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Pulmonary Pharmacology > Pulmonary Pharm > Flashcards

Pulmonary Pharm Flashcards

1
Q

What are the two main drug types for pulmonary?

A

Bronchodilators and Anti-inflammatories

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2
Q

What classes are in bronchodilators?

A

Beta2 Agonists, Anticholinergics, Xanthine derivatives

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3
Q

What classes are in Anti-inflammatories?

A

Leukotriene receptor antagonists (LTRAs), Inhaled glucocorticoids, Mast cell stabilizers

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4
Q

What drug classes are used to treat COPD?

A

Beta2 Adrenergic and Glucocorticoids

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5
Q

What do bronchodilators do?

A

Dilate the bronchioles. Give before giving an inhaled glucocorticoid to open airways and improve efficacy of steroid.

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6
Q

What do Glucocorticoids do?

A

Decrease inflammation of the bronchioles

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7
Q

How do bronchodilators works?

A

Relaxes the smooth muscle in the bronchial –> dilates bronchi and bronchioles

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8
Q

What meds are short acting Beta-adrenergic agonists?

A

Albuterol (PO or inhaled) and Levalbuterol (Inhaled)

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9
Q

What meds are long acting Beta-adrenergic agonists?

A

Salmeterol and Formoterol

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10
Q

What should be used in an asthma attack?

A

Short acting Beta-Adrenergic agonists. Albuterol or Levalbuterol.

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11
Q

Suffix for Beta-Adrenergic Agonists

A

-erol

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12
Q

What is a rescue drug?

A

Short acting beta-adrenergic agonists (SABA)

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13
Q

What is the duration for SABA?

A

Q4-6 hrs

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14
Q

What is the duration for LABA?

A

Q12-14 hrs. THIS IS GIVEN FOR PREVENTION

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15
Q

Beta-Adrenergic Agonists MOA

A

Mimics the action of the SNS to stimulate the fight or flight response. Relaxes and dilates the airway by stimulating the Beta2-adrenergic receptors in the LUNGS.

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16
Q

Non-selective adrenergic drugs

A

stimulate both beta 1 and beta 2 and alpha receptors. EPINEPHERINE

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17
Q

Non-selective beta-adrenergic drugs

A

stimulates both beta 1 and beta 3 receptors METAPROTERENOL.

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18
Q

Selective beta-2 receptors

A

stimulates only beta 2 in the lungs. ALBUTEROL.

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19
Q

Epinephrine MOA

A

Stimulates the alpha receptors, beta 1 in the heart and beta 2 in the lungs. Decreases edema and swelling in mucous membranes by vasoconstriction, has cardiovascular effects (Increases HR and BP) and stimulates CNS.

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20
Q

Where is the beta 1 receptor?

A

Heart

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21
Q

Where is the beta 2 receptor?

A

Lungs

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22
Q

Indication for Beta-adrenergic agonists

A

prevention or relief of bronchospasm related to asthma, bronchitis, or other pulmonary conditions

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23
Q

Contraindications for Beta-adrenergic agonists

A

uncontrolled HTN, cardiac dysrhythmias, high risk for TIA

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24
Q

What do you need to avoid while on Beta-adrenergics?

A

MAOIs and sympathomimetics (ephedrine/Sudafed) bc it increases risk for HTN

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25
Q

Effect of Beta-adrenergic agonists on DM pt?

A

May increase blood sugar. Need higher doses of the med and insulin to compensate.

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26
Q

Adverse effects of Beta-adrenergic agonists

A

Insomnia, restlessness, anorexia, cardiac stimulation, hyperglycemia, tremor, vascular headache, HTN or hypotension

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27
Q

What do you do if too many beta-adrenergic agonists are given? (Overdose)

A

Beta blocker

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28
Q

MDI

A

metered dose inhaler. Non-breath activated. Pt. must be coordinated. (Evohaler)

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29
Q

DPI

A

dry powder inhaler. Breath-activated and propellant not required. (Accuhaler and Terbuhaler)

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30
Q

Types of inhalers

A

MDI, DPI and nebulizer. Can give higher doses and doesn’t required pt coordination.

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31
Q

Albuterol delivery method

A

MDI or nebulizer

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32
Q

Albuterol indications

A

Asthma, bronchitis, and emphysema. ACUTE episodes of wheezing, chest tightness and SOA

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33
Q

Onset of Albuterol

A

minutes

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34
Q

What is the first line of defense for an asthma attack?

A

Albuterol

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35
Q

What indicates inadequate control of asthma?

A

If pt. is using more than one cannister of Albuterol per month. Need to be transitioned to anti-inflammatory therapy with possible PO med.

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36
Q

How many actuations are in a canister?

A

200

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37
Q

Indications for Salmeterol

A

Worsening of COPD, moderate to severe asthma - typically given twice daily

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38
Q

Do you give salmeterol alone?

A

NO. It’s given with an inhaled corticosteroid.

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39
Q

What is the warning for Salmeterol?

A

It has been associated with an increase in asthma-related deaths (more common in black/african americans)

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40
Q

Anticholinergic MOA

A

Blocks action of acetylcholine –> creates bronchodilation by preventing bronchoconstriction

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41
Q

KEY POINT for anticholinergic meds

A

By blocking the effect of acetylcholine, we inhibit the normal physiological response of bronchoconstriction and mucus production.

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42
Q

Indications for anticholinergics

A

prophylaxis and maintenance therapy

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43
Q

Type of anticholinergic

A

Ipratropium

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44
Q

What do we normally give with anticholinergics?

A

Albuterol

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45
Q

Anticholinergic adverse effects

A

dry as a bone (dry throat, dry mouth, constipation, dry eyes, urinary retention), hot as a hare (feeling hot and decreased sweating), blind as a bat (blurred vision), red as a beet (redness), mad as a hatter (sedation, dizziness, confusion, hallucinations), tachycardia

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46
Q

Xanthine Derivatives (Methylxanthines) MOA

A

Increases levels of the cAMP enzyme by inhibiting phosphodiesterase –> stimulates CNS and CVD systems

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47
Q

What are the meds for Xanthine derivatives

A

Theophylline and aminophylline

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48
Q

Suffix for Xanthine derivatives

A

-phylline

49
Q

What are xanthine derivatives used for?

A

second-line treatment

50
Q

Why are xanthine derivatives used as a second treatment?

A

High risk of toxicity and drug-drug interactions

51
Q

Indications for xanthine derivatives

A

preventative treatment for asthma attacks and COPD exacerbations

52
Q

What do high levels of cAMP do?

A

induce smooth muscle relaxation and inhibit IgE induced release of chemical mediators of an allergic reaction

53
Q

SE of xanthine derivatives

A

Toxicity –> N/V/D, Headache, tachycardia, dysrhythmias, seizure disorders, hyperthyroid, and peptic ulcers

54
Q

Interactions with xanthine derivatives

A

Caffeine may increase SE because the body processes it similarly to caffeine. Smoking can decrease absorption.

55
Q

Therapeutic index for xanthine derivatives

A

NARROW. Monitor the serum levels to watch for toxicity

56
Q

drug interactions of xanthine derivatives

A

macrolide antibiotics, allopurinol, cimetidine, quinolones, flu vaccine, and oral contraceptives

57
Q

What is the antidote for xanthine derivatives?

A

activated charcoal

58
Q

Leukotriene receptor agonists (LTRA) MOA

A

prevent leukotrienes from attaching to receptors located on immune cells and within the lungs –> prevent inflammation

59
Q

Normal function of leukotrienes

A

They are released by mast cells during the inflammatory response –> induce inflammation, bronchoconstriction and mucus production

60
Q

Route for leukotriene receptor antagonists

A

PO

61
Q

Meds for LTRAs

A

montelukast and zafirlukast

62
Q

suffix for LTRAs

A

-kast

63
Q

What LTRA can’t be given to children under 5?

A

Zafirlukast

64
Q

What LTRA is used for child over 12 months?

A

Montelukast

65
Q

Indication for LTRAs

A

Prophylaxis and chronic treatment of asthma in adults and children. Also used for allergies.

66
Q

AE of LTRAs

A

Headache, nausea, dizziness, insomnia, diarrhea

67
Q

When are corticosteroids given PO rather than inhaled?

A

Temporarily during a COPD exacerbation until switch to inhaled

68
Q

Inhaled corticosteroids MOA

A

Reduces inflammation and enhances activity of beta agonists, also helps with bronchodilation

69
Q

What are the meds for inhaled coritcosteroids?

A

beclomethasone diproprionate, budesonide, and fluticasone

70
Q

Downside of inhaled corticosteroids

A

Can take several weeks of continuous therapy before seeing full effect of steroids. May be started on PO med to bridge over.

71
Q

Inhale corticosteroid route

A

MDI or nebulizer

72
Q

What do you teach to asthma pts about inhaled corticosteroids?

A

This is not a PRN medication, you need to take it on a regular schedule. When you take it, take the bronchodilator first to increase absorption of the corticosteroid. Commonly given with beta-adrenergic med.

73
Q

AE of inhaled corticosteroid

A

Pharyngeal irritation, coughing, dry mouth, and oral fungal infections

74
Q

What do you do to prevent oral fungal infections with inhaled corticosteroids?

A

Rinse mouth after use

75
Q

What would you give to a pt with an oral fungal infection?

A

Nystatin rinse

76
Q

Combination inhaled glucocorticoid and bronchodilator meds

A

budesonide with formoterol and fluticasone with salmeterol

77
Q

KEY POINT for combination inhalers

A

Not for acute attacks

78
Q

Indications for combination inhalers

A

Moderate to severe asthma

79
Q

Mast cell stabilizer MOA

A

Stabilizes membranes of mast cells to prevent release of broncho-constrictive inflammatory substances

80
Q

Mast cell stabilizer med

A

Cromolyn

81
Q

Indication for Mast cell stabilizer

A

Prevention of acute asthma attacks. Given 15-20 minutes prior to known triggers.

82
Q

Monoclonal antibody anti-asthmatic MOA

A

monoclonal antibody which selectively binds to immunoglobulin IgE –> limits the release of mediators of allergic response (decreases hyperresponsiveness)

83
Q

Monoclonal antibody Anti-asthmatic med

A

omalizumab

84
Q

Route for monoclonal antibody therapy

A

injection – must be monitored for hypersensitivity reactions

85
Q

When is monoclonal antibody therapy used?

A

As an add-on therapy for asthma

86
Q

Selective PDE-4 Inhibitor MOA

A

Selectively inhibits PDE4 enzyme in the lung cells –> anti-inflammatory effects

87
Q

Indication for Selective PDE4 inhibitors

A

Prevention of COPD exacerbations. Works best for chronic bronchitis with hx of alot of exacerbations.

88
Q

Route for Selective PDE4 inhibitors

A

PO

89
Q

SE of Selective PDE4 inhibitors

A

N/V/D, headache, muscle spasm, decreased appetite, uncontrollable tremors

90
Q

What med is a selective PDE4 inhibitor?

A

roflumilast

91
Q

What is the PDE4 enzyme?

A

inflammation trigger

92
Q

What are the long-term control medications?

A

anticholinergics, xanthine derivatives, inhaled corticosteroids, leukotriene modifiers, mast cell stabilizers and LABA

93
Q

What are the short-term or quick relief medications?

A

SABA and albuterol

94
Q

Antitubercular drug categories

A

First-line, used to treat first; and second-line, used for more complicated cases that are resistant to primary meds

95
Q

Typical treatment for TB

A

Started on a 4 drug regimen and then tested to see what the pt is susceptible to and adjust from there. Treatment for rest of life.

96
Q

Most common medication for TB

A

Isoniazid or INH

97
Q

Isoniazid (INH) MOA

A

Disrupts the cell wall synthesis essential to the function of mycobacteria

98
Q

Route for INH

A

Oral

99
Q

SE of INH

A

Peripheral neuropathy, hepatoxicity, optic neuritis, visual disturbances, hyperglycemia

100
Q

What do you need to avoid while on INH?

A

Antacids. They can reduce the absorption.

101
Q

Black box warning for INH

A

Increased risk of hepatitis

102
Q

What do we monitor with INH?

A

Liver enzymes –> metabolized in the liver

103
Q

Rifampin MOA

A

Inhibits protein synthesis via attacking the hydrocarbon ring structure of mycobacteria

104
Q

What is Rifampin used for in addition to TB?

A

meningitis, HIV, and leprosy mycobacterium

105
Q

Why does rifampin decrease the effect of certain drugs?

A

It’s a CYP450 inhibitor

106
Q

SE of rifampin

A

hepatitis, hematologic disorders, red-brown discoloration of urine and other body fluids

107
Q

Route of rifampin

A

PO and IV

108
Q

Teaching point for rifampin

A

May change the color of body fluids, need to tell a pharmacist or HCP if taking because of the drug interactions

109
Q

Ethambutol MOA

A

Diffusing into the mycobacteria and suppresses RNA synthesis, which inhibits protein synthesis

110
Q

SE of ethambutol

A

retrobulbar neuritis (nerve neuritis in eye), blindness

111
Q

Route of ethambutol

A

PO

112
Q

Pyrazinamide (PZA) MOA

A

unknown - thought to inhibit lipid and nucleic acid synthesis necessary for DNA replication

113
Q

SE of PZA

A

hepatotoxicity and hyperuricemia

114
Q

Contraindication for PZA

A

people with severe hepatic disease or acute gout because gout is already high uric acid levels

115
Q

What TB drug is not safe for pregnant women in US but used in other countries?

A

PZA

116
Q

Streptomycin MOA

A

aminoglycoside –> interferes with the normal synthesis, causing production of faulty proteins within the bacteria

117
Q

SE of streptomycin

A

ototoxicity, nephrotoxicity, blood dyscrasias

118
Q

Streptomycin Route

A

IM injection only - given daily

119
Q

Antitubercular meds

A

Streptomycin, Pyrazinamide (PZA), Ethambutol, Rifampin, and Isoniazid (INH)

Pulmonary Pharmacology (3 decks)

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