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SBB > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

What is primary hemostasis?

A

Platelets adhere to exposed endothelium
Sub endothelium has collagen and vWF
Platelets aggregate and form platelet plug

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2
Q

What is secondary hemostasis?

A

Coagulation cascade results in fibrin cross links to form stable clot

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3
Q

What glycoproteins on the platelet are involved with aggregation?

A

GP IIb/IIIa - activated by fibrinogen binding to GP Ib; bridges plt’s together
Deficient in Glazmann’s Thrombasthenia

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4
Q

What glycoproteins on the platelet are involved with adhesion?

A

GP Ib/IX/V - vWF and thrombin binding
vWf acts as a bridge between endothelial collagen and platelet
Defective in Bernard Soulier Syndrome

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5
Q

What is platelet membrane called?

A

glycocalyx

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6
Q

What is released in the alpha granules of the platelets?

A 
Most numerous
Coagulation factors I, V, VIII
Thromboxane A2 = plt activator
Protein S = inhibits coagulation
vWF
β-thromboglobulin (BTG) 
PF4 - Inhibits heparan sulfate (promotes coagulation)
Platelet-derived growth factor (PDGF)
Thrombospondin - Stimulates TGFβ release; promotes wound healing
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7
Q

What is released in the dense granules of platelets?

A

ADP
ATP
Ca++
Serotonin

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8
Q

What happens when platelets are activated?

A

Platelets adhere to collagen > release Collagen > Increased Ca++ activate phospholipase A2 > catalyzes release of arachidonic acid (AA) > Cyclo-oxygenase and thromboxane synthase convert AA to the prostaglandin thromboxane A2 (TXA2)
TXA2 stimulates the release of dense granules

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9
Q

What are platelet activators?

A

ADP, Ca++ and serotonin are potent platelet activators

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10
Q

How does aspirin inhibit platelet function?

A

Aspirin is a potent cyclooxygenase inhibitor that prevents clotting by preventing the release of dense granules from activated platelets

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11
Q

What coag factors are in the prothrombin group?

A

Factors II, VII, IX, X

  • Serine proteases
  • Not consumed
  • Vitamin K dependent, adds carboxyl to glutamic acid residues required to bind calcium, Protein Induced in Vitamin K Absence (PIVKA)
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12
Q

What coag factors are in the fibrinogen group?

A

I (fibrinogen), V, VIII, XIII
V and VIII are heat labile, degrade rapidly in plasma
XIII covalently cross-links fibrin strands

Acute phase reactants increase during inflammation and pregnancy

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13
Q

What factors in the contact group?

A

Factors XII, XI, Prekallikrein (PK), High Molecular Weight Kininogen (HMWK)
Mediate contact with negatively charged surfaces

Only XI results in bleeding where there is a deficiency

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14
Q

What is half life for factor I (Fibrinogen)

A

3-6 days

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15
Q

What is half life for factor VIII?

A

8-12 hours

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16
Q

What is half life for factor IX?

A

18 - 24 hours

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17
Q

How does protein C and protein S regulate 2* hemostasis?

A

Thrombin activates F-V and F-VIII, butat high concentrations thrombin binds to thrombomodulin and activates Protein C that with protein S inactivates F-V and F-VIII.

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18
Q

What is the half life of factor VII?

A

2-5 hours

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19
Q

What is the half life of factor I (fibrinogen)?

A

3-6 Days

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20
Q

What is the half life of Factor II (prothrombin)?

A

2-5 Days

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21
Q

What is the role of antithrombin in 2* hemostasis?

A

Antithrombin suppresses serine proteases (thrombin, IX, X, XI, XII, PK, and plasmin. Heparin is cofactor; AT complexes with factor. Heparin works by increasing antithrombin activity 3-4x.
AT is produced in the liver

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22
Q

Where is heparan sulfate found?

A

Heparan sulfate is found in high concentrations in endothelial cell membranes

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23
Q

Where is heparin found in the body

A

Mast cells and basophils

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24
Q

What is fibrinolysis?

A

Normal clot break down mechanism

Functions to remove fibrin from the vascular system in a controlled manner to prevent excessive fibrin accumulation

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25
Q

What is the mechanism of the fibrinolytic system?

A

Plasminogen is converted to plasmin and plasmin breaks down fibrin in FDP.

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26
Q

What are the procoagulant functions of thrombin?

A
  • Forms fibrin from fibrinogen
  • Activates V, VIII, XIII to amplify its own production
  • Stimulates endothelial cells to release VWF, expose TF, and plasminogen activator inhibitor (PAI-1)
  • Activates platelets
  • Suppress fibrinolysis by activating thrombin activatable fibrinolysis inhibitor (TAFI)
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27
Q

What are the anticoagulant functions of thrombin?

A
  • Thrombin binds to thrombomodulin and activates protein C and S
  • Stimulates endothelial cells to release plasminogen activator and nitric oxide (NO) . tPA is produce to break down clot
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28
Q

What is the function of XIIIa?

A

Transglutaminase

Crosslinks fibrin stands to form stable clot

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29
Q

What are fibrinolytic inhibitors?

A

a2-antiplasmin
plasminogen activator inhibitor-2 (PAI-2)
Thrombin-activated fibrinolysis inhibitor (TAFI)

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30
Q

What do D-Dimers indicate?

A

Crosslinked fibrinogen is broken down

High in DIC, DVT and PE

31
Q

What do FDP’s indicate?

A

Fibrin and fibrinogen is broken down

32
Q

What is the effect of high concentrations of FDP’s?

A
  • Antithrombin activity
  • Fragment’s compete with fibrinogen for thrombin so less fibrin is formed
  • Inhibit polymerization of fibrin by competing with fibrin monomers
  • Interferes with platelet aggregation
33
Q

What pathway does the PT test measure?

A

Extrinsic

Factor VII and common pathway

34
Q

What pathway does the PTT test measure?

A

Intrinsic

VIII, IX, XI, XII, HMWK, PK

35
Q

What factors are in the common pathway?

A

F-I (fibrinogen), F-II (prothrombin), F-V, F-X, and F-XIII

36
Q

What is Glanzmann’s Thrombasthenia?

A

Autosomal recessive
GPIIb/IIIa deficiency ➔Hemorrhaging
No aggregation
Abnormal bleeding time, abn platelet aggregation with all except ristocetin, clot retraction

37
Q

What is Bernard Soulier Disease?

A

GPIB/IX deficiency - Adhesion
Symptoms similar to von Willebrand’s disease
Abnormal bleeding time, normal vWF assay, large platelets, abnormal aggregation normal with all except ristocetin.

38
Q

What is storage pool disease?

A

Decreased numbers of dense granules (⬇ADP, etc.)

No platelet aggregation

39
Q

What diseases are associated with ineffective platelets?

A

Kidney failure - Uremic toxins inhibit platelet function
Multiple myeloma - High plasma protein concentrations block platelet receptors
Immune Thrombocytopenic Purpura (ITP) -
Autoimmune anti-platelet antibodies
Drugs - Aspirin, anti-malarials, heroin

40
Q

What is the function of vWF?

A

Binds collagen to platelet GPIb/IX.
- Platelet Adhesion
Binds to and stabilizes FVIII:C.

41
Q

What are characteristics of vWF?

A

Autosomal dominant
Abnormal bleeding time (may be normal)
Abnormal platelet aggregation with Ristocetin

42
Q

What is the association of Group O and vWF?

A

Group O have 25% less vWF

43
Q

What are the characteristics of type 1 vWD?

A

Quantitative decrease of vWF
Also results in decreased FVIII
Most common

44
Q

What are the characteristics of Type 2 vWD?

A

Quantitatively normal, abnormal protein and function

FVIII can be normal

45
Q

What are the characteristics of Type 3 vWD?

A

Homozygous
Extremely low levels of vWF and FVIII:C
Most severe

46
Q

What is treatment for vWD?

A

Cryo or FFP to replace FVIII:C and vWF
Commercial preparations of vWF and FVIII
DDAVP (desmopressin) - Induces the release of vWF from endothelial cells > greatly increases plasma concentrations of FVIII:C via vWF stabilization of FVIII

47
Q

What is hemophilia A?

A 
FVIII deficiency
X-linked
85% of all hemophilia
Normal bleeding time, prolonged PTT, low F-VIII
Treatment = DDAVP (if mild), Cryo, or 
recombinant FVIII (rFVIII)
48
Q

What is hemophilia B?

A 
FIX deficiency
X-linked
14% of all hemophilia
Treatment = Purified plasma concentrate
rFIX (preferred)
49
Q

What is hemophilia C?

A 
FXI deficiency
Autosomal dominant 
Ashkenazi Jews <1% of all hemophilia
FXI is the only contact factor associated with bleeding
Treatment: FFP
50
Q

What are causes of fibrin deficiencies?

A 
Acquired hypofibrinogenemia
 - l-asparaginase impaies synthesis of fibrinogen by the liver
 - Antithymocyte globulin treatment of aplastic anemia
 - Corticosteroids
Inherited Disorders
 - Dysfibrinogenemia
 - Hypodysfibinogenemia
 - Afibrinogenemia
51
Q

What are some examples of acquired coagulation disorders?

A

Vitamin K Deficiency
Liver Disease
Secondary fibrinolysis
Disseminated Intravascular Coagulation

52
Q

How does vitamin K affect coagulation?

A

FII, VII, IX, X require Ca++ binding to function

Vitamin K adds carboxyl groups that bind Ca++

53
Q

How does liver disease affect coagulation?

A

FI (fibrinogen), II (thrombin), V, VII, IX and X are produced in the liver
Note: FVIII is made by endothelial cells
Decreased thrombopoietin produced by hepatocytes results in mild low PLT’s
Elevated fibrinolysis and premature clot dissolution can result in consumption of clotting factors

54
Q

What is most common cause of DIC?

A

Sepsis

Also seen in trauma, placenta abruption, myocardial infarction

55
Q

What is the mechanism of DIC?

A

Elevated thrombin, tissue factor or thromboblastin activates uncontrolled intravascular coagulation
Extensive formation of intravascular microthrombi frequently result in severe tissue hypoxia, organ failure and death
Consumptive coagulopathy that depletes platelets, fibrinogen and coagulation factors and can also result in hemorrhage

56
Q

How do Clopridogrel (Plavix) and Ticlopidine (Ticlid) affect platelets?

A

ADP receptor inhibitors
These drugs block the P2Y12 platelet receptors and prevent binding of ADP to the P2Y12 receptor.
Causes decrease in PLT aggregation

57
Q

How does coumadin work?

A 
Vitamin K antagonist
Slow acting, slow clearance time
Counteracted by high dose vitamin K 
Monitored by PT (2-2.5x longer)
Monitored by INR (2-3)
58
Q

How does heparin work?

A

Increases antithrombin activity ~1000 fold
Fast acting, fast clearance time
Counteracted by protamine sulfate
Monitored by APTT

59
Q

What is HIT type 1?

A

Non-immune-mediated and self-limiting

Between 1-3 days after start of heparin therapy

60
Q

What is HIT Type 2?

A

Immune-mediated; requires prior sensitization
5-14 days after start of heparin therapy
IgG antibodies against PF4-Heparin complex
High risk of thrombosis (DVT or PE)

61
Q

Why are platelets decreased in sepsis?

A

-Thrombin is increased > activates plt’s

62
Q

What is lupus anticoagulant?

A

Antibodies produced against phospholipis
Cause thrombosis not bleeding
Increased PTT result

63
Q

What does the thrombin time measure?

A 
Fibrinogen is converted to fibrin
Prolonged with:
 Heparin
 Low fibrinogen
 Abnormal fibrinogen
 FSP
64
Q

How much will a single cryo increase fibrinogen by?

A

1 unit of cryoprecipitate will increase the fibrinogen level by 5-10 mg/dL

65
Q

What causes TTP?

A

Deficiency of ADAMST-13, needed to cleave large vWF. Clotting occurs in microvascular. Due by autoimmune (antibody to ADAMST-13), hereditary, or secondary to disease.

66
Q

What causes PTP?

A

Occurs 5-12 after transfusion due to anti-HPA -1a. Antibodies destroy transfused and self platelets.

67
Q

Calculate rFVIII dose

A

1 IU rFVIII will increase the FVIII level 2%.

Weight (lbs) ÷ 4.4 × factor level increment desired = number of factor VIII units needed

68
Q

Calculate rFIX dose

A

1 IU rFIX will increase the FVIII level 1%

Weight (lbs) ÷ 2.2 × factor level increment desired = number of factor IX units needed

69
Q

How do you reverse warfin?

A

Oral vitamin K if INR > 10

70
Q

How do you reverse Heparin?

A

Protamine

71
Q

How do you calculate CCI?

A 
Post PLT CT - Pre PLT ct x BSA (2) /
PLT yield (# of PLT x Volume x 1000 mL) = CCI
72
Q

How does Desmopressin (DAVP) work?

A

DDAVP causes von Willebrand factor (VWF) to be released from the stores in the endothelial cells that line the blood vessels. VWF then binds to FVIII as it is released from the liver, protecting it from degradation. Following the administration of DDAVP, circulating FVIII and VWF levels may rise approximately three-fold in responsive patient

73
Q

What are Aminocaproic acid (Amicar) and Tranexamic acid (Lysteda)?

A

Antifibrinolytic - stops fibrinolysis in uncontrolled bleeding

SBB (37 decks)

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