Blood drugs Flashcards
(88 cards)
1
Q
What is thrombosis?
A
The formation of an unwanted clot within a blood vessel.
2
Q
List some thrombotic disorders.
A
- Acute myocardial infarction
- Deep vein thrombosis
- Pulmonary embolism
- Acute ischemic stroke
3
Q
What types of drugs are used to treat thrombotic disorders?
A
- Anticoagulants
- Fibrinolytics
4
Q
What is hemophilia?
A
A bleeding disorder treated with transfusion of Factor VIII prepared by recombinant DNA techniques.
5
Q
How is vitamin K deficiency treated?
A
With dietary supplements of vitamin K.
6
Q
What is iron-deficiency anemia?
A
Anemia caused by nutritional deficiencies that can be treated with dietary or pharmaceutical supplementation.
7
Q
What distinguishes a thrombus from an embolus?
A
A thrombus adheres to a vessel wall, while an embolus is a clot that floats in the blood.
8
Q
What is the primary risk associated with thrombi and emboli?
A
They may occlude blood vessels and deprive tissues of oxygen and nutrients.
9
Q
What typically triggers arterial thrombosis?
A
Surface lesions on endothelial cells caused by atherosclerosis.
10
Q
What is characteristic of arterial thrombosis?
A
It usually consists of a platelet-rich clot.
11
Q
What typically triggers venous thrombosis?
A
Blood stasis or inappropriate activation of the coagulation cascade.
12
Q
What is characteristic of venous thrombosis?
A
It typically involves a clot that is rich in fibrin, with fewer platelets.
13
Q
What initiates hemostasis after vascular injury?
A
A complex series of interactions between platelets, endothelial cells, and the coagulation cascade.
14
Q
What is vasospasm?
A
The initial response of a damaged blood vessel to prevent further blood loss.
15
Q
Name a platelet inhibitor.
A
- Abciximab (REOPRO)
- Aspirin (various)
- Cilostazol (PLETAL)
- Clopidogrel (PLAVIX)
- Dipyridamole (PERSANTINE)
- Eptifibatide (INTEGRILIN)
- Prasugrel (EFFIENT)
- Ticlopidine (TICLID)
- Tirofiban (AGGRASTAT)
16
Q
Name an anticoagulant.
A
- Argatroban (ARGATROBAN)
- Dabigatran (PRADAXA)
- Dalteparin (FRAGMIN)
- Enoxaparin (LOVENOX)
- Fondaparinux (ARIXTRA)
- Heparin (HEP-LOCK, HEPFLUSH-10)
- Lepirudin (REFLUDAN)
- Tinzaparin (INNOHEP)
- Warfarin (COUMADIN, JANTOVEN)
17
Q
What are thrombolytic agents?
A
- Alteplase (tPA) (ACTIVASE)
- Reteplase (RETAVASE)
- Streptokinase (STREPTASE)
- Urokinase (KINLYTIC)
18
Q
What is aminocaproic acid used for?
A
It is used in the treatment of bleeding.
19
Q
What is the role of vitamin K in treating bleeding disorders?
A
It is used as a dietary supplement for vitamin K deficiency.
20
Q
How is anemia treated?
A
- Cyanocobalamin (B12)
- Erythropoietin
- Folic acid
- Iron
21
Q
What medication is used to treat sickle cell anemia?
A
- Hydroxyurea (DROXIA, HYDREA)
- Pentoxifylline (TRENTAL)
22
Q
What are resting platelets?
A
Resting platelets are platelets that circulate freely in the absence of injury, monitoring the integrity of the endothelium.
23
Q
What do healthy, intact endothelial cells release?
A
Healthy, intact endothelial cells release prostacyclin into plasma.
24
Q
How does prostacyclin affect platelets?
A
Prostacyclin binds to platelet membrane receptors, causing the synthesis of cAMP, which stabilizes inactive GP IIb/IIIa receptors and inhibits the release of granules containing platelet aggregation agents.
25
What is the role of cAMP in resting platelets?
Elevated levels of intracellular cAMP are associated with a decrease in intracellular calcium, preventing platelet activation.
26
What happens when endothelial cells are damaged?
Damaged endothelial cells synthesize less prostacyclin, leading to lower levels of intracellular cAMP and increased platelet aggregation.
27
What are some chemical mediators synthesized by endothelial cells?
Prostacyclin and nitric oxide are synthesized by intact endothelial cells and act as inhibitors of platelet aggregation.
28
What is the effect of the drug dipyridamole?
Dipyridamole inhibits the enzyme phosphodiesterase, which inactivates cAMP, thereby prolonging its active life.
29
What triggers platelet activation?
Platelet activation can be triggered by thrombin, thromboxanes, and collagen.
30
What do activated platelets release?
Activated platelets release chemical mediators such as thromboxane A2, ADP, and serotonin.
31
What is the role of activated platelets in hemostasis?
Activated platelets cover and adhere to exposed endothelial surfaces, contributing to the formation of a hemostatic plug.
32
What are thromboxanes?
Thromboxanes are signaling molecules involved in platelet activation and aggregation.
33
What happens in an intact, normal vessel regarding thrombin and thromboxane levels?
Circulating levels of thrombin and thromboxane are low, and the intact endothelium covers the collagen in the subendothelial layers.
34
What is the result of unoccupied platelet receptors in a normal vessel?
Platelet activation and aggregation are not initiated.
35
What triggers platelet activation when the endothelium is injured?
Platelets adhere to and cover the exposed collagen of the subendothelium.
36
What occurs during platelet activation?
Receptors on the surface of adhering platelets are activated by collagen, causing morphologic changes and the release of granules.
37
What chemical mediators are released from activated platelets?
Adenosine diphosphate (ADP), thromboxane A2, serotonin, platelet-activation factor, and thrombin.
38
How do signaling molecules affect resting platelets?
They bind to receptors on resting platelets, activating them and leading to aggregation.
39
What messenger systems are involved in platelet activation?
These systems result in elevated levels of calcium and decreased concentration of cAMP within the platelet.
40
What is the role of thrombin in platelet activation?
Thrombin is a mediator that contributes to the activation of platelets.
41
What is the effect of elevated calcium levels in platelets?
It causes the release of platelet granules, activation of thromboxane A2 synthesis, and activation of GP IIb/IIIa receptors.
42
What is the formation of a hemostatic plug?
It involves the aggregation of activated platelets and the formation of a platelet-fibrin clot.
43
What is a resting platelet?
A platelet that is not activated and is in a resting state.
44
What is an activated platelet?
A platelet that has undergone activation and is involved in the aggregation process.
45
What role does fibrinogen play in platelet aggregation?
Fibrinogen binds to GP IIb/IIIa receptors on separate platelets, resulting in platelet cross-linking and aggregation.
46
What is the function of GP IIb/IIIa receptors?
They regulate platelet-platelet interaction and thrombus formation.
47
What is thromboxane A2?
A platelet activation agent that promotes aggregation.
48
What is the role of cyclooxygenase-1 (COX-1) in platelets?
COX-1 is involved in the synthesis of thromboxane A2, which promotes platelet activation.
49
How does aspirin affect platelet function?
Aspirin irreversibly inhibits platelet cyclooxygenase-1, reducing aggregation.
50
What is the significance of cytosolic calcium increase during platelet activation?
It leads to the release of granules containing mediators that activate other platelets.
51
What is the process of clot formation?
Thrombin catalyzes the hydrolysis of fibrinogen to fibrin, forming a hemostatic plug.
52
What is fibrinolysis?
The process where plasminogen is converted to plasmin, which dissolves the fibrin network.
53
What are platelet aggregation inhibitors?
Agents that decrease the formation or action of signals promoting platelet aggregation.
54
What is the role of ADP in platelet aggregation?
ADP is a platelet activation agent that promotes the conformational change necessary for GP IIb/IIIa receptor binding.
55
What are the therapeutic uses of platelet aggregation inhibitors?
They are used in the prevention and treatment of occlusive cardiovascular diseases.
56
What is the mechanism of action of aspirin?
Aspirin inhibits thromboxane A2 synthesis from arachidonic acid in platelets by irreversible acetylation of a serine, preventing arachidonate from binding to the active site of COX-1.
57
What is the effect of aspirin on platelet aggregation?
Aspirin shifts the balance of chemical mediators to favor the antiaggregatory effects of prostacyclin, thereby impeding platelet aggregation.
58
How long does the inhibitory effect of aspirin last?
The inhibitory effect lasts for the life of the anucleate platelet, which is approximately 7 to 10 days.
59
What are the therapeutic uses of aspirin?
Aspirin is used in the prophylactic treatment of transient cerebral ischemia, to reduce the incidence of recurrent myocardial infarction, and to decrease mortality in pre- and post-myocardial infarct patients.
60
What is the recommended dose range of aspirin?
The recommended dose of aspirin ranges from 50 to 325 mg.
61
What complications can arise from aspirin treatment?
Aspirin treatment can prolong bleeding time, leading to complications such as an increased incidence of hemorrhagic stroke and gastrointestinal bleeding.
62
How does ibuprofen interact with aspirin?
Ibuprofen can obstruct the access of aspirin to the serine residue, antagonizing the platelet inhibition by aspirin. Therefore, aspirin should be taken at least 30 minutes before ibuprofen or at least 8 hours after.
63
What is the mechanism of action of ticlopidine, clopidogrel, and prasugrel?
These drugs irreversibly inhibit the binding of ADP to its receptors on platelets, inhibiting the activation of GP IIb/IIIa receptors required for platelet aggregation.
64
What is the relationship between ticlopidine and clopidogrel?
Ticlopidine and clopidogrel are similar in both structure and mechanism of action, but they have different therapeutic uses.
65
What is unique about aspirin compared to other NSAIDs?
Aspirin is the only NSAID that irreversibly exhibits antithrombotic efficacy.
66
What is the mechanism of action of aspirin?
Aspirin inhibits thromboxane A2 synthesis from arachidonic acid in platelets by irreversible acetylation of a serine, preventing arachidonate from binding to the active site of COX-1.
67
What is the effect of aspirin on platelet aggregation?
Aspirin shifts the balance of chemical mediators to favor the antiaggregatory effects of prostacyclin, thereby impeding platelet aggregation.
68
How long does the inhibitory effect of aspirin last?
The inhibitory effect lasts for the life of the anucleate platelet, which is approximately 7 to 10 days.
69
What are the therapeutic uses of aspirin?
Aspirin is used in the prophylactic treatment of transient cerebral ischemia, to reduce the incidence of recurrent myocardial infarction, and to decrease mortality in pre- and post-myocardial infarct patients.
70
What is the recommended dose range of aspirin?
The recommended dose of aspirin ranges from 50 to 325 mg.
71
What complications can arise from aspirin treatment?
Aspirin treatment can prolong bleeding time, leading to complications such as an increased incidence of hemorrhagic stroke and gastrointestinal bleeding.
72
How does ibuprofen interact with aspirin?
Ibuprofen can obstruct the access of aspirin to the serine residue, antagonizing the platelet inhibition by aspirin. Therefore, aspirin should be taken at least 30 minutes before ibuprofen or at least 8 hours after.
73
What is the mechanism of action of ticlopidine, clopidogrel, and prasugrel?
These drugs irreversibly inhibit the binding of ADP to its receptors on platelets, inhibiting the activation of GP IIb/IIIa receptors required for platelet aggregation.
74
What is the relationship between ticlopidine and clopidogrel?
Ticlopidine and clopidogrel are similar in both structure and mechanism of action, but they have different therapeutic uses.
75
What is unique about aspirin compared to other NSAIDs?
Aspirin is the only NSAID that irreversibly exhibits antithrombotic efficacy.
76
What is ticlopidine approved for?
Ticlopidine is approved for the prevention of transient ischemic attacks and strokes for patients with a prior cerebral thrombotic event. It is also used as adjunct therapy with aspirin following coronary stent implantation to decrease the incidence of stent thrombosis.
77
What are the serious adverse reactions associated with ticlopidine?
Ticlopidine can cause life-threatening hematologic adverse reactions, including neutropenia/agranulocytosis, thrombotic thrombocytopenic purpura (TTP), and aplastic anemia.
78
When is ticlopidine generally reserved for use?
Ticlopidine is generally reserved for patients who are intolerant to other therapies.
79
What is clopidogrel approved for?
Clopidogrel is approved for prevention of atherosclerotic events following recent myocardial infarction, stroke, and established peripheral arterial disease. It is also approved for prophylaxis of thrombotic events in acute coronary syndrome.
80
How does clopidogrel compare to ticlopidine in ischemic heart disease events?
Clopidogrel is the preferred agent in ischemic heart disease events because there is more data to support its use in these cardiac patients.
81
What is prasugrel and its approval?
Prasugrel is the newest ADP receptor antagonist approved to decrease thrombotic cardiovascular events in patients with acute coronary syndrome.
82
How effective is prasugrel compared to clopidogrel?
In clinical trials, prasugrel was more effective than clopidogrel in reducing cardiovascular death, nonfatal heart attack, and nonfatal stroke.
83
What effect does food have on the absorption of these drugs?
Food interferes with the absorption of ticlopidine, but not with clopidogrel or prasugrel.
84
What is the elimination route for these drugs?
Elimination of the drugs and metabolites occurs by both the renal and fecal routes.
85
What is a significant warning for ticlopidine?
Ticlopidine has a FDA black box warning due to the severe hematologic adverse reactions associated with its use.
86
What are the major side effects of prasugrel?
The major side effect of prasugrel is bleeding, which can be more common compared to other agents.
87
What is the genetic factor affecting clopidogrel efficacy?
Genetic polymorphism of CYP450 2C19 leads to less active metabolite and reduced clinical response in patients who are poor metabolizers.
88
What should be done for poor metabolizers of clopidogrel?
It is recommended that other antiplatelets or different strategies be used for poor metabolizers.
