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Pharmacology > Cardiopulm > Flashcards

Cardiopulm Flashcards

1
Q

Drugs used for ischemic heart disease

A

Nitrates (nitrovasodilators)

Calcium channel blockers (non cardioactive and cardioactive)

Beta blockers

Ranolazine

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2
Q

Name nitrates

A

Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

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3
Q

Name calcium channel blockers

A

Non-cardioactive
Amlodipine
Nifedipine

Cardioactive
Dilitazem
Verapamil

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4
Q

Name beta blockers

A

Propranolol
Nadolol
Metoprolol
Atenolol

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5
Q

Ranolazine

A

Ok

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6
Q

What is ischemic heart disease

A

Partial occlusion of coronary artery

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7
Q

Classic angina (angina of effort, stable angina)

A

Occlusion of coronary arteries resulting from the formation of atherosclerotic plaque

  • most common
  • symptoms occur during exertion or stress
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8
Q

Variant angina

A

Episodes of vasoconstriction of coronary arteries

Likely genetic
Symptoms at rest
Much less common than classics angina

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9
Q

Angina

A

Imbalance between oxygen demand of the heart and oxygen supply via the coronary arteries

At rest oxygen demand=supply of oxygen through partially blocked artery
No symptoms

During exercise/stress
Oxygen demand> supply through partially blocked coronary artery
CHEST PAIN

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10
Q

How reduce oxygen demand

A

Decrease cardiac work load

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11
Q

How increase oxygen suppl

A

Increase blood flow through coronary arteries

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12
Q

What are approaches to increase coronary blood flow

A

Coronary artery bypass grafting

Percutaneous transluminal coronary angioplasty (PTCA)

Atherectomy-tip of catheter shears off the plaque
-reoclusion

Stent-expandable tube used as scaffolding to keep vessel open
-drug elating stents (antiproliferative drugs)

Vasodilator

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13
Q

Vasodilator to increase coronary blood flow

A

Useful in vasospastic (prinzmetal) angina

Relieves coronary spasm, restores blood flow to ischemic area, vasodilator

*spasm of proximal right coronary artery and its treatment with a vasodilator

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14
Q

When are vasodilator not useful in treating angina

A

Atherosclerotic (classic ) angina

-coronary steal phenomenon-redistribution of blood to non ischemic areas-associated with the dilation of small arterioles (example-potent arteriolar vasodilator, such as DIPYRIDAMOLE)

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15
Q

How reduce myocardial oxygen demand

A

HR, contractility, preload, afterload

Physic coronary flow

  • isovolumetric contraction
  • ejection
  • diastole
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16
Q

What drugs are used in chronic ischemic heart disease

A

Nitrates
Calcium channel blockers
Beta blockers
Ranolazine

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17
Q

How is vasculature relaxed

A

Release of ENDOTHELIUM derived relaxing factor (EDRF) by Ach
Endothelium is necessary

Endogenous NOS makes NO, a vasorelaxing agent …NO and citrulline activate GC to make cGMP

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18
Q

How are nitrates, NO donors

A

Organiz nitrates cause metabolic activation of NO (do do endothelial cells)
Outside cell then NO into cell

NO activates GC to turn GTP to cGMP In cell

GTP activates protein kinase G->myosin LC dephosphorylation->smooth muscle renalxation

PKG also opens K channels to allow K out and get hyperpolarization and reduced calcium entry

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19
Q

What are the nitrovasodilators

A

Nitroglycerin

Isosorbide

Isosorbide mononitrate

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20
Q

Pharmacokinetics of nitrovasodilators

A

Significant first pass metabolism-high nitrate reductase activity in the liver
-nitrate reductase activity in saturable

Bioavailability with oral route is low

Other routes that avoid first pass metabolism are used

Partially denigrated metabolites may still have activity and longer half lives

Isosorbide mononitrate is a poor substrate of nitrate reductase
-characterized by higher bioavailability

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21
Q

MOA nitrates

A

Unknown enzymatic reaction releases NO (or other active metabolite)
-the role of mitochondrial aldehyde dehydrogenase 2 (ADH2)

Thiopental compounds are needed to release NO from nitrates

Vascular smooth muscle-NO dilate veins and (at much higher concentrations) large arteries

Sensitivity of vasculature to nitrate-induced vasodilationL
Veins>large arteries>small arteries and arterioles
-no “coronary steal” phenomenon
-inhibit platelet aggregation

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22
Q

How do nitrates decrease myocardial oxygen demand

A

Relaxation of smooth msucle

  • dilation of veins major effect)
  • increased venous capacitance
  • reduced ventricular preload

Dilation of arteries-higher concentrations off nitrates are needed, as compared to venous dilation

  • may reduce afterload
  • may dilate large pericardial coronary arteries
  • there is no substantial increase inc ordinary blood flow into ischemic area in atherosclerotic angina
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23
Q

What turns nitrate into NO

A

ADH2 thinks

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24
Q

What does NO do

A

Vascular smooth muscle relaxation

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25
Q

How does NO help variant angina

A

Vascular smooth muscle relaxation->coronary artery dilation->coronary spasm relief

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26
Q

How do nitrates helps angina of effort

A

Vascular smooth muscle relaxation->venous dilation->reduced preload-> decreased O2 demand

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27
Q

Effects of NO beyond vasodilation

A

LDL oxidation

Superoxide radical

Smooth muscle cell proliferation

Platelet aggregation

Monocyte adhesion

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28
Q

Development of tolerance to nitrates

A

Depletion of thiol compounds

Increased generation of superoxide radicals

Reflex activation of sympathetic nervous system (tachycardia, decreased coronary blood supply)

Retention fo salt and water

-increased generation of superoxide radical depletes tissues of NO

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29
Q

What happens when NO joins superoxide

A

Becomes peroxynitrits or H2O2 and O2

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30
Q

Clinical use of nitrates

A

Short acting formulations are used to relieve the angina attack

Long acting preparations may be used to prevent attacks

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31
Q

Short acting nitrates

A

Nitroglycerin
Sublingual-10-30 min
Spray 10-30 min

Isosorbide dinitrate
Sublingual 30-60 min
Spray 90 min

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32
Q

Long acting nitrates

A

Nitroglycerin
Oral 4-8 hr
Ointment 3-6 hr
Patch 8-12 hr

Isosorbide dinitrate
Oral-4-6 hr

Isosorbide mononitrate
Oral 6-10 hr

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33
Q

Adverse effects of nitrates

A

HA (due to meningeal vasodilation; nitrates are contraindicated in intracranial pressure is elevated)

Orthostatic hypotension

Increased sympathetic discharge

  • tachycardia
  • increased cardiac contractility

Increased renal Na and H2O reabsorption

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34
Q

Drug interactions nitrate

A

ED meds (sildenafil, vardenadil, tadafil)

  • inhibit cGMP PDE-5, increase cGMP
  • minimal effects on hemodynamics when administered alone in men with coronary artery disease
  • combination with nitrates causes severe increase in cGMP and a dramatic drop in BP
  • acute MI have been reported
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35
Q

CGMP effect

A

Smooth muscle relaxation—-elective tissue and blood vessels

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36
Q

What calcium channel blockers are used in angina

A

Non cardioactive

  • amlodipine (long t1/2=30-50 hr)
  • nifedipine (short acting (t1/2=4 h)
  • nicardipine (short acting t1/2 2-4 hours)

Cardioactive

  • diltiazem
  • verapamil
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37
Q

How do ca channel blockers work

A

Ca enters cells via voltage dependent ca channels to mediate smooth msucle contraction

Ca binds calmodulin which activates MLCK to cause MLC contraction with actin

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38
Q

What drug class causes most vasodilation

A

Amlodipine -dihydropyridine

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39
Q

What drug causes most decrease inc Adrian contractility

A

Verapamil-phenylalkylamina

Least is amlodipine

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40
Q

What drug causes most decrease in SA node

A

Verapamil and dilitiazem

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41
Q

What drug causes most decrease in conduction of AV node

A

Verapamil and diltiazen

Non amlodipine

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42
Q

How do calcium channel blockers decrease myocardial O2 demand (atherosclerotic angina)

A

Dilation of peripheral arterioles

  • decrease PVR and afterload, decreased bp
  • arterioles affected more than veins (less orthostatic hypotension)
  • dihydropyridines are more potent vasodilator

Decreased cardiac contractility and HR (observed with cardioactive CCB)

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43
Q

How do calcium channel blockers increase blood supply (operates in variant angina)

A

Dilation of coronary arteries relieves local spasm

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44
Q

Major adverse effects of calcium channel blockers

A

Cardiac depression, cardiac arrest and acute heart failure (cardioactive)

Brady arrhythmias, atrioventricular block (cardioactive)

Short acting dihydropyridine CCB-vasodilation triggers reflec sympathetic activation

Nifedipine (immediate release) increases the risk of MI in patients with HTN-slow release and long acting dihydropyridines are better tolerated

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45
Q

Minor AE CCB

A

Flushing, headache, anorexia, dizzy

Peripheral edema

Constipation

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46
Q

Name beta blockers

A

Propranolol
Nadolol
Metoprolol
Atenolol

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47
Q

MOA beta blockers

A

Decreased myocardial oxygen demand

  • decrease in HR leads to improved myocardial perfusion and reduced oxygen demand at rest and during exercise
  • decrease inc interactivity
  • decrease in bp leads t reduced afterload
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48
Q

AE beta blockers

A

Reduce cardiac output
Bronchoconstriction
Impaired glucose mobilization
Produce an favorable blood lipoprotein profile (increase VLDL and decrease HDL)
Sedation, depression
Withdrawal syndrome associated with sympathetic hyperresponsiveness

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49
Q

Contraindications beta blockers

A 
Asthma
Peripheral vascular disease
Type I diabetics on insulin
Bradyarrhythmia and AV conduction abnormalities
Severe depression of cardiac function
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50
Q

Nitrates alone adverse effects

A

HR increase

Contractility increase

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51
Q

AE beta blockers or calcium channel blockers

A

Increase end diastolic volume

Increase ejection time

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52
Q

Combined nitrates with beta blockers or calcium channel blockers

A

None of those bad side effects

Decrease HR
Decrease arterial pressure
Decrease or no change in end diastolic volume

No changecontractility

No change in ejection time

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53
Q

Ranolazine (new) 2006

A

Inhibits late Na current in cardiomyocytes

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54
Q

MOA ranolazine

A

Ischemic myocardium is often partially depolarized

Na channel inc ardiomyocytes is voltage gated

Late Na current is enhanced in ischemic myocardium and brings about Ca overload and depolarizer abnormalities

RANOLAXINE normalizes depolarization of cardiac myocytes and reduces mechanical dysfunction

  • may reduce diastolic tension and compression of coronary vessel in diastole
  • may reduce cardiac contractility and oxygen demand
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55
Q

Does ranolazine affect hr, coronary blood flow and peripheral hemodynamics

A

No

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56
Q

Clinical use of ranolazine

A

Stable angina which is refractory to standard medications

Decreases angina episodes and improves exercise tolerance in patients taking nitrates, or amlodipine, or atenolol

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57
Q

Approaches to treatment of variant angina

A

Prevention of episodes1
CCB are the first choice drugs
If CCB are contraindicated (low BP, bradycardia, AV block), long acting nitrates *

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58
Q

Approach to treat stable (atherosclerotic angina

A

Lipid lowering , lifestyle, immediate release nitrates (SL or spray), antiplatelet therapy (asprin)

BB or CCB or LA nitrate

Add CCB or BB
Low BO: LA nitrate or ranolazine

Consider triple therapy (BB +CCB+LA nitrate or ranolazine)

CABG surgery

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59
Q

What drug classes are used for lipid disorders

A

HMG-CoA reductase inhibitors (statins)

Niacin (nicotonic acid, vitamin B3)

Fabric acid derivatives (fibrates)

Bile acid sequestration (resins)

Cholesterol absorption inhibitors

New-

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60
Q

Name HMG-CoA reductase inhibitors (statins)

A 
Atorvastatin
Fluvastatin
Lovastatin
Pitavastatin
Pravastastin
Rosuvastatin
Simvastatin
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61
Q

Name niacin

A

Niacin

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62
Q

Name fibrinic acid derivatives

A

Fenofibrate

Gemfibrozil

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63
Q

Name bile acid sequestration

A

Cholestyramine
Cholesevelam
Colestipol

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64
Q

Name cholesterol absorption inhibitors

A

Ezetimibe

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65
Q

Name new treatments

A

Lomitapide
Mipomersen
Evolocumab, alirocumab

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66
Q

Dietary management of hyperlipidemia: when do

A

1at! Unless patient has evident coronary or peripheral vascular disease; patients with familial hypercholesterolemias always require drug therapy in addition to diet

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67
Q

How do dietary management

A

Total fat, cruise, and fructose increase vldl; alcohol can cause significant hypertriglyceridemia by increasing hepatic secretion of vldl; synthesis and secretion of vldl are increased by excess calories; during weight loss, LDL and VLDL levels may be much lower than can be maintained during neutral caloric balance (concluding that dietary changes suffice for lipid management can only be made after weight has stabilized for 1 month)

Generally dietary recommendations : limit total calories from fat 20-25% of daily intake, saturated fats to less than 8% of daily intake, cholesterol to less than 200 mg.day; reductions in serum cholesterol range from 10-20% adhering to these recommendations

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68
Q

Name HMG Coa reductase inhibitors

A

Statins

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69
Q

What are statins

A

Most effective agents in reducing LDL levels and best tolerated class of lipid lowering agents

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70
Q

Pharmacokinetics

A

Oral absorption varies from 40-75% with the exception of fluvastatin (almost completely absorbed; statin absorption enhanced bt food)

Big first pass metabolism

Plasma half lives range

Most excreted in bile
Metabolized by CYP3A4(lovastatin, simvastatin, atorvastatin)

Metabolized by CYP2C9 (fluvastatin and rosuvastatin )

Metabolized by 450 (pitavastastin ) limited

Pravastatin not CYP450@ metabolized

Pravastatin

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71
Q

MOA statins

A

Structural analogs of HMG-CoA (initial precursor of cholesterol) and inhibit MHG-CoA reductase, the rate limiting enzyme in cholesterol synthesis; inhibiting de node cholesterol synthesis depletes the intracellular supply of cholesterol, which causes the cell to increase the number of specific cell surface LDL receptors that can bind and internalize circulating LDLs; increased expression of surface LDL receptors reduced circulating LDL levels; can reduce LDL levels 20-55%

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72
Q

Potency statin

A

Atorvastatin=rosuvastatin>simvastatin>pitavastatin=lovastatin=pravastatin?fluvastatin

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73
Q

Therapeutic benefits statins

A

Plaque stabilization, improvement of coronary endothelial function, inhibitoin of platelet thrombus formation, and anti-inflammatory effects

Statins are effective in lowering plasma cholesterol levels in all types of hyperlipidemia; used alone or with resins, niacin or ezetimibe; and are primarily taken night (cholesterol synthesis occurs at night) except the longer acting atorvastatin, pitavastatin, rosuvastatin

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74
Q

Why statin taken at night

A

Cholesterol synthesis occurs at night

Except longer acting atorvastatin , pitavastatin, rosuvastatin

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75
Q

Liver AE statin

A

Elevations of serum aminotransferase activity (up to 3x normal in patients with liver disease or a history of alcohol abuse); levels decrease upon suspension of drug therapy

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76
Q

Muscle AE statin

A

Creatinine kinase activity levels may increase, particularly in patients who have a high level of physical activity; rhabdomyolysis (leading to myoglobinuria) can occur rarely and lead to renal injury; myopathy can occur with monotherapy; increased incidence of myopathy in Athens concomitantly taking statins and fibrates

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77
Q

Statins and war fin

A

Increase warfarin levels

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78
Q

Contraindications statins

A

Pregnant, Lactation or likely to become pregnant,

Liver disease or skeletal muscle myopathy

Kids restricted to those with homozygous familial hypercholestermia and some patients with heterozygous

Caution with other agents that inhibit , compete with or induce CYP 450 enzymes (except pravastatina Nd pitavastatin)

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79
Q

What does niacin do

A

Decrease TG, LDL, LP; increase HDL

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80
Q

Pharmacokinetics niacin

A

Converted to nicotinamide and is incorporated into NAD; well absorbed; distributed to mainly hepatic, renal, and adipose tissues extensive first pass metabolism; half life approximately 60 minutes (2x or 3x daily dosing)

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81
Q

MOA niacin

A

Inhibits the lipolysis of TG in adipose tissue (the primary producer of circulating FFA)

By reducing circulating FFA, the liver produces less VLDL and LDL levels decreased

Catabolic rate for HDL is decreased

Fibrinogen levels are reduced ant tissue plasminogen activator levels are increased

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82
Q

AE niacin

A

Intense cutaneous flush accompanied by an uncomfortable feeling of warmth that occurs after each dose when drug is started or when the dose is increased (asprin taken before niacin or once daily ibuprofen can mitigate the flushing, which is prostagladin mediated)

Pruritis, rash, dry skin or mucous membranes, acanthosis nigricans
Hepatotoxicity (monied liver enzymes0

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83
Q

Contraindications niacin

A

Hepatic disease or active peptic ulcer

Causation with DM-niacin induced insulin resistance, which can cause hyperglycemia —see acanthosis nigricans due to elevated insulin)

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84
Q

Niacin adipose tissue effect

A

Decrease hormone sensitive lipase->decreases plasma FFA

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85
Q

Liver niacin

A

Decreases apoA-i clearance which increases plasma HDL which increases cholesterol delivery-> increased excretion of cholesterol in bile

The decrease in FFA from adipose causes decrease in TG synthesis which decreases VLDL/LDL plasma -> decreases cholesterol delivery to peripheral cells

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86
Q

Peripheral cells niacin

A

Decrease in VLDL /LDL causes decrease cholesterol delivery which

Increased cholesterol removal causes increase HDL plasma which increases cholesterol delivery to liver which increase excretion of cholesterol in bile

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87
Q

Name fabric acid derivatives (fibrates)

A

Gemfibrozil

Fenofibrate

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88
Q

Pharmacokinetics fabric acid derivatives

A

Well absorbed when taken with a meal but less when taken on an empty stomach; gemfibrozil half life is 1.5 hours;

Fenofibrate half life is 20 hours

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89
Q

MOA fabric acid derivatives (fibrates)

A

Agonists for peroxisome proliferator-activated receptor alpha (PPARa), when activated, PPARa binds to DNA, regulating the expression of genes encoding proteins involved in lipoprotein structure and function (lipoprotein lipase, app A-I, app A-II expression is increased and apo C-III is decreased)

Major effect is increased oxidation of FA in liver and striated muscle

Increased lipolysis of TG via lipoprotein lipase while intracellular lipolysis in adipose tissue is decreased

VLDL levels decrease, LAL modestly decrease in most patients (LDL levels can increase as TG are reduced), HDL increase moderately

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90
Q

Why use fibrates

A

Management of hypertriglyceridemias where VLDL predominates, dysbetalipoproteinemia, and hyperTG that results from treatment with viral protease inhibitors

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91
Q

AE GI fibrocartilage acid derivatives

A

Mild GI disturbances are msot common and usually subside; increased the risk of cholelithiasis (due to an increase int he cholesterol content of bile) and should be used with caution in patients with biliary tract disease or in those at high risk (women, obese, native Americans

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92
Q

Fibrates and liver

A

Increased serum transaminases (3x normal)

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93
Q

Muscle fibrates

A

Myositis can occur (evaluate for muscle weakness and tenderness) myopathy and rhabdomyolysis have been reported (increased risk when fibrates and statins combined)

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94
Q

Fibrates anticoagulants

A

Fibrates May potentiation the actions of anticoagulants

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95
Q

Fibrates contraindications

A

Avoided in part it’s with hepatic or renal dysfunctional safely has not been established in pregnant or lactating women

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96
Q

How do fabric acid derivatives work

A

PPARa activation

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97
Q

What is PPARa activation cause

A

Increased apoAI, aIII synthesis in hepatocytes
(Increase HDL)

Decrease apoCIII synthesis in hepatocytes increase lipoprotein lipase expression in muscle vascular beds
(Decrease plasma TG)
Increase FA oxidation in hepatocytes
(Decrease plasma TG)

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98
Q

Name bile acid sequesterants (resins)

A

Colestipol, cholestyramine, colesevelam

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99
Q

Pharmacokinetics bile acid sequestrants

A

Large polymeric cationic exchange resins that are insoluble in water; neighbor absorbed nor metabolically altered by the intestine; totally excreted int he feces

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100
Q

MOA bile acid sequestrants

A

Positively changed compounds bind to negatively charged bile acids (metabolites of cholesterol) and increase bile acid excretion up to tenfold; increased excretion of bile acids enhance the conversion of cholesterol to bile acids int he liver via 7a-hydrocylation (normally controlled by negative feedback via bile acids) the decline in hepatic cholesterol stimulates an increase in hepatic LDL receptor, which enhances LDL clearance and lowers levels; however this effect is partially offset by enhanced cholesterol synthesis caused by upregulation of HMG-CoA reductase (therefore, combined use of statin substantially increases the effectiveness of resins)

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101
Q

Why use bile acid sequestrants

A

Bile acid sequestrants are used to treat patients with primary hypercholesterolemia (reduces LAL by 20%);
Monotherapy or in combination with niacin for treatment of Type II a and type IIb hyperlipidemia; use to relieve pruritus in patients who have bile salt accumulation

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102
Q

AE GI bile acid sequestrants

A

The most common, high doses impair the absorption of fat soluble vitamins ADEK

Impaired absorption of numerous drugs, including tetracycline, phenobarbital, digoxin, warfarin , pravastatin, fluvastatin, asprin and thiazide diuretics

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103
Q

How give resins

A

Additional meds given at least 1 hour before or at least 2 hours after

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104
Q

Contraindications bile acid sequestrants

A

Avoid or use with caution in patients with diverticulitis, preexisting bowel disease, or cholestasis

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105
Q

Name cholesterol absorption inhibitors

A

Ezetimibe

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106
Q

Pharmacokinetics ezetimibe

A

Highly water insoluble
Majority is excreted int he feces

22 hr half life

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107
Q

MOA ezetimibe

A

Selectively inhibits intestinal absorption of cholesterol and phytosterols

Thought to inhibit the transport protein NPC1L1

Effective even in the absence of dietary cholesterol due to inhibition of reabsorption of cholesterol excreted in bile

On average, ezetimibe lowers LDL by 18% and TG by 6% while raising HDL levels slightly 1.3%

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108
Q

Uses of cholesterol absorption inhibitors

A

Treat various causes of elevated cholesterol levels (hypercholesterlmia), homozygous familial hypercholesterolemia
Mixed hyperlipidemia I

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109
Q

AE ezetimibe

A

Avoid with bile acid sequesterants due to impaired ezetimibe absorption

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110
Q

List drugs that decrease LDL most to least

A

Statin>bile acid sequesterants>niacin>fibrates=cholesterol absorption inhibitor

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111
Q

List drug effect of HDL increase most to least

A

Niacin>fibrates>statins>bile acid sequesterants=choesltol absorption inhibitor

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112
Q

Effect of drugs on TG lowering most to least

A

Fibrates>niacin>statins>cholesterol absorption inhibitor>bile acid sequesterants

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113
Q

What is homozygous familial hypercholesterolemia

A

Mutations leading to dysfunctional LDL receptors incapable of taking up LDL fromt he bloodstream; reductase inhibitors rely on functional LDL receptors to achieve a LDL lowering effect and will not work in patients with homozygous familial hypercholestermia

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114
Q

Lomitapide MOA

A

Directly binds to an inhibits microsomes TG transverse protein MTP which is located in the lumen of the endoplasmic reticulum. MTP inhibiton prevents the assembly of apo-B containing lipoproteins in enterocytes and hepatocytes resulting in reduced production of chylomicrons and VLDL and subsequently reduces plasma LDL-C concentrations

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115
Q

CYP3A4 lomitapide

A

Substrate and inhibitor of CYP3A4, causing interactions with a number of drugs; most common AE effects are GI symptoms, increased liver aminotransferase levels, and hepatic fat accumulation (>250000$ a year)

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116
Q

MOA mipomersen

A

Antisense oligonucleotide that targets apolipoprotein B-100 mRNA and disrupts its function; ApoB-100 is the ligand that binds LDL to its receptor and is important for the transport and removal of atherogenic lipids; elevated levels of apoB, LDL-c and VLDL are associated with increased risk of atherosclerosis and cardiovascular diseases

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117
Q

AE mipomersen

A

Injection site reactions (SQ injection one time a week)

Flu like symptoms, HA, elevation of liver enzymes>3 times the upper limit of normal (discontinue if elevations persist or are accompanied by clinical symptoms, such as hepatic steatosis) 176,000 a year

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118
Q

Statin MOA

A

Inhibit HMG-CoA reductase

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119
Q

Effects statin

A

Reduce cholesterol synthesis and upregulate LDL receptors on hepatocytes+modest reduction in TG

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120
Q

Clinical statins

A

Atherosclerotic vascular disease (primary and secondary prevention) + acute coronary disease

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121
Q

PK statins

A

Oral 12-24 hours

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122
Q

Toxicity statin

A

Myopathy , hepatic dysregulation

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123
Q

Interactions statin

A

CYP dependent metabolism (3A4, 2C9) interacts with CYP inhibitors/competitors

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124
Q

Fibrates MOA

A

Peroxisome proliferator activated receptor alpha PPARa agonist

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125
Q

Effects fibrates

A

Decreases secretion of vldl, increases lipoprotein lipase activity, increase HDL

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126
Q

Clinical fibrates

A

HyperTG, low HDL

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127
Q

PK fibrates

A

Oral duration 3-24 hours

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128
Q

Toxicity fibrates

A

Myopathy, hepatic dysfunction

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129
Q

Bile acid sequesterants MOA

A

Binds bile acids in gut and prevents reabsorption and increases cholesterol catabolism and upregulated LDL receptors

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130
Q

Effects bile acid sequesterants

A

Decrease LDL

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131
Q

Clinical bile acid sequesterants

A

Elevated LDL, digitalis toxicity, pruritis

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132
Q

PK bile acid sequesterants

A

Take with meals not absorbed

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133
Q

Toxicity bile acid sequesterants

A

Constipation, bloating, interferes with absorption of some drugs and vitamins

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134
Q

Cholesterol absorption inhibitor MOA

A

Blocks sterol transporter NPC1L1 in intestine brush border

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135
Q

Effects cholesterol absorption inhibitors

A

Inhibits reabsorption of cholesterol excreted in bile and decreased LDL and phytosterols

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136
Q

Clinical cholesterol absorption inhibitor

A

Elevated LAL, phytosterols is

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137
Q

PK cholesterol absorption inhibitor

A

Oral 24 hours

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138
Q

Toxicity cholesterol absorption inhibitor

A

Low incidence of hepatic dysfunction, myositis

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139
Q

Niacin MOA

A

Decrease catabolism of apo AI and reduced VLDL secretion from liver

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140
Q

Effects niacin

A

Increases HDL and decreases LDL

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141
Q

Clinical niacin

A

Low HDL , elevated VLDL, elevated LDL in statin unresponsive or intolerant patients

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142
Q

PK niacin

A

Oral large doses

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143
Q

Niacin toxicity

A

Gastric irritation, flushing, low incidence of hepatic toxicity, may reduce glucose tolerance

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144
Q

PCSK9 humanized monoclonal antibodies MOA

A

Complexes PCSK9

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145
Q

Effects PCSK9 humanized monoclonal antibodies

A

Inhibits catabolism of LDL receptor

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146
Q

Clinical PCSK9 humanized monoclonal antibodies

A

Familial hypercholesterolemia not responsive to oral therapy

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147
Q

PK PSCK9 humanized monoclonal antibodies

A

Parenteral

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148
Q

Cost PCSK9

A

14,000 a year

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149
Q

Toxicity PCSK9 humanized monoclonal antibodies

A

Injection site reactions, nasopharyngitis, flu like, rarely myalgia, neurocognitice and ophthalmologist events

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150
Q

Drug classes used in thromboembolic disorders

A

Parenteral anticoagulants

Oral anticoagulants

Antiplatelet drugs

Thrombocytosis (fibrinolytic) drugs

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151
Q

Name parenteral anticoagulants

A

Indirect thrombin and factor Xa inhibitors

Direct thrombin inhibitors

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152
Q

Name indirect thrombin and factor Xa inhibitors

A

Unfractioned heparin
-heparin sodium

Low molecular weight heparin

  • enoxaparin
  • tinzaparin
  • dalteparin
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153
Q

Name direct thrombin inhibitors

A

Lepirudin
Bivalirudin
Argatroban

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154
Q

What are oral anticoagulants

A

Coumadin anticoagulatnts

Direct oral anticoagulatnts

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155
Q

Name Coumadin anticoagulants

A

Warfarin

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156
Q

Name direct oral anticoagulatns

A

Factor Xa inhibitors
-rivaroxaban
-apixaban
—edoxaban

Direct thrombin inhibitor
-dabigatran

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157
Q

What are antiplatelet drugs

A

Inhibitors of thromboxane A2 synthesis

ADP receptor blockers

Platelet glycoproteins receptor blockers

Inhibitors of phosphodiesterases

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158
Q

Name inhibitors of thromboxane A2

A

Asprin

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159
Q

Name ADP receptor blockers

A

Clopidogrel

Prasugrel

Ticlopidine

Ticagrelor

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160
Q

Name platelet glycoproteins receptor blockers

A

Abciximab

Aptifibatide

Tirofiban

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161
Q

Inhibitors of phosphodiesterases

A

Dipyridamole

Cilostazol

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162
Q

What are thrombocytosis (fibrinolytic) drugs

A

Tissue type plasminogen activator drugs

Urokinase type plasminogen activator

Streptokinase

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163
Q

Name tissue type plasminogen activator drugs

A

Alteplase

Reteplase

Tenecteplase

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164
Q

Name urokinase type plasminogen activator

A

Urokinase

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165
Q

Name streptokinase preparations

A

Streptokinase

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166
Q

Blood clot

A

All clots involve both platelets and fibrin but the degree of involvement of platelet/fibrin in thrombus formation depends not he vascular location

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167
Q

White thrombus (platelet rich)

A

Forms in high pressure arteries and is the result of platelet binding to the damaged endothelium and aggregation with little involvement of fibrin

Pathological condition associated with white thrombi: local ischemia due to arterial occlusion (in coronary arteries: MIunstable angina)

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168
Q

Red thrombus (fibrin rich with trapped RBC)

A

Forms in low pressure veins and in heart; result of platelet binding and aggregation followed by formation of bulky fibrin tails in which red blood cells become enmeshed

Pathological conditions associated with red thrombi: pain and severe swelling, embolism and distal pathology (embolic stroke)

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169
Q

Anticoagulants

A

Regulate the function and synthesis of clotting factors

Used to prevent clots from forming in the venous system and heart (red thrombi)

170
Q

Antiplatelet drugs

A

Inhibit platelet fruition

Primarily used to prevent clots from forming in the arteries (white thrombi)

171
Q

Thrombocytosis

A

Destroy blood clots after they are formed

Re establish blood flow through vessels once clots have formed

172
Q

How do antiplatelet drugs work

A

ADP
TXA2
5-HT increase

173
Q

How do thrombolytics work

174
Q

How do anticoagulants work

A

Intrinsic and eextrinsic _>Xa turns prothrombin into thrombin

175
Q

Indirect parenteral anticoagulants

A

Unfractionated heparin
-heparin sodium

Low molecular weight heparin

  • enoxaparin
  • tinzaparin
  • dalteparin

Synthetic pentasaccharide
-fondaparinux

176
Q

Direct thrombin inhibitos

A

Lepirudin
Bivalirudin
Argatroban

177
Q

MOA indirect thrombin and FXa inhibitors

A

Indirect thrombin and FXa inhibitors-bind plasma serine protease inhibitor antithrombin III

Antithrombin III inhibits several clotting factor proteases, espicially thrombin (IIa), IXa, and Xa

In the absence of heparin, protease inhibition reactions are slow; heparin increases antithrombin III activity by 1000 fold

178
Q

MOA HMW heparin

A

Inhibits the activity of both thrombin and factor Xa

179
Q

MOA LMW heparin

A

Inhibitors factor Xa with little effect not hrombin

180
Q

MOA fondaparinux

A

Inhibits factor Xa activity with no effect not hrombin

181
Q

HMW vs LMW

A

Have practically equal efficiency in several thromboembolic conditions

LMW have increased bioavailability fromt he SC injection site and allow for less frequent injections and more predictable dosing

182
Q

How is heparin given

A

Very hydrophilic, must be given IV or SC

183
Q

What is heparin used to treat

A

Disorders secondary to red (fibrin rich) thrombi and reduce the risk of emboli

Protects against embolic stroke, pulmonary emboli

Administer to patients with DVT, atrial arrhythmias and other conditions that predispose towards red thrombi

Prevention of emboli during surgery or in hospitalized patients (reduce risk of emboli)

184
Q

Heparin looks

A

Prevents clots from forming inc athletes

185
Q

How monitor patients on heparin

A

Activated partial thrombophlebitis time (aPTT)
-measures the efficacy of the intrinsic (contact activation) pathway and a common pathways

  • in order to activate the intrinsic pathway, phospholipids, activator(kaolin or silica) , and Ca are mixed with patients plasma
  • evaluates serine protease factors (II, IX, X, XI, XII) affected by heparin

Anti-Xa assay
-designed to examine proteolytic activity of factor Xa

186
Q

AE heparin

A

Bleeding

Heparin induced thrombocytopenia
-immunogenicity of the complex of heparin with platelet factor 4 (PF4)

187
Q

What to look for in a patient on heparin

A 
Thrombocytopenia (platelet removal by splenic macrophages) 
and thrombosis (platelet aggregation)
188
Q

HIT

A

A systemic hypercoagulable state

Characterized by venous and arterial thrombosis

Relate to the immune response to heparin

189
Q

Treat HIT

A

To discontinue heparin and administer DTI

190
Q

Contraindications heparin

A

Severe HTN
Active tuberculosis
Ulcers of GI tract
Patients with recent surgeries

191
Q

How reverse heparin action

A

Protamine sulfate

192
Q

Indirect factor Xa inhibitors

A

Fondaparinux

193
Q

Fondaparinux

A

Synthetic pentasaccharide

194
Q

MOA fondaparinux

A

Binds to antithrombin to indirectly inhibit factor Xa

  • high affinity reversible binding to antithrombin III
  • conformational change in the reactive loop greatly enhances antithrombin basal rate of factor Xa inactivation
  • acts as an antithrombin III catalyst
195
Q

How is fondaparinux unlike heparin

A

Does not inhibit thrombin activity
Rarely induces HIT
It’s action is not reversed by protamine sulfate

196
Q

Clinical indications for heparin

A

Prevention of DVT

Treatment of acute DVT(in conjunction with warfain)

Treatment of pulmonary embolism

197
Q

MOA direct thrombin inhibitors

A

Direct inhibitoin of the protease activity of thrombin

198
Q

I valentines direct thrombin inhibitors (bind at both active site and substrate recognition site)

A

Lepirudin

Bivalirudin

199
Q

Direct thrombin inhibitos that bind only at the thrombin active site

A

Argatroban

200
Q

Lepirudin

A

Recombinant form of hirudin (which was originally purified from medicinal leeches)

Identical to natural hirudin except for substitution of leucine for isoleucine at the N terminal end of the molecule and the absence of a sulfate group on the tyrosinase at position 63

Irreversible inhibitor of thrombin

201
Q

Bivalirudin

A

A synthetic, 20 aa peptide

Reversible inhibitor of thrombin

Also inhibits platelet aggregation

202
Q

Argatroban

A

A small molecular weight inhibitor

Short acting drug-used intravenously

203
Q

Clinical indications for direct thrombin inhibitors -parenteral

A 
HIT
Coronary angioplasty (bivalirudin and argatroban)
204
Q

AE direct thrombin inhibitors

A

Bleeding (should be used with caution as no antidote exists)

Repeated lepirudin use may cause anaphylactic reaction

205
Q

Oral anticoagulatnts

A

Coumadin
-warfarin

Direct oral anticoagulants
-factor Xa inhibitors
—rivaroxaban
—apixaban
—edoxaban

Direct thrombin inhibitor
-dabigatran

206
Q

Warfarin

A

Most commonly prescribed anticoagulatn in USA

207
Q

MOA warfarin

A

Inhibits reactivation of vitamin K by inhibiting enzyme vitamin K episode reductase

Inhibits carboxylation of glutamate residues by GGCX in prothrombin and factors VII, IX, and X making them inactive

208
Q

What proteins are affected by warfarin

A

Factor II
Hemostasis factors VII, IX, and X
Other proteins that function in apoptosis, bone ossification, extracellular matric formation

Carboxylation of glutamate residues is one of the common mechanisms of posttranslational modification of proteins
-converts hypofunction OA hemostatic factors into functional ones

209
Q

Pharmacokinetics warfarin

A

Two stereoisomers: R and S

S isomer is 3 to 5 fold more potent

210
Q

R warfarin metabolization

211
Q

S warfarin metabolized

212
Q

OH derivatives are pumped out of hepatocytes by ABCB transporter into bile

A

Excreted with bile

213
Q

How administer warfarin

A

Administer orally

100% bioavailability

214
Q

Onset and half life of warfarin

A

12 hour onset delay

36 hour half life

215
Q

99% of warfarin is bound to __

A

Plasma albumin (responsible for its small volume of distribution and a long half life)

216
Q

Why do correct warfarin doses vary widely from patient to patient

A

Significant individual variability based on disease states and genetic make up

Multiple drug interactions

217
Q

Clinical uses warfarin

A

Prevent thrombosis or prevent/treat thromboembolism

A fib

Prosthetic heart valves

218
Q

AE warfarin

A

Teratogenic effect (bleeding disorder in fetus, abnormal bone formation)

Skin necrosis, infarction of breasts, intestines, extremities

Osteoporosis

Bleeding

219
Q

Warfarin dose is titrations based on laboratory testing

A

PT-time to coagulation of plasma after the addition of a tissue factor (TF or factor III)-used for the evaluation of the extrinsic pathway

INR
.9-1.3 normal
.5 high chance of thrombosis
4-5-high chance of bleeding
2-3-range for patients on warfarin
220
Q

PK warfarin

A

VKORC1 (vit K epoxied reductase complex subunit 1)-responsible for 30% variation in dose (low and high dose HaplotypE)

221
Q

Who has high dose HaplotypE warfarin

A

African Americans, more resistant to warfarin

222
Q

Who has low dose HaplotypE warfarin

A

Asian they are less resistant to warfarin

223
Q

___-responsible for 10% variation in dose, mainly among Caucasian patients

224
Q

Warfarin drug interactions PK

A

CYP enzyme induction

CYP enzymes inhibiton

Reduced plasma protein binding

225
Q

Pharmacodynamic warfarin interactions

A

Synergism with other antithrombotic drugs

Competitive antagonism (vit K)

Clotting factor concentration (diuretics)

226
Q

Warfarin a disease states

A

Liver disease (reduced clotting factor synthesis)

Thyroid status

Warfarin and diet

227
Q

What pharmacokinetics increase PT

A

Amiodarone

Cimetidine

Disulfiram

Metronidazole

Fluconazole

Phenylbutazone

Sulfinpyrazone

TMP-SMX

228
Q

Pharmacodynamic increase PT

A

Asprin
Cephalosporins, third gen
Heparin

Hepatic disease hyperthyroidism

229
Q

Pharmacokinetic decrease PT

A

Barbiturates
Cholestyramine
Rifampin

230
Q

Pharmacodynamic decreased PT

A

Diuretics
Vit K

Hypothyroidism

231
Q

Advantages of warfarin

A

Oral administration

Long duration of action

Drug clearance is independent of renal function

Reversal of action strategy has been developed

  • vit k administration usually reverses warfarin action 12-24 hours
  • if more rapid reversal is needed fresh frozen plasma or prothrombin complex concentrate are given
232
Q

Warfarin drawbacks

A

Very high dosing variability, maintaining optimal drug concentration is difficult

This may lead to bleeding complications, such as intracranial hemorrhages

Requires INR monitoring

233
Q

DOAC

A

Oral XA
Rivaroxaban
Apixaban
Edoxaban

Oral IIa
Dabigatran

Parenteral
XA
Fondaparinux LMWH

IIa
Argatroban
Bivalirudin

234
Q

Clinical use of rivaroxaban, apixaban, edoxaban

A

Prevention of thromboembolism

Treat thromboembolism

Prevention of stroke in patients with atrial fib

235
Q

Advantages rivaroxaban, apixaban, edoxaban

A

Given orally

Administered at fixed doses and do not require monitoring

Shown non inferiority compared with warfarin

Rapid onset of action as compared to warfain

236
Q

Drawbacks rivaroxaban, apixaban, edoxaban

A

Excreted by kidneys; dose adjustment is needed in renal patients

237
Q

Dabigatran

A

First oral DOAC approved by FDA

238
Q

Clinical use dabigatran

A

To reduce the risk of stroke and systemic embolism in patients with non valvular atrial fibrillation

Treatment of venous thromboembolism

239
Q

Advantages dabigatran

A

Predictable pharmacokinetics and bioavailability

Fixed dosing and predictable anticoagulant action (no INR monitoring required)

Rapid onset and offset of action
No interaction with P450 metabolized drugs

Antidote approved

240
Q

Antidote dabigatran

A

Idarucizumab-humanized antibody fragment that binds dabigatran with high affinity to prevent dabigatran inhibition of thrombin

241
Q

Disadvantages dabigatran

A

80% renal excretion-may not be suitable in renal patients

242
Q

Antidoes to HMV, LMW heparin

A

Protamine sulfate

243
Q

Antidote to warfarin

A

Vitamin K, prothrombin complex concentrate

244
Q

DOAC-FXa inhibitors antidote

A

Andexanet alfa

245
Q

DOAC-DTI antidote

A

Idarucizumab

246
Q

Heparin blood coagulation tests

A

APTT, anti Xa

247
Q

Warfarin blood coagulation tests

A

PT-based (INR)

248
Q

DOAC -FXa inhibitors blood coagulation tests

249
Q

DOAC -DTA blood coagulation tests

A

Diluted thrombin time (TT)

250
Q

APTT

A

Intrinsic pathway

251
Q

Anti Xa

252
Q

Extrinsic pathway

253
Q

IIa

A

Diluted TT

254
Q

Categories of antiplatelet drugs

A

Inhibitors of thromboxane A2

ADP receptor blockers

Platelet glycoprotein receptor blockers

Inhibitors of phosphodiesterase

255
Q

Inhibitors of thromboxane A2 synthesis

256
Q

ADP receptor blockers

A

Clopidogrel
Prasugrel
Ticlopidine
Ticagrelor

257
Q

Platelet glycoprotein receptor blockers

A

Abciximab
Eptifibatide
Tirofiban

258
Q

Inhibitors of phosphodiesterases

A

Dipyridamole

Cilostazol

259
Q

MOA asprin

A

Inhibiton of cyclooxygenase

Decreased TXA2 production

260
Q

Clinical use of asprin

A

Primary and secondary prevention of a heart attack and other vascular events (ischemic stroke, arterial thrombosis of the limbs resulting in intermittent claudication)

261
Q

AE asprin

A

Peptic ulcer

GI bleeding

262
Q

MOA antiplatelet drugs

A

Blockers of ADP receptors

  • inhibition of AC by a is relieved
  • increased production of cAMP

Inhibitors of phosphodiesterase

  • inhibition of cAMP degradation
  • levels of cAMP in platelets are increased
263
Q

Pharmacogenomics of clopidogrel

A

High variability of clopidogrel action

Related primary to metabolism by CYP2C19 isoenzymes

Nonfunctinal CYP2C19 allele is present in 50% Chinese, 34% african Americans, 25% caucasians, and 19% Mexican Americans

Cytochrome p450 status does not affect the use of other ADPKD receptor antagonists

264
Q

Platelet glycoprotein (GP) IIb/IIIa is an integrins binding to extracellular ligand: fibrinogen, vitronectin, fibronectin, Von Willie Randolph factor

265
Q

Platelet GP receptor antagonists

A

Target Arg-Glu-Asp (RGD) sequence

Prevent binding of ligand to the GP IIbIIIa receptor to inhibit platelet aggregation

266
Q

GP Iib/IIIa antagonists work

A

GP Iib/IIIa receptors

267
Q

What are the GP IIb/IIIa antagonists

A

Abciximab, tirofiban ,eptifibatide

268
Q

Clinical use of antiplatelet drugs

A

Prevention of thrombosis in unstable angina and other acute coronary syndromes

Prevention of ischemic stroke and arterial thrombosis in peripheral vascular disease

In patients undergoing percutaneous coronary angioplasty and stunting

Inhibitors of phosphodiesterase are considered adjunct antiplatelet agents and used in combination with other antiplatelet agents or anticoagulatns

  • dipyridamole with asprin to prevent cerebrovascular ischemia
  • dipyridamole with warfarin in patients with prosthetic heart valves
  • cilostazol is primarily used to treat intermittent claudication
269
Q

MOA thrombolytics drugs

A

Activate endogenous fibrinolytic system by converting plasminogen into plasminogen

270
Q

Plasminogen

A

Plasma zymogen that forms active enzyme upon cleavage of the peptide bond between arg-560 and val-561 by tPA or uPA

271
Q

Plasmin

A

Activate serine protease that cleaves and degrades fibrin and other proteins (fibronectin, laminin, thrombospondin, vWF)

272
Q

Types of fibrinolytic drugs (they alla ctivate plasminogen to plasmin)

A

Tissue type plasminogen activator (tPA)-endogenous protein that cleaves plasminogen, released by endothelium, needs fibrin as coactivator

Urokinase type plasminogen activator (urokinase, uPA)-endogenous protein , produced in kidneys; a human enzyme directly converting plasminogen to plasmin

Streptokinase-protein released by b-hemolytic streptococci, forms the complex with plasminogen, converts it into plasmin by non-proteolytic mechanism

273
Q

TPA tissue type plasminogen activator drugs

A

Alteplase:recombinant human protein

Reteplase:recombinant modified human protein

Tenecteplase:recombinant mutated human protein

274
Q

UPA urokinase type plasminogen activator

275
Q

Streptokinase preparations

A

Streptokinase: purified from bacteria

276
Q

Clinical uses thrombolytics (fibrinolytic) drugs

A

Acute ambolic/thrombotic stroke (within 3 h)

Acute MI

Pulmonary embolism

DVT

Ascending thrombophlebitis

277
Q

Clot in cerebral artery-stroke

A

Treat with t-PA to break down the clot and open up artery

Most effective within 3 hours after embolic and thrombotic stroke

Can exacerbate the damage produced by hemorrhagic stroke

278
Q

AE fibrinolytic drugs

A

Bleeding from the systemic fibrinogenolysis (streptokinase, urokinase)

Allergic reactions (streptokinase)

Systemic fibrinogenolysis with streptokinase and urokinase

279
Q

Streptokinase, urokinase

A

Nonfibrin specific or less fibrin specific plasminogen activators

280
Q

TPA

A

Fibrin specific plasminogen activators

281
Q

Treat acute angina of classic angina

Resting ekg is normal

A

Nitroglycerin

Normal HR normal BP sitting there and intermittent symptoms

And atorvastatin and asprin

282
Q

How administer nitroglycerin for acute angina

A

Sublingual so bypass the first pass effect

Quick to heart where need it to exerting effect

283
Q

Which body regulatory factor mimicked by nitroglycerin

A

NO (EDRF) comes from endothelial cells synthesized from arginine

284
Q

What does NO increase

285
Q

MOA nitroglycerinwhich of the following treats angina

A

Forms free radical NO which in smooth muscle activates soluble GC->increase cGMP->dephosphorylation of myosin light chains and smooth msucle relaxation

286
Q

Effects of nitroglycerin

A

Veins vasodilator

Reduced cardiac oxygen demand by decreasing preload

Modestly reduce afterload

Dilated coronary arteries/improves collateral flow

287
Q

Clinical nitroglycerin

A

Acute angina pectoris or prevention

Acute decompensated heart failure (espicially when associated with acute MI)

Perioperative HTN (espicially during surgery)

Induction of intraoperative hypotension

288
Q

Off label nitroglycerin

A

Intra anal treat anal fissure pain

Short term for GI and pulmonary arterial smooth muscle relaxation

289
Q

Toxicities

A

Reflex tachycardia

Flushing

Hypotension , orthostatic hypotension

Peripheral edema

HA

N/v/xerostermia

Paresthesia, weakness,

Dyspnea, pharyngitis, rhinitis, diaphoresis

290
Q

Direct consequence of nitroglycerin

A

Ok

Endothelial

291
Q

Isosorbide mono and donate similar drugs with

A

Slower onset of action

292
Q

Nifedipine MOA

A

Prototypical dihydropyridine CCB

Inhibits calcium ion channels or select voltage sensitive areas of vascular smooth muscle and myocardium during depolarization

293
Q

Effects nifedipine

A

Cause relaxation of coronary vascular SM muscle->coronary vasodilation

Increases myocardial oxygen delivery in patients with vasospastic angina

Negative inotropy but less so than verapamil

Reduces vascular resistance, producing a reduction in arterial bp

Frequency independent not cardioactive

294
Q

Clinical application nifedipine

A

Management of chronic stable or vasospastic angina

Treat HTN (sustained release products only)

First line for HTN

Non black without CKD

Black without CKD including those with diabetes, instead of an ACE or ARB

295
Q

Off label nifedipine

A

HTN emergency of pregnancy

Preterm labor

Raynaud phenomenon

Pulmonary HTN

296
Q

Pharmacokinetics nifedipine

A

Immediate and extended

Extensive hepatic metabolism via CYP34A

T1/2 2- 5hours increased by cirrhosis

Metabolites eliminated in urine

297
Q

Toxicities nifedipine

A

Common-Flushing , peripheral edema

Dizzy, HA, nausea, heart burn.

Rare-Palpations and gingival hyperplasia

298
Q

What if unstable and stable angina add after

A

Want drug exerts crease HR, myocardial contractility and wall tension

Dilitizam-decrease afterload, SA node,

But nadolol bc

299
Q

Amlodipine

A

Limited to CAD and HT, but very widely used in part due to long HL 30-50 hours

300
Q

Verapamil MOA

A

CCB non dihydropyridine

Inhibits Ca ion channels from entering the slow channels or select voltage sensitive areas of vascular smooth muscle and myocardium during depolarization

301
Q

Effects verapamil

A

Produces relaxation of coronary vascular SM and coronary vasodilation

Increases myocardial oxygen delivery in patients with VASOSPASTIC angina

Slows AV

Decrease myocardial contractility, more negative inotropy than nifedipine or dilitazam

Frequency dependent

302
Q

Clinical verapamil

A

IV: supraventricular tachycardia

Oral, treatment of
Primary HTN (CCB first line in JNC8)
Angina pectoris (vasospastic, chronic, stable, unstable)
Supraventricular tachycarrhythmia

303
Q

Off label verapamil

A

Episodic migraine prevention , hypertrophic cardiomyopathy

304
Q

Pharmacokinetics verampamil

A

Available as tablets with immediate and extended release as IV solution

Undergoes extensive hepatic metabolism via multiple YPs

Majority of metabolites are excreted in Irvine

T1/2 3-7 hours

305
Q

Toxicities verapamil

A

Common-HA, gingival hyperplasia, constipation

Rare-peripheral edema, CHF, pulmonary HTN, AV block, flush rash, dyspepsia, flu like

306
Q

Propranolol MOA

A

Nonselective competitive beta adrenergic blocker

Class II antiarrhythmic

Decrease camp

Block AC

307
Q

Effects propranolol

A

Beta 1 block
Decreased HR, decreased myocardial contractility, decrease blood pressure, myocardial oxygen demand

Beta 2 block
Blunting of bronchodilator less vasodilation

308
Q

What drug give instead b blocker if has asthma

A

Ok

Metroprolol it is selective b1

309
Q

Clinical propranolol

A

HTN
Angina pectoris
Pheochromocytoma

Essential tremor

Supraventricular arrhythmias

Ventricular tachycardia

Prevention of myocardial infarction

Migraine HA prophylaxis

310
Q

Off label propranolol

A

Akathisia, antipsychotic induced performance anxiety

311
Q

Pharmacokinetics propranolol

A

Given orally
25% reaches systemic circulation due to high first pass metabolism

Extended release formulation available

Also solutions for oral IV administration

312
Q

Toxicities propranolol

A

Bronchospasm,dyspnea

Cold extremities

Bradycardia, AV conduction disturbance

CHF, cardiogenic shock, hypotension, syncope

Disrupted sleep with nightmares

Hyperglycemia or hypoglycemia, hyperkalemia, hyperlipidemia

Abdominal pain, diarrhea, constipation

Conjunctival decreased vision

313
Q

What b blocker if cant sleep so tired

314
Q

MOA atenolol

A

B1 selective
Antagonist

Little or no effect on B2 receptors except at high doses

Less CNS effect

315
Q

Effects atenolol

A

B1 blocker

Decreased HR

Decreased myocardial contractility

Decreased blood pressure

Decreased myocardial oxygen demand

316
Q

Clinical atenolol

A

Treatment of HTN, alone or in combination with other agents

Management of angina pectoris

Secondary prevention postmyocardial infarction

317
Q

Vascular disease

A

Contraindication for b block decrease b2 mediated vasodilation and cold extremities

318
Q

Off label atenolol

319
Q

Pharmacokinetics atenolol

A

PO rapid but incomplete 50% absorption

Not lipophilic no cross BBB
T1/2 6-7 hours

Verampamil

Amlodipine-no reflex tachy

320
Q

AE atenolol

A

Bradycardia persistent

2, 3 degree atrioventricular block

Cardiac failure, chest pain, hypotension

Cold extremities edema, raynaud

Confusion fatigue HA insomnia, lethargy nightmare

Constipated

IMPOTENCE

321
Q

Metoprolol

A

Selective beta 1 blocker shorter HL than atenolol but available in extended release form; more lipid soluble so more likely to produce CNS effects

322
Q

Bishop roll

A

Notable for having highest b 1 selectivity

323
Q

Ranolazine MOA

A

Inhibits the late phase of the inward Na channel in ischemic cardiac myocytes during cardiac depolarization

Reducing intracellular sodium concentrations enhances calcium efflux via Na Ca exchange

Decreased intracellular calcium reduces ventricular tension and myocardial oxygen consumption

324
Q

Effects ranolazine

A

Exerts antianginal and anti ischemic effects without changing hemodynamic parameters

Presumed to occur bc ranolazine facilitates myocardial relaxation

325
Q

Clinical application ranolazine

A

Chronic angina

Stable ischemic heart disease

May be useful as substitute for beta blockers for relief of symptoms if initial treatment with beta blockers has unacceptable side effects, is ineffective, or contraindicated

May also be used in combination with beta blockers for relied of symptoms when initial treatment with beta blockers is not successful

326
Q

Verampamil work on veins

327
Q

Pharmacokinetics ranolazine

A

Administered as extended release tablets

Extensive hepatic metabolism CYP3A4major and 2D6minor …so be aware of other drugs

1/2=7 hours

328
Q

AE ranolazine

A

Bradycardia , hypotension , orthostatic hypotension, palpitation, peripheral edema

Prolonged QT interval (dose related), HA, dizziness, confusion, vertigo, syncope

Sweating , constipation, ab pain, anorexia, dyspepsia, nauseas, vomiting , xerostomia, hematuria, weakness, blurredvision, tinnitus, dyspnea

329
Q

What is not associated with ad of verapamil

Constipation
Facial flushing
Gingival hyperplasia
Reflex tachycardia
Worsening of heart failrue
A

Reflex tachycardia

330
Q

Coronary artery bypass

A

Often better option vs PCI when drug are inadequate

331
Q

But start with non surgical. What causes imbalance

A

Decrease o

Increase demand

Decrease supply and increase demand

Unlike skeletal msucles cant stop and rest

332
Q

What regions of the heart are more poorly perfused

A

Subendocardial regions

333
Q

Decrease preload

A

Decrease intraventrucular pressure->increase subendocardial perfusion

334
Q

When is the heart suckle perfused

A

Between beats,

Decrease time for coronary perfusion

335
Q

Patient no asthma or peripheral vascular disease, frequent predicable chest pain

A

Nitroglycerin patch-NO reflex stimulation of heart
Dilate veins not lower bp anymore potentiallly increase

Ranolazine -cause reflex tachycardia but drop BP

336
Q

Amlodipine

A

Frequent predictable chest pain been taking atenolol for 15 years due to HTN . Addition of

337
Q

Reflex tachycardia

A

CCB caused significant angina

Nifedipine

338
Q

Least likely to be useful for variant angina

Atenolol, dilitazem, nifedipine, nitroglycerin, verampamil

339
Q

without affecting traditional indices of heart work such as heart rate bp and rate pressure product

A

Ranolazine -potentiation relaxation of heart

Block late Na current —late Na current goes into heart continuous influx of Na normally need between beets to drive Na Ca exchanger to bring Ca out of cells.calsium stays in cell and accumulates. When heart not relax as fast, squish capillaries and not get as good a flow

340
Q

MOA unfractioned heparin

A

Prepared from lungs of cattle and intestines of pugs

Long polysaccharide chains with weight 300-30000

Pentasaccharide sequence found randomly along length that binds to/activates antithrombin III to inhibitic Xa and via formation of a ternary complex, thrombin

341
Q

Effects heparin

A

Blocks generation of thrombin from prothrombin and also inactivated thrombin

Prevents formation of red clots

342
Q

Clinical unfractioned heparin

A

Whenever there is a need for rapid onset anticoagulant effects including pulmonary embolism, stroke, DVT, disseminated intravascular coagulation acute MI

In preg bc doesn’t cross placenta

Extracorporeal circuits

343
Q

Antidote heparin unfractioned

A

Protamine, many positive change bonds ironically with the negative charges of heparin

344
Q

Pharmacokinetics heparin unfractioned

A

Partenterally

Highly negative

Can’t cross membranes

Binds nonspecificallyhighly variable plasma levels which require intensive monitoring via aPTT assay

He 1.5 hours

345
Q

AE unfractioned heparin

A

Don’t give thrombocytopenia and uncontrollable bleeding, avoid during surgery or brain eye or spine procedures

Bleeding!!

Monitor bp , hr buried

Spinal or epidural hematoma can cause paralysis

HIT
-potentially fatal immune mediated disorder characterized by reduced platelet counts with a paradoxical increase in thrombotic events

346
Q

MOA low molecular weight heparins

A

Heparin molecules of shorter length
Can’t form ternary complex with antithrombin III and thrombin that is need to inactivate this , but factor Xa is inhibitors

347
Q

Effects low molecular weight heparin

A

Block Xa

Prevents red clots

348
Q

Clinical low molecular weight heparin

A

Prevent DVT
Abdominal surgery or hip knee surgery

Treat DVT with or withou pulmonary embolism

Prevent ischemic complications

349
Q

Pharmacokinetics low molecular weight heparin

A

Easier oral dosing is predictable

PREVENT DVT

Longer HL

350
Q

AE low molecular weight heparin

A

Bleeding

HIT

Neurological injury in spinal puncture or spinal or epiduarla anesthesia

351
Q

Fondaparinux MOA

A

Synthetic pentassachharide identical to antithrombin binding structure of heparin

Selectively inhibits Xa

352
Q

Effects fondaparinux

A

Blocks coagulation by preventing conversion of prothrombin to thrombin

No effect on thrombin

More effective than enoxaparin but risk of bleeding

353
Q

Clinical fondaparinux

A

Prevent DVT

Treat acute pulmonary embolism in conjunction with warfarin

Treat acute DVT with warfarin

354
Q

Pharmacokinetics fondaparinux

A

SubQ

Predictable

HL17 hrs
Longer if renal impairment too long?

355
Q

AE fondaparinux

A

Bleeding

Not reversible with protamine

No HIT

356
Q

Bivalirudin MOA

A

Synthetic 20 aa peptide similar to hirudin directly blocks thrombin

357
Q

Effects bivalirudin

A

Reversible inhibits coagulation

358
Q

Clinical bivalirudin

A

With asprin for angioplasty

359
Q

Pharmacokinetics bivalirudin

A

IV expensive

360
Q

AE bivalirudin

A

Doesn’t require antithrombin and causes less bleeding

No antidote

361
Q

Lepirudin

A

Recombinant form of leech hirudin that binds thrombin irreversibly no longer marketed

362
Q

Argatroban MOA

A

Binds to catalytic site of thrombin

363
Q

Argabatran clncial

A

Prophylaxis treatment of thrombosis in patients with HIT

364
Q

How is efficacy of argatroban monitored

365
Q

Pharmacokinetics argatroban

A

IV

HL 45 min

366
Q

AE argatroban

A

Hemorrhage

367
Q

Warfain MOA

A

Vitamin K antagonist

368
Q

Effects warfarin

A

Decrease production of biologically active forms of calcium dependent clotting factors II VII IX X

Protein C and S

369
Q

Clinical warfarin

A

Prophylaxis thrombosis

Prevent venous thrombosis, thromboembolism with mechanical heart valves, prevent thrombosis in a fib, effects delayed so not for emergencies

370
Q

Pharmacokinetics warfarin

A

Oral 100% available

Bile elimination

Slow onset

Slow offset

INR monitor

371
Q

AE warfarin

A

Bleeding
Crosses placenta

Drug interactions
Liver disease

Cutaneous necrosis-protein c has a shorter half life than several othe clotting factors so warfarin administration can initially cause procoagulant state

Skin necrosis

372
Q

Reverse warfarin

A

Bit K

Fresh whole blood plasma concentrates

373
Q

Rivaroxaban MOA

A

Direct inhibitor of activated factor X

374
Q

Effects rivaroxaban

A

Directly inhibits the production of thrombin

375
Q

Advantages of rivaroxaban over warfarin

A 
Rapid onset
Fixed dose
Lower bleeding
Fewer drug interactions 
No need for INR monitoring
376
Q

Clinical rivaroxaban

A

Prevent DVT and pulmonary embolism

Prevent stroke with a fib

377
Q

Antidote rivaroxaban

378
Q

Pharmacokinetics rivaroxaban

A

Oral high bioavailability

379
Q

AE rivaroxaban

A

Bleeding

  • epidural hematoma
  • intracranial bleed
  • adrenal bleed
  • GI bleed

Don’t five renal or hepatic impairment

No preg

Not combined with anticoagulatnts other

CYP34A

380
Q

Dabigatran MOA

A

Reversible direct thrombin inhibitor

381
Q

Effects dabigatran

A

Directly blocks thrombin

382
Q

Advantages dabigatran over warfarin

A

Rapid onset
Don’t need monitor

Few drug interactions
Low risk bleeding
Same dose for all

383
Q

Clinical dabigatran

A

Prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation

384
Q

Contraindication dabigatran

A

Mechanical heart valves

385
Q

AE dabigatran

A

Bleeding

Antidote idarucizumab

386
Q

Asprin MOA

A

Irreversible inhibits cyclooxygenase

387
Q

Effects asprin

A

Blocks formation TXA2

Persists for lifetime of platelet 5-9 days

388
Q

Clinical asprin

A

TIA, chronic stable and unstable angina

MI prevention

Acute MI

Prevent restnosis after stent

389
Q

AE asprin

A

Bleed

Ulcer

390
Q

MOA clopidogrel

A

Irreversible block of P2Y12 receptors on platelets

Prevents its Gi protein driven decrease in platelet cAMP

391
Q

Effects clopidogrel

A

Prevent stenosis of coronary stents

Secondary prevention of MI and ischemic stroke

392
Q

Pharmacokinetics clopidogrel

A

Prodrug
CYP2c19

Some variants cant activate it-Chinese

393
Q

AE clopidogrel

A

Well tolerated

Bleeding

394
Q

Prasugrel

A

Close relative to clopidogrel more effective with fewer drug interactions, but also causes major bleeding

395
Q

Ticagrelor

A

Reversible P2Y12 blocker more effective but increase risk of hemorrhage stroke

396
Q

Ticlopidine

A

Similar to clopidogrel removed from marked due to AE

397
Q

Which needs cyp219 activation

A

Just clopidogrel move to others if issue

398
Q

Abciximab MOA

A

Purified Fab fragment monoclonal antibody

399
Q

Effects abciximab

A

Blocks final pathway of platelet aggregation
Inhibits aggregation caused by all factors

Most effective of antiplatelet drugs

400
Q

Lingual abciximab

A

Acute coronary syndromes

Percutaneous coronary intervention

401
Q

Dipyridamole MOA

402
Q

Effects dipyridamole

A

Suppresses platelet aggregation

403
Q

Clinical dipyridamole

A

Fixed dose with asprin for prevent recurrent ischemic stroke

404
Q

AE dipyridamole

A

Bleeding

HA, dizzy

405
Q

Cilostazol MOA

A

Type 3 phosphodiesterase inhibitors

Prolongs life of cAMP in platelets and cells

406
Q

Effects cilostazol

A

Platelet aggregation inhibitor

Vasodilator

407
Q

Clinical cilostazol

A

Intermittent claudication

408
Q

Alteplase MOA

A

Purified glycoprotein of 537 aa

Human tpa sequence identical generated in Chinese hamster ovary cells by recombinant dna technology

409
Q

Effects alteplase

A

Catalyze the conversion of clot bound plasminogen to plsmi

410
Q

Clinical alteplase

A

Acute MI

Acute ischemic stroke

Acute massive pulmonary embolism

411
Q

Pharmacokinetics alteplase

A

Large molecule parenteral

Short HL 5 min

412
Q

AE alteplase

A

Bleeding

Intracranial hemorrhage

Destroying persisting clots
By degrading clotting factors, interferes with clot formation

413
Q

Tenectaplase

A

Longer HL more effective for stroke

Good for MI

414
Q

Reteplase

A

Only MI HL 13-16 min

415
Q

Contraindications alteplase

A

Intracranial hemorrhage

Cerebral vascular lesion

Ischemic stroke recently in months unless past 5 hours$
Aortic dissection

416
Q

Urokinase MOA

A

Second physiologic plasminogen activator in urine

417
Q

Effects urokinase

A

Major activator of fibrinolytic in fluid phase/extravascular compartment

418
Q

Clinical urokinase

A

Pulmonary embolism

419
Q

Pharmacokinetics urokinase

420
Q

AE urokinase

A

Fatal hemorrhage

Anaphylactic shock

Pharmacology (52 decks)

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