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Pharmacology II > Coagulation Modifiers > Flashcards

Coagulation Modifiers Flashcards

1
Q

3 processes involving blood coagulation

A
  1. Vasoconstriction
  2. Platelet clumping
  3. Cascade of clotting factors (coagulation)
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2
Q

First reaction to blood vessel injury.

- If injury is small, this can close the blood vessel and arrest the bleeding and allow the vessel to heal.

A

Vasoconstriction

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3
Q
  1. Injury to blood vessel exposes collagen and other substances under the endothelial lining of blood vessels.
  2. Platelets stick to site of injury
  3. Collagen and platelets release chemicals (serotonin, adenosine di-phosphate and thromboxane A2 etc.) which causes vasoconstriction and more platelets to attach.
A

Platelet Aggregation

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4
Q

If platelet plug and vasoconstriction not enough to seal injury, ______ process may occur.

A

Coagulation

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5
Q

2 pathways of coagulation

A
  1. Intrinsic Pathway

2. Extrinsic Pathway

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6
Q

Coagulation Pathway.

a. XII is activated to become XIIa
b. XIIa activates XI which leads to the activation of other factors in the pathway until the conversion of prothrombin into thrombin is reached.
c. Thrombin activates fibrinogen, then fibrinogen activates fibrin that forms a clot (thrombus) into the vessel. The thrombus (platelet + fibrin) then seals the blood vessel.

A

Intrinsic Pathway

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7
Q

Coagulation Pathway.

  • Blood leaked out of the blood vessel into surrounding tissue also form a clot.
  • Injured cells release tissue “thromboplastin” (tTP), which activates clotting factors in the blood and starts clotting cascade to form a clot on the outside of the blood vessel.
  • The injury vessel is now vasoconstricted and has a platelet plug and clots on both sides of the injury.
A

Extrinsic Pathway

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8
Q

A chemical substance in the blood in which comes in contact with injured blood vessels.

A

Hageman Factor, XII

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9
Q

Chemical released by injured cells which activates clotting factors in the blood and starts clotting cascade to form a clot on the outside of the blood vessel.

A

Thromboplastin (tTP)

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10
Q

A clot that consists of platelets and fibrin that seals the blood vessel.

A

Thrombus

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11
Q

2 factors that inhibit blood clotting in the blood plasma.

A
  1. Anti-thrombin

2. Plasminogen

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12
Q

Factor that prevents the formation of thrombin.

A

Anti-thrombin

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13
Q

a. Activators converts plasminogen to plasmin.

b. Plasmin targets fibrin and dissolves clot.

A

The Plasminogen Mechanism

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14
Q

Activators that converts plasminogen to plasmin. (4)

A

ADH, NE, urokinase, streptokinase

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15
Q

A genetic deficiency or absence in clotting factor VIII, which causes increased bleeding and usually affects males.
- Regular drug Tx not required, concentrated mixture of factor use of severe bleed or bruising occurs.

A

Haemophilia A

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16
Q

Factor IX deficiency - low to absent.

A

Haemophilia B aka Christmas Disease

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17
Q

Clotting disorders can also be present in the absent or deactivation of what certain vitamin?

A

Vitamin K deficiency

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18
Q

The process that stops bleeding after injury to blood vessel.

A

Hemostasis

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19
Q

The process of formation of a fibrin blood clot (thrombus)

A

Thrombosis

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20
Q

A small fragment of a thrombus that breaks off and circulates until it becomes trapped in a capillary causing either ischemia or infarction to the area distal to the obstruction.

A

Embolus

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21
Q

Agents that inhibits the action or formation of clotting factors and therefore prevents clots from forming. No effect on clot that is already formed. For unstable angina, MI, atrial fib, indwelling devices. Reduce risk of venous thrombi (composed of fibrin and RBC) Most common is Heparin and Warfarin (Coumadin)

A

Anticoagulant

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22
Q

Agents that prevent platelet plugs from forming by inhibiting platelet aggregation. Reduce risk of arterial thrombi (due to platelet aggregation)

A

Anti-platelet agent

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23
Q

Agents that breakdown preformed clots.

A

Thrombolytic Agent (fibrinolytics)

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24
Q

Agents that promote blood coagulation and help in the management of conditions in which excessive bleeding would be harmful.

  • Stop bleeding
  • Prevention and Tx of excessive bleeding resulting from systemic hyperfibrinolysis or surgical complications such as repeated coronoary bypass surgery
A

Haemostatic Agent (antifibrinolytics)

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25
Q

Diseases associated with abnormal clotting within blood vessel.

A

thrombo-embolic diseases

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26
Q

Used to diagnose presence and aetiology of a thrombus and an embolism.

A
  1. Physical Exam
  2. Client History
  3. Doppler Ultrasound
  4. Phlebography
  5. Radiolabel fibrinogen studiees
  6. Angiogram
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27
Q

Lab tests for Heparin that are used to measure the effect of the drug on clotting. (2)

A

APTT (activated partial thromoplastin time) and/or ACT (activating clotting time)

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28
Q

Lab tests for “Oral Anticoagulants” that are used to measure the effect of the drug on clotting. (2)

A

PT (prothrombin time) or INR (international normalized ratio)

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29
Q

Amount of prothrombin in the blood is assessed by determining __________

A

Prothrombin Time (PT)

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30
Q
  • Thromboplastin and Ca+ are added to a sample of the patients plasma and to a control sample simultaneously.
  • The amount of time require for clot formation in both samples is measured.
  • Prolonged indicates deficiency of one of the factors.
  • Normal time is 11 to 12.5 s (vary from lab to lab)
A

Prothrombin Time

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31
Q

Test that is used to detect coagulation defect of the intrinsic system.

  • Activated partial thromboplastin is added to a sample of the patients blood plasma and a control sample.
  • Time required for formation of clot is measured.
  • Delayed clotting time suggests abnormality in one or more factors of intrinsic system.
  • Further tests require to identify specific abnormal factor.
  • Used in detecting haemophilia and monitor effect of heparin.
  • Normal 60-85 s after addition of reagent and Ca++ to blood (vary from lab to lab)
A

PTT Test

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32
Q

Test that determines the efficacy of various clotting factors.
- Normal time 32-51 s (vary from lab to lab)

A

APTT (activated partial thromboplastin time)

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33
Q

The prothrombin time ratio that would have been obtained if a standard reagent in the PT determination.

  • Patient prothrombin time/ mean of prothrombin time of reference interval.
  • a laboratory measurement of how long it takes blood to form a clot. It is used to determine the effects of oral anticoagulants on the clotting system.
A

International Normalized Ratio (INR)

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34
Q

Normal INR Value

A

1

35
Q

INR therapeutic range

A

2-3

36
Q

Ideal INR range for Warfarin therapy

A

2.5-3.5

37
Q

Drug class.

- Anagrelide, Anasindione, Dalteparin, enoxoparin, HEPARIN, WARFARIN.

A

Anticoagulants - inhibits certain clotting factors

38
Q

Drug class.

- abciximab, ASPIRIN, clopidogrel, dipyridamole, eptifibatide, pentoxifylline

A

Antiplatelets - prevent platelet plug formation

39
Q

Drug class.

- aminocaproic acid, tranexamic acid, aprotinin

A

Antifibrinolytics - prevent breakdown of fibrin

40
Q

Drug class.

- alteplase, anistreplase, reteplase, streptokinase

A

Thrombolytics (fibrinolytics) - Directly lyse the clot

41
Q

Reversal agent. Heparin Antagonist. Dissociates the heparin-antithrombin complex. Given IV over 10 min. immediate effect and lasts for 2 hrs. May cause hypotension and anaphylactoid reaction.

A

Protamine sulphate

42
Q

Reversal agent. Warfarin Na antagonist. Guideline does depend on INR and whether life-threatening bleeding is present.

A

Vitamin K

43
Q

What should the healthcare provider asses before administering parenteral anticoagulant?

A

APTT (activated partial thromboplastin time, normal time 32-51 s) and platelet count.

44
Q

During anticoagulant therapy, clotting profile for PT, INR, or APTT should be ____-____ times the normal value.

A

1.25-2.50

45
Q

Parenteral Anticoagulant.

  • Immediate onset (20-30min)
  • inhibit the conversion of prothrombin to thrombin.
  • Protein bound. Metabolized by the liver, excreted by urine.
  • 2 types, endogenous and exogenous.
  • Used for pt with DVT, PE. Risk for acute MI, HF, Stroke, TP
  • Preffered treatment for TP in pregnancy because it does not cross the placenta barrier or enter breast milk.
  • Combines with antithrombin III to inactivate factors IXa, Xa, XIa, XIIa.
A

Heparin

46
Q

Why must Heparin not be administered orally?

A

Its lipophoic - not soluble in lipids

Its not absorbed from the GIT. Inactivated by the stomach.

47
Q

Mucopolysaccharide found in various body tissues, most abundant in the liver and lung

A

Endogenous Heparin

48
Q

Heparin obtained from animal tissue.

A

Exogenous Heparin

49
Q

Inactivation of factor ___ prevents the conversion of prothrombin - thrombin, thereby inhibiting formation of fibrin from fibrinogen.

A

Xa

50
Q

Adverse effects of Heparin

A
  1. Heparin Induced thrombocytopenia (low amount of platelets)
  2. BLEEDING.
51
Q

Incase bleeding occurs?

A
  1. Whole blood and/or plasma may be administered.
  2. Slow IV injection of Protamine sulphate which dissociates the heparin-antithrombin complex (rapid injection may cause respiratory diff, bradycardia, hypotension)
52
Q

Safer and less side effects than Heparin.
Have longer half-life
Administered once a day, can give to pt to take home
Smaller dosage
Require less blood testing
Agents end in “PARIN”
Inactivate factor Xa

A

Low Molecular Weight Heparin (LMWH)

53
Q

Why isnt Heparin IM?

A

Muscles are very vascular, bleed easily.

54
Q

Tx for allergy to Heparin.

- management in cases with heparin inducd thrombocytopenia.

A

Lepirudin

& bivalirudin

55
Q

If pt switching from Heparin to Warfarin, make sure pt’s INR is _____.

A

2-3

56
Q

Heparin-like compound.

- used to treat TP and bruises (hematomas) and contusions

A

Heparinoid

57
Q

Heparin-like compound.

- present in OTC prep, used in sports injury

A

Hyaluronidase

58
Q

Used in pts with congenital deficiency during procedures that could lead to thromboembolism.

A

Antithrombin III

59
Q

Oral anticoagulant that acts on the liver to prevent the synthesis of Vitamin K-dependent clotting factors (ie. Factors II, VII, IX and X)

  • BLOCKS ACTIVATION OF VIT. K IN THE LIVER SO THERE IS NO CLOTTING FACTORS SYNTHESIZED
  • Onset 3-5 days
  • Longterm therapy
  • No effect in circulating clotting factor and platelets
  • Protein bound. Meatbolized in the liver and inactive metabolites excreted via kidney
  • Tx of DVT, PE, after stroke, MI, venous thrombo-embolism
A

Warfarin

60
Q

Anticoagulants used with caution with pts with? (5)

A

HTN, Hepatic + Renal disease, Hx of GI ulcerations, Drainage tubes, endometriosis

61
Q

Interactions with Warfarin

  1. Increase anticoagulation effect by affecting platelet func or causing GI upset
  2. Inhibits metabolism
A
  1. Penicillin

2. Cimetidine

62
Q

Anti-plateplet agent.

  • Inhibits enzyme called cyclo-oxygenase which is needed to produce thromboxane A2 (TXA) which is a potent vasoconstrictor and inducer and platelet aggregation.
  • Lack of TXA decrease platelet aggregation
  • 75-150 mg/daily
  • Alters hepatic synthesis of coagulation factors VII IX and X (same as warfarin)
  • Reduce risk of MI in clients with previous MI or unstable angina, taken during MI to limit damage to myocardium, used to reduce the risk of recurrent transient ischemic attacks ans stroke
A

Aspirin (ASA)

63
Q

Antiplatelet agent.
- Phosphodiesterase inhibitor, increase the concentration of cAMP in platelets and thus decrease platelets adhesiveness. It is used with warfarin or ASA to treat angina. Also used to prevent blood clot after cardiac valve surgery.

A

Dipyridamole

64
Q 
Antiplatelet Agent
- belongs to a class of drugs called monoclonal antibody prepared by tissue culture of cloned B lymphocytes, It binds to glycoprotein receptors on platelets causing inactivation of the platelet. receptor that cause the platelets to aggregate.
A

Abcixmab (ReoPro)

65
Q

Antiplatelet agent.

  • Inhibits platelet aggregation by preventing ADP-induced binding between platelets and fibrinogen.
  • USED TO PREVENT SECOND STROKE
A

Ticlopidine (Ticid)

66
Q

Antiplatelet agent.
- chemically relaed to ticlopidine but has a fewer adverse effects. Used to reduce stroke, MI, and other coronary syndrome.

A

Clopidogrel (Plavix)

67
Q

Antiplatelet agent.

- inhibit cyclooxygenase (reversibly). Their anti-platelets effect is gone once they are excreted from the body.

A

Ibuprofen and other ASA-related drugs

68
Q

Antiplatelet that blocks a receptor on the platelet and prevent it from binding with fibrinogen.

A

Glycoprotein IIb/IIa inhibitors

69
Q

Contraindications for anti-platelets

A

thrombocytopenia, active bleeeding, leukemia, traumatic injury and recent stroke

70
Q

Antiplatelet stop if platelet counts < _______ cells/mm3

- Use w/ caution with pts with Hx of bleeding in the last ___ wks and those with liver disease

A

80 000 cells/mm3

6 wks

71
Q

Antifibrinolytic agent

  • controls bleeding caused by overdoses of thrombolytic agents or bleeding disorder caused by hyperfibronolysis. PO ir IV.
  • It antagonizes plasminogen, thus decreasing the conversion of plasminogen to plasmin. Plasmin breaks up clot.
A

aminocaproic acid and tranexamic acid

72
Q

Antifibrinolytic agent
- inhibits trypsin, plasmin and kallikrein, which lyse protein that destroy fibrin clots. Mostly used in selective pts undergoing cardiovascular procedures

A

Aprotinin

73
Q

Adverse effects of antifibrinolytic agents

A

dysrythmia, OH, bradycardia, hallucination, psychosis, convulsions, GI problems

74
Q

Clot busters.

  • Works indirectly or directly to convert plasminogen (floats freely in the blood) to plasmin (breaks up fibrin clots)
  • Used to dissolve thrombi
  • tissue plasminogen activator (t-PA)
  • Stimulate plasminogen - plasmin conversion (fibrinolysin)
  • To re-establish blood fow ASAP and limit tissue damage
  • therapy followed by anticoagulant and antiplatelet therapy to limit reformation of clots
  • IV - onset in mins, t1/2 is 40-80 mins duration is 6 hr
  • in cases of coronary vessel occlusion, this therapy must begin within 6 hours
  • DVT, PE, MI, Stroke
A

Thrombolytic Agents (fibribolytics)

75
Q

A naturally occuring substance secreted by the endothelial clls in response to injury to the artery

A

Plasminogen

76
Q

Enzyme that breaks down proteins. It degrades fibrin, fibrinogen and other pro-coagulating proteins.

A

Plasmin

77
Q

The natural occuring plasminogen activator secreted by vascular endothelial cell in blood vessel walls. These are stimulated by fibrin clots.

A

tissue plasminogen activator (t-PA)

78
Q

After fibrinolytic agent injection, what nursing interventions should the nurse apply?

A

Apply manual pressure followed by application of pressure dressing.

79
Q

Main thrombolytic enzyme.

  • along with urokinase are used mainly to lyse coronary clots in acute MI cases
  • antigenic, leading to allergic reaction.
  • cause bleeding
  • APTT is usually
A

Streptokinase *Streptase

80
Q

Thrombolytic enzyme used when pt allergic to streptokinase

A

Urokinase (Abbokinase)

81
Q

t-PA made by recombinant DNA technology

A

exogenous t-PA

82
Q

exogenous t-PA is available in 3 forms

A

alteplase, reteplase, tenecteplase (TNKase)

83
Q

t-PAs used to treat thrombus associated with acute MI.

  • bind to fibrin in the clot and act locally to dissolve the clot
  • adverse effect include: intracranial, GI, genitourinary bleeding, and bleeding from tissue punctured sites
A

alteplase, reteplase, tenecteplase (TNKase)

84
Q

Contraindication for thromolytic agents

A

severe HTN, pts risk for severe bleeding (aneurysm, active bleeding, brain tumor)
Cautin with pts with GI bleeding, organ biopsy and severe trauma in the past 10 days

Pharmacology II (11 decks)

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