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Asthma

Asthma & COPD

QuestionAnswer
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