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Internal Medicine > Part 11 - Pulmonology > Flashcards

Part 11 - Pulmonology Flashcards

1
Q

True or false: Asthma can present at any age

A

True

p. 1669

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2
Q

_____ variant in the beta2-receptor has been associated with reduced response to beta 2 agonists in asthma

A

Arg-Gly-16

p. 1670

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3
Q

Genetic predisposition to asthma: the most consistent findings have been associations with polymorphism of genes on what chromosome?

A

5q

p. 1670

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4
Q

What is the “hygiene hypothesis” in asthma?

A

Lack of infections in early childhood preserves the T helper 2 (TH2) cell bias at birth, while exposure to infections and endotoxins result in a shift towards a predominant protective TH1 immune response
(p. 1670)

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5
Q

True or false: The presence of intestinal parasite infection may be associated with a reduced risk for asthma

A

True

p. 1670

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6
Q

Diets low in what substances/vitamins are associated with an increased risk for asthma?

A 
Vitamins A, C, D
Magnesium
Selenium
Omega-3 polyunsaturated fats
(p. 1670)
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7
Q

Diets high in what substances/vitamins are associated with increased risk for asthma?

A

Sodium
Omega-6 polyunsaturated fats
(p. 1670)

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8
Q

True or false: Obesity is an independent risk factor for asthma

A

True

p. 1670

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9
Q

When is occupational asthma suspected?

A

When symptoms improve during weekends and holidays

p. 1670

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10
Q

Endogenous risk factors for asthma

A 
Genetic predisposition
Autopsy
Airway hyperresponsiveness
Gender
Ethnicity
Obesity
Early viral infections
(p. 1670)
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11
Q

Environmental risk factors for asthma

A 
Allergens (Indoor and outdoor)
Occupational sensitizers
Passive smoking
Respiratory infections
Diet
Acetaminophen (Paracetamol)
(p. 1670)
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12
Q

Asthma triggers

A 
Allergens
Upper respiratory tract viral infections
Exercise and hyperventilation
Cold air
Sulfur dioxide and irritant gases
Drugs (beta blockers, aspirin)
Stress
Irritants (household sprays, paint fumes)
(p. 1670)
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13
Q

True or false: Patients with nonatopic or intrinsic asthma usually show later onset of disease and have more severe, persistent asthma

A

True

p. 1671

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14
Q

What is the most common allergen to trigger asthma?

A

Dermatophagoides species

p. 1671

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15
Q

What is thunderstorm asthma?

A

When pollen grains are disrupted in thunderstorms and particles that may be released can trigger severe asthma exacerbations
(p. 1671)

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16
Q

True or false: The use of beta blockers in asthma is dangerous, including topical medications

A

True

p. 1671

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17
Q

Mechanism for worsening asthma with the use of beta blockers

A 
Cholinergic bronchoconstriction
(p. 1671)
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18
Q

When does exercise-induced asthma typically begin and when does it resolve?

A

Begins after exercise has ended and resolves spontaneously within about 30 minutes
(p. 1671)

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19
Q

How can exercise-induced asthma be prevented?

A

Prior administration of beta 2 agonists and anti-leukotrienes
Regular treatment with ICS (best)
(p. 1671)

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20
Q

True or false: Laughter may be an asthma trigger

A

True

p. 1671

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21
Q

Food preservative that may trigger asthma through the release of sulfur dioxide gas in the stomach

A

Metabisulfite

p. 1671

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22
Q

In occupational asthma, there is usually complete recovery if removed from exposure within the first ____ months of symptoms

A

6

p. 1671

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23
Q

True or false: Very severe stress (eg. bereavement) may improve asthma symptoms

A

True

p. 1671

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24
Q

Inflammation in asthma is found in what anatomical structures?

A

Respiratory mucosa from the trachea to the terminal bronchioles, with predominance in the bronchi (cartilaginous airways)
(p. 1672)

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25
Q

Mast cells are activated by allergens through what mechanism?

A

IgE-mediated

p. 1672

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26
Q

Bronchoconstrictor mediators released by mast cells

A

Histamine
Prostaglandin D2
Cysteine-leukotrienes
(p. 1672)

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27
Q

What cytokine is released from epithelial cells in asthmatic patients and instructs dendritic cells to release chemokines that attract T helper 2 cells?

A

Thymic stromal lymphopoietin (TSLP)

p. 1672

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28
Q

What cytokine/s released from T helper 2 cells is/are associated with eosinophilic inflammation?

A

IL-5

p. 1673

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29
Q

What cytokine/s released from T helper 2 cells is/are associated with increased IgE formation?

A

IL-4
IL-13
(p. 1673)

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30
Q

What is the action of inflammatory mediators (eg. histamine, prostaglandin D2, cysteinyl-leukotrienes) in asthma?

A

1) Contract airway smooth muscle
2) Increase microvascular leakage
3) Increase airway mucus secretion
4) Attract other inflammatory cells
(p. 1673)

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31
Q

What are the pathophysiologic mechanisms in asthma?

A

1) Hypertrophy/hyperplasia of airway smooth muscle cells
2) Mucus hyperplasia
3) Angiogenesis
4) Subepithelial fibrosis
(p. 1673)

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32
Q

Anti-inflammatory cytokine/s that may be deficient in asthma

A

IL-10
IL-12
(p. 1674)

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33
Q

Evidence for increased oxidative stress in asthma

A

Increased concentrations of 8-isoprostane and increased ethane
(p. 1674)

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34
Q

What proinflammatory transcription factors are activated in asthmatic airways and orchestrate the expression of multiple inflammatory genes?

A

Nuclear factor-KB
Activator protein-1
GATA-3
(p. 1674)

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35
Q

Subepithelial fibrosis in asthma is due to deposition of what type/s of collagen?

A

Type III and V

p. 1674

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36
Q

What cytokine induces mucus hypersecretion in asthma?

A

IL-13

p. 1674

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37
Q

What is the characteristic physiologic abnormality of asthma?

A

Airway hyperresponsiveness

p. 1675

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38
Q

What are examples of direct bronchoconstrictors (in asthma)?

A

Histamine
Metacholine
(p. 1675)

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39
Q

Spirometry findings in asthma

A

Reduced FEV1, FEV1/FVC, PEF

p. 1675

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40
Q

Spirometry: Reversibility in asthma is demonstrated by?

A

1) >12% and 200 ml increase in FEV1 15 minutes after an inhaled SABA OR
2) 2-4 week trial of oral corticosteroids (prednisone or prednisolone 30-40 mg daily)
(p. 1675)

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41
Q

What test can be used for differential diagnosis of chronic cough or when suspecting asthma but with normal pulmonary function tests?

A

Metacholine or histamine challenge

p. 1675

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42
Q

CXR finding/s in asthma

A

Usually normal
Hyperinflated lungs (in more severe patients)
Possible pneumothorax (in exacerbations)
(p. 1675)

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43
Q

Non-invasive test to measure airway inflammation

A

Exhaled nitric oxide (FeNO)

p. 1676

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44
Q

Pharmacologic therapy for rapid relief of symptoms of asthma but has little or no effect on the underlying inflammatory process

A

Bronchodilators

p. 1676

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45
Q

Three classes of bronchodilators in current use for asthma

A

Beta 2 adrenergic agonists
Anti-cholinergic
Theophylline
(p. 1676)

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46
Q

Mode of action of beta 2 agonists for treatment of asthma

A

1) Relax airway smooth muscle cells of ALL airways
2) Inhibition of mast cell mediator release
3) Reduction in plasma exudation
4) Inhibition of sensory nerve activation
(p. 1676)

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47
Q

What is the duration of action of SABAs?

A

3-6 hours

p. 1676

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48
Q

What is the duration of action of LABAs?

A

Over 12 hours

p. 1676

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49
Q

For asthma treatment, how many times is Indacaterol given per day?

A

Once daily

p. 1676

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50
Q

Common side effects of beta 2 agonists

A

Muscle tremor
Palpitations
(p. 1676)

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51
Q

What can be used as an additional bronchodilator in patients with asthma that is not controlled by ICS and LABA combinations?

A

Anticholinergics

p. 1676

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52
Q

Most common side effect of anticholinergics (used in asthma)?

A

Dry mouth

p. 1677

53
Q

Side effects of anticholinergics (seen in asthma treatment)?

A

Dry mouth
Urinary retention
Glaucoma
(p. 1677)

54
Q

What is the mechanism of action of theophylline in asthma treatment?

A

Inhibition of phosphodiesterases in airway smooth muscle cells
Activates the key nuclear enzyme histone deacetylase-2 (HDAC2)
(p. 1677)

55
Q

IV medication that may be used in patients with severe asthma exacerbations that are refractory to SABA

A

IV aminophylline

p. 1677

56
Q

What is/are the most effective controller medication/s for asthma?

A

Inhaled corticosteroids

p. 1677

57
Q

Local side effects of use of inhaled corticosteroids in asthma

A

Hoarseness (dysphasia)
Oral candidiasis
(p. 1677)

58
Q

How can local side effects of inhaled corticosteroids be reduced?

A

Use of a large-volume spacer device

p. 1677

59
Q

Course of oral corticosteroids used to treat exacerbations of asthma with no tapering of the dose needed (according to Harrison’s)

A

Prednisone or prednisolone 30-45 mg once daily for 5-10 days

p. 1677

60
Q

Asthma controller drugs that inhibit mast cell and sensory nerve activation

A

Cromones (Cromolyn sodium and nedocromil sodium)

p. 1678

61
Q

Asthma medication used to neutralize circulating IgE and thus inhibits IgE-mediated reactions

A

Omalizumab

p. 1678

62
Q

Asthma medication usually given as a subcutaneous injection every 2-4 weeks

A

Omalizumab

p. 1678

63
Q

Arterial blood gas finding/s indicating impending respiratory failure in asthma

A

Normal or rising PCO2

p. 1679

64
Q

What is the most common reason for poor control of asthma?

A

Non-compliance with medications

p. 1679

65
Q

What is type 1 brittle asthma?

A

Persistent pattern of variability that may require oral corticosteroids or continuous infusion of beta 2 agonists
(p. 1680)

66
Q

What is type 2 brittle asthma?

A

1) Generally normal or near normal lung function but precipitous unpredictable falls in lung function that may result in death
2) Do not respond well to corticosteroids
3) Worsening of asthma does not reverse well with inhaled bronchodilators
(p. 1680)

67
Q

What is the most effective therapy for type 2 brittle asthma?

A

Subcutaneous epinephrine

p. 1680

68
Q

True or false: Anti-TNF therapy is effective in severe asthma

A

False

p. 1680

69
Q

Aspirin-sensitive asthma responds to usual therapy with what medication?

A

Inhaled corticosteroids

p. 1680

70
Q

Which drugs used in asthma therapy for pregnant patients have been shown to be safe and without teratogenic potential?

A

SABA
ICS
Theophylline
(p. 1680)

71
Q

What oral corticosteroid can be used safely in treatment for asthma in pregnant patients?

A

Prednisone (rather than prednisolone)

p. 1680

72
Q

What treatment is beneficial in preventing exacerbations of bronchopulmonary aspergillosis?

A

Oral itraconazole

p. 1681

73
Q

What are the leading causes of transudative pleural effusion?

A

Left ventricular failure
Cirrhosis
(p. 1716)

74
Q

What are the leading causes of exudative pleural effusion?

A 
Bacterial pneumonia
Malignancy
Viral infection
Pulmonary embolism
(p. 1716)
75
Q

What is the Light’s criteria? (Components)

A

1) Pleural fluid protein/serum protein > 0.5
2) Pleural fluid LDH/serum LDH > 0.6
3) Pleural fluid LDH more than 2/3 the normal upper limit for serum
(p. 1716)

76
Q

What is the most common cause of pleural effusion?

A

Left ventricular failure

p. 1716

77
Q

What test is diagnostic that a pleural effusion is secondary to congestive heart failure?

A

Pleural fluid N-terminal pro-brain natriuretic peptide (NT-proBNP)
(p. 1717)

78
Q

A pleural fluid NT-proBNP level of ______ is diagnostic that effusion is secondary to congestive heart failure.

A

> 1500 pg/ml

p. 1717

79
Q

What is the most common cause of exudative pleural effusion?

A

Parapneumonic effusion

p. 1717

80
Q

In parapneumonic effusion, a therapeutic thoracentesis should be performed if the free fluid separates the lung from the chest wall by ____ mm.

A

> 10

p. 1717

81
Q

In parapneumonic effusion, what factors indicate the likely need for an invasive procedure (rather than thoracentesis)?

A

1) Loculated pleural fluid
2) Pleural fluid pH <7.2
3) Pleural fluid glucose < 3.3 mmol/L (<60 mg/dl)
4) Positive gram stain or culture of the pleural fluid
5) Presence of gross pus in the pleural space
(p. 1717)

82
Q

What is the second most common cause of exudative pleural effusion?

A

Malignancy

p. 1717

83
Q

What are the three common malignant etiologies of exudative pleural effusion?

A

Lung carcinoma
Breast carcinoma
Lymphoma
(p. 1717)

84
Q

What procedures should be considered in a patient with malignant pleural effusion and dyspnea, relieved by thoracentesis?

A

1) insertion of a small indwelling catheter
2) tube thoracostomy with the instillation of a sclerosing agent such as doxycycline (500 mg)
(p. 1717)

85
Q

Most mesotheliomas are related to exposure to?

A

Asbestos

p. 1717

86
Q

CXR findings in mesothelioma

A

Pleural effusion
Generalized pleural thickening
Shrunken hemithorax
(p. 1717)

87
Q

Pleural effusion secondary to pulmonary embolism is almost always ______ (transudative/exudative)?

A

Exudative

p. 1717

88
Q

The diagnosis of pleural effusion secondary to pulmonary embolism is established by what test/imaging study?

A

Spiral CT scan or pulmonary arteriography

p. 1717

89
Q

Pleural effusion secondary to TB is due to what mechanism?

A

Hypersensitivity reaction to tuberculous protein in the pleural space
(p. 1718)

90
Q

The diagnosis of pleural effusion secondary to tuberculosis is established by what test/imaging study?

A

Adenosine deaminase >40 IU/L OR
Interferon gamma >140 pg/ml
(p. 1718)

91
Q

What is the most common cause of chylothorax?

A

Trauma

p. 1718

92
Q

Pleural fluid findings in chylothorax

A

Milky fluid with triglyceride level >1.2 mmol/L (110 mg/dl)

p. 1718

93
Q

What is the treatment of choice for most chylothoraxes?

A

Insertion of chest tube plus administration of octreotide

p. 1718

94
Q

Why shouldn’t patients with chylothorax undergo prolonged tube thoracostomy with chest tube drainage?

A

Because this will lead to malnutrition and immunologic incompetence
(Pp. 1718)

95
Q

When a diagnostic thoracentesis reveals bloody pleural fluid, what test should be obtained?

A

Pleural fluid hematocrit

p. 1718

96
Q

How is a hemothorax diagnosed through pleural fluid findings?

A

If pleural fluid hematocrit is more than 1/2 of that in the peripheral blood
(p. 1718)

97
Q

When should thoracoscopy or thoracotomy be considered in the setting of hemothorax/pulmonary hemorrhage?

A

If pulmonary hemorrhage exceeds 200 ml/hr

p. 1718

98
Q

What should be considered if pleural fluid amylase level is elevated?

A

Esophageal rupture
Pancreatic disease
(p. 1718)

99
Q

What is Meigs’ syndrome?

A

Benign ovarian tumor + ascites + pleural effusion

p. 1718

100
Q

Primary spontaneous pneumothorax is usually due to what?

A

Rupture of apical pleural blebs

p. 1719

101
Q

What is the initial recommended treatment for primary spontaneous pneumothorax?

A

Simple aspiration

p. 1719

102
Q

What is the usual cause of secondary pneumothorax?

A

COPD

p. 1719

103
Q

Tension pneumothorax usually occurs during what conditions?

A

Mechanical ventilation
Resuscitative efforts
(p. 1719)

104
Q

Why is there reduced cardiac output in tension pneumothorax?

A

The positive pressure is transmitted to the mediastinum resulting in decreased venous return to the heart
(p. 1719)

105
Q

In OSAHS, the airway may collapse at various anatomical levels, which are?

A

1) Soft palate (most common)
2) Tongue base
3) Lateral pharyngeal walls
4) Epiglottis
(p. 1723)

106
Q

OSAHS is most severe during what phase of sleep?

A

REM

p. 1724

107
Q

What are the major risk factors of OSAHS?

A

Obesity
Male sex
(p. 1724)

108
Q

A 10% weight gain is associated with how many % increase in apnea-hypopnea index (AHI)?

A

30%

p. 1724

109
Q

What are the risk factors for OSAHS?

A

1) Obesity
2) Male sex
3) Mandibular retrognathia and micrognathia
4) Positive family history of OSAHS
5) Genetic syndromes that reduce upper airway patency
6) Adenotonsillar hypertrophy
7) Menopause
8) Various endocrine syndromes
(p. 1724)

110
Q

What is the most common complaint in OSAHS?

A

Snoring

p. 1724

111
Q

What is the most common daytime symptom of OSAHS?

A

Sleepiness

p. 1724

112
Q

What is the gold standard for diagnosis of OSAHS?

A 
Overnight polysomnogram (PSG)
(p. 1725)
113
Q

What are key physiologic information collected during a sleep study for OSAHS assessment?

A

1) Measurement of breathing
2) Oxygenation
3) Body position
4) Cardiac rhythm
(p. 1725)

114
Q

In a polysomnogram, apnea is defined as what?

A

Cessation of airflow for > or = to 10 seconds during sleep, accompanied by persistence/absence of respiratory effort
(p. 1725, Table 319-1)

115
Q

In a polysomnogram, hypopnea is defined as what?

A

A > or = to 30% reduction in airflow for at least 10 seconds during sleep accompanied by a > or = to 3% desaturation or an arousal
(p. 1725, Table 319-1)

116
Q

In a polysomnogram, how is respiratory effort-related arousal (RERA) defined?

A

Partially obstructed breath that does not meet the criteria for hypopnea but with evidence of increasing inspiratory effort punctuated by an arousal
(p. 1725, Table 319-1)

117
Q

In a polysomnogram, flow-limited breath is defined as what?

A

Partially obstructed breath, typically within a hypopnea or RERA, identified by a flattened or “scooped out” inspiratory flow shape
(p. 1725, Table 319-1)

118
Q

Definition of mild OSAHS by number of AHI

A

5-14 events/hr

p. 1725, Table 319-2

119
Q

Definition of moderate OSAHS by number of AHI

A

15-29 events/hr

p. 1725, Table 319-2

120
Q

Definition of severe OSAHS by number of AHI

A

> or = to 30 events/hr

p. 1725, Table 319-2

121
Q

True or false: OSAHS can raise blood pressure to prehypertensive and hypertensive ranges

A

True

p. 1725

122
Q

True or false: Depression is commonly reported in OSAHS

A

True

p. 1726

123
Q

What is the standard medical therapy with the highest level of evidence for efficacy in OSAHS?

A

CPAP

p. 1727

124
Q

Oral appliances can also be used to treat OSAHS however its side effects include what?

A

Temporomandibular joint pain
Tooth movement
(p. 1727)

125
Q

True or false: Bariatric surgery is an option for obese patients with OSAHS

A

True

p. 1727

126
Q

Central sleep apnea is often caused by what?

A

1) Increased sensitivity to pCO2 –> hyperventilation alternating with apnea
2) Prolonged circulation delay between the pulmonary capillaries and carotid chemoreceptors
(p. 1727)

127
Q

What do you call the condition wherein central apnea is induced by the use of CPAP?

A

Complex sleep apnea

p. 1727

128
Q

What is a form of ventilatory support used for treatment of central sleep apnea that dynamically changes inspiratory support levels across periods of apnea and hypopnea?

A

Adaptive seroventilation

p. 1727

129
Q

Elevations in blood pressure in OSAHS is due to what mechanism/s?

A

1) Augmented sympathetic nervous system activation
2) Alterations in RAAS and fluid balance
(p. 1725)

Internal Medicine (20 decks)

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