37: Pathology of the Lung Part 1 and 2- Carnevale Flashcards

1
Q

incomplete expansion of lungs (neonatal) or collapse of previously inflated lungs

A

atelectasis

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2
Q

what type of atelectasis: follows complete airway obstruction, excessive secretions, mediastinal shift toward the atelectatic lung

A

resorption atelectasis

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3
Q

what is the most common form of atelectasis?

A

compression

excessie air, fluid, blood, or tumor in pleural space. t

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4
Q

where does the mediastinum shift with compression atelectasis?

A

away from the affected lung

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5
Q

what type of atelectasis occurs with loss of surfactant, RDS or post-surgically?

A

patchy atelectasis

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6
Q

fibrosis around the lung –> ______ atelectasis

A

contraction

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7
Q

2 primary causes of pulmonary congestion and edema

A
  • hemodynamic disturbances

- microvascular injury

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8
Q

most common cause of hemodynamic pulmonary edema

A

increased hydrostatic pressure from things such as L CHF

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9
Q

heart-failure cells may indicate ….

A

hemodynamic pulmonary edema

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10
Q

injury to capillaries of alveolar septa –>

A

hemodynamic pulmonary edema caused by micorvascular injury

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11
Q

group of diseases with common symptoms of dyspnea and recurrent airway obstruction

A

obstructive pulmonary disease

ex: emphysema, chronic bronchitis, asthma, bronchiectasis

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12
Q

emphysema and chronic bronchitis =

A

COPD

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13
Q

mucus hypersecretion and inflammation in large airways =

A

chronic bronchitis

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14
Q

loss of elastic recoil in respiratory bronchioles and alveolar ducts (small airways) =

A

emphysema

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15
Q

irreversible airway obstruction in contrast to asthma

A

COPD

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16
Q

limitation of airflow due to increased resistance caused by partial or complete obstruction from trachea to respiratory bronchioles

A

obstructive airway disease

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17
Q

decreased FEV1 and decreased FEV1/FVC ratio

TLC and FVC normal

A

obstructive airway disease

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18
Q

decreased expansion of the lung

A

restrictive lung disease

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19
Q

decreased TLC and FVC

normal FEV/FVC ratio

A

restrictive lung disease

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20
Q

emphysema is more common and severe in ____

A

males

generally not disabling until 5-8th decades

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21
Q

symptoms of emphysema are generally not apparent until _ of pulmonary parenchyma incapacitated

A

1/3

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22
Q

irreversible enlargement of airspaces distal to terminal bronchiole accompanied by non-fibrotic destruction of airway walls

A

emphysema

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23
Q

smoking stimulates release of ________ from both neutrophils and macrophages

A

elastase

macrophage elastase is not inhibited by alpha1-AT

ALSO free radicals inhibit the antiprotease leading to even more damage

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24
Q

proposed mechanism for emphsema

A

protease-antiprotease mechanism

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25
a person develops emphysema at an earlier age... what might they have?
alpha1-AT deficiency
26
do you have too little or too much protease/elastase in emphysema?
too much ---> collagen and elastin destruction
27
PiZZ phenotype =
80% develop symptomatic panacinar emphysema this genotype leads to misfolded prtns which can not get out of the liver
28
acinus =
lung distal to terminal bronchiole
29
emphysema adjacent to areas of fibrosis, scarring or atelectasis
paraseptal emphysema
30
airspace enlargement with fibroiss associated with scarring
irregular emphysema
31
most common type of emphysema
centriacinar emphysema
32
emphysema with respiratory bronchioles affected and distal alveoli spared
centriacinar emphysema greatest severity in apical segments of upper lobes
33
emphysema with acini uniformly enlarged from respiratory bronchioles to terminal blind alveoli
panacinar emphysema most common in basilar portions of lung can occur together with centriacinar emphysema
34
emphysema enlargement with destructiono of distal portion of acinus
distal acinar/ paraseptal emphysea usually adjacent to pleura, septae, lobule margins and areas of scarring
35
what type of emphysema is associated with sponstaneous pneumothorax and bullous disease of lung in young adults NOT smoking
paraseptal emphysema
36
what causes death from emphysema?
- respiratory acidosis and coma - R HF - massive collapse of lungs secondary to pneumothorax
37
"pink puffers"
severe emphysema - barrel chest, DOE, pursed-lip breathing, weight loss
38
"blue bloaters"
chronic bronchitis --> cor pulmonale and CF purulent sputumm hypoxia
39
chronic bronchitis = persistent cough with production of sputum for at least _____ months of a year for at least ___ consecutive years; may have airflow decrease (FEV1)
3 | 2
40
morphologic correlates of chronic bronchitis
- chronic inflammation of airways - hypertrophy of submucosal glands - goblet cell metaplasia - plugging from mucus - epithlium metaplasia and dysplasia
41
what is bronchiolitis obliterans?
obliterationof lumen secondary to fibrosis leads to narrowing of bronchioles morphologic correlate of chronic bronchitis
42
normal v. chrnic bronchitis reid index
normal = less than 0.4 chronic is more than 0.4
43
pulomonary HTN and HF caused by chronic bronchitis occur ________ than from severe emphysema
earlier and more severe
44
why does chronic bronchitis provide ground for cancer development?
causes squamous metaplasia and dysplasia of bronchial epithelium
45
how does cigarette smoke predispose to infection with chronic bronchits?
- interfering with ciliary action - directly damaging the epithelium - inhibitng the ability of bronchial and alveolar leukocytes to clear bacteria
46
younger, late dyspnea, copious sputum, infections, episodic, HF, airway resistance, large heart, "blue bloater"
bronchitis
47
older, early dyspnea, little sputum, progressively worse, low elastic recoil, "pink puffer"
emphysema
48
observe: lumen filled with mucus, tall epitheliu, with goblet cell metaplasia, fibrous thickening of wall, and increased prominence of smooth muscle
chronic bronchitis
49
chronic inflammatory disorder of airways; causes recurrent episodes of wheezing, breathlessness, chest tightness and cough particularly at night or early morning
asthma
50
inflammation --> _______ --> episodes of reversible bronchoconstriction
hyperreactive airways = asthma
51
unremitting and fatal asthma =
status ashtmaticus
52
initiated by a type I hypersensitivity rxn after exposure to an extrinisc allergen; triggered by environmental allergens
atopic (extrinisc) asthma nonatopic would be initiated by a diverse nonimmune mechanism such as ingestion of aspirin, pulmonary infection, inhalants and exercise
53
Describe the hypersensitivity rxn of asthma
- initial sensitization to inhaled antigens stimulates induction of CD4+ cells of TH2 type - TH2 releases cytokines IL4 and IL5 - IG-E mediated eosinophilic reaction can make this early and a later response
54
what response is fundamental for allergic asthma?
TH2 response
55
early v. late phase asthma
early: antigen exposure, 30 min, asthmatic attack, goes away by itself in hours late: 4-8 hrs later recruited cells arrive in bronchus, binding to left over IgE triggers another attack bronchoconstriction is vagal a direct effect of mediators on smooth muscle
56
how do autonomic nerves play a role in asthma?
the discharge of eosinophilic granules further impairs mucociliary function and damages epithelial cells; stimulating n. endings in the mucosa, thereby initiating an autonomic discharge that contributes to airway narrowing and mucous secretion
57
what are curshmann spirals?
asthma indication whorls of shed epithelium
58
what are charcot-leyden crystals?
asthma indication crystalloids made of eosinophilic prtns
59
permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue, resulting from or assoc. with chronic necrotizing infections
bronchiectasis -- IRREVERSIBLE
60
two requisite conditions for bronchiectasis
obstruction and chronic persistent infection
61
what is kartagener syndrome?
genetic disorder causing abnormal cilia and loss of radial spokes
62
complications of bronchiectasis?
pulmonary HPT brain abscesses rarely cor pulmonale amyloidosis
63
``` chronic productive cough hemoptysis foul smelling sputum dyspnea pneumonia lung abscess fever weight loss weakness ```
bronchiectasis
64
mechanism of bronchiectasis
obstruction --> airway damaged, dilates and distorts infection --> causes fibrosis around distorted airway and locks it in that position IRREVERSIBLE