Exam 2: Pulmonary Patho Flashcards Preview

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Flashcards in Exam 2: Pulmonary Patho Deck (127):
1

Orthopnea is usually a sign of:

Pulmonary edema or pleural effusion

2

Describe Kussmaul respirations:

Rapid rate to ↓ CO2

3

Describe Cheyne-Stokes respirations:

Alternative apnea and tachypnea

4

Cause of Cheyne-Stokes respirations:

Dying cardiorespiratory center in the brainstem

5

Pulmonary pain is usually:

Pleuritis causing rubbing of pleura

6

Acute respiratory failure is:

Inadequate gas exchange

7

Two broad causes of pulmonary edema:

↑ vascular pressure
↑ vascular permeability

8

Two types of atalectasis:

Compression
Absorption

9

Define bronchiectasis:

Chronic abnormal dilation of bronchi

10

Define bronchiolitis:

Inflammatory obstruction of bronchioles

11

Define open pneumothorax:

Communication between pleural space and outside

12

Define tension pneumothorax:

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

13

Transudative effusion is:

Low protein content; plasma escaping capillaries d/t pressure

14

Exudative effusion is:

High protein content; usually d/t local inflammation

15

Hemothorax, chylothorax, and empyema are:

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

16

Examples of acute intrinsic restrictive lung disease:

ARDS, pulmonary edema

17

Example of chronic intrinsic restrictive lung disease:

Pulmonary fibrosis

18

Example of chronic extrinsic restrictive lung disease:

Spinal cord damage

19

Examples of obstructive lung diseases:

Asthma
COPD

20

Four examples of respiratory tract infections:

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

21

Gas exchange/diffusion measured using:

CO because concentration gradient is zero and it diffuses easily

22

Primary problem with restrictive d/o's:

Loss of compliance - cannot get air in

23

PFT changes in restrictive d/o's:

↓ FVC

24

Primary problem with obstructive d/o's:

Loss of recoil - obstructed airways

25

PFT changes in obstructive d/o's:

↓ FEV1
↓ FEV1/FVC ratio

26

Obstruction is worse on:

Expiration

27

S/s of obstructive d/o:

Dyspnea
Wheezing

28

S/s of asthma:

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

29

Airway changes in asthma episode:

Widespread but variable airflow obstruction, reversible spontaneously or with medication

30

Define atopy:

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

31

Strongest predisposing factor for asthma:

Atopy

32

Pathogenesis of asthma:

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

33

Epithelial damage in asthma caused by:

Eosinophil products

34

Small-airway disease in chronic bronchitis results in:

Airflow obstruction

35

Large-airway disease in chronic bronchitis results in:

Mucus hypersecretion

36

Genetic abnormality leading to COPD:

Alpha1-antitrypsin deficiency (< 1% of cases)

37

Criteria for chronic bronchitis:

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

38

Characteristics of chronic bronchitis mucus:

↑ size/# of mucus glands
Thicker mucus

39

Emphysema is:

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

40

Pathogenesis of emphysema:

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

41

Pores between alveoli called:

Pore of Kohn

42

PFTs that are unchanged in restrictive lung disease:

Exp flow rate
FEV1/FVC ratio

43

S/s of restrictive lung disease:

↑ WOB
Dyspnea
Rapid, shallow breathing

44

Change in dead space in restrictive d/o:

Increased dead space ventilation

45

Change in gas exchange in restrictive d/o:

Normal gas exchange until disease is advanced

46

S/s of advanced restrictive d/o:

↑ PaCO2, ↓ PaO2, pulm HTN, cor pulmonale

47

Pathogenesis of pulmonary edema:

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

48

CXR of pulmonary edema will show:

Bilateral symmetrical opacities

49

Three pathogenic pathways for pulmonary edema to form:

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

50

ARDS is:

Diffuse pulmonary endothelial injury

51

Pathogenesis of ARDS:

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

52

Four main "issues" in ARDS:

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

Pathogenesis of aspiration pneumonitis:

Gastric secretions destroy type II pneumocytes, damage endothelium

54

Clinical s/s of aspiration pneumonitis:

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

55

Tx of aspiration pneumonitis:

INCREASED FIO2!
PEEP
B2 agonists for bronchospasm

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

56

Pathogenesis of cardiogenic pulmonary edema:

LV failure --> ↑ pulm vascular pressures

57

SNS activation s/s in cardiogenic pulmonary edema:

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

58

Type of effusion in cardiogenic pulmonary edema:

Transudative

59

Pathogenesis of neurogenic pulmonary edema:

2/2 massive SNS discharge in response to CNS insult
Generalized vasoconstriction shifts blood volume into pulmonary vessels, ↑ pressure, vessel injury, transudation

60

Tx of neurogenic pulmonary edema:

Control ICP, ↑ FiO2, PPV, PEEP, etc
Diuretics not indicated

61

Describe heroin-induced pulmonary edema:

Permeability of capillaries

62

Describe cocaine-induced pulmonary edema:

Pulm vasoconstriction or MI

63

Pathogenesis of high altitude pulmonary edema:

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

64

Tx for high altitude pulmonary edema:

O2, descent and inhaled NO
Hyperbaric "sleeping bag" at 760mmHg

65

Pathogenesis of reexpansion pulmonary edema:

Follows evacuation of big pneumothorax or pleural effusion
Negative pressure on capillaries enhances their permeability

66

Pathogenesis of negative pressure pulmonary edema:

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

Causes of NPPE:

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

68

Tx of NPPE:

Usually self-limited (12-24 hrs)
O2 support, airway maintenance, mechanical ventilation if needed

69

Progressive chronic intrinsic disease leads to:

Pulmonary HTN, cor pulmonale

70

Common complication of advanced chronic intrinsic disease:

Pneumothorax

71

Breathing pattern in chronic intrinsic disease:

Dyspnea

72

Population prone to sarcoidosis:

Young black females

73

Sarcoidosis is:

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

74

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

Laryngeal sarcoid

75

Non-pulm structures often affected by sarcoidosis:

Liver
Spleen
Optic nerve
Facial nerve

76

Electrolyte imbalance seen in sarcoidosis:

Hypocalcemia

77

Stress dose steroids for minor surgery:

2x normal dose

78

Stress dose steroids for moderate surgery:

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

79

Stress dose steroids for major surgery:

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

80

Hypersensitivity pneumonitis is:

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

81

Pneumoconiosis is:

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

82

Compressed lungs result in:

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

83

Cardiac dysfunction common with thoracic deformity:

RV dysfunction d/t chronic compression of pulmonary vasculature

84

Impaired cough leads to:

Chronic infection
Development of obstruction

85

Obesity affects pulmonary status by:

Restricting diaphragm and chest wall movement

86

PFT changes seen in obesity:

↓ FRC
V/Q mismatch

87

Obesity pulmonary changes exacerbated by:

Supine position

88

Define scoliosis:

Lateral curvature of the spine with rotation of the vertebral column

89

Define kyphosis:

Anterior flexion of vertebral column

90

Scoliotic angle of 60º causes:

Dyspnea with exercise

91

Scoliotic angle of 100º causes:

Alveolar hypoventilation
↓ PaO2
Erythrocytosis
Pulmonary HTN
Cor pulmonale

92

Scoliotic angle >110º causes:

Vital capacity < 45% normal
Respiratory failure

93

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

CNS depressants

94

Cause of flail chest:

Rib fx or sternotomy dehiscence

95

Presentation of flail chest:

Paradoxical movement of the unstable portion of the chest wall

96

Clinical manifestations of flail chest:

↓ PaO2
↑ PaCO2

Due to alveolar hypoventilation

97

Tx of flail chest:

PPV until thoracic stabilization

98

Useful measure of impact of NM disease on ventilation:

Vital capacity

99

S/s of pneumothorax:

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

100

Tx of tension pneumothorax:

Small-bore plastic catheter into 2nd anterior intercostal space

101

FiO2 ↑ in pneumothorax tx because:

Improves rate of air resorption by pleura 4x

102

Define pleurodesis:

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

103

FVC/FEV1/ratio in obstructive lung disease:

FVC: Normal
FEV1: Decreased
Ratio: Decreased

104

FVC/FEV1/ratio in restrictive lung disease:

FVC: Decreased
FEV1: Normal or decreased
Ratio: Normal

105

Flow-volume loop for obstructive lung disease:

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

106

Flow-volume loop for restrictive lung disease:

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

107

Lungs receive their O2 from:

Breathing, not blood flow
Very resilient during ischemia

108

Microemboli and lungs:

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

Define pulmonary embolism:

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

110

Virchow's Triad:

Venous stasis
Hypercoagulability
Injuries to endothelial cells

111

Conditions that predispose to Virchow's triad:

Post-op
Long flights
Immobility

112

Pathogenesis of pulmonary embolism:

Hypoxic vasoconstriction
↓ surfactant
Inflammation
Pulmonary edema
Atalectasis

113

Define pulmonary HTN:

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

114

Two types of endothelial dysfunction in pulmonary HTN:

Overproduction of vasoconstrictors
Underproduction of vasodilators

115

Pulmonary vasoconstrictors from the epithelium:

Thromboxane
Endothelin

116

Pulmonary vasodilators from the epithelium:

Prostacyclin
NO

117

Lung disease --> pulmonary HTN pathogenesis:

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

118

Smoking related to cancers of:

Lungs
Larynx
Oral cavity
Esophagus
Bladder

119

Types of lung cancer:

Small cell carcinoma (oat cell)
Non-small cell: squamous cell, adenocarcinoma, large cell carcinoma

120

Describe squamous cell carcinoma:

Slow growing
Near hilus
Obstructive - cough, hemoptysis

121

Describe small cell carcinoma:

Rapidly growing
Smoking-related
Very high mortality
Produces ectopic hormones

122

Describe adenocarcinoma:

Moderate growth
Least correlated with smoking
Peripheral in lung

123

Describe large cell carcinoma:

Rapid growth

124

Basic problem with CF:

Defective Cl- channels in gallbladder, pancreas, and lungs

125

CF in gallbladder:

Bile becomes too concentrated and GB becomes fibrotic

126

CF in lungs:

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

127

Transporters involved in CF:

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