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DRUGS FOR COAGULATION DISORDERS AND DYSLIPEDEMIA > COAGULATION DISORDERS > Flashcards

COAGULATION DISORDERS Flashcards

1
Q

Inciting event: epithelial vascular injury

A

Clotting mechanism

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2
Q

Also known as primary hemostasis

A

Platelet aggregation

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3
Q

Also known as secondary hemostasis

A

Attachment of other blood cells

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4
Q

In platelet aggregation it has:

A

White thrombus
Platelet plug
Unstable clot

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5
Q

In attachment of other blood cells it has:

A

Red thrombus
Stable clot

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6
Q

Clot that adheres to a blood vessel wall

A

Thrombus

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7
Q

Detached thrombus

A

Embolus

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8
Q

The coagulation process that generates thrombin that is essential in the formation of fibrin used in clot formation involves coagulation cascade

A

Clotting mechanism

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9
Q

Drugs for coagulation disorders

A

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

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10
Q

Anticoagulants site of action

A

Synthesis of or directly against clotting factors (II, IIa)

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11
Q

Anticoagulants types of PARENTERAL

A

-Hirudin
- Heparin

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12
Q

Anticoagulants types of ORAL

A

-Dicumarol
-Warfarin

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13
Q

Obtained from medicinal leeches (Hirudo medicinalis)

A

Hirudin

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14
Q

Used in the management of HIT (Heparin-Induced Thrombocytopenia)

A

Hirudin

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15
Q

Produced by recombinant DNA technology

A

Lepirudin

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16
Q

Heterogenous mixture of sulfated mucopolysaccharides

A

Heparin

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17
Q

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

A

Regular or Unfractionated Heparin

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18
Q

Inactivates IIa and Xa

A

Low Molecular Weight Heparin

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19
Q

Low MW Heparin drugs are:

A

-Enoxaparin
-Fraxiparin
-Dalteparin

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20
Q

Low MW Heparin route is

A

SQ or subcutaneous

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21
Q

Regular or Unfractionated Heparin Route is

A

SQ/IV

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22
Q

Initiation of anticoagulant therapy and is the management of MI or Unstable Angina. It is also a treatment and prevention of pulmonary embolism & DVT

A

Heparin

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23
Q

An anticoagulation in pregnancy (APAS)

A

Heparin

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24
Q

Side effects of heparin are:

A

-Hemorrhage
-Thrombocytopenia

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25
Q

How to monitor the hemorrhage?

A

Monitor aPTT

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26
Q

Activated partial thromboplastin site

A

Monitor aPTT

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27
Q

Contraindications of Heparin

A

-Hypersensitivity
-Active Bleeding
-Thrombocyptopenia
-Severe HPN
-Active TB

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28
Q

Also known as bis-hydroxycoumarin

A

Dicumarol

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29
Q

High incidence of GI side effects

A

Dicumarol

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30
Q

Anti-Platelet Drugs

A

-Thromboxane Synthesis Inhibitors
- Phosphodiesterase Inhibitors
- ADP Inhibitors
- Glycoprotein IIb/IIIa Inhibitors

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31
Q

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

A

Thromboxane Synthesis Inhibitors

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32
Q

Aspirin is in a class of

A

Thromboxane Synthesis Inhibitors

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33
Q

Primary prophylaxis for MI and a secondary prophylaxis for MI and stroke

A

Aspirin

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34
Q

Given together with antiplatelet; ineffective when alone

A

Dypiridamole

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35
Q

Side effects of dypiridamole

A

Coronary steal phenomenon

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36
Q

Dypiridamole is in a class of

A

Phosphodiesterase Inhibitors

37
Q

ADP Inhibitors drugs

A

-Ticlopidine
- Clopidogrel

38
Q

A class of ADP Inhibitors and the side effects are thrombocyptopenia, purpura, neutropenia, N/V and diarrhea

A

Ticlopidine

39
Q

Much safer than ticlopidine

A

Clopidogrel

40
Q

Glycoprotein Inhibitors Drugs

A

-Abciximab
-Eptifibatide
-Tirofiban

41
Q

Catalyse activation of plasminogen to plasmin (serine protease)

A

Fibrinolytic Agents/Thrombolytics

42
Q

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

A

Fibrinolytic Agents/ Thrombolytics

43
Q

A class of fibrinolytic agents that destroy fibrin that is either bound to clots or is in the unbound form

A

Streptokinase

44
Q

Class of fibrinolytic agent that binds to fibrin bound to a clot

A

Tissue plasminogen activator

45
Q

from the kidneys

A

Urokinase

46
Q

Fibrinolytic Agents/Thrombolytics Drugs

A

-Streptokinase
-Tissue plasminogen activator
-Anistreplase
-Urokinase

47
Q

Management of bleeding disorders

A

Pro-coagulant Drugs

48
Q

Phytonadione (in plants, useful clinically)

A

K1

49
Q

Menaquinone (intestinal bacteria)

A

K2

50
Q

Menadione (synthetic)

A

K3

51
Q

Used for vitamin K deficiency; hemorrhagic disorders in newborns

A

K3- menadione (synthetic)

52
Q

Prevents activation of plasminogen

A

Aminocaproic Acid

53
Q

Increase in LDL and decrease in HDL

A

Hypercholesterolemia

54
Q

Increase TG, Increase VLDL, chylomicrons

A

Hypertriglyceridemia

55
Q

The only organ in the body that efficiently uses cholesterol

A

Liver

56
Q

Converts it to bile salts

A

Liver

57
Q

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

A

Atherosclerosis

58
Q

Atherosclerosis could lead to

A

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

59
Q

Minor risk factors

A

-Chronic Infection
- Sedentary Lifestyle

60
Q

Modifiable risk factors

A
  • By therapy
  • By lifestyle change
61
Q

Drugs for Dyslipidemia

A
  • HMG-CoA Reductase Inhibitors
  • Nicotinic Acid
  • Bile Acid Sequestrants
    -Fibric Acid Derivatives
    -Probucol
62
Q

First line drugs for dyslipidemia

A

HMG-CoA Reductase Inhibitors

63
Q

Inhibit the enzyme HMG-Coa Reductase, thereby inhibiting the first step (rate-limiting step) in cholesterol synthesis

A

HMG-Coa Reductase

64
Q

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

A

HMG-CoA Reductase

65
Q

As a result Statins reduce LDL by up to

A

60% reduce TG up to 40% and increase HDL up to 10%

66
Q

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

A

Diurnal Pattern of Cholesterol Synthesis

67
Q

Short-acting HMG-CoA Reductase Inhibitors

A

-Simvastatin
-Lovastatin
-Fluvastatin

68
Q

Long-acting HMG-CoA Reductase Inhibitors

A

-Atorvastatin
-Rosuvastatin

69
Q

Side Effects of HMG-CoA Reductase Inhibitors

A

-Hepatotoxicity
-Myositis
-Rhabdomyolysis (Muscle Wasting)

70
Q

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

A

Nicotinic Acid

71
Q

A reduction in the VLDL production leads to:

A

decrease LDL levels; the result therefore is decrease TC and TG while HDL is increased.

72
Q

Used in the management of hypertriglyceridemia

A

Nicotinic Acid

73
Q

Side Effects of Nicotinic Acid

A

-Flushing (due to percutaneous vasodilation), myositis

74
Q

Also known as Bile-Acid- Binding Resins

A

Bile Acid Sequestrants

75
Q

These drugs cause substantial

A

Bile Acid Sequestrants

76
Q

Decrease in LDL and modest increase in HDL but minimal effects on TG

A

Bile Acid Sequestrants

77
Q

Bile Acid Sequestrant Drugs

A

-Cholestyramine
-Colestipol

78
Q

Side Effects of Bile Acid Sequestrant Drugs

A

-Constipation
- Impaired absorption of certain drugs
- may increase incidence/risk of biliary stone formation

79
Q

First line drug in hypertriglyceridemia

A

Fibric Acid Derivatives

80
Q

Stimulate lipoprotein lipase which decreases triglycerides

A

Fibric Acid Derivatives

81
Q

Fibric Acid Derivatives Drugs

A

Gemfibrozil
Fenofibrate
Clofibrate (withdrawn)

82
Q

Fibric Acid Derivatives Side Effects

A

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

83
Q

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

A

Cholesterol absorption inhibitors

84
Q

Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) comprise 30% of the fatty acids in fish oil, EPA & DHA are potent inhibitors of VLDL TG formation

A

High polyunsaturated long chain (n=3) fatty acids (Fish oil) (omega fatty acids)

85
Q

Anti-oxidant

A

Probucol

86
Q

Side effects of probucol

A

-increase risk of arrhythmia
- produces fetid odor

87
Q

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

A

Fish Oil

88
Q

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

A

Fibric Acid Derivatives

DRUGS FOR COAGULATION DISORDERS AND DYSLIPEDEMIA (1 decks)

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