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Block 7 Week 4 > Le Blanc: Pharm > Flashcards

Le Blanc: Pharm Flashcards

1
Q

Under normal physiological conditions, little or no intravascular coagulation occurs. This is primarily due to three effects - what are they?

A

dilution (of factors)
presence of plasma inhibitors
activated clotting factors are rapidly removed by the liver

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2
Q

When vascular damage occurs, several physiologic reactions participate to control blood loss. What are they?

A 
platelet adhesion reaction
platelet activation
platelet aggregation
formation of a clot
fibrinolysis
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3
Q

Briefly describe platelet aggregation and formation of the platelet plug

A

damage to vessel endothelium exposes collagen - vWF comes in and binds - platelets bind to GPIb (platelet adhesion)- when platelets bind they undergo shape change and degranulate - degranulation releases enzymes like ADP and thromboxane A2 which draw in more platelets (aggregation) to create the platelet plug

**no activation of coag cascade yet, just formation of weak platelet plug

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4
Q

2 contents released by platelets that trigger powerful constrictions of blood vessels (transient reaction)

A

thromboxane A2

serotonin (5HT)

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5
Q

Coagulation occurs due to trauma originating from the extra-vascular space (formation of a macromolecular complex involving Thromboplastin or Tissue Factor, and Factor VII); the most important in vivo

A

Extrinsic pathway

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6
Q

Coagulation is triggered by trauma to the blood itself (from large glycoprotein complexes released by platelets)

A

Intrinsic pathway

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7
Q

What does plasmin do?

A

degrades a fibrin clot

**this produces D-dimer

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8
Q

What are the three categories of drugs used to treat coagulation disorders? Give an example of each

A
  1. direct acting anticoagulants: calcium chelatlors like EDTA, heparin, factor IIa and 10a inhibitors)
  2. indirect acting anticoagulants: Warfarin (coumadin)
  3. antiplatelet agents: aspirin
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9
Q

What is a normal platelet count?

A

150,000 - 400,000

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10
Q

What does prothrombin time reflect?

A

reflects alterations in the EXTRINSIC pathway (~12 sec)

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11
Q

What is the INR measuring?

A

PT of the patient/PT reference

**normal is 1.0
2-3 is therapeutic INR

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12
Q

What does the activated PTT reflect?

A

reflects alterations in the INTRINSIC pathway (normal 24-34 secs)

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13
Q

Where is heparin derived from? Why is this important to consider?

A

from bovine lung and porcine intestinal mucosa; important to consider bc some people develop allergy

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14
Q

What does heparin bind to and form a complex with to inhibit blood coagulation? What does this essentially do?

A

alpha2-globulin (antithrombin III); antithrombin III is a natural anti-coagulant, and when bound by heparin it just accelerates the anti-coag effects by like 100x

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15
Q

At low doses, Heparin primarily neutralize Factor (blank). At high doses, it prevents the thrombin-induced activation of (blank), and activation Factors V and VIII

A

Xa; platelets

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16
Q

What is one concern with heparin use?

A

may cause moderate to severe thrombocytopenia **heparin-induced thrombocytopenia

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17
Q

How is heparin administered?

A

IV infusion

**not effective orally

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18
Q

Does heparin cross the placenta and pass into the maternal milk?

A

No!

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19
Q

Contraindications with heparin use?

A 
active bleeding
patients with low platelets or history of heparin-induced thrombocytopenia
patients with severe allergy
severe HTN
older patients, esp women
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20
Q

What to do if there is a heparin overdose?

A

simple withdrawal;

use Protamine Sulfate to bind heparin and neutralize its effects

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21
Q

What are 4 advantages of using low molecular weight heparin?

A
  1. more predictable outcome, 2x longer half life
  2. less frequent dosing requirements
  3. increased bioavailability from the subcutaneous site of injection
  4. less frequent bleeding
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22
Q

What would you use for any of these?

Blood transfusions
Atrial fibrillation
Disseminated intravascular coagulation (DIC)
Open heart surgery
Pulmonary embolism
Venous thromboembolism
Venous catheter occlusion
A

heparin

23
Q

How do thrombin inhibitors work as anticoagulants? How are they administered?

A

they block the enzyme by binding to the catalytic site; given IV

24
Q

When would you want to use thrombin inhibitors instead of heparin?

A

in patients that are susceptible to developing heparin induced thrombocytopenia and in coronary angioplasty or coronary bypass surgery

25
Q

Another type of anticoagulatant is a factor 10a inhibitor. Name two.

A

rivaroxaban

apixaban

26
Q

This is the most common oral anticoagulant, only active in vivo after 12-24 hours

A

Warfarin (coumadin)

27
Q

How does coumadin work?

A

it is a structural analog of Vitamin K, so it causes the same effects as Vitamin K depletion

**need Vitamin K for formation of clotting factors

28
Q

What is Vit K used for in the synthesis of clotting factors?

A

it causes post-ribosomal carboxylation of specific glutamic acid residues; when carboxylated, these amino acid residues bind Ca++ making it less available for the Coag pathway

29
Q

Warfarin inhibits blood clotting mechanisms by interfering with the hepatic synthesis of (blank)

A

vitamin K-dependent clotting factors

**VII, IX, X, prothrombin

30
Q

Warfarin also down-regulates protein C. What effect does this have? What does protein C normally do?

A

Protein C promotes the degradation of factors 5a and 8a, rendering them inactive. If this is downregulated, you will have increased 5a and 8a and this explains the pro-coagulant activity of warfarin seen in early stages of therapy

31
Q

So early on in warfarin treatment, what will you observe in regards to coagulation?

A

first, increased coagulant activity due to increased levels of factor 5a and 8a

32
Q

What are two measures used to monitor the anticoagulant effects of warfarin?

A

prothrombin time

INR

33
Q

What are 3 things you could do if you overdose a patient on warfarin?

A
  1. withdraw the drug
  2. give vit K supplements
  3. tranfuse with whole blood or plasma if major bleeding noted
34
Q

When should warfarin NOT be used?

A

when you need to avoid active bleeding
Vit K deficiency
pregnant women!!!
severe hepatic/renal disease

35
Q

Does warfarin pass the placental barrier?

A

YES; don’t use in pregnant women!

**may lead to abortion and birth defects

36
Q

Why are newborns more sensitive to oral anticoagulants than adults?

A

they have lower vitamin K levels (things like warfarin will decrease vit K) and also they have lower rates of metabolism

37
Q

What is one drug that is known to increase the response to warfarin?

A

aspirin **any drug that decreases platelet aggregation

38
Q

What is desmopressin? What is it used for?

A

synthetic analogue of ADH; stimulates factor 8; used for hemophilia A or in pts with factor 8 antibodies

**think of this: hemophilia a-ate (8 - factor 8)

39
Q

How does aspirin inhibit platelet aggregation?

A

aspirin inhibits platelet release of ADP which prevents aggregation; it also acetylates COX, which prevents the formation of thromboxane A2; thromboxane A2 causes platelet aggregation and is a potent vasoconstrictor

40
Q

Aspirin inhibits the release of (blank) by platelets and their aggregation by acetylating the enzymes (cyclo-oxygenases or COX) of the platelet that synthesize the precursors of (blank), a labile inducer of platelet aggregation and a potent vasoconstrictor

A

ADP; thromboxane A2

41
Q

Is the effect of aspirin reversible?

A

no; it causes a covalent modification due to acetylation of the enzymes (COX)

42
Q

How do the antiplatelet drugs Ticlopidine and Clopidogrel bisulfate work? When are they used?

A

they inhibit ADP-mediated platelet aggregation; prevent aggregation by impairing the GPIIb/IIIa receptor; they are used as an alternative to aspirin for recurrent stroke patients

43
Q

How does abciximab work? When is it used?

A

it is a chimeric monoclonal antibody that blocks the glycoprotein IIb/IIIa receptor - prevents platelet aggregation;
used in acute coronary syndromes and percutaneous coronary intervention

44
Q

The Fibrinolytic System dissolves intravascular clots as a result of the action of (blank), an enzyme that digests Fibrin

Plasminogen, an inactive precursor, is converted to (blank) by cleavage of a single peptide bond. (blank) is a relatively non-specific protease, which digests fibrin clots and other plasma proteins, including several coagulation factors

A

plasmin; plasmin

45
Q

Therapy with thrombolytic drugs tends to dissolve both pathological thrombi and also fibrin deposits at sites of vascular injury. What can these drugs cause as a result?

A

hemorrhage

46
Q

What should patients with the following conditions receive?

extensive pulmonary emboli
severe iliofemoral thrombophlebitis
acute coronary occlusion

A

thrombolytic therapy to break up clots

47
Q

This is released from endothelial cells in response to various signals, including stasis produced by vascular occlusion

A

tissue plasminogen activator (t-PA)

48
Q

What does t-PA bind to? Its binding causing the conversion of what to what?

A

t-PA binds to FIBRIN and converts plasminogen (also binds to fibrin) to plasmin

49
Q

What does fibrin bind to in the plasma to inhibit its action?

A

an alpha2-antiplasmin

50
Q

t-PA is a serine protease. It is a poor Plasminogen activator in the absence of (blank). t-PA binds to (blank) and activates bound Plasminogen several hundred-fold more rapidly than it activates Plasminogen in the circulation.

A

fibrin; fibrin

51
Q

a protein produced by β-hemolytic streptococci. It has no intrinsic enzymatic activity, but forms a stable non-covalent 1:1 complex with Plasminogen. This produces a conformational change that exposes the active site on Plasminogen that cleaves a peptide bond on free Plasminogen molecules to form free Plasmin

A

streptokinase

52
Q

When should you NOT use thrombolytic therapy?

A

surgery w/i 10 days
serious GI bleeding w/i 3 months
history of HTN
active bleeding or hemorrhagic disorder

53
Q

prevents the binding of Plasminogen and Plasmin to Fibrin. It is a potent inhibitor for Fibrinolysis and can reverse states that are associated with excessive Fibrinolysis

A

aminocaproic acid

Block 7 Week 4 (8 decks)

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