16 Asthma Flashcards Preview

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Flashcards in 16 Asthma Deck (63):
1

What is a recurrent episodic bout of coughing and difficult breathing from airway inflammation?

asthma

2

What 2 things is asthma associated with?

genetic linkage
environmental factor related to immunological challenge

3

Which T cell response is associated with asthma?

TH2

4

Infections from what 2 organisms lead to no asthma?

helminth
hep A

5

What is allergic asthma triggered by?

allergen-induced mast cell activation and release of inflammatory mediators[histamines/leukotrienes]

6

True or false--asthmatic initiation is characterized by airway constriction and decreased mucus secretion? Why?

False, increased mucus secretion

7

What do inflammatory mediators do once released from mast cell activation?

recruit additional inflammatory cells (eosinophil and neutrophils)THIS LEADS TO A SECOND WAVE OF INFLAMMATION

8

What can chronic airway inflammation perpetuate? what is the result?

-airway hyperresponsiveness to environmental irritants-asthmatic episodes are triggered in the absence of the original aggravating allergen

9

What are the 2 clinical features of asthmatic airway?

1. bronchial hyperreactivity to aerosolized histamine/adenosine as measured by reduced FEV2. Increased eosinophil numbers beneath the airway epithelium, and sputum/lavage

10

What can control the early reaction of allergic asthma response?

prophylactic corticosteroids and cromolyn?

11

What can palliate symptoms once the early reaction of asthma is initiated?

B2 adrenergic receptor agonists

12

What can reduce the late reaction?

inhaled corticosteroids at or before initiation of the early reaction

13

Asthma therapies target (try to do) what 2 things?

1. acute symptoms (quick relief)2. Reduce airway hyper-responsiveness (long term control)

14

What is the general job of a quick reliever in asthma? Key example?

promote relaxation of smooth muscle which leads to dilation For example: B2 adrenergic receptor agonist

15

What are the long term controllers of asthma?

-anti-inflammatories that target leukotriene and mast cells degranulation-long acting agents to reduce probability of airway constriction

16

What are 2 examples of a way to prevent airway constriction long term?

longer acting B2-adrenergic receptor agonists, methylxanthines)

17

What creates arachidonic acid?

phospholipase A2 acts on phospholipids

18

What key enzyme initially allows production of leukotriene?

5-lipoxygenase

19

What does LTB4 do to blood vessels?

nothing

20

What does LTB4 do in smooth muscle?

nothing

21

What does LBT4 do in regards to leukocytes?

neutrophil chemotaxis

22

What does LTC4 do in blood vessels?

decreased coronary blood flow increase capillary permeability

23

What does LTC4 due on smooth muscle

constrict bronchial

24

What does LTC4 do in regards to a leukocytes?

eosinophil chemotaxis an degranulation

25

What does LTD4 do on blood vessels?

decrease coronary blood flow, increase capillary permeability

26

What does LTD4 do with smooth muscle?

constrict bronchial

27

What effect does LTD4 have on leukocytes?

eosinophil chemotaxis and degranulation.

28

How are long-term controllers: corticosteroids for asthma typically administered?

topically to the airway by aerosol inhalation

29

Beclomethasone, Budesonide, fluticasone, triamcinolone are examples of what?

long-term controllers: corticosteroids

30

When is oral or intravenous administration of corticosteroids necessary?

symptoms are not adequately controlled by maintenance therapy and treatment with bronchodilators

31

What are the 2 main oral corticosteroids?

prednisone
methylprednisolone

32

What are the 3 main mechanisms by which corticosteroids work?

1. inhibit PLA2 expression-->reduced mediators by mast.2. reduced synthesis of chemotactic factors--->reduced recruitment3. inhibition of cytokine expression-->reduce TH2 response and leukocyte prolif.

33

Why can't corticosteroids provide immediate release?

effects are delayed because the mech. is dependent on altered gene expression

34

Why are inhaled corticosteroids generally well tolerated?

low bioavailability outside of airway

35

What are the adverse side effects of systemic administration of corticosteroids? [5]

1. abnormal glucose metabolism
2.diabetes
3. hypertension
4. Cushing's
5.immune compromised individuals
[short term treatment is usually not a big deal 5-10 days]

36

LTD4 is chemotactic for what?

eosinophils

37

LTB4 is chemotactic for what?

neutrophils

38

What is the drug example for long term control from inhibition of leukotriene pathways thats main effect is on synthesis inhibiting?

zileuton

39

What is the mech of zileuton?

inhibits 5-lipoxygenase-->inhibits LTB4 and LTD4 in mast/eosinophils

40

How is zileuton administered?

orally

41

What side effect is zileuton associated with?

liver toxicity and can inhibit P450s effecting metabolism of other drugs

42

What are the examples for long term control from inhibition of leukotriene pathways thats main effect is as a receptor antagonist?

zafirlukast, montelukast

43

What drugs can allow for corticosteroid reduction in asthma patients?

zafirlukast, montelukast

44

How does zafirlukast, montelukast work?

LTD4 receptor antagonists that reduce bronchoconstriction and edema associated with inflammation

45

What percent of asthmatics exhibit severe sensitive to aspirin and other NSAIDS, resulting in profound bronchoconstriction?

5-10%

46

IS sensitivity of asthma patients to NSAIDs associated with allergic responses to the drug? How?

NO, likely caused by shifting arachidonic metabolism from prostaglandin to leukotriene synthesis

47

Why must cromolyn and nedocomil be absorbed topically?

they are poorly soluble salts

48

When is cromolyn and nedocomil only active?

prophylactically

49

What are the 2 mech behind cromolyn and nedocomil?

1. inhibits degranulation of mast cells, possibly from inhibition of Ca channels
2.Inhibit Cl channels to reduce nerve activity and cough

50

How does muscarinic antagonists change bronchial tone?

less bronchoconstriction

51

How does theophylline change bronchial tone?

less bronchoconstriction, and increased bronchodilation through cAMP pathway

52

Why is an inhaled form preferred over systemic administration for Beta-2 agonists? [2 reasons]

faster onset for short term relief and fewer side effects.

53

Increased usage of Beta-2 agonist for asthma might signify what?

lack of effective control by maintenance therapy

54

T_F--long acting Beta-2 agonists can be used for short term relief?

False

55

What bronchodilator is a muscarinic antagonist?

ipratropium

56

IS ipratropium faster or slower than beta-2 agonists for asthma?

slower [may be most useful in patients intolerant to beta-2 agonists.

57

What is the mech. of theophylline?

inhibit phosphodiesterase degradation of cAMP and thus increasing levels and creates relaxation o bronchial smooth muscles

58

Why must serum levels of theophylline be monitored?

minimize side effects- therapeutic plasma level =10-20 micrograms/ml

59

What are the key side effects of theophylline?

tachycardia, CNS stim

60

What is the best treatment option for mild-intermittent asthma patients?

quick relief only with beta-2 agonist

61

Do mild-persistent asthma patients need long acting bronchodilators?

No, just corticosteroid or cromolyn use, [moderate persistent patients do]

62

Which asthma patients are usually treated with oral corticosteroids as well as everything else?

severe-persistent

63

What are the major long term beta-2 agonists that must be combined with corticosteroids?

1. Salmeterol combined with fluticasone