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CPR Exam 1 > Pulm Path Pt 1 > Flashcards

Pulm Path Pt 1 Flashcards

1
Q

What are capillaries associated with in normal alveolar structure?

A

endothelium

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2
Q

What is the basement membrane associated with in normal alveolar structure?

A

interstitium

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3
Q

What do Type 1 pneumocytes do?

A

facilitate gas exchange

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4
Q

What do Type 2 pneumocytes do?

A

produce surfactant and replace Type 1 pneumocytes (are modified stem cells)

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5
Q

What do alveolar pores (of Kohn) do?

A

allow aeration but also bacteria/cells/exudate to travel between alveoli

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6
Q

What causes pulmonary hypoplasia?

A
  • reduced pace in thoracic cavity (diaphragmatic hernia)

- impaired ability to inhale (oligohydramnios/renal agenesis/chest wall motion disorders)

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7
Q

What is a foregut cyst?

A
  • detached outpourings of foregut, seen along hilum and mediastinum
  • can be respiratory, esophageal, or gastroenteric
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8
Q

What are the complications of a foregut cyst?

A

rupture, infection, or airway compression

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9
Q

What is Congenital Pulmonary/Cystic Adenomatoid Malformation (CPAM/CCAM)?

A

“arrested development” of pulmonary tissue with the formation of intrapulmonary cystic masses

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10
Q

Can CPAM/CCAM be detected on fetal US?

A

yes

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11
Q

Why is CPAM/CCAM deadly?

A

due to hydrops or pulmonary hypoplasia

- can also get infected later in life

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12
Q

What are pulmonary sequestrations?

A

nonfunctioning lung tissue that forms an accessory lung bud

- typically in the region of lower left lobe

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13
Q

What are pulmonary sequestrations characterized by?

A
  • lack of connection to the tracheobronchial tree

- independent (systemic) arterial supply

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14
Q

What determines if a pulmonary sequestration is intralobar or extralobar?

A

depends on whether the budding occurs before or after the pleura is established

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15
Q

What makes intralobar pulmonary sequestration (ILS) susceptible to infection and abscess formation?

A

lack of airway perfusion

- may present in older children and adults

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16
Q

When does extralobar pulmonary sequestration (ELS) usually present?

A

after birth with other congenital anomalies

- come to attention as mass lesions in the chest or abdomen

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17
Q

Which type of pulmonary sequestration has independent vessels, pleura and possibly airways?

A

extralobar (ELS)

- no connection to pulmonary vasculature or tracheobronchial tree

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18
Q

What are the 3 types of atelectasis discusses?

A
  1. resorption
  2. compression
  3. contraction
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19
Q

What is resorption atelectasis?

A

airway obstruction with gradual resorption of air

- reduces lung expansion

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20
Q

What is compression atelectasis?

A

accumulated material in the pleural cavity compresses the lung parenchyma
- not a direct lung issue

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21
Q

What is contraction atelectasis?

A

fibrotic or other innate restrictive process in the pleura or peripheral lung
- restricts lung expansion

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22
Q

What is pulmonary edema?

A

interstitial fluid (proteinaceous material) accumulates in alveolar spaces

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23
Q

What are the examples given of “pushing out” pulmonary edema?

A
  • left sided heart failure
  • volume overload
  • pulmonary vein obstruction
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24
Q

What are the examples given of “leaking out” pulmonary edema?

A
  • hypoalbuminemia
  • nephrotic syndrome
  • liver disease
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25
Q

What types of injury to alveolar wall can cause pulmonary edema?

A
  • bacterial pneumonia
  • sepsis
  • smoke inhalation
  • aspiration
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26
Q

What are the two physiologic mechanisms behind pulmonary edema?

A
  1. increased hydrostatic pressure -> forces fluid out

2. decreased oncotic pressure -> loses fluid through equilibrium across a semipermeable membrane

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27
Q

What is acute lung injury (ALI)?

A

acute onset, hypoxemia, bilateral infiltrates

- no evidence of cardiac failure

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28
Q

What is acute respiratory distress syndrome (ARDS)?

A

worsening hypoxemia

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29
Q

What is diffuse alveolar damage (DAD)?

A

the histologic manifestation of ARDS

- what pathologists diagnose, NOT physicians!

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30
Q

Which respiratory disorder presents with abrupt onset of symptoms, hypoxemia, bilateral infiltrates, and is non-cardiac in nature?

A

ARDS

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31
Q

What is the mechanism behind ARDS?

A
  1. endothelial activation
  2. adhesion/extravasion of neutrophils
  3. accumulation of intraalveolar fluid, formation of hyaline membranes
  4. resolution of injury
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32
Q

What makes up a hyaline membrane?

A

edema + fibrin + cell debris (dead cells) -> forms a sticky hyaline membrane

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33
Q

What leads to a decreased PaO2/FiO2 ratio?

A

decreased aeration -> ventilation-perfusion mismatch

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34
Q

What are the stages of progression of ARDS?

A
  1. exudative
  2. proliferative
  3. fibrotic
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35
Q

What can be seen in the exudative stage of ARDS?

A

edema, hyaline membranes, neutrophils

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36
Q

What can be seen in the proliferative stage of ARDS?

A

fibroblast proliferation, organizing pneumonia, early fibrosis

37
Q

What can be seen in the fibrotic stage of ARDS?

A

extensive fibrosis, loss of normal alveolar architechture

38
Q

What are the 2 possible pathways after the fibroproliferative phase of ARDS?

A
  1. resolution: restoration of normal cellular structure/function
  2. fibrosis: destruction and distortion of normal cellular structure -> IRREVERSIBLE
39
Q

What is the difference between ARDS and acute interstitial pneumonia (AIP)?

A

AIP has same clinical presentation and histology as ARDS

** BUT CANNOT BE ATTRIBUTED TO A SPECIFIC CAUSE/ETIOLOGY**

40
Q

What type of lung disease would you see:

  • volume restriction
  • normal FEV1/FVC ratio
  • FVC reduced
A

restrictive

41
Q

What type of lung disease would you see:

  • decreased flow
  • low FEV1/FVC ratio
A

obstructive

42
Q

What is the most common cause of COPD/chronic bronchitis

A

smoking

43
Q

What does the airway of someone with chronic bronchitis look like?

A
  • increased mucus (and extra goblet cells)
  • damaged cilia
  • thickened smooth muscle (narrowed lumen)
44
Q

How do physicians make the diagnosis of chronic bronchitis?

A

persistent cough with productive sputum for ** 3 months out of 2 consecutive years**

45
Q

What is the predominant pathophysiologic mechanism of chronic bronchitis?

A

mucus glad hyperplasia -> damage to airway epithelium

46
Q

What are the complications of chronic bronchitis?

A
  • *squamous metaplasia** -> dysplasia -> carcinoma
  • bronchiectasis (bronchi walls thickened d/t inflammation and infection)
  • death from respiratory infection
47
Q

Why is emphysema considered an obstructive disease?

A

because chronic bronchitis has left the bronchiole ducts narrowed/compressed -> ducts feeding into alveoli are obstructed

48
Q

Pt presents with enlarged lungs and flattened diaphragm on CXR, “barrel chest”, reduced FEV1/FVC ratio
- severa/painful dyspnea

A

emphysema

49
Q

What is the clinicoradiographic/pathologic diagnosis of emphysema?

A

permanent enlargement and destruction of airspaces distal to the terminal bronchiole

50
Q

What can a deficiency in alpha-1 antitrypsin lead to?

A

emphysema

51
Q

What does a1-antitrypsin do in the lungs?

A

it coats the lungs, and inhibits neutrophil elastase

-when left uninhibited, neutrophil elastase can cause lung damage

52
Q

Where is a1-antitrypsin synthesized?

A

liver

- secreted into bloodstream to inhibit neutrophil elastase

53
Q

What does neutrophil elastase do?

A

produced by WBC to break down harmful bacteria

- potentially damaging to lungs if left uninhibited

54
Q

What are the 4 types of emphysema discussed?

A
  1. a1-antitrypsin deficiency
  2. COPD
  3. spontaneous
  4. localized
55
Q

What is panacinar/panlobular swelling?

A

widespread swelling throughout

56
Q

What is centroacinar/centrilobular swelling?

A

starts in the central part of the lung, alveoli are spared

57
Q

What gene encodes a1-antitrypsin?

A

Pi gene (proteinase inhibitor) on xsome 14

58
Q

What is the primary means of diagnosis for a1-AT def?

A

serum testing

- often diagnosed as adult

59
Q

What are the 3 components of asthma?

A
  1. recurrent airway obstruction with a reversible component
  2. airway hyper-responsiveness
  3. airway inflammation
60
Q

What is considered atopic (extrinsic) “classic” asthma?

A
  • 2/3 of patients
  • any age, typically children
  • family hx of asthma
  • ** elevated IgE levels (Type 1 hypersensitivity)**
  • variety of allergen triggers
61
Q

What cell types are seen in Type 1 hypersensitivity?

A

eosinophils, mast cells, lymphocytes

62
Q

What is considered non-atopic (intrinsic) asthma?

A
  • 1/3 of patients
  • often older** patients
  • typically normal IgE levels
  • triggers include cold, exercise, infection
63
Q

What cell types are seen in non-atopic asthma?

A

T lymphocytes, neutrophils

64
Q

What immune response is seen in the immediate phase of an asthma attack?

A

bronchoconstriction, increase in mucus secretion, increase in vascular permeability

65
Q

What is the immunologic mechanism behind an asthma attack?

A

antigen/allergen stimulates Th2 cell -> IgE activation -> mast cell activation -> eosinophil recruitment

66
Q

What response does an increase in leukotrienes C/D/E, histamine, prostaglandin D and ACh cause?

A

bronchoconstriction

67
Q

What does an increase in leukotrienes C/D/E cause?

A

mucus secretion and increased vascular permeability

68
Q

What does an increase in interleukins case?

A

recruitment of inflammatory cells

69
Q

What is status asthmaticus?

A

when asthma attacks follow each other without pause, potentially fatal

70
Q

What is aspirin-sensitive asthma?

A

associated with nasal polyps and recurrent rhinitis (Samter’s triad)**

  • a unique sensitivity to aspirin
  • cross reacts with other NSAIDs

NOTE: COX 1/2 pathway inhibited by aspirin! Leave leukotrienes C/D/E in excess -> bronchospasm

71
Q

What is bronchiectasis?

A

necrotizing inflammatory response

- the end stage process of multiple infections/obstructions

72
Q

What are the examples given where bronchiectasis is seen?

A
  • allergic bronchopulmonary aspergillosis (ABPA)
  • cystic fibrosis
  • chronic infection (Tb)
  • primary ciliary dyskinesia
73
Q

What is Kartagener’s syndrome?

A

primary ciliary dyskinesia

- dysfunction of dynein arm of microtubules

74
Q

What is the triad seen in Kartagener’s syndrome?

A
  • sinusitis
  • bronchiectasis
  • situs inversus (visceral organs are reversed)

NOTE: often male infertility involved

75
Q

What is primary ciliary dyskinesia?

A

immobility of cilia and flagella due to microtubule defect

76
Q

What is allergic bronchopulmonary asperigillosis (ABPA)?

A

exaggerated hypersensitivity response to Aspergillus infection overlying chronic lung disease

77
Q

Pt presents with a background of asthma or cystic fibrosis, increased IgE on serum testing, positive skin test, thick mucus in bronchi

A

allergic bronchopulmonary aspergillosis

78
Q

What is fungal hyphae a characteristic of?

A

Aspergillus

- leads to bronchiectasis over time

79
Q

What stain demonstrates aggregates of fungal hyphae?

A

silver stain

80
Q

What is pneumoconiosis?

A

reaction by the lungs to inhaled mineral or organic dust

  • occupational exposure***
  • air pollution

NOTE: exaggerated response in some individuals indicates a possible genetic component

81
Q

What makes pneumoconiosis worse?

A
  • exposure is high and repetitive
  • size of particles is small
  • smoking (impaired ciliary clearance)
82
Q

What is Coal worker’s pneumoconiosis?

A

disease due to inhaled coal dust, with a spectrum of disease

  1. anthracosis
  2. coal macules/nodules
  3. progressive massive fibrosis
83
Q

What is silicosis?

A

disease resulting from inhales silicon dioxide

  • mining/quarry work
  • concrete repair/demolition

NOTE: has insidious onset, it can progress after exposure is no longer present

84
Q

What can silicosis progress to?

A

massive pulmonary fibrosis

- also a two-fold risk of developing cancer

85
Q

What presents as dense collagenous nodules on histo slides, and eggshell calcifications on CXR?

A

silicosis

86
Q

What is asbestosis?

A

interstitial and pleural disease resulting from inhalation of asbestos fibers

  • isulation workers
  • shipyard workers
  • paper mill workers
  • oil or chemical refinery workers
87
Q

What are the disease manifestations of asbestosis?

A
  • pleura: fibrosis/fibrous plaques, effusions, mesothelioma
  • lung: interstitial fibrosis, carcinoma
  • extrapulmonary neoplasms
88
Q

When do you see feruginous bodies on a histo slide and “candlewax drippings” grossly?

A

asbestosis

89
Q

What is mesothelioma associated with?

A

asbestos exposure

  • may occur decades after exposure
  • lifetime exposure risk as high as 10%

CPR Exam 1 (18 decks)

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