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ARCHIVED: Pathophysiology > Exam 2: Pulmonary Patho > Flashcards

Exam 2: Pulmonary Patho Flashcards

1
Q

Orthopnea is usually a sign of:

A

Pulmonary edema or pleural effusion

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2
Q

Describe Kussmaul respirations:

A

Rapid rate to ↓ CO2

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3
Q

Describe Cheyne-Stokes respirations:

A

Alternative apnea and tachypnea

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4
Q

Cause of Cheyne-Stokes respirations:

A

Dying cardiorespiratory center in the brainstem

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5
Q

Pulmonary pain is usually:

A

Pleuritis causing rubbing of pleura

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6
Q

Acute respiratory failure is:

A

Inadequate gas exchange

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7
Q

Two broad causes of pulmonary edema:

A

↑ vascular pressure

↑ vascular permeability

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8
Q

Two types of atalectasis:

A

Compression

Absorption

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9
Q

Define bronchiectasis:

A

Chronic abnormal dilation of bronchi

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10
Q

Define bronchiolitis:

A

Inflammatory obstruction of bronchioles

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11
Q

Define open pneumothorax:

A

Communication between pleural space and outside

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12
Q

Define tension pneumothorax:

A

Gas enters pleural space during inhalation, can’t escape during exhalation

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13
Q

Transudative effusion is:

A

Low protein content; plasma escaping capillaries d/t pressure

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14
Q

Exudative effusion is:

A

High protein content; usually d/t local inflammation

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15
Q

Hemothorax, chylothorax, and empyema are:

A

Hemothorax: blood in pleural space
Chylothorax: lymph in pleural space
Empyema: pus in plural space

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16
Q

Examples of acute intrinsic restrictive lung disease:

A

ARDS, pulmonary edema

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17
Q

Example of chronic intrinsic restrictive lung disease:

A

Pulmonary fibrosis

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18
Q

Example of chronic extrinsic restrictive lung disease:

A

Spinal cord damage

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19
Q

Examples of obstructive lung diseases:

A

Asthma

COPD

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20
Q

Four examples of respiratory tract infections:

A

Pneumonia (6th most common cause of death in US)
TB
Bronchitis
Abscess

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21
Q

Gas exchange/diffusion measured using:

A

CO because concentration gradient is zero and it diffuses easily

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22
Q

Primary problem with restrictive d/o’s:

A

Loss of compliance - cannot get air in

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23
Q

PFT changes in restrictive d/o’s:

A

↓ FVC

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24
Q

Primary problem with obstructive d/o’s:

A

Loss of recoil - obstructed airways

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25
Q

PFT changes in obstructive d/o’s:

A

↓ FEV1

↓ FEV1/FVC ratio

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26
Q

Obstruction is worse on:

A

Expiration

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27
Q

S/s of obstructive d/o:

A

Dyspnea

Wheezing

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28
Q

S/s of asthma:

A

Episodes of wheezing
Breathlessness
Chest tightness/cough, esp. at night and morning
Hyperresponsive to stimuli

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29
Q

Airway changes in asthma episode:

A

Widespread but variable airflow obstruction, reversible spontaneously or with medication

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30
Q

Define atopy:

A

The genetic predisposition for development of IgE-mediated response to aeroallergens

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31
Q

Strongest predisposing factor for asthma:

A

Atopy

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32
Q

Pathogenesis of asthma:

A

Immune activation (IgE –> T cells) leads to mast cell degranulation and production of vasoactive mediators, which produce vasodilation/↑ capillary permeability (runny nose/lungs)

Mast cell degranulation also releases chemotactic mediators which attract WBCs

Short-term result: Bronchospasm, congestion, airway swelling, etc

Long-term result: Epithelial fibrosis, bronchial hyperresponsiveness/obstruction

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33
Q

Epithelial damage in asthma caused by:

A

Eosinophil products

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34
Q

Small-airway disease in chronic bronchitis results in:

A

Airflow obstruction

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35
Q

Large-airway disease in chronic bronchitis results in:

A

Mucus hypersecretion

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36
Q

Genetic abnormality leading to COPD:

A

Alpha1-antitrypsin deficiency (< 1% of cases)

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37
Q

Criteria for chronic bronchitis:

A

Hypersecretion of mucus/productive cough at least 3mo/yr for at least 2 yrs

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38
Q

Characteristics of chronic bronchitis mucus:

A

↑ size/# of mucus glands

Thicker mucus

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39
Q

Emphysema is:

A

Abnormal enlargement of gas exchange airways and destruction of alveolar walls without fibrosis

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40
Q

Pathogenesis of emphysema:

A

ROS from tobacco inactivates antiproteases, which leads to ↑ neutrophil elastase and loss of recoil

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41
Q

Pores between alveoli called:

A

Pore of Kohn

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42
Q

PFTs that are unchanged in restrictive lung disease:

A

Exp flow rate

FEV1/FVC ratio

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43
Q

S/s of restrictive lung disease:

A

↑ WOB
Dyspnea
Rapid, shallow breathing

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44
Q

Change in dead space in restrictive d/o:

A

Increased dead space ventilation

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45
Q

Change in gas exchange in restrictive d/o:

A

Normal gas exchange until disease is advanced

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46
Q

S/s of advanced restrictive d/o:

A

↑ PaCO2, ↓ PaO2, pulm HTN, cor pulmonale

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47
Q

Pathogenesis of pulmonary edema:

A

Fluid leakage from intravascular space into lung interstitium/alveoli either from ↑ pressure or ↑ permeability

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48
Q

CXR of pulmonary edema will show:

A

Bilateral symmetrical opacities

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49
Q

Three pathogenic pathways for pulmonary edema to form:

A

Pressure from LH failure, valvular disease, etc
Injury to capillary endothelium (permeability)
Blockage of lymphatic vessels

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50
Q

ARDS is:

A

Diffuse pulmonary endothelial injury

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51
Q

Pathogenesis of ARDS:

A

Insult leads to cytokine release and influx of inflammatory cells to lung/release of ROS and more cytokines

52
Q

Four main “issues” in ARDS:

A

Damage to type II pneumocytes –> atalectasis
Disruption of alveolar-capillary membrane –> pulmonary edema, intrapulmonary shunting, washed away surfactant
Microthrombi in pulm circulation –> pulm hypertension
Release of fibroblast growth factors –> pulm fibrosis

Dry spots - membrane’s shot - lots of clots - fibroblasts hot

53
Q

Pathogenesis of aspiration pneumonitis:

A

Gastric secretions destroy type II pneumocytes, damage endothelium

54
Q

Clinical s/s of aspiration pneumonitis:

A 
Hypoxia
Tachypnea
Bronchospasm
Pulm vascular constriction/HTN
RLL changes in CXR
55
Q

Tx of aspiration pneumonitis:

A

INCREASED FIO2!
PEEP
B2 agonists for bronchospasm

Possible tx:
Lavage
Bronchoscopy (for solids)
ABX, steroids

56
Q

Pathogenesis of cardiogenic pulmonary edema:

A

LV failure –> ↑ pulm vascular pressures

57
Q

SNS activation s/s in cardiogenic pulmonary edema:

A 
Usually more dramatic than with edema d/t permeability
Dyspnea
Tachypnea
HTN
Tachycardia
Diaphoresis
58
Q

Type of effusion in cardiogenic pulmonary edema:

A

Transudative

59
Q

Pathogenesis of neurogenic pulmonary edema:

A

2/2 massive SNS discharge in response to CNS insult

Generalized vasoconstriction shifts blood volume into pulmonary vessels, ↑ pressure, vessel injury, transudation

60
Q

Tx of neurogenic pulmonary edema:

A

Control ICP, ↑ FiO2, PPV, PEEP, etc

Diuretics not indicated

61
Q

Describe heroin-induced pulmonary edema:

A

Permeability of capillaries

62
Q

Describe cocaine-induced pulmonary edema:

A

Pulm vasoconstriction or MI

63
Q

Pathogenesis of high altitude pulmonary edema:

A

Hypoxic pulmonary vasoconstriction after 48-96 hrs at 2500-5000m altitude
↑ pulm vascular pressures result in edema

64
Q

Tx for high altitude pulmonary edema:

A

O2, descent and inhaled NO

Hyperbaric “sleeping bag” at 760mmHg

65
Q

Pathogenesis of reexpansion pulmonary edema:

A

Follows evacuation of big pneumothorax or pleural effusion

Negative pressure on capillaries enhances their permeability

66
Q

Pathogenesis of negative pressure pulmonary edema:

A

2-3 minutes after acute upper airway obstruction in spontaneously breathing patient; negative pressure caused by attempts to breathe against obstruction leads to “pulling” fluid into alveoli

67
Q

Causes of NPPE:

A 
Post-extubation laryngospasm*
Obstructive sleep apnea*
Epiglottitis
Tumors
Obesity
Hiccups
68
Q

Tx of NPPE:

A

Usually self-limited (12-24 hrs)

O2 support, airway maintenance, mechanical ventilation if needed

69
Q

Progressive chronic intrinsic disease leads to:

A

Pulmonary HTN, cor pulmonale

70
Q

Common complication of advanced chronic intrinsic disease:

A

Pneumothorax

71
Q

Breathing pattern in chronic intrinsic disease:

A

Dyspnea

72
Q

Population prone to sarcoidosis:

A

Young black females

73
Q

Sarcoidosis is:

A

Systematic granulomatous disorder, often found in thoracic lymph nodes and lungs

74
Q

1-5% of pts with sarcoidosis have this airway complication:

A

Laryngeal sarcoid

75
Q

Non-pulm structures often affected by sarcoidosis:

A

Liver
Spleen
Optic nerve
Facial nerve

76
Q

Electrolyte imbalance seen in sarcoidosis:

A

Hypocalcemia

77
Q

Stress dose steroids for minor surgery:

A

2x normal dose

78
Q

Stress dose steroids for moderate surgery:

A

25mg hydrocortisone pre-op
75mg IV hydrocortisone intraop
50mg IV hydrocortisone post-op
Taper to usual dose

79
Q

Stress dose steroids for major surgery:

A

50mg IV hydrocortisone pre-op
100mg IV hydrocortisone intraop
100mg IV hydrocortisone post-op Q8hr x 24hrs
Taper to usual dose

80
Q

Hypersensitivity pneumonitis is:

A

Granulomatous diffuse rxn in the lungs after inhalation of immunogenic proteins (fungi, spores, animal protein, etc)

81
Q

Pneumoconiosis is:

A

Non-immunogenic irritant in the lungs (silicosis, black lung, asbestosis, etc)

82
Q

Compressed lungs result in:

A

Increased WOB
↓ lung volumes and ↑ airway resistance
Abnormal chest wall mechanics

83
Q

Cardiac dysfunction common with thoracic deformity:

A

RV dysfunction d/t chronic compression of pulmonary vasculature

84
Q

Impaired cough leads to:

A

Chronic infection

Development of obstruction

85
Q

Obesity affects pulmonary status by:

A

Restricting diaphragm and chest wall movement

86
Q

PFT changes seen in obesity:

A

↓ FRC

V/Q mismatch

87
Q

Obesity pulmonary changes exacerbated by:

A

Supine position

88
Q

Define scoliosis:

A

Lateral curvature of the spine with rotation of the vertebral column

89
Q

Define kyphosis:

A

Anterior flexion of vertebral column

90
Q

Scoliotic angle of 60º causes:

A

Dyspnea with exercise

91
Q

Scoliotic angle of 100º causes:

A 
Alveolar hypoventilation
↓ PaO2
Erythrocytosis
Pulmonary HTN
Cor pulmonale
92
Q

Scoliotic angle >110º causes:

A

Vital capacity < 45% normal

Respiratory failure

93
Q

Increased risk of hypoventilation/pneumonia using which drugs along with vertebral deformities:

A

CNS depressants

94
Q

Cause of flail chest:

A

Rib fx or sternotomy dehiscence

95
Q

Presentation of flail chest:

A

Paradoxical movement of the unstable portion of the chest wall

96
Q

Clinical manifestations of flail chest:

A

↓ PaO2
↑ PaCO2

Due to alveolar hypoventilation

97
Q

Tx of flail chest:

A

PPV until thoracic stabilization

98
Q

Useful measure of impact of NM disease on ventilation:

A

Vital capacity

99
Q

S/s of pneumothorax:

A 
Acute dyspnea
Ipsilateral chest pain
↓ PaO2, ↑ PaCO2
Hypotension
Tachycardia
↓ chest wall movement
↓ or absent breath sounds
Hyperresonant percussion
100
Q

Tx of tension pneumothorax:

A

Small-bore plastic catheter into 2nd anterior intercostal space

101
Q

FiO2 ↑ in pneumothorax tx because:

A

Improves rate of air resorption by pleura 4x

102
Q

Define pleurodesis:

A

Procedure in which talcum powder is used to irritate & fuse the pleura for someone with recurrent effusions

103
Q

FVC/FEV1/ratio in obstructive lung disease:

A

FVC: Normal
FEV1: Decreased
Ratio: Decreased

104
Q

FVC/FEV1/ratio in restrictive lung disease:

A

FVC: Decreased
FEV1: Normal or decreased
Ratio: Normal

105
Q

Flow-volume loop for obstructive lung disease:

A

Shifted left (higher volumes) with flattened or concave expiration phase (slow expiration)

106
Q

Flow-volume loop for restrictive lung disease:

A

Shifted right (low volumes) with relatively normal shape (normal ratio)

107
Q

Lungs receive their O2 from:

A

Breathing, not blood flow

Very resilient during ischemia

108
Q

Microemboli and lungs:

A

Lungs act as filter for microemboli!
Catch and heparinize microclots
Small blocked blood flow won’t hurt lungs - don’t get ischemic from hypoxemia

109
Q

Define pulmonary embolism:

A

Occlusion of portion of pulmonary vascular bed by thrombus, embolus, tissue, lipid, air

110
Q

Virchow’s Triad:

A

Venous stasis
Hypercoagulability
Injuries to endothelial cells

111
Q

Conditions that predispose to Virchow’s triad:

A

Post-op
Long flights
Immobility

112
Q

Pathogenesis of pulmonary embolism:

A 
Hypoxic vasoconstriction
↓ surfactant
Inflammation
Pulmonary edema
Atalectasis
113
Q

Define pulmonary HTN:

A

Mean PAP 5-10mmHg above normal (or above 20mmHg)

114
Q

Two types of endothelial dysfunction in pulmonary HTN:

A

Overproduction of vasoconstrictors

Underproduction of vasodilators

115
Q

Pulmonary vasoconstrictors from the epithelium:

A

Thromboxane

Endothelin

116
Q

Pulmonary vasodilators from the epithelium:

A

Prostacyclin

NO

117
Q

Lung disease –> pulmonary HTN pathogenesis:

A 
Disease --> chronic hypoxemia, acidosis
PA vasoconstriction
↑ PAP
Fibrosis (intima) and hypertrophy of vascular smooth muscle
Chronic HTN
118
Q

Smoking related to cancers of:

A 
Lungs
Larynx
Oral cavity
Esophagus
Bladder
119
Q

Types of lung cancer:

A

Small cell carcinoma (oat cell)

Non-small cell: squamous cell, adenocarcinoma, large cell carcinoma

120
Q

Describe squamous cell carcinoma:

A

Slow growing
Near hilus
Obstructive - cough, hemoptysis

121
Q

Describe small cell carcinoma:

A

Rapidly growing
Smoking-related
Very high mortality
Produces ectopic hormones

122
Q

Describe adenocarcinoma:

A

Moderate growth
Least correlated with smoking
Peripheral in lung

123
Q

Describe large cell carcinoma:

A

Rapid growth

124
Q

Basic problem with CF:

A

Defective Cl- channels in gallbladder, pancreas, and lungs

125
Q

CF in gallbladder:

A

Bile becomes too concentrated and GB becomes fibrotic

126
Q

CF in lungs:

A

Cl- unable to leave cells, Na+ and H2O enter and dehydrate mucus

127
Q

Transporters involved in CF:

A

CFTR: cystic fibrosis transmembrane conductance regulator
ENaC: epithelial Na channel

ARCHIVED: Pathophysiology (18 decks)

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