Respiratory Meds Flashcards

1
Q

How many muscarinic receptors are there?

A

5

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2
Q

Which muscarinic receptors are inhibitory? Stimulatory?

A

M2 and M4 are inhibitory

M1, M3, M5 are stimulatory

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3
Q

Which muscarinic receptors’ function is cardiac inhibition?

A

M2

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4
Q

Which Muscarinic receptors increase Inositrol triphosphate?

A

M1, M3, M5

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5
Q

What does Inositrol triphosphate cause the release of?

A

Ca++

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6
Q

M2 and M4 receptors cause an inhibition of _______ which causes a _____ in cAMP?

A

Adenylate cyclase and decrease

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7
Q

What is atropine’s effects on the respiratory system?

A
  1. Antagonizes ACh effects on large/medium sized airways smooth muscle
  2. Affects airways that respond to vagal stimulation
  3. Decreases airway resistance
  4. Increases dead space
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8
Q

Which medication did Emily consider “Atropine Lite”?

A

Ipratropium

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9
Q

What situation is ipratropium most effective in treating bronchospasm?

A

Bronchospasm due to beta antagonism

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10
Q

Which is slower and more selective- Atropine or Ipratropium?

A

Ipratropium

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11
Q

T/F: Ipratropium is more effective than beta agonists in treating bronchial asthma?

A

False; not useful in acute attacks

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12
Q

T/F: Ipratropium is more effective than beta agonists in chronic bronchitis or ephysema?

A

True

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13
Q

T/F: Ipratropium should never be used in combination with beta agonists?

A

False; almost always used in combo with a beta agonist

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14
Q

Does ipratropium have a low or high systemic absorption rate?

A

Low= <1%

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15
Q

T/F: Both ipratropium and atropine reach a ceiling effect as more medication is administered?

A

False; tolerance has NOT been observed to the bronchodilator effects of ipatropium; however, atropine reaches a ceiling effect around 3mg

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16
Q

What class of medications does ipratropium/tiotropium belong to?

A

Anticholinergic bronchodilators

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17
Q

What is an example of a long acting anticholinergic bronchodilator?

A

Tiotropium (spiriva)

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18
Q

Which muscarinic subtypes does tiotropium (Spiriva) block?

A

M1 and M3

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19
Q

What two major effects does tiotropium (Spiriva) have when blocking M1 and M3?

A
  1. Facilitates bronchodilation

2. Reduces mucous secretion

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20
Q

How does aclidinium (Tudorza) compare to tiotropium (Spiriva)?

A

Given twice daily (vs once daily), but has faster onset to peak (2d vs 7d).

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21
Q

What are 4 examples of adrenergic agents used as respiratory medications?

A
  1. Ephedrine/Epinephrine
  2. Isoproterenol
  3. Albuterol
  4. Terbutaline
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22
Q

What is the primary reason why adrenergic agents (specifically epi,ephedrine,isoproterenol) are used less frequently and should be used with caution?

A

Significant amount of non-respiratory side effects

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23
Q

Why do selective Beta 2 agonists have a sustained duration of action compared to non-selective like (epi, isoproteronol, ephedrine, etc)?

A

Their chemical structure makes them resistant to COMT

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24
Q

What are the 4 FDA approved uses of Beta 2 agonists?

A
  1. Status asthmaticus
  2. Prevention of exercise induced asthma
  3. Improved airflow and exercise tolerance in COPD
  4. Tocolytic to stop premature uterine contractions
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25
Q

What is the preferred route of administration for Beta 2 Agonists?

A

Inhaled via M.D.I. or Ultrasonic/Jet aerosol

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26
Q

What percent of medication actually reaches the lungs with proper technique?

A

12%

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27
Q

Dosage of nebulized Beta 2 Agonist must be increased or decreased by how much to equal M.D.I. dosing?

A

Nebulizer required 6-10x that of a MDI dose to produce the same degree of bronchodilation

28
Q

By how much does the presence of an ETT reduce the amount of drug delivered?

A

50-70%

29
Q

Side effects of Beta 2 Agonists?

A
  1. Tremor
  2. Tachycardia
  3. Metabolic responses such as hyperglycemia, hypokalemia, hypomagnesemia
30
Q

What is more effective in treatment of bronchospasm due to non-selective beta blocker- beta 2 agonist or anticholinergic?

A

Anticholinergic like atropine, ipratropium

31
Q

What are the four SABAs (short acting beta 2 agonists)?

A
  1. Albuterol
  2. Levoalbuterol (xopenex)
  3. Metaproterenol
  4. Terbutaline
32
Q

What are the two LABAs (long acting beta 2 agonists)?

A
  1. Salmeterol (Serevent/Advair)

2. Vilanterol (Anoro/Breo)

33
Q

What is the Black Box warning for LABAs and why?

A

Increase risk of asthma related death if not used in combo with something else. Some think it is related to the drug inhibiting the way the body can respond normally to bronchoconstriction/asthma flair ups

34
Q

MOA of Cromolyn Sodium (Intal)?

A

Inhibits antigen-induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses

35
Q

There is not great data behind the drug (Cromolyn sodium: Intal) because of what three things?

A
  1. Suppresses the secretory repsonse NOT the Ag-Ab interaction
  2. Does NOT relax bronchial or vascular smooth muscle
  3. NO use in an acute asthma attack
36
Q

What drug class does cromolyn sodium (Intal) belong to?

A

Membrane Stabilizer (also called Mast Cell Stabilizer)

37
Q

What is the FDA approved use for Cromolyn Sodium (Intal)?

A

Prophylactic treatment of Bronchial asthma

38
Q

What three drugs belong to the methylxanthines class?

A
  1. Theophylline/Aminophylline
  2. Caffeine
  3. Theobromine
39
Q

MOA of methylxanthines?

A
  1. Non-selective Phosphodiesterase inhibitors

2. Competitive antagonists of adenosine receptors

40
Q

Which methylxanthine is most active as a competitive antagonist of adenosine receptors?

A

Theophylline/aminophylline

41
Q

Which PDE isoenzyme is largely responsible for bronchodilation when inhibited?

A

PDE-4

To a lesser degree PDE-3 and PDE-7

42
Q

Why are PDE-4 selective inhibitors not used more frequently?

A

Very expensive

43
Q

Why does caffeine (and other methylxanthines) produce wakefulness?

A

Adenosine attaches to the receptor, it allows GABA to be released which promotoes sleepiness (think propofol). Caffeine promotes adenosine antagonism which promotes CNS stimulation

44
Q

What other way do methylxathines promote wakefulness?

A

Inhibit reuptake of NE/Epi

45
Q

For what reason are the CNS stimulating properties of methylxanthines used specifically?

A

Treat apnea of prematurity in infants

46
Q

T/F: Theophylline is preferred due to its wide therapeutic index

A

False; Must be used with caution due to its narrow therapeutic window

47
Q

What toxic side effects are associated with theophylline at a given serum level?

A

15-25=GI upset, N/V, tremor
25-35=Tachycardia, PVCs
>35=VTach, Seizures

48
Q

T/F: Caffeine is a cerebral vasodilator and inhibits secretion of gastric acid?

A

False; it is a cerebral vasoconstrictor and promotes secretion of gastric acid

49
Q

What is histamine?

A

Low molecular weight, naturally occurring hydrophillic endogenous amine that produces a variety of physiologic and pathologic responses

50
Q

Where are the main location for Mast Cells in the body?

A

Skin, lungs, GI tract, and in circulating basophils

51
Q

What two things can cause a release of histamine from mast cells?

A
  1. Certain drugs

2. Ag-Ab reactions

52
Q

Does histamine cross the blood-brain barrier

A

Does not easily cross the blood-brain barrier

53
Q

What must be administered to completely block the vasodilatory effects of histamine release?

A

H1 and H2 blocker

54
Q

What is considered the “Triple Response” (Wheal and Flare) to histamine?

A
  1. Edema due to increased permeability
  2. Dilated arteries around the edema (Flare)
  3. Pruritus due to histamine in the superficial layers of the skin
55
Q

What is H2 receptor activation do to bronchial smooth muscle?

A

Relaxes bronchial smooth muscle (H1 constricts bronchial smooth muscle)

56
Q

Histamine receptor antagonists are competive/non-competitive and reversible/non-reversible antagonists of histamine receptors?

A

Competive and reversible

57
Q

Do histamine receptor antagonists inhibit the release of histamine?

A

Do NOT inhibit the release of histamine, but rather attache to receptors and prevent the responses mediated by histamine

58
Q

Are first or second generation H1 Receptor antagonists sedating?

A

H1 1st generation are sedating

59
Q

What are examples of first generation H1 antagonists?

A
  1. Dramamine

2. Benadryl

60
Q

What are examples of second generation H1 antagonists?

A
  1. Allegra
  2. Claritin
  3. Zyrtec
61
Q

H1 Receptor Antagonists can also be “re-classified” as what?

A

Inverse agonists because they combine and stabilize the inactive from of the H1 receptor which shifts the equilibrium toward the inactive state

62
Q

What are side effects seens with first generation H1 Antagonists?

A
  1. CNS- somnolence, decreased alertness, slowed reaction times, and impaired cognitive function
  2. Anticholinergic- dry mouth, blurred vision, urinary retention, and constipation
  3. CV- tachycardia, QT prolongation, heart block,and cardiac dysrrhthmias
63
Q

Why would you see tachycardia with first generation H1 antagonists?

A

Due to anticholinergic (anti-muscarinic) properties

64
Q

Why might H1 blockers not be ideal for treating nasal congestion?

A

Because they thicken the secretions and can cause dryness that would make it more difficult to expel drainage

65
Q

What is dramamine’s MOA?

A

Inhibits the integrative functioning of vestibular nuclei by decreasing vestibular and visual input

66
Q

What are side effects that can be seen clinically with long term 1st gen H1 Blocker use?

A
  1. Agitation
  2. Thick secretions
  3. Other anti-cholinergic side effects
67
Q

What is the benefit of xoponex (levoalbutirol) over albuterol?

A

Does not cause tachycardia. Better choice for patients with atrial fibrillation or ventricular dysrhythmias