontrolled for long periods of time?

A

Progressive structural changes to airways with characteristic histologic findings = fibrosis, smooth muscle hyperplasia, increased goblet cells and submucosal glands

Changes may be IRREVERSIBLE! There will also be a decreased response to therapeutic agents like bronchodilators and corticosteroids

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39
Q

Unremitting, possibly fatal asthma attack resulting from bronchial occlusion by thick mucus

A

Status asthmaticus

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40
Q

Characteristic histologic findings associated with status asthmaticus

A

Coiled mucus plugs: “Curshchmann spirals”

Eosinophils and breakdown product — Charcot Leyden crystals

41
Q

Other conditions and genetic factors associated with atopic asthma

A

Associated with seasonal allergies and eczema

May be linked to various alleles controlling factors like IgE, cytokines (IL-4), adrenergic receptors, etc.

42
Q

Environmental factors impacting asthma

A

Disease of industrialized societies — pollution, lack of allergen exposure at early age

Early infection

43
Q

Samter’s triad includes what specific type of asthma? What are the other 2 disease associations?

A
  1. Aspirin-sensitive asthma
  2. Nasal polyps
  3. Recurrent rhinitis
44
Q

Pathologic mechanism of aspirin sensitive asthma

A

When COX enzymes inhibited by aspirin or other NSAID, arachidonic acid is shunted into 5-lipoxygenase pathway which results in some production of leukotrienes C4-D4-E4, which are responsible for bronchoconstriction, mucus secretion, and increased vessel permeability resulting in asthmatic symptoms

45
Q

End stage process of multiple chronic respiratory conditions (infection, obstruction, ABPA, CF, etc.) charcterized by a necrotizing inflammatory response

A

Bronchiectasis

46
Q

What condition is defined by dysfunction of dynein arm of microtubules resulting in characteristic triad of respiratory symptoms as well as male infertility?

A

Kartagener’s syndrome: Primary Ciliary Dyskinesia

47
Q

Triad of sx associated with Kartagener’s syndrome: Primary Ciliary Dyskinesia

A

Sinusitis

Bronchiectasis

Situs inversus

48
Q

Difference in ciliary ultrastructure between PCD and CF

A

PCD has abnormal ciliary ultrastructure

CF has normal ciliary ultrastructure; damage of cilia occurs secondary to other disease processes

49
Q

Difference in etiology of male infertility in CF vs. PCD

A

CF — congenital bilateral absence of vas deferens

PCD — immotile sperm (this disease results in abnormal cilia AND flagella!)

[can also differentiate from Young’s syndrome male infertility which results from retained sperm in epididymis]

50
Q

What is ABPA?

A

Allergic bronchopulmonary aspergillosis: exaggerated hypersensitivity response to aspergillus infection overlying chronic lung disease (asthma or cystic fibrosis)

51
Q

ABPA results in increased ____ on serum testing, as well as positive _____ test. There is thick mucus in bronchi as well as ________ characteristic of aspergillus infection. It is associated with _______ in advanced disease

A

IgE; skin; fungal hyphae; bronchiectasis

52
Q

Histologic findings with ABPA

A

Silver stain demonstrates aggregates of fungal hyphae characteristic of Aspergillus spp. (characteristic septations of hyphae and narrow angle branching)

53
Q

5 categories of restrictive lung disease

A

Fibrosing: idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, cryptogenic organizing pneumonia, connective tissue disease-associated, pneumoconiosis, drug reactions, radiation pneumonitis

Granulomatous: sarcoidosis, hypersensitivity pneumonitis

Eosinophilic

Smoking related: desquamative interstitial pneumonia, respiratory bronchiolitis-associated ILD

Other: Langerhans cell histiocytosis, pulmonary alveolar proteinosis, lymphoid interstitial pneumonia

54
Q

Factors involved in pathogenesis of idiopathic pulmonary fibrosis

A

Environmental factors — industrialized societies, smoking

Genetic factors

Age — typically 50+

55
Q

Clinical findings of idiopathic pulmonary fibrosis

A

Dyspnea

Crackles on exam = “Velcro-like”

Restrictive pattern on PFT’s — decrease in DLco, FVC

Basilar infiltrates - progression to “honeycomb” lung

56
Q

Classic findings on what test is required for diagnosis of idiopathic pulmonary fibrosis?

A

High-resolution CT scan OR pulmonary biopsy

[biopsy shows usual interstitial pneumonia (UIP) characterized by normal and fibrotic areas, fibroblast foci, peripheral honeycombing]

57
Q

T/F: Honeycomb fibrosis is specific to interstitial pulmonary fibrosis

A

False, it is just the end-stage of IPF

58
Q

Prognosis of idiopathic pulmonary fibrosis

A

It is progressive, most pts expire from respiratory disease 3-5 years after diagnosis

Potential therapies: lung transplant, medication to arrest fibrosis (tyrosine kinase inhibitors, TGF-beta inhibitors)

59
Q

Idiopathic lung condition with unique histology consisting of uniform infiltrates and fibrosis, no heterogeneity, no fibroblast foci, no granulomata, and it has an overall better prognosis than UIP

A

Non-specific interstitial pneumonia (NSIP)

[note that NSIP is NOT non-specific because it has unique histology]

60
Q

Respiratory condition that presents with pneumonia-like consolidation in 5-6th decades and exists as a diagnosis of exclusion when there is no infection, drug or toxin, or relation to CT disorders

A

Cryptogenic Organizing Pneumonia (COP)

[formerly BOOP — bronchiolitis-obliterans-organizing pneumonia]

61
Q

Histologic findings and prognosis associated with cryptogenic organizing pneumonia

A

Fibroblast (Masson bodies) — organizing plugs of CT

Good prognosis - pts tend to have full recovery with oral steroids

62
Q

What autoimmune diseases can manifest as ILD (UIP, NSIP, organizing pneumonia, bronchioloitis)?

A

Rheumatoid arthritis
Systemic sclerosis
Lupus erythematosus

[note that if ILD occurs as a manifestation of these conditions, they are not diagnosed as pure diseases, but the prognosis is linked to treatment of the underlying condition]

63
Q

Of the interstitial lung diseases, which ones are considered granulomatous diseases?

A

Sarcoidosis

Hypersensitivity pneumonia

64
Q

Systemic disease manifesting non-caseating (non-necrotizing) granulomata that presents as incidental abnormal radiograph, or with c/o dyspnea

A

Sarcoidosis

65
Q

Clinical presentation of sarcoidosis

A

In addition to incidental radiograph findings or dyspnea, pts also tend to have:

Elevated serum ACE levels

Pts also tend to be <40 y/o, 10-fold predominance in african americans, commonly involves the lungs (also LNs or anywhere around the body)

[etiology is likely immune-related; possible genetic predisposition]

66
Q

Characteristic granuloma inclusions seen in sarcoidosis

A

Asteroid body

Schaumann bodies

[in addition to other granulomata findings like histiocytes, multinucleated giant cells, some lymphocytes, fibrotic sclerotic stroma, tight formation]

67
Q

The stages of sarcoidosis do not occur in order. 20% of patients have progressive lung disease. Death may occur via involvement of what systems?

A

Pulmonary, cardiac, or neurologic

68
Q

Respiratory condition caused by immune reaction to inhaled antigen resulting in airway-centered granulomata with associated lymphocytes

A

Hypersensitivity pneumonitis

69
Q

Diagnosis of hypersensitivity pneumonitis requires a detailed history. What are some environmental exposures that might trigger this disease?

A

Pigeon breeder’s lung — protein from bird feces

Farmer’s lung — actinomycetic spores in hay

Hot tub lung — reaction to mycobacterium avium complex (MAC)

70
Q

Disease affecting smokers in 4-5th decades with restrictive lung disease presentation and shows characteristic “stuffed” alveolar spaces full of macrophages on histology

A

Desquamative interstitial pneumonia (DSIP)

71
Q

Treatment and prognosis of desquamative interstitial pneumonia (DSIP)

A

Treatment: stop smoking, corticosteroids

Good prognosis: >95% survival at 5 years

72
Q

Disease that exists as part of a spectrum with DSIP, but less symptomatic and earlier presentation (3rd-4th decades) and has dose-dependent relationship to smoking; radiographic abnormalities prompt biopsy for diagnosis

A

Respiratory brionchiolitis interstitial lung disease (RB-ILD)

73
Q

Histologic findings associated with RB-ILD

A

Macrophages present to lesser extent

“Peribronchiolar” metaplasia (abnormally located ciliated cells)

May have fibrosis in advanced cases

74
Q

T/F: RB-ILD is often reversible with smoking cessation if caught early

A

True

75
Q

Lung disease found in young smokers and characterized by stellate lung lesions, progressive scarring leads to cysts and peripheral cysts may rupture and present with pneumothorax

A

Langerhans Cell Histiocytosis (LCH)

76
Q

Histologic findings associated with Langerhans Cell Histiocytosis (LCH)

A

Eosinophils

Langerhans cells (immature dendritic cells) — S-100 and CD1a positive!!!

Varying fibrosis and cysts

77
Q

What is the best way to reverse Langerhans Cell Histiocytosis?

A

Smoking cessation!

78
Q

Respiratory disease characterized by impairment of surfactant metabolism due to defect of GM-CSF resulting in accumulation of surfactant proteins throughout alveoli and airspaces

A

Pulmonary alveolar proteinosis

79
Q

Pulmonary alveolar proteinosis may be autoimmune (>90%), secondary to other disease, or hereditary (very rare). It can be treated with ______

A

Subcutaneous GM-CSF

80
Q

Histologic and bronchioloalveolar lavage findings with pulmonary alveolar proteinosis

A

Histology: proteinaceous collections in alveolar spaces (appears similar to pulmonary edema on histology, need history to make dx)

Fluid from bronchioalveolar lavage shows copious milky fluid

81
Q

Reaction by the lungs to inhaled mineral or organic dust - often due to occupational exposure or air pollution (exaggerated response in some individuals indicates possible genetic component)

A

Pneumoconiosis

82
Q

Aggravating factors of pneumoconiosis

A

Worse if exposure is high and repetitive, size of particles is small (means they can reach alveoli), and impaired ciliary clearance d/t smoking

83
Q

Coal worker’s pneumoconiosis is a disease due to inhaled coal dust, with a spectrum of disease including what 3 components?

A

Anthracosis
Coal macules/nodules
Progressive massive fibrosis

[most pts will not have progressive dz]

84
Q

What is silicosis?

A

Disease resulting from inhaled silicon dioxide — occurs in mining/quarry work, concrete repair, demolition, etc.

Insidious in onset, can occur after exposure is no longer present

May progress to massive pulmonary fibrosis and has 2x risk of developing cancer (as opposed to CWP)

85
Q

Histologic and radiographic findings characteristic of silicosis

A

Histology: dense collagenous nodules

Radiographic: eggshell calcifications (calcified hilar LNs)

86
Q

Interstitial and pleural disease resulting from inhalation of asbestos fibers in which risk correlates with exposure (insulation, shipyards, paper mills, oil or chemical refinery)

A

Asbestosis

87
Q

Disease manifestations of asbestosis

A

Pleura — fibrosis/fibrous plaques, effusions, mesothelioma

Lung — interstitial fibrosis, carcinoma

Possibly extrapulmonary neoplasms

88
Q

2 types of asbestos fibers and which one is most dangerous

A

Serpentine

Amphibole — most dangerous, able to be inhaled deeper into lungs

89
Q

Characteristic histologic finding associated with asbestosis

A

Asbestos bodies (consist of central filament, asbestos itself, and macrophage debris)

Pleural plaque formation (known as “candlewax drippings”) manifests on histology as hyalinized collagen

90
Q

Pulmonary emboli may be defined as obstruction of pulmonary vessels by what structures?

A

Blood clot (“true” thromboembolism)

Bone marrow/fat

Cancer (tumor embolus)

Septic emboli

Air

Foreign material

Parasites (dorofilaria)

91
Q

In what patient populations might you see talc embolism?

A

IV drug users

92
Q

Describe appearance of pulmonary infarcts

A

Wedge shaped lesions

Begin as hemorrhagic, then fibrosis sets in (red—> white infarct)

93
Q

Define pulmonary hypertension

A

Pulmonary artery pressure (PAP) greater than 25 mmHg

94
Q

Histologic findings associated with pulmonary HTN

A

Plexiform lesion — very characteristic!

Medial hypertrophy (smooth muscle in small arteries is good indicator)

95
Q

3 pulmonary hemorrhage syndromes

A

Goodpasture syndrome

Polyangiitis with granulomatosis (Wegener’s)

Idiopathic pulmonary hemosiderosis

96
Q

What does Goodpasture syndrome show on immunofluorescence?

A

Linear pattern of deposition d/t anti-basement membrane Abs

97
Q

Pulmonary hemorrhage syndrome typically found in male smokers in their teens/20s, characterized by heavy red-brown lungs with necrosis, hemorrhage, and hemosiderin-laden macrophages, as well as linear deposits of Ig along basement membrane; clinical features include hemoptysis, focal pulmonary consolidation, renal failure, and possibly death d/t uremia

A

Goodpasture syndrome

98
Q

Pulmonary hemorrhage syndrome d/t autoimmune dz associated with hemoptysis, capillaritis, and scattered, poorly formed granulomas unlike those seen in sarcoidosis

A

Polyangiitis with granulomatosis

99
Q

Pulmonary hemorrhage syndrome associated with intermittent, diffuse alveolar hemorrhage of which the cause and pathogenesis is unknown; it is most often seen in young children, with insidious onset of productive cough, hemoptysis, and anemia, plus diffuse pulmonary infiltration

A

Idiopathic pulmonary hemosiderosis

Respiratory Medicine Exam I (9 decks)

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