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Pharmacology - Coggle Diagram

- - - - Agonist
      - Early phase
      - BD + increased mucous clearance
    - - antagonist
      - Prevents PSNS ACh contraction of SMCs
      - Less effective than B2
      - Inhibits constriction and mucus
  - - - inhibition of immune mediators froom
    - - SABA + extended side chain
    - - Leukotrine activation = constriction of bronchial smooth muscles
    - - Reduces stimulation of mast cells and release of inflammatory mediators
  - - - Activation = bronchodilation
    - - ACh receptors
      - Activation = constriction
        Antagonism = dilation
- - - - Nitroglyceryn
        
        Sublingual
        
        Oral
        
        Transdermal
        
        Converted to NO by liver;
        dilates veins and arteries
        
        NO relaxes SMCs
        
        Low dose
        
        Dilates veins
        
        Decreases venous return
        
        High dose
        
        dilates arteries and veins
    - - Reduce myocardial O2 demand
        by reducing cardiac work d/t negative
        ionotropic effects
    - - Bind reversibly to alpha subunit of L-Ca2+ channels
      - Inhibit Ca2+ movement --> inhibits contraction
      - Nodal and myocardial effects
        
        Smooth muscles of coronary and peripheral muscles
        
        Coronary artery dilation
        
        peripheral arteriole contraction
        
        Systemic decrease in TPR and BP
      - Effects on cardiac conduction
        
        Blocks inward Ca2+ current in SA node.
        
        Decreases automaticity --> decreases HR
        
        Slow AV conduction; prolong AV refractory time
        
        Fewer atrial impulses --> rate of contraction slowed
    - - Tx
        
        VD -> increase O2 supply
        
        Ca2+ blockers; statins
        
        Decrease HR -> decrease O2 demand
        
        Organic nitrates; Ca2+ blockers
    - - Reduces cardiac muscle stiffness
      - Used when other Rx fail
      - Blocks inward Na currents in cardiomyocytes
  - - - -statin
      - Inhibit HMG-coA reductase
        
        rate limiting step in cholesterol synthesis
        
        Reduces mevalonate
        
        reduced LDL-C
        c = cholesterol
      - Effects
        
        Reduce LDL, improve lipid profile
        
        Increased NO production
        
        Antiplatelet
        
        Stabilize plaques
    - - -fibrate
      - PPAR alpha agonists
      - Reduction of inflammation
      - Effects
        
        Large VLDL and TG reduction
        
        modest LDL reductions
        
        modest HDL increases
        
        used when issues d/t DM
      - Contraindication: renal issues
    - - Effects
        
        Cholesterol converted to bile acid by liver, which are then re-absirbed
        BABRs prevent re-absorption of bile acids, and promote excretion
      - SE
        
        ?
      - Used in severe disease
    - - Effect
        
        Inhibits sterol transporter at brush border
        
        blocks ~50% of C absorption
        
        10 - 20% reduction in LDL
      - SE
        
        Malabsorption syndrome.
        Joint pain.
    - - Pro drug. Upstream inhibition of cholesterol synthesis
      - Reduces LDL-C 18% when used with Statins; reduces MIs by 23%
    - - PCSK9 secreted by liver. Degrades LDL receptors when cholesterol too high
        
        Causes increase in serum cholesterol
      - Given as injection x2/year
      - Increases LDL receptors on cell by increasing recycling
  - - - Na channel blocker
      - 1a
        
        disopyramide
        
        Tx for VTac
        
        medium speed dissociation
        
        Slows phase 0
        
        qunidine
      - 1c
        
        Slowest dissociation form Na channels
        
        flecainide
        
        Slow conduction in ventricles
        
        works on tissue and nodes
        
        Prolongs QT and QRS
        
        uses
        
        Afib
        
        Aflut
        
        SVT
        
        contra with HB
      - 1b
        
        Fastest dissociation
        
        limited effect on conduction v elocity
        
        binds active and refractory channels
        
        Greatest effect in depolarized tissue. Limited impact on nodes
        
        lignocaine
        
        Used for MI related ventricular arrhythmia
        
        More specific for voltage gated channels.
        Frequency dependent. Works best with high HR
    - - Beta-2 channel antagonist
        
        reduces HR
      - Blocks sympathetic stim of heart
        
        Depress SA and AV node activity
      - beta 1 selective
        
        Atenolol
        
        Metoprolol
        
        Tx
        
        Post MI
        
        tachyarrhythmias
      - Reduce calcium influx
        
        coralan
      - Negative ionotrope (shorter plateau phase)
    - - K+ channel blocker
      - Prolonged AP by delaying
        repolarization by increasing Na
        channel refractory period
      - amiodarone
      - Sotalol
    - - Ca2+ channel blocker
      - Drugs
        
        Verapamil
        
        Diltiazem
        
        Adenosine
    - - Rx
        
        Atropine
        
        Isoprenaline
    - - Digoxin
  - - - LV Hypertrophy
      - Stroke/MI
      - Endothelial damage
      - Renal Failure
      - Retinal Damage
    - - ACE inhibitors OR ARB
      - CCB
      - Thiazide diruetics
- - - - Increase synthesis of anti-inflammatory proteins
      - decrease synthesis of pro-inf mediators
      - Inhibits PLA2
        
        REDUCES PGD
      - Reduces COX enzyme expression
      - Suppresses Th2
  - - - COX1
        
        Protective prostaglandin
        
        Permanently inhibited by aspirin
        
        inhibits thromboxane = prolongs clotting time
        
        INHIBITORS
        
        IRREVERSIBLY INHIBITED BY ASPIRIN
        COX1 x10 > COX 2
        
        Effects
        
        Anti-platelet
        
        anaglesic
        
        antipyretic
        
        Indomethacin
        COX 1 x7 > COX 2
        competitive/reversible
        
        Effects
        
        Most potent anti inflammatory
        
        10x better analgesic than aspirin
        
        ++ toxicity; cant use in kids <14 and preg
        
        Ibuprofen
        competitive, reversible inhibitor
        
        COX 1 = COX 2
        Slightly COX 2 selective
        
        Analgesic
        Antipyretic
        Menstrual pain analgesic
        RA
        
        Risks: Thrombosis, mild GI irritation
        Well tolerated.
        Safe for children.
        
        Diclofenac
        Competitive
        reversible
        inhibitor
        
        COX 2 > COX 1
        
        Potent NSAID
        ++ pain relief
        
        Longest lasting NSAID
        
        Chronic inflammation. Topical
        
        CVD, GI, Renal, hypersensitivity risks
        
        Naproxen
        competitive reversible inhibitor
        
        COX 1 and 2 Inhibitor 2:1
        
        Good for menstrual pain
        (lasts longer than ibuprofen as well)
        
        Well tolerated. Less SEs. Can increase thrombosis risk
      - COX2
        
        Inflammatory prostaglandin
        
        COX 2 inhibitors
        
        Celecoxib
        
        COX 1: COX2 = 1:30
        
        SE
        
        Stroke, MI
        GI bleeding
        
        CV effects d/t inhibition of PGl2
        leads to platelet aggregation
        
        Inhibition of COX2 reduces PGl2 and PGE2 --> HTN and edema as arterial pressure hemostasis is disrupted
        
        RA and OA
    - - Analgesic
      - Anti-pyretic
      - Anti-inflammatory
    - - Not a traditional NSAID
      - Selective COX 3 inhibitor in CNS
      - Strong anti-pyretic
        Good analgesic for mild pain
        Weak anti-inflammatory
        most well tolerated analgesic
      - Good for those with GI problems.
      - AEs
        
        highly hepatotoxic when overdosed
        
        Chronic use can be hepatotoxic over time
        d/t toxic intermediate
        liver enzymes and bili rises
        Hepatic dmg appears in 2 - 4 days
  - - - PLA generates cytosolic AA
        
        COX 1
        
        PGD + thromboxane
        
        5LP
        
        Leukotriene
        
        COX 2
        
        Inhibitors
        
        Exogenous glucocorticoids
        
        Hydrocortisone
        Prednisolone
        Dexamethasone
        
        Endogenous corticosteroids