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Pharm blk4-Asthma


what are characteristics of acute obstrucitve disease episodes (time course - 2) 1) intermittent; 2) reversible
what is asthma characterized by reversible inflammation of airway wall
what age/sex is asthma incidence highest boys in early childhood
what is happening to overall asthma incidence increasing
when in the day are asthma symptoms the worst night and early morning
what are the two main types of asthma 1) extrinsic/allergic; 2) intrinsic/idiopathic
which is more common in adults intrinsic/idiopathic (allergic asthma begins in childhood, less common in adults)
what does the hygiene hypothesis suggest that allergic asthma is due to an imbalance in Th1/Th2 cells
when will children have the right balance of Th1/Th2 cells when they are exposed to childhood infections
what are Th1 cells and Th2 cells responsible for protective immunity, inflammation/cytokines
what immune response (Th1 or Th2) predominates if children are not exposed to infections early Th2 - asthma is more likely
patients with what problems often experience intrinsic/idiopathic asthma those with nasal polyps or sinusitis
what is the most common asthma trigger exercise
when is strenuous exercise particularly likely to trigger asthma cold weather
what drugs/classes were said to trigger asthma (2) 1) NSAIDs; 2) aspirin
what else are asthma triggers (list) pollen, dander, mites, cigarette smoke, sulfites (preservatives) food coloring, chemicals, cleaners
define: asthma asthma is a narrowing of the bronchi due to an underlying chronic inflammatory disorder
what cells play a role in the inflammation of asthma (list) mast cells, eosinophils, T-cells, macrophages, neutrophils, and epithelial cells
what are the three important featuers of asthma 1) chronic airway inflammation; 2) airway hyper-reactivity; 3) airflow obstruction
what spirometry measurements are relevant to asthma (3) 1) FEV1 (forced expiratory volume in one second); 2) FVC (total volume expired from one expiration); 3) PEFR (maximum flow rate during forced expiration)
how can one test the reversibility of an obstructive lung condition (test and result) perform spirometry before and after inhaling a short-acting bronchodilator - one should see an increase of 12% or 180 ml in FEV1 after inhaling the drug - patients with asthma are hyper-responsive to these stimuli
who is spirometry not good for (3) 1) young; 2) very old; 3) very sick
what does PEFR measure diurnal variation in airway obstruction - indicator of asthma control
what worsens hyper-responsiveness to irritable stimuli in asthma patients exposure to allergen
for diagnosis, what test is done, related to hyper-responsiveness asthma patients are challenged with irritable stimuli and fall in FEV1 is measured
what are children challenged with, and adults challenged with children: exercise; adults: bronchoconstrictor (histamine, methacholine)
what measurement is obtained in adults, besides FEV1 the amount of bronchoconstrictor needed to reduce FEV1 by 20%
how is sputum induced for the sputum test by inhalation of hypertonic saline
what is done with the sputum analyze the inflammatory cells in the airways
what cells are predominant in normal individuals (2) 1) macrophages; 2) neutrophils
in asthma patients, what inflammatory cells will be most increased eosinophils (and also neutrophils, sometimes)
what drug, and type of response, is increased eosinophilia associated with good response to corticosteroids
what happens in the acute immediate response intense bronchoconstriction
what causes the late phase reaction prolonged bronchoconstriction
what occurs in the late phase reaction (4) 1) edema; 2) increased mucous secretion; 3) hyper-reactivity; 4) thickening of airway wall
what innervation mediates bronchoconstriction cholinergic nerve (vagal) innervation
what receptors mediate bronchoconstriction adenosine
what receptors mediate bronchodilation beta-2 adrenergic - these are present on bronchial smooth muscle and throughout the respiratory tract
what is the "traditional asthma theory" asthma comes from altered balance between adrenergic/cholinergic stimulation, and is based on the fact that beta-2 agonists as well as cholinergic muscarinic antagonists provide relief
what is evidence against this theory inhibiting beta-adrenergic receptors does not induce bronchial hyper-reactivity or asthma symptoms in normal individuals
what is the role of the vagus nerve it senses allergens and sends a signal to the CNS, which sends a signal back, causing the release of acetylcholine, which binds muscarinic receptors on airway smooth muscle and induces bronchial constriction
what cytokines cause bronchoconstriction (2) 1) IL-4; 2) IL-5
what other mediators cause broncohconstriction (3) 1) histamine; 2) leukotrienes; 3) prostaglandins
what cells do these inflammatory mediators recruit, that are most specifically related to asthma migration and activation of eosinophils
what do T helper cells secrete in response to antigen lymphokines
what is the role of Th2 cells in asthma induce inflammation
what does Th2 cell release that activates eosinophils IL-5
what other cells do Th2 cells activate neutrophils
what do Th2 cells induce B cells to do, related to asthma secrete IgE, which binds to surface of mast cells
what do substances released by eosinophils and neutrophils cause (5) 1) damage to epithelial cells; 2) mucus secretion; 3) hyper-reactivity; 4) bronchospasm; 5) smooth muscle contraction
what two types of cells are most associated with leukotriene release 1) eosinophils; 2) mast cells
at what point does airway remodeling occur after prolonged allergen exposure and long-term airway inflammation
what happens to epithelial cells in remodeling (2) 1) desquamation; 2) disruption
what remodeling change causes increased mucus secretion goblet cell hyperplasia
what cells are recruited in airway remodeling (3) 1) mast cells; 2) T cells; 3) eosinophils
what happens to smooth muscle increaesd thickness due to hyperplasia or hypertrophy
what is deposited in airway remdoeling, and why matrix (collagen) deposition due to increased fibroblasts
what may all of these structural changes eventually cause obstruction may be only partly reversible
what is asthma classification based on, mainly frequency of symptoms
how many classes are there, and what are they called four - "steps"
what is step 1 known as mild, intermittent
how often are symptoms, and what is FEV <2x/week, >80%
what was said about exacerbations brief
what is step 2 known as mild, persistent
how often are symptoms, and what is FEV >2x/week, >80%
what was said about symptoms and exacerbations may affect activity and sleep
what is step 3 known as moderate, persistent
how often are symptoms, and what is FEV daily, 60-80%
what was said about symptoms and exacerbations affect activity and sleep
what is step 4 known as severe, persistent
how often are symptoms, and what is FEV continuous, <60%
what was said about exacerbations frequent
what things are important in management besides pharmacologic therapy (3) 1) reduce exposure to allergens/irritants; 2) monitor lung function (step 3 and 4); 3) patient education
what is done to monitor lung function (2) 1) record daily PEFR; 2) use personal best and danger zones to manage asthma in home (important to decrease hospital admissions)
what is one advantage of aerosol over systemic delivery fewer serious side effects
what % of patients use inhaler devices, and which patient groups do not (2) about 90% (except small children, and elderly)
what size parrticles are deposited in the airway 1-5 um (smaller are inhaled and exhaled, larger deposited in mouth)
what is the use of spacers (2) 1) limits larger particles; 2) limits need to coordinate inhalation with inhaler activation
what other factor affects deposition breathing rate - need slow, deep breath, held for 5-10 seconds
what types of inhalers are used (3) 1) metered-dose inhalers (MDI); 2) nebulizers; 3) dry powder inhalers
which type is most effective all are equally effective and deliver 1-5 um particles
what is a disadvantage of metered dose inhalers contain chlorofluorocarbons as propellants (but are currently changing over to hydrofluoroalkane for environmental reasons)
what are nebulized used for, and in who severe asthma exacerbations
what are two advantages 1) don't require hand-breathing coordination; 2) can be used with face mask for young children and older patients
what are disadvantages (3) 1) requires power source; 2) requires pressurized gas supply; 3) takes longer to administer
what are powders made of that carry drugs in dry powder inhalers (2) 1) lactose; 2) glucose
what are disadvantages of dry powder inhalers (3) 1) high airflow needed to suspend powder, so bad for young and elderly; 2) poweder can be irritating; 3) temperature and humidity can affect its performance
what does activation of beta-2 receptors first cause within the airway smooth muscle cell activation of adenylyl cyclase and increase in cAMP
what does this result in activated protein kinase A
what does protein kinase A cause (2) 1) inhibits myosin light chain kinase; 2) opens K+ channels
what does opening K+ channels lead to muscle relaxation
what other cells do beta-2 agonist affect, and how prevent mediator release from mast cells by inhibiting function of inflammatory cells through upregulation of cAMP
what were these drugs said not to affect, and why they do not decrease hyper-responsiveness, possibly due to desensitization of receptors after prolonged use
how effective are short-acting, inhaled beta-2 agonists, and what are they the DOC for most effective asthma drugs, DOC for acute asthma
how long do they take to work, and how long does effect last work in 1-5 minutes, duration 2-6 hours
by what method(s) are they administered 1) MDI; 2) nebulizer
what inhaled, short-acting beta-2 agonists must we know (3) 1) albuterol (salbutamol); 2) terbutaline; 3) levalbuterol
how does levalbuterol compare to albuterol it is the R-isomer of albuterol (albuterol has both R and S enantiomers, but only the R enantiomer is pharmacologically active)
what is its advantage slightly lower incidence of adverse effects, but no more effective
what are its disadvantages (2) 1) price; 2) requires nebulizer administration
which beta-2 adrenergic agonists can be given orally in slow release forms (2) 1) salbutamol; 2) terbutaline
how does their efficacy compare to inhaled forsm less efficacceous
who are they effective for young children who can't use MDI or are irritated by nebulizer
what other disadvantes do they have (2) 1) more adverse effects; 2) shorter onset of action
how else can these slow-release forms be administered subcutaneous injection
what inhaled, long-acting beta-2 agonists must we know (2) 1) salmeterol; 2) formoterol
which of these drugs may act the soonest, and how quick formoterol - may work in five minutes
what is the duration of these drugs 12 hours
what should these drugs be used for breakthrough attacks, good for controlling nocturnal asthma - not acute attacks
why do they have longer duration they have long side chains that insert into lipid bilayer of plasma membrane and gradually diffuse
what was said about the selectivity of salmeterol 50X more selective to beta-2 receptors than albuterol
what is the dosing regimen for the long-acting inhaled beta-2 agonists twice daily
what is a disadvantage of long-acting inhaled beta-2 agonists mask worsening airway inflammation
what is the consequence of this problem not recommended as monotherapy
what can long-acting inhaled beta-2 agonists be used in conjunction with corticosteroids
what other beta-2 agonists must we know (3) 1) epinephrine; 2) ephedrine; 3) isoproterenol
how can epinephrine be administered (2) 1) inhaled; 2) injected subcutaneously
when does it provide maximum relief, and how long does it last 15 minutes, 60-90 minutes
why is it rarely prescribed more adverse effects (cardiac)
why does it have more adverse effects it stimulates beta-1 and alpha receptors as well as beta-2
what receptors is ephedrine an agonist at both alpha and beta
what does it function as, besides a bronchodilator decongestant
in what way is it used for asthma to prevent mild to moderate asthma
why is it used less extensively now beta-2 agonists are better
what are its adverse effects mentioned (2) 1) insomnia; 2) hypertension
what effect does isoproterenol have, and how is it given potent bronchodilator which is in microaerosol preparation
what side effect may it have cardiac arrhythmias
what effects of the beta-2 receptor were mentioned, besides bronchodilation (4) 1) vasodilation; 2) decreased GI tone; 3) uterine relaxation; 4) hepatic gluconeogenesis
what type of adverse effects arise from beta-1 stimulation cardiac via stimulation of beta-1 receptors on heart muscle - tachycardia, increased contractility, and conduction
what are adverse effects like for inhaled beta-2 agonists uncommon
what skeletomuscular adverse effect arises from oral/IV beta-2 agonists muscle tremor
how can muscle tremor be decreased starting with low doses
what CNS adverse effects arise from oral/IV beta-2 agonists (3) 1) nervousness; 2) restlessness; 3) anxiety
what cardiac adverse effects arise from oral/IV beta-2 agonists (4) 1) tachycardia; 2) palpitations; 3) arrhythmias; 4) angina
which oral/IV beta-2 agonist produces less cardiac effects than some other drugs albuterol
what drugs, if coadministered, increase cardiac adverse effects MAOIs
what additional adverse effects may MAOIs cause nausea/vomiting
why is overutilizing beta-2 agonists dangerous prolonged use may be associated with near-death from asthma - overuse associated with worsening
what criteria determines whether a patient requires more aggresssive anti-inflammatory therapy if they use the inhaler over 3x/day
what underlying mechanisms does long-term use of beta-2 agonists result in (2 problems) 1) downregulation of receptors; 2) increased hyperreactivity
what should be used to monitor the disease daily PEFR
what other misuse of beta-2 agonists has caused death using a long-acting beta-2 inhaler to treat an acute attack
what is the MOA of anticholinergic agents inhibit muscarinic (M3) acetylcholine receptors, blocking contraction of airway smooth muscle
how does bronchodilation compare to beta-2 agonists bronchodilation is slower and less intense - use has declined with advent of beta-2 agonists
what bronchoconstrictor stimuli were anticholinergics said to protect against (2) 1) dust; 2) cold air
what do they not protect against (3) 1) allergens; 2) exercise triggers; 3) inflammatory cells
what anticholinergics must we know (2) 1) ipratropium bromide; 2) triotropium bromide
which is available as a dry powder triotropium bromide
how is ipratropium bromide available inhaler or nebulizer forms
what is ipratropium derived from, and what is the difference between it and its derivative it is a more selective derivative of atropine
which anticholinergic has an advantage, what is it, and what is the magnitude of the advantage triotropium bromide has a 24 hour duration rather than 6 hopurs
why does it have a longer duration it dissociates from receptors more slowly than ipratropium bromide
is the response to anticholinergics consistent among patients no, it is variable
what can anticholinergics be combined with, and what combined form must we know beta-2 agonists - albuterol + ipratropium (combivent)
what is the incidence of side effects with anticholinergic inhalers low, because of little systemic absorption
what adverse effects occur (4) 1) dry mouth; 2) blurred vision; 3) urinary retention; 4) bitter taste
what may these drugs precipitate in the elderly glaucoma
what patients are corticosteroids drugs of choice for for patients who need to use a beta-2 agonist inhaler >3x/week, and who are step 2-4
are they useful for acute attacks, prophylaxis, or both prophylactically only
how long does it take for them to be effective 6-12 hours
why are they administered at ER visits to prevent recurrence after acute attacks
how can they be administered (3) 1) oral; 2) IV; 3) inhaled
how long may it take for maximal improvement to occur Several weeks
what is the mechanism of action of corticosteroids inhibit airway inflammation by binding to the glucocorticoid receptor in cells
what happens when the GR receptor is activated (2) 1) heat shock proteins are released; 2) GR goes to nucleus and binds genes containing GRE element in promoter and affects transcription of inflammatory genes
what is the effect of corticosteroids on smooth muscle activity no direct effect
how do they affect bronchial reactivity by reducing inflammation
how do they interact with beta-2 agonists they restore sensitivity to beta-2 agonists
what is the long term effect of corticosteroids on bronchial reactivity unlike beta-2 agonists, prolonged use reduces bronchial reactivity
what is the effect of corticosteroids on late-phase inflammatory response, and what specific example was given decrease late-phase response, such as scar formation
what is the mechanism of the effect of corticosteroids on inflammation (list of many effects) modulate cytokine/chemokine production, inhibit chemotaxis, prevent leukotriene release, prevent basophil, eosinophil, and leukocyte accumulation in lung tissue
how does effectiveness vary among corticosteroids all are equally effective
which corticosteroids can be given by metered dose inhaler (5) 1) beclomethasone; 2) budesonide; 3) flunisolide; 4) trimacinolone; 5) fluticasone
which of these have a nebulizer formulation (2) 1) budesonide; 2) fluticasone
what corticosteroid is given IV, and for what patients hydrocortisone, for patients with respiratory failure or GI upsets
what other oral-systemic corticosteroid is given, and how long is the treatment course oral-systemic prednisolone for 5-10 days
what local effects can inhaled corticosteroids have, at normal doses (2) 1) voice (loss, hoarseness, weakness); 2) oral candidiasis
at higher doses, what adverse effects can happen (3) 1) suppression of hypothalamic/pituitary axis and adrenal suppression; 2) osteoporosis; 3) cataracts
what can reduce voice effects reduction of dose
what can be done to protect against candidiasis (2) 1) rinse mouth and throat after use; 2) use a spacer (reduces incidence)
what can systemic use of oral corticosteroid cause (long list of adverse effects) fluid retention, weight gain due to increased appetite, osteoporosis, skin bruising (dermal thinning) hypertension, cataracts, diabetes, peptic ulcers, psychosis, susceptibility to infections, HPA suppression and adrenal suppression, inhibition of growth
what is important to do with these drugs to avoid adrenal suppression taper off drug
why are these drugs used, despite all of the adverse effects the small risk of adverse effects is outweighed by the risk of inadequately controlling severe asthma
what type of prophylactic preparation (mixed with corticosteroids) can be used for patients not adequately controlled by steroids alone use of long acting beta-agonist with low to medium doses of inhaled corticosteroids
what example of this combination (name and two drugs used) is available in the US advair - combination of salmeterol and fluticasone
what mast cell degranulation inhibitor is available for all ages cromolyn sodium
which is available for adults only (12 years and up) nedocromil sodium
what is the mechanism of action of these drugs (2) 1) inhibit activation of delayed chloride channels in cell membrane of mast cells and eosinophils, which inhibits their activation; 2) inhibits coughing by inhibiting airway nerves
what other cells was it said to inhibit, and what is the result inhibits eosinophils, preventing inflammatory response to inhaled allergens
what components of asthma were mast cell degranulation inhibitors said to affect (2) 1) reduce bronchial reactivity; 2) inhibit late-phase asthma responses to allergens/exercise
are they effective in acute attacks no - no effect on smooth muscle tone, and do not inhibit bronchospasms
what forms are mast cell degranulation inhibitors given in 1) aerosol spray; 2) nebulizer
what was said about their absorption and excretion poorly absorbed (1%) and excreted unchanged in urine and bile
when does peak concentration occur, and how long does it last occurs 15 minutes after inhalation and last 45 to 100 minutes
how effective are mast cell degranulation inhibitors less effective than corticosteroids - used as alternative to oral or inhaled beta-agonists - use in US is decreasing due to limited efficacy
how common are adverse effects well-tolerated
what effects can occur (6) 1) laryngeal edema; 2) joint swelling; 3) headache; 4) rash; 5) nausea; 5) rarely, anaphylaxis
which drug must we know in this class [anti inflam] obalizumab
what is its mechanism of action, and what does it act upon biological drug - recombinant humanized monoclonal antibody against IgE - binds free IgE so it cannot bind mast cells
what is the bioavailability of obalizumab (%) 60%
how long does it take to reach peak serum levels 7-8 days
how long does it take for the drug to be eliminated 26 days
what are the disadvantages (2) 1) expensive; 2) single SQ injection every 2-4 weeks
who should this drug be given to patients with severe asthma that is not well controlled by standard drugs (corticosteroids + long-acting beta-2 agonists)
what is the incidence of side effects like well-tolerated
what side effects can occur (3) 1) low antibody titers; 2) injection site reaction; 3) anaphylaxis (0.1%); 4) higher frequency of malignancies occur in patients taking it (but not sure that this is due to the drug)
what is secreted from mast cells after activation, but later than histamine, and what is caused in the lungs leukotrienes are secreted - induces SM contraction in airways, but slower rate than histamine
what are leukotrienes synthesized from, and where arachadonic acid in the nuclear membrane of inflammatory cells
what leukotrienes were said to be potent bronchoconstrictors (class) and how potent were they said to be cysteinyl leukotrienes (cysLT) - 1000x as potent as histamine
what leukotrienes belong to this class (cysLTs - 3) LTC4, LTD4, LTE4
so, what induces the secretion of the cysLTs IgE crosslinking
what induces eosinophils to produce cysLTs adhesion, migration
where can these cysLTs be detected in asthma patients (2) 1) bronchoalveolar lavage fluid; 2) urine
what were asthmatics said to be 25-100 fold more sensitive to than non-asthmatics LTD4
what are the effects of leukotrienes, besides potent bronchoconstriction (4) 1) induce vascular leakage; 2) edema of airway wall; 3) stimulate mucus secretion; 4) cause eosinophil chemotaxis
what classes of leukotriene modifiers must we know (2) 1) leukotriene receptor antagonists (LTRAs); 2) leukotriene synthesis inhibitors
what LTRAs must we know (2) 1) zafirlukast; 2) montelukast
what receptor do LTRAs antagonize cys-LT1 receptor
what three things do they block leukotriene action on 1) mast cells; 2) eosinophils; 3) airway smooth muscle
what actions do they inhibit (4) 1) bronchoconstriction; 2) inflammation; 3) edema; 4) leukocyte chemotaxis
what types of asthma are these drugs useful for 1) exercise-induced; 2) nocturnal
what spirometric measurements were they said to improve (2) and how strong is the effect 1) FEV1; 2) PEFR - modest effect
what were they said not to be effective as bronchodilators
are LTRAs used for acute or prophylactic treatment, or both prophylactic
what % of patients will not respond 50% - many nonresponders
how efficaceous are these drugs considered to be, and when are they used not as efficaceous as moderate to high dose steroids - considered second-line therapy for moderate to severe asthma
what can LTRAs be used in conjunction with (2) 1) beta-agonists; 2) steroids
which can be used for children montelukast
which can be given just once daily montelukast
which has higher bioavailability zafirlukast (90% vs 60%)
which has a longer half life zafirlukast (but effect is not as long, as the parent drug is responsible for effects, rather than the metabolites)
which LTRA must be taken on an empty stomach zafirlukast
why is compliance better with LTRAs than with inhaled steroids don't have to learn to use an inhaler
which one of these drugs has a drug interaction, and what is it zafirlukast may interact with warfarin
which LTRA has fewer adverse effects montelukast
what rare adverse effect may occur Churg-Strauss syndrome
what is Churg-Strauss syndrome, and what is it characterized by (3) a rare autoimmune syndrome characterized by: 1) eosinophilia in lungs; 2) vasculitis; 3) flu-like syndromes
what other adverse effects may occur (5) 1) abnormal liver function tests; 2) nausea/vomiting; 3) GI upset; 4) rash; 5) headaches
what can Churg-Strauss syndrome be treated with corticosteroids
when in asthma treatment might this syndrome arise unmasked when patients reduce or eliminate the amount of oral corticosteroids
what leukotriene synthesis inhibitor must we know zileuton
what is the MOA of zileuton inhibits 5' lipoxygenase and inhibits lipoxygenation of arachidonic acid
what does this in turn inhibit synthesis of all leukotrienes
besides bronchoconstriction, what other function does zileuton inhibit chemoattraction of WBC
which leukotriene was said to be a WBC chemoattractant B4
what is the effects of zileuton on cysLT production (what % blocked) 70% blocked
what is the dosing regimen and mode of administration has to be administered four times daily, orally, as it is a short-acting drug
what is the main side effect associated with zileuton acute liver disease
what test indicates liver toxicity with zileuton elevation of liver enzymes within the first two months
what drug interactions does zileuton have, and how does it affect these drugs 1) theophylline; 2) warfarin - decreases clearance
what precaution should be taken if theophylline is used with zileuton dose should be reduced by half
how often is zileuton used not used in US due to pharmacologic/safety issues
what drug is theophylline related to, and what class are these drugs in closely related to caffeine - both are methylxanthines
what is the main effect of theophylline bronchodilator - smooth muscle relaxant
what other beneficial effects does it have anti-inflammatory
what other effects does theophylline have, that are not related to asthma (3) 1) CNS stimulant; 2) cardiovascular stimulant; 3) decreases peripheral vascular resistance
what are the three mechanisms of action of theophylline 1) blocks adenosine receptors; 2) activates histone deacetylaces; 3) inhibits phosphodiesterase
what is the function of adenosine in asthmatics bronchoconstrictor (but not in normal individuals)
when is adenosine released into the circulation in asthmatics, and what is its effect released into circulation following allergen challenge, and enhances mast cell activation
where were adenosine receptors said to be present (2) 1) SM cells; 2) inflammatory cells
what are the function of HDACs (histone deacetylases) that are blocked by theophylline HDACs bind HAT/CBP complexes, and prevent them from binding to histones and acetylating them
what is the effect represses gene transcription of proinflammatory genes
besides HDACs, what else binds HAT/CBP complexes, and represses these same genes glucocorticoids
what proinflammatory genes were mentioned (2) 1) GM-CSF; 2) IL-8
what drugs does theophylline potentiate the effect of corticosteroids (both inhibit HAT/CBP complexes, and corticosteroids bring HDACs in close proximity to HAT complexes)
what is the effect of theophylline blocking phosphodiesterase (increases 2 substances) 1) cAMP; 2) cGMP
what effects does blockage of phosphodiesterase have on asthma (2) 1) bronchodilation; 2) blocks synthesis/release of inflammatory mediators
how does it block release of inflammatory mediators, and from what cells (2) by inhibition of PDE4 - blocks synthesis/release from mast cells, basophils
how can theophylline be given (2) 1) oral (liquid, coated, sustained release); 2) parenteral
what dosing strategy is used to minimize side effects low dose for three days, with increase if tolerated, and necessary
what slows the rate of absorption (2) 1) food; 2) sleep
what was said about theophylline and pregnant/nursing mothers secreted into breast milk, crosses placenta
how is theophylline eliminated liver
how does half-life of theophylline differ between adults and children longer in adults (8-9 hours) than young children (3-4 hours)
what medical conditions can increase half-life of theophylline (3) 1) CHF; 2) cirrhosis; 3) pulmonary edema
what drug increases its half life erythromycin
what drugs decrease the half-life of theophylline (3) 1) cigarettes; 2) barbiturates; 3) oral contraceptives
why can theophylline be toxic and even fatal if administered too fast cardiac arrhythmias
what can occur prior to signs of toxicity seizures
what are signs of toxicity (list) headache, palpitation, nausea, dizziness, hypotension, tachycardia, restlessness, agiation, emesis
what are behavioral signs of toxicity panic, anxiety, fear
when is theophylline used as an add-on/second line therapy for patients who are not controlled with low dose corticosteroids
what drugs are better, and have fewer side effects beta-2 agonists
how well does theophylline work when combined with corticosteroids (what can it be compared to) works as well as doubling steroid amount
what does cAMP promote in asthma treatment bronchodilation
what drug classes affect cAMP levels, and how does each work 1) beta-agonists increase cAMP by increasing adenyl cyclase activity; 2) PDE inhibitors slow rate of degradation
what drug classes inhibit bronchoconstriction (2) 1) muscarinic antagonists; 2) adenosine antagonists
what definitive evidence exists that alterantive therapies work for asthma none
what alternative drugs were shown to decrease airway resistance 1) oral THC; 2) ivy leaf extract
what alternative therapy may worsen the disease black tea/coffee
what alternative therapy increased FEV1 in one study ginkgo biloba
ASTHMA MANAGEMENT FOR CHILDREN UNDER FIVE for young children, what drugs should be used for quick relief for children under five use short-acting beta-2 agonist inhalers
what is standard treatment for children with step 1 asthma none
what is the standard treatment for children with step 2 asthma low dose corticosteroid (inhaled or nebulizer)
what are alternative treatments for children with step 2 (2) 1) cromolyn; 2) leukotriene antagonist
what are standard treatments for children with step 3 asthma (2) 1) low dose corticosteroid + long acting inhaled beta-2 agonist; 2) medium dose ICS
if these treatments are insufficient for children with step 3, what should be used medium dose ICS + long acting beta-2 agonist
alternatively for children with step 3, what can be combined with medium dose ICS (2) 1) leukotriene antagonist; 2) theophylline
what is standard treatment for children with step 4 asthma 1) high dose ICS; 2) long acting beta-2 agonist
if necessary, what can be added oral corticosteroid syrup
ASTHMA MANAGEMENT FOR ADULTS AND OLDER CHILDREN for adults, what should be used for quick relief short-acting beta-2 agonist inhalers
what is the standard treatment for step 2 asthma low dose ICS
what are alternative treatments for step 2 for adults (4) 1) cromolyn; 2) leukotriene antagonist; 3) nedocromil; 4) sustained release theophylline
what are standard treatments for adults with step 3 asthma (3) 1) low dose ICS + long acting inhaled beta-2 agonist; 2) medium dose ICS; 3) low dose ICS + theophylline; 4) low dose ICS + leukotriene modifier
if needed, what change can be made increase to medium dose ICS + long acting beta-2 agonist
what are alternative treatments for step 3 asthma in adults (2) 1) meduim dose ICS + leukotriene antagonist; 2) medium dose ICS + theophylline
what is the standard treatment for step 4 asthma in adults high dose ICS + long acting beta-2 agonist
what can be added, if necessary oral corticosteroid syrup or tablets long-term
what change should be made in drug strategy if control is maintained when review is made 1-6 months later stepwise reduction
when should a low-dose ICS be added to a beta-2 agonist in mild asthma if the beta-2 agonist is used >3x / week
what less-effective alternative can be added to the beta-2 agonist leukotriene modifiers
if adding a low dose ICS isn't effective, what can be added (2) 1) long-actinb beta agonist; 2) leukotriene modifier
how does the effectiveness of adding a second drug compare to increasing ICS dose tends to be more effective
what other therapy can be considered if low dose ICS isn't effective for mild asthma obalizumab
who can it be used in patients over 12 who are not controlled by other drugs
besides fast-acting beta-2 agonists, what else were said to be helpful for acute exacerbations oral corticosteroids
what is most common cause of asthma death under-treatment
what measurement should be used by patients to monitor asthma PEFR
when should it be monitored AM and PM
how is PEFR characterized (what are categories called) and what does each category represent 1) green zone: 80-100% of personal best; 2) yellow zone: 50-79%; 3) red zone: <50%
what is the strategy if PEFR is in the yellow zone adjust medication if PEFR stays in yellow zone after two puffs of beta-2 agonist
what should be done if PEFR is in the red zone call provider immediately if beta-agonist doesn't bring PEFR out of red zone
what should be the first step when someone enters hospital with asthma exacerbation assess asthma severity - FEV or PEFR, respiratory rate, oxygen saturation
what should be done if there is impending respiratory arrest (5 things - 3 drugs, 2 actions - do all) 1) intubate; 2) give nebulized beta-2 agonist; 3) give anticholinergic; 4) IV corticosteroid; 5) admit to ICU
what should initial treatment be if FEV or PEFR is <50% (severe exacerbation - 2 drugs, frequency of dosing) give by nebulizer every 20 minutes: 1) inhaled beta-2 agonist; 2) anticholinergic
what else should be given if FEV <50% (2) 1) oxygen; 2) oral corticosteroid
what oxygen saturation should be reached 90%
what should be done if FEV or PEFR >50% (2) 1) beta agonist (up to 3 doses in first hour); 2) oxygen to achieve >90% saturation
what should be added if no immediate response oral corticosteroids
what is considered to be a good response to treatments PEFR > 70% for one hour
what should be done if good response is seen send patient home with treatment
what drugs should be given (2) 1) beta-2 agonist; 2) ICS
what is considered to be incomplete response PEFR 50-70%
what should be done admit to hospital, continue treatment
what is considered to be poor response PEFR < 50%
what drugs should be given if response is poor (3) 1) inhaled beta-2 agonist hourly; 2) anti-cholinergic; 3) IV corticosteroid
what other actions shuld be taken (2) 1) admit to ICU; 2) possible intubation
what classes of drugs are used for COPD (4) 1) long acting beta-2 agonists; 2) long acting anti-cholinergics; 3) glucocorticoids; 4) theophylline
what long-acting beta-2 agonists are used (2) 1) salmeterol; 2) formoterol
what long-acting cholinergics is the longer acting tiotropium bromide
which long-acting cholinergic was said to be used for patients with a partially reversible component ipratropium bromide
how effective are glucocorticoids for COPD, what treatment course is used, and when are they most effective some respond to short course -mixed results as to efficacy, except if there is an acute bronchospasm episode
what is theophylline used with in COPD beta-2 agonist
what is the treatment for emphysema in patients with alpha-1-antitrypsin deficiency (AKA alpha-1-antiproteinase) purified alpha-1-antiprotease (prolastin) - IV
Created by: mcafej02