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IHO Mike Rose > Treatments and Test for Final > Flashcards

Treatments and Test for Final Flashcards

1
Q

Template bleeding time

A

Evaluates response to vascular injury. Some platelet disorders have a long bleeding time.

Inflate blood pressure cuff –> make incision –> Time how long it takes to stop bleeding

Doesn’t test coagulation, only platelet plug formation.

Only test that tests in vivo platelet funciton.

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2
Q

Closure Time

A

An alternative to bleeding time

“in-vitro bleeding time”

Better than bleeding time at detecting aspirin-related bleeding and von Willebrand disease.

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3
Q

Platelet Aggregation

A

Why - to find platelet function abnormalities

How - Add aggregating agents to patient’s sample. See if platelets aggregate. Measure decrease in sample turbidity.

Aways repeat an abnormal test.

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4
Q

Coagulation Lab Tests

A

How - Draw blood into citrate tube. Spin tube, decant plasma. Add reagants to plasma and watch for formation of fibrin.

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5
Q

Prothrombin Time (PT)

A

Plasma + Thromboplastin

Measures External pathways.

Always order an INR over a PT.

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6
Q

INR

A

A corrected PT for various thromboplastin manufacturers. . (International normalized ratio)

Order to:

  • Assess liver function
  • Monitor Warfarin therapy
  • Dx DIC
  • To assess pre-op status.
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7
Q

Partial Thromboplastin Time (PTT)

A

Plasma + Phospholipid

Measure Intrinsic pathway

APTT= same thing

PTT increased: Hemophilia A & B, DIC, heparin, and inhibitors.

Should order when:

  • Investigate hx of abnormal bleeding
  • Monitor heparin therapy
  • Dx DIC
  • Dx antiphospholipid antibody
  • To assess pre-op status.
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8
Q

Thrombin Time

A

Plasma + Thrombin

Measures conversion of fibrinogen to fibrin

Bypasses intrinsic and extrinsic pathway.

When to order?:
When PTT is prolonged and you want to rule out fibrinogen problem (Rare!)

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9
Q

PTT Mixing Study

A

Pooled plasma + patient plasma + phospholipid.

Order when PTT is prolonged, but TT is normal.

If PTT corrects –> something is missing

If PTT doens’t correct –> inhibitor present (antibody that messes up the test)

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10
Q

Fibrin Degredation Product Assay

A

Measures FDPs (including D-dimers)

Very sensitive! Used to rule out, not rule in.

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11
Q

D-Dimer Assay

A

Similar to FDP assay, but specific to D-dimers only.

Also very sensitive.

Used to rule out, not rule in.

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12
Q

Fibrinogen Assay

A

Measure fibrinogen

Decreased in DIC and massive bleed. (think if patient was given packed cells in place of whole blood and patient continued to bleed).

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13
Q

Clopidogrel

A

Class - Antiplatelet; ADP Receptor Antagonist

MOA: Irreversible ADP P2Y Receptor Antagonist.

PK: Oral drugs w/ duration of days. Activation by CYP2C19.

Use: Used during stenting and recommended for patients that don’t tolerate aspirin.

A.E. Bleeding, nausea, diarrhea, rash, severe leukopenia (1% or patients)

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14
Q

Ticlopidine

A

Class - Antiplatelet; ADP Receptor Antagonist

MOA: Irreversible ADP P2Y Receptor Antagonist.

PK: Oral drugs w/ duration of days.

Use: Used during stenting and recommended for patients that don’t tolerate aspirin.

A.E. Bleeding, nausea, diarrhea, rash, severe leukopenia (1% or patients), TTP (very rare)

Worst A.E. of the 3.

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15
Q

Prasugrel

A

Class - Antiplatelet; ADP Receptor Antagonist

MOA: Irreversible ADP P2Y Receptor Antagonist.

PK: Oral drugs w/ duration of days.

Use: Used during stenting and recommended for patients that don’t tolerate aspirin.

A.E. Bleeding, nausea, diarrhea, rash, severe leukopenia (1% or patients)

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16
Q

Abciximab

A

Class - Antiplatelet; GPIIB/IIIA Receptor Inhibitors

MOA - Humanized MAB against GPIIB/IIIA receptor. Inhibits the final common pathway of platelet aggregation.

PK: IV

Uses: With aspirin and heparin during angioplasty. For acute coronary syndromes.

Adverse effects: Bleeding, thrombocytopenia (chronic use)

17
Q

Eptifibatide

A

Class - Antiplatelet; GPIIB/IIIA Receptor Inhibitors

MOA - Fibrinogen analogue that inhibits the GPIIB/IIIA receptor. Inhibits the final common pathway of platelet aggregation.

PK: IV

Uses: With aspirin and heparin during angioplasty. For acute coronary syndromes.

Adverse effects: Bleeding, thrombocytopenia (chronic use)

18
Q

Tirofiban

A

Class - Antiplatelet; GPIIB/IIIA Receptor Inhibitors

MOA - Non-peptide competitive inhibitor of GPIIB/IIIA receptor. Inhibits the final common pathway of platelet aggregation.

PK: IV

Uses: With aspirin and heparin during angioplasty. For acute coronary syndromes.

Adverse effects: Bleeding, thrombocytopenia (chronic use)

19
Q

Dipyridamole

A

Class - Antiplatelet

MOA: Increases cAMP and inhibits platelet activation. Phosphodiesterase 3 inhibitor. Inhibits platelet uptake of adenosine and thus increases adenosine interaction with Adenosine A2 recpetor –> increases cAMP.

Also a vasodilator.

Little to no beneficial effect by itself –> used in combination with aspirin or warfarin.

20
Q

Unfractionated Heparin

A

= High molecular weight heparin (HMW). Often just called heparin.

Class - Indirect Thrombin Inhibitors

MOA: Bind to antithrombin III which causes it to do a better job incactivating thrombin and factor Xa and IIA.

PK - Parenteral; binds to plasma proteins (highly variable anticoagulant response). Short half life (1 hour)

Requires close monitoring of PTT.

A.E. - Bleeding, thrombocytopenia (2x likely in women)

21
Q

Low molecular weight heparin

A

Class - Indirect Thrombin Inhibitors

Commonly used form: Lovenox = Enoxaparin sodium

PK - Parenteral; more predictable than HMW (less plasma protein binding) Medium half life (4 hours)

MOA: Bind to antithrombin III which causes it to do a better job incactivating thrombin and factor Xa amd IIA.

Monitoring of PTT (less than HMW)

A.E. - Bleeding, thrombocytopenia (2x likely in women)

22
Q

Fondaparinux

A

Class - Indirect Thrombin Inhibitors

PK - Parenteral

MOA: Bind to antithrombin III which causes it to do a better job incactivating thrombin and factor Xa.

Synthetic. Longer half life (17 hours).

23
Q

Bivalirudin

A

Class - Direct Thrombin Inhibitors

PK - Parenteral

MOA- Directly binds and inhibits thrombin.

24
Q

Argatroban

A

Class - Direct Thrombin Inhibitors

PK - Parenteral

MOA - Directly binds and inhibits thrombin.

25
Q

Dabigatran etexilate

A

Class - Direct Thrombin Inhibitors

PK - Oral

MOA - Directly binds and inhibits thrombin.

26
Q

Protamine

A

MOA - Binds heparin to form a stable complex that lacks anitcoagulant activity. Completely reverses HMW; paritally LMW; and no reversal activity of Fondaparinux.

27
Q

Warfarin

A

Class- Anticoagulant

PK - Oral. MANY DRUG-DRUG INTERACTIONS. Requires constant monitoring. Very narrow TI. Dosing varies based on VKORC1 and CYP2C9 polymorphisms,

MOA: Inhibits Vitamin K dependent epoxide reductase in turn blocking synthesis of Vitamin K dependent clotting factors. Inhibits gamma-carboxylation of factors II, VII, IX, and X and protein C and S.

Crucial note: Initially creates hypercoaguable state due to blocking protein C and S; thus we must use a “bridge” to treatment.

Adverse effects: BLEEDING, flatulence and diarrhea, cutaneous necrosis, chondrodysplasia punctata.

Racemic mixture of R and S enantiomers. S is the more active enantiomer. They are metabolized differently.

If bleeding too much: Stop the drug. Add vitamin K (phytonadione), prothrombin complex concentrates, recombinant factor VIIa

28
Q

Rivaroxaban

A

Class - Xa inhibitor

PK - Oral

MOA: Inhibit factor Xa

PK: Rapid onset of action and shorter half-life than warfarin. Don’t require monitoring.

No antidote!

29
Q

Apixaban

A

Class - Xa inhibitor

PK - Oral

MOA: Inhibit factor Xa

PK: Rapid onset of action and shorter half-life than warfarin. Don’t require monitoring.

No antidote!

30
Q

Edoxaban

A

Class - Oral Xa inhibitor

PK - Oral

MOA: Inhibit factor Xa

PK: Rapid onset of action and shorter half-life than warfarin. Don’t require monitoring.

No antidote!

31
Q

Phytonadione

A

Vitamin K

Class - Coagulant

Antidote for Warfarin caused bleeding

32
Q

Streptokinase

A

Class - Fibrinolytic

Rarely used clinically.

Complexes w/ plasminogen wherever it is and facilitates formation of plasmin.

Can only be used once due to antibody formation?

From Strep bacteria.

33
Q

Urokinase

A

Class - Fibrinolytic

MOA: Kidney enzyme that directly converts plasminogen to plasmin. Occurs primarily in response to inflammatory stimuli. Promotes extravascular fibrinolysis.

34
Q

Alteplase

A

Class - TPA

MOA - Preferentially acitvates plasminogen to plasmin that is bound to firbrin which confines it to the thrombus rather than systemic activation.

Dissolve EXISTING life-threatening thrombi. Given IV. 3-4 hour window.

Only thrombolytics approved for use in stroke

PK: Given IV; can be given with IR

A.E. Bleeding, Cost

35
Q

Reteplase

A

Class - TPA

MOA - Preferentially acitvates plasminogen to plasmin that is bound to firbrin which confines it to the thrombus rather than systemic activation.

Dissolve EXISTING life-threatening thrombi. Given IV. 3-4 hour window.

Only thrombolytics approved for use in stroke

PK: Given IV; can be given with IR

A.E. Bleeding, Cost

36
Q

Tenecteplase

A

Class - TPA

MOA - Preferentially acitvates plasminogen to plasmin that is bound to firbrin which confines it to the thrombus rather than systemic activation.

Dissolve EXISTING life-threatening thrombi. Given IV. 3-4 hour window.

Only thrombolytics approved for use in stroke

PK: Given IV; can be given with IR

A.E. Bleeding, Cost

37
Q

Fresh Frozen Plasma

A

All coag factors in normal levels.

Used to reverse warfarin’s effect (very high INR/risk of hemorrhage patients) or replace factors missing due to liver disease or DIC.

38
Q

Cryoprecipitent

A

1U = 10 FFP
-Provides fibrinogen, vWF, factor VIII, factor XIII, fibronectin.

Use when very deficient and volume for FFP is going to be a problem.

IHO Mike Rose (20 decks)

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