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Respiratory Drugs Flashcards

(47 cards)

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1
Q

What do the SNS fibers in the lung innervate and what do they do?

A

They pass from the thoracic ganglia to the lungs to innervate smooth muscles of bronchi and pulmonary blood vessels - they bronchodilate via B2ARs

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2
Q

What do the PSNS fibers innervate in the lung and what do they do?

A

innervates lung smooth muscle of the bronchi and pulmonary blood vessels and causes bronchoconstriction via muscarinic M3 receptors

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3
Q

beta 2 agonism causes and is morse sensitive to which NT

A
  • bronchodilation
  • increased intracellular cAMP
  • more sensitive to epi than NE
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4
Q

M3 receptors do what

A

mediate bronchoconstriction and mucus secretion via the activation of IP3 which increases intracellular calcium concentration

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5
Q

What is asthma?

A

chronic inflammatory disorder of the airway characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli

creates airways that are inflamed and edematous

characterized by: irritation, hyper-reactivity, and REVERSIBLE airway obstruction (air outflow problem)

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6
Q

signs and symptoms of asthma

A 
wheezing
breathlessness
chest tight
cough (night and early AM)
tachypnea
prolonged expiratory phase
fatigue
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7
Q

primary histologic mediators for asthma

A

eosinophils, mast cells, cytokines, interleukins (3,4,5), leukotrienes, and histamine

**some asthmatics are atopic and have IgE synthesis = extrinsic asthma

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8
Q

primary histologic mediators for COPD

A

neutrophils, macrophages, and T lymphocytes

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9
Q

What is COPD?

A

Obstructive pulmonary disease that is not reversible

causes cell death and destruction of alveoli due to impaired lung parenchyma and toxic actions of inflammatory cells

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10
Q

Treatment steps for airway outflow disorders

A
  1. short acting bronchodilators
  2. regular inhaled corticosteroids
  3. long acting bronchodilators
  4. phosphodiesterase inhibitors, methylxanthines, leukotriene inhibitors
  5. oral corticosteroid
    other: cromolyns
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11
Q

Name the three types of bronchodilators (classes)

A

beta-adrenergic agonists (increase cAMP = bronchodilation)
anticholinergics (inhibit Ach and PSNS response = bronchodilation/stop constriction)
methylxanthines (stop cAMP breakdown = bronchodilation)

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12
Q

How much more selective to beta2ARs than beta1ARS are our selective B2ARs?

A

200-400x more selective

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13
Q

MOA for beta adrenergic agonists

A

BARs = gpcrs
agonist activates adenlyl cyclase to INCREASE cAMP = bronchodilation
reduced intracellular calcium alters membrane conduction

WHAT HAPPENS?

  • smooth muscle relaxation and bronchodilation
  • inhibited mediator release from mast cells
  • increased mucus clearance by action on cilia
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14
Q

onset of action/duration of action of short acting beta adrenergic agonists

A

onset within minutes

duration 4-6 hours

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15
Q

side effects of beta adrenergic agonists

A

tremor, increased HR, vasodilation, metabolic changes (hyperglycemia, hypokalemia, hypomagnesemia)

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16
Q

Albuterol dosing

A

administered via metered dose

  • 100 mcg/puff
  • 2 puffs q4-6h

nebulizer = 2.5-5mg in 5ml of saline

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17
Q

anesthesia considerations for albuterol

A
  • has an additive effect with our VAs on bronchomotor tone
  • 4 puffs blunt airway response to tracheal intubation in asthmatic patients
  • remember that the medicine sticks to the tubes of the circuit so you have have to give more
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18
Q

Metaproterenol-Alupent

  1. what is it?
  2. how is it administered?
  3. max dose?
A
  1. B2 agonist for asthma (less selective than Maxair)
  2. administered via metered dose
  3. not to exceed 16 puffs/day
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19
Q

Pirbuterol-Maxair

  1. what is it?
  2. dosing info
Study These Flashcards
A
  1. beta 2 agonist (more selective than alupent)

2. 2 puffs (400 mcg) via metered dose/ not to exceed 12 inhalations/day

20
Q

Terbutaline

  1. admin
  2. indication
  3. dose
Study These Flashcards
A
  1. administered oral, subq, or inhalation
  2. used to treat asthma - subq admin resembles epi
  3. Doses
    - child subq = .01 mg/kg
    - adult subq = .25 mg q 15 min
    - metered dose inhaler = 16-20 puffs per day (1 puff = 200 mcgs)
21
Q

Long acting beta agonists

  1. what are they?
  2. why are they long acting?
  3. duration
Study These Flashcards
A
  1. salmeterol (there is a combo drug with fluticasone and salmeterol also) and formoterol
  2. lipophillic side chain that resists degradation
  3. good for 12-24 hours but longer onset so not good for acute situations
22
Q

MOA anticholinergics/muscarinic receptor antagonists

Study These Flashcards
A
  • competitive antagonists at mAChR
  • M1 and M3 subtypes are the targets of the antagonists to mediate smooth muscle relaxation and decreased mucus secretion
  • drugs antagonize endogenous Ach
23
Q

what are the common uses for muscarinic antagonists

Study These Flashcards
A
  1. COPD treatment

2. Second line treatment for asthma in patients resistant to beta agonist or patients with significant cardiac disease

24
Q

Atropine

  1. what is it
  2. how is it administered/dosed
  3. PK highlight
  4. SE
Study These Flashcards
A
  1. naturally occuring alkaloid, muscarinic receptor antagonist (anticholinergic), used now for COPD
  2. administered 1-2mg in 3-5ml saline vie neb
  3. highly absorbed across respiratory endothelium
  4. tachycardia, nausea, dry mouth, GI upset
25
ipratropium bromide 1. MOA 2. Dose 3. onset/DOA 4. PK highlights 5. SE
1. antagonizes effect of Ach at M3 receptor 2. MDI 40-80mcg in 2-4 puffs via neb 3. onset = 30 min/DOA = 4-6 hours "short acting" 4. not as well absorbed compared to atropine (This is a good thing because less systemic side effects) 5. accidental oral admin = dry mouth and GI upset
26
tiotropium 1. What is it? 2. PK highlights 3. use
1. long acting anticholinergic 2. not well absorbed across resp epithelium, so less side effects 3. FDA approved for COPD
27
rank the anticholinergics for COPD
1. tiotropium 2. ipratropium 3. atropine
28
Methylxanthines - Phosphodiesterase Inhibitors 1. MOA 2. clinical applications 3. types and routes
1. nonspecific inhibition of phosphodiesterase isoenzymes to prevent cAMP degradation in airway smooth muscle cells as well as in inflammatory cells leading to airway relaxation and bronchodilation 2. clinical applications = copd and asthma 3. theophylline = PO/aminophylline = IV
29
what are the big problems with methylxanthines-phosphodiesterase inhibitors
they have multiple MOAs and are nonselective so they have multiple side effects and a tight therapeutic index TOX LEVELS - theophylline = therapeutic level = 10-20mcg/ml -TOXIC at >20mcg/ml they are metabolized by CYP450, so be careful with drugs that are inhibitors renal excretion caution with halothane?
30
side effects of PDIs
``` headache N/V irritability/restlessness insomnia arrhythmias seizures - lowers threshold SJS ```
31
what are the mechanisms of bronchodilation?
agonistic effects on beta2ARs = increase cAMP antagonistic effects to Ach at M3 receptor sites = increased cAMP inhibiting breakdown of cAMP via targeting phosphodiesterase = increased cAMP
32
Inhaled corticosteroids 1. use 2. MOA
1. major preventative treatment for patients with asthma 2. MOA = alter gene transciption by increasing B2ARs and anti-inflammatory proteins, decreasing pro-inflammatory proteins, inducing apoptosis in inflammatory cells, inhibits mast cells indirectly over time SUPPRESSIVE THERAPY - not a cure
33
what is the major preventative treatment for patients with asthma/their most important drug in asthma management
inhaled corticosteroids suppressive therapy = not a cure
34
what are the 3 major actions of inhaled corticosteroids
1. decrease inflammatory cells and thereby damage to lungs 2. decreases vascular permeability = less airway edema 3. reduces airway hyper-responsiveness
35
what are the types of inhaled corticosteroids?
beclomethasone triamcinolone fluticasone budesonide
36
inhaled corticosteroid considerations for surgery (3)
1. administer 1-2 hours preop 2. may prolong response of beta agonists 3. may consider 5 day course of combined corticosteroid and albuterol to minimize the risk of intubation evoked bronchospasm
37
how much of your inhaled coricosteroid reaches the airway
25%
38
side effects of inhaled corticosteroids
1. thrush 2. osteopenia/osteoporosis 3. delayed growth in kids 4. hoarseness 5. hyperglycemia
39
Cromolyn MOA
stabilized mast cells by inhibiting release of histamine and other inflammatory mediators ***it inhibits immediate allergic response to antigen, but does not stop an allergic response that has already been activated
40
administration of cromolyn
administered by inhalation 8-10% enters systemic circulation give 4x a day
41
what do we use cromolyn for
prophylactic therapy of bronchial asthma NOT FOR RESCUE OR TO STOP AN ALLERGIC RESPONSE ALREADY STARTED
42
cromolyn side effects
laryngeal edema angioedema urticaria anaphylaxis
43
leukotriene inhibitors
used for bronchial asthma (not for acute attack) MOA: leukotrienes are synthesized from arachadonic acid when inflammatory cells are activated, these drugs inhibit that pathway montelukast, zileuton
44
Zileuton
leukotriene inhibitor that blocks biosynthesis of leukotrienes from arachiodonic acid to produce bronchodilation and improve asthma symptoms shown long term improvement in PFT HEPATOTOXIC - not commonly used
45
montelukast
leukotriene inhibitor that blocks the leukotriene receptors (antagonists) to stop bronchoconstriction caution with co-administration of warfarin, because could result in prolonged PT
46
Anti-IgE Antibodies
by removing these antibodies from circulation, you mitigate acute response of inhaled allergen
47
Omalizumab
monoclonal antibody derived from DNA (anti-IgE antibody) binds to IgE to decrease quantity of circulating IgE down regulation of receptors RARE adverse effect = triggers immune response

Advanced Pharm (11 decks)

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