Allergy and inflammation
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1 Allergy and inflammation 1
2 Allergy Allergic population hyper-producers of IgE consistently increasing western societies: ~20% of general population 2
3 Allergy Allergic population 3
4 Allergy Allergic triggers 4
5 Allergy Allergic triggers abnormal over-reaction to normal exposures 5
6 Allergy Allergic reactions basophils, blood cells tissue cells 6
7 Allergy Allergic reactions 7
8 Allergy Allergic symptoms food allergies mouth/pharynx itching abdominal pain nausea, vomiting BP respiratory symptoms dermatological symptoms airborne allergies runny nose mucus production sneezing itching eyes, nose, throat watering eyes conjunctivitis 8
9 Allergy Allergy types/presentations allergic rhinitis inflammation of nasal mucous membranes allergic conjunctivitis atopic eczema/contact dermatitis anaphylactic reaction (shock) asthma 9
10 Allergy Allergic rhinitis local exposure to allergen (inhaled) interaction with mast cells release of hisatmine, leukotrienes, chemotactic factors local edema, cellular infiltration, mucosal thickening signs and symptoms of allergic rhinitis sneezing, nasal irritation, watery nose, congestion 10
11 Allergy Allergic rhinitis allergic rhinitis asthma 11
12 Allergy Non-pharmacological Tx 12
13 Allergy Non-pharmacological Tx avoiding/minimizing exposure to allergen immunotherapy = desensitization ( IgE, IgG) 13
14 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 14
15 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 15
16 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) block histamine binding to H 1 receptors most effective vs. sneezing and watery nose ineffective vs. congestion oral/nasal administration 1 st generation: additional anticholinergic properties and CNS ADEs 2 nd generation: less anticholinergic/cns ADEs, longer action 16
17 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) - 1 st generation chlorpheniramine (Ahiston, Acamol-Tsinun, Dexamol-Cold ) diphenhydramine (various combination products) hydroxizine (Otarex ) anticholinergic properties: - sedation, drowsiness, dry mouth/eyes, urinary hesitance CNS effects (lipophillic): - memory, confusion, motor function 17 - children, rare: stimulation
18 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) - 2 nd generation cetirizine (Zytrec, Histazine ) loratadine (Lorastine ) desloratadine (Aerius ) metabolites: less CNS ADEs than parent? fexofenadine (Telfast ) (terfandine metabolite) azelastine (Rhinolast ) - spray (antiinflammatory: vs. congestion; rapid onset: rescue ; bitter taste) 18
19 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) - 2 nd generation lesser anticholinergic effects (dry eyes) less CNS penetration (lipophobic): less/non-sedating less effective against congestion (vs. INCs) 19
20 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 20
21 Allergy Pharmacotherapy - allergic rhinitis α-adrenergic agonists (AAAs) nasal decongestants, sympathomimetics phenylephrine (combinations: Alnase, Vibrocil, Sinaf ) oxymetazoline (Alrin, Rhinoclir ) xylometazoline (Otrivin ): long-acting pseudoephedrine (Sinufed, various combinations), 21
22 Allergy Pharmacotherapy - allergic rhinitis α-adrenergic agonists (AAAs) vasoconstrictors: reduce edema, congestion mostly intranasal use (pseudoephedrine - oral) pseudoephedrine: additional beta-agonist effect: bronchial relaxation, HR AAA phenylephrine xylometazoline pseudoephedrine duration 0.5-4hr 10hr 6-8hr frequency 4-6/day 2/day 2-4/d 22
23 Allergy Pharmacotherapy - allergic rhinitis α-adrenergic agonists (AAAs) ADEs: limited with intranasal administration; potential: - CNS effects: headache, insomnia, excitability - BP, HR - local effect: dryness, irritation, itching PD DDIs (low probability with local administration) 23
24 Allergy Pharmacotherapy - allergic rhinitis α-adrenergic agonists (AAAs) high dose/prolonged use down-regulation of local α 1 receptors loss of pharmacological effect rebound congestion 24 rhinitis medicamentosa
25 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 25
26 Allergy Pharmacotherapy - allergic rhinitis Intranasal corticosteroids (INCs) fluticasone (Flixonase, Allegro ) mometasone (Nasonex ) budesonide (Nasocort ) betamethasone (Betnesol ) 2 nd generation 1 st generation 3 rd generation 26
27 Allergy Pharmacotherapy - allergic rhinitis Intranasal corticosteroids (INCs) inhibition of allergic inflammation advanced INCs (mometasone, fluticasone): lipophilicity systemic bioavailability (<2%) systemic adverse effects 27
28 Allergy Pharmacotherapy - allergic rhinitis Intranasal corticosteroids (INCs) inhibition of allergic inflammation 1998 meta-analysis: significantly greater relieve of congestion, nasal discharge, sneezing, nasal itch, postnasal drip, and total nasal symptoms than oral antihistamines. ADEs: - systemic - rare - local - irritation, itching, dryness, burning sensation once-daily: prefer at night 28
29 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 29
30 Allergy Pharmacotherapy - allergic rhinitis Cromolyn/nedocromil mast-cell stabilizers effective only as prevention/prophylaxis - prior to allergy season - prior to exposure to known allergen in mild cases may be corticosteroid-sparing (young children) frequent dosing required (3-4/day) main advantage: safety (children, pregnancy, elderly) 30
31 Allergy Pharmacotherapy - allergic rhinitis H 1 -recpetor blockers (antihistamines) α-adrenergic agonists (AAAs) intranasal corticosteroids (INCs) cromolyn/nedocromil leukotriene modifiers 31
32 Allergy Pharmacotherapy - allergic rhinitis Leukotriene modifiers mainly effective vs. congestion useful in patients - intolerant of intranasal administration - with concomitant asthma 32
33 Allergy Pharmacotherapy - allergic rhinitis Therapeutic considerations INCs usually 1 st -line: superior efficacy vs. all symptoms antihistamines ineffective vs. congestion 2 nd -generation ( non-sedating ) safer than 1 st generation AAAs for short-term use only cromolyn ineffective for acute relief leukotriene modifiers: limited data combination products 33
34 Allergy Pharmacotherapy - allergic rhinitis Therapeutic considerations - special populations population 1 st -line 2 nd -line 3 rd line children <3yr cromolyn 2 nd -gen. AH INC concomitant asthma leukotriene modifier elderly INC 2 nd -gen. AH pregnancy cromolyn 2 nd -gen. AH (budesonide?) AH - antihistamine; INC - intranasal corticosteroid 34
35 Allergy Pharmacotherapy allergy DRUGS FOR EXAM chlorpheniramine loratadine oxymetazoline pseudoephedrine (fluticasone) (cromolyn) (montelukast) 35
36 Anti-inflammatory drugs 36
37 Inflammatory process 1. stimulus (cut) 2. Initial local vasoconstriction( blood loss) 3. vasodilation, local immune/inflammatory reaction (heat, redness) 4. swelling and pain 5. damage repair, inflammatory response gradually subsides 6. healing 37
38 Inflammatory process calor dolor rubor tumor 38
39 Inflammation - presentation 39
40 Prostaglandins in inflammation COX unrelated to leukotriene production 40
41 COX-1 vs. COX-2 41
42 Anti-inflammatory drug classes classical NSAIDs COX-2 inhibitors leukotriene modifiers corticosteroids (Olga ) 42
43 Classical NSAIDs inhibition of COX enzymes decreased PG synthesis suppression of inflammatory processes 43
44 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) 44
45 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) prototypic NSAID synthesized 1853, introduced as Aspirin 1899, mechanism elucidated
46 Allergy Acute allergic inflammation COX active site Ser OH acetylsalicylic acid (aspirin) COOH O O C CH 3 Acetyl group attacks Ser hydroxyl residue Ser O C O CH 3 46 Acetylated COX [INACTIVE]
47 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) acetylsalicylic acid + COX salicylate + acetyl-cox acetyl: irreversible binding 47
48 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) acetylsalicylic acid + COX acetyl + salicylate-cox acetyl group salicylate salicylate: reversible binding 48 probably plays a minor role in salicylate PG-inhibition effect
49 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per action site anti-inflammatory effect: peripheral target sites inhibition of PG-mediated inflammatory cascade inflammatory process PG release inflammation: pain, swelling, heat, redness 49
50 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per action site antipyretic effect: central thermoregulation infection, inflammation, hypersensitivity elevated by pyrogens reset by aspirin inhibition of PGE2 synthesis and release 50
51 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) resultant effect varies per site analgesic effect: peripheral sites inflammatory process PG release histamine, bradykinin, other mediators 51 sensitization of sensory nerve endings
52 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) undesired effects: respiratory: elevated CO 2, increased ventilation (high-dose: respiratory alkalosis; toxic doses: respiratory acidosis) GI: increased gastric acid secretion, nausea, vomiting (PGs gastric acid secretion and secretion of protective mucus) kidney: Na + /H 2 O retention, edema, hyperkalemia (PGs regulate and maintain renal blood flow) 52
53 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) undesired effects: platelets irreversible aggregation inhibition bleeding complications 53
54 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) PK/PD: oral administration (food, fluids) peak: min platelets inactivation evident: 1hr irreversible inactivation long PD T 1/2 non-cyp hepatic metabolism renal excretion 54
55 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) additional ADEs: dermatological Reye s syndrome (<15yr) [?] hypersensitivity (allergic) reactions tinnitus/hearing loss hepatotoxicity (reversible) rebound headache in chronic use vs. headache 55
56 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) salicylism: Mild Moderate Severe headache, drowsiness, dizziness, tinnitus/hearing loss thirst, visual impairment, uncontrolled hand movements seizures, hallucinations, severe nervousness, excitement, confusion, wheezing/shortness of breath, unexplained fever 56
57 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) lethal 150 severe vasomotor collapse, coma, dehydration intoxication 100 mild tinnitus, central hyperventilation salicylate plasma concentration 57 mg/dl anti-inflammatory analgesic, antipyretic, antiplatelet
58 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) DDIs: PD other drugs affecting renal function other NSAIDs other drugs affecting platelets/coagulation hypoglycemics ( insulin secretion) corticosteroids ( salicylate clearance) antihypertensives (sodium/water retention) SSRIs/SNRIs (antiplatelet effect) 58
59 Classical NSAIDs Aspirin (acetylsalicylic acid, ASA) place in therapy diminishing use as antipyretic/analgesic (safety) other salicylates used for several inflammatory states (such as rheumatoid arthritis, inflammatory bowel disease) local use vs. cutaneous inflammation (methyl salicylate) 59
60 Classical NSAIDs Other NSAIDs propionic acid derivatives: - ibuprofen (Nurofen, Advil, Adex,Artofen ) - naproxen (Narocin, Naxyn, Point ) acetic acid derivatives: - indomethacin (Indomed, Indocin, Indovis ) - diclofenac (Voltaren, Abitren ) 60
61 Classical NSAIDs Other NSAIDs oxicams: - piroxicam (Brexin, Feldene Gel ) - norloxicam (Xefo ) naphthylalkylanone: nabumetone (Relifex, Nabuco ) pyranocarboxylic acid: etodolac (Etopan ) nimesulide (Mesulid ) 61
62 Classical NSAIDs Other NSAIDs mechanism: similar to that of aspirin - reversible binding to COX - differing COX-1/COX-2 selectivity 62
63 aspirin Classical NSAIDs Other NSAIDs simple vs. time-dependent competition irreversible binding COX competitive binding ibuprofen naproxen piroxicam simple competitors tight binding, slow self-dissociation arachidonic acid 63 time-dependent competitors diclofenac indomethacin
64 Classical NSAIDs Other NSAIDs potent anti-inflammatory effect effective antipyretics relatively mild analgesic effect 64
65 Classical NSAIDs GI toxicity presentation frequency minor endoscopic lesions 65% symptomatic 3-6mo 1% ulcer, bleeding, perforation 1yr 2-4% probably safer: nabumetone, etodolac, oxicams 65
66 Classical NSAIDs GI toxicity local effect (acidity) GI TOXICITY systemic effect (COX inhibition) nabumetone (non-acidic prodrug) increased COX-2 selectivity 66
67 Classical NSAIDs T 1/2 NSAID specific ADEs effect of effect of short ibuprofen indomethacin aseptic meningitis GI/CNS effects dig, warf, Li, Li diuretics furosemide anti-htns intermediate diclofenac etodolac naproxen LFTs --- pulmonary infiltrates warf, dig, Li, hypogly dig, Li warf, Li, ACEIs diuretics diuretics --- long nabumatone piroxiacm warf, Li diuretics diuretics 67 dig - digoxin; warf - warfarin; Li - lithium; hypogly hypoglycemics; PK PD
68 Classical NSAIDs Choosing an NSAID indication clinical data (evidence-based) ADEs/DDIs patient factors cost trial and error similar properties - varying effects 68
69 Cyclooxygenase pathway 69
70 COX-1 vs. COX-2 70
71 COX-2 selectivity 71
72 Selective COX-2 inhibitors celecoxib (Celebra, Celcox ) etoricoxib (Arcoxia ) rofecoxib (Vioxx ) valdecoxib (Bextra ) 72
73 COX-2 selectivity is relative some NSAIDs are more COX-2 selective than COX-2 selective inhibitors 73
74 Selective COX-2 inhibitors etoricoxib oral administration, good absorption heaptic CYP metabolism mostly-renal clearance T 1/2 ~ 22hr (once-daily) minor GI ADEs, dizziness, peripheral edema, BP DDIs - lithium, theophylline levels - warfarin effect - anti-htn effect of diuretics, ACEIs 74
75 Selective COX-2 inhibitors similar efficacy to that of NSAIDs main advantage: decreased GI toxicity other ADEs: generally similar to NSAIDs no anti-platelet effect CV risk: small BP increase, edema, renal effects caution if combined with aspirin (CHD/CVA prevention) 75
76 Selective COX-2 inhibitors some COX-2 selective inhibitors withdrawn: - rofecoxib (cardivascular/renal toxicity in long-term use) - valdecoxib (cardivascular/renal toxicity in short-term use, severe skin reactions) [ - nimesulide (hepatotoxicity) ] 76
77 Selective COX-2 inhibitors some COX-2 selective inhibitors withdrawn: an over-simplification COX-2 NSAIDs COX-1 complex, dynamic inter-relations incomplete mechanistic data limited long-term clinical data 77
78 Prostaglandins in inflammation choosing an anti-inflammatory 78
79 Pharmacotherapy anti-inflammatory drugs DRUGS FOR EXAM aspirin naproxen etoricoxib Anti-inflammatory drugs 79
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