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Pharmacology > Pharm Unit 4 > Flashcards

Pharm Unit 4 Flashcards

1
Q

Heparin is found in _____ along with histamine and serotonin

A

Mast cells

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2
Q

Is heparin acidic or basic?

A

Strongly acidic!

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3
Q

What is the function of the heparin pentasaccharide sequence?

A

Allows heparin to bind to ATIII (co-factor)

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4
Q

How many units of heparin are in a 1 mg dose?

A

120 USP units; 1 unit = 12 micrograms

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5
Q

What are the actions of heparin?

A

Inhibits actions of Factor IIa and Factor Xa Also inhibits other serine proteases (IVa, XIa, XIIa) Inhibits platelet aggregation at high concentrations Causes release of tissue factor pathway inhibitor

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6
Q

Heparin MOA

A

Binds to ATIII - induces conformational change in ATIII - 1000x greater affinity for clotting factors Acts as an anticoagulant

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7
Q

Actions of heparin

A

Plasma clearing effect - plasma cleared of fat chylomicrons by release of lipase from vessels Causes release of tissue factor pathway inhibitor (TFPI)

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8
Q

How is heparin administered?

A

IV or subcutaneous injection

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9
Q

Therapeutic range for heparin is achieved when the APTT is ___x baseline

A

2-2.5x baseline value

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10
Q

Endogenous modulator of heparin action

A

ATIII - heparin co-factor TFPI - released from endothelial cells Platelet factor 4 - released by activated platelets; binds to heparin and neutralizes it

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11
Q

Heparin side effects

A

Hemorrhagic complications - adrenal, gut Heparin induced thrombocytopenia - patient develops antibody to heparin-platelet factor 4 complex; activation of platelets leads to thrombus formation Osteoporotic manifestations Alopecia after long term use

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12
Q

Clinical uses of heparin

A

Therapeutic anticoagulation Surgical anticoagulation - only drug used for coronary bypass Prophylactic anticoagulation Thrombotic and ischemic stroke

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13
Q

What compound neutralizes heparin?

A

Protamine sulfate

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14
Q

Protamine is acidic or basic?

A

Strongly basic - combines with strongly acidic heparin to form a stable salt Need to give protamine as slow infusion - may cause bradycardia and hypotension

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15
Q

Benefits of LMW heparin

A

Increased bioavailability (100% vs 30%) and longer course of action; only need to give one injection per day

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16
Q

Example of LMW heparin

A

Enoxaparin

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17
Q

Indications for antithrombin concentrates

A

Treating patients with acquired or congenital antithrombin deficiency Also useful in sepsis and DIC

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18
Q

R-hirudin

A

Used in the treatment of heparin induced thrombocytopenia

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19
Q

Argatroban

A

Synthetic antithrombin agent used in patient who cannot be treated with heparin; special usage in heparin induced thrombocytopenia

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20
Q

Bivalirudin

A

Synthetic antithrombin agent; used for PTCA anticoagulation

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21
Q

What is warfarin used for?

A

Prophylactically used to prevent thrombotic disorders and to treat established thrombi

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22
Q

Warfarin MOA

A

Vitamin K analogue Warfarin inhibits Factors II, VII, IX, and X; inhibits carboxylation of glutamic acid and formation of gamma carboxyl glutamic acid (blocks vitamin K epoxide reductase)

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23
Q

What test is used to measure effects of warfarin?

A

PT/INR As level of clotting factors decrease, INR value increases Therapeutic effect achieved at 1.5x baseline value

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24
Q

Warfarin pharmacokinetics

A

Given orally - 100% bioavailability T 1/2 - 36 hours Highly protein bound - drugs with high binding may displace warfarin and lead to bleeding Undergoes hepatic metabolism

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25
Q

Factors that affect dose of oral anticoagulants

A

Nutrition - foods that contain vitamin K Anemia - high plasma volume, drug will be more diluted Liver disease - decreased coagulation proteins means greater effects of warfarin Biliary obstruction - decreased absorption of warfarin Drug interactions - especially highly protein bound drugs

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26
Q

Warfarin toxicity

A

Hypoprothrombinemia - echymosis, purpura, hematuria, hemorrhage All oral anticoagulants pass placental barrier and may cause fetal malformation Necrosis - due to impaired functionality of protein C

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27
Q

Treatment of warfarin toxicity

A

Replacement of 4 factors Recombinant Factor VIIa Vitamin K and related agents (used to treat warfarin induced hypoprothrombinemia)

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28
Q

Vitamin K and related agents

A

Uses: Drug induced hypoprothombinemia; intestinal disorders and surgery; hypoprothrombinemia of newborns

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29
Q

What are the oral anti-Xa agents?

A

Rivaroxaban Edoxaban Apixiban

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30
Q

What are the oral anti-thrombin agents?

A

Dabigatran

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31
Q

Rivaroxaban

A

Anti-Xa agent Fixed once daily dosing - good for elderly patients Renal clearance - adjust for patients with RI Potent CYP 3A4 inhibitor

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32
Q

Apixiban

A

Anti-Xa agent Used more often than rivaroxaban due to less renal clearance Potent CYP 3A4 inhibitor

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33
Q

Dabigatran

A

Anti-IIa agent Renal clearance - adjust for patient in RI Interferes with protein pump

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34
Q

Edoxaban

A

Half-life is 10-14 hours Decreased plasma protein binding 35% excreted by kidney 62% bioavailability

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35
Q

Light granules release:

A

Fibrinogen Factors V and VIII Platelet factor 4 - neutralizes heparin PDGF

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36
Q

Dark granules release:

A

Calcium Serotonin Histamine ADP/ATP

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37
Q

ADP receptor inhibitors (anti-platelet drugs)

A

Ticlopidine Clopidogrel Prasugrel Ticagrelor* Cangrelor* ** denotes drug that is already converted; the rest are prodrugs - better for patients with hepatic insufficiency

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38
Q

Dipyridamole

A

MOA - increases cAMP in platelets, prevents platelets from being used in thrombotic transformation Phosphodiesterase inhibitor and coronary vasodilator

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39
Q

Cilostazol

A

Phosphodiesterase inhibitor - anti-platelet agent Used for management of intermittent claudication

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40
Q

Abciximab

A

Gp IIb/IIIa inhibitor - prevents platelet aggregation Most commonly used IV agent in coronary and neurologic indications

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41
Q

Aspirin and NSAIDs

A

COX-1 and COX-2 inhibitors Prevent conversion of arachidonic acid to thromboxane - decrease platelet aggregation

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42
Q

Clopidogrel

A

ADP receptor inhibitor Prevents platelet activation Polymorphisms exist that make individuals less sensitive to clopidogrel - NOT SEEN WITH PRASUGREL

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43
Q

Antiplatelet drugs - clinical uses

A

Cerebrovascular disease - transient ischemic attack; stroke

Coronary artery disease - Acute MI; unstable angina

Peripheral vascular disease - venous thrombosis; peripheral arterial disease

Small vessel disease - membrane proliferative glomerulonephritis; thrombotic thrombocytopenic purpura

Prevention of thrombus formation on artificial surfaces

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44
Q

Zileuton

A

Inhibits lipoxygenase pathway - prevents conversion of arachidonic acid to leukotrienes

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45
Q

Montelkast

A

Leukotriene antagonist - used in treatment of asthma and seasonal allergies

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46
Q

Zarirlukast

A

Leukotriene antagonist - used in treatment of asthma

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47
Q

Omega-3 fatty acids

A

Lead to thromboxane A3 formation - not a potent vasoconstricting and platelet aggregating agent; decreases platelet aggregation

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48
Q

What compounds are capable of converting plasminogen into plasmin?

A

TPA Urokinase Streptokinase Factor XIIa

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49
Q

What are the physiological inhibitors of thrombolytics?

A

Plasminogen activator inhibitor 1 (PAI-1) TAFI Alpha 2 antiplasmin Alpha 2 macroglobulin

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50
Q

What is produced when stabilized fibrin clots are degraded by plasmin?

A

D dimers!

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51
Q

Factors which promote fibrinolysis

A

Plasminogen incorporation into thrombus Release of TPA by endothelial cells Binding of TPA to fibrin - TPA is an activator of thrombolysis; activates plasminogen

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52
Q

Factors which limit fibrinolysis

A

Fibrin crosslinking via Factor XIIIa Binding of alpha-2 antiplasmin to fibrin

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53
Q

Alteplase

A

Recombinant form of human TPA - most commonly used fibrinolytic agent

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54
Q

Reteplase

A

Mutant form of human TPA More fibrin specific Longer half life Comparable to tenecteplase

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55
Q

Clinical uses of thrombolytic agents

A

Acute MI - thrombus in coronary artery Peripheral arterial occlusion DVT Pulmonary embolism - only urokinase and streptokinase Thrombotic stroke - MCA occlusion Catheter clearance

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56
Q

Complications of thrombolytic therapy

A

Bleeding Re-occlusion due to free split products Stroke

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57
Q

Contraindications of thrombolytic therapy

A

Intracranial bleeding Massive hemorrhage

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58
Q

Pharmacological antagonists for thrombolytic agents

A

EACA - epsilon amino caproic acid Transexemic Acid Aprotonin

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59
Q

Ancrod

A

Snake venom-like drug that can digest fibrinogen

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60
Q

Statins - Clinical effects

A

20-60% reduction in LDL Modest reduction in triglycerides Modest increase in HDL

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61
Q

Statin MOA

A

Statins completely inhibit HMG-CoA reductase - inhibit endogenous cholesterol synthesis Activates SREBP - increases expression of LDL receptor at plasma membrane - leads to increased clearance of serum LDL and excretion in bile

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62
Q

Therapeutic uses of statins

A

Drug of choice for treating patients with increase LDL-C Drug of choice for both primary and secondary prevention of coronary heart disease

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63
Q

Statin adverse effects

A

Mostly mild GI disturbances Increase liver enzymes - rare Small increased risk of T2DM but benefits outweigh risks Major effects are on the muscles - 5-10% experience myalgia and myopathy Most serious side effect - rhabdomyolysis

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64
Q

Statin pharmacokinetics

A

Absorbed in intestine - 30-85% Lovastatin, simvastatin, atorvastatin metabolism by CYP 3A4 (grapefruit juice increased bioavailability of statins) Pravastatin - not metabolized by CYP 450 enzymes; good choice for patients with hepatic impairment or drug interactions

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65
Q

Ezetimibe

A

Cholesterol absorption inhibitor

MOA - Lowers LDL concentration, increased LDL receptor density

Therapeutic uses - decreases LDL in patients with primary hypercholesterolemia; further lowers LDL when used with statins

Adverse effects - generally well tolerated; flatulence; diarrhea

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66
Q

What are the bile acid binding resins used to treat hypercholesterolemia?

A

Cholestyramie

Colestipol

Colesevelam

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67
Q

Bile acid bindings resins

A

Cholestyramine, Colestipol, Colesevelam

Decrease LDL but may cause slight increase in triglycerides

MOA - bind bile acids and prevent their reabsorption; leads to increased bile acid synthesis and decreased cholesterol synthesis (via cholesterol -7a-hydroxylase); increased expression of LDL receptors

Therapeutics uses - combination with statins (dramatic decrease in LDL); used in patients in whom statins are contraindicated (pregnancy, liver dysfunction)

Adverse effects - high concentrations impair absorption of Vitamins A, D, E, K; may impair absorption of other drugs

Contraindications - patients with high triglycerides

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68
Q

What are the PCSK9 inhibitors indicated in the treatment of hypercholesterolemia?

A

Avrilocumab

Evolocumab

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69
Q

PCSK9 inhibitors

A

Avirlocumab, Evolocumab

MOA - binds PCSK9, prevent internalization and degradation of LDL rececptor; increases LDL receptor density on plasma membrane

Uses - familial hypercholesterolemia and patients that have not achieved goals with statins

Avirlocumab leads to decrease in LDL even in presence of high dose statins

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70
Q

Elevated triglycerides place someone at risk of what conditions?

A

Cardiovascular disease and pancreatitis

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71
Q

What is the most effective drug at raising HDL?

A

Niacin - 10-30% increase in HDL with a 50-80% decrease in triglycerides

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72
Q

Niacin

A

50-80% reduction in triglycerides, 10-30% increase in HDL

Most effective drug for raising HDL

MOA - complex; increased LDL clearance; increased HDL synthesis; decreased levels of Lp (a) - leads to increased thrombolysis and destruction of plaques

Indications - patients with elevated triglycerides and cholesterol - familial combined hyperlipidemia

Adverse Effects - skin flushing and pruritis; can predispose gout; can exacerbate peptic ulcer disease

Contraindications - gout; peptic ulcer disease; impaired liver function; T2DM

73
Q

Fibrates

A

Fenofibrate, Gemfibrozil

MOA - decrease VLDL and increase HDL

Therapeutic Uses - high LDL associated with high triglycerides

Adverse effects - predisposition to gallstones; Gemfibrozil inhibits statin glucuronidation and predisposes to rhabdomyolysis (increases concentration of all statin drugs)

Drug interactions - highly protein bound, can displace other protein bound drugs; Gemfibrozil should not be used with statins

Contraindications - patients with renal dysfunction of pre-existing gallbladder disease

74
Q

Omega 3 fatty acids

A

Reduce triglycerides 30-50%; minor increase in HDL; can increase LDL in some individuals

Therapeutic uses - adjunct to diet in individuals with triglycerides over 500 mg/dL

75
Q

What are some common ACE inhibitors?

A

Captopril, Enalapril, Lisinopril

76
Q

What are some common angiotensin receptor blockers?

A

Losartan, Valsartan

77
Q

What is/what are the physiological effects of Desmopressin?

A

Desmopression - ADH analogue

Effects - increases Factor VIII and vWF in plasma; used in blood banking; used to control minor surgical bleeding

78
Q

What drug is used to inhibit endothelin function?

A

Bosentan

79
Q

What are some vasopeptide inhibitors and what do they do?

A

Omapatrilat, Sampatrilat, Fasidotrilat

Increase levels of natriuretic peptides and decrease formation of angiotensin II - leads to increase vasodilation and sodium excretion (decreases intravascular volume)

80
Q

What receptor does Icatibant bind to and what does it do?

A

Binds to bradykinin B2 receptor - inhibits actions of bradykinin (can be used to treat hypotension)

81
Q

What does Aprotonin do?

A

Aprotonin is a kallikrein inhibitor - prevents formation of bradykinin (inhibits vasodilation)

82
Q

What are the thiazide diuretics used to treat hypertension?

A

Hydrochlorothiazide and chlorthalidone; diuretics are drugs of choice for treating uncomplicated hypertension

83
Q

Hydrochlorothiazide

A

MOA - inhibit Na/Cl transporter on lumenal side of distal convoluted tubule Side effects - hyponatremia, hypokalemia, metabolic alkalosis, hyperglycemia, increased LDL/HDL ration Contraindications - hyperkalemia Drug interactions - NSAIDs, beta blockers

84
Q

Furosemide

A

MOA - inhibits Na/K/2Cl transporter in loop of Henle Side effects - hyponatremia, metabolic alkalosis, hypokalemia, impaired diabetes control, increased LDL/HDL ratio, ototoxicity Drug interactions - NSAIDs, aminoglycosides (worsen ototoxicity)

85
Q

What are the potassium sparing diuretics used to treat hypertension?

A

Spironolactone, eplerenone, triamterene, and amiloride

86
Q

Spironolactone

A

MOA - aldosterone receptor antagonist (prevents insertion of Na channels in collecting duct; more sodium excreted, less potassium excreted) Side effects - hyperkalemia, gynecomastia Drug interactions - NSAIDs, ACE inhibitors and angiotensin receptor blockers (potentiate hyperkalemia) Contraindications - renin-angiotensin-aldosterone system inhibitors (potentiate hyperkalemia)

87
Q

What are the two types of calcium channel blockers?

A

Dihydropyridines - block calcium channels in vascular smooth muscle Non-dihydropyridines - block calcium channels in vascular smooth muscle and cardiac muscle

88
Q

Calcium channel blocker MOA

A

All reduce vascular resistance by reducing calcium influx in vascular smooth muscle Non-dihydropyrides also reduce pacemaker potential, AV node conduction, and contractility *ND blockers contraindicated in patients with conduction disturbances, use with caution in patients on beta blockers, avoid use for chronic hypertension

89
Q

Nifedipine

A

Dihydropyridine calcium channel blocker (limited effect on pacemaker or conduction/contractility) Side effects - acute tachycardia, peripheral edema

90
Q

Diltiazem

A

Non-dihydropyridine calcium channel blocker Side effects - bradycardia

91
Q

Verapamil

A

Non-dihydropyridine calcium channel blocker Side effects - bradycardia and constipation

92
Q

Clonidine

A

MOA - alpha 2 adrenergic receptor agonist (decreases sympathetic outflow from CNS) Withdraw drug slowly to avoid rebound hypertension Side effects - sedation, dry mouth, bradycardia Guanfacine - similar, longer half life and less chance of rebound

93
Q

Methyldopa

A

MOA - converted to methylnorepinephrine (alpha 2 agonist, decreases sympathetic CNS outflow); also competes with L-DOPA for dopamine carboxylase (decreases dopamine production) Interactions - Levodopa Side effects - sedation (decreased sympathetic activation)

94
Q

Reserpine

A

MOA - blocks VMAT vesicular transport (prevents NE storage in vesicles) Combined with diuretics, used for patients who are resistant to many other drugs Side effects - depression, nasal congestion Drug interactions - CNS depressants, MAOIs

95
Q

Phenoxybenzamine

A

MOA - non-selective alpha adrenergic receptor antagonist Side effects - tachycardia (NE binding to beta-1 receptors since alpha are blocked)

96
Q

Prazosin

A

MOA - selective alpha-1 adrenergic antagonist; less tachycardia than direct vasodilators Side effects - hypotension Terazosin and doxazosin have longer half lives

97
Q

Propranolol

A

MOA - non-selective beta blocker Used as adjunct to prevent tachycardia

98
Q

Nadolol

A

MOA - non-selective beta blocker Longer half life than propranolol

99
Q

Pindolol

A

MOA - non-selective partial agonist beta blocker Less bradycardia than other beta blockers

100
Q

Metoprolol

A

MOA - selective beta-1 blocker, somewhat lipophilic (can get into brain and decrease anxiety)

101
Q

Atenolol

A

MOA - selective beta-1 blocker Hydrophilic, eliminated by kidneys

102
Q

Labetolol

A

MOA - beta blocker with some alpha blocking capacity Lipophilic

103
Q

Carvedilol

A

MOA - non-selective beta blocker and alpha receptor antagonist Acts as a vasodilator

104
Q

Beta blocker side effects

A

Bradycardia

Increased triglycerides

Hyperglycemia

Impaired exercise tolerance

Increased airway resistance (non-selectives)

Insomnia and chronic fatigue - lipophilic beta blockers

Can mask and prolong insulin-induced hypoglycemia

Less efficacious as monotherapy in African Americans but efficacious when combined with beta blockers

105
Q

Hydralazine

A

MOA - vasodilator, used in drug resistant hypertension or emergency

Side effects - tachycardia, angina aggravation, fluid retention

NSAIDs reduce effectiveness

106
Q

Minoxidil

A

MOA - vasodilator, used to treat drug resistant hypertension

107
Q

Nitroprusside

A

MOA - vasodilator, used in emergencies

Side effects - cyanide poisoning

108
Q

ACE inhibitors

A

MOA - block production of angiotensin II (vasoconstrictor and aldosterone releasing agent); increases circulating levels of bradykinin

Side effects - increased bradykinin may lead to dry cough, hyperkalemia, angioedema

Captopril - short half life

Enalapril - converted to active metabolite, longer half life, longer onset of action

Lisinopril - water soluble

Contraindications - pregnancy, bilateral renal stenosis

ACE inhibitors prolong survival in patients with heart failure or left ventricular dysfunction after MI

Preserve renal function in diabetic patients

109
Q

Losartan

A

MOA - angiotensin receptor blocker (mediate vasoconstriction and sodium retention)

Side effects - hyperkalemia

Contraindications - pregnancy

Drug interactions - K sparing drugs

110
Q

Good combinations of hypertensive medications

A

Thiazide/loop diuretic + potassium sparing diuretic

Thiazide diuretic + beta blocker

Calcium channel blocker + ACE inhibitor

111
Q

Preferred therapy for DM

A

ACE inhibitors

112
Q

Preferred therapy for heart failure

A

ACE inhibitors

113
Q

Preferred therapy for MI

A

ACE inhibitors, beta blockers

114
Q

Consideration for pregnancy

A

Avoid ACE inhibitors or ARBs

115
Q

Considerations for AA

A

Monotherapy with diuretics or calcium channel blockers most efficacious; avoid monotherapy with beta blockers, ACE inhibitors

116
Q

Considerations for elderly

A

Give drugs in small increments, monitor side effects closely

117
Q

Considerations for obstructive airway disease

A

Avoid non-selective beta blockers

118
Q

Procainamide

A

Class IA sodium channel blocker

Slows upstroke of the AP, conduction, prolongs QRS complex Indications - atrial and ventricular arrhythmia

Side effects - risk of hypotension; can induce torsades de pointes (ventricular tachycardia); long term use can lead to lupus erythematosus

119
Q

Quinidine

A

Class IA sodium channel blocker

Rarely used because of cardiac and extra-cardiac adverse effects

Side effects - can induce V-fib and torsades de pointes; cinchonism - headache, dizziness, tinnitus

120
Q

Lidocaine

A

Class IB sodium channel blocker

Selective depression of conduction in depolarized cells

First choice for treating ventricular tachycardia and fibrillation after cardioversion in ischemia/infarct

Metabolism - extensive first pass metabolism (increased concentration in liver disease)

Side effects - least cardiotoxic of class I drugs; may induce hypotension (decreased contractility); some neuro side effects due to anesthetic properties (nausea, lightheadededness, hearing disturbances)

121
Q

Mexiletine

A

Class IB sodium channel blocker

Orally available lidocaine analogue

Can be used off label for chronic pain

122
Q

Flecainide

A

Class IC sodium channel blocker

Used to treat supraventricular arrhythmia in patients with otherwise normal hearts

Increases mortality in patients with ventricular tachyarrhythmia, MI, ventricular ectopy

123
Q

Propafenone

A

Class IC sodium channel blocker

Used to treat supraventricular arrhythmia in patients with otherwise normal hearts

Side effects - same effects as flecainide plus bradycardia, bronchospasm

124
Q

Amiodarone

A

Class III drug - prolongs AP duration

Structural analogue of thyroid hormone

Effects - blocks K and Na channels, weakly blocks Ca channels, inhibits beta receptors; prolongs refractoriness and slows conduction

Indications - recurrent v-tach or fibrillation; atrial fibrillation; drug of choice for out of hospital cardiac arrest, termination of ventricular tachycardia or fibrillation

Adverse effects - bradycardia/heart block; pulmonary toxicity (may lead to fibrosis); blocks conversion of T4 to T3

125
Q

Dronedarone

A

Similar to amiodarone but without effects on thyroxine metabolism

Contraindicated in severe or recently decompensated symptomatic heart failure

126
Q

Verapamil

A

Class IV calcium channel blocker

High cardiac selectivity; directly slows AV node conduction and refractorines; slows SA node automaticity

Indications - supraventricular arrhythmia (drug of choice); re-entry arrhythmia, tachycardia involving AV node; slows ventricular rate in atrial flutter/fibrillation

Side effects - negative inotropic effects; contraindication in ventricular tachycardia (can lead to hypotension); vasodilation; peripheral edema

127
Q

Diltiazem

A

Class IV calcium channel blocker

Similar effects as verapamil

128
Q

Adenosine

A

Acts via purinergic receptors to increase K+ conductance (leads to hyperpolarization)

Primary action on atrial tissue - slows AV node conduction and increases AV node refractoriness

Drug of choice for converting paroxysmal SVT to sinus rhythm

Side effects - bradycardia, sinus pauses, AV block, hypotension

129
Q

What effect on the heart do vagal maneuvers have? (diving reflex/Valsalva maneuver)

A

Slow conduction through the AV node - acute treatment for paroxysmal SVT

130
Q

What are the drugs of choice for treating uncomplicated hypertension?

A

Diuretics

131
Q

Hydrochlorothiazide/Chlorthalidone

A

MOA - inhibit Na/Cl cotransporter in distal convoluted tubule; decrease blood volume

Side effects - hyponatremia; hypokalemia; hyperglycemia; increased LDL/HDL ratio

Contraindications - hypokalemia

Relative contraindication - pregnancy (patient can stay on if previously on it but needs to be monitored)

Can be combined with beta-blockers, ACE inhibitors, aldosterone receptor blockers, centrally acting hypertensives

Drug interactions - NSAIDs

132
Q

Furosemide

A

Loop diuretic - inhibits Na/K/2 Cl transporter in thick ascending loop

Side effects - hyponatremia; hypokalemia; metabolic alkalosis; impaired diabetes control; increased LDL/HDL ratio; ototoxicity

Drugs interactions - NSAIDs; aminoglycosides (worsens ototoxicity)

133
Q

Spironolactone

A

Potassium sparing diuretic

MOA - aldosterone receptor antagonist

Side effects - hyperkalemia; gynecomastia

Drugs interactions - NSAIDs; ACE inhibitors and angiotensin receptor blockers (exacerbate effects, hyperkalemia due to less aldosterone activation and less potassium excretion)

Contraindications - RAS inhibitors (can exacerbate hyperkalemia)

134
Q

Nifedipine

A

Dihydropyridine calcium channel blocker (specific for vascular smooth muscle)

Side effects - acute tachycardia (baroreflex); peripheral edema (vasodilator effect)

135
Q

Diltiazem

A

Non-dihydropyridine calcium channel blocker (vascular and cardiac smooth muscle)

Side effects - bradycardia

136
Q

Verapamil

A

Non-dihydropyridine calcium channel blocker (vascular and cardiac smooth muscle)

Side effects - bradycardia and constipation

137
Q

Who are non-dihydropyridines contraindicated in?

A

Patients with conduction disturbances; use with caution in patients who are taking beta-blockers (can cause severe bradycardia)

138
Q

Clonidine

A

MOA - alpha 2 receptor agonist; decreases sympathetic outflow from CNS (acts as a vasodilator, decreased action at alpha 1 receptors)

Must withdraw drug slowly to avoid rebound hypertension

Side effects - sedation; dry mouth (sympathetic NS leads to salivation); bradycardia

Guanfacine has longer half life and less chance of rebound

139
Q

Methyldopa

A

MOA - competes for DOPA decarboxylase with L-DOPA; acts as an alpha 2 agonist following metabolism

Most extensively used anti-hypertensive in pregnancy

Side effects - sedation; decreased dopamine production

Interactions - levodopa (decreases dopamine production)

140
Q

Reserpine

A

MOA - blocks VMAT vesicular transport (prevents storage of NE centrally and peripherally; less NE = less alpha 1 activation = lower BP)

Combined with other diuretics - used for patients who are resistant to other drugs

Side effects - depression; nasal congestion

Drug interactions - CNS depressants; MAOIs (buildup of NE in the cytosol leads to inappropriate release)

141
Q

Phenoxybenzamine

A

Non-selective alpha adrenergic antagonist

Side effects - tachycardia (blockade of alpha receptors causes NE to bind to beta-1 receptors)

142
Q

Prazosin

A

MOA - selective alpha 1 adrenergic antagonist

Less tachycardia than direct vasodilators

Terazosin and Doxazosin have longer half lives than Prazosin

Side effects - hypotension (blockade of alpha 1 receptor); may decrease LDL/HDL ratio - good for patients with hyperlipidemia

143
Q

Beta-blockers

A

MOA - decrease contractility, reduce cardiac output, decrease renin release (less vasoconstriction)

Side effects - bradycardia, hyperglycemia (can mask and prolong insulin-induced hypoglycemia), increased airway resistance in non-selectives

Drug interactions - calcium channel blockers (decreased contractility and conduction)

Contraindications - cardiogenic shock, sinus bradycardia, asthma, severe heart failure Less efficacious as monotherapy in AA, efficacious when combined with diuretic

144
Q

When should vasodilators be indicated in hypertension?

A

Used for patients who are resistant to other therapies or in emergencies

145
Q

Hydralazine

A

Used in drug resistant hypertension or in emergency

Side effects - tachycardia (baroreflex to low BP); angina aggravation (decreased venous return); fluid retention

146
Q

ACE inhibitors

A

Captopril, Enalapril, Lisinopril

MOA - block production of angiotensin II and downstream aldosterone; increase levels of bradykinin Captopril - short half life Enalapril - longer half life, has to be converted to metabolite Lisinopril - water soluble, excreted unchanged by kidney

Side effects - hyperkalemia; dry cough (associated with bradykinin); angioedema (allergic reaction, skin and mucosal swelling)

Drug interactions - exacerbates hyperkalemia with potassium sparing diuretics

Contraindications - pregnancy (need ATII for normal development); bilateral renal stenosis

Prolong survival in patients with HF or LV dysfunction following MI (prevent remodeling)

Preserve renal function in diabetics

147
Q

Losartan

A

MOA - angiotensin II receptor blocker (decreased vasoconstriction and sodium retention)

Selectively blocks AT1 receptor

Side effects - hyperkalemia

Contraindications - pregnancy

Drug interactions - K+ sparing diuretics

148
Q

What is the mechanism of action of nitrates in vivo?

A

Decrease venous return

Decrease LV wall tension

Reduce afterload

Direct coronary artery vasodilation

149
Q

Clinical uses of nitrates

A

Angina pectoris (stable, unstable, Prinzmetal)

Hypertensive crisis

Congestive heart failure (decrease venous return to heart)

150
Q

Side effects of nitrates

A

Exaggeration of therapuetic effects - orthostatic hypotension; reflex tachycardia; headache

Nitrate tolerance - leads to nitrosylation of proteins

151
Q

Clinical uses of calcium channel blockers

A

Angina pectoris

Hypertension

Arrhythmias (slow SA node conduction)

Hypertrophic cardiomyopathy

Migraine

152
Q

What are the dihydropyridine calcium channel blockers and what do they do?

A

Nifedipine Amlodipine Nicardipine

Act on vascular smooth muscle calcium channels - lead to vasodilation

153
Q

What are the non-dihydropyridine calcium channel blockers and what do they do?

A

Verapamil Diltiazem Bepridil

Act on vascular but also cardiac calcium channels - have negative inotropic and chronotropic effects (decrease HR and contractility)

154
Q

Side effects of calcium channel blockers

A

Bradycardia (verapamil)

CHF (verapamil - due to decreased contractility)

Heart block

Hypotension

Reflex tachycardia

Peripheral edema

155
Q

Clinical effects of beta blockers

A

Decreased HR

Decreased contractility

Decreased myocardial oxygen demand

Increased diastolic perfusion

Increased oxygen supply

156
Q

Clinical uses of beta blockers

A

Angina pectoris

Hypertension

Arrhythmia

Dissecting aortic aneurysm

Mitral valve prolapse

Post MI prophylaxis (prevents remodeling)

Hyperthyroidism

Migraine

157
Q

Nonselective beta blockers with intrinsic sympathomimietic activity

A

Pindolol Labetalol

158
Q

Cardioselective beta blockers with intrinsic sympathomimetic activity

A

Acebutolol

159
Q

Side effects of beta blockers

A

Bronchospasm

Peripheral vasospasm

Exaggeration of therapeutic effects - heart block; bradycardia

CNS effects - insomnia; depression; fatigue

160
Q

Beta blocker contraindications

A

Insulin-dependent diabetes

Acute CHF

Advanced AV nodal block

Peripheral vascular disease

Bronchospasm

Marked bradycardia

Sexual impotence

161
Q

Ivabradine

A

MOA - funny current inhibitor; indicated in patients who cannot take beta blockers

Side effects - luminous phenomenon; bradycardia; AV nodal block

162
Q

What are common causes of acute CHF?

A

Large MI (involving over 40% ventricle)

Myocarditis

Arrhythmia

Cardiac tamponade

Pulmonary embolism

Acute valvular regurgitation

163
Q

What are common causes of chronic CHF?

A

Ischemic cardiomyopathy (most common in US)

Hypertrophic cardiomyopathy (HTN, stenosis, cor pulmonale)

Dilated cardiomyopathy (regurgitation, alcohol, genetic causes, idiopathic)

164
Q

What are the treatment objectives in acute CHF?

A

Reduce symptoms

Decrease pulmonary congestion (loop diuretics, venodilators)

Increase cardiac contractility (beta agonists)

Reduce afterload (nitroprusside)

165
Q

Diuretics used in acute CHF

A

Furosemide (Na/K/2Cl blocker - potent diuretic, rapid onset of action)

Thiazides - weaker, can be used with loop diuretics in patients resistant to furosemide

166
Q

Side effects of diuretics

A

Overdiuresis

Hyponatremia

Hypokalemia

Ototoxicity

Allergies (loop and thiazides are sulfa drugs)

Diuretic resistance (overcome by using drugs in combinations)

167
Q

Niseritide

A

MOA - promotes natriuresis and vasodilation; used to treat acute congestive heart failure

168
Q

Beta agonists used to treat acute CHF

A

MOA - increase cardiac contractility (contractility depressed in many forms of CHF)

Isoproterenol Dopamine Dobutamine NE

169
Q

Beta agonists increase cAMP in cardiac myocytes. What do increased cAMP levels lead to?

A

Increased opening of L type calcium channels

Increase reuptake of calcium into the SR

Increased pacemaker current

Increased rate of conduction

170
Q

What class of drugs is contraindicated in acute CHF?

A

Calcium channel blockers - lead to decreased contractility

171
Q

What are the treatment objectives in chronic CHF?

A

Reduce pulmonary congestion

Reduce afterload

Increase contractility (digitalis)

Prevent ventricular remodeling

Increase survival

172
Q

What drug is used in chronic CHF to increase contractility?

A

Digitalis

173
Q

What is the MOA of digitalis?

A

Partial inhibitor of Na/K ATPase; leads to increase intracellular and SR calcium; more calcium released with each contraction

174
Q

Mechanical effects of digitalis

A

Increased velocity of fiber shortening and force of contraction

Increased ventricular emptying

Decreased end-systolic and end-diastolic volumes

175
Q

Systemic effects of digitalis

A

Increased cardiac output

Increased renal perfusion

Decreased sympathetic activity

176
Q

What are some side effects associated with digitalis use?

A

DADs and abnormal automaticity

VPBs

V tach

Junctional tach

Side effects treated by administering digibind antibodies

177
Q

What patient population is digitalis primarily used in?

A

Used in patients with CHF and atrial fibrillation with rapid ventricular response

178
Q

What is the MOA whereby ACE inhibitors prevent ventricular remodeling in CHF?

A

ACE inhibitors prevent formation of angiotensin II - angiotensin II is a potent cardiomyocyte growth factor and fibroblast mitogen Leads to reduced systolic and diastolic wall stress

Angiotensin II is also a potent vasoconstrictor - blockade leads to vasodilation and reduction in afterload

179
Q

Are beta blockers indicated in chronic CHF?

A

YES! Beta blockers increase survival and prevent deterioration of LV performance in patients with mild-moderate CHF

Prevents deleterious effects of chronic sympathetic activation

Pharmacology (5 decks)

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