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IC 1.0 > Treating Asthma > Flashcards

Treating Asthma Flashcards

1
Q

Which disease is the leading cause of lost school days in children and work days among adults is what?

A

asthma

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2
Q

How do we differentiate mild from severe asthma?

A
  • mild: occasional symptoms, usually upon some sort of exposure
  • sever: frequent attacks, especially at hight, which limit activity
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3
Q

Describe airway changes in those suffering an asthma attack.

A
  • bronchial and tracheal constriction
  • mucosal thickening from edema and cellular infiltration
  • the net result is narrow airways filled with thick mucous plugs
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4
Q

During an asthma attack, what measures of airflow are likely to be reduced?

A

all indices of expiratory flow:

  • FEV1
  • FVC
  • FEV1/FVC
  • peak expiratory flow rate
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5
Q

What is FEV1?

A

the volume of air expired in the first second of forced expiration

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6
Q

What is FVC?

A

the volume breathed out from a maximally forced expiratory effort

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7
Q

During an asthma attack, which measures of airflow are likely increased?

A
  • total lung capacity
  • functional residual capacity
  • residual volume
  • DLCO (diffusion capacity for CO)
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8
Q

What is the difference between functional residual capacity and residual volume?

A
  • functional residual capacity is the residual volume left during normal breathing
  • residual volume is the residual volume left after maximally forced expiratory effort
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9
Q

What role do bronchodilators and anti-inflammatory agents play in the treatment of asthma?

A
  • bronchodilators are short-term relievers

- anti-inflammatory agents are long-term controllers

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10
Q

How does the airway of an asthmatic individual differ from that of a healthy individual?

A

the airway of an asthmatic is hyper-responsive to inflammatory mediators released in response to allergens, cold, exercise, etc.

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11
Q

Which inflammatory cells are involved in the early and late phase of an asthma attack?

A
  • early: primarily mast cells

- late: T-cells, mast cells, eosinophils, and neutrophils

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12
Q

Why do severe asthmatics often experiences more symptoms at night?

A

because PNS tone is highest at night, which means that bronchoconstriction is more likely

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13
Q

How is bronchoconstriction mediated by the autonomic nervous system?

A

vagal efferents release acetylcholine onto muscarinic receptors on bronchial smooth muscle

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14
Q

Through what two mechanisms can inhaled irritants cause bronchoconstriction?

A
  • they can induce release of chemical mediators from mast cells
  • they can stimulate afferent vagal nerves to initiate reflex bronchoconstriction
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15
Q

What second messenger system regulates bronchial tone?

A

cAMP

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16
Q

Through what mechanism does the sympathetic nervous system act on bronchial smooth muscle?

A
  • B2-adrenergic receptors are activated, activating AC

- cAMP levels rise and induce bronchodilation

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17
Q

Do high intracellular cAMP levels support bronchodilation or bronchoconstriction?

A

bronchodilation

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18
Q

What role does PDE play in regulating bronchial tone?

A

it degrades cAMP, promoting bronchoconstriction

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19
Q

How do phosphodiesterase inhibitors function in the treatment of asthma?

A

they inhibit the degradation of cAMP, promoting bronchodilation

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20
Q

How does theophylline function in the treatment of asthma?

A

it is an adenosine receptor antagonists that inhibits adenosine from inducing bronchoconstriction

21
Q

Name two molecular signals that serve to initiate bronchoconstriction.

A
  • acetylcholine

- adenosine

22
Q

Bronchodilators fail to treat what aspect of asthma pathology?

A

mucous formation, edema, and cellular infiltration

23
Q

Why are inhaled B2 agonists like albuterol relatively safe with few side effects?

A
  • because inhalation, if done correctly, is essentially a topical administration without systemic effects of the drug
  • that which is swallowed is either poorly absorbed or subject to a high first pass effect
24
Q

What effect does albuterol have on potassium?

A

it increases insulin release and therefore induces a hypokalemia

25
Q

What role do sympathomimetics play in the treatment of asthma?

A
  • selective B2 agonists like albuterol are first line therapy
  • however, less selective sympathomimetics like epinephrine and ephedrine have too many off target cardiovascular effects and are thus reserved for resolution of severe attacks
26
Q

Drugs ending in the suffice “-phylline” are part of what class?

A

the methylxanthine bronchodilators

27
Q

Why aren’t muscarinic antagonists a first line therapy for acute asthma given their bronchodilator effects?

A

because they have unpredictable efficacy due to varying involvement of parasympathetics in the bronchospasm of different people

28
Q

What role do muscarinic antagonists play in the treatment of asthma?

A
  • they relax bronchial smooth muscle and decrease mucus secretion
  • however, they are only effective in those for whom parasympathetic involvement contributes significantly to their bronchospasms
  • most useful for those with symptoms at night (symptoms often induced by increased PNS tone)
29
Q

Through what mechanism of action do glucocorticoids function in the treatment of asthma?

A
  • they inhibit the production of inflammatory cytokines

- they have no direct effect on bronchodilation

30
Q

List three benefits of using glucocorticoids in those with asthma?

A
  • reduce bronchial reactivity
  • increase airway caliber by reducing edema
  • reduce frequency of attacks
31
Q

Many asthmatics require daily corticosteroids to prevent asthma attacks. How do we avoid the systemic symptoms of these treatments?

A

by prescribing inhaled corticosteroids

32
Q

What are the side effects that accompany long-term inhaled corticosteroid use?

A

oropharyngeal candidiasis or hoarseness from vocal cord irritation

33
Q

Drugs with the suffix “-lukast” act in what way?

A

they are leukotriene inhibitors used in the treatment of asthma

34
Q

What role do leukotrienes play in asthma?

A

they especially help mediate the late phase of asthma

  • LTB4 is a chemoattractant for eosinophils, monocytes, and neutrophils
  • LTC4 and LTD4 are eosinophil chemoattractants, potent broncho-constrictors, and promoters of vascular permeability and mucous secretion
35
Q

What is zileuton?

A

a 5-lipoxygenase inhibitor which impairs leukotriene synthesis and is used in the treatment of asthma

36
Q

Leukotriene antagonists are most specific for which receptor?

A

the LTD4 receptor

37
Q

What is omalizumab?

A
  • an antibody against IgE, which inhibits binding of IgE to mast cells (doesn’t inactivate already bound IgE)
  • lowers plasma IgE levels and reduces bronchospasms
  • lessens asthma severity and reduces the need for corticosteroids
38
Q

Which two monoclonal antibody drugs are useful in the treatment of asthma? What do they target?

A
  • omalizumab: anti-IgE

- mepolizumab/reslizumab: anti-IL-5

39
Q

What role do mepolizumab and reslizumab play in the treatment of asthma?

A
  • inhibit binding of IL-5 to mast cells
  • reduces severe asthma attacks by reducing number of eosinophils in the blood
  • used for refractory asthma
40
Q

What is the goal of asthma prophylaxis treatments?

A

reduce mast cell degranulation, thereby reducing the number of asthma attacks

41
Q

What is cromolyn sodium?

A

a drug used to stabilize mast cells and prevent degranulation, thereby inhibiting asthma attacks

42
Q

When are asthma prophylactic drugs used?

A

just before exercise or allergen exposure

43
Q

For what kinds of asthma are prophylactic drugs like cromolyn sodium best?

A

allergen- and exercise-induced asthma

44
Q

What is nedocromil sodium?

A

a mast cell stabilizer used as asthma prophylaxis

45
Q

How do asthma prophylactics differ from daily anti-inflammatory drugs?

A
  • prophylactics offer acute protection when an exposure is expected soon
  • anti-inflammatory drugs are used daily to reduce the responsiveness of the airway and to prevent asthma attacks or limit their severity all the time
46
Q

How do cromolyn sodium and nedocromil sodium stabilize mast cells?

A
  • they alter delayed chloride channels in the cell membrane

- this inhibits mast cell activation and reduces release of histamine and other mediators

47
Q

How is cromolyn sodium administered?

A

via inhalation since it experiences poor GI absorption

48
Q

Describe the asthma treatment pyramid.

A
  • offer a short-acting B2 agonist for symptom relief
  • add a low dose ICS
  • then add a long-acting B-agonist (oral formulation)
  • then increase the dose of ICS
  • finally, add an OCS if necessary

IC 1.0 (24 decks)

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