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Pharmacology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Definition of COPD

A

Progressive lung cell destruction; characterized by persistent airflow limitation

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2
Q

Is COPD reversible?

A

No, not fully

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3
Q

Most common modifiable treatment to COPD?

A

Quit smoking

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4
Q

What are some causes of COPD?

A

Persistent exposure to noxious particles/chemicals, which make the lung parenchyma susceptible and causes an enhanced or chronic inflammatory response

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5
Q

Which disease is CHRONIC and PROGRESSIVE?

A

COPD

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6
Q

How common is COPD? And is it preventable/treatable?

A

Pretty common, and yes, it is preventable and treatable

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7
Q

Two presentations of COPD? Which can occur separately or together?

A
  1. Narrowing of small airways (obstructive bronchiolitis)

2. Parenchymal destruction (emphysema)

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8
Q

What causes chronic bronchitis? (physiologically-wise?)

A

Chronic inflammation and excess mucus plugging

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9
Q

Chronic inflammation leads to ______ ______ and/or ________ ________.

A

airway narrowing; parenchymal destruction

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10
Q

What happens to the alveoli in emphysema?

A

Loss of alveolar membrane attachments and decreased elastic recoil

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11
Q

When the airways are narrowed via obstructive bronchiolitis, there is increased ________.

A

resistance

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12
Q

Breath stacking is more common in what kind of patients?

A

Asthma

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13
Q

What’s one way to test whether or not a pt has COPD or asthma? And what would be the results in each case?

A

Use a bronchodilator - for an asthma pt, it will bring them back to baseline, it will have a minimal response for a COPD pt

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14
Q

Which disease is reversible?

A

Asthma

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15
Q

What characterizes asthma?

A

Airway hyper-responsiveness

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16
Q

Patient picture for a COPD diagnosis?

A

Onset in midlife, symptoms have been slowly progressive, history of tobacco smoking or exposure to other types of smoke

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17
Q

Patient picture for an asthma diagnosis?

A

Onset early in life (childhood, usually); symptoms vary widely day-to-day; symptoms worse at night and/or early morning; allergy, rhinitis, and/or eczema often present; family history of asthma

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18
Q

Modifiable risk factors?

A

Smoke, occupational dusts and chemicals, air pollution

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19
Q

Non-modifiable risk factors?

A

Genetic predisposition (AAT deficiency), airway hyper-responsiveness, impaired lung growth/infections

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20
Q

What does AAT involve?

A

Issue with lung surfactant

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21
Q

Pack history calculation?

A

cigarettes a day x years of smoking

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22
Q

Percentages of smokers who develop COPD? Percentages of COPD patients who are/were smokers?

A

15-20%

85%

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23
Q

Primary cause of COPD?

A

Cigarette smoking

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24
Q

What could impair lung growth?

A

low birth weight, prematurity, childhood illnesses

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25
Q

Why is it bad if your lungs scar?

A

Because they won’t be able to properly oxygenate and you get more lung rigidity (you lose elasticity and compliance) which increases risk of breath stacking

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26
Q

Repeated injury and repair of the lungs leads to what?

A

Inflammatory and destructive changes - leads to air trapping and airflow limitation

Disrupted normal defense/repair - leads to scarring and fibrosis

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27
Q

What can you see on a CXR by counting ribs?

A

Hyperinflation of the lungs

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28
Q

Hyperinflation causes what?

A

Flatttening of diaphragmatic muscles

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29
Q

Why is hyperinflation bad in the lungs?

A

less efficient ventilation; requires more work to contract; muscle fatigue; changes in lung volume; limits inspiratory reserve capacity while increases functional residual capacity; increases intrathoracic pressure

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30
Q

What is hypercapnia?

A

Excessive CO2 in the bloodstream due to inadequate respiration

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31
Q

Due to hyperinflation, what happens to the gas exchange in our bodies?

A

Reduced gas transfer including hypoxemia, hypercapnia

Reduced ventilation including obstruction, hyperinflation, ventilatory muscle impairment

Reduced ventilatory drive with CO2 retentino

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32
Q

Problems with chronic productive cough?

A

Impairs ciliary mobility

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33
Q

Clinical presentaitons of chronic bronchitis?

A

Overweight and cyanotic, elevated hemoglobin, peripheral edema, rhonchi and wheezing

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34
Q

Clinical presentations of emphysema?

A

Older and thin, severe dyspnea, quiet chest, CXR will show hyperinflation with flattened diaphragm

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35
Q

COPD clincial presentation

A

Dyspnea (progressive, worsens with activity, persistent), chronic cough** (intermittent, often productive)

Physical Exam: increased RR/shallow breathing, use of accessory respiratory muscles, cyanosis of mucosal membranes, barrel chest (due to hyperinflation)

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36
Q

Progress of COPD?

A

Pulmonary effects: hypoxemia, hypercapnia

Extrapulmonary effects: skeletal muscle wasting (cachexia), lower extremity edema

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37
Q

Gold standard for COPD?

A

Spirometry

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38
Q

Hallmark of COPD

A

Reduction in post-bronchodilator FEV1/FVC < 0.70

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39
Q

What is tidal volume?

A

Volume of air that is breathed in and out in a normal quiet breath

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40
Q

What is residual volume?

A

Amount of air that remains in the lungs after maximum exhalation

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41
Q

What is vital capacity?

A

Maximum volume of air exhaled after maximum inhalation

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42
Q

What is total lung capacity?

A

Maximum amount of air that the lung can hold

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43
Q

What is FEV1?

A

Amount of air that the patient exhales in 1 second

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44
Q

What is FEV1/FVC?

A

Ratio of FEV1 relative to the full volume patient exhaled in 6 seconds

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45
Q

Acute exacerbations of COPD can be due to what?

A

Bacterial and viral infections; tobacco or pollutant triggers

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46
Q

What occurs more frequently in severe chronic COPD?

A

acute exacerbations

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47
Q

What symptoms occur in an acute exacerbation?

A

Dyspnea, cough, sputum production and purulence, worsened hyperinflation

Worsening ABG, increased muscle fatigue

hypoxemia/hypercapnia may result in repiratory acidosis and respiratory failure

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48
Q

Why do we treat COPD agressively?

A

Many are readmitted, it takes several weeks to return to baseline

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49
Q

To assess COPD, what three things do you do?

A
  1. Symptoms
  2. Degree of airflow limitation
  3. Risk of exacerbations
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50
Q

GOLD 1 severity and spirometry results?

A

Mild ; FEV1 > or = 80% predicted

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51
Q

GOLD 2 severity and spirometry results?

A

Moderate; 50% < or = FEV1 < 80% predicted

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52
Q

GOLD 3 severity and spirometry results?

A

Severe; 30% < or = FEV1 < 50% predicted

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53
Q

GOLD 4 severity and spirometry results?

A

Very severe; FEV1 < 30% predicted

54
Q

COPD Stage 1 lung function?

A

80%

55
Q

COPD Stage 2 lung function?

A

50-80%

56
Q

COPD Stage 3 lung function?

A

30-50%

57
Q

COPD Stage 4 lung function?

A

<30%

58
Q

When respiratory symptoms worsen beyond normal day-day variations, what do you do for treatment?

A

Change in medication

59
Q

Comorbid conditions include?

A

CVD, osteoporosis, depression/anxiety, skeletal muscle dysfunction, metabolic syndrome, lung cancer

60
Q

Non-pharmalogical therapy for COPD management includes?

A

Quit smoking, reduce occupational exposure and indoor/outdoor pollution, possible CBT counseling to quit smoking

Nutrition counseling, education, exercising training

61
Q

Preventative measures for COPD management?

A

vaccines - especially flu, pneumococcal, and covid

62
Q

What is not generally recommended for COPD prophylaxis?

A

antibiotics

63
Q

What antibiotic does seem to help with preventing COPD?

A

Azithromycin

Decreased exacerbations, but increases ADRs and lung resistance

64
Q

The three goals of pharmacothearpy for COPD?

A
  1. Reduce COPD symptoms
  2. Reduced freqency and severity of symptoms
  3. Improve health status and exercise tolerance
65
Q

What medications include SABA and LABA?

A

Beta 2 agonists

66
Q

What medications include SAMA and LAMA?

A

Anti-cholinergics

67
Q

What combination is usually used for ICS?

A

LABA/ICS

68
Q

What are the three classe of bronchodilators?

A

Beta 2 agonists; anti-muscarinics, methylxanthines

69
Q

MOA for Beta 2 agonists?

A

Stimulate beta receptors on the lung to relax smooth muscles in the airway

70
Q

ADRs for Beta 2 agonists?

A

Tachycardia, palpiations, tremor

71
Q

SABAs?

A

Albuterol and levalbuterol

72
Q

LABAs?

A

Salmeterol, Formoterol, Arformoterol, Indacaterol, Olodaterol, Vilanterol

73
Q

MOA for anticholinergics?

A

Blocks ACh effects on muscarinic receptors leading to bronchodilation; M3 receptor on airway smooth muscle mediating bronchoconstriction and mucous secretion

74
Q

What’s the benefit of SAMAs over SABAs?

A

Slower onset, but typically longer duration

75
Q

ADRs for anticholinergics?

A

Dry mouth, hoarseness, blurred vision, metallic taste

76
Q

Benefit of LAMAs over LABAs?

A

LAMAs seem to have a greater effect in reducing exacerbations

77
Q

SAMAs?

A

Ipratropium

78
Q

LAMAs?

A

Tiotropium, Aclidinium, Umeclidinium

79
Q

What is methylxanthine structurally related to?

A

Caffeine

80
Q

MOA for methylxanthine?

A

Non-selective PDE inhibitor (3/4) causing bronchodilation, decreases airway reactivity

81
Q

ADRs for methylxanthine?

A

NTD, arrhythmias, convulsions

HA, insomnia, N/V, heartburn (at thearpeutic concentrations)

Many drug interactions (smoking induces metabolism)

82
Q

If someone stops smoking while taking methylxanthine, what do you need to do to their medication?

A

Reduce the dose

83
Q

ICSs?

A

Fluticasone, mometasone, budesonide

84
Q

First line asthma treatment?

A

ICs

85
Q

What gets added later in COPD treatment as compared to asthma treatment?

A

ICs

86
Q

Use of ICs?

A

Improved symptoms, lung function, reduced exacerbations

87
Q

ADRs for ICs?

A

Hoarseness, oral candidiasis

Increased risk of PNA in COPD pts

88
Q

When are oral steroids used for respiratory illnesses?

A

Refractor disease (really severe COPD)

89
Q

PDE 4 Inhibitor?

A

Roflumilast

90
Q

MOA for PDE 4 Inhibitors?

A

Anti-inflammatory effects via cAMP accumulation

91
Q

PDE 4 inhibitors improve FEV1 in combination with what other drug?

A

LABAs

92
Q

ADRs for PDE4 inhibitors?

A

N/V decreased appetitie, diarrhea, weight loss, mood disturbances, night terrors, suicidality

93
Q

What virus can exacerbate asthma?

A

RSV

94
Q

What is the strongest predictor of asthma?

A

Genetic predisoposition with atopic dermatitis

95
Q

What is asthma?

A

variable airway obstruction that if often REVERSIBLE

96
Q

What are some environmental triggers for asthma?

A

Secondhand smoking, urban vs rural living, RSV infection, occupational hazards

97
Q

What two things can occur with asthma?

A

Airway edema (due to mast cell activation, which is elevated in allergic conditions)

Eosinophilia (releases cytokines and proinflammatory mediators)

98
Q

Problem with asthma exacerbations?

A

If you have one, you’ll likely have more, and if you get more, you can get permanent damage

99
Q

Asthma presentations

A

Episodic dyspnea, wheezing, chest tightenss, coughing

100
Q

Asthma symptoms occur when?

A

Spontanteous, allergen exposure, exercise induced

101
Q

You can premedicate with what before exercise with asthma?

A

Albuterol (SABA)

102
Q

Gold standard for asthma?

A

spirometry

103
Q

Asthma reversibility indicated by spirometry?

A

FEV1 > 12% AFTER SABA administration

104
Q

FEV1/FVC in both asthma and COPD

A

< 70%

105
Q

Spirometry results from exercise induced bronchospasm

A

Drop FEV1 > 15% after an exercise challenge

This is measured at baseline and 5 min intervals x 20-30 min

106
Q

Asthma initial visit goals?

A

Diagnose, assess severity, initiate medicine and demonstrate use, develop written asthma action plan, schedule follow up

107
Q

Why are follow-ups important for asthma patients?

A

Because pts will often stay on the same medication dose for a very long time, so we need to make sure they are on the right dose

108
Q

Why don’t we use LABA monotherapy for asthma?

A

It can reduce the pt’s own susceptibility to SABA thearpy (the body develops a tolerance for it) and increases risk of DEATH

109
Q

Treatment for asthma?

A

low dose ICs (can be in combination with LABAs) and SABA for rescue

110
Q

What are the two Leukotriene receptor antagonists?

A

Montelukast (Singulair) and Aarfirlukast (Accolate)

111
Q

MOA for Leukotriene receptor antagonists

A

Decreases response from the allergic/hypersensitivity reactions

112
Q

When would you use a leukotriene receptor antagonist?

A

Asthma with allergic components

113
Q

What biologics are available for asthma treatment?

A

Omalizumab, Mepolizumab

114
Q

When would you use a biologic in asthma treatment?

A

pts with high amounts of eosinophils and IgE

115
Q

Doseage for Omalizumab?

A

Dosed q2-4 weeks SQ based on eosinophil counts

116
Q

Mepolizumab dosage?

A

q4 weeks SQ

117
Q

ADRs for biologics?

A

hypersensitivity, injection site pain, HA, edema, increased risk of infection/parasitic infection

118
Q

Preferred drug choice for asthma in pregnancy?

A

Albuterol

119
Q

Preferred long term control ICs during pregnancy?

A

Budesonide

120
Q

What other drugs appear to be safe in pregnancy to treat asthma?

A

LABAs and Montelukast (Singulair)

121
Q

What drug can also help with allergic rhinitis in asthma with pregnancy?

A

Cromolyn

122
Q

Precipitating Factors to asthma exacerbation?

A

allergen, pollutant exposure, respiratory infections including viral and bacterial (H. influenzae, Strep. pneumoniae, Moraxela catarrhalis), medication non-adherence

123
Q

Treatment for COPD exacerbation?

A

Rapid labs and imaging work ups; treating the underlying cause, deciding outpatient vs inpatient treatment appropriation

124
Q

AECOPD treatment?

A

SABA +/- SAMA treatment (Albuterol/Ipratropium nebulized solution)

Oral corticosteroid treatment - Prednisone 40mg x 5 days

Antibiotics - use with increased cough and sputum purulence, mostly azithromycin or doxycycline most commonly used

125
Q

What are the 3 cardinal symptoms with antibiotics?

A

Increased dyspnea, sputum volume, sputum purulence

126
Q

Gold standard dosing for oral contraceptives for AECOPD?

A

Prednisone 40 mg x 5 days

127
Q

What is used for asthma pts to measure their PEF?

A

Peak flow meters

128
Q

Early signs of asthma exacerbation

A

Breathlessness at rest, drowsiness, agitation, inability to speak full sentences, PEF < 50% personal best

129
Q

Asthma exacerbation treatment?

A

SABA administration
Oral/IV steriod - Prednisone 40-60 mg/dose equivalent x 5-7 days
Oxygen
Increase maintenance therapy (ICs/LABA dose)

130
Q

What drug can you also use in combination to treat an asthma exacerbation?

A

SAMA combination

131
Q

Proper technique for using inhaler? MDI vs DPI?

A

MDI: Slowed inhalation of medication (that’s why it needs a spacer)
DPI: Deep forceful inhalation to get the medication into the lungs

Pharmacology (6 decks)

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