Exam 2: Pulmonary Patho Flashcards
(127 cards)
1
Q
Orthopnea is usually a sign of:
A
Pulmonary edema or pleural effusion
2
Q
Describe Kussmaul respirations:
A
Rapid rate to ↓ CO2
3
Q
Describe Cheyne-Stokes respirations:
A
Alternative apnea and tachypnea
4
Q
Cause of Cheyne-Stokes respirations:
A
Dying cardiorespiratory center in the brainstem
5
Q
Pulmonary pain is usually:
A
Pleuritis causing rubbing of pleura
6
Q
Acute respiratory failure is:
A
Inadequate gas exchange
7
Q
Two broad causes of pulmonary edema:
A
↑ vascular pressure
↑ vascular permeability
8
Q
Two types of atalectasis:
A
Compression
Absorption
9
Q
Define bronchiectasis:
A
Chronic abnormal dilation of bronchi
10
Q
Define bronchiolitis:
A
Inflammatory obstruction of bronchioles
11
Q
Define open pneumothorax:
A
Communication between pleural space and outside
12
Q
Define tension pneumothorax:
A
Gas enters pleural space during inhalation, can’t escape during exhalation
13
Q
Transudative effusion is:
A
Low protein content; plasma escaping capillaries d/t pressure
14
Q
Exudative effusion is:
A
High protein content; usually d/t local inflammation
15
Q
Hemothorax, chylothorax, and empyema are:
A
Hemothorax: blood in pleural space
Chylothorax: lymph in pleural space
Empyema: pus in plural space
16
Q
Examples of acute intrinsic restrictive lung disease:
A
ARDS, pulmonary edema
17
Q
Example of chronic intrinsic restrictive lung disease:
A
Pulmonary fibrosis
18
Q
Example of chronic extrinsic restrictive lung disease:
A
Spinal cord damage
19
Q
Examples of obstructive lung diseases:
A
Asthma
COPD
20
Q
Four examples of respiratory tract infections:
A
Pneumonia (6th most common cause of death in US)
TB
Bronchitis
Abscess
21
Q
Gas exchange/diffusion measured using:
A
CO because concentration gradient is zero and it diffuses easily
22
Q
Primary problem with restrictive d/o’s:
A
Loss of compliance - cannot get air in
23
Q
PFT changes in restrictive d/o’s:
A
↓ FVC
24
Q
Primary problem with obstructive d/o’s:
A
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
