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CPR > First Aid Pharmacology > Flashcards

First Aid Pharmacology Flashcards

1
Q

Nifedipine

A
  • Dihydropyridine Calcium channel blocker
  • Blocks volt-dependent Ca2+ channels of cardiac & smooth m.
  • Reduces muscle contractility
  • Of CCBs nifedipine has most action of vessels and least on heart
  • Use: HTN, angina, Prinzemetal angina, Raynaud’s
  • Toxicity: Cardiac depression, AV block, edema, flushing, dizzy, constipation
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2
Q

Nitroprusside

A
  • Short acting
  • Increase cGMP via direct release of NO
  • Used for Malignant HTN
  • Tox: can cause cyanide toxicity
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2
Q

Fenoldapam

A
  • Dopamine D1 receptor agonist
  • Relaxes renal vascular smooth muscle
  • Used for Malignant HTN
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3
Q

Diazoxide

A
  • K+ channel opener
  • Hyperpolarizes and relaxes vascular smooth muscle
  • Used for malignant HTN
  • Tox: hyperglycemia by reducing insulin release
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4
Q

Verapamil

A
  • Non-dyhidropyradine Calcium channel blocker
  • Blocks volt-dependent Ca2+ channels of cardiac & smooth m.
  • Reduces muscle contractility
  • Of CCBs Verapamil has most action on heart and least on vessel
  • Use: Arrhythmias, HTN, angina, Prinzemetal angina, Raynaud’s
  • Toxicity: Cardiac depression, AV block, edema, flushing, dizzy, constipation
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5
Q

Diltiazem

A
  • Non-dyhidropyradine Calcium channel blocker
  • Blocks volt-dependent Ca2+ channels of cardiac & smooth m.
  • Reduces muscle contractility
  • Of CCBs Diltiazem has equal action on heart and vessel
  • Use: Arrhythmias, HTN, angina, Prinzemetal angina, Raynaud’s
  • Toxicity: Cardiac depression, AV block, edema, flushing, dizzy, constipation
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6
Q

Amlodipine

A
  • Long acting Dihydropyradine Ca2+ channel blocker
  • Blocks volt-dependent Ca2+ channels of cardiac & smooth m.
  • Reduces muscle contractility
  • Of CCBs Verapamil has most action on heart and least on vessel
  • Use: Arrhythmias, HTN, angina, Prinzemetal angina, Raynaud’s
  • Toxicity: Cardiac depression, AV block, edema, flushing, dizzy, constipation
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7
Q

Nitroglycerine

A
  • Vasodilate by releasing NO in smooth muscle
  • Increases cGMP-> smooth muscle relaxation
  • Dilates veins»arteries: decrease preload
  • Use: Angina, pulmonary edema, ED
  • TOX: reflex tachycardia, flushing, headache, tolerance for vasodilating action during workweek and loss over weekend resulting in tachycardia, dizziness, and headache on re-exposure in industrial setting
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8
Q

Isosorbide

A
  • Vasodilate by releasing NO in smooth muscle
  • Increases cGMP-> smooth muscle relaxation
  • Dilates veins»arteries: decrease preload
  • Use: Angina, pulmonary edema, ED
  • TOX: reflex tachycardia, flushing, headache, tolerance for vasodilating action during workweek and loss over weekend resulting in tachycardia, dizziness, and headache on re-exposure in industrial setting
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9
Q

Dinitrate

A
  • Vasodilate by releasing NO in smooth muscle
  • Increases cGMP-> smooth muscle relaxation
  • Dilates veins»arteries: decrease preload
  • Use: Angina, pulmonary edema, ED
  • TOX: reflex tachycardia, flushing, headache, tolerance for vasodilating action during workweek and loss over weekend resulting in tachycardia, dizziness, and headache on re-exposure in industrial setting
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10
Q

Statins: Lovastatin, pravastatin, simvastatin, etc

A
  • HMG-CoA Reductase inhibitors
  • Inhibits cholesterol precursor, mevalonate
  • Huge decrease in LDL
  • Mild increase in HDL
  • Mild decrease in TG
  • TOX: hepatotoxicity, rhabdo
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11
Q

Niacin

A
  • direct decrease in hepatic synthesis of VLDL
  • Inhibits lipolysis in fat
  • Decreases LDL
  • Increases HDL
  • Slight decrease TG
  • TOX: red, flush, hyperglycemia, hyperuricemia
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12
Q

Cholestyramine

A
  • Bile acid resins
  • binds bile acids in the intestinal lumen; inhibits the reabsorption of bile acid.
  • cholesterol is the precursor of bile acid
  • Inhibition of bile reabsorption causes increased channeling of cholesterol to the production of bile acids
  • Decreases LDL
  • Slightly increases HDL
  • Slightly increases TG
  • Tox: patients hate it…bad taste, GI upset, Decreased absorption of fat soluble vitamins, cholesterol gallstones
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13
Q

Colestipol

A
  • Bile acid resins
  • binds bile acids in the intestinal lumen; inhibits the reabsorption of bile acid.
  • cholesterol is the precursor of bile acid
  • Inhibition of bile reabsorption causes increased channeling of cholesterol to the production of bile acids
  • Decreases LDL
  • Slightly increases HDL
  • Slightly increases TG
  • Tox: patients hate it…bad taste, GI upset, Decreased absorption of fat soluble vitamins, cholesterol gallstones
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14
Q

Colesvelam

A
  • Bile acid resins
  • binds bile acids in the intestinal lumen; inhibits the reabsorption of bile acid.
  • cholesterol is the precursor of bile acid
  • Inhibition of bile reabsorption causes increased channeling of cholesterol to the production of bile acids
  • Decreases LDL
  • Slightly increases HDL
  • Slightly increases TG
  • Tox: patients hate it…bad taste, GI upset, Decreased absorption of fat soluble vitamins, cholesterol gallstones
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15
Q

Ezetimibe

A
  • works on the brush border of the gut wall to prevent cholesterol absorption through the intestinal villi
  • Decreases LDL
  • No effect on HDL or TG
  • Rare increase on liver function test
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16
Q

Gemfibrozil

A
  • binds to PPARα (peroxisome proliferator activated receptor α) in liver & brown fat.
  • PPARα activation regulates gene transcription resulting in:
    1. increased lipoprotein lipase activity -VLDL & TG catabolism
    2. decreased VLDL synthesis and excretion by liver
    3. increased HDL cholesterol (due to increased synthesis of apoA-I and apoA-II)
  • Decrease LDL, Increase HDL
  • HUGE decrease in TG
  • TOX: Myositis, hepatotoxicity, cholesterol gallstones
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17
Q

Fenofibrate

A
  • binds to PPARα (peroxisome proliferator activated receptor α) in liver & brown fat.
  • PPARα activation regulates gene transcription resulting in:
    1. increased lipoprotein lipase activity -VLDL & TG catabolism
    2. decreased VLDL synthesis and excretion by liver
    3. increased HDL cholesterol (due to increased synthesis of apoA-I and apoA-II)
  • Decrease LDL, Increase HDL
  • HUGE decrease in TG
  • TOX: Myositis, hepatotoxicity, cholesterol gallstones
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18
Q

Digoxin

A

-Cardiac Glycosides
-Direct inhibition of Na/K ATPase-> Indirect inhibition of Na/Ca exchanger
-Increases [Ca]i
-Positive inotropy (Contractility)
-Stimulates vagus nerve
-Use: CHF (increased contractility), Afib (decreased conduction at AVN and depression of SAN
-TOX: N/V/D blurry vision, Increased PR, Decreased QT, swooping T wave inversion, arrhythmia, hyperkalemia
*Worsened by renal failure: decreased excretion
*Hypokalemia: allow dig binding on Na/K ATPase
*Quinidine: decreased clearence
Antidote: Normalize K+, lidocaine, pacer, anti-dig Fab fragment

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19
Q

Quinidine

A
  • Class 1a Na+ channel blocker
  • Antiarrhythmetic
  • Increased AP duration
  • Increased effective refractory period
  • Increased QT interval
  • Affect both atrial and ventricular arrhythmias
    • especially reentrant and ectopic SVTs and VT
  • Tox: cinchonism- headache and tinnitus, thrombocytopenia, torsades de pointes
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20
Q

Procainamide

A
  • Class 1a Na+ channel blocker
  • Antiarrhythmetic
  • Increased AP duration
  • Increased effective refractory period
  • Increased QT interval
  • Affect both atrial and ventricular arrhythmias
    • especially reentrant and ectopic SVTs and VT
  • Tox: Reversible SLE like symptoms, thrombocytopenia, torsades de pointes
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21
Q

Disopyramide

A
  • Class 1a Na+ channel blocker
  • Antiarrhythmetic
  • Increased AP duration
  • Increased effective refractory period
  • Increased QT interval
  • Affect both atrial and ventricular arrhythmias
    • especially reentrant and ectopic SVTs and VT
  • Tox: , thrombocytopenia, torsades de pointes
22
Q

Lidocaine

A
  • Class 1b Na+ channel blocker
  • Anti arrhythmic
  • Decreased AP duration
  • Preferentially affects ischemic or depolarized purkinje and ventricular tissue
  • Useful in acute ventricular arrhythmias (post-MI) and digoxin-induced arrhythmias
  • TOX: local anesthetic, CNS stim/depression, CV depression
23
Q

Mexiletine

A
  • Class 1b Na+ channel blocker
  • Anti arrhythmic
  • Decreased AP duration
  • Preferentially affects ischemic or depolarized purkinje and ventricular tissue
  • Useful in acute ventricular arrhythmias (post-MI) and digoxin-induced arrhythmias
  • TOX: local anesthetic, CNS stim/depression, CV depression
24
Q

Tocainide

A
  • Class 1b Na+ channel blocker
  • Anti arrhythmic
  • Decreased AP duration
  • Preferentially affects ischemic or depolarized purkinje and ventricular tissue
  • Useful in acute ventricular arrhythmias (post-MI) and digoxin-induced arrhythmias
  • TOX: local anesthetic, CNS stim/depression, CV depression
25
Q

Flecainide

A
  • Class 1c Na+ channel blocker
  • Antiarrhythmic
  • No effect on AP duration
  • Useful in VT that progresses to VF, and in intractable SVT
  • Used only as last resort in refractory tachyarrhytmias
  • For pts w/o structural abnormalities
  • TOX: Contraindicated post-MI b/c proarrhythmic, prolongs refractory period in AVN
    • Hyperkalemia increases toxicity in all class 1 drugs
26
Q

Propafenone

A
  • Class 1c Na+ channel blocker
  • Antiarrhythmic
  • No effect on AP duration
  • Useful in VT that progresses to VF, and in intractable SVT
  • Used only as last resort in refractory tachyarrhytmias
  • For pts w/o structural abnormalities
  • TOX: Contraindicated post-MI b/c proarrhythmic, prolongs refractory period in AVN
    • Hyperkalemia increases toxicity in all class 1 drugs
27
Q

Beta blockers “-olols”

A
  • Class II antiarrythmics
  • Decreases cAMP
  • decrease Ca2+ currents
  • Suppressing abnormal pacemakers by decreasing phase 4 slope
  • AVN most sensitive
  • Use: VT, SVT, slowing ventricular rate during Afib/flutter
  • Tox: impotence, asthma, bradycardia, AV block, CHF
28
Q

Ibutilide

A
  • Class III Antiarrhythmics: K+ channel blocker
  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval
  • Used with other antiarrhythmic fail
  • Tox: torsades de pointes
29
Q

Sotalol

A
  • Class III Antiarrhythmics: K+ channel blocker
  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval
  • Used with other antiarrhythmic fail
  • Tox: torsades de pointes, excessive beta block
30
Q

Bretylium

A
  • Class III Antiarrhythmics: K+ channel blocker
  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval
  • Used with other antiarrhythmic fail
  • Tox: new arrhythmias, hypotension
31
Q

Amiodarone

A
  • Class III Antiarrhythmics: K+ channel blocker
  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval
  • Used with other antiarrhythmic fail
  • Tox: pulmonary fibrosis, hepatotoxicity, thyroid problems, corneal and skin deposits, neurologic effects, constipation, bradycardia, heart block, CHF
32
Q

Dofetilide

A
  • Class III Antiarrhythmics: K+ channel blocker
  • Increase AP duration
  • Increase effective refractory period
  • Increased QT interval
  • Used with other antiarrhythmic fail
  • Tox: torsades de pointes
33
Q

Adenosine

A
  • Antiarrhythmic
  • Increases K+ out of cells: hyperpolarizing cell
  • Decreases Ca2+ current
  • Drug of choice for SVT
  • Very short acting
  • TOX: flush, hypotension, chest pain
    • Blocked by thephylline
34
Q

Captopril

A
  • Inhibits ACE
  • Reduces levels of Angiotensin II (vasoconstrictor)
  • prevents inactivation of bradykinin (vasodilator)
  • Renin release increase b/c loss of feedback inhibition
  • Use: HTN, CHF, diabetic renal disease, prevents heart remodeling as result of chronic HTN
  • TOX: cough, angioedema, proteinuria, taste change, hypotension, fetal renal damage, rash, increased renin, decrease angiotension II, hyperkalemia
    • Avoid w/ bilateral renal artery stenosis
35
Q

Enalapril

A
  • Inhibits ACE
  • Reduces levels of Angiotensin II (vasoconstrictor)
  • prevents inactivation of bradykinin (vasodilator)
  • Renin release increase b/c loss of feedback inhibition
  • Use: HTN, CHF, diabetic renal disease, prevents heart remodeling as result of chronic HTN
  • TOX: cough, angioedema, proteinuria, taste change, hypotension, fetal renal damage, rash, increased renin, decrease angiotension II, hyperkalemia
    • Avoid w/ bilateral renal artery stenosis
36
Q

Lisinopril

A
  • Inhibits ACE
  • Reduces levels of Angiotensin II (vasoconstrictor)
  • prevents inactivation of bradykinin (vasodilator)
  • Renin release increase b/c loss of feedback inhibition
  • Use: HTN, CHF, diabetic renal disease, prevents heart remodeling as result of chronic HTN
  • TOX: cough, angioedema, proteinuria, taste change, hypotension, fetal renal damage, rash, increased renin, decrease angiotension II, hyperkalemia
    • Avoid w/ bilateral renal artery stenosis
37
Q

Spironolactone

A
  • K+sparing diuretic
  • Competitive aldosterone receptor antagonist
    • Blocks Na retention & K excretion
  • Use: HTN and CHF
  • TOX: hyperkalemia
38
Q

Eplerenone

A
  • K+sparing diuretic
  • Competitive aldosterone receptor antagonist
    • Blocks Na retention & K excretion
  • Use: HTN and CHF
  • TOX: hyperkalemia
39
Q

Losartan

A
  • AT1 receptor blocker
  • Interferes w/ binding of Angiotensin II to receptor (no effect on bradykinin)
  • Use: HTN (less effective in blacks) , CHF
40
Q

Aliskiren

A

-Renin inhibitor

41
Q

Heparin

A
  • Cofactor for the activation of antithrombin
  • Decreases thrombin and Factor Xa
  • Short half life
  • Use: anticoagulation for PE, stroke, acute coronary syndrome, MI, DVT, and can be used during pregnancy
  • TOX: bleeding, HIT, osteoporosis, interactions
    • antidote: protamine sulfate binds - charged heparin
42
Q

Enoxaprin

A
  • Low Molecular Weight Heparin
  • acts more on Xa
  • Better availability and longer half life
  • Can be administered subQ w/o labs
  • Used for the same stuff as heparin
43
Q

Lepirudin

A
  • Hirudin derivative (from leeches)
  • directly inhibits thrombin
  • Used as alternate to heparin in patients w/ HIT
44
Q

Bivalirudin

A
  • Hirudin derivative (from leeches)
  • directly inhibits thrombin
  • Used as alternate to heparin in patients w/ HIT
45
Q

Warfarin

A
  • Interferes w/ normal synth and gamma carboxylation of Vit. K dependent clotting factors (II, VII, IX, X, protein C and S)
  • Metabolized by p450s
  • Effects extrinsic pathway
  • Increases PT
  • Use: chronic anticoagulation (post STEMI, venous thromboembolism)
  • Can’t use if pregnant (crosses placenta)
  • TOX: bleeding, teratogenic, interactions
46
Q

Streptokinase

A
  • Thrombolytic
  • Indirectly aids conversion of plasminogen to plasmin
  • Plasmin cleaves thrombin and fibrin clots
  • Increased PT and PTT, no change in platelet count
  • Use: MI, early ischemic stroke
  • TOX: bleeding, HTN, (don’t use w/ active bleeding, hx of intracranial bleeds, recent surgery)
    • Treat tox w/ aminocaprotic acid that inhibits fibrinolysis
47
Q

tPA

A
  • Thrombolytic
  • Indirectly aids conversion of plasminogen to plasmin
  • Plasmin cleaves thrombin and fibrin clots
  • Increased PT and PTT, no change in platelet count
  • Use: MI, early ischemic stroke
  • TOX: bleeding, HTN, (don’t use w/ active bleeding, hx of intracranial bleeds, recent surgery)
    • Treat tox w/ aminocaprotic acid that inhibits fibrinolysis
48
Q

Aspirin

A
  • Acetylates and irreversibly inhibits COX1 and COX2
  • Prevents conversion of Arachidonic acid to thromboxane A2
  • Increases bleeding time
  • No effect on PT or PTT
  • Use: antipyretic, analgesic, anti-inflammatory, antiplatelet drug
  • TOX: gastric ulceration, bleeding, hyperventilation, Reye’s syndrome in kids
49
Q

Clopidogrel

A
  • Inhibits platelet aggregation
  • Irreversibly blocks ADP receptors
  • Inhibits fibrinogen binding by preventing GP IIb/IIIa expression
  • Use: acute coronary syndrome, coronary stenting
50
Q

Ticlopidine

A
  • Inhibits platelet aggregation
  • Irreversibly blocks ADP receptors
  • Inhibits fibrinogen binding by preventing GP IIb/IIIa expression
  • Use: acute coronary syndrome, coronary stenting
  • TOX: neutropenia
51
Q

Cilostazol

A
  • PDE III inhibitor
  • Increases cAMP in platelets
    • inhibits platelet aggregation
  • Vasodilator
  • Use: intermittant claudication, coronary vasodilation, prevent stroke/TIA, angina prophylaxis
  • TOX: nausea, headache, flushing, hypotension, abdominal pain
52
Q

Dipyridamole

A
  • PDE III inhibitor
  • Increases cAMP in platelets
    • inhibits platelet aggregation
  • Vasodilator
  • Use: intermittant claudication, coronary vasodilation, prevent stroke/TIA, angina prophylaxis
  • TOX: nausea, headache, flushing, hypotension, abdominal pain
53
Q

Abciximab

A
  • Monoclonal antibody that binds GP IIb/IIIa on activated platelets
  • Prevents platelet aggregation
  • Use: acute coronary syndrome, coronary angioplasty
  • TOX: bleeding, thrombocytopenia

CPR (13 decks)

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