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Final Exam Flashcards

1
Q

Organic Nitrates MOA

A

compound denitrated by ntALDH, forms NO which signals for release of cGMP, leading to decreased [Ca++]i and vasodilation

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2
Q

Effects of Organic Nitrates

A

Primary action is venodilation - significant decrease in preload.
Coronary artery dilation
Some arteriolar dilation - decreased afterload
Net result: decreased oxygen demand, and in some situations, increased oxygen supply

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3
Q

Organic Nitrate metabolism

A

high 1st pass effect = limited oral bioavailability

metabolized by glutathione-organic nitrate reductase

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4
Q

Sub-lingual and nasal Organic Nitrates

A

EX: SL nitroglycerin, SL isosorbide dinitrate, inhalant amyl nitrite
ra[id onset, short DOA
used to relieve acute angina

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5
Q

Oral and Dermal Organic Nitrates

A

nitroglycerin ointment, nitroglycerin dermal patches, oral isosorbide dinitrate.
slow onset, longer DOA
used for prophylaxis of angina

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6
Q

Organic Nitrates Side Effects

A

Orthostatic hypotension
Tachycardia (SNS activation)
Throbbing headache (“Monday disease”, can develop tolerance)
Dizziness, flushing of skin

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7
Q

Organic Nitrates Contraindications

A

PDE5 inhibitors (ED) - both promote vasodilation via separate mechanisms = potentiated effects

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8
Q

Main Uses of Organic Nitrates

A

Stable angina and Variant angina that is not associated with atherosclerosis

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9
Q

Effects of Calcium Channel Blockers

A

blocks receptor-mediated Ca++ channel, decreases [Ca++]i. Voltage-gated channel can still be activated
Decreases oxygen consumption by decreasing contractility and heart rate and causing relaxation of coronary smooth muscle cells (relieves vasospasms)

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10
Q

“Others” class of Ca Channel Blockers

A

Verapamil and Diltizem
Cardiac&raquo_space; Vascular effects
Primary effects are to decrease HR, contractility, and conduction velocity, all of which decrease oxygen demand on the heart.
Safer choice for pts with stable angina than dihydropyridines

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11
Q

Dihydropyridines

A

Nifedipine, amlodipine, felodipine
Primary effect is to decrease afterload, which decreases oxygen demand.
BUT if you lower BP too fast, trigger SNS response = increased oxygen demand. (tempers effectiveness)
short acting nifedipine should not be used as monotherapy for unstable or chronic stable angina
long acting nifedipine, amlodipine, and felodipine are more slowly absorbed, and are not as likely to cause reflex tachycardia.
This class CAN be used for angina, just have to be cautious of what type is used

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12
Q

Net Effects of Ca Channel Blockers

A

Decreased oxygen demand

Decreased vasospasms

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13
Q

Main Uses of Ca Channel Blockers

A

Variant and Stable Angina

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14
Q

Ca Channel Blockers Side Effects

A 
Bradycardia
Heart Block (AV node)
Dizziness and edema
Flushing (vasodilation)
Constipation (reduced GI motility)
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15
Q

Beta-Blockers used in Angina

A

B1 Selective - metoprolol and atenolol
Nonselective - propranolol and nadolol
Do not usually use ones with ISA

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16
Q

Effects of Beta blockers

A

reduces inotropy (contractility) and chronotropy (HR), leading to overall reduction in oxygen demand.
Slight increase in coronary flow to ischemic areas, not consistent (increased oxygen supply)
Net: decreases oxygen demand, slight increase in blood flow (and oxygen supply)
28-40% reduction in mortality

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17
Q

Main anti-anginal uses of B-blockers

A

Stable and Unstable angina.

CAUTIOUS use in pts with ischemia induced CHF

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18
Q

Contraindications of B-blockers

A

Variant angina (unchecked alpha-receptor effects)

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19
Q

B-blocker side effects

A

Cardiovascular effects: bradycardia, heart failure, low exercise tolerance
Rebound effect: upregulated receptor number can cause an increase in HR or BP, causing more angina
Bronchospasms (B2 antagonists)
CNS effects (lipophilic B2 antag): fatigue, depression, vivid dreams/nightmares

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20
Q

Ranolazine (Ranexa) MOA

A

blocks the “late Na+ current” curing cardiac AP.

Decreasing [Na+]i will decrease [Ca++]i, reduces ventricular stiffness and therefore oxygen consumption

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21
Q

Angina Pectoris

A

Pain resulting from myocardial ischemia, usually originates in chest and ratiates to arm

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22
Q

Myocardial Ischemia

A

oxygen demand&raquo_space; oxygen supply in heart

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23
Q

Myocardial Infarction

A

Myocardial Cell Death following prolonged ischemia

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24
Q

Stable Angina (classical or effort)

A

Most common type of angina
Etiology: atherosclerosis
Symptoms: angina with exertion, relief at rest
Goal of therapy is to decrease oxygen demand
Drugs: long-acting nitrates, Ca blockers, B blockers, combo therapy, surgery

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25
Q

Variant angina (Prinzmetal’s)

A

Etiology: vasospasms of coronary artery, which may or may not be associated with atherosclerosis.
Symptoms: pain independent of rest or exertion. Length depends on how long the vasospasm lasts.
Therapy goal is to decrease severity and frequency of vasospasms.
Drugs: nitrates, Ca blockers, combo therapy

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26
Q

Unstable Angina

A

Etiology: recurrent formation of platelet clots, usually associated with plaque and often compounded by local vasospasms.
Symptoms: prolonged pain at rest, change in character, frequency, or duration of stable angina
goal of therapy is aggressive anticoagulants, vasodilators, etc.
This type of angina usually signifies an impending MI
Drugs: anticoagulants, thrombolytics, nitrates, Ca blockers, B blockers, combo therapy, surgery.

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27
Q

Uses of anticoagulants

A

Diseases: unstable angina (and acute coronary syndromes), Afib, Pulmonary embolism, DVT, HF, stroke
Procedures: angioplasty, valve replacement, hemodialysis, indwelling catheters, assist devices, heart/lung machine

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28
Q

Pathophysiology of Acute Coronary Syndromes

A

fibrous cap covering plaque ruptures, causing platelet activation and aggregation, leading to thrombus

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29
Q

Important drug targets in clotting pathway

A

Vitamin K
Factor Xa
Factor IIa (thrombin)

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30
Q

Heparins MOA

A

binds to circulating antithrombin and increases affinity for thrombin and factors IXa and Xa 1000x. This complex is then rapidly removed by liver.
Not orally active, given IV/SC. Active site is the pentasaccharide sequence (has to be sulfated in a certain order to be active)

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31
Q

Fondaparinux (Arixtra)

A

Most basic form of heparin, only consists of the pentasaccharide sequence, therefore only binds and inactivates Xa.
Given SC
Eliminated primarily unchanged in urine
Contraindicated in pts with CrCl <30mL/min (and pts with animal allergies, isolated from pigs)
-T1/2 17-21h, effect lasts 2-4 days after discontinuing
less likely to cause thrombocytopenia

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32
Q

Types of Heparins

A

Unfractionated: full length heparin. Inactivates Xa and IIa equally. Increased risk of allergies, major bleeding, and thrombocytopenia. F=0.3
Low Mol-Wt Heparin: fractionated heparin, inactivates factor Xa > IIa. slightly lower risk of allergies, major bleeding, and thrombocytopenia. F=0.9
Fondaparinux: smallest version of heparin (pentasaccharide sequence only). Only inactivates Xa. Greatly reduced risk of allergic reactions, major bleeding, or thrombocytopenia. F = 1. Much more expensive than others.

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33
Q

(unfractionated) heparin side effects

A

Bleeding - dose related
Thrombocytopenia
Osteoporosis with long term use (relatively rare)

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34
Q

(unfractionated) heparin contraindications

A

Active bleeding (ulcers, tumors, trauma, etc.)
Coagulopathies
Hypersensitivity to pork products

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35
Q

Apixaban (Eliquis)

A

Newer, Direct acting, reversible Xa inhibitor
In phase 3 trials (delayed approval)
Prevent venous thromboembolism
no routine monitoring required

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36
Q

Rivaroxiban (Xarelto)

A

First orally active direct Xa inhibitor, once daily dosing is possible
approved for prophylaxis of DVT in pts undergoing knee or hip replacement surgery
slightly higher bleeding incidence than heparin
does not require routine monitoring

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37
Q

Lepirudin (Refludan)

A

Direct thrombin inhibitor, recombinant version of hirudin (leeches)
most potent thrombin inhibitor known
neutralizes clot-bound thrombin (unlike heparin)
Main use: pts with heparin induced thrombocytopenia

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38
Q

Bivalirudin (Angiomax)

A

direct thrombin inhibitor
small synthetic peptide (20aa’s)
beter tissue/clot penetration
main use: pts with unstable angina undergoing angioplasty (alternative to heparin)

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39
Q

Dabigatran (Pradaxa)

A

Orally available, direct thrombin inhibitor, for prevention of stroke in pts with afib.
Just as effective as warfarin, may challenge warfarin as dominant oral anticoagulant.
(GI bleeding significantly higher with 150mg vs 110mg or warfarin)

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40
Q

Warfarin MOA

A

Vitamin K antagonist - inhibits Vitamin K epoxide reductase. reduces amount of VitK available for biological synthesis of clotting factors (II, VII, IX, X)
30-50% effective decrease of functional clotting factors. takes 3-5 days to reach full effect, lasts several days after stopping

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41
Q

Warfarin metabolism

A

extensively metabolized by CYP2C9. Genetic variations lead to variable pt response.

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42
Q

Warfarin Interactions

A

Has a narrow therapeutic index. 99% protein bound.
Dietary Vit K changes
Inhibitors/Inducers of CYP enzymes
All result in variable pt response. Therapy requires constant INR monitoring

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43
Q

Warfarin Side Effects

A

Bleeding - can be correct with Vitamin K administration and/or blood transfusions
Birth defects/abortion

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44
Q

Warfarin Contraindications

A

pregnancy and pre-existing bleeding

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45
Q

Anti-platelet drugs

A

Aspirin
Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor
Tirofiban, Abciximab, Eptifibatide
Effects: prevent platelet activation/aggregation. Mechanisms differ

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46
Q

Aspirin MOA

A

irreversibly acetylates and inhibits COX-1 in platelets. Decreases amount of thromboxane A2 (TXA2) = reduced platelet activation and adhesion.
81mg/day will effectively inhibit platelet formation without causing additional effects

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47
Q

ADP antagonists

A

Inhibit ADP dependent activation and aggregation of platelets, and blocks ADP receptor on platelets
Irreversible: Ticlopidine and Clopidogrel
Reversible: Prasugrel and Ticagrelor (quicker onset than irreversible, greater and more predictible inhibition of ADP0induced platelet activation. Less PG variability, greater efficacy for preventing stent thrombosis. But, greater incidence of life threatening bleeding)

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48
Q

Clopidogrel

A

generally more potent than Ticlopidine, better safety profile. (rare thrombocytopenia/leukopenia)
Prodrug, requires oxidation by CYPs.
Genetic variations in CYP2C19 are associated with reduced drug responsiveness.

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49
Q

Prasugrel

A

MOA: thienopyridine, antiplatelet agent
Reduces rate of thrombotic CV events in pts with unstable angina, NSTEMI or STEMI managed with PCI
Contraindications: pts with history of intracranial hemorrhage, active bleeding, or severe hepatic impairment
BBW: May cause significant or fatal bleeding; contraindicated in pts with active bleeding or history of TIA or stroke
Reversal: platelet concentrate of desmopressin

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50
Q

Ticagrelor

A

Newest oral antiplatelet agent
MOA: reversibly inhibits platelet ADP receptor
Used for prevention of stent thrombosis, cardiovascular death, heart attack in adults with ACS
Contraindications: pts with historyof intracranial hemorrhage, active bleeding, or severe hepatic impairment.

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51
Q

Abciximab (Reopro)

A

Monoclonal antibody against fibrinogen receptor. Approved for high risk post-angioplasty thrombosis. Noncompetitive inhibition, long half life, slow to reverse

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52
Q

Eptifibatide (Integrilin)

A

blocks fibrinogen binding to activated platelets. Proven success in PTCA and unstable angina trials. competitive inhibition, 2.5h half life. quickly reversible.

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53
Q

Tirofiban (Aggrastat)

A

Blocks fibrinogen binding to activated platelets. Short acting, IV use in high risk ACS pts. competitive inhibition, 2h half life, quickly reversible

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54
Q

Anti-platelet drugs Side Effects

A 
Bleeding (all classes, all drugs) especially in GI tract (aspirin)
GI upset (aspirin)
Ticlopidine: Nausea, Vomiting, Neutropenia, Thrombocytopenia, Skin rashes.
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55
Q

Fibrinolytic agents

A

Streptokinase, Alteplase recombinant tPA, Tenecteplase

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56
Q

Uses of fibrinolytic agents

A

dissolve existing fibrin clots by converting circulating plasminogen to plasmin

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57
Q

streptokinase MOA

A

binds to plasminogen, forms enzyme complex which catalyzes conversion of plasminogen to active plasmin

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58
Q

Alteplase and Tenecteplase MOA

A

similar MOAs. Binds to fibrin first, then complex binds plasminogen forming triad.
alteplase = longer infusion time
tenecteplase = shorter infusion time

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59
Q

Side Effects of Fibrinolytic agents

A

bleeding and allergic reactions

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60
Q

Contraindications of Fibrinolytic agents

A

Recent bleeding
Recent surgery or invasive procedures
Severe hypertension
History of stroke.

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61
Q

Sources of LDL

A 
from VLDLs (endogenous)
From diet (exogenous)
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62
Q

Removal of LDLs

A

LDL receptor activity, serves as the mechanism for LDL’s to enter cells, thus reducing plasma concentrations.
HDLs also transport LDLs back to liver for enterohepatic recycling

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63
Q

Lipoprotein disorders

A

genetic: familial hypocholesterolemia (defective LDL receptor)
Most common - polygenic hypercholesterolemia (multiple genetic and environmental factors)

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64
Q

HMG CoA Reductase Inhibitors MOA

A

“statins”

Reversible, competitive inhibitors of HMG CoA reductase activity (converting HMG CoA to intermediates and then to cholesterol etc.)

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65
Q

Physio Effects of HMG CoA Reductase Inhibitors

A

reduce cholesterol synthesis in liver
reduce plasma VLDL concentration
reduce plasma LDL concentration
increase LDL receptor # (increased removal from plasma)
results in 20-55% decrease in plasma [LDL]

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66
Q

HMG CoA reductase Inhibitor optimal dosing

A

take at bedtime, cholesterol synthesis increased at night

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67
Q

HMG CoA reductase Inhibitor side effects

A

usually well tolerated, relatively few side effects
Increased liver transaminase
Rhabdomyolysis (rare) with secondary renal failure - can be fatal

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68
Q

HMG CoA reductase Inhibitor contraindications

A

pregnancy (need cholesterol for fetus to make new cells

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69
Q

Net result of HMG CoA reductase Inhibitor

A

decreased cholesterol synthesis in liver, increased LDL receptor activity inliver
20-55% decrease in LDL
5-15% increase in HDLs

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70
Q

Bile Acid Binding Resins

A

cholestyramine, colestipol HCl

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71
Q

Bile Acid Binding Resin MOA

A

resins positively charged, bile salts/acids negatively charged. Resins bind to cholesterol-containing bild acids/salts in intestine.
reduces enterohepatic recirculation of cholesterol

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72
Q

Effects of Bile Acid Binding Resin

A

decreased reabsorption of bild acids/salts
increased bile (and cholesterol) excretion in feces
increased hepatic LDL receptor expression (decrease plasma [LDL])
increased hepatic cholesterol synthesis (tempers therapeutic effect)

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73
Q

Bile Acid Binding Resin useful dosing

A

usually supplied as powder, and drunk as slury. take with meal (more bile secreted into SI)

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74
Q

Side Effects of Bile Acid Binding Resin

A

no direct systemic SE

Local: bloating, abdominal discomfort, constipation, all leading to compliance issues

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75
Q

Bile Acid Binding Resin Drug interactions

A

binds to other anionic drugs/compounds. Need to dose other drugs 1 hour before or 3 hours after

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76
Q

Net Result of Bile Acid Binding Resin

A 
increases LDL receptor activity
Increases cholesterol synthesis in liver (limits efficacy)
increases cholesterol loss in feces
15-30% reduction in LDLs
3-5% increase in HDLs
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77
Q

Ezetimibe MOA

A

inhibits cholesterol absorption at brust border of intestines. DOES NOT effect absorption of anionic drugs (vit A, D, E, Warfarin, OC’s etc.)

78
Q

Ezetimibe clinical use

A

10mg once a day, with or without food
13% decrease TC
18% decrease LDL
1% increase HDL

79
Q

Ezetimibe Side Effects

A

rare allergic RXNs, otherwise well tolerated

80
Q

Ezetimibe Combo therapy with statins (Vytorin)

A

additional 25% decrease in cholesterol
additional 33% decrease in TGs
7-9% increase in HDL

81
Q

Niacin MOA

A

inhibits TG synthesis in liver, leads to reduced VLDL, which leads to reduced LDL
Increases lipoprotein lipase activity which promotes the clearance of chylomicrons and VLDL TGs

82
Q

Niacin Physio Effects

A

10-15% decrease LDLs
15-35% increase HDLs (unknown mechanism)
35-50% decrease TGs

83
Q

Niacin Side Effects

A 
50% of pts
intense cutaneous flushing (can develop tolerance to this or give aspirin to decrease effect)
GI irritation (large frequent dosing)
hepatic dysfunction (jaundice)
Hyperglycemia
84
Q

Niacin use/dosing

A

often used as adjunct therapy to raise HDLs

available OTC

85
Q

Niacin contraindications

A

liver dysfunction
peptid ulcers
diabetic pts
pregnancy

86
Q

Fibric Acid Derivatives

A

gemfibrozil, clofibrate

87
Q

Fibric Acid Derivative MOA

A

stimulates the PPAR-alpha, reduces TGs by 50%

88
Q

Fibric Acid Derivatives Physio effects

A

decreases VLDL synthesis
9% decrease in LDLs
10-20 increase in HDLs
Effective in pts with hypertriglyceridemia

89
Q

Fibric Acid Derivative side effects

A

gall stones
GI irritation
GI/hepatic tumors

90
Q

Fibric Acid Derivative contraindications

A

pts on warfarin - increases anticoag effect

91
Q

NEW CETP inhibitors in development: Anacetrapib

A

40% decrease in LDL
138% increase in HDLs
Acceptable SE profile
Did not produce adverse CV effects and mortality observed with predecessors

92
Q

Class 1A Na Channel Blockers

A

Procainamide, Quinidine, Disopyramide

93
Q

Class 1A Na Channel Blocker Effects

A

moderate potency to block Na channel
slows upstroke of AP, Increase AP duration (increases phase 0 and 3)
reduce conduction felocity
increase refractoriness

94
Q

Class 1A Na Channel Blocker uses

A

atrial and ventricular arrhythmias

95
Q

Important features of Class 1A Na Channel Blockers

A

drugs preferentially target rapidly depolarizing tissue more than normal tissue
prolonging repolarization = increased refractory period (effective in stopping re-enterant arrhythmias

96
Q

Class 1B Na Channel Blockers

A

Lidocaine

97
Q

Class 1B Na Channel Blocker Effects

A

Low potency Na blockers
have highest affinity for Na channels in ischemic cells
reduce phase 0 slope and slows conduction
reduces automaticity and phase 4 slope
increase refractoriness

98
Q

Class 1B Na Channel Blocker uses

A

ventricular arrhythmias

ineffective in atrial tissue

99
Q

Class 1B Na Channel Blockers unique features

A

lidocaine - highly lipophilic
reduces ventricular tachycardias or Vfib after cardioversion
clinical trials = decreased survival after MI when used long term

100
Q

Class 1C Na Channel Blockers

A

Flecainamide, Propafenone

101
Q

Class 1C Na Channel Blocker effects

A

high potency Na blockers with some K blocking potential
decreases phase 0 slope and AP conduction
increases AP duration and refractoriness especially in atrial cels at fast rates and AV nodes

102
Q

Class 1C Na Channel Blocker uses

A

supraventricular arrhythmias (nodal arrhythmias)

103
Q

Class 1C Na Channel Blocker unique features

A

increases AP duration disporportionately more in atria at fast rates
increases mortality in patients recovering from MI

104
Q

Class 1 Antiarrhythmic Side Effects

A 
provoke or increase arrhythmias
exacerbate congstive heart failure
heart block (block AV node)
Hypotension
GI distress
Sedation, tremor, dizziness, blurred vision
nausea, vomiting
105
Q

Class 2 antiarrhythmics (B-blockers)

A

propranolol, sotalol, esmolol

106
Q

Class 2 antiarrhythmic effects

A

increases AV refractoriness
decreases conduction velocity
increases AP duration (atria, nodal tissue)

107
Q

Class 2 antiarrhythmic uses

A

atrial tachycardia and ventricular tachycardia

108
Q

Class 2 antiarrhythmic unique features

A

reduces mortality after MI (new studies say maybe not)

109
Q

Class 2 antiarrhythmic side effects

A 
relatively well tolerates
CV: bradycardia, HF, low exercise tolerance
Rebound effect
Bronchospasm (B2)
Sedation (lipophilic B2)
Metabolic effects (increased TGs)
110
Q

Class 3 antiarrhythmics

A

amiodarone (most freq), dronederone, dofetilide

111
Q

Class 3 antiarrhythmic effects

A

blocks K channels

increases repolarization phase and AP duration

112
Q

Class 3 antiarrhythmic uses

A

nost arrhythmias (atrial/ventricular)

113
Q

Class 3 antiarrhythmic unique features

A

highly lipophilic, concentrates in tissues, therefore very long t1/2 (25-110 days)
SLIGHTLY decreases mortality after MI

114
Q

Class 3 antiarrhythmic Side Effects

A

75% of pts
hypotension and decreased LV contractility
muscle weakness
hypo/hyperthyroidism
pulmonary fibrosis (rare but can be fatal)

115
Q

Class 4 antiarrhythmics

A

verapamil, diltiazem (no dihydropyridines)

116
Q

Class 4 antiarrhythmic effects

A

blocks Ca channels
decreases slope of phase 4, increases AP, decreases automaticity
decreases HR
decreases AV conduction

117
Q

Class 4 antiarrhythmic uses

A

atrial tachycardias, Afib, AV node arrhythmias

118
Q

Class 4 antiarrhythmic unique features

A

do not reduce mortality after MI (do not increase either)

Dihydropyridines are ineffective

119
Q

Class 4 antiarrhythmic side effects

A 
mostly with concomitant therapy
hypotension (w/ vasodilators)
sinus bradycardia (w/ B blockers)
Heart block (w/ B blockers)
decreased contractility
constipation
120
Q

Adenosine MOA

A

stinulates adenosine receptors
opens K channels, hyperpolarizes membrane
inhibits pacemaker current in Ca channels

121
Q

Adenosine use

A

supraventricular rhythms, must be given IV, usually in hospital setting

122
Q

Adenosine side effects

A

Asystole (transient)

hypotension

123
Q

Digoxin MOA

A

increases AV node refractoriness

124
Q

Digoxin uses

A

AV re-entrant rhythms, atrial fibrilation (HF)

125
Q

Digoxin side effects

A 
triggered rhythms
AV block (reduced coordination of contraction)
126
Q

Sources of LDL

A 
from VLDLs (endogenous)
From diet (exogenous)
127
Q

Removal of LDLs

A

LDL receptor activity, serves as the mechanism for LDL’s to enter cells, thus reducing plasma concentrations.
HDLs also transport LDLs back to liver for enterohepatic recycling

128
Q

Lipoprotein disorders

A

genetic: familial hypocholesterolemia (defective LDL receptor)
Most common - polygenic hypercholesterolemia (multiple genetic and environmental factors)

129
Q

HMG CoA Reductase Inhibitors MOA

A

“statins”

Reversible, competitive inhibitors of HMG CoA reductase activity (converting HMG CoA to intermediates and then to cholesterol etc.)

130
Q

Physio Effects of HMG CoA Reductase Inhibitors

A

reduce cholesterol synthesis in liver
reduce plasma VLDL concentration
reduce plasma LDL concentration
increase LDL receptor # (increased removal from plasma)
results in 20-55% decrease in plasma [LDL]

131
Q

HMG CoA reductase Inhibitor optimal dosing

A

take at bedtime, cholesterol synthesis increased at night

132
Q

HMG CoA reductase Inhibitor side effects

A

usually well tolerated, relatively few side effects
Increased liver transaminase
Rhabdomyolysis (rare) with secondary renal failure - can be fatal

133
Q

HMG CoA reductase Inhibitor contraindications

A

pregnancy (need cholesterol for fetus to make new cells

134
Q

Net result of HMG CoA reductase Inhibitor

A

decreased cholesterol synthesis in liver, increased LDL receptor activity inliver
20-55% decrease in LDL
5-15% increase in HDLs

135
Q

Bile Acid Binding Resins

A

cholestyramine, colestipol HCl

136
Q

Bile Acid Binding Resin MOA

A

resins positively charged, bile salts/acids negatively charged. Resins bind to cholesterol-containing bild acids/salts in intestine.
reduces enterohepatic recirculation of cholesterol

137
Q

Effects of Bile Acid Binding Resin

A

decreased reabsorption of bild acids/salts
increased bile (and cholesterol) excretion in feces
increased hepatic LDL receptor expression (decrease plasma [LDL])
increased hepatic cholesterol synthesis (tempers therapeutic effect)

138
Q

Bile Acid Binding Resin useful dosing

A

usually supplied as powder, and drunk as slury. take with meal (more bile secreted into SI)

139
Q

Side Effects of Bile Acid Binding Resin

A

no direct systemic SE

Local: bloating, abdominal discomfort, constipation, all leading to compliance issues

140
Q

Bile Acid Binding Resin Drug interactions

A

binds to other anionic drugs/compounds. Need to dose other drugs 1 hour before or 3 hours after

141
Q

Net Result of Bile Acid Binding Resin

A 
increases LDL receptor activity
Increases cholesterol synthesis in liver (limits efficacy)
increases cholesterol loss in feces
15-30% reduction in LDLs
3-5% increase in HDLs
142
Q

Ezetimibe MOA

A

inhibits cholesterol absorption at brust border of intestines. DOES NOT effect absorption of anionic drugs (vit A, D, E, Warfarin, OC’s etc.)

143
Q

Ezetimibe clinical use

A

10mg once a day, with or without food
13% decrease TC
18% decrease LDL
1% increase HDL

144
Q

Ezetimibe Side Effects

A

rare allergic RXNs, otherwise well tolerated

145
Q

Ezetimibe Combo therapy with statins (Vytorin)

A

additional 25% decrease in cholesterol
additional 33% decrease in TGs
7-9% increase in HDL

146
Q

Niacin MOA

A

inhibits TG synthesis in liver, leads to reduced VLDL, which leads to reduced LDL
Increases lipoprotein lipase activity which promotes the clearance of chylomicrons and VLDL TGs

147
Q

Niacin Physio Effects

A

10-15% decrease LDLs
15-35% increase HDLs (unknown mechanism)
35-50% decrease TGs

148
Q

Niacin Side Effects

A 
50% of pts
intense cutaneous flushing (can develop tolerance to this or give aspirin to decrease effect)
GI irritation (large frequent dosing)
hepatic dysfunction (jaundice)
Hyperglycemia
149
Q

Niacin use/dosing

A

often used as adjunct therapy to raise HDLs

available OTC

150
Q

Niacin contraindications

A

liver dysfunction
peptid ulcers
diabetic pts
pregnancy

151
Q

Fibric Acid Derivatives

A

gemfibrozil, clofibrate

152
Q

Fibric Acid Derivative MOA

A

stimulates the PPAR-alpha, reduces TGs by 50%

153
Q

Fibric Acid Derivatives Physio effects

A

decreases VLDL synthesis
9% decrease in LDLs
10-20 increase in HDLs
Effective in pts with hypertriglyceridemia

154
Q

Fibric Acid Derivative side effects

A

gall stones
GI irritation
GI/hepatic tumors

155
Q

Fibric Acid Derivative contraindications

A

pts on warfarin - increases anticoag effect

156
Q

NEW CETP inhibitors in development: Anacetrapib

A

40% decrease in LDL
138% increase in HDLs
Acceptable SE profile
Did not produce adverse CV effects and mortality observed with predecessors

157
Q

Class 1A Na Channel Blockers

A

Procainamide, Quinidine, Disopyramide

158
Q

Class 1A Na Channel Blocker Effects

A

moderate potency to block Na channel
slows upstroke of AP, Increase AP duration (increases phase 0 and 3)
reduce conduction felocity
increase refractoriness

159
Q

Class 1A Na Channel Blocker uses

A

atrial and ventricular arrhythmias

160
Q

Important features of Class 1A Na Channel Blockers

A

drugs preferentially target rapidly depolarizing tissue more than normal tissue
prolonging repolarization = increased refractory period (effective in stopping re-enterant arrhythmias

161
Q

Class 1B Na Channel Blockers

A

Lidocaine

162
Q

Class 1B Na Channel Blocker Effects

A

Low potency Na blockers
have highest affinity for Na channels in ischemic cells
reduce phase 0 slope and slows conduction
reduces automaticity and phase 4 slope
increase refractoriness

163
Q

Class 1B Na Channel Blocker uses

A

ventricular arrhythmias

ineffective in atrial tissue

164
Q

Class 1B Na Channel Blockers unique features

A

lidocaine - highly lipophilic
reduces ventricular tachycardias or Vfib after cardioversion
clinical trials = decreased survival after MI when used long term

165
Q

Class 1C Na Channel Blockers

A

Flecainamide, Propafenone

166
Q

Class 1C Na Channel Blocker effects

A

high potency Na blockers with some K blocking potential
decreases phase 0 slope and AP conduction
increases AP duration and refractoriness especially in atrial cels at fast rates and AV nodes

167
Q

Class 1C Na Channel Blocker uses

A

supraventricular arrhythmias (nodal arrhythmias)

168
Q

Class 1C Na Channel Blocker unique features

A

increases AP duration disporportionately more in atria at fast rates
increases mortality in patients recovering from MI

169
Q

Class 1 Antiarrhythmic Side Effects

A 
provoke or increase arrhythmias
exacerbate congstive heart failure
heart block (block AV node)
Hypotension
GI distress
Sedation, tremor, dizziness, blurred vision
nausea, vomiting
170
Q

Class 2 antiarrhythmics (B-blockers)

A

propranolol, sotalol, esmolol

171
Q

Class 2 antiarrhythmic effects

A

increases AV refractoriness
decreases conduction velocity
increases AP duration (atria, nodal tissue)

172
Q

Class 2 antiarrhythmic uses

A

atrial tachycardia and ventricular tachycardia

173
Q

Class 2 antiarrhythmic unique features

A

reduces mortality after MI (new studies say maybe not)

174
Q

Class 2 antiarrhythmic side effects

A 
relatively well tolerates
CV: bradycardia, HF, low exercise tolerance
Rebound effect
Bronchospasm (B2)
Sedation (lipophilic B2)
Metabolic effects (increased TGs)
175
Q

Class 3 antiarrhythmics

A

amiodarone (most freq), dronederone, dofetilide

176
Q

Class 3 antiarrhythmic effects

A

blocks K channels

increases repolarization phase and AP duration

177
Q

Class 3 antiarrhythmic uses

A

nost arrhythmias (atrial/ventricular)

178
Q

Class 3 antiarrhythmic unique features

A

highly lipophilic, concentrates in tissues, therefore very long t1/2 (25-110 days)
SLIGHTLY decreases mortality after MI

179
Q

Class 3 antiarrhythmic Side Effects

A

75% of pts
hypotension and decreased LV contractility
muscle weakness
hypo/hyperthyroidism
pulmonary fibrosis (rare but can be fatal)

180
Q

Class 4 antiarrhythmics

A

verapamil, diltiazem (no dihydropyridines)

181
Q

Class 4 antiarrhythmic effects

A

blocks Ca channels
decreases slope of phase 4, increases AP, decreases automaticity
decreases HR
decreases AV conduction

182
Q

Class 4 antiarrhythmic uses

A

atrial tachycardias, Afib, AV node arrhythmias

183
Q

Class 4 antiarrhythmic unique features

A

do not reduce mortality after MI (do not increase either)

Dihydropyridines are ineffective

184
Q

Class 4 antiarrhythmic side effects

A 
mostly with concomitant therapy
hypotension (w/ vasodilators)
sinus bradycardia (w/ B blockers)
Heart block (w/ B blockers)
decreased contractility
constipation
185
Q

Adenosine MOA

A

stinulates adenosine receptors
opens K channels, hyperpolarizes membrane
inhibits pacemaker current in Ca channels

186
Q

Adenosine use

A

supraventricular rhythms, must be given IV, usually in hospital setting

187
Q

Adenosine side effects

A

Asystole (transient)

hypotension

188
Q

Digoxin MOA

A

increases AV node refractoriness

189
Q

Digoxin uses

A

AV re-entrant rhythms, atrial fibrilation (HF)

190
Q

Digoxin side effects

A 
triggered rhythms
AV block (reduced coordination of contraction)

PDA (2 decks)

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