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DRUGS FOR COAGULATION DISORDERS AND DYSLIPEDEMIA > COAGULATION DISORDERS > Flashcards

COAGULATION DISORDERS Flashcards

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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
How to monitor the hemorrhage?
Monitor aPTT
26
Activated partial thromboplastin site
Monitor aPTT
27
Contraindications of Heparin
-Hypersensitivity -Active Bleeding -Thrombocyptopenia -Severe HPN -Active TB
28
Also known as bis-hydroxycoumarin
Dicumarol
29
High incidence of GI side effects
Dicumarol
30
Anti-Platelet Drugs
-Thromboxane Synthesis Inhibitors - Phosphodiesterase Inhibitors - ADP Inhibitors - Glycoprotein IIb/IIIa Inhibitors
31
Irreversibly acetylates COX-inhibition of TXA2 synthesis, lasts for 8-10 days
Thromboxane Synthesis Inhibitors
32
Aspirin is in a class of
Thromboxane Synthesis Inhibitors
33
Primary prophylaxis for MI and a secondary prophylaxis for MI and stroke
Aspirin
34
Given together with antiplatelet; ineffective when alone
Dypiridamole
35
Side effects of dypiridamole
Coronary steal phenomenon
36
Dypiridamole is in a class of
Phosphodiesterase Inhibitors
37
ADP Inhibitors drugs
-Ticlopidine - Clopidogrel
38
A class of ADP Inhibitors and the side effects are thrombocyptopenia, purpura, neutropenia, N/V and diarrhea
Ticlopidine
39
Much safer than ticlopidine
Clopidogrel
40
Glycoprotein Inhibitors Drugs
-Abciximab -Eptifibatide -Tirofiban
41
Catalyse activation of plasminogen to plasmin (serine protease)
Fibrinolytic Agents/Thrombolytics
42
Management of severe pulmonary embolism, heart attack, acute MI, DVT
Fibrinolytic Agents/ Thrombolytics
43
A class of fibrinolytic agents that destroy fibrin that is either bound to clots or is in the unbound form
Streptokinase
44
Class of fibrinolytic agent that binds to fibrin bound to a clot
Tissue plasminogen activator
45
from the kidneys
Urokinase
46
Fibrinolytic Agents/Thrombolytics Drugs
-Streptokinase -Tissue plasminogen activator -Anistreplase -Urokinase
47
Management of bleeding disorders
Pro-coagulant Drugs
48
Phytonadione (in plants, useful clinically)
K1
49
Menaquinone (intestinal bacteria)
K2
50
Menadione (synthetic)
K3
51
Used for vitamin K deficiency; hemorrhagic disorders in newborns
K3- menadione (synthetic)
52
Prevents activation of plasminogen
Aminocaproic Acid
53
Increase in LDL and decrease in HDL
Hypercholesterolemia
54
Increase TG, Increase VLDL, chylomicrons
Hypertriglyceridemia
55
The only organ in the body that efficiently uses cholesterol
Liver
56
Converts it to bile salts
Liver
57
Condition associated with cholesterol deposition in vascular in vascular smooth muscles (arthroma) with consequent narrowing of the lumen of the affected blood vessels
Atherosclerosis
58
Atherosclerosis could lead to
-CAD -Cerebrovascular disease -Aortic disease - Renal Artery Disease
59
Minor risk factors
-Chronic Infection - Sedentary Lifestyle
60
Modifiable risk factors
- By therapy - By lifestyle change
61
Drugs for Dyslipidemia
- HMG-CoA Reductase Inhibitors - Nicotinic Acid - Bile Acid Sequestrants -Fibric Acid Derivatives -Probucol
62
First line drugs for dyslipidemia
HMG-CoA Reductase Inhibitors
63
Inhibit the enzyme HMG-Coa Reductase, thereby inhibiting the first step (rate-limiting step) in cholesterol synthesis
HMG-Coa Reductase
64
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
HMG-CoA Reductase
65
As a result Statins reduce LDL by up to
60% reduce TG up to 40% and increase HDL up to 10%
66
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
67
Short-acting HMG-CoA Reductase Inhibitors
-Simvastatin -Lovastatin -Fluvastatin
68
Long-acting HMG-CoA Reductase Inhibitors
-Atorvastatin -Rosuvastatin
69
Side Effects of HMG-CoA Reductase Inhibitors
-Hepatotoxicity -Myositis -Rhabdomyolysis (Muscle Wasting)
70
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
Nicotinic Acid
71
A reduction in the VLDL production leads to:
decrease LDL levels; the result therefore is decrease TC and TG while HDL is increased.
72
Used in the management of hypertriglyceridemia
Nicotinic Acid
73
Side Effects of Nicotinic Acid
-Flushing (due to percutaneous vasodilation), myositis
74
Also known as Bile-Acid- Binding Resins
Bile Acid Sequestrants
75
These drugs cause substantial
Bile Acid Sequestrants
76
Decrease in LDL and modest increase in HDL but minimal effects on TG
Bile Acid Sequestrants
77
Bile Acid Sequestrant Drugs
-Cholestyramine -Colestipol
78
Side Effects of Bile Acid Sequestrant Drugs
-Constipation - Impaired absorption of certain drugs - may increase incidence/risk of biliary stone formation
79
First line drug in hypertriglyceridemia
Fibric Acid Derivatives
80
Stimulate lipoprotein lipase which decreases triglycerides
Fibric Acid Derivatives
81
Fibric Acid Derivatives Drugs
Gemfibrozil Fenofibrate Clofibrate (withdrawn)
82
Fibric Acid Derivatives Side Effects
-myositis -rhabdomyolysis -increase risk of bile stone formation -hepatobiliary cancer (clofibrate)
83
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
84
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
High polyunsaturated long chain (n=3) fatty acids (Fish oil) (omega fatty acids)
85
Anti-oxidant
Probucol
86
Side effects of probucol
-increase risk of arrhythmia - produces fetid odor
87
Also inhibit platelet aggregation and have been shown to decrease mortality from CHD(coronary heart disease)
Fish Oil
88
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

DRUGS FOR COAGULATION DISORDERS AND DYSLIPEDEMIA (1 decks)

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