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Pulmonary > PHARM: Drugs for Asthma/COPD > Flashcards

PHARM: Drugs for Asthma/COPD Flashcards

1
Q

What do adrenergic agonists do? (broad)

A

Bronchodilator

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2
Q

List 3 non-specific adrenergic agonists.

A

Epinephrine (beta1, beta2, alpha)
Ephedrine (beta1, beta2, some alpha)
Isoproterenol (beta1, beta2)

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3
Q

List 2 beta-2 specific agonists with quick onset/short duration.

A

Albuterol
Xopenex
Terbutaline (IV)

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4
Q

List 2 beta-2 specific agonists with slow onset/long duration.

A

Salmeterol

Formoterol (used with steroids)

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5
Q

What do cholinergic antagonists do? (broad)

A

bronchodilator

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6
Q

Name 2 cholinergic antagonists.

A

Atropine

Ipratropium

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7
Q

What are methylxanthines?

A

bronchodilators with anti-inflammatory activity

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8
Q

Name 2 methylxanthines.

A

Aminophylline

Theophylline

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9
Q

Name 4 classes of drugs used for inflammation associated with asthma.

A

1) Cromolyns
2) Corticosteroids
3) Leukotriene receptor blockers
4) Leukotriene synthesis inhibitors

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10
Q

Name an example of a cromolyn.

A

Cromolyn sodium

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11
Q

Name some examples of corticosteroids.

A

Budesonide
Fluticasone
Prednisone (oral)
(ones, ides, or compined with “ols”)

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12
Q

Name 2 leukotriene receptor blockers.

A

Monteleukast

Zafirlukast

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13
Q

Name a leukotriene synthesis inhibitor.

A

Zileuton

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14
Q

What is the anti-IgE antibody used for asthma/COPD treatment?

A

Omalizumab

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15
Q

Which class of drugs are used as “rescue medication”? How long is the duration?

A

selective, quick-onset beta-2 agonists with intermediate duration (3-6 hours)

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16
Q

What class of drugs are used only in combination with inhaled steroids? How long is the duration?

A

LABAs (long-acting beta2 agonists) that last for over 12 hours

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17
Q

List some LABA + steroid combinations.

A

Advair (salmeterol + fluticasone)

Symbicort (formoterol fumarate + Budesonide)

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18
Q

How do beta agonists lead to bronchodilation (help asthma)?

A
  • Increase levels of cAMP
  • Inhibit release of mediators from mast cells
  • Inhibit microvascular permeability
  • promote some mucociliary transport
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19
Q

How does increasing cAMP lead to bronchodilation?

A

Gs Pathway: cAMP activates PKA which inhibits myosin light chain kinase (along with decreased levels of calcium from activation of calcium-activated K+ channels) leading to relaxation

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20
Q

What is the “alternative signaling” pathway of beta2 agonists?

A

Gq pathway: Increased phospholipase C and input from beta-arrestin2 leads to increased inflammation

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21
Q

What are some adverse reactions to beta agonists?

A
  • N/V
  • Headache
  • Decreased BP, Increased HR (cardiac arrhythmias)
  • Decreased PaO2
  • CNS effects (coma, convulsions, agitation, etc)
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22
Q

What is the MOA of antimuscarinics?

A

Block Ach receptors to reduce airway muscle constriction, decrease mucus secretion, and enhance beta2-mediated bronchodilation

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23
Q

What are some adverse effects of antimuscarinics?

A

Pupillary dilation

Cycloplegia (on contact)

24
Q

What is interesting about ipratropium?

A

it is a tertiary compound (antimuscarinic) that is poorly absorbed and has no significant systemic effects

25
Q

What is combivent?

A

combined anti-cholinergic and beta-2 agonist (albuterol + ipratropium bromide)

26
Q

What is the indication for combivent?

A

COPD

27
Q

Methylaxanthines are related to what chemical?

A

caffeine

28
Q

What are the major actions of methylaxanthines?

A
  • Increase levels of cAMP (bronchodilation)
  • Decrease release of inflammatory mediators
  • Block muscle adenosine receptors (prevent bronchoconstriction)
29
Q

How do methylxanthines increase levels of cAMP?

A

they block the conversion of cAMP into AMP (breakdown)

30
Q

The adverse effects of methylxanthines depend on what?

A

the serum levels

31
Q

What adverse reactions occur with 5-10 microgram/mL serum levels of methylxanthines?

A

N/V
Nervousness
Headache
Insomnia

32
Q

What adverse reactions occur with over 20 microgram/mL serum levels of methylxanthines?

A 
Vomiting
Hypokalemia
Hyperglycemia
Tachycardia
Tremor
Seizures
33
Q

Cromolyns may alter the activity of what type of channels?

A

chloride channels

34
Q

What are the 4 major actions of cromolyns?

A
  • Inhibit mast cell degranulation
  • Inhibit inflammatory response (act on eosinophils)
  • Inhibit cough (act on airway nerves)
  • Reduce bronchial hyperactivity
35
Q

What is a reason people may not be adherent to cromolyns?

A

they taste bad

36
Q

List some adverse reactions to cromolyns.

A 
COUGH and bronchospasm after inhalation (irritation of trachea)
Chest pain (rare)
Restlessness (rare)
Hypotension (rare)
N/V (rare)
37
Q

List 4 actions of glutocorticoids.

A

1) Decrease production of inflammatory cytokines
2) Reduce mucus secretions
3) Reduce bronchial hyperactivity
4) Enhance effect of Beta-2 agonists (by increasing transcription of the receptors)

38
Q

Which syndrome can result from use of glucocorticoids? List some symptoms.

A

Cushingoid Syndrome

  • Weight gain (abdomen, buffalo hump, moon face)
  • Thinning and leg/arm muscle weakness
  • Thin skin
  • Increased acne, facial hair growth, scalp hair loss in women
  • Ruddy complexion
  • Acanthosis (neck skin darkening)
  • Child obesity and poor growth
  • High BP
39
Q

What is the role of LTB4?

A

neutrophil chemoattractant

40
Q

Which leukotrienes mimic asthma symptoms (bronchial hyper-reactivity and constriction, mucosal edema, increased mucus secretion)?

A

LTC4

LTD4

41
Q

What leukotriene receptor do Zafirlukast and Monteleukast block?

A

LTD4 receptors

42
Q

Leukotriene receptor blockers are “effective in some patients” of what subtype of asthma?

A

aspirin-induced asthma

43
Q

What are some adverse effects associated with zafirlukast?

A

GI problems
headache
elevation of liver enzymes (liver and bladder cancer in rodents)

44
Q

What are some adverse effects associated with monteleukast?

A 
GI problems
laryngitis/pharyngitis
nausea
otitis/sinusitis
viral infections increased
possible suicidal ideation*
45
Q

What is the effect that leukotriene synthesis blockers have in asthma patients?

A
  • Decrease smooth muscle contraction

- Decrease blood vessel permeability/leukocyte migration to damaged area

46
Q

Which CYP is inhibited by (and a substrate for) Zileuton?

A

CYP1A2 (interacts with theophylline!)

47
Q

What must be checked when on Zileuton?

A

LFTs are required, because it causes hepatic enzyme elevation

48
Q

Use of Zileuton could be connected to what sort of conditions?

A

inflammation-related conditions like RA and acne

49
Q

Omalizumab is used for what?

A
  • Reduce severity/frequency of asthma attacks by decreasing the allergic response to triggers
  • Reduce requirement for inhaled corticosteroids
50
Q

What are some adverse effects of omalizumab?

A
  • Serious allergic RXN
  • Redness, warmth, itching, bruising in injection site
  • Sore throat/cold symptoms
  • Increase CV complications
51
Q

How does the treatment approach differ for asthma and COPD?

A

corticosteroids do not help and bronchodilators are only partially helpful

52
Q

What are the 3 main-lines of treatment for COPD?

A

1) Smoking cessation
2) Bronchodilators
3) Antimuscarinics

53
Q

What 5 drug classes are contraindicated in airway diseases?

A

1) Sedatives
2) Beta-blockers
3) Aspirin
4) ACE Inhibitors
5) Local anesthetics with EPI

54
Q

What is doxapram?

A

a short-acting respiratory stimulant given IV

55
Q

What is the MOA of doxapram?

A

activates peripheral carotid receptors to increase respirations to treat acute hypercapnia in COPD or post-anesthesia respiratory depression

56
Q

What is the “best” glucocorticoid? Why?

A

Ciclesonide

  • High lipophilicity
  • Rapidly cleared from mouth
  • Good binding to receptor
  • Good brinding to protein

Pulmonary (34 decks)

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