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CRRAB II > Respiratory Path lecture 1 > Flashcards

Respiratory Path lecture 1 Flashcards

1
Q

Pulmonary system sole purpose

A

Ventilation

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2
Q

2 metabolic functions of pulmonary system

A
  1. Oxygenate blood

2. Expire CO2

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3
Q

Obstructive disorders

A
  • -Expiratory flow limitation

- -Typically smaller airways

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4
Q

Obstructive disorder examples

A
  • -Asthma
  • -COPD
  • -Bronchiectasis
  • -Bronchiolitis
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5
Q

How is degree of obstruction tested?

A
  • -Pulmonary function testing

- -Often decreased FEV1

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6
Q

Restrictive diseases

A

–Reduced total lung capacity/reduced ventilatory elasticity

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7
Q

Restrictive disease examples

A
  • -Diffuse parenchymal/interstitial lung disease (idiopathic pulmonary fibrosis, occupation lung diseases )
  • -Chest wall/pleural disease
  • -Massive obesity
  • -Neuromuscular disease
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8
Q

Measuring degree of restriction?

A

Pulmonary function testing (Total lung capacity)

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9
Q

Pulmonary vascular disease

A
  • -Thromboembolism (from DVT usually)
  • -Pulmonary HTN
  • -Pulmonary hemorrhage/vasculitis syndromes
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10
Q

Pulmonary edema (from L sided CHF)

A

–Cardiogenic pulmonary edema (chronic coronary artery disease, MI, hypertensive heart disease, cardiomyopathies, aortic or mitral stenosis

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11
Q

Non-cardiogenic pulmonary edema

A

Microvascular/alveolar capillary injury (acute respiratory distress syndrome (trauma/shock, sepsis)

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12
Q

Pulmonary infectious disease (definition)

A

Infection of distal/alveolar lung (pneumonia/lung abscess or in the airways)

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13
Q

Pneumonia

A

Most common infectious disease leading to hospital admission and death in US

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14
Q

Diagnosis of pneumonia

A

Need to see pulmonary infiltrates on CT or CXR

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15
Q

Subtypes of pneumonia

A
  • -Community-acquired
  • -Hospital/institution acquired
  • -Immunosuppressed forms
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16
Q

Space occupying effect

A

Restricting lung expansion or causing lung collapse

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17
Q

Effusions

A
  • -Transudates (CHF)
  • -Exudates (para-pneumonic, malignant)
  • -Hemothorax (trauma, aortic aneurysm, dissection rupture)
  • -Chylous
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18
Q

Pneumothorax

A

–Visceral, pleural air leak secondary to underlying lung pathology

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19
Q

Atelectasis

A

Pulmonary collapse (segment, lobe, entire lung)

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20
Q

Atelectasis causes

A
  • -Usually obstructed bronchus or pleural effusion

- -If unrelieved: risk of pneumonia

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21
Q

Bronchiectasis

A

Chronic infection/inflammation of larger airways

  • -Irreversible bronchial dilation
  • -Chronic micropurulent sputum production
  • -Eventual bronchial collapse/obstructive symptoms
  • -Unrelated to cigarette smoking
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22
Q

Congenital lung disease

A

–Associated w/perinatal death, neonatal respiratory distress with variable survival, delayed symptoms/discovery into adulthood

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23
Q

Dyspnea

A

Increased work of breathing due to decreased compliance, increased resistance to flow, impair gas exchange (alveolar injury)

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24
Q

Causes of acute onset dyspnea

A
  • -Laryngeal edema/anaphylaxis
  • -Bronchospasm
  • -MI
  • -Large PE
  • -Pneumothorax
  • -Aspiration
  • -Inhaled toxic substance
  • -Massive hemorrhage or hemolysis
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25
Q

Causes of progressive/chronic dyspnea

A
  • -Chronic obstructive or restrictive pulmonary disease
  • -CHF
  • -Worsening anemia
  • -Obesity/deconditioning
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26
Q

Expiratory wheezing causes

A

Suggests airway obstruction (esp. asthma, can occur with peribronchial edema due to CHF

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27
Q

Chest pain secondary to respiratory diseases (causes)

A
  • -Irritation of parietal pleura
  • -Pneumonia w/secondary pleuritis
  • -PE w/lung infection
  • -Pneumothorax
  • -Lung CA invading chest wall
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28
Q

Expiratory wheeze causes

A

Bronchospasm vs CHF

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29
Q

Rhonchi causes

A

Obstruction of medium -size bronchi w/secretions (bronchitis, bronchiectasis, COPD)

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30
Q

Stridor (inspiratory wheezes) causes

A

Upper airway obstruction (larynx/trachea)

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31
Q

Crackles/rales causes

A

Alveolar disease (pneumonia, pulmonary edema, interstitial/fibrosing disease)

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32
Q

Causes of decreased breath sounds

A

Emphysema, pneumothorax, pleural effusion, pulmonary consolidation

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33
Q

Arterial blood gases

A

Gold standard for assessing adequacy of gas exchange

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34
Q

ABG normal values

A 
PaO2: 80-95 mmHg
PaCO2: 35-45 mmHg
pH: 7.35-7.45
HCO3: 22-28 meq/L
SaO2: 95-100%
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35
Q

What are you looking for on CXR?

A

Pulmonary pleural disease, cardiac enlargement, mediastinal pathology

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36
Q

What disease states are usually normal on CXR?

A

Larger airways disease and pulmonary vascular disease

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37
Q

What can you see on CT?

A
  • -Better detail

- -Small lung lesions, larger airways, lymph nodes, aorta, esophagus, mediastinal masses/cysts

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38
Q

What are you looking for on high res CT?

A

Chronic interstitial and diffuse parenchymal lung disease. Gold standard for these

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39
Q

Pulmonary function testing (PFT) use

A

Est. dx and severity of chronic or restrictive lung disease

40
Q

Spirometry

A

Look at FEV1/FVC especially

41
Q

What if FEV1/FVC less than 70% of predicted?

A

Obstructive lung disease (esp. COPD and asthma)

42
Q

What if the FEV1:FVC ratio reverses some w/bronchodilator?

A

Asthma or asthmatic component to COPD

43
Q

What does it mean if TLC less than 80% of predicted?

A

Restrictive pathology w/poor respiratory compliance.

44
Q

How do you make dx of atelectasis?

A

CXR: shows volume loss + pulmonary opacification

45
Q

Primary atelectasis (neonatal)

A

Rare

Incomplete expansion of lungs at birth (inadequate surfactant)

46
Q

Secondary atelectasis types

A
  • -99%

- -Obstructive, resorptive, compression, contraction types

47
Q

Obstructive secondary atelectasis

A

–Resorption of alveolar gas distal to bronchial obstruction (MUCUS plugging, foreign body aspiration, tumor, extrinsic bronchial compression)

48
Q

What is the most common cause of atelectasis in children?

A

Obstructive from mucus plugging (asthma, cystic fibrosis)

49
Q

Resorptive secondary atelectasis

A

Alveolar collapse from pneumonia, poor lung ventilation (neuromuscular weakness/poor cough reflex), post-general anesthesia all compounded by MUCUS SECRETIONS

50
Q

Compression secondary atelectasis

A

Pulmonary collapse due to mass effect: pleural effusion, pneumothorax, tumor, cysts, congenital abnormalities, lobar hyperinflation/large emphysematous blebs

51
Q

Contraction secondary atelectasis

A

Pulmonary shrinkage from pleural fibrosis or fibrotic pulmonary interstitial disease

52
Q

What happens with failure to relieve atelectasis?

A

Increased risk of pneumonia

53
Q

Prophylaxis to reduce risk of atelectasis post-anesthesia

A

Deep ventilation exercises

54
Q

Asthma

A
  • -Reversible airflow obstruction

- -Associated with bronchial inflammation and bronchoconstriction

55
Q

Asthma epidemiology

A
  • -300 million people worldwide
  • -8% of US pop.
  • -90% cases triggered by allergic/atopic disease
  • -10% from nonatopic/”intrinsic” causes (such as cold air, exercise, drugs, stress, inhaled irritants)
  • -Occupational asthma: 1/3 of occupational lung disease
56
Q

Asthma symptoms

A
  • -Episodic wheezing, dyspnea, cough

- -+/- mucus/sputum, kids often have cough (predominant sx)

57
Q

Asthma Dx

A
  • -Symptom based
  • -Typically no CXR findings
  • -PFT: decreased FEV1 and FEV1/FVC with >12% increase w/inhaled B2 agonist or post-steroid trial
58
Q

Asthma histology

A

Bronchial/bronchiolar mucosal/submucosal inflammation: eosinophils/T lymphocytes, mucosal edema, mucus hypersecretion/plugging, hypertrophied bronchial smooth muscle

59
Q

What % of COPD patients have asthma features?

A

10%. With response to corticosteroids–probably both diseases present

60
Q

Asthma rx

A
  1. Relief of bronchoconstriction w/beta-2 agonists
  2. Inflammation control/suppression: inhaled +/- oral corticosteroids
  3. May need 2nd/3rd line drugs for refractory cases
61
Q

Asthma complications

A
  • -Status asthmaticus
  • -Allergic bronchopulmonary aspergillosis
  • -Chronic eosinophilic pneumonia
62
Q

COPD gen. info

A
  • -4th leading cause of death in US
  • -Expiratory airflow obstruction, not fully reversible
  • -Slowly progressive/persistent w/ acute exacerbations (often due to infection)
  • -80-90% of cases associated with smoking
63
Q

COPD etiology

A

Abnormal inflammatory response to noxious gas/particles

64
Q

Toxic effects of cigarette smoke on trachea/bronchi

A

–Submucosal glandular hyperplasia w/abundant mucus production/cough (chronic bronchitis)

65
Q

Toxic effects of cigarette smoke on distal small airways

A

Mucosal goblet cell hyperplasia and bronchiolitis w/inflammation, increased mucus, edema, fibrosis

66
Q

Alveolar destruction in COPD

A

Neutrophils/macrophages release elastolytic proteinases and degrade natural anti-proteinase protection

67
Q

Emphysema

A

Progressive acinar destruction w/permanent air space enlargement

68
Q

Centriacinar emphysema

A

Vast majority of cases. Predominantly affecting upper lobes

69
Q

Panacinar emphysema

A

Upper and lower lung field involvement of equal severity.

70
Q

Causes of panacinar emphysema

A
  • -Very advanced common emphysema

- -Alpha-1 antitrypsin deficiency (may also have associated liver disease

71
Q

Subpleural blebs in emphysema

A

Can cause pneumothorax or space-occupying mass effect

72
Q

Types of mechanisms of airflow obstruction in COPD

A
  • -mucus plugging
  • -decreased alveolar tethering of respiratory bronchioles
  • -mixed
73
Q

Mechanism of airflow obstruction w/predominant Bronchitis component in COPD

A

Mucus plugging

74
Q

Mech. of airflow obstruction w/predominant emphysema component

A

Decreased elastic/alveolar “tethering” of respiratory bronchioles–airway collapse during expiration w/alveolar air trapping, loss of elastic recoil, hyperinflation.

75
Q

COPD clinical presentation

A
  • -Sedentary lifestyle (avoiding exertional dyspnea)
  • -Progressive dyspnea on exertion
  • -Evolving cough w/sputum production (mucoid or purulent)
  • -Acute chest illness
76
Q

Acute chest illness

A

Increased cough, purulent sputum, wheezing/dyspnea, episodically occurring (may resemble asthma, CHF, bronchiectasis)

77
Q

Physical exam w/severe COPD disease

A
  • -Systemic wasting
  • -Hyperinflated lungs w/barrel chest
  • -Decreased breath sounds, wheezes, lung base crackles, distant heart sounds.
  • -Use of accessory muscles to breathe
  • -Cyanosis
  • -Cor pulmonale
78
Q

COPD diagnosis

A
  • -PFT

- -FEV1/FVC

79
Q

ABG’s in mild and severe COPD

A
  • -Mild: mild/mod. hypoxemia w/o hypercarbia (hypercapnea)

- -Severe: worsening hypoxemia w/hypercarbia

80
Q

Hemogram results in COPD

A

–If polycythemia present implies chronic hypoxemia.

81
Q

Clinical course of COPD

A
  • -Slowly progressive sx (stable phase) w/periodic exacerbations
  • -Chronic hypoxemia induces vasoconstriction/HTN and eventual cor pulmonale
82
Q

COPD exacerbation causes (common)

A

50% due to bacterial pneumonia (Moraxella, H. influenzae, S. pneumo) w/50% triggered by viral infection

83
Q

Bronchiectasis

A

Permanent dilation of bronchi/bronchioles

84
Q

Common causes of bronchiectasis

A
  • -Recurrent bronchial infection due to impaired drainage/airway obstruction, host defense deficits
  • -Secondary to bacterial pneumonia
85
Q

Bronchiectasis symptoms

A
  • -Cough
  • -Daily micropurulent sputum (months to yrs)
  • -+/- dyspnea/wheezing.
  • -May see sinusitis and hemoptysis
86
Q

Bronchiectasis findings on CT scan

A

Dilated bronchi (diffuse or focal)

87
Q

Classic bronchiectasis disease associations

A
  • -Cystic fibrosis
  • -Airway obstruction from foreign body or tumor
  • -Primary ciliary dyskinesia
  • -Primary pulmonary infection
  • -Connective tissue disease
  • -Immune deficiencies
  • -Uncertain/unknown (25-50% cases)
88
Q

Pneumonia

A

Infection involving pulmonary alveolar or interstitial parenchyma
–Most common lethal adult infection

89
Q

Pneumonia sx

A
  • -Acute, rapidly evolving

- -Cough, fever, pleuritic chest pain, dyspnea, sputum production +/- chills/rigors, GI sx, mental status changes

90
Q

Pneumonia physical exam findings

A

Rales or evidence of pulmonary consolidation

91
Q

Pneumonia diagnosis

A

CXR or CT: must see pulmonary infiltrate!!!
–Can have lobar or whole lung consolidation, patchy alveolar infiltrates, interstitial infiltrates, cavitation +/- pleural effusion/empyema.

92
Q

Alveolar exudate inflammation (neutrophilic) pathology in pneumonia

A

Common bacterial pneumonia

93
Q

Interstitial/alveolar wall inflammation pathology in pneumonia

A
  • -Usually lymphocytic type

- -Seen in “atypical pneumonia” (mycoplasma, viruses, chlamydophylia)

94
Q

Necrotizing granuloma pathology in pneumonia

A

Fungi or mycobacteria cause

95
Q

Pulse oximetry findings in pneumonia

A

Desaturation

96
Q

Inflammatory disease markers in pneumonia

A

Leukocytosis (usually neutrophilic), increased ESR, CRP.

CRRAB II (13 decks)

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