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96 Cards in this Set
- Front
- Back
Diagram of lipid pathways and where drugs act at:
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Which Apoprotein is the one that takes LDL back to the liver?
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ApoB
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If a patient is deficient in lipoprotein lipase what will be elevated?
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Triglycerides
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Treatment goals for lipid therapy:
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Common Lipid Disorders:
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What do the statins do?
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Inhibit HmgCoA, the enzyme and rate limiting step responsible for endogenous production of cholesterol
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Statins:
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How do resins work?
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By binding to bile acids and preventing recycling
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Resins:
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What does Ezetimibe do?
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Decreases dietary absorption of cholesterol; Inhibits intestinal sterol transporter
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Ezetimibe:
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How does niacin work?
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- Reduces hormone sensitive lipase activity
- Decreases free fatty acids & triglycerides - Reduces catabolism of HDL |
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Niacin:
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Can also increase blood glucose levels and worsen insulin resistance in type II diabetics!
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How do fibrates work?
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- Activator of peroxisome proliferator activating receptor- a
- Increases synthesis of adipose lipoprotein lipase VLDL & triglyceride breakdown, fatty acid oxidation in liver - Increase ApoA = increases HDL |
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Fibrates:
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Chart of lipid lowering drug effectiveness:
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Niacin =greatest increase HDL
Statins=greatest decrease in LDL Most favorable increase HDL:LDL ratio = niacin Bile binders & ezetimibe can increase triglycerides |
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Niacin and gemfibrozil
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Lipid treatment exercise:
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Answers:
P1: Familial Combined Hyperlipoproteinemia (metabolic syndrome) - ideal = statin, niacin, fenofibrate P2: Familial Hypercholesterolemia –heterozygous (likely cause : LDL receptor or Apo B) = start on statin (HDL good) P3: Familial Hypertriglyceridemia (likely cause: disorder ApoA-V)= gemfibrozil, niacin (helps bring up HDL) |
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Name the drug class under the boxes:
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Secondary causes of lipid disorders:
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Highlites in the formation of a clot:
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Review of platelet aggregation:
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Aspirin:
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Other antiplatelet agents:
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Heparin:
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Lepirudin:
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Dabigatran: newly approved oral direct thrombin inhibitor
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Warfarin:
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MAO: Competitively inhibits vitamin K epoxide reductase (VKOR) to decrease regeneration of vitamin K supply necessary for these clotting factors
Vitamin K necessary co-enzyme in activating clotting factors Reduces activation of factors II, VII, IX |
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What is the anticoagulant of choice in pregnancy?
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Heparin
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Clot Busters:
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- Streptokinase-less expensive but:
severe allergic rxn in some people. recommended to have corticosteroids available to trt such rxn. - Alteplase, tenecteplase, reteplase: Severe bleeding possible, esp with longer-acting. Reverse excessive bleeding with aminocaproic acid |
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Clinical indications for anticoagulant drugs:
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Aggrenox is aspirin + dipyridamole
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Review of Autonomic (sympathetic and parasympathetic) Nervous System:
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Basic review of autonomic receptors:
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Which receptors increase coronary blood flow? B2 adrenergic receptors
During a stress response, which transmitter exerts the greatest stimulatory effects on B2 adrenergic receptors? Epinephrine |
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More autonomic review:
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Review of receptors and second messengers:
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*Arterial pressure is a function of cardiac output and peripheral vascular resistance
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Baroreceptor reflex to increased BP:
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Baroreceptor reflex to low BP:
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Overview of sympathomimetic agents:
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Effects of NE vs Isoproterenol:
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Why would NE decrease the heart rate? Compensatory baroreceptor effect.
So…isoproterenol does the opposite – it decreases blood pressure so to compensate the heart beats faster. What best explains why ISO produces a drop in blood pressure while producing an increase in HR? Vasodilation via B2 without vasoconstriction via A1 activation. |
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Epinephrine:
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Epinephrine Part 2:
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Epi increases renin release and activates the renin-angiotensin-aldosterone system through activation of which receptor? B1
Adenyl cyclase and cAMP 2nd messenger system is activated and renin levels are elevated |
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Norepinephrine:
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Dopamine:
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α1 effect : Seen only at very high doses = vasoconstriction.
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Alpha agonists:
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*Note: FYI: Selective uses of selective α1 agonists = tend to decrease HR via baroreceptor effect –use of phenylephrine could be a concern in situations where one needs to get BP up but also needs to get the heart pumping (eg…hypovolemic shock after massive blood loss).
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Beta agonists:
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Selective Beta agonist:
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Summary of receptors involved in heart rate and vessel tone:
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α1 =vasoconstrictor increases TPR
α2 offsets = auto-inhibition β1 receptor activation = inotropic & chronotropic β2 receptor activation vasodilates coronory vessels (FEEDs the heart O2)/ offsetting vasodilation LAST NOT LEAST = baroreceptor to keep it all in line….if compensatory systems get “reset” get…hypertension/disease |
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Overview of MOA of Beta Blockers:
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Treatment plans for stage I and II hypertension:
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Blocking the a2 receptor decreases release of what neurotransmitter?
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Norepinephrine
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Hypertension Drugs and thier sites of action:
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Orthostatic hypotension
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Pharmacology of Alpha 2 agonists part 1:
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Practical issues – Per Dr. Asmar, these patients are always trying to drink something (some may overdo it on the volume injested . Dry mouth can a problematic side effect for many patients.
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Compensatory response to anti-hypertensive medication:
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alpha-2 receptor downregulation
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Trimethapan and Reserpine:
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B-adrenergic receptors
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Overview of alpha blockers:
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Adrenergic A1 stimulation without compensatory B2 vasodilation
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Overview of beta blockers:
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Propranolol:
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Propranolol Part 2:
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Beta 1 selective antagonists:
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Mixed Alpha antagonist Beta agonists:
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Why choose these over other beta blockers???
- Beta block/partial β agonist sympathomimetic activity (labetalol): Beneficial to certain patients with compromised cardiac function – less negative inotropic / chronotropic effects. - Less effect on airway resistance Less block of coronary vessels (if CAD) Still relative contraindication in asthma - Possess adverse effects of α1 antagonism |
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What is the initial treatment recommendation for hypertension?
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Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes
If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic. |
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MOA of thiazide diuretics:
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Decrease cardiac preload volume
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Thiazides:
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Adverse effects of thiazide diuretics:
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Notes:
Friendly mnemonic for thiazide adverse if you like it: Thia=“Hy UGLi” (hyperUricemia, Glycemia, Lipidemia) Differential effects on potassium – if patients eat too much salt (common in this country), see thiazide induced hypokalemia. If patient restricts salt intake, thiazides may not cause hypokalemia |
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MOA of loop diuretics:
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Loop diuretics:
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Adverse effects of loop diuretics:
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Potassium sparing diuretics:
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COX inhibition reduces vasodilating prostacyclin
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MOA of ACE inhibitors:
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Low renin levels
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Adverse effects of ACE Inhibitors part 1:
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Adverse effects of ACE Inhibitors part 2:
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Lower aldosterone levels reduce K+ excretion
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Angiotensin receptor blockers:
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Renin Antagonist:
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Therapeutic goals of treatment with vasodilators and calcium channel blockers:
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MOA of calcium channel blockers:
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Bodywide effects of calcium channel blockers:
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Comparison between effects of CCB and CCB-DHP type on vasculature:
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Comparison of CCB types:
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Afterload
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Common uses for CCB's:
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Adverse effects of regular CCB's:
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Adverse effects of DHP CCB's:
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Vasodilators used for severe hypertension:
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Hydrochlorthiazide
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Nitroprusside:
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Hydralizine and Minoxidil:
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*Hydralazine=lmmunologic reaction more common in slow acetylators = Drug-induced lupus-like syndrome –serious. Detect with positive antinuclear antibody test. Symptoms include arthralgia, serum sickness with fever, vasculitis, hemolytic anemia. Dose-dependent, up to 10% of patients after years hydralazine.
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Other indications for vasodilators:
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Metoprolol
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