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phar 301 > 2: Lecture 2 Drugs > Flashcards

2: Lecture 2 Drugs Flashcards

1
Q

What to use for immediate pain relief and ischemia in the heart

A

Nitrates
ex. Nitroglycerin (rapid-acting) and isosorbide dinitrate
Eliminates pain but not pathology

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2
Q

Mechanism of Nitrates (symptomatic)

A

Increases production of nitric oxide–>increase in levels of cGMP within blood vessels of heart–>vasodilation
This vasodilation reduces venous returns, cardiac size, and diastolic myocardial oxygen consumption
Vasodilation brings more blood flow to the heart–>increasing oxygen supply to the heart

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3
Q

Side effects of Nitrates (symptomatic)

A

Orthostatic hypotension, tachycardia reflex, headache

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4
Q

Mechanism of Calcium channel blockers

A

Block calcium channels and adjust contractility of the blood vessels in heart tissue (peripheral vasodilation and reduction of cardiac work)
Can be given as prophylactic
ex. Verapamil, Nifedipine, and Diltiazem

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5
Q

Side effects of Calcium channel blockers

A

Orthostatic hypotension, AV blockade, edema

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6
Q

Mechanism of Beta blockers

A

Reduce blood pressure and cardiac work by reducing force of contraction of heart

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7
Q

Side effects of beta blockers

A

Orthostatic hypotension, tachycardia, headache

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8
Q

Target when reducing de novo cholesterol synthesis

A

HMG CoA-reductase enzyme

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9
Q

Function of HDL

A

Good cholesterol
Transports cholesterol to liver to be expelled from body
CHOLESTEROL OUT OF BODY
Helps eliminate excess cholesterol to reduce buildup (plaques)

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10
Q

Function of LDL

A

Bad cholesterol
Transports cholesterol to arteries where it can accumulate leading to atherosclerosis (plaque formation)

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11
Q

Main action of Statins

A

ex. Iovastatin
Inhibit cholesterol synthesis

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12
Q

Mechanism of Statins

A

ex. Iovastatin
Target HMG CoA-reductase (enzyme used for production of cholesterol in liver)
Most commonly administered

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13
Q

Side effects of Statins

A

Damage skeletal muscle (affects amount of cholesterol absorbed by skeletal muscle) or liver, interference with myelination of infants
Avoided during pregnancy (fetus needs all cholesterol synthesis pathways for myelination)

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14
Q

Main action of Resins

A

ex. cholestyramine
Block cholesterol reabsorption

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15
Q

Mechanism of Resins

A

ex. Cholestyramine
Non-absorbable macromolecules bind to cholesterol preventing reabsorption from the gut (acts as a macromolecular sponge)
(allows for more cholesterol to be excreted than absorbed)

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16
Q

Side effects of Resins

A

More side effects than statins
Unpleasant gritty taste, GI tract discomfort, interference of vitamin or drug absorption

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17
Q

Main action of Niacin

A

ex. nicotinic acid, vitamin B3
Decrease VLDL (very low density lipoprotein) secretion
Mechanism unknown

18
Q

Side effects of Niacin

A

Occasional flush with itching (reduced with aspirin)
Rarely causes glucose intolerance

19
Q

Main action of Fibrates

A

ex. Gemfibrozil
Increased synthesis of lipoprotein lipase

20
Q

Mechanism of Fibrates

A

ex. Gemfibrozil
Activates peroxisome proliferation-activated receptor-a which increases lipoprotein lipase synthesis

21
Q

Side effects of Fibrates

A

May cause nausea and skin rashes

22
Q

3 Ways to target plaque formation

A

1) Anticoagulants
2) Fibrinolysis
3) Platelet aggregation inhibition

23
Q

Why use anticoagulants?

A

Prevent and treat venous clotting (especially deep vein thrombosis)

24
Q

2 Types of Anticoagulants

A

1) Warfarin
2) Heparin

25
Q

Main action of Warfarin (anticoagulant)

A

Vitamin K antagonist, binds coagulation factors II,VII,IX, and X

26
Q

Mechanism of Warfarin (anticoagulant)

A

Replaces Vitamin K and blocks reactivation of Vitamin K epoxide, binds to coagulation factors II, VII, IX, and X

27
Q

Test with Warfarin and High MW Heparin (anticoagulants)

A

Prothrombin time test to monitor effect since people’s coagulation abilities vary

28
Q

Main action of Heparin (anticoagulant)

A

Binds coagulation factors Xa and Antithrombin III

29
Q

2 Types of Heparin (anticoagulant)

A

High molecular weight (MW)–>less expensive, unfractionated, variable effect that requires monitoring
Low molecular weight (MW)–>more expensive, fractionated, predictable

30
Q

Side effects of anticoagulants

A

Bleeding
teratogenic (warfarin)

31
Q

Main action of Fibrinolytic drugs

A

Break up fibrin inside blood clots (at level of plasmin the enzyme that breaks down firbin)

32
Q

2 Types of Fibrinolytic drugs

A

1) Streptokinase
2) Tissue plasminogen activators

33
Q

Mechanism of Streptokinase (fibrinolytic drug)

A

Converts plasminogen to plasmin (enzyme)
Cost-effective
Treats pulmonary embolism and myocardial infarction
Possible bleeding and allergic response

34
Q

Mechanism of Tissue plasminogen activators

A

Activates plasminogen bound to fibrin
Expensive
Treats pulmonary embolism and myocardial infarction
Possible bleeding

35
Q

What activates platelets and what do they release

A

A break in collagen wall activates platelets which release thromboxane A2 (from arachidonic acid) and secretes adenosine diphosphate (ADP)

36
Q

Function of Thromboxane A2 and adenosine diphosphate (ADP)

A

Reduce blood flow and increase platelet aggregation
Stimulate appearance of fibrinogen binding sites on platelet membranes
Thromboxane A2 is a potent aggregating agent and vasoconstrictor

37
Q

Mechanism of Cyclooxygenase Inhibitors (Antiplatelet drug)

A

ex. Aspirin and Ibuprofen
Inhibit cyclooxygenase enzyme that synthesizes thromboxane A2 (to counteract its effect)
Differences
Aspirin–>Binds irreversibly to the enzyme
Ibuprofen–>binds reversibly

38
Q

Why use cyclooxygenase inhibitors (antiplatelet drug)

A

Treatment for transient ischemic attacks and myocardial infarction
Aspirin as prophylactic drug to reduce chance of person having a second heart attack (relatively safe over long term)

39
Q

Side effects of cyclooxygenase inhibitors (antiplatelets)

A

Bleeding
GI ulceration (aspirin)

40
Q

Mechanism of Adenosine Receptor Blockers (antiplatelets)

A

ex. Ticlopidine
Inhibit the platelet response (aggregation) by blocking ability of secreted ADP to bind to adenosine receptors
ADP (adenosine diphosphate)–>potent platelet aggregating agent

41
Q

Why use Adenosine Receptor blockers (antiplatelet drugs)

A

ex. Ticlopidine
Treat transient ischemic attacks and myocardial infarction
Alternative to asprin if patient is allergic

42
Q

Side effects of adenosine receptor blockers (antiplatelet drugs)

A

Bleeding
Skin rashes

phar 301 (23 decks)

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