Respiratory medications Flashcards
(45 cards)
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
2
Q
use of glycopyrrolate
A
- anticholinergic for COPD
- not for acute symptoms
- no significant tachycardia
3
Q
ipratropium
A
- paradoxical bronchospasm may occur
- most effective in treating bronchospasm due to beta antagonist
- slow onset
- less effective than beta agonists
4
Q
tiotropium
A
- long-acting bronchodilator
- maintenance of bronchospasm associated with COPD
- long-acting end in “ium”
5
Q
warnings with inhaled anticholinergics
A
- narrow angle glaucoma
- urinary retention
6
Q
beta-2 agonists actions
A
- relax bronchial smooth muscle
- non-catecholamine structure (resistant to COMT) = increased DOA
7
Q
beta-2 agonists uses
A
- acute asthma treatment
- prevents exercise induced asthma
- stop premature uterine contractions
- treatment of hyperkalemia
8
Q
primatene mist
A
- inhaled epinephrine
- treatment of mild asthma
9
Q
albuterol uses and action
A
- preferred for acute bronchospasm
- short-acting beta agonist (SABA)
- levoalbuterol is a SABA
10
Q
terbutaline
A
- treatment of asthma
- tocolytic- reduces contractions to postpone labor
11
Q
long-acting beta agonist (LABA)
A
- work > 12hrs
- salmeterol (frequently administered with a steroid)
- end in “erol”
12
Q
side effects of beta2 agonists
A
- tremor (increased Ca in the muscle
- tachycardia
- metabolic response (hyperglycemia, hypokalemia, hypomagnesemia)
13
Q
black box warning with LABAs
A
- increased risk of asthma related death
- should not be used alone
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)
15
Q
methylxanthines names
A
- theophylline/ aminophylline
- caffeine
- theobromine
16
Q
effects of methylxanthines
A
- stimulates the CNS
- increases BP
- increased myocardial contractility and HR
- relax smooth muscle
17
Q
methylxanthines MOA
A
- nonselective phosphodiesterase inhibitors
- competitive antagonists of adenosine receptors
- theophylline is the most active
18
Q
theophylline uses
A
- treatment of bronchospasm due to acute exacerbation of asthma
- CNS stimulant
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
histamine airway effects
- H1 = bronchial constriction
- H2 = bronchial dilation
26
histamine gastric effects
- evokes secretion of gastric fluid containing high H+
27
histamine receptor antagonists effects
- competitive and reversible
- do not inhibit histamine release but prevent response mediated by histamine
28
H1 receptor antagonists generations
- first gen are sedating
- second gen are non-sedating
29
first gen H1 histamine antagonists effects
- decreased alertness
- anticholinergic effects
- tachycardia, QT prolong
30
second gen histamine antagonists side effects
- unlikely to produce CNS side effects or any of the first gen side effects
31
uses of H1 histamine receptor antagonists
- prevent and relieve symptoms of allergies
- antiemetic
- antipruritic
32
Diphenhydramine
- H1 antagonist
- for anaphylaxis
- blocks histamine mediated vasodilation
- prevents motion sickness and PONV
33
cortisol
- produced by adrenal cortex
- released by stimulation of HPA axis due to stress
- inhibits inflammatory/ allergic response
34
aldosterone
- secreted secondary to increased K and decreased Na, BP
- causes increased K excretion and Na and H2O retention
35
glucocorticoid effect
- anti-inflammatory response
36
mineralocorticoid effect
- evoke distal renal tubular re-absorption of Na+ in exchange for K+
37
electrolyte and metabolic changes from corticosteroids
- 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
CNS dysfunction with steroid use
- neurosis and psychosis
- manic depression and suicidal tendencies
- cataracts can develop with long term use
39
blood changes with steroids
- tend to increase hematocrit and leukocytes
40
suppression of HPA axis
- 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
therapies unlikely to suppress HPA axis
- prednisone 5mg/ day or less
- long-term every other day dosing
- glucocorticoids admin < 3 weeks
42
prednisone or dexamethasone & HPA suppression
- given as a single daily dose at bedtime is associated more commonly with HPA axis suppression
43
therapies assumed to suppress HPA axis
- prednisone 20 mg/day for > 3 weeks
- pts with signs of cushings syndrome
- no need to test, just supplement with stress dose steroids
44
1st degree adrenal insufficiency
- addisons disease
- adrenals do not secrete cortisol or aldosterone
- must replace with glucocorticoid and mineralocorticoids
45
2nd degree adrenal insufficiency
- due to chronic use and suppression of the HPA axis
- aldosterone secretion maintained
- usually only requires glucocorticoid replacement
