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Pathopharm Exam 3 > Module 8: Part 2 > Flashcards

Module 8: Part 2 Flashcards

28-52

1
Q

Bronchiolitis

A
  • Diffuse inflammation of small airways or bronchioles
  • Occurs in adults with chronic bronchitis or those with a viral infection or who have inhaled toxic gases
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2
Q

Bronchiolitis
Most common in…

A

children

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3
Q

Bronchiolitis
manifestations

A
  • Rapid RR
  • significant use of accessory muscles
  • low fever
  • dry, nonproductive cough
  • hyperinflated chest
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4
Q

Bronchiolitis
Treatment

A
  • Antibiotics
  • steroids
  • chest physical therapy
    (humidified air, coughing and deep breathing, postural drainage)
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5
Q

Bronchiolitis obliterans

A
  • Late-stage fibrotic disease of the airways
  • Causes permanent scarring of the lungs
  • Can occur with all causes of bronchiolitis
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6
Q

When is Bronchiolitis obliterans most likely to occur?

A
  • Most common after lung transplantation
  • D/t acute rejection and infection
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7
Q

Bronchiolitis obliterans
treatment

A

Corticosteroids other immunomodulatory agents

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8
Q

What is true about Pulmonary fibrosis?
A) From exposure to toxic gases like urea
B) Effectively treated with steroids alone
C) Late-stage fibrotic disease of the airways
D) Causes permanent scarring of the lungs
E) None of these

A

E) None of these

toxic gases:
Ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide

Treatment: Corticosteroids; combined treatment with cytotoxic drugs; antifibrotic drugs (such as N-acetylcysteine and pirfenidone), interferon, and anticoagulant agents; lung transplantation

Bronchiolitis obliterans:
* Late-stage fibrotic disease of the airways
* Causes permanent scarring of the lungs

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9
Q

Pulmonary fibrosis

A
  • Excessive fibrous or connective tissue
  • Idiopathic pulmonary fibrosis: No specific cause
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10
Q

Pulmonary fibrosis
manifestations

A

Increasing dyspnea on exertion

When d/t exposure:
* Burning eyes, nose, and throat
* coughing
* chest tightness
* dyspnea
* hypoxemia

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11
Q

Pulmonary fibrosis
causes

A

Exposure to toxic gases:
* Ammonia
* hydrogen chloride
* sulfur dioxide
* chlorine
* phosgene
* nitrogen dioxide

idiopathic pulmonary fibrosis: No specific cause

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12
Q

Pulmonary fibrosis
Treatment

non-exposure vs exposure to toxic gases

A

Corticosteroids combined with:
* cytotoxic drugs
* antifibrotic drugs (N-acetylcysteine, pirfenidone)
* interferon
* anticoagulant agents
* lung transplantation

If d/t Gas exposure
* O2
* mechanical ventilation + PEEP
* CV support
* Steroid effectiveness questionable

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13
Q

T/F
Steroids are effective treatment for Pulmonary fibrosis resulting from exposure to toxic gases.

A

False
questionable
but
used for pulmonary fibrosis not d/t toxic gas exposure

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14
Q

Oxygen toxicity

A
  • Prolonged exposure to high O2 concentrations
  • Severe inflammatory response
  • mediated primarily by oxygen radicals
  • damage to alveolocapillary membranes
  • disrupts surfactant production
  • interstitial and alveolar edema
  • decreased compliance
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15
Q

oxygen toxicity causes what types of edema?

A

interstitial and alveolar

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16
Q

What is false about Oxygen Toxicity?
A) Prolonged exposure to high O2 concentrations
B) mediated primarily by CO2 radicals
C) alveolocapillary membrane damage
D) inhibits surfactant production
E) none of these

A

B) mediated primarily by CO2 radicals

should be oxygen radicals

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17
Q

Oxygen toxicity
Treatment

A
  • Ventilatory support
  • inspired O2 concentration <60% ASAP
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18
Q

Oxygen toxicity
Wean to FiO2 of ____ as soon as tolerated.

A

<60%

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19
Q

Any change in lung caused by the inhalation of inorganic dust particles

A

Pneumoconiosis

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20
Q

Pneumoconiosis
Most common causes

A
  • usually from the workplace
  • Silica, asbestos, and coal

Any change in lung caused by the inhalation of inorganic dust particles

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21
Q

Pneumoconiosis
Clinical manifestations

A
  • Cough
  • sputum production
  • dyspnea
  • decreased lung volumes
  • hypoxemia
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22
Q

Pneumoconiosis
Treatment

A
  • Palliative
  • prevention of further exposure
  • Improve working conditions
  • Pulmonary rehabilitation
  • manage associated hypoxemia & bronchospasm
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23
Q

Which condition is known to have associated bronchospasm?
A) Oxygen toxicity
B) Allergic alveolitis
C) Pulmonary fibrosis
D) Pneumoconiosis
E) None of these

A

D) Pneumoconiosis

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24
Q

Pneumoconiosis
Types

A
  • Silicosis: inhale free silica (silicon dioxide) & containing compounds (mining); No cure
  • Coal worker pneumoconiosis (coal miner’s lung, black lung): coal dust deposits
    No specific treatment
  • Asbestosis: Asbestos exposure; factory workers; if nearby asbestos emission; Supportive treatment; Link to mesothelioma
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25
Q

Pneumoconiosis Types:
Silicosis

A
  • inhale free silica (silicon dioxide) & containing compounds
  • mining
  • No cure
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26
Q

Pneumoconiosis Types:
Black lung

A
  • Coal worker pneumoconiosis/coal miner’s lung/black lung)
  • coal dust deposits
  • No specific treatment
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27
Q

T/F
The effects Asbestosis are limited to those who work in the prescence of it.

A

False
affects not only factory workers but it also affects individuals who live in areas of asbestos emission

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28
Q

T/F
Silicosis is a form of Pneumoconiosis that is linked to mesothelioma.

A

False
Asbestosis is the form of Pneumoconiosis that is linked to mesothelioma

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29
Q

Allergic alveolitis

A
  • Extrinsic allergic alveolitis (hypersensitivity pneumonitis)
  • Hypersensitivity to allergens
  • Inhalation of organic particles or fumes
  • Acute, subacute, chronic
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30
Q

T/F
Allergic alveolitis can occur by inhalational insult.

A

True
Inhalation of organic particles or fumes

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31
Q

AKA hypersensitivity pneumonitis

A

Allergic alveolitis/Extrinsic allergic alveolitis

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32
Q

Allergic alveolitis
Treatment

A
  • Avoid the trigger agent
  • Corticosteroids
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33
Q

Systemic disorders and the lungs
Affect the…

A

airways, pleurae, or lung parenchyma

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34
Q

Systemic disorders that affect the lungs

A
  • Granulomatous disorders
  • connective tissue diseases
  • Goodpasture syndrome (autoimmune attack of lungs)
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35
Q

autoimmune attack of lungs occurs in…

A

Goodpasture syndrome

attacks lining of lungs and kidneys

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36
Q

Systemic disorder lung involvement
-manifestations
-treatment

A
  • usually nonspecific
  • diagnose based on involvement of other organs
  • Usually no specific treatment
  • corticosteroids often used
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37
Q

Pulmonary edema:
Excess water in the lung d/t disturbances of …
(3)

A
  • capillary hydrostatic pressure
  • capillary oncotic pressure
  • capillary permeability
38
Q

Most common cause of pulmonary edema

A

Left-sided heart disease

39
Q

Postobstructive pulmonary edema (POPE)

A
  • Negative pressure pulmonary edema
  • rare & life-threatening
  • complication after relief of upper airway obstruction
40
Q

Negative pressure pulmonary edema is called

A

Postobstructive pulmonary edema (POPE)

41
Q

When does Postobstructive pulmonary edema (POPE) occur?

A

can occur after relief of upper airway obstruction

42
Q

Pulmonary edema
Clinical manifestations

A
  • Dyspnea
  • orthopnea
  • hypoxemia
  • increased work of breathing
43
Q

Pulmonary edema pathophysiology

A

Can start with
* valve/LV dysfxn; CAD
* injured capillary endothelium
* blocked lymph vessels

44
Q

T/F
Pulmonary edema may have cardiac, pulmonary or lymphatic etiology.

A

True

45
Q

Pulmonary edema
Treatment

A

heart failure:
* Improve CO & volume status
* diuretics, vasodilators, inotropes

Increased capillary permeability d/t injury:
* Remove trigger agent
* maintain oxygenation, ventilation, circulation

POPE (Post-Obstructive Pulmonary Edema)
* PEEP ventilation

Any type:
* O2 and/or mechanical ventilation

46
Q

T/F
Heart failure can cause pulmonary edema by increasing oncotic pressure.

A

False
Increased hydrostatic pressure

47
Q

Regardless of the cause of pulmonary edema, what should be used as treatment?

A

O2 and/or mechanical ventilation

48
Q

Which type of pulmonary edema treatment is characterized by using PEEP ventilation?
A) secondary to heart failure
B) Lung injury
C) Post-Obstructive Pulmonary Edema
D) None of these

A

C) Post-Obstructive Pulmonary Edema

Mechanical ventilation can be used with all types but Negative pressure pulmonary edema especially needs PEEP

Ie: when pt breathes against closed cords when waking up = negative pressure pulmonary edema; we combat this by squeezing that bag continuosly to pop it back open

49
Q

What do Acute lung injury (ALI) & acute respiratory distress syndrome (ARDS) have in common?

A
  • Forms of respiratory failure
  • characterized by acute lung inflammation & diffuse alveolocapillary injury
  • Injured pulmonary capillary endothelium
  • Increased capillary permeability
  • Inflammation
  • Surfactant inactivation
  • Edema and atelectasis
50
Q

Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) include:
A) Decreased capillary permeability
B) Over production of surfactant
C) Fibrosis of the pulmonary capillary endothelium
D) localized alveolocapillary injury
E) None of these

A

E) None of these

  • Forms of respiratory failure
  • characterized by acute lung inflammation & diffuse alveolocapillary injury
  • Injured pulmonary capillary endothelium
  • Increased capillary permeability
  • Inflammation
  • Surfactant inactivation
  • Edema and atelectasis
51
Q

Acute Lung Injury &
Acute Respiratory Distress Syndrome
-Phases
-Timeline for each?

A
  • Exudative/Inflammatory: Within 72 hours
  • Proliferative: 4-21 days
  • Fibrotic: 14-21 days
52
Q

Exudative/Inflammatory Phase:
A) Is the second stage of ALI/ARDS
B) 4 to 21 days after onset
C) Edema resolves
D) involves alveolar destruction
E) Surfactant is inactivated

A

E) Surfactant is inactivated

all other options belong to latter stages

53
Q

Asthma is (restrictice/obstructive) disease.

A

obstructive

54
Q

Which ALI/ARDS stage includes acute respiratory failure?

A

Fibrotic
14 to 21 days

55
Q

Hyopexmia develops in which ALI/ARDS stage ?

A

Proliferative
4 to 21 days

56
Q

Some specific features of ARDS

A
  • Macrophage involvement
  • Alveolar consoildation
  • atelactasis
57
Q

ARDS
chain of events

A
58
Q

Which attribute of ARDS occurs first?
A) Decreased tissue perfusion
B) Dyspnea and hypoxemia
C) poor response to supplemental O2
D) Hyperventilation
E) More than one correct answer

A

More than one correct answer:
B) Dyspnea and hypoxemia
C) poor response to supplemental O2

59
Q

T/F
In ARDS, repiratory alkalosis will precede respiratory acidosis.

A

True
metabolic acidosis occurs in between

60
Q

T/F
Decreased cardiac output and hypotension occur in early to mid ARDS.

A

False
end stage

61
Q

ARDS Treatment

A
  • Mechanical ventilation with PEEP
  • high oxygen %
  • Low-volume ventilation
  • noninvasive positive pressure ventilation
  • permissive hypercapnia
  • prone
  • extracorporeal gas exchange
  • partial liquid ventilation
  • Low-dose steroid administration
62
Q

ARDS treatment should include all of these EXCEPT:
A) Mechanical ventilation with PEEP
B) noninvasive positive pressure ventilation
C) permissive hypercapnia
D) partial liquid ventilation
E) Aggressive steroid therapy

A

E) Aggressive steroid therapy

  • Mechanical ventilation with PEEP
  • high oxygen %
  • Low-volume ventilation
  • noninvasive positive pressure ventilation
  • permissive hypercapnia
  • prone
  • extracorporeal gas exchange
  • partial liquid ventilation
  • Low-dose steroid administration
63
Q

Obstructive Pulmonary Diseases show worsening airway obstruction during (inspration/expiration)

A

expiration

64
Q

T/F
In restrictive pulmonary diseases, more force or more time is required to expire a given volume of air & emptying the lungs is slower.

A

False
Obstructive

65
Q

Obstructive Pulmonary Disease
Unifying signs & symptoms

A

Wheezing and dyspnea

66
Q

Wheezing is a symptoms a/w (obstructive/restrictive) respiratory diseases.

A

Obstructive

Obstructive Diseases
* Asthma
* Chronic bronchitis
* Emphysema
* Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

67
Q

Obstructive Pulmonary Disease
Manifestations

A
  • Increased work of breathing
  • ventilation-perfusion mismatch (VQ mismtach)
  • ↓ forced expiratory volume in one second (FEV1)
68
Q

V/Q mismatch is a/w (obstructive/restrictive) respiratory diseases.

A

obstructive

Obstructive Diseases
* Asthma
* Chronic bronchitis
* Emphysema
* Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

69
Q

The Obstructive Diseases

A
  • Asthma
  • Chronic bronchitis
  • Emphysema
  • Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

Restrictive:
* Aspiration
* Atelectasis
* Bronchiectasis, bronchiolitis
* Pulmonary fibrosis
* Inhalational disorders
* Pneumoconiosis
* Allergic alveolitis
* Pulmonary edema
* Acute respiratory distress syndrome

70
Q

T/F
Asthma is a chronic inflammatory disorder of the alevolar mucosa.

A

False
bronchial

Asthma is disease of the airways, not really the lungs

71
Q

Asthma
How much of the occurrence is during childhood?

A

50%

72
Q

T/F
Asthma is a familial disorder, with over 100 identified genes.

A

True

73
Q

Asthma causes…

A
  • bronchial hyperresponsiveness
  • airway constriction
  • airways variable airflow obstruction
74
Q

T/F
The variable airflow obstruction seen in asthma is reversible.

A

True

75
Q

For Asthma, a ___ hypothesis is suggested.

A

Hygiene

suggests that early exposure to certain microorganisms helps children develop healthy immune systems and protects against allergies.

76
Q

Asthma includes episodic attacks of:

A
  • bronchospasm
  • bronchial inflammation
  • mucosal edema
  • increased mucous production
77
Q

Early asthmatic response
-Immunoglobulin
-its effects

A

Immunoglobulin E (IgE): mast cells degranulate & release lot of inflammatory mediators

  • Vasodilation
  • Increased capillary permeability
  • Mucosal edema
  • Bronchial smooth muscle contraction (bronchospasm)
  • Tenacious mucous secretion
78
Q

The early asthmatic response includes all of the following except:
A) Tenacious mucous secretion
B) Vasodilation
C) Immunoglobulin E (IgE)
D) Increased capillary permeability
E) Alveolar edema

A

E) Alveolar edema

Immunoglobulin E (IgE): mast cells degranulate & release lot of inflammatory mediators

  • Vasodilation
  • Increased capillary permeability
  • Mucosal edema
  • Bronchial smooth muscle contraction (bronchospasm)
  • Tenacious mucous secretion
79
Q

Immunoglobulin E (IgE) in the Early asthmatic response

A

causes the mast cells to degranulate, releasing a large number of inflammatory mediators

80
Q

All of the following occur in asthma EXCEPT
A) smooth muscle constriction
B) Mast cell granulation
C) Mucus production & accumulation
D) Alveoli hyperinflation
E) Mucus plugs

A

B) Mast cell granulation

should be DEgranulation

81
Q

Early asthmatic response
endogenous substances involved

A
  • dendritic cells
  • CD4+ T cells
  • Interleukin 4 (IL-4)
  • B-cell activation
  • IgE
  • IL-5
  • eosinophils
  • IL-8
  • IL-13
  • IL-17
  • IL-22
82
Q

Which interluekin (IL) causes the activation of eosinophils, contributing to bronchial hyperresponsiveness?

A

IL-5

83
Q

Antigen exposure to the bronchial mucosa activates…

A

dendritic cells (antigen-presenting cells) to present the antigen to CD4+ T cells

84
Q

Early asthmatic reponse
steps

A

E (IgE): masts cells degranulate; release inflammatory mediators
⬇️
Antigen exposure: dendritic cells
(antigen-presenting cells) present antigen to CD4+ T cells
⬇️
Interleukin 4: B-cell activation & produce antigen-specific IgE
⬇️
IL-5: activates eosinophils (bronchial hyperresponsiveness, fibroblast proliferation, epithelial injury, and airway scarring)
⬇️
IL-8: neutrophils (exaggerate inflammation)
⬇️
IL-13: impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction
⬇️
IL-17 increases neutrophilic inflammation
⬇️
IL-22 stimulates airway epithelial cells
(further innate & adaptive immune responses)

85
Q

Which interleukin activates neutrophils that cause a more exaggerated inflammatory response?

A

IL8

IL-5: activates eosinophils
IL-8 activates neutrophils
IL-13: impairs mucociliary clearance, enhances fibroblast secretion, and contributes to bronchoconstriction
IL-17: increases neutrophilic inflammation
IL-22: stimulates airway epithelial cells

86
Q

Which interleukin enhances fibroblast secretion, and contributes to bronchoconstriction?

A

IL-13

87
Q

Which interluekin stimulates airway epithelial cells?

A

IL-22

88
Q

eosinophils vs eosinophils
in asthma

A

eosinophils
* bronchial hyperresponsiveness
* fibroblast proliferation
* epithelial injury
* airway scarring

neutrophils
* more exaggerated inflammatory response

89
Q

Which is obstructive?
A) Pulmonary fibrosis
B) Inhalational disorders
C) Pneumoconiosis
D) Emphysema
E) Pulmonary edema

A

D) Emphysema

Obtructive:
* Asthma
* Chronic bronchitis
* Emphysema
* Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

Restrictive:
* Aspiration
* Atelectasis
* Bronchiectasis, bronchiolitis
* Pulmonary fibrosis
* Inhalational disorders
* Pneumoconiosis
* Allergic alveolitis
* Pulmonary edema
* Acute respiratory distress syndrome

90
Q

Which are restrictive?
Which are obstructive?
-Bronchiectasis
-Bronchitis
-Bronchiolitis

A

restrictive: Bronchiectasis, bronchiolitis

obstructive: bronchitis

91
Q

Her lung disorder is:
A) restrictive
B) obstructive

A

B) obstructive

  • Asthma
  • Chronic bronchitis
  • Emphysema
  • Chronic bronchitis plus emphysema equals chronic obstructive pulmonary disease (COPD)

Pathopharm Exam 3 (18 decks)

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