Section 6: Anti-Thrombotic Therapy Flashcards
1
Q
Thrombosis versus embolus
A
Thrombosis: clot forms where it shouldn’t and stays there in the vessel
Embolus: clot dislodges and travels somewhere else
2
Q
Thrombosis consequences
A
- obstruct flow in critical vessels
- obliterate valves and other structures that are essential to normal hemodynamic function
3
Q
List principle clinical syndromes that result from thrombosis
A
- AMI
- DVT
- PE
- acute ischemic stroke
- acute peripheral arterial occlusion
- occlusion of indwelling catheters
4
Q
part of purpose to issue anti-thromboticc therapy
A
to avoid DIC
5
Q
Causes of DIC
A
- septicemia
- obstetric complication
- severe burns
- trauma
- casting of legs
- snake venoms
- APL (acute promyelocytic leukemia)
6
Q
Describe DIC process
A
- Extensive endothelial damage or release of tissue thromboplastin
- Start out-of-control clotting process, which uses up clotting factors and formation of many thrombi/platelet aggregates everywhere in the body
- Platelet aggregation contributes to thrombocytopenia and excessive clot formation results in ischemia and multiple infarctions -> organ failure from lack of oxygen
- Overwhelming clotting leads to excessive fibrinolysis, coupled with reduced serum fibrinogen -> excessive bleeding and hemorrhage
- Simultaneous excessive clotting and bleeding at same time (it’s a mess)
7
Q
List obstetric complications that can lead to DIC
A
- Dead fetus syndrome (dies in utero without removal from mom -> release TF3)
- Amniotic fluid embolus
- Abruptio placentae (placenta pulls from uterine wall)
- Preeclampsia, eclampsia, HELLP
- Increase in FVII, VIII, IX, XII, and I (increase at end of term)
- Decrease Protein S
- Abortion
8
Q
Clinical signs of DIC
A
- Oozing
- Bleeding from multiple sites due to using up clotting factors (GIT, UR tract, IV sites, nose…etc)
- Organ damage from fibrin deposition
9
Q
Purpose of anti-thrombotics (“not blood thinners””
A
- Limit or prevent clotting by suppressing synthesis/function of various hemostatic constituents
- Prevent thrombosis without causing hemorrhage
10
Q
List 3 categories of anti-thrombotics and what they do
A
- anti-platelets (inhibit aggregation)
- anti-coagulants (inhibit cascade)
- thrombolytics (dissolve clot)
11
Q
Warfarin (Coumadin/Jantoven)
A
- Oral anti-coagulant
- Arrests vit K in storage form and makes it unavailable to add second carboxyl group to produce complete factors II, VII, IX, and X
12
Q
How to monitor Warfarin and interfering factors
A
- Monitor by PT and INR monthly
- Vit K rich foods interfere (green tea, bananas)
13
Q
How are patients with venous thrombosis usually treated?
A
- Unfractionated heparin (UFH) and then Warfarin
- Low MW heparin (LMWH) getting popular bc difficulties monitoring UFH/Warfarin
14
Q
UFH or standard heparin drug mechanism
A
- Heparin causes conformational change in the anti-thrombin (AT) molecule, thus increasing AT’s inhibitory effect
- AT forms an irreversible complex with factors IIa, IXa, Xa, XIa, XIIa, and plasmin
- Heparin not consumed, so dissociates and serves as cofactor for more AT molecules
- Also inhibits factor Xa
15
Q
Heparan sulfate
A
Heparin-like substances made by endothelial cells
