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CS1 Exam 3 > 37: Pathology of the Lung Part 1 and 2- Carnevale > Flashcards

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
Q

a person develops emphysema at an earlier age… what might they have?

A

alpha1-AT deficiency

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26
Q

do you have too little or too much protease/elastase in emphysema?

A

too much —> collagen and elastin destruction

27
Q

PiZZ phenotype =

A

80% develop symptomatic panacinar emphysema

this genotype leads to misfolded prtns which can not get out of the liver

28
Q

acinus =

A

lung distal to terminal bronchiole

29
Q

emphysema adjacent to areas of fibrosis, scarring or atelectasis

A

paraseptal emphysema

30
Q

airspace enlargement with fibroiss associated with scarring

A

irregular emphysema

31
Q

most common type of emphysema

A

centriacinar emphysema

32
Q

emphysema with respiratory bronchioles affected and distal alveoli spared

A

centriacinar emphysema

greatest severity in apical segments of upper lobes

33
Q

emphysema with acini uniformly enlarged from respiratory bronchioles to terminal blind alveoli

A

panacinar emphysema

most common in basilar portions of lung

can occur together with centriacinar emphysema

34
Q

emphysema enlargement with destructiono of distal portion of acinus

A

distal acinar/ paraseptal emphysea

usually adjacent to pleura, septae, lobule margins and areas of scarring

35
Q

what type of emphysema is associated with sponstaneous pneumothorax and bullous disease of lung in young adults NOT smoking

A

paraseptal emphysema

36
Q

what causes death from emphysema?

A
  • respiratory acidosis and coma
  • R HF
  • massive collapse of lungs secondary to pneumothorax
37
Q

“pink puffers”

A

severe emphysema

  • barrel chest, DOE, pursed-lip breathing, weight loss
38
Q

“blue bloaters”

A

chronic bronchitis

–> cor pulmonale and CF
purulent sputumm
hypoxia

39
Q

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)

A

3

2

40
Q

morphologic correlates of chronic bronchitis

A
  • chronic inflammation of airways
  • hypertrophy of submucosal glands
  • goblet cell metaplasia
  • plugging from mucus
  • epithlium metaplasia and dysplasia
41
Q

what is bronchiolitis obliterans?

A

obliterationof lumen secondary to fibrosis

leads to narrowing of bronchioles

morphologic correlate of chronic bronchitis

42
Q

normal v. chrnic bronchitis reid index

A

normal = less than 0.4

chronic is more than 0.4

43
Q

pulomonary HTN and HF caused by chronic bronchitis occur ________ than from severe emphysema

A

earlier and more severe

44
Q

why does chronic bronchitis provide ground for cancer development?

A

causes squamous metaplasia and dysplasia of bronchial epithelium

45
Q

how does cigarette smoke predispose to infection with chronic bronchits?

A
  • interfering with ciliary action
  • directly damaging the epithelium
  • inhibitng the ability of bronchial and alveolar leukocytes to clear bacteria
46
Q

younger, late dyspnea, copious sputum, infections, episodic, HF, airway resistance, large heart, “blue bloater”

A

bronchitis

47
Q

older, early dyspnea, little sputum, progressively worse, low elastic recoil, “pink puffer”

A

emphysema

48
Q

observe: lumen filled with mucus, tall epitheliu, with goblet cell metaplasia, fibrous thickening of wall, and increased prominence of smooth muscle

A

chronic bronchitis

49
Q

chronic inflammatory disorder of airways; causes recurrent episodes of wheezing, breathlessness, chest tightness and cough particularly at night or early morning

A

asthma

50
Q

inflammation –> _______ –> episodes of reversible bronchoconstriction

A

hyperreactive airways

= asthma

51
Q

unremitting and fatal asthma =

A

status ashtmaticus

52
Q

initiated by a type I hypersensitivity rxn after exposure to an extrinisc allergen; triggered by environmental allergens

A

atopic (extrinisc) asthma

nonatopic would be initiated by a diverse nonimmune mechanism such as ingestion of aspirin, pulmonary infection, inhalants and exercise

53
Q

Describe the hypersensitivity rxn of asthma

A
  • 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
Q

what response is fundamental for allergic asthma?

A

TH2 response

55
Q

early v. late phase asthma

A

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
Q

how do autonomic nerves play a role in asthma?

A

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
Q

what are curshmann spirals?

A

asthma indication

whorls of shed epithelium

58
Q

what are charcot-leyden crystals?

A

asthma indication

crystalloids made of eosinophilic prtns

59
Q

permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue, resulting from or assoc. with chronic necrotizing infections

A

bronchiectasis – IRREVERSIBLE

60
Q

two requisite conditions for bronchiectasis

A

obstruction and chronic persistent infection

61
Q

what is kartagener syndrome?

A

genetic disorder causing abnormal cilia and loss of radial spokes

62
Q

complications of bronchiectasis?

A

pulmonary HPT
brain abscesses
rarely cor pulmonale
amyloidosis

63
Q 
chronic productive cough
hemoptysis
foul smelling sputum
dyspnea 
pneumonia
lung abscess
fever
weight loss
weakness
A

bronchiectasis

64
Q

mechanism of bronchiectasis

A

obstruction –> airway damaged, dilates and distorts

infection –> causes fibrosis around distorted airway and locks it in that position

IRREVERSIBLE

CS1 Exam 3 (17 decks)

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