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Asthma
Asthma & COPD
| Question | Answer |
|---|---|
| What is asthma? | hyper-responsive airway (exposed to trigger) bronchoconstriction marked airway inflammation |
| Asthma is triggered by? | Antigenic: pollen, smoke, bacteria, viruses, pet dander, mold, fungi Non-antigenic: cold air, exercise |
| Asthma is what type of reaction? | Type 1 IgE |
| What is the early phase of asthma? | fast, bronchoconstriction of smooth muscle, quick, histamine mediated |
| What is the late phase of asthma? | slow, inflammation, prostaglandins, leukotrienes, IL, TNF, cytokines, edema, takes time for mediators to activate |
| Asthma triggers may also activate what in the respiratory tract? | sensor/pain neurons: Ach, substance P |
| What is the problem with asthma? | constant remodeling, bronchoconstriction, mucus production |
| Activation of vagal output release what neurotransmitter? | Ach (acetylcholine) which in turn activate the PNS: bronchoconstriction and mucus production |
| What is substance P? | released in airways contributing to bronchoconstriction, swelling, painful tissue pain neuron, found in airways |
| How do you treat the effects of PNS-Ach effects of bronchoconstriction and increased mucus production? | anti-muscarinics/anticholinergic |
| What is the drawback of using anti-muscarinics/anticholinergics? | lots of side effects |
| What form of respiratory treatment to use to avoid the anti-muscarinic side effects/systemic reaction? | use an inhaler for asthma patients |
| Acute S&S of asthma? | bronchospasm air trapping (hyperinflation of lungs, increase CO2, and ph-acidosis) dyspnea & fatigue of respiratory muscles hypoxemia hypercapnia |
| Long-term S&S of asthma? | airway injury airway remodeling (irreversible) respiratory failure if severe status asthmatics: chronic condition of long term untreated asthma |
| 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) |
| 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 |
| 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) |
| What are the short acting sympathomimetics? | terbutaline metaproterenol albuterol (salbutamol) |
| 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 |
| Can you use short acting sympathomimetics with a steroid? | yes |
| Beta 2 receptors are found where? | lungs, liver, skeletal muscles, kidneys |
| What are the adverse effects of Beta 2 selective agents? | tachyphylaxis, down regulation, densensitization |
| 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) |
| 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 |
| Sympathomimetics (B2 selective) | Formoterol, terbutaline, metaproterenol, albuterol (salbutamol), salmeterol |
| Formoterol, terbutaline, metaproterenol, albuterol (salbutamol), salmeterol | Sympathomimetics (B2 selective) |
| Theophylline is found in what foods? | caffeine, ephedrine, lobella, theobromine |
| Theophylline can be given in what form to reduce systemic effects? | powder inhaler gets absorbed pretty well in bloodstream |
| Adenosine in the airways causes? | bronchoconstriction increased release of histamine from mast cells |
| Adenosine is blocked by? | theophylline (methylxanthine) |
| The side effects of Methylxanthine (theophylline) of CNS? | CNS: mild stimulation, insomnia (like caffeine), nervousness & tremor at higher doses, seizures & convulsions & death with overdose |
| 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: |
| 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 |
| The side effects of Methylxanthine (theophylline) of Kidneys? | weak diuretic like caffeine |
| Monitoring theophylline? | narrow therapeutic index liver metabolized half-life 3-16 hrs dosing requires monitoring blood levels 10-20mcg/ml penetrates CNS limited use |
| Anti-muscarinic Agents: Atropine, Ipratropium Bromide lots of side effects | inhibits bronchoconstriction of Ach at muscarinic receptors M3 |
| inhibits bronchoconstriction of Ach at muscarinic receptors M3 | Anti-muscarinic Agents: Atropine, Ipratropium Bromide |
| Atropine | anti-muscarininc, bronchodilator at low doses but cardiac effect with increasing blood levels |
| 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 |
| 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 |
| 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 |
| 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 |
| SE of Ipratropium Bromide? | minimum due to poor absorption from bronchi and inhaled ability to penetrate CNS |
| Beclomethansone, Budesonide, Fluticasone | corticosteroids, highly lipid soluble, delivered via airways with minimal systemic absorption |
| Which 2 corticosteroids do not have extensive first-pass metabolism? | beclomethansone, triamcinolone |
| Which corticosteroids have extensive first-pass metabolism? | Budesonide, Fluticasone, Fluticasone this is good b/c it gets metabolize first before getting to circulation |
| 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 |
| What is the benefit of esterases for ciclesonide? | clips the ester linkage to allow drug to stay in tissues/airways |
| 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 |
| Advair treats both bronchostriction & inflammation | salmeterol + fluticasone (B2 long acting) (steroid) |
| Symbicort treats both bronchostriction & inflammation | Fomoterol + Budesonide (B2 long acting) (steroid) |
| 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 |
| What effects do mast cells cause? | mast cell granulates influx of ions (Ca,Cl) release of histamine inflammation |
| Test question Which drug does not cause bronchodilation? | mast cell stabilizers Cromylyn and Nedocromil Sodium |
| 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 |
| 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 |
| Zileuton | leukotriene inhibitor, PO, short half-life so use sustained release formulation, block synthesis (5-COX), SE: hepatotoxicity |
| Montelukast, Zafirlukast | blocks LT to its receptor (blocks receptor), leukotriene inhibitor, PO, 1-2x per day, liver metabolized (no liver toxicity), minimal SE |
| What is -lukast? | leukotriene receptor antagonist |
| 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 |
| 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) |
| What is the consequence/drawback of using Omalizumab? | it reduces the levels of coticosteriods, SQ, expensive, some antibodies formation against omalizumab |
| Which type of asthma would Omalizumab not be useful for? | non-antigenic : exercise induced, ASA-induced, cold induced asthma |
| Side effects of Omalizumab? | injection site reactions, anaphylactic rxn rare but possible so monitor pt. several hours after injection, some antibody formation against omalizumab |
| What is the role of PNS activation in asthma? | bronchoconstriction and mucus production |
| 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 |
| Can't use corticosteroids for what disease? | RA cause you get give it topically |
| Leukotrienes cause what? | bronchoconstriction, vascular permeability |
Created by:
cburrows
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