Drugs for Coagulation Disorders Flashcards by Kate Carmie

Clot that adheres to a blood vessel wall

Thrombus

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Detached thrombus

Embolus

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Generates thrombin that is essential in the formation of fibrin used in clot
formation involves coagulation
cascade

Clotting Mechanism

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Drugs for Coagulation Disorders are:

-Anticoagulants
-Anti-Platelet Drugs
-Fibrinolytic Agents
-Pro-coagulant Drugs

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Parenteral Anticoagulants Drugs

-Hirudin
-Heparin

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Oral Anticoagulants Drugs

-Dicumarol
-Warfarin

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Obtained from medicinal leeches (Hirudo medicinalis)

Hirudin

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Produced by recombinant DNA technology

Lepidurin

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Heterogenous mixture of sulfated mucopolysaccharides

Heparin

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Activates antithrombin III which in turn inactivates thrombin (IIa); Ixa, Xa, Xia

Regular or Unfractionated Heparin

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Also known as bis-hydroxycoumarin and high incidence of GI side-effects

Dicumarol

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Its mechanism of action blocks carboxylation of X, IX, VII, II

Warfarin

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Onset of Warfarin

8-12 hrs maximum after 1 to 3 days

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Irreversibly acetylates COX- inhibition of TXA2 synthesis, lasts for 8-10 days

Thromboxane Synthesis Inhibitors

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Primary prophylaxis for MI and secondary prophylaxis for MI and stroke

Aspirin

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Aspirin is in what kind of inhibitors?

Thromboxane Synthesis Inhibitors

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Phosphodiesterase Inhibitors is

Dypiridamole

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Given together with antiplatelet; ineffective when alone

Dypiridamole

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ADP Inhibitors are

-Ticlopidine
-Clopidogrel

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Safer than ticlopidine

Clopidogrel

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Glycoprotein Inhibitors

-Abciximab
-Eptifibatide
-Tirofiban

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Management of severe pulmonary embolism, heart attack, acute MI and DVT

Fibrinolytic Agents/Thrombolytics

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Destroy fibrin that is either bound to clots or is in the unbound form

Streptokinase

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Binds to fibrin bound to a clot

Tissue plasminogen activator

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Management of bleeding disorders

Pro-coagulant drugs

Phytonadione (in plants, useful clinically)

Menaquinone (intestinal bacteria)

Menadione (synthetic)

Prevents activation of plasminogen

Aminocaproic Acid

Increase LDL, decrease HDL

Hypercholesterolemia

Increase TG, inc VLDL, chylomicrons

Hypertriglyceridemia

Only organ in the body that efficiently uses cholesterol

Liver

Condition associated with cholesterol deposition in vascular smooth muscles (arthroma) with consequent narrowing of the lumen of the affected blood vessels

Atherosclerosis

Atherosclerosis could lead to

-CAD -Cerebrovascular Disease -Aortic Disease -Renal Artery Disease

Major Risk Factors of Atherosclerosis

– Age (males: > 45; females: > 55) – Smoking – DM – HPN – Dyslipidemia – Obesity – Family history of premature heart attack

Minor Risk Factors of Atherosclerosis

-Chronic Infection -Sedentary Lifestyle

Modifiable Risk Factors of Atherosclerosis

-By therapy -By lifestyle changes

Drugs for Dyslipidemia

-HMG- Coa Reductase Inhibitors -Nicotinic Acid -Bile Acid Sequesterants -Fibric Acid Derivatives -Probucol

First line drug for dyslipidemia

HMG-CoA Reductase Inhibitors

These drugs inhibit cholesterol synthesis by competing effectively to inhibit the HMG CoA reductase the rate limiting step in the cholesterol synthesis thus depleting the intracellular supply of cholesterol

HMG-CoA Reductase Inhibitors

Means that the biosynthesis of cholesterol in the body occurs at night thus most statins are given at bedtime (esp the short-acting ones)

Diurnal Pattern of Cholesterol Synthesis

Short-acting drugs of HMG-CoA Reductase Inhibitors

-Simvastatin -Lovastatin -Fluvastatin

Long-acting drugs of HMG-CoA Reductase Inhibitors

-atorvastatin -rosuvastatin

In adipose tissue, niacin inhibits the lipolysis of triglycerides by hormone sensitive lipase, which reduces transport of free fatty acids to the liver and decreases hepatic triglyceride synthesis

Nicotinic Acid

Used in the management of hypertriglyceridemia

Nicotinic Acid

Side Effects of Nicotinic Acid

Flushing (due to percutaneous vasodilation), myositis

Also known as Bile Acid-Binding Resins

Bile Acid Sequesterants

Inhibit reabsorption of bile acid

Bile Acid Sequesterants

Bile Acid Sequesterants are

-Cholestyramine -Colestipol

Side effects of bile acid sequesterants are

-constipation -impaired absorption of drugs -may increase incidence/ risk of biliary stone formation

First line drug in hypertriglyceridemia

Fibric Acid Derivatives

Its mechanism of action stimulates lipoprotein lipase which decreases triglycerides

Fibric Acid Derivatives

Fibric Acid Drugs are

-Gemfibrozil -Fenofibrate -Clofibrate (withdrawn)

Side Effects of Fibric Acid Derivatives

-myositis -rhabdomyolysis -increase risk of bile stone formation -hepatobiliary cancer (clofibrate)

These inhibit the intestinal mucosa transporter NPC1L1 that absorbs dietary and biliary cholesterol. The resultant depletion of hepatic cholesterol up regulates hepatic LDL receptor activity.

Cholesterol absorption Inhibitors

This mechanism is synergistic with statins, LDL is reduced by 17%, TG is reduced by 6% While HDL is increased by 1.3%

Cholesterol absorption Inhibitors

Eicosapentanoic acid (EPA) and Docosahexanoic acid (DHA) comprise of ____ of the fatty acids in fish oil

30%

Anti-oxidant

Probucol

Side Effects of Probucol

-increase risk of arrhytmia -produces fetid odor

Epithelial vascular injury

Clotting Mechanism inciting event

Fibrates stimulate the Peroxisome proliferator-activated receptor alpha (PPAR)-α which controls the expression of gene products that mediate the metabolism of TG & HDL

Fibric Acid Derivatives

Fibrates reduce TG up to

up to 50%, and ↑HDL by 20% but LDL changes are variable

Also inhibit platelet aggregation and have been shown to decrease mortality from CHD(coronary heart disease)

Fish Oil