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CR&R > Quiz 4 drugs + B&B OLD > Flashcards

Quiz 4 drugs + B&B OLD Flashcards

1
Q

Which four medications fall into the designation of asthma “relievers”?

A

Albuterol
Levalbuterol
Epinephrine
Ipratropium

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2
Q

What two medications are designated as short-acting beta-2 agonists?

A

Albuterol
Levalbuterol

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3
Q

What medication for asthma relief is designated a short-acting beta-1&2 alpha-1&2 agonist?

A

Epinephrine

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4
Q

What medication for asthma relief is designated a short-acting muscarinic antagonist?

A

Ipratropium

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5
Q

What is the MoA of SABAs?

A

B2 receptor -> AC -> cAMP -> decreased IC Ca2+ -> MLCK inactivation -> SM relaxation

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6
Q

How are SABAs used clinically?

A

Relief of acute sx/attacks
Prevention of exercise-induced bronchiospasm (EIB)

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7
Q

What SABA standard is used to determine good asthma control?

A

Less than one MDI/month

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8
Q

What are potential side effects of SABA use? Rank the liklihood of adverse effects by doseage form:
-Nebulizer
-Oral
-MDI
-Parenteral

A
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9
Q

What additional measure should be taken to care for patients using a SABA more than 2x a week consistantly?

A
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10
Q

What is the MoA of SAMAs?

A
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11
Q

Are SABAs or SAMAs more effective to treat asthma?

A

SABAs by far; they work much quicker and are more effective at airway dilation; SAMAs are rarely ever used by themselves

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12
Q

What is the brand name for ipratropium?

A

Atrovent HFA

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13
Q

What is the most common adverse effect seen with SAMAs?

A

Dry mouth

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14
Q

What is the main FDA approved LABA? Do the MoA and adverse effects differ from SABA? Can LABAs be used for monotherapy for long-term control?

A
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15
Q

What is the FDA approved LAMA currently used? What are some adverse effects?

A
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16
Q

What are the five primary inhaled corticosteroids (ICS) that are used as asthma controllers?

A
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17
Q

Besides ICS or combination medications, What are 2 drug classes and 2 individual drugs that are also used as “asthma controllers”?

A
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18
Q

What are the four major inflammatory mediators inhibited by ICS? Which notable immune cells are inhibited from migrating in large numbers?

A
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19
Q

What immune cell response is highly associated with asthma?

A

Eosinophils

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20
Q

Corticosteroids are responsible for blocking the leukotriene synthesis pathway by directly interfering with the synthesis of what compound?

A

Arachidonic acid (inhibition of PLA2)

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21
Q

What are three possible side effects of ICS use?

A

*Rinsing, gargling and spitting water each time the medicine is used can reduce the chance of SE

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22
Q

What is the MoA of theophylline?

A

*Not really used anymore
**Same MoA as beta-agonists after PDE triggers cAMP activation

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23
Q

What are several notable side effects of theophylline?

A

*Many adverse effects are similar to excess caffeine

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24
Q

What are the two MoA of leukotriene modifiers?

A
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25
Q

What are the two notable leukotriene receptor antagonists (with brand names)?

A

Montelukast (Singulair)
Zafirlukast (Accolate)

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26
Q

What is the notable 5-lipoxygenase inhibitor (leukotriene modifer)?

A

Zileuton (Zyflo)

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27
Q

Which leukotriene modifiers are notable for hepatotoxicity and drug interactions?

A

Zafirlukast & Zileuton (all except montelukast)

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28
Q

Why is montelukast not considered a first line agent for asthma?

A

It is not very potent

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29
Q

What is Cromolyn? What is the MoA? What are adverse effects?

A

Mast-cell stabilizer
*It is not really used at all; not very potent

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30
Q

What antibody treatment is anti-IgE? Which is an IL5 RA? Which are anti IL5? Which is an IL4RA (anti IL13?)?

A
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31
Q

What is the brand name for omalizumab? What is its MoA? What is the doseage form and frequency?

A
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32
Q

What black box warning is associated with Omalizumab (Xolair)?

A

*Also notable for injection SE

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33
Q

When are biological treatments (i.e. antibody treatments) administered to asthma patients?

A

For uncontrolled step 5 therapy

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34
Q

Which two drugs are anti-IL5 treatments for asthma?

A

Mepolizumab and Reslizumab

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35
Q

What is the brand name of Mepolizumab? What is the MoA? What is the doseage route and frequency?

A
36
Q

What are some adverse side effects of Mepolizumab (Nucala)?

A

*Anaphylaxis is not a BBW, but could occur
*Also notable for injection SE

37
Q

What is the brand name for Reslizumab? What is its MoA? What is the doseage form and frequency?

A

*Not used as often due to IV route; inconvenient and potentially costly

38
Q

What is the significant BBW for use of Reslizumab? What is another notable SE?

A

*Myalgia is other notable

39
Q

What is the brand name of Benralizumab? What is the MoA? What is the doseage route?

A
40
Q

What is the doseage frequency of Benralizumab (Fasenra)? What are notable adverse effects?

A
41
Q

What is the brand name of Dupilumab? What is the MoA?

A
42
Q

What is the doseage route and frequency (general description) of Dupilumab (dupixent)? What are potential adverse effects?

A
43
Q

Which notable drug used for asthma is a thymic stromal lymphopoietin (TSLP) antagonist?

A

Tezepelumab (Tezspire)

44
Q

What is the brand name for Tezepelumab? What is the MoA? What is the doseage form?

A
45
Q

What is the doseage philosophy for Tezepelumab (Tezspire)? What are some adverse effects?

A
46
Q

What happens to residual volume and total lung volume in restrictive lung disease? What happens in obstructive lung disease?

A
47
Q

What are the four main obstructive lung diseases? What can differentiate asthma from chronic lung disease (other 3 OLDs)?

A
48
Q

What is the largest risk factor associated with chronic lung disease?

A

Smoking

49
Q

What are the clinical indications for a diagnosis of chronic bronchitis (3 items)?

A
50
Q

What pathology of the respiratory tract (RT) occurs in chronic bronchitis? What value on the Reid index may indicate chronic bronchitis? What is the significance of “mucous plugging”? Why does CB cause increased risk of infection?

A

Reid index taken from autopsy
**Mucous plugging can result in loss of ventilation to areas of the lung
**Impaired mucus clearance can increase risk of infection

51
Q

Chronic bronchitis leads to poor lung ventilation causing hypoxic vasoconstriction which can progress to what further pathologies?

A
52
Q

What are the two most common etiologies of emphysema? What are the pathologies of both causes? Which leads to more upper lung damage vs lower lobe damage?

A

*a1-anti-trypsin deficiency is very rare

53
Q

How does emphysema lead to destruction of the alveoli?

A
54
Q

What are several notable symptoms of emphysema? Which is most classic?

A

*Barrel chest

55
Q

What anatomic structures make up the respiratory acinus? Where does damage to the acinus tend to differ between smokers and patients with a1 anti-trypsin deficiency?

A

Centriacinar- mostly damage to bronchioles, alveoli mostly intact

Panacinar- entire acinus sustains damage

56
Q

What are two notable histological findings for emphysema?

A

-Thin septa
-Large air spaces

57
Q

What describes the pathology seen in a CXR of a patient with emphysema?

A

Hyperinflated lungs

58
Q

What happens to functional residual capacity (FRC) in patients with emphysema?

A

It increases

*Meaning more air is left in the lungs after each quiet breath, which extra capacity contributes to the barrel chest

59
Q

T/F: Patients with chronic bronchitis are known as pink puffers, and patients with emphysema are known as blue bloaters

A

False, it is the opposite

60
Q

Why are patients with chronic bronchitis referred to as blue bloaters?

A
61
Q

Why are patients with emphysema referred to as pink puffers?

A
62
Q

Which diseases fall under the umbrella of chronic obstructive pulmonary disorders (COPD)? Why are they grouped together?

A

*Asthma is considered separate in all scenarios but the one involving severe, refractory asthma that is no longer reversible; in that case it is considered part of COPD

63
Q

What is the pathology of a1 anti-trypsin deficiency? How is it inherited? What is an example of a protease balanced by AAT?

A
64
Q

What two organs are primarily affected by an a1 anti-trypsin deficiency? How are the lungs affected? How is the liver affected? Which organ damage only occurs in some phenotypes?

A
65
Q

In a classic case of a1 anti-trypsin deficiency, What PFT values would be expected (normal, restrictive, etc)? What type of acinar involvement would be expected? Why is smoking so dangerous for these patients?

A
66
Q

Why is the bronchoconstriction seen in asthma different from other obstructive disorders? What type of stimulus usually triggers asthma? In what patient population is it most common?

A
67
Q

What are 6 common triggers of asthma?

A

*Aspirin is rare

68
Q

What is the classic triad of Aspirin exacerbated respiratory disease (AERD)?

A
69
Q

What is the pathology of AERD? How is it treated?

A
70
Q

What can happen to the I/E ratio in an asthma episode?

A

The I/E ratio decreases, as the expiratory phase becomes prolonged due to obstruction (down from 1/2 to 1/4 or 1/5)

71
Q

What two elements are usually used to diagnose asthma? What prominant test can be done in order to further test for asthma?

A
72
Q

What pathology finding is visible in this sputum sample? What disease process is it indicative of?

A

Curschmann’s spirals

It is indicative of asthma

73
Q

What pathology finding is visible in this sputum sample? What disease process is it indicative of?

A

Charcot-Leyden crystals

It is indicative of asthma

74
Q

What two classic sputum findings are indicative of asthma?

A
75
Q

What is the most frequent non-cardiac cause of pulsus paradoxus?

A

Asthma/COPD

76
Q

What is the pathology of bronchiectasis? Why is it obstructive if the airways are permanently dilated?

A

Large airways are dilated, but most of the bronchial tree involves small/medium airways, which experience thickened walls

77
Q

What pathology is notable on this CT scan? What disease process is it indicative of?

A

Large, circular, dilated airways

Bronchiectasis

78
Q

What are 3 notable symptoms of bronchiectasis? What fourth symptom/pathology is shared with other obstructive lung diseases?

A

*Cor pulmonale
**Bronchiectasis is rare cause of amyloidosis

79
Q

What are five notable causes of bronchiectasis?

A

*Kartagener and ABA are RARE causes but notable for step 1

80
Q

What is the pathology of Primary Ciliary Dyskinesia? What protein is mutated? What is the inheritance?

A
81
Q

Patients with Primary Ciliary Dyskinesia are at risk for developing what syndrome?

A
82
Q

What are the four main characteristics of Kartagener’s syndrome?

A
83
Q

What characterizes Allergic bronchopulmonary aspergillosis (ABPA)? What happens to the lungs?

A
84
Q

What two types of patients are at highest risk for ABPA? What are four notable blood chemistry findings in patients with ABPA?

A
85
Q

Which of these symptoms would be indicative of another pathology beyond asthma or CF? What is the most likely diagnosis? How is it diagnosed/treated?

A

-High IgE level
-Peripheral blood eosinophilia
-Brownish mucus plugs, hemoptysis

86
Q
A

CR&R (8 decks)

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