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Pharm 2 > Final, Lecture 3 > Flashcards

Final, Lecture 3 Flashcards

1
Q

Hemostasis Tripod

A

Primary hemostasis- mediated by platelets
Coagulation (chemical)
Vasoconstriction (mechanical)

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2
Q

Platelets adhere to disrupted vessel wall via

A
  • Surface membrane glycoprotein receptor Ib

- Von Willebrand Factor

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3
Q

Platelets adhere to eachother via

A
  • Surface receptor glycoprotein IIb/IIIa

- Fibrinogen

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4
Q

Platelet actions

A

Primary hemostasis
Arachidonic acid vasoconstriction
Release of proteins from platelet storage granules
Site for generation of thrombin and then fibrin

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5
Q

Coagulation: Extrinsic Pathway

A

Tissue factor exposed to blood and forms complex w/ Factor VII –> activates factor X –> converts prothrombin to thrombin (factor V is a required cofactor for this)

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6
Q

Coagulation: Alternate/Secondary Pathway

A

Tissue factor-Factor VIIa complex activates Factor IX –> along w/ cofactor VI it activates Factor X –> converts prothrombin to thrombin

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7
Q

Coagulation: 3rd Pathway

A

Thrombin activates Factor XI –>activates Factor IX –> converts prothrombin to thrombin

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8
Q

Thrombin- what does it do?

A

Essential for conversion of fibrinogen to fibrin
Activates coagulation factors and cofactors facilitating its own formation
Activates platelet aggregation
Mediates fibrinogen cleavage

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9
Q

Factor responsible for crosslinking of Fibrin in ultimate step of coag cascade

A

Factor XIII

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10
Q

Anticoagulation processes

A

TFPI
Protein C
Antithrombin III

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11
Q

TFPI

A

Acts on Tissue Factor-Factor VIIa complex

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12
Q

Protein C

A

Activated by thrombomodulin and Protein S

Degrades Factors V and VIII

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13
Q

Antithrombin III

A

Forms complexes and inactivates Thrombin and Factor Xa

Enhanced by presence of heparin

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14
Q

Fibrinolysis

A

tPA and uPA in endothelial cells- released due to several stimuli like hypoxia, acidosis

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15
Q

Inactivation of fibrinolysis

A

PAI’s inactivate it

circulating protease inhibitors

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16
Q

Most common congenital coagulation disease

A

von Willebrand disease

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17
Q

Occurence of milder von Willebrand disease

A

1-5:1000

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18
Q

3 Types of von Willebrand Disease

A

1: Reduced conc of vWF’s
2: Dysfunctional vWF’s
3. Absent vWF- homozygous for gene defectTr

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19
Q

Treatment for von Willebrand Disease

A

Types I and IIa - Desmopressin - stimulates release of more vWF. Contraindicate in type IIb vWD
More severe types - replacement w/ transfuced factors
Continue treatment for 4-7 days after surgery

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20
Q

Most commonly inherited coagulation disorder

A

Hemophilia A - sex-linked recessive - 1:100,000 male births

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21
Q

Hemophilia A

A

Varied levels of Factor VIII - mild up to 40% of normal, severe less than 1%
Severe cases will develop anti-factor VIII antibodies

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22
Q

Hemophilia A Treatment

A

Mild to moderate - DDAVP (desmopressin) –> release of Factor VIII and vWF
Severe disease - Factor VIII transfusion

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23
Q

Hemophilia B

A

Like Hemophilia A but affects Factor IX

If severe- factor transfusion

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24
Q

Protein C or Protein S Deficiency

A

Causes hypercoagulation - can predispose to thrmobosis

Both proteins are liver synthesized, Vit K dependant

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25
Q

Factor V Leiden

A

Causes hypercoagulation
Polymorphic factor V which resists inactivation by Protein C–> deep venus thrombosis
Present in about 5% of North American Caucasians

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26
Q

Source of coagulation factors

A

Liver

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27
Q

Source of protein C, S, and fibrinogen

A

Liver

28
Q

Liver Disease complications

A

Decreased coagulation factors
Thrombocytopenia may exist
Thrombocyte function impaired

29
Q

MELD

A

Formula based on serum bilirubin, creatinine, and INR

Predicts 3 mo mortality- the higher the score the better

30
Q

Renal failure complications

A

Often has coagulation abnormalities, at risk for enhanced bleeding- impaired platelet adhesion, aggregation and release
Impaired primary hemostasis w/ a low hematocrit

31
Q

Treatment for coagulation problems due to renal disease

A

DDAVP (Desmopressin)

32
Q

Aspirin

A

Irreversible inhibitor of platelet membrane-associated cyclooxygenase –> blocks formation of thromboxane A2

33
Q

Aspirin - consequences

A

Can cause significant impairment of primary hemostasis and mild enhancement of bleeding
Platelet life span: 10 days
5-7 days usually required after termination of aspirin use to achieve platelet function and effective hemostasis

34
Q

most important adverse effects of aspirin

A

Bleeding and hemorrhagic gastritis or gastric ulceration

35
Q

Clopidogrel (Plavix)

A

Blocks ADP receptor on the platelet
Causes more bleeding than aspirin
Generally safe to continue through surgery

36
Q

Dypyramidole

A

Inhibits phosphodiesterase–> accumulation of cyclic AMP–> anti-aggregating effect
No significant efficacy in fighting thromboembolic disease tho

37
Q

Glycoprotein Receptor IIb/

IIIA Inhibitors

A

Most potent platelet aggregation inhibitors
Competitively inhibit fibrinogen binding to platelet IIb/IIIa receptor
Oral forms are not effective- use IV

38
Q

Antiplatelet Drugs

A

Aspirin, Clopidogrel (Plavix), Dipyramidole, Glycoprotein Receptor IIb/IIIA inhibitors

39
Q

Coumadin

A

Blocks vit K dep carboxylation of coagulation factors II, VII, IX, and X- formation of inactive proteins

40
Q

Coumadin - when effects kick in and how long they last

A

Takes 2-3 days to work

Takes 3-5 days after termination of Coumadin before normal coagulation

41
Q

Coumadin - how to monitor drug effect

A

PT and INR

42
Q

May cause skin necrosis

A

Coumadin

Often assoc w/ protein C deficiency

43
Q

Factor Xa Inhibitors

A

oxaban’s, dabigatran

44
Q

Oxabans/dabigatran characteristics

A 
Inhibit factor Xa
Don't require regular lab monitoring- not affected by diet ,etc
Rapid onset and short half life
Prevents strokes like Coumadin
Same risk for extracranial bleeding
45
Q

Factor Xa Inhibitors and dental surgery

A

May be prudent to discontinue them for 1-2 days before procedure

46
Q

Reversal of oxabans/dabigatran

A

Idarucizamab
For emergency surgery or life-threatening/uncontrollable bleeding
Reverses anticoagulation immediately
Solution contains Sorbitol- can’t give to fructose intolerant people

47
Q

Other reversal options for oxabans/dabigatran

A

Andexanet Alfa- reverses anticoagulation in less than 5 min
PER977- nonspecific agent
Both in early clinical trials

48
Q

Heparin

A

Parental
Binds to antithrombin III–> potentiates inhibition of factors IIa (thrombin) and Xa 1000 fold
Dose-dependant half-life
Mix of glycosaminoglycans from pig, cow lungs

49
Q

Heparin consideration

A

Anticoagulation effect may be variable–> frequent lab monitoring is required

50
Q

Low Molecular Weight Heparins

A

4-6 kDa
More favorable response than w/ unfractionated heparin
Longer half life and more predictable
Effective in preventing venous thromboembolism in surgical patients

51
Q

Pentasaccharides

A

Fondaparinux
synthetic
antithrombin exlcusive inhibition of Factor Xa
Good for hip/knee surgery

52
Q

Heparin derivatives complications

A

Most frequent adverse effect is bleeding
HIT- 5-7 days after initial exposure
Long-term use–> osteopenia

53
Q

Thrombolytic agents

A

Plasminogen activators

54
Q

Signs that point to possible defect in coaguation

A

Abnormal bruising
Petechiae
Splenomegaly

55
Q

Pts that have negative med history

A

Don’t need lab tests

56
Q

Pt that have signs/symptoms of bleeding tendency

A

Get platelet count, PTT, PT and INR

57
Q

If abnormality in primary hemostasis is suspected

A

Check bleeding time and measure vWF

58
Q

PT/INR

A

Add Ca and thromboplastin to blood and time for clot formation
Normal is 12+-2 sec
INR accounts for differences in labs

59
Q

Prolonged PT due to deficiencies in

A 
Factor VII
Factor X
Factor V
Prothrombin
Fibrinogen
60
Q

PTT

A

Measures the intrinsic, slower pathway
Normal is 25-40 sec
Requires presence of all factors other than Factor VII
Deficiencies in factors VII and XIII will not be detected

61
Q

When PT is used more and when PTT is used more

A

PT- coumadin drugs

PTT - heparin drugs

62
Q

aPTT

A

if prolonged, may indicate use of heparin, hemophilia, sepsis, antiphospholipid antibody, presense of antibodies against coagulation

63
Q

Bleeding time test

A

Not used anymore- not sensitive or specific, poorly reproducible, can be affected by skill of performer and often leaves scars

64
Q

PFA-100

A

Measures platelet function

Runs blood sample through tube- promotes platelet adherence and aggregation- measure closure time

65
Q

PFA-100 tests

A

First run collagen/EPI- if negative, no platelet dysfunction

If positive, then do collagen/ADP test to confirm

66
Q

Gold standard for platelet function analysis

A

PAA

67
Q

PAA

A

shows response of blood to specific aggregation inducing agents
As platelet aggregation occurs, light transmission increases

Pharm 2 (11 decks)

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