Respiratory medications Flashcards

1
Q

what does atropine do

A
  • antagonizes Ach on airway smooth muscle
  • effects airways that respond to vagal stimulation
  • increases dead space
  • decreases airway resistance
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2
Q

use of glycopyrrolate

A
  • anticholinergic for COPD
  • not for acute symptoms
  • no significant tachycardia
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3
Q

ipratropium

A
  • paradoxical bronchospasm may occur
  • most effective in treating bronchospasm due to beta antagonist
  • slow onset
  • less effective than beta agonists
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4
Q

tiotropium

A
  • long-acting bronchodilator
  • maintenance of bronchospasm associated with COPD
  • long-acting end in “ium”
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5
Q

warnings with inhaled anticholinergics

A
  • narrow angle glaucoma
  • urinary retention
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6
Q

beta-2 agonists actions

A
  • relax bronchial smooth muscle
  • non-catecholamine structure (resistant to COMT) = increased DOA
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7
Q

beta-2 agonists uses

A
  • acute asthma treatment
  • prevents exercise induced asthma
  • stop premature uterine contractions
  • treatment of hyperkalemia
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8
Q

primatene mist

A
  • inhaled epinephrine
  • treatment of mild asthma
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9
Q

albuterol uses and action

A
  • preferred for acute bronchospasm
  • short-acting beta agonist (SABA)
  • levoalbuterol is a SABA
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10
Q

terbutaline

A
  • treatment of asthma
  • tocolytic- reduces contractions to postpone labor
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11
Q

long-acting beta agonist (LABA)

A
  • work > 12hrs
  • salmeterol (frequently administered with a steroid)
  • end in “erol”
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12
Q

side effects of beta2 agonists

A
  • tremor (increased Ca in the muscle
  • tachycardia
  • metabolic response (hyperglycemia, hypokalemia, hypomagnesemia)
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13
Q

black box warning with LABAs

A
  • increased risk of asthma related death
  • should not be used alone
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14
Q

cromolyn sodium

A
  • membrane stabilizer
  • inhibits antigen induced release of histamine and other mediators from pulmonary mast cells during antibody mediated allergic responses
  • does not relax bronchial smooth muscle
  • not for acute asthma attack (prophylactic)
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15
Q

methylxanthines names

A
  • theophylline/ aminophylline
  • caffeine
  • theobromine
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16
Q

effects of methylxanthines

A
  • stimulates the CNS
  • increases BP
  • increased myocardial contractility and HR
  • relax smooth muscle
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17
Q

methylxanthines MOA

A
  • nonselective phosphodiesterase inhibitors
  • competitive antagonists of adenosine receptors
  • theophylline is the most active
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18
Q

theophylline uses

A
  • treatment of bronchospasm due to acute exacerbation of asthma
  • CNS stimulant
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19
Q

theophylline toxicity

A
  • 15-25 = GI upset, N/V, tremor
  • 25-35 = tachycardia, PVCs
  • > 35 = Vtach, seizures
20
Q

caffeine effects

A
  • CNS stimulant
  • cerebral vasoconstrictor
  • secretion of gastric acid
21
Q

caffeine uses

A
  • apnea of prematurity
  • post-dural puncture headache
  • cold remedies
22
Q

histamine H1 receptors

A
  • evoke smooth muscle contraction in resp and GI tract
  • pruritis and sneezing
  • nitric oxide vasodilation
  • slow HR (decreases A-V nodal conduction)
  • coronary vasoconstriction
  • usually think respiratory
23
Q

histamine H2 receptors

A
  • activates adenyl cyclase and increase cAMP
  • activates proton pump to secrete H+
  • increases contractility and HR
  • coronary vasodilation
  • usually think stomach and GI tract
24
Q

histamine triple response (wheal and flare)

A
  • edema (increased capillary permeability)
  • dilated arteries (flare)
  • pruritis
25
Q

histamine airway effects

A
  • H1 = bronchial constriction
  • H2 = bronchial dilation
26
Q

histamine gastric effects

A
  • evokes secretion of gastric fluid containing high H+
27
Q

histamine receptor antagonists effects

A
  • competitive and reversible
  • do not inhibit histamine release but prevent response mediated by histamine
28
Q

H1 receptor antagonists generations

A
  • first gen are sedating
  • second gen are non-sedating
29
Q

first gen H1 histamine antagonists effects

A
  • decreased alertness
  • anticholinergic effects
  • tachycardia, QT prolong
30
Q

second gen histamine antagonists side effects

A
  • unlikely to produce CNS side effects or any of the first gen side effects
31
Q

uses of H1 histamine receptor antagonists

A
  • prevent and relieve symptoms of allergies
  • antiemetic
  • antipruritic
32
Q

Diphenhydramine

A
  • H1 antagonist
  • for anaphylaxis
  • blocks histamine mediated vasodilation
  • prevents motion sickness and PONV
33
Q

cortisol

A
  • produced by adrenal cortex
  • released by stimulation of HPA axis due to stress
  • inhibits inflammatory/ allergic response
34
Q

aldosterone

A
  • secreted secondary to increased K and decreased Na, BP
  • causes increased K excretion and Na and H2O retention
35
Q

glucocorticoid effect

A
  • anti-inflammatory response
36
Q

mineralocorticoid effect

A
  • evoke distal renal tubular re-absorption of Na+ in exchange for K+
37
Q

electrolyte and metabolic changes from corticosteroids

A
  • hypokalemic metabolic alkalosis from enhanced absorption of Na and loss of K
  • inhibit glucose and promote gluconeogenesis
  • contributes to edema and weight gain
  • redistributes body fat
38
Q

CNS dysfunction with steroid use

A
  • neurosis and psychosis
  • manic depression and suicidal tendencies
  • cataracts can develop with long term use
39
Q

blood changes with steroids

A
  • tend to increase hematocrit and leukocytes
40
Q

suppression of HPA axis

A
  • any admin may result in suppression
  • can blunt release of cortisol in stress and = hypotensive shock
  • the longer the use the longer it takes for HPA to work on its own
41
Q

therapies unlikely to suppress HPA axis

A
  • prednisone 5mg/ day or less
  • long-term every other day dosing
  • glucocorticoids admin < 3 weeks
42
Q

prednisone or dexamethasone & HPA suppression

A
  • given as a single daily dose at bedtime is associated more commonly with HPA axis suppression
43
Q

therapies assumed to suppress HPA axis

A
  • prednisone 20 mg/day for > 3 weeks
  • pts with signs of cushings syndrome
  • no need to test, just supplement with stress dose steroids
44
Q

1st degree adrenal insufficiency

A
  • addisons disease
  • adrenals do not secrete cortisol or aldosterone
  • must replace with glucocorticoid and mineralocorticoids
45
Q

2nd degree adrenal insufficiency

A
  • due to chronic use and suppression of the HPA axis
  • aldosterone secretion maintained
  • usually only requires glucocorticoid replacement