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Pharmacology > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Tidal volume for normal adults is _________. If normal adults take a deep breath, volume is ______.

A

1/2 L (500cc)

4-5L

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2
Q

3 predictors of lung volume

A

1) Gender
2) Height
3) Age

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3
Q

1 risk factor for COPD

A

smoking

80-90% of COPD in U.S. are linked to smoking. However, only 15-20% of smokers have COPD sx to degree that leads to MD visit

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4
Q

what are the implications of chronic mucous production in COPD?

A

leads to colonization of lungs with bacteria which induces neutrophilic inflammation, which responds less well to steroid therapy

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5
Q

Do steroids work better on eosinophils or neutrophils?

A

eosinophils

why we use steroids to tx asthma but not pneumonia

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6
Q

Do asthma pt. need to take medications daily?

A

Yes

it has been shown that there is not a big correlation btwn how lungs are doing and how pt. feels

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7
Q

You will prevent more fatal lung incidents if you __________ is asthmatics

A

monitor lung volume (can also have pt. do at home monitoring)

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8
Q

What are the two broad classifications of pharmacotherapy drugs used in lung dz?

A

1) Relievers: bronchodilate

2) Controllers: aimed at inflammatory pathways to control underlying dz

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9
Q

When using an inhaler, spacers help by

A

making sure more medicine actually gets into the lungs

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10
Q

With some inhalers you can put the device directly in your mouth if you are having trouble using the inhaler with spacing. However, do not do this with _______.

A

Steroids

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11
Q

When should you recommend a nebulizer?

A

pt. cannot use the handheld device well

(many downsides to nebulizers: device is big, particle size is bigger so doesn’t go to lungs as well, larger dose of drug is needed)

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12
Q

Metered-dose inhaler (MDI) is recommended when

A

pt. is >/= 5 y/o

if < 5 y/o can add a spacer or valved holding chamber mask

(in general MDIs are better than nebulizers)

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13
Q

Reliever medications include

A

1) Beta agonists (short and long acting)

2) anticholinergics

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14
Q

Short-acting beta agonist (SABA) MOA

A

relax bronchial smooth muscle

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15
Q

Short-acting beta agonist (SABA) pharmacokinetics

A

1) onset: 1-2 min

2) DOA: 3-6 hr

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16
Q

Which drugs is used in a rescue inhaler?

A

Short-acting beta agonist (SABA)

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17
Q

Albuterol (salbutamol) class

A

Short-acting beta agonist (SABA)

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18
Q

What is the MC Short-acting beta agonist (SABA)?

A

Albuterol (MC by far)

other SABA only make up 2-3% of what we use, and include: metaproterenol, pirbuterol, terbutaline

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19
Q

T/F: regular daily use of SABA is recommended

A

FALSE

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20
Q

T/F: if you need to use SABA > 2 days per week for sx relief, asthma is poorly controlled

A

TRUE

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21
Q

Short-acting beta agonist (SABA) ADRs

A
  • tachycardia
  • HTN (large doses)
  • “jitteriness” or mild anxiety with larger doses via nebulizer
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22
Q

T/F: Asthmanefrin is a new drug on the market that is very helpful in controlling asthma

A

FALSE

this literally is epinephrine, it works in 30 sec but only lasts 5 min

not a safe drug to use

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23
Q

Long-Acting Beta Agonists (LABA) come in ________ forms

A

inhaled and oral

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24
Q

Inhaled Long-Acting Beta Agonists (LABA)

A

Salmeterol (**MC)
Formoterol
Arformoterol

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25
Q

Long-Acting Beta Agonists (LABA) are used for

A

exercise or adjunct to anti-inflammatory drugs; chronic tx of asthma or bronchospasm, not for acute exacerbations

dosed at nighttime

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26
Q

Oral Long-Acting Beta Agonists (LABA)

A

albuterol, metaproterenol, terbutaline in SR tablets dosed at nighttime; can also come in syrup for children

**Rarely, rarely done in practice

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27
Q

Long-Acting Beta Agonists (LABA) pharmacokinetics

A

1) onset: 20 min

2) DOA: 12 hr

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28
Q

T/F: LABA are considered controllers in regards to asthma

A

FALSE

they do not control disease progression, the FDA put a black box warning on LABA for asthma w/out a controller

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29
Q

Short acting inhaled anticholinergic

A

Ipratropium (Atrovent HFA)

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30
Q

Ipratropium (Atrovent HFA) MOA

A

blocking acetylcholine (Ach) in lungs relaxes bronchial smooth mm.

(same clinical effect as beta agonist)

31
Q

Ipratropium (Atrovent HFA) pharmacokinetics

A

1) onset: 5 min (slower than SABA)

2) DOA: 4-8 hr (longer than SABA)

32
Q

Ipratropium (Atrovent HFA) ADRs

A
  • dry mouth

- blurred vision (local effect from aerosol)

33
Q

Do SABA or short-acting anticholinergics have a greater role in tx COPD?

A

short-acting anticholinergics

e.g. Ipratropium (Atrovent HFA)

34
Q

long-acting anticholinergic

A

Tiotropium (Spiriva)

35
Q

What does Tiotropium (Spiriva) primarily tx?

A

COPD (recently approved for asthma)

this is a long-acting anticholinergic

36
Q

T/F: The short-acting anticholinergic, Ipratropium, can be used as a rescue inhaler

A

FALSE

relatively short-acting (5 min), but not as short-acting as albuterol (1-2 min)…asthma attack can cz death w/in 5 min

37
Q

do inhaled anticholinergics cause anti-SLUD s/e?

A

No

they have very, very low bioavailability, so s/e are only local (dry mouth; blurred vision from misfiring)

38
Q

What is a benefit of long-acting anticholinergics over LABA?

A

pt. don’t build a tolerance over time with anticholinergics (i.e. they have persistent LT effects)

also with tiotropium you only need to do 1 puff per day (easier to use)

39
Q

What types of drugs are considered controllers in asthma tx?

A

1) Inhaled steroids (MC)
2) Leukotriene antagonists
3) Misc.

40
Q

Which drugs are inhaled corticosteroids used to control asthma?

A

1) Beclomethasone HFA (QVAR)
2) Budesonide HFA (Pulmincort)
3) Flunisolide HFA (Aerospan)
4) Fluticasone (Flovent and generic)

41
Q

Inhaled corticosteroids ADRs

A

minimal since inhaled and given in very low doses

  • thrush (can prevent by rinsing mouth after inhale)
  • in COPD there is a slight incr. in pneumonia risk
  • in peds may have small effect on long bones and growth
42
Q

Which inhaled steroid is the best tx for asthma/COPD?

A

one steroid is NOT better than another

what matters is using the proper dose of whatever steroid you choose

43
Q

How much of an MDI or DPI dose gets into the lung?

A

about 1/3

if you use inhaler really well, about 1/2 can get to lungs

44
Q

What happens to MDI or DPI dose that doesn’t make it into lungs?

A

gets stuck in mouth or swallowed (absorbed in gut)

however, we use such small doses, this isn’t a big concern

45
Q

Zileuton (Zyflo) class

A

Leukotriene Antagonist - lipooxygenase inhibitor (controller)

46
Q

Zileuton (Zyflo) ADRs

A

rare liver toxicity and a lot of drug interactions so likely to never see in practice

47
Q

Zafirlukast (Accolate) class

A

Leukotriene Antagonists - receptor blockers (controllers)

48
Q

Montelukast (Singulair) class

A

Leukotriene Antagonists - receptor blockers (controllers)

49
Q

Zafirlukast (Accolate) MOA

A

LTD4 and LTE4 antagonists

50
Q

Zafirlukast (Accolate) pharmacokinetics

A

metabolized by CYP2C9 and CYP3A4

51
Q

Zafirlukast (Accolate) drug interaction

A

warfarin

many other theoretical interactions

52
Q

Montelukast (Singulair) MOA

A

LTD4 and LTE4 receptor antagonists

53
Q

Montelukast (Singulair) pharmacokinetics

A

metabolized by CYP2C9 and CYP3A4

54
Q

Montelukast (Singulair) ADRs

A

essentially non-existent; GI upset maybe a minor s/e

55
Q

Zafirlukast (Accolate) ADRs

A

less liver toxicity than predecessor LTRA, but some reports

56
Q

What is an advantage of leukotriene antagonists over inhaled steroids?

A

Pill is easier for some to use

however, they are not as effective in controlling asthma

57
Q

Roflumilast class

A

Phosphodiesterase inhibitor (controller)

58
Q

Roflumilast MOA

A

block metabolisms of c-AMP to directly relax bronchiole sm. mm.

*may reduce COPD exacerbations but no defined role is asthma

59
Q

Theophylline class

A

methylated xanthine (bronchodilator)

60
Q

Theophylline MOA

A

mild stimulant

MOA for asthma improvement unclear (bronchodilation vs. antiinflammatory vs. diaphragmatic inotrope)

61
Q

Theophylline ADRs

A
  • toxicity (requires periodic concentration monitoring)
  • variability in dose based on age, other drugs, smoking, liver dz, and maybe HF
  • toxicity signs = hyperstimulation (diarrhea, GI cramping, tremor, tachycardia, seizures)

**alternative bronchodilator that has a lot more s/e than other bronchodilators

62
Q

Preferred controller drugs in (1) COPD and (2) asthma

A

inhaled steroids (ICS) for both!

63
Q

When might you use oral or injectable steroids in pulmonary tx?

A

primary role is as “burst therapy” for exacerbations of asthma or COPD and may be a very last resort in chronic asthma

64
Q

Which medication(s) can stop or slow the LT decline in lung fn or prolong survival in COPD?

A

NONE - not even inhaled steroids

although medications can improve QOL

65
Q

When would you choose to stop a COPD medication?

A

COPD meds are rarely stopped after being added b/c it is a progressive dz (unlike intermittent asthma)

66
Q

When is dual bronchodilator therapy of beta-agonist + anticholinergic therapy usually seen?

A

tx of COPD b/c bronchodilation is the primary therapeutic approach

67
Q

Tx of Stage 0 COPD

A

educate regarding avoidance of risk fx (smoking, flu vaccine)

68
Q

Tx of Stage 1 COPD

A

add PRN short-acting bronchodilator (albuterol, ipratropium, combivent)

69
Q

Tx of Stage 2 COPD

A

add one or more scheduled long acting bronchodilator (formoterol, arformoterol, salmeterol, tiotropium, theophylline SR)

70
Q

Tx of Stage 3 COPD

A

add inhaled steroid, esp. if multiple acute exacerbations (beclomethasone, budesonide, fluticasone)

71
Q

Tx of Stage 4 COPD

A

oxygen if indicated (PO2 < 88%)

surgery (emphysema)

72
Q

Frequent, severe EIB may indicate

A

poorly controlled asthma

however, it is also true that exercise may be the only precipitant of asthma for a pt.

73
Q

________ will prevent EIB in more than 80% of pt.

A

pretreatment before exercise of inhaled B2-agnosist (SABA or LABA)

Pharmacology (14 decks)

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