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PHRM 5001 > 2. Anticholinergic Bronchodilators > Flashcards

2. Anticholinergic Bronchodilators Flashcards

1
Q

what are the two autonomic nerve fibers?

A

cholinergic fibers and adrenergic fibers

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2
Q

what are the two main autonomic neurotransmitters? which autonomic nerve fiber are they released by?

A

acetylcholine released by cholinergic fibers and norepinephrine (noradrenaline) released by adrenergic fibers

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3
Q
  1. what is the parasympathetic system responsible for?
  2. which region of the spinal cord is it innervated by?
  3. describe the length of the pre and post ganglionic fibers, are they short or long?
A
  1. “rest and digest” response
  2. craniosacral region
  3. long pre ganglionic and short postganglionic
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4
Q
  1. why must the body oppose the parasympathetic system? (hint: 1 answer)
  2. what do drugs do when they block the parasympathetic system? (hint: 1 answer)
  3. what are the drugs called that block the parasympathetic system? (hint: 3 answers)
A
  1. to counteract effects of the sympathetic system
  2. cause relaxation of airway smooth muscle
  3. anticholinergics or antimuscarinics, parasympatholytics, parasympathetic antagonists
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5
Q

anticholinergic drugs will oppose the parasympathetic responses, what does the acronym SLUDGE stand for?

A 
S = salivation 
L = lacrimation 
U = Urination 
D = defecation 
G = gastrointestinal motility 
E = excretions
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6
Q

what other sympathetic responses do anticholinergics inhibit? (hint: 4 answers)

A
  • bronchoconstriction
  • decreased HR
  • miosis (constriction of pupil)
  • contraction (thickening) of lens
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7
Q
  1. where are M1 receptors found? what do they facilitate?

2. where are M2 receptors found? what do they inhibit?

A
  1. parasympathetic nerve ganglia, facilitate cholinergic neurotransmission and bronchoconstriction
  2. cholinergic nerve endings, inhibit further acetylcholine release from postganglionic neuron
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8
Q

where are M3 receptors found? what do they cause? what do they stimulate?

A

found on airway smooth muscle, cause bronchoconstriction and stimulation of mucus glands (exocytosis)

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9
Q
  1. what is the vagally-mediated reflex triggered by?
  2. what are some of the triggers? (hint:4 answers)
  3. which cranial nerve is this bronchoconstriction reflex associated with? what does this control?
A
  1. nonspecific stimuli
  2. irritant aerosols, cold dry air, inflammatory mediators and pathogens/allergens
  3. cranial nerve 10 (vagus nerve), controls innervation of the heart, lungs, GI tract
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10
Q
  1. what is the mechanism of action of anticholinergic drugs?
  2. what does this inhibit? what does this suppress?
  3. what does this prevent?
A
  1. competitive antagonism of Ach at M3 - muscarinic cholinergic receptors
  2. inhibits guanylyl cyclase –> cGMP suppression
  3. decrease cGMP prevents: airway smooth muscle contraction, glandular secretions, histamine release
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11
Q

what are antimuscarinic bronchodilators effective in treating? (hint: 3 answers)

A
  • chronic bronchitis
  • emphysema
  • vagally-mediated asthma
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12
Q
  1. what are the tertiary ammonium compound prototypes for current anticholinergic inhaled therapy for managing?
  2. what are the 2 naturally occurring belladonna alkaloids?
  3. what do these compounds differ by?
A
  1. managing asthma and COPD
  2. atropine and scopolamine
  3. oxygen molecule bridging carbon-7
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13
Q
  1. where are the tertiary compounds absorbed? where are they widely distributed?
  2. can they cross the blood brain barrier? what does this cause?
A
  1. in the bloodstream, distributed throughout the body

2. yes! causing significant systemic side effects

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14
Q

which organs/organ systems are affected by tertiary ammonium compounds? (hint: 6 answers)

A
  • respiratory tract
  • CNS
  • eyes
  • cardiovascular
  • gastrointestinal
  • genitourinary
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15
Q
  1. what are the respiratory tract effects of tertiary ammonium compounds?
  2. what are the CNS effects?
  3. what can increasing doses lead to?
A
  1. inhibits mucociliary clearance and relaxes airway smooth muscle
  2. restlessness, irritability, drowsiness, fatigue, mild excitement
  3. disorientation, hallucinations or coma
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16
Q
  1. what are the eye effects of tertiary compounds?

2. cardiovascular effects?

A
  1. pupil dilation, blurred vision, increased intraocular pressure in glaucoma pts
  2. decrease in HR with small doses and an increase in HR with large doses
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17
Q
  1. what are the GI effects of tertiary compounds?

2. what are the GU effects?

A
  1. mouth dryness, dysphagia, decrease GI motility

2. inhibition of urinary sphincter leads to: urinary retention and male impotency

18
Q
  1. are Quaternary ammonium compounds absorbed in the body?
  2. do they cross the BBB? what does this cause?
  3. where are they not rapidly removed from?
A
  1. poorly absorbed in the bloodstream
  2. no! causing less systemic side effects (wider therapeutic margin)
  3. not rapidly removed from aerosol deposition site
19
Q
  1. ipatropium bromide (atrovent) is what class of medication?
  2. what type of derivative is this med? potent or nonpotent?
  3. onset of action? peak? duration?
  4. what does ipatropium lack? where is this med most effective in the respiratory tract?
A
  1. SAMA
  2. atropine derivative, potent bronchodilator
  3. 15 mins, 1-2 hrs, 4-6 hrs
  4. lacks selectivity for muscarinic recptors, most effective on large diameter proximal airways
20
Q
  1. what does ipatropium (atrovent) minimize compared to atropine? what does this result in?
  2. what are the methods of delivery for ipatropium? including dose.
A
  1. minimizes adverse side effects compared to atropine, resulting in: decrease drying secretions, decrease ocular effects and CNS effects
  2. MDI (20 mcg/puff), inhaled solution (0.2 mg/ml) or premixed nebules (500 microg)
21
Q
  1. what is the onset of action for anticholinergics (SAMA)? beta agonists (SABA)? (very general)
  2. peak effect?
  3. duration?
  4. presence of a tremor?
  5. decrease in PaO2?
  6. tolerance?
  7. sit of action?
A
  1. slightly slower for anticholinergics, faster for beta agonists
  2. slower for anticholinergics, faster for beta agonists
  3. anticholinergics longer and shorter for beta agonists
  4. none for anticholinergics, present with beta agonists
  5. none for anticholinergics, yes for beta agonists
  6. none for anticholinergics, yes for beta agonists
  7. larger/central airways for anticholinergics and central/peripheral airways for beta agonists
22
Q
  1. is tiotropium (spiriva) a potent or nonpotent bronchodilator?
  2. onset of action? peak? duration?
  3. what is tiotropium good at versus ipatropium? what does this mean?
A
  1. potent bronchodilator
  2. 30 mins, 1-3 hours, 24 hours
  3. good selectivity for M3 muscarinic receptors meaning, dissociates from M1,M2,M3 receptors at different rates
23
Q
  1. what is tiotropium (spiriva) available as?
  2. what dosing improves treatment compliance?
  3. what is the dosing for a DPI? what type of DPI is normally used? what is deposition dependent on?
A
  1. MDI or DPI
  2. once daily dosing
  3. 18 microg/inhalation, capsule for handihaler device, deposition dependent on inspiratory effort
24
Q
  1. what is the MDI device for tiotropium (spiriva)? how does this improve compliance?
  2. what are the two doses available?
  3. what dose is recommended for COPD maintenance?
  4. what dose is recommended for asthma maintenance?
A
  1. respimat - improved compliance through ease of use
  2. 1.25 mcg/actuation OR 2.5 mcg/actuation
  3. 2 puffs (5.0 mcg) OD
  4. > 12 years = 2 puffs (2.5 mcg) OD
25
Q
  1. what type of med is Umeclidinium (Incruse)?
  2. does it act locally or systemically? what does this cause? duration of action?
  3. what does this med inhibit?
  4. what delivery device is available for this med? how often should it be taken?
A
  1. LAMA
  2. locally to produce prolonged bronchodilation, 24 hour duration of action
  3. competitively inhibits binding of Ach at M3 receptors on airway smooth muscle
  4. DPI - take once daily via Ellipta
26
Q
  1. what type of med is Aclidinium Bromide (Tudorza)?
  2. what population of patients is this med for?
  3. duration? how often is this taken? what type of device is used?
  4. what is this med not used for? (hint: 3 answers)
A
  1. LAMA
  2. long term maintenance in COPD patients
  3. 12 hours, taken BID, Genuair device
  4. not used for acute deterioration, not used in patients with glaucoma or urinary retention
27
Q
  1. what type of drug is Glycopyrronium (Seebri)?
  2. what type of patients is this med intended for?
  3. duration? how often should this be taken? onset?
  4. what is the treatment not used for?
A
  1. LAMA
  2. long term maintenance of COPD patients
  3. 24 hours, taken OD, 5 minutes
  4. not for acute deterioration
28
Q
  1. what does salbutamol + ipatropium (combivent) combine?
  2. what is this med available as?
  3. what is the common delivery device used? include dosage.
A
  1. combines short acting B2 agonists and antimuscarinic effects (SABA + SAMA)
  2. MDI, inhalational solution, and fixed dose drug in unit dose vials (UDV’s)
  3. respimat - 20 mcg of ipatropium and 100 mcg salbutamol per actuation
29
Q
  1. what does Vilanterol + Umeclidinium (Anoro) combine?
  2. what is the only population this drug is designed for? how often is it taken?
  3. what type of delivery device is used?
A
  1. combinees long acting B2 agonist and antimuscarinic effects (LABA + LAMA)
  2. long term maintenance therapy for COPD only, taken once daily
  3. DPI - Ellipta
30
Q
  1. how do we monitor ongoing effectiveness of treatment?

2. what does long term effectiveness rely on?

A
  1. ongoing respiratory assessment –> RR/pattern, breath sounds before/after treatment, assess WOB
    - monitor flow rates –> peak flow meters, bedside spirometry
    - monitor ABG and/or pulse oximetry
  2. relies on good bedside education
31
Q
  1. what is a xanthine?

2. what is a methylxanthine? list examples

A
  1. nitrogenous compound found in many organs and bodily fluids (blood and urine)
  2. methylated drug (CH3 + group) derived from xanthines (caffeine, theophylline and theobromine)
32
Q
  1. what do methylxanthines promote? (hint: 2 answers)
  2. what is epinephrine fast asthma?
  3. what do methylxanthines delay? which mediators?
A
  1. relaxation of airway smooth muscle and inhibit glandular secretions in cases of refractory asthma
  2. patients no longer respond to B2 agonists
  3. delay release/formation of allergic mediators (histamine and leukotrienes)
33
Q
  1. what additional benefits do methylxanthine bronchodilators provide?
  2. what is methylxanthine known as?
A
  1. increased CO2 sensitivity in medullary respiratory centres leading to increase alveolar ventilation and increase diaphragmatic responses
  2. known as a respiratory stimulant
34
Q

what are the proposed mechanisms of action of methylxanthines? (hint: 3 answers)

A
  1. inhibition of cAMP phosphodiesterase –> increase intracellular cAMP induces bronchial relaxation and anti-inflammatory effects
  2. antagonism of adenosine –> block A1 receptors that inhibit cAMP
  3. Catecholamine release –> possible production and release of endogenous catecholamines causing bronchial relaxation
35
Q

what are the clinical indications for using methylxanthine bronchodilators (2 answers)

A
  1. second/third line of treatment for COPD and asthma

2. treat apnea of prematurity in neonates (caffeine citrate - Cafcit)

36
Q

what are the general pharmacologic properties of methylxanthines? (hint: 6 answers)

A
  • CNS stimulation
  • cardiac muscle stimulation
  • diuresis
  • smooth muscle relaxation
  • peripheral and coronary vasodilation
  • cerebral vasoconstriction
37
Q
  1. what type of med is theophylline?
  2. what is special about this drug?
  3. is the therapeutic margin narrow or large?
  4. what degrades theophylline?
  5. what are the routes of administration?
A
  1. xanthine bronchodilator
  2. only xanthine derivative with practical therapeutic value
  3. narrow therapeutic margin, must monitor serum concentrations carefully
  4. hepatic enzymes
  5. orally, rectally and IV
38
Q
  1. what factors enhance theophylline clearance?

2. what factors inhibit theophylline clearance?

A
  1. cigarette smoking, certain drugs (corticosteroids, B agonists, benzodiazepines)
  2. liver disease, alcoholism, CHF, certain drugs (Ca 2+ channel blockers, leukotriene modifiers, some diuretics, vaccinations)
39
Q
  1. what are some signs of toxic effects of theophylline? (hint: 10)
  2. what are the signs of severe toxicity? (hint: 2)
A
  1. nausea/vomiting, gastric bleeding, decrease BP, increase HR, palpitations, increase RR, headache, dizziness, agitation
  2. seizures and arrhythmias
40
Q
  1. what is aminophylline?
  2. what is the solubility of this med? what is it ideal for?
  3. what is this drug designed to treat?
  4. what else can this drug be used for? what does this stimulate?
A
  1. theophylline (85%) dissolved in solvent
  2. water soluble, ideal for IV administration
  3. treat status asthmaticus (acute bronchoconstriction/life threatening)
  4. cheyne-stokes breathing (stimulate central respiratory control centers)
41
Q
  1. what is the goal for combining xanthine bronchodilators?
  2. what can this help to minimize?
    3 what do fixed dose combinations lack?
  3. what are the 4 component drugs?
A
  1. goal - drug synergism
  2. minimize amount of theophylline and unwanted side effects
  3. lack versatility
  4. theophylline, ephedrine, CNS depressants and expectorants

PHRM 5001 (12 decks)

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