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Pharmacology Exam 2 > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Regulation of respiration involves what?

A
  • Control of the respiratory center

- Balance maintained between para and sympathetic nervous systems

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2
Q

Control of the respiratory involves:

  • Medullary rhymicity center
  • Vagul Input from lungs
  • _____
A

ABGs- arterial blood gases

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3
Q

The PNS mainly produces ___________ and mucus __________

The SNS mainly involves B2 receptors _________ smooth muscle and _________ mucociliary clearance

A
  • bronchoconstriction, secretion

- relaxing, increasing

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4
Q

What does clenbuterol do?

A

Helps build muscle, can cause cardiac issues

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5
Q

Our respiratory tract is divided into _____ and ______

A

Upper and lower

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6
Q

What is the function of our upper respiratory tract?

A
  • consists of our nasal and oral cavity, larynx, pharynx, and trachea
  • warms, humidifies, and filters inspired air (1st line of pulm immune defense)
  • mucocilliary escalator-lines conduction airways for 2nd line of defense
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7
Q

What does the lower respiratory tract consist of?

A
  • trachea, bronchi, bronchioles, and alveoli

- immune cells complete pulmonary defense

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8
Q

Function of the trachea and bronchial tree?

A

Warm/moisten air

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9
Q

Function of the alveoli?

A

Primary gas exchange site

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10
Q

What does V stand for?
What does Q stand for?
Together they make what?

A
  • V=ventilation
  • Q=perfusion
  • V/Q ratio:
    • amount of air breathing in/amount of blood to lungs
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11
Q

What is dead space?

What is shunt?

A

Dead space

  • When ventilation is in excess of perfusion
  • The alveoli are ventilated but not perfused

Shunt

  • When perfusion is in excess of ventilation
  • The alveoli is perfused but not ventilated
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12
Q

What is considered regular breathing in terms of volumes?

A

Tidal volume

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13
Q

What are the categories of drugs used to treat respiratory tract irritation and control respiratory secretions?

A
  • Decongestants
  • Antitussives
  • Antihistamines
  • Mucolytics and Expectorants
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14
Q

Deongestants MOA?

AE?

A
  • MOA (usually alpha-1 adrenergic agonists)
    • cause vasoconstriction
    • reduce blood flow and hence outflow from capillaries
  • HA, dizziness, nerevousness, nausea, CV irregularities
  • *can mimic the effects of increased sympathetic NS activity
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15
Q

Who shouldn’t take decongestants?

What drugs does this counteract?

A
  • People with high BP, can raise BP

- beta-blockers

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16
Q

Antitussives MOA?

AE?

A
  • MOA-decrease afferent nerve activity or decrease cough center sensitivity
  • sedation, dizziness, GI upset
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17
Q

Antitussives are usually recommended for ______

A

short-term use

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18
Q

Antitussives are used to suppress a __________ as opposed to a ____________

A
  • dry cough

- productive cough

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19
Q

Benadryl is an example of a _________

A

antihistamine

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20
Q

Antihistamines are used to manage respiratory _________ responses

A

allergic

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21
Q

Antihistamines block histamine receptors reducing what?

A
  • Mucosal irritation
  • Decreases sneezing caused by histamine associated sensory neural stimulation
  • Decreased nasal congestion
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22
Q

What are the primary AE of antihistamines?

A
  • Sedation
  • Fatigue
  • Dizziness
  • Blurred vision and incoordination
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23
Q

Whats the difference between 1st gen and 2nd gen antihistamines?

A

1st gen cross the BBB while 2nd gen do not easily cross

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24
Q

Is there a higher risk of side effects with 2nd gen antihistamines?

A

No, but they are not devoid of side effects

  • Side effects can include same as 1st gen plus:
    • dry mouth
    • sore throat
    • cough
    • nausea
    • HA
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25
Q

Can antihistamines be used on people with asthma?

A

Yes, will not dry up the airways and aggravate asthma

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26
Q

Mucolytics MOA?

A

-split disulfide bonds

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27
Q

Mucolytics are drugs which _______ the viscosity of respiratory secretions (mucus)

A

decrease

-in doing so they loosen and clear mucus from the airways

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28
Q

Expectorants act to facilitate the __________ and ___________ of mucus.
How does it do this?

A

-production and ejection

  • causes a thinning of mucus
  • promotes a productive cough
  • lubricates respiratory tract
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29
Q

-Expectorants are used to treat both _____ and ______ conditions ranging from common colds to emphysema

A

acute and chronic

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30
Q

Decongestants can ______ effects of the SNS.

A

increase

-vasoconstriction can increase BP

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31
Q

Who should avoid OTC decongestant products?

A

HTN patients

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32
Q

What is emphysema?

A

A accumulation of air in the tissues, particularly in the lungs

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33
Q

What is emphysema commonly associated with?

A

Smoking

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34
Q

Lungs with emphysema don’t ______ and _______ as well as a regular lung.

A

stretch and recoil

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35
Q

People with emphysema have a decrease in _____ volume but an increase in ______ volume.

A
  • tidal

- residual

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36
Q

What are the clinical manifestations of emphysema?

A
  • Exertional dyspnea progresses to dyspnea at rest
  • Tachypnea (increases RR)
  • Use of accessory breathing muscles for ventilation
  • Barrel Chest
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37
Q

What classifies someone as having chronic bronchitis?

A

Someone who has a really productive cough, lasting for at least 3 months per year for 2 consecutive years

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38
Q

What are the clinical manifestations of chronic bronchitis?

A
  • Persistent cough and sputum production
  • Shortness of breath
  • Prolonged expiration

-Late effects including pulmonary hypertension leading to cor pulmonale, severe disability and death

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39
Q

What is cor pulmonale?

A

Right sided heart failure caused by increase in pulmonary artery BP

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40
Q

S28 Changes in Chronic Bronchitis and Emphysema

A

S28

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41
Q

Goals of treatment for COPD

A
  • reduce airway edema secondary to inflammation and bronchospasm through the use of BRONCHODILATOR medication
  • elimination of bronchial secretion
  • prevent and treat respiratory infection
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42
Q

Inhaled beta agonists:

  • If acting in the lungs, B1 or B2 receptor?
  • What type of receptor is this?
  • What neurotransmitter typically binds this type of receptor?
  • Is this sympathetic or parasympathetic activity?
A
  • B2
  • Adrenergic
  • Epi and NE
  • Sympathetic
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43
Q

Inhaled beta agonists are divided into ____ and ____.

A
  • SABA (short acting)

- LABA (long acting)

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44
Q

What do inhaled beta agonists usually end in?

A

-end in -terol

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45
Q

What is the MOA for both SABA and LABA?

A

-agonize B2 receptors= bronchodilation

46
Q

SABA onset?
Duration?
Use?

A
  • onset- 5 minutes
  • duration- 4-6 hours
  • use as needed for SOB (shortness of breath)
47
Q

LABA Duration?

Dosage?

A
  • duration- 12-24 hours

- once or twice daily

48
Q

SABA is generally used for _____ reasons while LABA is typically taken on an _______ basis

A
  • acute

- ongoing

49
Q

What are the AE of Inhaled beta agonists?

A
  • generally well tolerated

- can cause tachycardia, tremor, hypokalemia

50
Q

Inhaled antimuscarinics (anticholinergic) are divided into ____ and ____.

A
  • SAMA (short acting muscarinic antagonist)

- LAMA (long acting muscarinic antagonist)

51
Q

What is the MOA for both SAMA and LAMA?

A

-primarily binds M3 in airway smooth muscle; antagonizes ACh actions at these sites = bronchodilation

52
Q

SAMA Onset?

Duration?

A
  • 15-20 minutes

- 6-8 hours

53
Q

LAMA Duration?

Dosage?

A
  • 12-24 hours

- once or twice daily

54
Q

What are the most common AE of SAMA and LAMAs?

A

generally well tolerated but can cause dry mouth

55
Q

What are inhaled corticosteroids typically used for?

A

In COPD they are typically used for exacerbations or more severe diseases

56
Q

What do inhaled corticosteroids typically end in?

A

-end in -asone

57
Q

What are some of the many AE of inhaled corticosteroids?

A
  • oral candidiasis (prevent by rinsing mouth)
  • hoarse voice
  • skin bruising
  • increased risk pneumonia
58
Q

What is the benefit of using combination of products with treatment?

A

Combining bronchodilators may increase effect with lower AE as compared to increasing dose of a single product

  • SABA and SAMA
  • LABA and LAMA
  • LABA and ICS
  • LABA and LAMA and ICS
59
Q

What are the goals of COPD treatment?

A
  • decrease symptoms
  • increase exercise tolerance
  • improve health status
  • prevent disease progression
60
Q

Can someone be on one class of drug and still have advanced COPD?

A

Yes

61
Q

What can be the causes of inhalers not working?

A
  • Disease progression
  • Incorrect inhaler or nebulizer use
  • Nonadherance(need edu on PRN vs maintanence meds)
  • In COPD, may not be able to produce force necessary
62
Q

Phosphodiesterase-4 (PDE-4) Inhibitor MOA?

AE?

A

-MOA- decrease breakdown of intracellular cyclic AMP = decrease in inflammation

  • AE-present in 5% or less of patients
    • diarrhea (10%)
    • nausea (5%)
    • weight loss (up to 20%)
63
Q

PDE-4 is generally used for what?

A

more severe COPD

64
Q 
When are antibiotics used for COPD?
What class ends in -mycin?
A

used in acute exacerbations
- extended treatment only in patients prone to exacerbations

-macrolide

65
Q

What is bronchial asthma?

A

-A reversible obstructive lung disease characterized by infammation and increased smooth muscle reaction of the airways to various stimula

66
Q

Is bronchial asthma chronic or acute?

A

Both

-Its a chronic condition with acute exacerbations

67
Q

Unlike chronic bronchitis and emphysema it can affect what?

A

All ages

-Most common chronic disease in adults and children

68
Q

What is the difference between extrinsic asthma and intrinsic asthma?

A

Extrinsic:
-caused by allergic exposure

Intrinsic:

  • non-allergenic
  • no known trigger
69
Q

What is EIA?

A

Exercise induced asthma

-especially in cold, dry air that may cause bronchoconstriction

70
Q

Clinical manifestation of asthma?

A
  • S/Sx differ in presentation, degree, and frequency
  • Sensation of chest constriction
  • Inspiratory and expiratory wheezing
  • Nonproductive cough
  • Prolonged expiration
  • Tachypnea and cardia
71
Q

What is status asthmaticus?

A

An acute attack that cannot be altered with routine care; medical emergency; can be fatal

72
Q

Asthma treatment goals?

A
  • decrease impairement

- decrease risk

73
Q

What is the maintenance of treatment?

A

1st line- ICS and LABAs

74
Q

What is the difference between asthma and other COPD disorders in regards to medication?

A

Inhaled corticosteroids are added into treatment earlier than any other. (2nd step) S49

75
Q

ICS and LABA
ICS used as maintanence to decrease ________ and risk of __________.
PO is only taken when?

Why is LABA used in combo with ICS?
Do NOT use for _______ symptoms, _________ or long term monotherapy.

A
  • impairement and risk of exacerbation
  • PO only taken for acute exacerbation or severe persistent asthma
  • Used with ICS to maintain lower ICS dose to prevent ICS AE
  • acute symptoms, exacerbations
76
Q

Leukotriene modifiers are split into ______ and __________.

A
  • LTRA (leukotriene receptor antagonist)

- 5-lipoxygenase inhibitor

77
Q

Leukotrienes receptor antagonist (LTRA) MOA?

What do they do?

A
  • MOA- competitively antagonize leukotriene receptors
  • released from mast cells and eosinophils to play a role in airway edema, smooth muscle contraction, inflammatory process
78
Q

Leukotriene receptor antagonist (Montelukast) for asthma are taken _____ daily (for allergies can only be used in the __).
They are alternative agents for ____ and ________

A
  • once
  • AM

-kids and adults

79
Q

5-lipoxygenase inhibitor MOA?

AE?

A
  • selectively inhibits 5-lipoxygenase, a key enzyme in the conversion of arachnoid acid to leukotrienes
  • rare hepatotoxicity
80
Q

5-lipoxygenase inhibitor are only an alternative for ______.

A

adults

81
Q

Immunomodulators: Anti IgE MOA?

AE?

A
  • MOA- binds IgE antibody→ prevents IgE binding to receptors on mast cells and basophils→ limits activation and release of allergic response mediators
  • AE- headache, injection site reaction
82
Q

Are Anti IgE becoming more commonly used?

A

Yes

83
Q

Immunomodulators: Interleukin Antagonists MOA?

AE?

A
  • MOA- monoclonal antibodies that binds interleukins→ results in decrease inflammatory responses; inhibiting IL-5 specifically decreases eosinophils which are specifically associated with asthma pathogenesis
  • AE- injection site reaction, headache, increased creatine kinase
84
Q

Cromolyn Sodium MOA?

AE?

A
  • MOA- prevents mast cell release of histamine, leukotrienes, and slow reacting substance of anaphylaxis by inhibiting degranulation after contact with antigens
  • AE-transient cough, wheezing
85
Q

Is cromolyn sodium commonly used?

A

No

86
Q

Methylxanthines MOA?

AE?

A
  • MOA-inhibits phosphodiesterase= bronchodilation

- AE- insomnia, gastric upset, tremor, increased hyperactivity in some children

87
Q

Methylxanthines are only used as _______ maintenance treatment, not as effective or commonly used

A

adjunct

-has a NTI

88
Q

Acute symptom relief and exacerbation.

A

SABA
-for acute symptom relief or exercise-induced bronchoconstriction (EIB)

SAMA
-may be used in combo with SABA in emergency care setting

PO steroids
-moderate-severe exacerbations

89
Q

What is used in pediatrics to ensure med delivery?

A

Spacers

90
Q

Elite athletes with asthma often time requires this to use their medication.

A

Therapeutic Use Exemption

91
Q

What does WADA stand for?

A

World Anti Doping Agency

92
Q

What is cystic fibrosis?

A

-Cystic fibrosis affects the cells that produce mucus, sweat, and digestive juices. It causes these fluids to become thick and sticky. They then plug up tubes, ducts, and passageways.

93
Q

What drugs are used for maintanence of cystic fibrosis?

A

-LABA

  • SABA used prior to:
    • chest physiotherapy
    • other inhaled meds that may produce bronchospasm
    • exercise
94
Q

What do CFTR modulators do?

A

Regulate sodium and water which helps keep mucous thin

95
Q

What are the main drugs and their functions?

A
  • Ivacaftor- improves CFTR activity by keeping chloride channels open longer
  • tezacaftor/lumacaftor- facilitate trafficking of CFTR to cell membrane surface
96
Q

What is the overall function of the CFTR modulators?

A

Sodium and water regulation for mucous thinning

97
Q

Do CFTR modulators interact with CYP enzymes?

CFTR Modulators must be taken with what?

A
  • Yes, DDI interactions

- High fat meals to increase absorption

98
Q

What are the AE of CFTR Modulators?

A
  • HA
  • GI
  • Respiratory

Less common:

  • dizziness
  • HTN
99
Q

How do Mucolytics help to treat Cystic Fibrosis?

A
  • decrease risk of exacerbation

- increase lung function and QOL

100
Q

What are the 2 main Mucolytic drugs used for Cystic Fibrosis?

A
  • hypertonic saline

- dornase alfa

101
Q

How does hypertonic saline work?

A

-increase salt in airways to draw more water into airways

102
Q

How does dornase alfa work to treat cystic fibrosis?

A

-cleaves DNA which decreases mucous viscocity

103
Q

What are the AE of dornase alfa?

A
  • chest pain
  • cough
  • voice disorder
  • skin rash
104
Q

Can anti-inflammatory be used to treat Cystic Fibrosis?

A

Yes

105
Q

When can ibuprofen be used for treatment?

A
  • If <18 yo, can take high dose. Not beneficial in adults.

- Not common due to required monitoring.

106
Q

Can we use inhaled antibiotics for treatment of Cystic Fibrosis?
How?

A

Yes

-Benefit > Risk because P. aeruginosa increases morbidity and mortality

107
Q

What is different about the treatment of inhaledantibiotics?

A

-Nebulized 2 or 3 times daily for 28 days, then 28 days off

108
Q

What is the nutritional support aspect of treatment of Cystic Fibrosis?

A
  • Supplement vitamins A,D,E,K

- Pancreatic enzyme replacement therapy (PERT)

109
Q

What are the additional complications related to Cystic Fibrosis?

A
  • Cystic Fibrosis related Diabetes (CFRD)
  • Bone Disease
  • Liver Disease
  • Lung Transplant
110
Q

Overall therapeutic concerns with drugs for respiratory conditions.

A

Anticholinergic drug

  • Tachycardia
  • HTN
  • Dry Mouth

Steroids

  • Inhaled drugs: oral candidiasis
  • Infection risk
  • HTN
  • Hyperglycemia
  • Osteoporosis
  • Muscle Weakness

B2 agonists

  • Tremor
  • Tachycardia
  • Hypokalemia
  • Hyperglycemia

Pharmacology Exam 2 (7 decks)

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