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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
What types of injury to alveolar wall can cause pulmonary edema?
- bacterial pneumonia - sepsis - smoke inhalation - aspiration
26
What are the two physiologic mechanisms behind pulmonary edema?
1. increased hydrostatic pressure -> forces fluid out | 2. decreased oncotic pressure -> loses fluid through equilibrium across a semipermeable membrane
27
What is acute lung injury (ALI)?
acute onset, hypoxemia, bilateral infiltrates | - no evidence of cardiac failure
28
What is acute respiratory distress syndrome (ARDS)?
worsening hypoxemia
29
What is diffuse alveolar damage (DAD)?
the histologic manifestation of ARDS | - what pathologists diagnose, NOT physicians!
30
Which respiratory disorder presents with abrupt onset of symptoms, hypoxemia, bilateral infiltrates, and is non-cardiac in nature?
ARDS
31
What is the mechanism behind ARDS?
1. endothelial activation 2. adhesion/extravasion of neutrophils 3. accumulation of intraalveolar fluid, formation of hyaline membranes 4. resolution of injury
32
What makes up a hyaline membrane?
edema + fibrin + cell debris (dead cells) -> forms a sticky hyaline membrane
33
What leads to a decreased PaO2/FiO2 ratio?
decreased aeration -> ventilation-perfusion mismatch
34
What are the stages of progression of ARDS?
1. exudative 2. proliferative 3. fibrotic
35
What can be seen in the exudative stage of ARDS?
edema, hyaline membranes, neutrophils
36
What can be seen in the proliferative stage of ARDS?
fibroblast proliferation, organizing pneumonia, early fibrosis
37
What can be seen in the fibrotic stage of ARDS?
extensive fibrosis, loss of normal alveolar architechture
38
What are the 2 possible pathways after the fibroproliferative phase of ARDS?
1. resolution: restoration of normal cellular structure/function 2. fibrosis: destruction and distortion of normal cellular structure -> IRREVERSIBLE
39
What is the difference between ARDS and acute interstitial pneumonia (AIP)?
AIP has same clinical presentation and histology as ARDS | ** BUT CANNOT BE ATTRIBUTED TO A SPECIFIC CAUSE/ETIOLOGY**
40
What type of lung disease would you see: - volume restriction - normal FEV1/FVC ratio - FVC reduced
restrictive
41
What type of lung disease would you see: - decreased flow - low FEV1/FVC ratio
obstructive
42
What is the most common cause of COPD/chronic bronchitis
smoking
43
What does the airway of someone with chronic bronchitis look like?
- increased mucus (and extra goblet cells) - damaged cilia - thickened smooth muscle (narrowed lumen)
44
How do physicians make the diagnosis of chronic bronchitis?
persistent cough with productive sputum for ** 3 months out of 2 consecutive years**
45
What is the predominant pathophysiologic mechanism of chronic bronchitis?
mucus glad hyperplasia -> damage to airway epithelium
46
What are the complications of chronic bronchitis?
* *squamous metaplasia** -> dysplasia -> carcinoma - bronchiectasis (bronchi walls thickened d/t inflammation and infection) - death from respiratory infection
47
Why is emphysema considered an obstructive disease?
because chronic bronchitis has left the bronchiole ducts narrowed/compressed -> ducts feeding into alveoli are obstructed
48
Pt presents with enlarged lungs and flattened diaphragm on CXR, "barrel chest", reduced FEV1/FVC ratio - severa/painful dyspnea
emphysema
49
What is the clinicoradiographic/pathologic diagnosis of emphysema?
permanent enlargement and destruction of airspaces distal to the terminal bronchiole
50
What can a deficiency in alpha-1 antitrypsin lead to?
emphysema
51
What does a1-antitrypsin do in the lungs?
it coats the lungs, and inhibits neutrophil elastase | -when left uninhibited, neutrophil elastase can cause lung damage
52
Where is a1-antitrypsin synthesized?
liver | - secreted into bloodstream to inhibit neutrophil elastase
53
What does neutrophil elastase do?
produced by WBC to break down harmful bacteria | - potentially damaging to lungs if left uninhibited
54
What are the 4 types of emphysema discussed?
1. a1-antitrypsin deficiency 2. COPD 3. spontaneous 4. localized
55
What is panacinar/panlobular swelling?
widespread swelling throughout
56
What is centroacinar/centrilobular swelling?
starts in the central part of the lung, alveoli are spared
57
What gene encodes a1-antitrypsin?
Pi gene (proteinase inhibitor) on xsome 14
58
What is the primary means of diagnosis for a1-AT def?
serum testing | - often diagnosed as adult
59
What are the 3 components of asthma?
1. recurrent airway obstruction with a reversible component 2. airway hyper-responsiveness 3. airway inflammation
60
What is considered atopic (extrinsic) "classic" asthma?
- 2/3 of patients - any age, typically children - family hx of asthma - ** elevated IgE levels (Type 1 hypersensitivity)** - variety of allergen triggers
61
What cell types are seen in Type 1 hypersensitivity?
eosinophils, mast cells, lymphocytes
62
What is considered non-atopic (intrinsic) asthma?
- 1/3 of patients - often older** patients - typically normal IgE levels - triggers include cold, exercise, infection
63
What cell types are seen in non-atopic asthma?
T lymphocytes, neutrophils
64
What immune response is seen in the immediate phase of an asthma attack?
bronchoconstriction, increase in mucus secretion, increase in vascular permeability
65
What is the immunologic mechanism behind an asthma attack?
antigen/allergen stimulates Th2 cell -> IgE activation -> *mast cell activation* -> eosinophil recruitment
66
What response does an increase in leukotrienes C/D/E, histamine, prostaglandin D and ACh cause?
bronchoconstriction
67
What does an increase in leukotrienes C/D/E cause?
mucus secretion and increased vascular permeability
68
What does an increase in interleukins case?
recruitment of inflammatory cells
69
What is status asthmaticus?
when asthma attacks follow each other without pause, potentially fatal
70
What is aspirin-sensitive asthma?
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
What is bronchiectasis?
necrotizing inflammatory response | - the end stage process of multiple infections/obstructions
72
What are the examples given where bronchiectasis is seen?
- allergic bronchopulmonary aspergillosis (ABPA) - cystic fibrosis - chronic infection (Tb) - primary ciliary dyskinesia
73
What is Kartagener's syndrome?
primary ciliary dyskinesia | - dysfunction of dynein arm of microtubules
74
What is the triad seen in Kartagener's syndrome?
- sinusitis - bronchiectasis - situs inversus (visceral organs are reversed) NOTE: often male infertility involved
75
What is primary ciliary dyskinesia?
immobility of cilia and flagella due to microtubule defect
76
What is allergic bronchopulmonary asperigillosis (ABPA)?
exaggerated hypersensitivity response to Aspergillus infection overlying chronic lung disease
77
Pt presents with a background of asthma or cystic fibrosis, increased IgE on serum testing, positive skin test, thick mucus in bronchi
allergic bronchopulmonary aspergillosis
78
What is fungal hyphae a characteristic of?
Aspergillus | - leads to bronchiectasis over time
79
What stain demonstrates aggregates of fungal hyphae?
silver stain
80
What is pneumoconiosis?
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
What makes pneumoconiosis worse?
- exposure is high and repetitive - size of particles is small - smoking (impaired ciliary clearance)
82
What is Coal worker's pneumoconiosis?
disease due to inhaled coal dust, with a spectrum of disease 1. anthracosis 2. coal macules/nodules 3. progressive massive fibrosis
83
What is silicosis?
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
What can silicosis progress to?
massive pulmonary fibrosis | - also a two-fold risk of developing cancer
85
What presents as dense collagenous nodules on histo slides, and eggshell calcifications on CXR?
silicosis
86
What is asbestosis?
interstitial and pleural disease resulting from inhalation of asbestos fibers - isulation workers - shipyard workers - paper mill workers - oil or chemical refinery workers
87
What are the disease manifestations of asbestosis?
- pleura: fibrosis/fibrous plaques, effusions, mesothelioma - lung: interstitial fibrosis, carcinoma - extrapulmonary neoplasms
88
When do you see feruginous bodies on a histo slide and "candlewax drippings" grossly?
asbestosis
89
What is mesothelioma associated with?
asbestos exposure - may occur decades after exposure - lifetime exposure risk as high as 10%

CPR Exam 1 (18 decks)

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