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Pharm 2 > Final, Lecture 3 > Flashcards

Final, Lecture 3 Flashcards

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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
Factor V Leiden
Causes hypercoagulation Polymorphic factor V which resists inactivation by Protein C--> deep venus thrombosis Present in about 5% of North American Caucasians
26
Source of coagulation factors
Liver
27
Source of protein C, S, and fibrinogen
Liver
28
Liver Disease complications
Decreased coagulation factors Thrombocytopenia may exist Thrombocyte function impaired
29
MELD
Formula based on serum bilirubin, creatinine, and INR | Predicts 3 mo mortality- the higher the score the better
30
Renal failure complications
Often has coagulation abnormalities, at risk for enhanced bleeding- impaired platelet adhesion, aggregation and release Impaired primary hemostasis w/ a low hematocrit
31
Treatment for coagulation problems due to renal disease
DDAVP (Desmopressin)
32
Aspirin
Irreversible inhibitor of platelet membrane-associated cyclooxygenase --> blocks formation of thromboxane A2
33
Aspirin - consequences
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
most important adverse effects of aspirin
Bleeding and hemorrhagic gastritis or gastric ulceration
35
Clopidogrel (Plavix)
Blocks ADP receptor on the platelet Causes more bleeding than aspirin Generally safe to continue through surgery
36
Dypyramidole
Inhibits phosphodiesterase--> accumulation of cyclic AMP--> anti-aggregating effect No significant efficacy in fighting thromboembolic disease tho
37
Glycoprotein Receptor IIb/ | IIIA Inhibitors
Most potent platelet aggregation inhibitors Competitively inhibit fibrinogen binding to platelet IIb/IIIa receptor Oral forms are not effective- use IV
38
Antiplatelet Drugs
Aspirin, Clopidogrel (Plavix), Dipyramidole, Glycoprotein Receptor IIb/IIIA inhibitors
39
Coumadin
Blocks vit K dep carboxylation of coagulation factors II, VII, IX, and X- formation of inactive proteins
40
Coumadin - when effects kick in and how long they last
Takes 2-3 days to work | Takes 3-5 days after termination of Coumadin before normal coagulation
41
Coumadin - how to monitor drug effect
PT and INR
42
May cause skin necrosis
Coumadin | Often assoc w/ protein C deficiency
43
Factor Xa Inhibitors
oxaban's, dabigatran
44
Oxabans/dabigatran characteristics
``` 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
Factor Xa Inhibitors and dental surgery
May be prudent to discontinue them for 1-2 days before procedure
46
Reversal of oxabans/dabigatran
Idarucizamab For emergency surgery or life-threatening/uncontrollable bleeding Reverses anticoagulation immediately Solution contains Sorbitol- can't give to fructose intolerant people
47
Other reversal options for oxabans/dabigatran
Andexanet Alfa- reverses anticoagulation in less than 5 min PER977- nonspecific agent Both in early clinical trials
48
Heparin
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
Heparin consideration
Anticoagulation effect may be variable--> frequent lab monitoring is required
50
Low Molecular Weight Heparins
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
Pentasaccharides
Fondaparinux synthetic antithrombin exlcusive inhibition of Factor Xa Good for hip/knee surgery
52
Heparin derivatives complications
Most frequent adverse effect is bleeding HIT- 5-7 days after initial exposure Long-term use--> osteopenia
53
Thrombolytic agents
Plasminogen activators
54
Signs that point to possible defect in coaguation
Abnormal bruising Petechiae Splenomegaly
55
Pts that have negative med history
Don't need lab tests
56
Pt that have signs/symptoms of bleeding tendency
Get platelet count, PTT, PT and INR
57
If abnormality in primary hemostasis is suspected
Check bleeding time and measure vWF
58
PT/INR
Add Ca and thromboplastin to blood and time for clot formation Normal is 12+-2 sec INR accounts for differences in labs
59
Prolonged PT due to deficiencies in
``` Factor VII Factor X Factor V Prothrombin Fibrinogen ```
60
PTT
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
When PT is used more and when PTT is used more
PT- coumadin drugs | PTT - heparin drugs
62
aPTT
if prolonged, may indicate use of heparin, hemophilia, sepsis, antiphospholipid antibody, presense of antibodies against coagulation
63
Bleeding time test
Not used anymore- not sensitive or specific, poorly reproducible, can be affected by skill of performer and often leaves scars
64
PFA-100
Measures platelet function | Runs blood sample through tube- promotes platelet adherence and aggregation- measure closure time
65
PFA-100 tests
First run collagen/EPI- if negative, no platelet dysfunction | If positive, then do collagen/ADP test to confirm
66
Gold standard for platelet function analysis
PAA
67
PAA
shows response of blood to specific aggregation inducing agents As platelet aggregation occurs, light transmission increases

Pharm 2 (11 decks)

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