PHARM of COPD AND ASTHMA Flashcards

1
Q

what do M2 receptors do?

A

they are autoreceptors that respond to ACh, provide negative feedback for M3 receptors

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2
Q

why arent muscarinic antagonists as effective as beta agonists?

A

they only work in the large airways (which is not the site of the greatest resistance)

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3
Q

what protein can bind M2 receptors and make them dysfunctional?

A

major basic protein made by eosinophils

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4
Q

albuterol MOA

A

newer selective beta 2 agonist “rescue medication” causes bronchodilation for early asthma response

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5
Q

how fast does albuterol work?

A

quick onset w/ 3-6 hr duration

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6
Q

Name the newer long-acting beta2-agonists that are together w/ inhaled steroids

A

salmeterol xinofoate
salmeterol fluticasone (advair)
formoterol fumarate
formoterol fumarate + budesonide (symbicort)

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7
Q

what is the onset and duration of action of the long acting beta2 agonists?

A

slower onset, 12 hr duration

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8
Q

what is the MOA of the sympathomimetics?

A

increase levels of cAMP (causing bronchodilation)
inhib. effect on release of mediators from mast cells
some inhib. effect on microvascular permeability
promotes mucociliary transport

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9
Q

name an antimuscarinic drug

A

Ipratropium

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10
Q

what are some adverse effects of the sympathomimetics?

A

N/V & headache
fall in BP, increased HR & arrhythmias
PaO2 may decrease
CNS effects like agitation convulsions, coma, resp. and vasomotor collapse

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11
Q

adverse effect of ipratropium?

A

pupillary dilation and cycloplegia

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12
Q

how do antimuscarinic drugs like ipratropium work?

A

competitive ACh block
reduce smooth muscle constriction
decrease mucous secretion
enhance beta-2 mediated bronchodilation

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13
Q

what is combivent and what does it treat?

A

anti-cholineric (ipratropium) and beta-2 agonist (albuterol), combined therapy has greater improvement, treats COPD

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14
Q

How does theophylline work?

A

increases levels of cAMP by inhibiting PDE (vasodilation), and blocks adenosine receptors (which would normally produce vasoconstriction)
-anti-inflamm., inotrope, chronotrope, increased CNS activity
-

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15
Q

what are some adverse effects of theophylline at low doses?

A

5-10 micrograms, may cause N/V, nervousness, headache, insomnia

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16
Q

what are some adverse effects of theophylline at higher doses?

A
serum greater than 20 micrograms/mL
vomiting
hypokalemia
hyperglycemia
tachycardia
arrhythmias
tremor
neuromuscular irritability and seizures
17
Q

how do cromolyns work?

A

alters chloride ion channels
prevents degranulation of mast cells in lung
inhibit inflamm. response by acting on eosinophils
inhib cough by action on nerves
reduce bronchial hyperactivity associated w/ exercise and antigen-inhaled asthma

18
Q

When are cromolyns used in time course of disease?

A

prophylactically

19
Q

MOA of glucocorticoids

A
  • binds to GRalpha and translocates to nucleus
  • uses GRE to transcribe anti-inflamm. genes
  • recruits HDAC to block transcription of inflamm. genes
  • causes trancription of TTP which destablilizes inflamm. mRNA
20
Q

what are the pharmacologic effects of glucocorticoids?

A
  • decrease prod. of inflamm. cytokines
  • reduce mucus secretion
  • reduce bronchial hyperactivity
  • enhance effect of beta-2 agonists
21
Q

what are some side-effects of inhaled corticosteroids?

A

oropharyngeal candidiasis
decreased bone density in premenopausal women
decreased growth in children

22
Q

MOA of monteleukast

A

LTD4 receptor antagonists

  • decrease bronchial reactivity and bronchoconstriction
  • mucosal hypersecretion and mucosal edema
  • decrease airway inflamm
23
Q

what are some systemic side-effects of steroids therapy?.

A
glucose intolerance
cushing syndrome
cataracts
immunosuppression
retarded growth
bone demineralization
24
Q

adverse effects of monteleukast

A
GI probs
laryngitis
pharyngitis
otitis
sinusitis
25
Q

how does zileuton work?

A

blocks the 5-LO path preventing the synth. of LTs

  • decreases smooth muscle contraction and blood vessel perm.
  • reduces wbc migration to the damage area
26
Q

what are some adverse effects of zileuton?

A

CYP1A2 interacts w/ theophylline

hepatic enzyme elevation

27
Q

MOA omalizumab

A

anti-IgE mAb, prevents release of inflamm. mediators–>decreased allergic response

28
Q

what are some important treatment options for COPD pts?

A
  1. nicotine replacement therapy (nicotine causes dopamine release=pleasure)
  2. bronchodilators
  3. antimuscarinics
  4. theophylline
  5. combination therapy
  6. corticosteroids
  7. O2 therapy
  8. mucolytics
29
Q

why dont you give sedatives to pts w/ airway disease?

A

depress respiratory drive

30
Q

why dont you give beta blockers to pts w/ airway disease?

A

negative inotropic effect on heart, nonspecific interaction will cause bronchoconstriction of airway

31
Q

why don’t you use local anesthetics w/ epinephrine on pts w/ airway disease?

A

epinephrine causes bronchodilation, vasoconstriction and tachycardia

32
Q

why dont you give aspirin and NSAIDs to pts w/ airway disease?

A

block COX and shunt pathway to produce LTs which cause bronchoconstriction

33
Q

why dont you give ACE inhibitors to pts w/ airway disease?

A

stops the breakdown of bradykinin (stimulates cough)

34
Q

what is beclamethasone?

A

inhaled corticosteroids

35
Q

what is prednisolone?

A

oral corticosteroid

36
Q

explain the pathogenesis of asthma with eosinophils

A

eosinophils (late response) secrete major basic protein–>binds M2 receptors and makes them dysfunctional–>too much ACh–>bronchoconstriction

37
Q

what are some adverse effects of ipratropium

A

pupillary dilation and cyloplegia on contact

38
Q

what are the pharmacologic effects of omalizumab?

A

reduces severity and freq. of asthma attacks

-requires inhaled steroids which improves long term asthma control