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100 Cards in this Set

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  • Back
  • 3rd side (hint)
List the steps leading to "Phase 1 Platelet Plug"
1. Vessel damage
2. Vasospasm
3. Platelet adhesion
4. Platelet aggregation
5. Viscous metamorphosis
6. Temporary Hemostasis
Upon damage, what do endothelial cells release to cause Vasospasm (vessel constriction)?
Platelets bind to damaged vessels via __1__, which binds to __2__; and __3__, which binds __4__
1. GP 1a
2. Collagen
3. GP 1b
4. von Willebrand factor

Platelets: GP 1a and 1b
Endothelial cells: Collagen and von Willebrand factor
In platelet aggregation, platelets bind to themselves via __1__, which also bind __2__ and other macromolecules
1. GP IIb / IIIa
2. Fibrinogen
What is "Viscous Metamorphosis" of platelets?
loss of individual platelet membranes to form a gelatinous mass
Thrombin formation induces these 3 events in platelets
1. release of ADP = further platelet aggregation
2. Serotonin release
3. Prostaglandin synthesis from platelet AA
Phase 2 Fibrin Plug:
Increased __1__ synthesis in platelet with decreased __2__ synthesis in damaged vessel wall
1. Thromboxane (TXA2)= platelet aggregation and vasoconstriction

2. Prostacycline (PGI2)
- vasodilator and platelet inhibitor
- but is decreased in damage
What induces the conversion of Fibrinogen to Fibrin?
Activation of both the intrinsic and extrinsic coagulation systems leads to teh conversion of ________ to ________
Prothrombin (factor II)

Thrombin (Factor IIa)
Prothrombin is bound by __1__ to __2__ on the platelet surface, whereas thrombin is __3__
1. calcium
2. phospholipids
3. released into circulation
What initiates the Intrinsic Coagulation Pathway?
Collagen from the damaged blood vessel
What measures the Intrinsic system of coagulation?
Partial Thromboplastin time (PTT)
What is PTT used to monitor?
Heparin therapy
Extrinsic Coagulation system:
1. Requires these factors for initiation
2. These Factors are limiting (why?)
3. What is it measured by?
4. What is it used to monitor?
1. Tissue Factor (Tissue Thromboplastin or Factor 3
2. Factors 2, 7, 9, and 10
3. Prothrombin time
4. Warfarin therapy
What are the 3 groups of things that are risk factors for Thromboembolism?
1. abnormalities of blood flow (anything that slows the blood)
2. abnormalities of surface in contact with blood
3. abnormalities of clotting factors
List 6 examples of things that cause abnormalities of blood flow
1. Left ventricular dysfunction
2. Ischemic cardiomyopathy
3. CHF
4. Bed rest/immobilization
5. Venous obstruction from tumor/obesity/pregnancy
6. Atrial fibrillation
List 6 things that can cause abnormalities of surface in contact with blood (risk factors for thromboembolism)
1. Vascular injury
2. Heart valve disease
3. Heart valve replacement
4. Atherosclerosis
5. Acute myocardial infarction
6. Indwelling catheters
List 3 Endogenous Anticoagulant deficiencies that can lead to Thromboembolism
1. Protein C ***
2. Protein S ***
3. Antithrombin III

*** Vitamin K - dependent
What syndrome could lead to Thromboembolism?
Antiphospholipid antibody syndrome
What 3 things lead to an increase in clotting factors and increase the risk for Thromboembolism?
1. Estrogen therapy -> affects the synthesis of coagulation factors
2. Pregnancy -> increased estrogen
3. Malignancy
Arterial Thrombosis:
__1__ > __2__ = __3__ thrombus
1. Platelets
2. Fibrin
3. White
What 4 events/things can cause Arterial Thrombosis?
1. Local ischemia
2. MI
3. Unstable angina
4. Stroke
What is a prophylaxis for Arterial Thrombosis?
Antiplatelet therapy (aspirin)

* b/c platelet are more prominent than fibrin in arterial side
Venous Thrombosis:
__1__ > __2__ = __3__ thrombus
1. Fibrin
2. Platelets
3. Red
Prophylaxis for Venous Thrombosis
Anticoagulant therapy
- Heparin
- Warfarin
Chemical name for Aspirin
Acetylsalicylic Acid
Aspirin inhibits the synthesis of __1__ by IRREVERSIBLE __2__ of __3__ in Platelets
1. Thromboxane (TXA2)
2. acetylation
3. COX-1
TXA2 increases the __1__ pathway in platelets causing __2__

*reduced by aspirin
1. PIP2 -> increases expression of Gp IIb/IIIa

2. aggregation
-TXA2, ADP, and Serotonin cause expression of Gp IIb/IIIa
TXA2 is a potent stimulator of __1__ and __2__
1. Platelet activation

2. Vasoconstriction
COX-1 is in __1__ and is inhibited by low doses of aspirin

COX-2 is in __2__ and produces __3__
1. Platelets

2. Endothelial cells

3. Prostacyclin (PGI2)
COX-2 is inhibited by high or low doses of aspirin?
Aspirin is useful in preventing or reduing the risk of __1__ and __2__ due to its antithrombotic effects
1. MI

2. transient ischemic attacks
Aspirin's antithrombotic effects on platelets are seen __1__ days after administration and lasts for the duration of the platelets life-span, usually __2__ days
1. 1-2

2. 7-10
Stop Aspirin __1__ before surgery

Stop other NSAIDs __2__ before surgery
1. 1 week

2. 2-3 days
What is Ticlopidine's mechanism of action?
1. inhibits platelet activation by irreversibly blocking ADP receptors

2. Inhibits Fibrinogen binding by preventing GP IIb/IIIa expression = blocks platelet-platelet binding

*ADP antagonist
What 3 things is Ticlopidine used as?
1. alternative to Aspirin to prevent initial or recurrent thromboembolic stroke
2. Post-MI reinfarction prophylaxis
3. Unstable angina
How is Ticlopidine administered?

*rapidly and well (>80%) absorbed
*extensively metabolized
Why is Ticlopidine only given to patients who are intolerant or unresponsive to aspirin?
b/c in rare cases it causes SEVERE BONE MARROW TOXICITY

*also increases Liver Functional Enzymes
Ticlopidine causes increased bleeding when given with these drugs
1. Warfarin
2. Heparin
3. other antiplatelet drugs
4. NSAID drugs
__1__ decreases its clearance

It decreases the clearance of __2__

T or F: Usually Clopidogrel is preferred over Ticlopidine as an ADP antagonist

**Clopidogrel has lower incidence of adverse skin, GI, or HEMATOLOGIC rxns
Clopidogrel or Ticlopidine:
Which has less drug-drug interactions?
Clopidogrel trade name
Clopidogrel has a similar mechanism to Ticlopidine but has a lower incidence of these 3 adverse effects
1. Cutaneous rxns
2. GI effects
Clopidogrel is used to reduce ______ in patients with a history of recent stroke, recent MI, or established peripheral vascular disease
Clopidogrel inhibits the activity of ______ and therefore increase the plasma concentrations of drugs
Clopidogrel may increase the plasma concentrations of these 6 drugs
1. Fluvastatin
2. Phenytoin
3. Tamoxifen
4. Tolbutamide
6. many NSAIDS
Eric Clopidogrel inhibits 2C9. His gf TAMMI has the FLU and she wears a PHENY-pack with her NSAIDS in it. Their country goes to WAR with the TOLBUT's
Abciximab is a new class of drugs called _________?
Platelet-receptor glycoprotein inhibitors
What is the mechanism of actions of Abciximab?
monoclonal antibody that binds to glycoprotein receptor IIb/IIIa on activated plates preventing platelet aggregation
- inhibits fibrinogen, vWF, and others from cross-linking platelets
How, what for, and with what is Abciximab given?
How = IV

What for = Angioplasty, atherectomy, stent placement

What with = Clopidogrel
What is the most common adverse effect of Abciximab?
Non-peptide Platelet-receptor glycoprotein inhibitor similar to Abciximab, but not a monoclonal antibody
Cyclic peptide platelet-receptor glycoprotein inhibitor similar to Abciximab, but not a monoclonal antibody

*Circular peptide Epithet inhibits of Gp IIb/IIIa
What is the main use of Dipyridamole?
In combo with Warfarin -> inhibits embolism from prosthetic heart valves
What 2 things does Dipyridamole do?
Coronary vasodilator

Inhibits platelet aggregation
Why is Dipyridamole not used to treat angina?
Even though it is a coronary vasodilator, it dilates healthy vessels instead of diseased ones and makes angina worse
Dipyridamole's mechanism is not clear, but it is in part due to increase in _____ because of inhibition of _____

In combination with aspirin, Dipyridamole reduces __1__ in patients with __2__ disease
1. thrombosis

2. thrombotic
Antithrombotic, antiplatelet, and vasodilatory drug that inhibits Phosphodiesterase III and thereby increases cAMP levels which prevents platelet aggregation
What is Cilostazol used for?
Intermittent claudication and peripheral vascular disease

*Buerger's disease
Drug that reduces elevated platelet counts in patients with essential thrombocytosis (too many platelets)
What is Anagrelide's mechanism of action?
inhibits Megakaryocyte development in the late postmitotic stage = inhibits formation of platelets
Anagrelide is approved for the treatment of __1__ secondary to __2__ disorders, such as __3__ and __4__ to reduce the risk of Stroke and MI
1. Thrombocytosis
2. Myeloproliferative
3. Polycythemia vera
4. Chronic Myelogenous leukemia
Give 3 examples of Calcium chelators
1. Oxalic acid
2. Sodium Citrate
3. Disodium edetate

*inhibit blood coagulation IN VITRO, not in humans!!!
Accelerate the action of Antithrombin III to neutralize thrombin and other coagulation factors
Direct thrombin inhibitors
Interfere with the hepatic synthesis of functional Vitamin K-dependent clotting factors
Coumarin derivatives = Warfarin
What is the source of Heparin?
Pig intestinal mucosa

Bovine lung
What is the chemical structure of Heparin?
Sulfated mucopolysaccharide = acidic = negatively charged
What are the routes of administration of heparin?

How is it never given and why?
Continuous IV drip or Intermittent Subcutaneous

Never Intramuscular due to risk of hematoma at injection site
Oral lacks absorption
What is the advantage of Heparin over Warfarin?
Heparin's action is IMMEDIATE
What is the problem with Heparin and its pharmacokinetics?
Large charged molecule -> sticky -> binds extensively to endothelial cells and plasma proteins
Is Heparin clearance Dose-dependent or dose-independent?

Dose-dependent b/c plasma levels of heparin increase considerably once binding sites are saturated

*most drugs are Dose-INDEPENDENT
What is the Therapeutic goal of Heparin?
to prolong the Partial Thromboplastin Time (PTT) to 1.5-2.5 times normal

*measured just before the next dose for intermittent therapy
-The protease inhibitor, __1__, forms a 1:1 complex with clotting factor proteases
-This interaction is slow, but is stimulated 1000-fold by __2__, which binds to Antithrombin III
1. Antithrombin III
2. Heparin
-The heparin-antithrombin complex inactivates __1__ (main mechanism)

-The heparin-antithrombin III complex also inactivates __2__, which occurs earlier in the cascade
1. Thrombin (IIa)

2. Xa
During active thrombosis, the anticoagulant effect of heparin is primarily due to inactivation of __1__

With little or no thrombosis, the anticoagulant effect is largely due to inactivation of __2__
1. Thrombin (IIa)

2. Factor Xa
What are the Contraindications for Heparin use? (4)
1. Bleeding disorders and disorders that predispose to bleeding (hemophilia, thrombocytopenia)
2. Patients with advanced liver or kidney disease
3. Severe HTN -> bleeding into brain
4. Infections -> active TB, infective endocarditis
Heparin is preferable to other anticoagulants during __1__ due to lack of __2__
1. pregnancy

2. placental transfer

*in contrast to Warfarin
With bleeding as an adverse effect of Heparin, what can be done to minimize it?
Careful monitoring of PTT and Platelet counts
1. Since Heparin is an animal product, what adverse can happen?

2. Long-term use of Heparin can cause this adverse effect
1. Allergic reaction

2. Osteoporosis
Describe Type I Thrombocytopenia caused by Heparin
-Immediate, transient, and reversible heparin-induced platelet sequestration

-heparin binds to platelet and causes them to lyse
Describe Type II Thrombocytopenia caused by Heparin

What is the name for it?
IgG develops to Heparin bound to Factor 4 on Platelets

Heparin-induced Thrombocytopenia (HIT)
What is a paradoxical effect related to Heparin-induced thrombocytopenia (HIT)?

*paradoxical b/c Heparin is an anticoagulant
**caused by IgG/Heparin/Platelet complex
What is the antidote to Heparin?
Protamine Sulfate
Protamine sulfate is a __1__ peptide that binds to Heparin

Excessive antidote must be avoided b/c protamine itself is an __2__
1. basic (acid/base or anion/cation interaction)

2. Anticoagulant
Administer __1__ protamine sulfate IV for each __2__ units of heparin remaining in the patient
1. 1 mg

2. 100 units
What is the disadvantage of Low Molecular Weight Heparin (LMWH)?
Protamine is much less capable of reversing its effects
What are the 3 Low Molecular Weight Heparins (LMWH)?


LMwH's were first approved for primary prevention of __1__ after __2__ therapy
1. deep vein thrombosis

2. hip replacement
When are LMWH's contraindicated?
in Heparin-induced Thrombocytopenia
How are LWMH's monitored?
When are they more often monitored?
-anti-Xa activity assay
-when used in pregnancy

*more expensive than PTT
What is an advantage of LMWH's over Unfractionated Heparin (UFH)?
Pharmacokinetics = dose-independent = are not sticky to endothelial cells or plasma proteins
What do LMWH's have more activity against, Factor Xa or IIa?
Is a synthetic pentasaccharide anticoagulant that only exerts antithrombotic activity as a result of ATIII-mediated selective inhibition of Factor Xa
*Has no effect on Thrombin (IIa)

Fondles Factor 10a
How is Fondaparinux different from Heparin and LMWH?
Selectively inhibits Factor Xa

*does not affect Thrombin (IIa)
What is the elimination half-life of Fondaparinux?

How is it administered?
18 hours = allows once-daily dosing


***Fondles factor 10a for 18 hours under the skin
Clinical trials are needed to determine if Fondaparinux is a safe alternative to heparin in patients at risk for what?
Heparin-induced Thrombocytopenia

*does not bind to Platelet Factor 4
What 3 things is Fondaparinux being used for?
1. Venous thromboembolism prophylaxis following orthopedic surgery
2. Treatment of Pulmonary Embolism
3. Treatment of Deep Vein Thrombosis