Asthma & COPD
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| What is asthma? | hyper-responsive airway (exposed to trigger)
bronchoconstriction
marked airway inflammation
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| Asthma is triggered by? | Antigenic: pollen, smoke, bacteria, viruses, pet dander, mold, fungi
Non-antigenic: cold air, exercise
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| Asthma is what type of reaction? | Type 1 IgE
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| What is the early phase of asthma? | fast, bronchoconstriction of smooth muscle, quick, histamine mediated
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| What is the late phase of asthma? | slow, inflammation, prostaglandins, leukotrienes, IL, TNF, cytokines, edema, takes time for mediators to activate
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| Asthma triggers may also activate what in the respiratory tract? | sensor/pain neurons: Ach, substance P
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| What is the problem with asthma? | constant remodeling, bronchoconstriction, mucus production
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| Activation of vagal output release what neurotransmitter? | Ach (acetylcholine) which in turn activate the PNS: bronchoconstriction and mucus production
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| What is substance P? | released in airways contributing to bronchoconstriction, swelling, painful tissue pain neuron, found in airways
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| How do you treat the effects of PNS-Ach effects of bronchoconstriction and increased mucus production? | anti-muscarinics/anticholinergic
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| What is the drawback of using anti-muscarinics/anticholinergics? | lots of side effects
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| What form of respiratory treatment to use to avoid the anti-muscarinic side effects/systemic reaction? | use an inhaler for asthma patients
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| Acute S&S of asthma? | bronchospasm
air trapping (hyperinflation of lungs, increase CO2, and ph-acidosis)
dyspnea & fatigue of respiratory muscles
hypoxemia
hypercapnia
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| Long-term S&S of asthma? | airway injury
airway remodeling (irreversible)
respiratory failure if severe
status asthmatics: chronic condition of long term untreated asthma
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| Sympathomimetics (B2 selective): Formoterol, terbutaline, metaproterenol, albuterol (salbutamol), salmeterol | mimic SNS: NE
act via B2 receptors to increase cAMP to cause bronchodilation
use w/metered inhaler to target B2 in airways (vasodilation)
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| Why don't we use non-specific beta agonists? adrenaline (epinephrine) isoproterenol | because it will activate alpha1 (vasoconstriction) and beta1 (increase heart rate) which will lead to arrhythmias, stroke HTN
example: Isoproterenol-nonspecific beta1 (increase HR) and B2 (dilate) agonist, Epinepherine-alpha1(vasoconstriction) & B1
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| What are the long acting sympathomimetics? AKA LABA = long acting beta agonists | formoterol, salmeterol, >12hrs, highly lipophilic, dissolve in smooth muscle cell membranes, use with a corticosteroid to stop both inflammation (steroid) & bronchoconstriction (sympathomimetics)
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| What are the short acting sympathomimetics? | terbutaline
metaproterenol
albuterol (salbutamol)
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| What is the problem with long acting sympathomimetics if used alone? | long acting sympathomimetics AKA LABA, will cause constant remodeling, slow onset, long term changes, status asthmatics when used alone
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| Can you use short acting sympathomimetics with a steroid? | yes
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| Beta 2 receptors are found where? | lungs, liver, skeletal muscles, kidneys
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| What are the adverse effects of Beta 2 selective agents? | tachyphylaxis, down regulation, densensitization
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| Methylxanthines inhibits PDE (phosphodiesterase, prevents cAMP to break down) = increase cAMP = bronchodilation anti-inflammatory: inhibition of PDE inflammatory cell decrease cytokines release blocks adenosine receptors | theophylline(aminophylline)
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| theophylline(aminophylline) | Methylxanthines
inhibits PDE (phosphodiesterase, prevents cAMP to break down) = which causes cAMP to rise = increase cAMP = bronchodilation
anti-inflammatory: inhibition of PDE inflammatory cell decrease cytokines release
blocks adenosine receptors
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| Sympathomimetics (B2 selective) | Formoterol, terbutaline, metaproterenol, albuterol (salbutamol), salmeterol
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| Formoterol, terbutaline, metaproterenol, albuterol (salbutamol), salmeterol | Sympathomimetics (B2 selective)
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| Theophylline is found in what foods? | caffeine, ephedrine, lobella, theobromine
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| Theophylline can be given in what form to reduce systemic effects? | powder
inhaler
gets absorbed pretty well in bloodstream
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| Adenosine in the airways causes? | bronchoconstriction
increased release of histamine from mast cells
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| Adenosine is blocked by? | theophylline (methylxanthine)
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| The side effects of Methylxanthine (theophylline) of CNS? | CNS: mild stimulation, insomnia (like caffeine), nervousness & tremor at higher doses, seizures & convulsions & death with overdose
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| The side effects of Methylxanthine (theophylline) of Cardio? | Cardio: ST, increase cardiac output, possible arrhythmia in sensitive individuals, increase heart rate (chronotropic), increase force of contraction (inotropic), tachycardia
GI:
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| The side effects of Methylxanthine (theophylline) of GI? | stimulates secretion of gastric acid and digestive enzymes; this will be a problem for ulcer and GI patients: GERD, PUD
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| The side effects of Methylxanthine (theophylline) of Kidneys? | weak diuretic like caffeine
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| Monitoring theophylline? | narrow therapeutic index
liver metabolized
half-life 3-16 hrs
dosing requires monitoring blood levels
10-20mcg/ml
penetrates CNS
limited use
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| Anti-muscarinic Agents: Atropine, Ipratropium Bromide lots of side effects | inhibits bronchoconstriction of Ach at muscarinic receptors M3
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| inhibits bronchoconstriction of Ach at muscarinic receptors M3 | Anti-muscarinic Agents:
Atropine, Ipratropium Bromide
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| Atropine | anti-muscarininc, bronchodilator at low doses but cardiac effect with increasing blood levels
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| Side effects of anti-muscarinic? | dry mouth, difficulty swallowing, thirsty, dilation of pupils, increase intraocular pressure, hot and flushed skin, dry skin, bradycardia followed by tachy, palpitations, arrhythmias, constipation, urinary retention, CNS effects, sleepy drowsy
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| Ipratropium Bromide | anti-muscarinic, derived from atropine, given by inhaler as a poorly absorbed salt by the airways = less systemic effects, localized, bronchodilator, doesn't cross BBB, stays topically in airways, doesn't reach high levels to effect heart/CNS
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| Can you use Ipratropium Bromide with an Beta 2 agonists? | yes to enhance the effects of bronchodilation in more severe asthma patients; less effective than beta 2 agonists
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| Corticosteroids Beclomethansone, Budesonide, Fluticasone, triamcinolone, ciclesonide | block eicosanoid (arachidonic acid) synthesis
broad anti-inflammatory effects
lots of SE
potent
can minimize SE if given topically/aerosol or in other forms that don't get absorbed in blood
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| SE of Ipratropium Bromide? | minimum due to poor absorption from bronchi and inhaled ability to penetrate CNS
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| Beclomethansone, Budesonide, Fluticasone | corticosteroids, highly lipid soluble, delivered via airways with minimal systemic absorption
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| Which 2 corticosteroids do not have extensive first-pass metabolism? | beclomethansone, triamcinolone
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| Which corticosteroids have extensive first-pass metabolism? | Budesonide, Fluticasone, Fluticasone this is good b/c it gets metabolize first before getting to circulation
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| Ciclesonide | cotricosteriod, ester prodrug, activated by esterases in the respiratory epithelium, tightly bound to plasma proteins in circulation = inactive drug to keep in airways to prevent systemic effects
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| What is the benefit of esterases for ciclesonide? | clips the ester linkage to allow drug to stay in tissues/airways
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| Side effects of corticosteriods | Inhaled: RTI,oropharyngeal candidiasis, slows growth in children (long term), osteoporosis (long-term)
Oral (for short term exacerbation): immune suppression, infections, adrenal gland suppression
hyperglycemia, weight gain, GI bleed/ulcers
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| Advair treats both bronchostriction & inflammation | salmeterol + fluticasone
(B2 long acting) (steroid)
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| Symbicort treats both bronchostriction & inflammation | Fomoterol + Budesonide
(B2 long acting) (steroid)
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| Cromylyn and Nedocromil Sodium AKA Mast cell stabilizers | prevents release of inflammatory mediators from mast cells and other immune cells,involves inhibition of Cl- and Ca+ channels, less SE, anti-inflammatory, not a bronchodilator
no effect on airway smooth muscle
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| What effects do mast cells cause? | mast cell granulates
influx of ions (Ca,Cl)
release of histamine
inflammation
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| Test question Which drug does not cause bronchodilation? | mast cell stabilizers
Cromylyn and Nedocromil Sodium
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| Cromylyn and Nedocromil Sodium AKA Mast cell stabilizers | used QID for asthma prophylaxis and exercise-induced asthma, good for exercise induced asthma and childhood asthma r/t less side effects, less effective than inhaled corticosteriods
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| Leukotriene inhibitors | Zileuton: inhibit 5-COX (5-lipoxygenase), block synthesis
Montelukast, Zafirlukast: block receptor (block LT to receptor)
can cause ASA induced asthma (bronchospasm) by blocking cyclooxygenase pathway,increase arachidonic acid=increase leukotrienes
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| Zileuton | leukotriene inhibitor, PO, short half-life so use sustained release formulation, block synthesis (5-COX), SE: hepatotoxicity
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| Montelukast, Zafirlukast | blocks LT to its receptor (blocks receptor),
leukotriene inhibitor, PO, 1-2x per day, liver metabolized (no liver toxicity), minimal SE
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| What is -lukast? | leukotriene receptor antagonist
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| Using Montelukast, Zafirlukast can result in what complication? | Churg-Strauss Syndrome (autoimmune/antigenic/drug induced): systemic vasculitis - when dose of corticosteroid is reduced & pt. starts on LT receptor antagonist
Unmasking: vascuilitis suppressed by the corticosteroids;remove steroid vasculitis will appear
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| Anti-IGE Antibodies: Omalizumab (Xoliar) binds to soluble IgE not bound to mast cell | monoclonal antibody that inhibits IGE to mast cells, do not activate any IGE already bound to mast cells = do not cause degranulation, SQ q.2-4wks, only used w/pts w/IGE-mediated bronchial hypersensitivity (pre-test first)
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| What is the consequence/drawback of using Omalizumab? | it reduces the levels of coticosteriods, SQ, expensive, some antibodies formation against omalizumab
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| Which type of asthma would Omalizumab not be useful for? | non-antigenic : exercise induced, ASA-induced, cold induced asthma
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| Side effects of Omalizumab? | injection site reactions, anaphylactic rxn rare but possible so monitor pt. several hours after injection, some antibody formation against omalizumab
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| What is the role of PNS activation in asthma? | bronchoconstriction and mucus production
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| So how do beta agonist work? | beta agonist bind to 7TMS receptor activate G-proteins which activates AC (adenylyl cyclase) which activates cAMP (causing it to rise) = bronchodilation
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| Can't use corticosteroids for what disease? | RA cause you get give it topically
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| Leukotrienes cause what? | bronchoconstriction, vascular permeability
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