Inflammation 4 PDF

Inflammation 4 H. Schaefer, MN See readings in course schedule H. Schaefer, MN 1 IBD H. Schaefer, MN 2 IBD - chronic inflammatory bowel disease: Crohn’s disease & Ulcerative Colitis (UC) risk factors: family hx + triggers (environmental, bacterial) autoimmune effect:...

Inflammation 4 H. Schaefer, MN See readings in course schedule H. Schaefer, MN 1 IBD H. Schaefer, MN 2 IBD - chronic inflammatory bowel disease: Crohn’s disease & Ulcerative Colitis (UC) risk factors: family hx + triggers (environmental, bacterial) autoimmune effect: GI cells targeted by an atypical immune response systemic S&S: fever, anemia, fatigue, wt loss, rash Crohn’s disease: anywhere within the GI tract UC: large intestine Tx: Drugs classes Glucocorticoids Aminosalicylates DMARDs (Methotrexate) stem cell research mesenchymal stem cells H. Schaefer, MN 3 Inflammatory bowel disease (IBD) H. Schaefer, MN 4 Colonoscopy: scope inserted into lower GI for imaging H. Schaefer, MN 5  Drug class: Aminosalicylates drug: Sulfasalazine (Azulfidine, Salazopyrin) PO administered – metabolized in the colon => active metabolites: ○ 5-ASA: salicylate (NSAID) ○ Sulfapyridine: immunomodulary activity (DMARD) Drug: 5-ASA (Asacol, Teva, Mesalamine) ○ Route of administration: PO, rectal ○ NSAID Asthma (aka bronchial asthma) chronic inflammatory airway disorder (not autoimmune) incidence: upto 10% Canadians risk factors: family hx, atopy etiology: noxious stimuli trigger (allergens, particles, infection, stress, ….) reactivity of the airways to the stimuli => chronic hypersensitivity chronic inflammatory changes: epithelial injury high goblet cell activity (mucous) presentation: bronchial inflammation bronchoconstriction mucous production Asthma: challenges 1. chronic bronchial inflammation 2. risk of acute attacks (e.g. sudden extreme inflammatory response) Tx focus: stabilizing the bronchial inflammation & minimizing the number of attacks avoidance of triggers daily ‘maintenance’ drugs to decrease bronchial inflammation: ‘controllers’ correct administration technique (inhalation equipment: inhalers) immunizations to decrease respiratory infection risk (e.g. Prevnar) recognizing the s&s of an attack asthma attack drugs: ‘rescue’ drugs (aka ‘relievers’) 911 if attack persists 8 anti-inflammatory drugs, inhaled: 1st line ’maintenance’ tx prophylaxis against ‘attacks’ Drug class: Glucocorticoids Drugs: Pulmicort (Budenoside), Qvar (Beclomethasone), Flovent (Fluticasone) Adjunct tx: Mast cell stabilizers E.g. Cromolyn (cromoglicic acid) Leukotrine modifiers E.g. Singulair (montelukast) H. Schaefer, MN long term maintenance: biologics (antibodies) Drug: Xolair (omalizumab) SC high affinity for free IgE => decreases expression of mast cell- bound IgE => reduction in mast cell response => reduction in allergic inflammation H. Schaefer, MN 11  Asthma attack: S&S: ○ wheezing, shortness of breath, decreased/no air entry into lung lobes ○ tachycardia ○ anxiety, panic ○ fatigue Patho: limited inspiration + longer expiration phase => trapping of air in alveoli: ○ hyper-inflated lungs with low gas exchange  ‘ventilation-perfusion’ mismatch  hypoxemia & hypercarbia  high pulmonary pressures => increased RVEDP => low CO  Tx: rescue bronchodilator drugs, inhaled Drug class: Beta 2 adrenergic agonists ○ Drug class: Anticholinergics ○ potent, high receptor less potent affinity antagonize PNS ○ stimulate SNS’s B2 slower onset of action ○ fast acting synergy with Beta2 Drugs: adrenergic agonists ○ Salbutamol (Ventolin) ○ Albuterol (Ventolin) ○ Drug: Atrovent ○ Formoterol (Oxeze, (Ipratropium) Turbohaler) Severe attack, ER admission s&s: life threatening O2 Beta2 adrenergic agonists, inhalation (nebulizer) ○ Ventolin Calcium channel blocker (smooth muscle) ○ Magnesium sulfate (MgSO4), IV Anticholinergics, inhalation (nebulizer) ○ Synergy tx Adrenergics/Sympathomimetics, IV ○ Epinephrine (Adrenalin) Glucocorticoids, IV ○ Dexamethasone Adjunct tx: Antihistamines, IV (e.g. Benadryl) Magnesium sulfate (MgSO4), IV Drug classes: electrolyte; enzymatic activator; Calcium channel blocker inhibition of Ca channels in smooth muscle => reduced cellular excitability => bronchodilation stabilization of mast cells & T-cells => decreased pro/inflammatory mediators enhanced release of NO => vasodilation, pulmonary vasodilation = improved gas exchange ○ s/e: hypotension titrate to effect for severe bronchoconstriction anaphylaxis: systemic vasodilation & bronchoconstriction; Tx: ABCs asthma: airway/breathing; Tx: AB H. Schaefer, MN 16