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44 Cards in this Set

  • Front
  • Back
Name the sympathomimetic drugs.

--produces bronchoconstriction via direct stimulation of B2 adrenoreceptors
--vasoconstriction via a-adrenoceptors decreases local congestion and edema
--also acts in the CNS to increase resp rate and tidal volume and thus decrease CO2 in the alveoli

**very rapid onset of action when given s.c. (30s)
salmeterol, terbutaline and albuterol effects, use?
1. bronchodilation via B2-adrenoceptor stimulation
2. preferentially dilate smaller and more periph airways
3. inhib release of inflamm cmpds from mast cells
4. inhib accumulation of eosinophils
5. improve mucociliary transport in prox and distal airways
6. tolerance develops due to down-regulation of B2-adrenoceptors
What is special about salmeterol?
It has a very slow onset of action, but is very long acting
-- bronchodilation may persist for 24h
-- therapy w/ short-acting B2-agonist is STILL req'd
-- do NOT use in patients with deteriorating asthma
-- NOT a substitute for corticosteroids
Side effects of the B-adrenoceptor agonists?
- few adverse effects when given via inhaler
- may cayse paradoxical bronchospasm after excessive inhalation
- When given p.o.:
-- cardiac arrhythmias, hyperglycemia, hypokalemia, dizziness, headache, nervousness, and tremor may occur
Corticosteroids used in respiratory pharmacology?
budesonide (high "first pass" metab)
corticosteroid MOA?
1. inhibit recruitment of leukocytes and monocytes-macrophages into affected areas and prevent autocoid release from these cells
2. prevent and reverse the early phase of inflamm process (edema, fibrin deposition, capillary dilation, migration)
3. prevent and reverse late phase inflamm response (prolif of capillaries and fibroblasts, collagen deposition)
4. inhib synth and/or release of PGs and LTs, PAF, TNF, IL-1, and plasminogen activator
aerosol formulations of corticosteroids?
direct application of corticosteroids to the lungs by inhalation is usually effective in the treatment of asthma and obviates the adverse effects of systemic admin

**if inhaled response inadequate, may be increased 4-fold before resorting to p.o. therapy with corticosteroids
How long is normal for systemic admin of corticosteroids?
treat acute exascerbations for 5-10 days -- will exert little toxicity and any adrenal suppression dissipates within 1-2wks
Adverse effects of corticosteroid use via inhalation?
- NO growth retardation
- bone resorption may occur, but is dose-dependent
- NO CHO/lipid metabolism
- adrenal suppression with higher doses
- purpura may occur, dose-related
- NO cataracts
MAJOR adverse effects:
- dysphonia
- oropharyngeal candidiasis
- BOTH can be mitigated by rincing mouth and throat with water after use ane by using spacers or reservoirs
Adverse effects of corticosteroid use systemically?
Long-term therapy requires alternate day therapy and the usual precautions upon cessation.

Many possible effects PREDNISONE mnemonic.
General properties of ipratroprium?
--poorly lipid-soluble quarternary cmpd
--does not enter CNS or cross placenta
--Bronchodilation w/in 10m of inhalation, peaks at 1-2h and persists for 4-8h
Ipratropium MOA?
-- Muscarinic receptor blockade in smooth muscle of large and small airways prevents vagally induced bronchoconstriction
-- no antihistaminic or anti-inflamm effects
-- does not inhib mast cell degran
Iprotropium effect on lungs?
-- dilates large and small sized airways
-- does NOT effect mucus production, viscosity, or clearance (no ciliary affect)
-- No effect on pulmonary gas exchange or arterial CO2
Ipratropium clinical use?
--a secondary therapeutic agent
--used prophylactically to prevent attacks in patients with either a poor response or intolerance to the B-adrenoceptor agonists
-- patiente response is highly variable but tolerance DOES NOT develop
-- After FEV1 is increased by ipratropium, a B2-adrenoceptor agonist will elicit a further increase in FEV1
Ipratropium toxicity and S/Es?
-- Most common are dry mouth and bitter taste
-- use with caution in presence of angle-closure glaucoma, GI or GU obstruction, and prostatic hypertrophy
How do leukotrienes (LTs) exhibit pulmonary toxicity?
-- bronchoconstriction
-- increased mucus production
-- increased vasc permeability
-- chemotaxis for eosinophils/PMNs
-- increased leukocyte adhesion
Name the 5-LO inhibitor.
Zileuton action, use?
-- prevents LT synth
-- increases FEV1, decreases asthma symptoms and use of B2-agonists and corticosteroids
-- used in prophylaxis and chronic tx of mild/moderate asthma
-- prevents aspirin induced asthma
Zileuton interactions?
Can increase plasma conc. of other drugs by inhibiting CYP450
Name the LT receptor antagonists.
zafirlukast and montelukast action, use?
-- both drugs are competitive receptor antag of receptors for LTC4 and LTD4 (SRS-A cmpds)
-- decrease late bronchoconstriction caused by allergen challenge
-- max therapeutic effect occurs after one week of therapy and is assoc w/ decreased need for rescue B-agonist like albuterol
-- alternative to low-dose corticosteroids or cromolyn sodium
zafirlukast, montelukast S/Es?
major S/E is headache (13%)
zafirlukast interactions?
can increase plasma conc. of other drugs by inhibiting CYP450
cromolyn sodium general properties?
-- lipid soluble, but only 10% absorbed from lungs and GI tract
-- available as powder in capsules for inhalation, powder in aerosol, nasal spray, and opthalmic drops
Chromolyn sodium MOA?
***prevents immediate and delayed Ag-induced degranulation of mast cells
-- prevents release of chemical mediators from mast cells by preventing increase in intracellular Ca conc induced by formation of IgE-Ag bridges on cell surface
-- Does NOT affect binding of IgE to mast cells or binding of Ag to IgE
-- No effect on basal tone of bronchial smooth muscle or the bronchoconstriction caused by ACh, LTs, or histamine
-- No direct antihist or anti-inflamm effects
-- Must be used prophylactically (10-15min) prior to exposure of Ag
Chromolyn sodium pharm effects?
-- reduces freq and severity of bronchospasm
-- beneficial effect may take 3-4 wks to develop
-- long-term therapy can reduce overall bronchial reactivity to histamine and LTs by preventing bronchial damage caused by mast cell products
Chromolyn sodium toxicity, S/Es?
-- no contraindications
-- use aerosol with care in patients with CAD or arrhythmias b/c hydrpcarbon propellants can elicit adverse cardiac effects
-- few adverse effects during long-term therapy
- may cause throat irritation, cough, dry mouth, wheezing
What is a good adjunctive therapy for asthma?
antihistamines -- block actions of histamine at H1 receptors, and the older drugs also block muscarinic receptors and aid in bronchodilation
Name the PDEase inhibitors used in asthma treatment?
theophylline and aminophylline general properties?
-- elim by hepatic metab and half-life decreased in cigarette smokers
-- crosses placenta
-- secreted in milk; usually no effect on nursing children but may cause irritability/excitation
-- aminophylline is more water soluble than theophylline
-- found in OTC asthma remedies
theophylline and aminophylline MOA?
-- inhibition of PDEase which degrades cAMP
-- increased cAMP allows increased excitability
-- a specific adenosine receptor antagonist
theophylline and aminophylline effects in the lungs?
--dilates large and periph airways by relaxation of smooth m.
-- improves ventilation by increasing contraction of the diaphragm and accessory resp m.
-- produces dose-related increase in FEV1 and FVC
-- tolerance DOES NOT develop
theophylline and aminophylline effects in the mast cell?
***iinhibit mast cell degran
-- prevents histamine release and LT synth
theophylline and aminophylline effects in the CNS?
-- increases ventilation by increasing the sensitivity of the medullary resp centers to CO2
-- causes central stim
-- can produce nervousness, excitation, insomnia, tremor, and seizures
theophylline and aminophylline effects on the heart and blood vessels?
-- slight decrease in TPR w/ increased HR and dp/dt elicits a transient rise in CO and organ perfusion
-- central venous pressure and cardiac preload decrease
-- direct effect on adrenal increases plasma epi
-- causes cerebral vasoconstriction, possibly by release of NE
theophylline and aminophylline effects on kidney, GI?
kidney - transient diuresis and weak natriuresis via a decrease in the filtration fraction

GI - enhances gastric acid secretion
theophylline and aminophylline toxicity and S/Es?
**serious toxicity is NOT always preceded by less severe S/Es
-- careful dose titration necessary to max benefit and min S/Es
-- monitor plasma conc b/c 5-8mg/L min conc for therapeutic effect while toxic effects appear at 15mg/L and are prominent at 20+mg/L
-- contraindicated in presence of active ulcer
-- use with care in presence of CAD ore recent MI, and CHF or hepatic disease
-- GI tract
- nausea, GI discomfort common b/c both meds are highly alkaline and cause direct gastric irritation
- emesis if conc >15mg/L via action on chemoreceptor trigger zone
-- CNS - restlessness, nervousness, excitation, headache and tremor
- seizures usually occur at 40+mg/L; control w/ diazepam
-- CV - rapid i.v. injection can cause hypotension and arrhyhmias
theophylline and aminophylline drug interactions?
cimetidine, diltiazem, ERYTHROMYCIN, verapamil, and OCP's increase plasma theophylline by blocking hepatic metab
What is Cheyne-Stokes breathing?
--periodic deep and shallow breathing which occurs in cycles of 45 seconds to 3 minutes

-- usually occurs in heart failure or after CNS injury
How do you treat Cheyne-Stokes?
aminophylline (i.v.) often normalizes respiration b/c it sensitizes respiratory center to CO2
What is neonatal apnea?
--apnea of greater than 15 seconds in duration which can cause recurrent cerebral hypoxia and may produce serious neurological damage
Tx for neonatal apnea?
aminophylline or caffeine (i.v.) increases resp rate and improves blood gasses in preterm infants w/ intermittent apnea
Neonatal hypoxic respiratory failure...
-- assoc w/ signs/symptoms of pulm HTN die to increased pulm vasc resistance

-- treat with NO gas given by inhalation
-- improves pulmonary perfusion by decreasing pulmonary vascular resistance