Respiratory medications Flashcards
what does atropine do
- antagonizes Ach on airway smooth muscle
- effects airways that respond to vagal stimulation
- increases dead space
- decreases airway resistance
use of glycopyrrolate
- anticholinergic for COPD
- not for acute symptoms
- no significant tachycardia
ipratropium
- paradoxical bronchospasm may occur
- most effective in treating bronchospasm due to beta antagonist
- slow onset
- less effective than beta agonists
tiotropium
- long-acting bronchodilator
- maintenance of bronchospasm associated with COPD
- long-acting end in “ium”
warnings with inhaled anticholinergics
- narrow angle glaucoma
- urinary retention
beta-2 agonists actions
- relax bronchial smooth muscle
- non-catecholamine structure (resistant to COMT) = increased DOA
beta-2 agonists uses
- acute asthma treatment
- prevents exercise induced asthma
- stop premature uterine contractions
- treatment of hyperkalemia
primatene mist
- inhaled epinephrine
- treatment of mild asthma
albuterol uses and action
- preferred for acute bronchospasm
- short-acting beta agonist (SABA)
- levoalbuterol is a SABA
terbutaline
- treatment of asthma
- tocolytic- reduces contractions to postpone labor
long-acting beta agonist (LABA)
- work > 12hrs
- salmeterol (frequently administered with a steroid)
- end in “erol”
side effects of beta2 agonists
- tremor (increased Ca in the muscle
- tachycardia
- metabolic response (hyperglycemia, hypokalemia, hypomagnesemia)
black box warning with LABAs
- increased risk of asthma related death
- should not be used alone
cromolyn sodium
- 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)
methylxanthines names
- theophylline/ aminophylline
- caffeine
- theobromine
effects of methylxanthines
- stimulates the CNS
- increases BP
- increased myocardial contractility and HR
- relax smooth muscle
methylxanthines MOA
- nonselective phosphodiesterase inhibitors
- competitive antagonists of adenosine receptors
- theophylline is the most active
theophylline uses
- treatment of bronchospasm due to acute exacerbation of asthma
- CNS stimulant
theophylline toxicity
- 15-25 = GI upset, N/V, tremor
- 25-35 = tachycardia, PVCs
- > 35 = Vtach, seizures
caffeine effects
- CNS stimulant
- cerebral vasoconstrictor
- secretion of gastric acid
caffeine uses
- apnea of prematurity
- post-dural puncture headache
- cold remedies
histamine H1 receptors
- 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
histamine H2 receptors
- activates adenyl cyclase and increase cAMP
- activates proton pump to secrete H+
- increases contractility and HR
- coronary vasodilation
- usually think stomach and GI tract
histamine triple response (wheal and flare)
- edema (increased capillary permeability)
- dilated arteries (flare)
- pruritis
histamine airway effects
- H1 = bronchial constriction
- H2 = bronchial dilation
histamine gastric effects
- evokes secretion of gastric fluid containing high H+
histamine receptor antagonists effects
- competitive and reversible
- do not inhibit histamine release but prevent response mediated by histamine
H1 receptor antagonists generations
- first gen are sedating
- second gen are non-sedating
first gen H1 histamine antagonists effects
- decreased alertness
- anticholinergic effects
- tachycardia, QT prolong
second gen histamine antagonists side effects
- unlikely to produce CNS side effects or any of the first gen side effects
uses of H1 histamine receptor antagonists
- prevent and relieve symptoms of allergies
- antiemetic
- antipruritic
Diphenhydramine
- H1 antagonist
- for anaphylaxis
- blocks histamine mediated vasodilation
- prevents motion sickness and PONV
cortisol
- produced by adrenal cortex
- released by stimulation of HPA axis due to stress
- inhibits inflammatory/ allergic response
aldosterone
- secreted secondary to increased K and decreased Na, BP
- causes increased K excretion and Na and H2O retention
glucocorticoid effect
- anti-inflammatory response
mineralocorticoid effect
- evoke distal renal tubular re-absorption of Na+ in exchange for K+
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
CNS dysfunction with steroid use
- neurosis and psychosis
- manic depression and suicidal tendencies
- cataracts can develop with long term use
blood changes with steroids
- tend to increase hematocrit and leukocytes
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
therapies unlikely to suppress HPA axis
- prednisone 5mg/ day or less
- long-term every other day dosing
- glucocorticoids admin < 3 weeks
prednisone or dexamethasone & HPA suppression
- given as a single daily dose at bedtime is associated more commonly with HPA axis suppression
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
1st degree adrenal insufficiency
- addisons disease
- adrenals do not secrete cortisol or aldosterone
- must replace with glucocorticoid and mineralocorticoids
2nd degree adrenal insufficiency
- due to chronic use and suppression of the HPA axis
- aldosterone secretion maintained
- usually only requires glucocorticoid replacement