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PHARM 1 Self > 16 > Flashcards

16 Flashcards

1
Q

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

A

asthma

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2
Q

What 2 things is asthma associated with?

A

genetic linkage

environmental factor related to immunological challenge

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3
Q

Which T cell response is associated with asthma?

A

TH2

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4
Q

Infections from what 2 organisms lead to no asthma?

A

helminth

hep A

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5
Q

What is allergic asthma triggered by?

A

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

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6
Q

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

A

False, increased mucus secretion

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7
Q

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

A

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

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8
Q

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

A
  • airway hyperresponsiveness to environmental irritants

- asthmatic episodes are triggered in the absence of the original aggravating allergen

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9
Q

What are the 2 clinical features of asthmatic airway?

A
  1. bronchial hyperreactivity to aerosolized histamine/adenosine as measured by reduced FEV
  2. Increased eosinophil numbers beneath the airway epithelium, and sputum/lavage
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10
Q

What can control the early reaction of allergic asthma response?

A

prophylactic corticosteroids and cromolyn?

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11
Q

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

A

B2 adrenergic receptor agonists

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12
Q

What can reduce the late reaction?

A

inhaled corticosteroids at or before initiation of the early reaction

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13
Q

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

A
  1. acute symptoms (quick relief)

2. Reduce airway hyper-responsiveness (long term control)

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14
Q

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

A

promote relaxation of smooth muscle which leads to dilation

For example: B2 adrenergic receptor agonist

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15
Q

What are the long term controllers of asthma?

A
  • anti-inflammatories that target leukotriene and mast cells degranulation
  • long acting agents to reduce probability of airway constriction
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16
Q

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

A

longer acting B2-adrenergic receptor agonists, methylxanthines)

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17
Q

What creates arachidonic acid?

A

phospholipase A2 acts n phospholipids

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18
Q

What key enzyme initially allows production of leukotriene?

A

5-lipoxygenase

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19
Q

What does LTB4 do to blood vessels?

A

nothing

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20
Q

What does LTB4 do in smooth muscle?

A

nothing

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21
Q

What does LBT4 do in regards to leukocytes?

A

neutrophil chemotaxis

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22
Q

What does LTC4 do in blood vessels?

A

decreased coronary blood flow increase capillary permeability

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23
Q

What does LTC4 due on smooth muscle

A

constrict bronchial

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24
Q

What does LTC4 do in regards to a leukocytes?

A

eosinophil chemotaxis an degranulation

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25
Q

What does LTD4 do on blood vessels?

A

decrease coronary blood flow, increase capillary permeability

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26
Q

What does LTD4 do with smooth muscle?

A

constrict bronchial

27
Q

What effect does LTD4 have on leukocytes?

A

eosinophil chemotaxis and degranulation.

28
Q

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

A

topically to the airway by aerosol inhalation

29
Q

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

A

long-term controllers: corticosteroids

30
Q

When is oral or intravenous administration of corticosteroids necessary?

A

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

31
Q

What are the 2 main oral corticosteroids?

A

prednisone

methylprednisolone

32
Q

What are the 3 main mechanisms by which corticosteroids work?

A
  1. inhibit PLA2 expression–>reduced mediators by mast.
  2. reduced synthesis of chemotactic factors—>reduced recruitment
  3. inhibition of cytokine expression–>reduce TH2 response and leukocyte prolif.
33
Q

Why can’t corticosteroids provide immediate release?

A

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

34
Q

Why are inhaled corticosteroids generally well tolerated?

A

low bioavailability outside of airway

35
Q

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

A
  1. abnormal glucose metab.,
    2.diabetes,
  2. hypertension,
  3. Cushing’s,
  4. potential increased infect susceptibility
    [short term treatment is usually not a big deal 5-10 days]
36
Q

LTD4 is chemotactic for what?

A

eosinophils

37
Q

LTB4 is chemotactic for what?

A

neutrophils

38
Q

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

A

zileuton

39
Q

What is the mech of zileuton?

A

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

40
Q

How is zileuton administered?

A

orally

41
Q

What side effect is zileuton associated with?

A

liver toxicity and can inhibit P450s effecting metabolism of other drugs

42
Q

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

A

zafirlukast, montelukast

43
Q

What drugs can allow for corticosteroid reduction in asthma patients?

A

zafirlukast, montelukast

44
Q

How does zafirlukast, montelukast work?

A

LTD4 receptor antagonists that reduce bronchoconstriction and edema associated with inflammation

45
Q

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

A

5-10%

46
Q

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

A

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

47
Q

Why must cromolyn and nedocomil be absorbed topically?

A

they are poorly soluble salts

48
Q

When is cromolyn and nedocomil only active?

A

prophylactically

49
Q

What are the 2 mech behind cromolyn and nedocomil?

A
  1. inhibits degranulation of mast cells, possibly from inhibition of Ca channels
  2. Inhibit Cl channels to reduce nerve activity and cough
50
Q

How does muscarinic antagonists change bronchial tone?

A

less bronchoconstriction

51
Q

How does theophylline change bronchial tone?

A

less bronchoconstriction,

and increased bronchodilation through cAMP pathway

52
Q

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

A

faster onset for short term relief and fewer side effects.

53
Q

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

A

lack of effective control by maintenance therapy

54
Q

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

A

False

55
Q

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

A
  1. Salmeterol combined with fluticasone

2. Formoterol combined with budesonide

56
Q

What bronchodilator is a muscarinic antagonist?

A

ipratropium

57
Q

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

A

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

58
Q

What is the mech. of theophylline?

A

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

59
Q

Why must serum levels of theophylline be monitored?

A

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

60
Q

What are the key side effects of theophylline?

A

tachycardia, CNS stim

61
Q

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

A

quick relief only with beta-2 agonist

62
Q

Do mild-persistent asthma patients need long acting bronchodilators?

A

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

63
Q

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

A

severe-persistent

PHARM 1 Self (6 decks)

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