antiarrythmics antihtn adrenergics cholesterol

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antiarrythmics antihtn adrenergics cholesterol
2015-02-07 18:14:33
antiarrythmics antihtn adrenergics cholesterol
antiarrythmics, antihtn, adrenergics, cholesterol
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  1. receptors on heart? affects of binding?
    beta 1 on heart at nodal cells increase hr,increases renal flow also
  2. what would happen if we gave the same amount of epi and norepi?
    norepi would vasoconstrict via a1 receptors while epi will counter and keep in check the vasoconstriction via beta 2 vasodilation
  3. norepi binding
    • primarliy alpha 1 to elevate blood pressure
    • does not bind to b2- no vasodilation, no counteract for norepi just vasoconstriict via a1
  4. epi
    • affects a1,a2,b1,b2
    • cardiac arrest, anaphylaxis
    • low dose-beta vascular predom
    • high dose alpha strongest
  5. dopamine
    • low dose- renal vasodilation D1 receptors
    • high doses- b1 activation( increases HR and contractility) and a1mediated vasoconstirct, increase bp
  6. Name a pure alpha2 agonist – that shuts off sympathetic outflow
    • clonidine, methyldopa
    • presynaptic terminal shuts off norpi- for refractory htn
  7. Name a pure alpha1 antagonist
    prazosin- SIN- vasodilation for HTN, BPH
  8. What is a mixed alpha and beta receptor antagonist?
    • able to stimulate both adrenoreceptors directly and stim NE release from the neuron
    • ephedrine, pseudoephedrine, metraminol
  9. Non-specific beta receptor antagonists vs. beta1 selective – in relation to side effects
    • non sepcific- 
    • b2 causes vasodilation, locate don the lungs also so if we antagonize beta 2 with a non selective beta blocker we will antagonize the lung and they will not be able to breathe and constrict asthma copd pts
    • we like the beta 1 selectives for cardi dx they are more selective
  10. Epinephrine
    • – decreases blood flow to the skin, increases blood flow to the skeletal muscle, increases force and rate of contraction
    • alpha 1 more in the skin, beta 2 a lot in the vascular beds of skeletal muscle
  11. isoproterenol untreated control
    pre treat with alpha1 blocker
    pre treat with beta2 blocker
    • pure beta agonist- stimulate beta receptors
    • no alpha effect, beta receptors still stimulated
    • very little beta receptor stim
  12. epinephrine untreated control
    pretreat with alpha1 blocker
    pretreat with beta2 blocker
    • epi has both alpha and beta stim
    • get more of a beta response
    • get more alpha response
  13. norepi untreated control
    pre treat with alpha1 blocker
    pre treat with beta2 blocker
    • no beta activity
    • get small alpha response
    • get alpha response with no inhibition
  14. Effective Refractory Period – what is it, what part of the action potential does it represent?
  15. Class I anti-arrhythmics –what channel is inhibited
  16. disopyramide
    – negative inotropic effects
  17. Lidocaine
    - Decreases action potential duration
  18. Quinidine
    - Associated with torsades de Pointes, Increase threshold, decrease automaticity, increases action potential duration, vagal inhibition, alpha receptor blocker
  19. Procainamide
    - Reversible lupus syndrome
  20. Class II Drugs What type Major effect
  21. Class III Drugs What type Major effect
  22. Amiodarone: side effect
    • low heart rate, low thyroxin, elevated thyroid stimulating hormone
    • Drug that has class II actions
  23. Class IV Drugs Channel affected Major adverse effect Useful in what arrhythmia and why
  24. Atrial vs Ventricular Action Potential
  25. Non-action potential antiarrhythmic drugs
    • Adenosine
    • Digitalis
    • Atropine
    • Electrolyte solution
  26. CCB- example and arrhythmia
    • verapamil
    • dilitiazam
    • PST and AFib
  27. Effective refractory period- which drugs act on it?
    • 1a greatly increased
    • 1b decreased
    • 1c no change
    • 2 increased
    • 3 greatly increased
    • 4 no effect
  28. Initial treatment for mild hypertension
    is life alterations
  29. Diuretics
    • MOA – vasodilation secondary to Na and water loss
    • Side effect – causes increased plasma lipids (cholesterol)
    • Potassium depletion – how to treat
    • Loop diuretics (furosemide) useful for controlling severe hypertension good for renal pts
  30. k sparing diuretic
  31. Centrally acting drug used for pregnant women
  32. ISA intinsic sympathomimetic activity
    pt with low heart and htn, give them ISA drug like acebutolol can maintain hr because beta blocker will slightly activate beta receptors slightly and block action of strong agonists helps reduce bradycardia
  33. Beta antagonists
    • Cardioselective
    • ISA intinsic sympathomimetic activity– to reduce bradycardia- 
    • Sudden withdrawal can produce arrhythmias
    • Fatigue, lethargy, decreased libido, impotence- affects compliance
  34. Agents used for hypertensive emergencies
    • – sodium nitroprusside- fast on fast off
    • no long lasting effects- does have cyanide- so in high doses may be bad
  35. Calcium Channel Blockers
    • Produce bradycardia and AV block as side effects
    • Verapamil – more cardio
    • Nifedipine – more vascular smooth muscle
  36. Alpha Blocking Agents for refractory pts
    • Cause fall in blood pressure, reflex tachycardia, fainting on initial dose
    • prazasin
  37. Vasodilators
    • Hydralazine
    • Minoxidil – increase fluid retention and may cause hypertrichosis- need to add diuretic prob
    • direct acting to increase cGMP and cause vasodilation
  38. Angiotensin system
    • – reduce peripheral resistance, prevent NaCl and water retention
    • act as a diuretic and vasodilator
  39. ACE inhibitors
    • Reduce AngII production, increase bradykinin production
    • Favorable side effects – dry cough is an annoying side effect
  40. renin inhibitors
    • alskiren
    • lowers bp effectively
    • contra in pregant 
    • causes diarrhea, dry cough, angioedema
  41. Ang Receptor Antagonist
    • Blocks AngII receptors
    • vasodilator
  42. Treatment of Coronary Artery Disease. Primary and secondary
    • If no evidence of coronary artery disease change lifestyle – weight, smoking, exercise, etc
    • Drug intervention – risk plays a significant role in how much to lower cholesterol
  43. Statins
    • HMG CoA reductase inhibitors (decreases synthesis of cholesterol)
    • Highly effective
    • Side effects – liver problems and myopathy
    • Drug interactions based on metabolism by P450 isozyme
  44. Fibrates
    • has fibro in the name
    • Prime action is to decrease triglycerides and increase HDL
    • PPAR transcription factor agonist- increase triglyceride enzyme
    • Increase FA oxidative enzymes such as lipoprotein lipase
    • warnings: increase mortality, hepatoxicity, cholelithiasis, interaction with oral anticoagulants
  45. Bile acid-binding resins
    • (cholestyramine)- decrease ldl
    • Promote secretion of bile acids into intestine
    • Drug interactions
    • Digoxin, warfarin, thyroxin, thiazides, vitamin K
    • May increase triglycerides- may need to add fibrate
  46. Nicotinic acid
    • Cheap, bought over the counter
    • Best drug to increase HDL
    • Decrease mobilization of FFA from adipose tissue by inhibiting lipolysis
    • Lots of side effects- flushing
  47. Cholesterol absorption inhibitors
    • zetia- ezetimide
    • interrupt intestinal absorption
    • Fairly safe
    • Use with statins
    • Coadministration with resin may decrease the bioavailability
    • gi discomfort