Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GS Pharmacology > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

Primary Hemostasis

A
  1. Platelet Adhesion
    • platelets stick to damaged epithelial wall of blood vessels
  2. Granule Release
  3. Aggregation & Consolidation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Platelet Granule Release

A

Lead to

  1. ADP, epinepherine, & collagen activation
  2. increased GPIIb/IIIa expression
  3. phospholipase A2 cleavage of arachidonic acid (AA) from phospholipid
  4. AA converted by cycloolygenase (COX) enzyme to thromboxane A2 (TXA2)
  5. 5-hydroxytryptamine (5HT) also produced & released

**Stimulate Platelet Aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Primary Hemostatic Plug

A

reversible

bridging molecule between molecule is fibrinogen, which binds GPIIb/IIIa receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

White Thrombus

A

mostly platelets

can form in high pressure arteries

can reduced blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Red Thrombus

A

can form around a white thrombus

in low pressure veins

coloring is from RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Secondary Hemostasis

A

activation of coagulation casacade

concurrent with platelet aggregation

Aims:

  1. generate fibrin
  2. produce thrombin
    • direction platelet aggregation action
    • helps sustain aggregation
    • makes irreversible secondary hemostatic plug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thrombin

A

avtivator of many steps in coagulation cascade

most important is the transformation of fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Partial Thromboplastin Time

A

aPTT

measurement of the intrinsic coagulation pathway

think of PTT blood test in blue tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Prothombin Time

A

PT

measurement index for the extrinsic coagulation pathway

PT test in blue blood tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Prostacyclin

A

PGI2

arachidonic acid metabolite secreted by endothelium

antiaggregtory

increases cAMP in platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Antithrombin III

A

ATIII

inhibits factor VIIa, factor IXa, factor Xa, & thrombin

activated by intact endothelium

NOT very active on its own, only in complex coagulation factor (thus stopping them from their purpose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Proteins C & S

A

negative feedback to prevent excessive enlargement of fibrin clot

protein C & S work together to inactivate facotrs Va & VIIIa

protein C is activated by binding to thrombomoldulin with thrombin when thrombin levels are in excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Thrombomodulin

A

enzyme that binds both thrombin and protein C

binds both together to activate protein C when thrombin is in excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tissue Factor Pathway Inhibitor

A

TFPI

activated by TF:VIIa complex

part of negative feedback mechanism to inactivate TF:VIIa complex & prevent excessive activation of factors IX & X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Predisposition for Thrombus (clot) Formation

A
  1. endothelial injury
    • blood vessel damage
  2. abnormal blood flow
    • usually in arrythmia patients
  3. hypercoagulability
    • RA
    • Lupus
    • mutations of protein C & S
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Unfractionated Heparin

A
  1. Other names:
  2. Uses:
    • DVT
    • prevent propagation of PEs (rapid onset)
    • post MI to prevent venous thromboembolism
    • initially in unstable angina
    • maintain patency in vascular catheters
  3. Mechanism:
    • binds to antithrombin III (ATIII) conformationally changing it
    • new complex has higher affinity for clottin facotrs
    • prolongation of aPTT
  4. Contraindications: none mentioned
  5. Adverse Effects:
    • bleeding
    • heparin-induced thrombocytopenia
    • long term use can cause osteoporosis
    • excessive anticoagulation can be treated by discontinuation or protamine sulfate
  6. Other:
    • negatively charged sulfated mucoplysaccharide found naturally in mast cells
    • MUST monitor aPTT
17
Q

Low Molecular Weight Heparins

A
  1. Names: Enoxaparin (Lovenox), Dalteparin, Tinzaparin
  2. Uses:
    • DVT
    • acute coronary syndromes (Enoxaparin & Dalteparin only)
  3. Mechanism:
    • less anti-thrombin activity
    • equal amount of anti-factor X activity/molecule
    • prolongation of aPTT
  4. Contraindications: renal insufficient patients
  5. Adverse Effects:
    • bleeding
    • heparin-induced thrombocytopenia
    • long term use may cause osteoporosis
    • MUST monitor aPTT
  6. Other:
    • more expensive
    • more favorable benefit to risk ratio
18
Q

Lepirudin

A
  1. Other names: none mentioned
  2. Uses: patients that develop heparin-induced thrombocytopenia
  3. Mechanism: inactivates thrombin in thrombi
  4. Contraindications: renal insufficiency
  5. Adverse Effects: bleeding
  6. Other:
    • monitored by PTT
    • cleared by kidneys
19
Q

Bivalirudin

A
  1. Other names: none mentioned
  2. Uses: percutaneous coronary angioplasty (balloon sx) & unstable angina
  3. Mechanism: inactivates thrombin in thrombi
  4. Contraindications: none mentioned
  5. Adverse Effects: bleeding
  6. Other: monitored by PTT
20
Q

Argotroban

A
  1. Other names: none mentioned
  2. Uses: heparin-induced thrombocytopenia in renal insufficient patients
  3. Mechanism: inactivates thrombin in thrombi
  4. Contraindications: none mentioned
  5. Adverse Effects: bleeding
  6. Other:
    • monitored by PTT
    • cleared by liver
21
Q

Warfarin

A
  1. Other names: Coumadin
  2. Uses: in conjunction with heparin for longer term
    • DVT
    • PE
    • systemic embolism post MI or Afib
  3. Mechanism: blockade coupled to metabolism of vitamin K, which aides in prothrombin formation
  4. Contraindications: none mentioned
  5. Adeverse Effects:
    • readily crosses the placenta & can cause hemorrhagic fiver in fetus
    • serious birth defects by abnormal bone formation
    • cutaneous necrosis in first few weeks
    • rarely can cause clotting
  6. Other:
    • class of delayed-acting anticoagulants
    • others in class include: dicumarol & phenindione
    • monitored by PT
    • 36h half life (long)
    • highly bound to albumin
    • 8-12hr delay bc of degradation rate of circulating vitamin K
22
Q

Warfarin Enhancers

A
  • clopidogrel (Plavix)- decreases warfarin metabolism
  • fluconazole (Diflucan- antifungal)- decreases earfarin metabolism
  • broad spectrum antibiotics- reduces vitamin K availability
23
Q

Warfarin Diminishers

A
  • Cholestyramine (lowers cholesterol)- inhibits warfarin absorption in GI tract
  • Vitamin K- bypasses warfarin’s inhibition of epoxide reductase
24
Q

Fibrinolytic Drugs

A
  1. Use:
    • lyse already existing clots in multiple PE & central DVT
    • early treatment acute MI (must be less than 6 hours)
  2. Adverse Effect: may cause lysis of physiologically important fibrin clots
25
Q

Streptokinase

A
  1. Other names/class: none mentioned/ fibrinolytic drug
  2. Uses:
    • acute PE
    • DVT
    • acute MI
    • arterial thrombosis
  3. Mechanism:
    • combines with proactivator plasminogen
    • catalyzes the degradation of fibrinogen, factors V & VII
  4. Contraindications: none mentioned
  5. Adverse Effects:
    • bleeding disorders
    • systemic fibrinolysis
  6. Other:
    • protein synthesized from streptococci
    • for MI, use w/in 4h & continue 1-3days thenuse heparin or oral anticoagulation
26
Q

Urokinase

A
  1. Other Names/ Class: n/m, fibrinolytic
  2. Uses: severe PE & DVT
  3. Mechanism: activates plasminogen, thus degrading both fibrin and fibrinogen
  4. Contraindications:n/m
  5. Adverse Effects: bleeding
  6. Other:
    • originally isolated from human urine
    • obtained from human fetal renal cells
    • more expensive than Streptokinase
    • bc of human origin, will NOT cause allergic rxn
27
Q

Tissue Plasminogen Activator

A
  1. class of sering protease drugs
  2. Uses:
    • MI
    • PE
    • peripheral arterial thromboembolism
    • stroke
  3. Mechanism:
    • rapidly binds to and activated plasminogen bound to fibrin in a thrombus or hemostatic plug
    • low affinity for free plasminogen
    • ***advantage: only lysing fibrin & no degredation of other proteins
  4. Contraindications: recent hemorrhagic stroke
  5. Adverse Effects: bleeding, including hemorrhagic stroke
  6. Other:
28
Q

Alteplase

A
  1. Other names/class: nm/ t-PA (tissue plasminogen activator)
  2. Uses:
    • MI
    • stroke
    • PE
    • peripheral arterial thromboembolism
  3. Mechanism:
    • fibrin selective
    • activates plasminogen in a thrombus of hemostatic plug
  4. Contraindications: recent hemorrhagic stroke
  5. Adeverse Effects: bleeding, including hemorrhagic stroke
  6. Other:
    • most common in t-PA family
    • unmodified human t-PA
29
Q

Reteplase

A
  1. Other name/class: nm/ t-PA
  2. Uses:
    • MI
    • PE
    • peripheral arterial thromboembolism
    • stroke
  3. Mechanism:
    • activates plasminogen bound fibrin in thrombus or hemostatic plug
  4. Contraindications: recent hemorrhagic stroke
  5. Adverse Effects: bleeding, including hemorrhagic stroke
  6. Other:
    • genetically engineered t-PA w/ several aminoacis deletions
    • longer half-life due to increased specificity
30
Q

Tenecteplase

A
  1. Other names/Class: nm/ t-PA
  2. Uses:
    • MI
    • Stroke
    • PE
    • peripheral arterial thromboembolism
  3. Mechanism: plasminogen activator when bound to fibrin; fibrin lysis
  4. Contraindications: recent hemorrhagic stroke
  5. Adverse Effects: bleeeding, including hemorrhagic stroke
  6. Other: similar to Reteplase
31
Q

Anisetreplase

A
  1. Other names/Class: nm/ t-PA
  2. Uses:
    • MI
    • stroke
    • PE
    • peripheral arterial thromboembolism
  3. Mechanism: activator of plasminogen bound to fibrin; lysis of fibrin
  4. Contraindications: recent hemorrhagic stroke
  5. Adverse Effects: bleeding, including hemorrhagic stroke
  6. Other:
    • complex of purified plasminogen & streptokinase
    • long half-life **sinlge bolus achieves reperfusion
32
Q

Aspirin

A
  1. Other Name/Class: ASA/?
  2. Uses:
    • antiplatelet therapy
    • prevention of arterial thrombosis leading to MI & stroke
  3. Mechanism: inhibition of COX enzyme through acetylation
  4. Contraindication: nm
  5. Adverse Effects:
    • GI disturbances
    • Renal toxicity (rare in low doses)
    • prolonged bleeding time
  6. Other:
    • **low dose must be used **
    • most often 81mg/day, but up to 325 mg/day
    • high 1st pass effect
    • higher doses may inhibit beneficial postacyclin production
33
Q

Ticlopidine

A
  1. Other names/Class: nm/ ADP receptor inhibitor
  2. Uses:
    • secondary prevention of thrombotic stroke (ASA intolerant pts)
    • in combo with ASA to prevent stent thrombosis
  3. Mechanism: ADP receptor inhibitor
  4. Contraindications: nm
  5. Adverse Effects: thrombocytopenia
  6. Other: must monitor blood counts
34
Q

Clopidogrel

A
  1. Other names/Class: Plavix/ ADP receptor inhibitor
  2. Uses:
    • prevention in MI, stroke & vascular patients
    • post coronary bypass
  3. Mechanism: inhibits ADP receptors
  4. Contraindications: nm
  5. Adverse Effects:
    • less than Ticlopidine
    • GI disturbances
35
Q

Dipyridamole

A
  1. Other names/Class: phosphodiesterase inhibitor
  2. Uses:
    • w/warfarin: prevention of thrombosis in prosthetic heart valves
    • w/ASA: patients w/ thrombotic diathesis (predisposed to blood clot)
  3. Mechanism: inhibits phosphodiesterase by increasing cAMP & vasodilator of arteries
  4. Contraindications: nm
  5. Adverse Effects: bleeding
  6. Other: ***no longer given***
36
Q

Abciximab

A
  1. Other names/Class: nm/ GPIIb/IIIa antibody
  2. Uses: acute coronary syndromes
  3. Mechaninsm:
    • GPIIb/IIIa inhibitor
    • new class of platelet inhibitor
    • directed against IIb/IIIa complex
  4. Contraindications:
  5. Adverse Effects: bleeding, especially when used with thrombolytics
  6. Other:
    • administered IV
    • humanized monoclonal antibody
37
Q

Eptifibatide & Tirofiban

A
  1. Other names/class: GPIIb/IIIa inhibitor
  2. Uses: acute coronary syndromes
  3. Mechanism: they are fibrinogen analogs that reviersible inhibit binding of fibrinogen to receptor
  4. Contraindications: nm
  5. Adverse Effects: bleeding, especially when given with thrombolytics
  6. Other: administered by IV
38
Q

Post MI treatment

A
  1. low dose ASA- reduces secondary coronary thrombosis
  2. nitrates- reduce preload
  3. beta blockers (do NOT use alone)
  4. ACE inhibitors- reduces mortality after thrombolytics

GS Pharmacology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions