Blood (m) Flashcards
most common abnormality; formation of an unwanted clot within a blood vessel
Thrombosis
intravascular clot that floats in the blood
Embolus
failure of hemostasis
Bleeding
loss of blood, increased destruction of RBC or decreased production of RBC
Anemia
inhibit the coagulation of platelets
Antiplatelet Drugs
attenuate fibrin formation
Anticoagulants
degrade fibrin or dissolve the clot
Fibrinolytic Drugs
T/ F
All antithrombotic drugs increase the risk of bleeding
T
T/ F
Thrombus and emboli are dangerous because they may occlude the blood vessel and deprive tissues of oxygen and nutrients which may lead to myocardial infarction, cardiovascular accidents or stroke, and pulmonary embolism which are fatal conditions.
T
T/ F
prostaglandin I2 or prostacyclin binds to platelet receptors that are coupled to the synthesis of cAMP (second messenger).
T
regulates platelet-platelet interaction & thrombus formation
glycoprotein IIb/IIIa receptor
inhibition of thromboxane A2 synthesis from arachidonic acid in platelets by blocking COX-1 → suppression of platelet aggregation
ASPIRIN
T/f
ASPIRIN
action on COX-1 is temporary, lasting for the life of the platelet (7-10 days)
False
(action on COX-1 is PERMANENT, lasting for the life of the platelet (7-10 days)
T/f
ASPIRIN
can be used in combination with other drugs having anti-clotting action
T
more potent
CLOPIDOGREL
in combination with Aspirin:
o superior to Aspirin alone for prevention of recurrent ischemia in patients with unstable angina
CLOPIDOGREL
lesser side effects than Ticlopidine
CLOPIDOGREL
T/f
food interferes with absorption of Ticlopidine but not with Clopidogrel
T
Fab fragment of humanized monoclonal Ab
ABCIXIMAB
T/f
ABCIXIMAB given through IV along with Heparin or Aspirin
T
increasing the intracellular levels of cAMP → decreasing
thromboxane A2 synthesis
DIPYRIDAMOLE
may potentiate the effect of prostacyclin in antagonizing platelet aggregation
DIPYRIDAMOLE
T/f
ANTICOAGULANTS
The extrinsic pathway is initiated by the activation of the clotting factor VII by tissue factor or thromboplastin
T
T/f
ANTICOAGULANTS
The intrinsic pathway is triggered by clotting factor XII.
T
is a glycoprotein that forms the mesh-like matrix of the blood clot.
fibrin
inhibit the action of coagulation factors (thrombin inhibitors)
Heparin
interfere with synthesis of coagulation factors (Vit. K antagonists)
Warfarin
T/F
Vitamin K is responsible for the synthesis of certain coagulation factors like factor II, VII, IX, and X.
T
found in secretory granules of mast cells
HEPARIN
T/ f
HEPARIN has no intrinsic anticoagulant activity
T
drug of choice for anticoagulation during pregnancy (does not cross placenta barrier)
HEPARIN
given parenterally because it is not absorbed through GI mucosa
HEPARIN
→ limit expansion of thrombus by preventing fibrin formation
→ acute deep vein thrombosis & pulmonary embolism
→ used in extracorporeal devices to prevent thrombosis
→ prevention of post-op thrombosis in patients undergoing elective
surgery and in acute MI
HEPARIN
→ longer half-life in patients with hepatic cirrhosis
HEPARIN
→ excreted in urine PHARMACOKINETICS
→ does not cross placental barrier
→ degraded primarily by reticuloendothelial system (mononuclear
phagocytes)
HEPARIN
HEPARIN
ADVERSE EFFECTS
→ hemorrhage
(Txt)?
Protamine sulfate
T/ F
Protamine sulfate is given by IV infusion
T