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Pharmacology > Part 8-2 Cardiovascular Pharmacology > Flashcards

Part 8-2 Cardiovascular Pharmacology Flashcards

1
Q

Coagulation disorders

A
  • Inadequate clotting: hemorrhage

- Excessive clotting: thrombogenesis

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2
Q

Clotting Mechanism Intrinsic System

A

Begins when factor XII contacts damaged vessel

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3
Q

Clotting Mechanism Extrinsic system

A

Begins when damaged vessel releases tissue factor (Thromboplastin)

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4
Q

Clotting Mechanism sequence

A

CF XII and CF VII lead to CF X

CF X turns prothrombin into Thrombin

Thrombin turns fibrinogen to Fibrin

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5
Q

Clot Breakdown

A

Tissue Plasminogen Activator turns plasminogen into plasmin

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6
Q

Drugs for overactive clotting

A

Anticoagulants
Antithrombotics
Thrombolytics

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7
Q

Anticoagulants

A

Used primarily in venous thrombosis

  1. Heparin
  2. Oral anticoagulants
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8
Q

Heparin

A

Acts by increasing effects of antithrombin III

  • rapid effects
  • Administered parenterally
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9
Q

Types of heparin

A

Unfractionated heparin

Low molecular weight heparins

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10
Q

Unfractioned heparin

A
  • IV administration, several injections per day

- Unpredictable effects

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11
Q

Low molecular weight heparins

A

Administered sub-Q, usually 1/day
Preferentially inhibit factor Xa
More predictable, safer effect

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12
Q

Heparin induced thrombocytopenia

A

Heparins can decrease platelets
Type I HIT
Type II HIT

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13
Q

Type I HIT

A

Asymptomatic, resolves spontaneously

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14
Q

Type II HIT

A

Immune reaction…causes serious thrombosis, life/limb threatening

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15
Q

Oral anticoagulants

A

Warfarin (Coumadin)
Dicumarol
-Inhibit vitamin K function in liver
-Decreased synthesis of certain clotting factors

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16
Q

Oral anticoagulants administration

A

Oral administration
Time lag of 3-4 days
Typically used after heparin

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17
Q

Other Anticoagulants

A

Can be used as primary or if other anticoagulants aren’t tolerated

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18
Q

Other anticoagulant examples

A

Direct Thrombin inhibitors

Factor Xa Inhibitors

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19
Q

Antithrombotics

A

-Inhibit platelet activity; decrease platelet induced clot
Primary agents
-aspirin
-Newer antiplatelet drugs

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20
Q

Aspirin anticlotting effects

A
  • Aspirin inhibits PG & Thrombozane (TX) biosynthesis

- Decreased TXs means less platelet induced clots

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21
Q

Thromboxanes (TX)

A

Increase platelet activity/aggregation

22
Q

Aspirin

A
  • Inhibits platelet function
  • Prevents arterial thrombogenesis in MI, Ischemic stroke
  • Therapeutic effects occur at very low doses
23
Q

Aspirin is….

A

Better at preventin MI in men

Better against stroke in women

24
Q

Newer antiplatelet drugs

A

ADP inhibitors

Glycoprotein IIb-IIa inhibitors

25
Q

ADP inhibitors

A

Block effects of ADP on platelets

26
Q

Glycoprotein IIa-IIb inhibitors

A

Block effects of fibrinogen, other activators on platelets

27
Q

Thrombolytics

A
  • Initiate clot breakdown by activating plasmin
  • Help dissolve clots in coronary/carotid arteries
  • Can restore blood flow
  • Prevent/reverse damage during MI, ischemic stroke
28
Q

Typical Thrombolytic agents

A
  • Tissue plasminogen activator (activase)
  • Urokinase
  • Reteplase
  • Tenecteplace
29
Q

Thrombolytics for MI

A
  • No agent is best for MI
  • Can decrease mortality by 50% if given within 1 hr of symptoms
  • May still be helpful within 3-12 hrs
30
Q

Thrombolytics use in ischemic stroke

A
  • Rule out hemorrhage first
  • Activase may be preferred
  • Administor within 2 hrs of symptoms
  • Benefits must balance risk of intracranial hemorrhage
31
Q

Anticlotting drugs rehab concerns

A 
Risk of hemorrhage
Use care when:
-Dressing changes
-Debridement
-Aggressive manual techniques
32
Q

Treatment of clotting deficiencies…hemophilia

A
  • Clotting factor replacement
  • CFs usually obtained from rDNA techniques
  • Pts can also develop alloantibodies to synthetic clot factors….tx with rituximab
33
Q

Hemophilia type A factor replacement

A

Factor VIII

34
Q

Hemophilia Type B factor replacement

35
Q

Fibrinolysis Inhibitors

A

Can be used in hemophilia and hyperfibrinolysis syndromes

36
Q

Vitamin K supplements

A
  • Administered to newborns or in severe vitamin K deficiency

- Can also help tx excessive warfarin

37
Q

Treatment of hyperlipidemia

A

Statins
Fibric Acids
Others

38
Q

Statin mechanism

A

Inhibit HMG-Co A reductase enzyme

  • Decreased cholesterol biosynthesis
  • Increased hepatic LDL breakdown
39
Q

Statins primary effects

A
  • Decreased LDL, VLDL cholesterol
  • Decreased triglycerides
  • Increased HDL
40
Q

Statins other beneficial effects

A 
Enhance vasodilation by NO
Anti-inflammatory
Anti-oxidant
Neuroprotection? 
Anticancer?
41
Q

Fibric Acids mechanisms

A

Activate nuclear receptor that effects gene controlling lipid metabolism

42
Q

Fibric Acid primary effects

A

Decreased triglycerides

Increased VLDL breakdown

43
Q

Niacin

A

Decreases VLDL % LDL synthesis

Decreases triglyceride levels

44
Q

Ezetimibe (Zetia)

A

Inhibits cholesterol absorption from GI tract

Can be combined with a statin

45
Q

Bile acid binding drugs

A

Increase GI excretion of bile acids

Decrease plasma cholesterol

46
Q

Antilipid agents adverse effects

A

Nausea, diarrhea, bloating

Liver toxicity, pancreatitis, blood dyscrasias, arrythmias

47
Q

Antilipid agents primary concern for rehab

A

Myalgia, Myositis, weakness, parasthesias

48
Q

Statin induced myopathy

A

5-7% of patients taking statins

Reasons unclear

49
Q

Fixed predisposing factors for statin induced myopathy

A

Renal/hepatic disease
Genetic factors
Advanced age
Female

50
Q

Modifiable predisposing factors for statin induced myopathy

A

Concurrent meds
High dose
Lipophilic statin
Heavy exercise

Pharmacology (15 decks)

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