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Health Assessment - Autumn > Coagulation - Final Exam > Flashcards

Coagulation - Final Exam Flashcards

1
Q

Normal Hemostasis is a balance b/w what 3 things?

A
  1. clot generation
  2. thrombus formation
  3. counter-regulatory mechanisms that inhibit uncontrolled thrombogenesis (clot formation) or premature thrombus degradation
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2
Q

What are the 3 goals of hemostasis?

A
  1. limit blood loss from vascular injury
  2. maintain intravascular blood flow
  3. promote revascularization after thrombosis
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3
Q

Stages of Hemostasis

What is primary hemostasis?

What does it lead to?
What kind of injury is it adequate for?

A
  • immediate platelet deposition at the endovascular injury site
  • leads to initial platelet plug formation
  • minor injuries
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4
Q

Stages of Hemostasis

What is secondary hemostasis?

A
  • where clotting factors are activated & a stabilized clot is formed w/ crosslinked fibrin
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5
Q

Hemostasis

Vascular endothelial cells have ________, ________, and ________ effects that inhibit clot formation.

A
  1. antiplatelet
  2. anticoagulant
  3. profibrinolytic
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6
Q

Hemostasis

Vascular endothelial cells are ________ charged to repel ________.

A
  1. negatively
  2. platelets
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7
Q

Hemostasis

What platelet inhibitors do vascular endotheloal cells produce?

A
  1. Prostacyclin
  2. Nitric Oxide
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8
Q

Hemostasis

What do vascular endothelial cells excrete that degrades ADP?

What is ADP’s role in hemostasis?

A
  • they excrete adenosine diphosphatase
  • ADP is a platelet activator
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9
Q

Hemostasis

True or False?

Vascular endothelial cells inactivate protein C?

  • what is protein C’s role in anti-clotting?
A

False. They increase protein C, which is an anticoagulant

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10
Q

Hemostasis

True or False?

Vascular Endothelial cells produce tissue factor pathway inhibitor (TFPI).

What does TFPI inhibit?

A
  • True
  • TFPI inhibits factor Xa and TF-VIIa complex
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11
Q

Hemostasis

Where is tissue plasminogen activator (t-PA) synthesized?

A

in vascular endothelial cells

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12
Q

Hemostasis

Where are platelets derived from?

A

bone-marrow megakaryocytes

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13
Q

Hemostasis

What do inactive platelets circulate as? What is their lifespan?

A
  • discoid anuclear cells
  • lifespan: 8-12 days
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14
Q

Hemostasis

In normal conditions 10% of platelets are consumed to support ________ ________.

How many platelets are formed daily?

A
  1. vascular integrity
  2. 1.2-1.5 x 10^11 (1 billion)
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15
Q

Hemostasis

What does the platelet membrane contain that increases the surface area?

A
  1. numerous receptors
  2. surface canalicular system (channels in the membrane that help the platelet function)
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16
Q

Hemostasis

What expose the extracellular matrix?

A

Damage to the endothelium

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17
Q

Hemostasis

What 3 things are found in the extracellular matrix?

A
  1. collagen
  2. Von Willebrand’s Factor
  3. other platelet adhesive glycoproteins
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18
Q

Hemostasis

What are the 3 phases that platets undergo after exposure to the extracellular matrix?

A
  1. Adhesion
  2. Activation
  3. Aggregation
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19
Q

Platelet phases

What initiates adhesion of platelets?

A
  • exposure to extracellular matrix proteins
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20
Q

Platelet phases

Activation of the platelet is stimulated when the platelet interacts with ________ & ________ ________.

What does activation of the platelet cause?

A
  • Collagen & tissue factor (TF)
  • Activation causes release of granular contents of the platelets
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21
Q

What are the 2 types of storage granules in platelets?

A
  1. alpha granules
  2. dense bodies
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22
Q

Platelets

What contents are release from alpha granules?

A
  • fibrinogen
  • Factors V & VIII
  • vWF
  • Plt-derived growth factor
  • & more
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23
Q

Platelets

What contents are released from dense bodies?

A
  • ADP
  • ATP
  • Calcium
  • Serotonin
  • Histamine
  • Epinephrine
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24
Q

Platelet Phases

When does platelet aggregation occur?

What does this recruit and activate?

Then ________ ________ coagulation is propagated.

A
  1. Occurs when granular contents are released
  2. this recruits and activates more platelets
  3. plasma-mediated coagulation propagated
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25
Q

Platelet Aggregation

What binds to fibrinogen and promotes fibrin crosslinking?

A
  • activated glycoprotein IIb/IIIa receptors on the platelet’s surface
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26
Q

Hemostasis

What does each stage of the clotting cascade require assembly of?

A
  • membrane-bound activation tenase complexes
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27
Q

What 4 things are each membrane-bound activation tenase-complex composed of?

A
  1. substrate (inactive precursor)
  2. enzyme (activated coagulation factor)
  3. cofactor (accelerator or catalyst)
  4. calcium
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28
Q

Clotting Factors

Factor I

A

Fibrinogen

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29
Q

Clotting Factors

Factor II

A

Prothrombin

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30
Q

Clotting Factors

Factor III

A

Tissue Thromboplastin

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31
Q

Clotting Factors

Factor IV

A

Calcium Ions

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32
Q

Clotting Factors

Factor V

A

Labile Factor

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33
Q

Clotting Factors

Factor VII

A

Stable Factor

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34
Q

Clotting Factors

Factor VIII

A

Antihemophilic Factor

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35
Q

Clotting Factor

Factor IX

A
  • Christmas Factor
    or
  • Plasma Thromboplastin Component (PTC)
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36
Q

Clotting Factors

Factor X

A

Stuart-Prower Factor

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37
Q

Clotting Factors

Factor XI

A

Plasma Thromboplastin Antecedent (PTA)

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38
Q

Clotting Factors

Factor XII

A

Hageman Factor

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39
Q

Clotting Factors

Factor XIII

A

Fibrin Stabilizing Factor

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40
Q

Picture from Miller of Clotting Cascade

41
Q

Which pathway is the initiation phase of plasma-mediated hemostasis?

A

Extrinsic Pathway

42
Q

What does the extrinsic pathway begin with? What does this expose?

A
  1. endothelial injury
  2. exposes TF to the plasma
43
Q

Extrinsic Pathway

After the TF is exposed to the plasma, what does TF form?

A

an active complex w/ VIIa (TF/VIIa complex)

44
Q

Extrinsic Pathway

What 2 factors does the TF/VIIa complex bind to & activate?

A
  1. Factor X —– Factor Xa
  2. Factor IX —– Factor IXa (intrinsic path)
45
Q

In the intrinsic pathway what does activated IXa and Calcium convert?

A

Factor X —- Factor Xa (intrinisc)

46
Q

What factor begins the final common pathway?

47
Q

Intrinsic Pathway

What factor does the intrinsic pathway begin with?

48
Q

Intrinsic Pathway

What was the intrinsic pathway initially thought to occur in response to?

A

endovascular contact w/ negatively charged substances (glass, dextran)

k

49
Q

intrinsic Path

Current Understanding - the intrinsic path plays a more minor role in ____________________.

It is more of an amplification system to propagate what??

A

Initiation of hemostasis

  • propagates thrombin generation initiated by the extrinsic path
50
Q

Most thrombotic events follow which path?

What path do lab coag studies rely on to activate cascade?

A
  1. extrinsic path
  2. lab studies rely on intrinsic path
51
Q

Intrinsic Path

What does the intrinsic path begin with?

What factor does this activate?

A
  • contact w/ a negatively charged surface
  • activates factor XII — factor XIIa
52
Q

Intrinsic path

What does Factor XIIa convert?

A

Factor XI to XIa

53
Q

Intrinsic Path

IXa + VIIIa + platelet membrane phospholipid + Ca… activate what?

A

Factor X to Xa

54
Q

Intrinsic Pathway Propagation

What 4 factors does activated thrombin (IIa) activate?

What does this amplify?

A
  • Factor V, VII, VIII, XI
  • amplifies thrombin generation
55
Q

Intrinsic Pathway Propagation

What is the powerhouse of clot formation?

A
  • activated thrombin (IIa) activating factor V, VII, VIII, & XI – amplifying thrombin generation
  • this process activates plts leading to propagation of the final common pathway
56
Q

Common Pathway

Factor X becomes Xa & binds w/ Va to form “________ ________.”

A

prothrombinase complex

57
Q

Common Pathway

What is the prothrombinase complex made of?

What does prothrombinase complex convert?

A
  • (Xa + Va) + Calcium
    Prothrombin (II) into thrombin (IIa)
58
Q

Common Pathway

What does the thrombin (IIa) attach to & convert?

A

attaches to plts converts fibrinogen (I) to fibrin (Ia)

59
Q

Common Pathway

What do fibrin molecules do?

A

Crosslink to form a mesh that stabilizes the clot

60
Q

Common Pathway

Thrombin cleaves ____________ from fibrinogen. This generates ________ ________.

A

Fibrinopeptides A & B

Fibrin Monomers

61
Q

Common Pathway

What do fibrin monomers do?

A

Polymerize into fibrin strands to form basic clot

62
Q

Common Pathway

What factor crosslinks the fibrin strands to stabilize and make an insoluble clot that is resistant to fibrinolytic degradation?

63
Q

What is the key step in regulating hemostasis?

A

Thrombin Generation

64
Q

Image depicting thrombin generation & fibrin formation

65
Q

What 4 things make up the intrinsic tenase complex?

A
  1. activator
  2. IXa
  3. VIIIa
  4. Calcium
66
Q

What 4 things make up the Extrinsic Tenase Complex?

A
  1. injury
  2. TF
  3. VIIa
  4. Calcium
67
Q

What initiates the intrinsic & extrinsic pathways?

A
  • A catalyst
  • Extrinsic: tissue injury
  • Intrinsic: activator
68
Q

Anticoagulation

What are the 4 major coagulation counter-mechanisms?

A
  1. Fibrinolysis
  2. Tissue Factor Pathway Inhibitor (TFPI)
  3. Protein C System
  4. Serine Protease Inhibitors (SERPINs)
69
Q

Coagulation Counter-Mechanism

Fibrinolysis

A

Endovascular tissue plasminogen activator (tPA) & urokinase convert plasminogen into plasmin

70
Q

Fibrinolysis

What does plasmin break down?
What does it degrade?

A
  • breaks down clots enzymatically
  • degrades V & VIII
71
Q

Anticoagulation

What does Tissue Factor pathway inhibitor form?

A
  • a complex w/ Xa that inhibitsTF/VIIa complex
  • downregulating the extrinsic pathway
72
Q

Anticoagulation

What 3 factors does the Protein C System inhibit?

A
  1. II
  2. Va
  3. VIIIa
73
Q

Anticoagulation

What 3 things are Serine protease inhibitors (SERPINs)?

A
  1. Antithrombin (AT)
  2. Heparin
  3. Heparin cofactor II
74
Q

SERPINs

What 5 factors does Antithrombin inhibit?

A
  1. thrombin
  2. IXa (9a)
  3. Xa (10a)
  4. XIa (11a)
  5. XIIa (12a)
75
Q

SERPINs

What does heparin bind to?

What does that cause?

A
  1. Heparin binds to antithrombin
  2. causes a conformational change - accelerates AT activity
76
Q

SERPINs

What does Heparin Cofactor II inhibit?

A

thrombin alone

77
Q

Pre-op Eval

What is the most effective predictor of bleeding?

What things should we inquire about?

A
  1. carefully performed bleeding history
  2. inquire about nose bleeds, bleeding gums, easy bruising
78
Q

Pre-op Eval

What procedures should we ask about for excessive bleeding?

A
  1. dental extractions
  2. surgery
  3. trauma
  4. child birth
  5. blood transfusion requirements
79
Q

Pre-op Eval:

Common Blood Thinners

A
  • ASA
  • NSAIDs
  • Vitamin E
  • Gingko
  • Ginger
  • Garlic Supps
80
Q

Pre-op Assessment

What 4 coexisting diseases lead to increased bleeding times?

A
  1. Renal Disease
  2. Liver Disease
  3. Thryoid Disease
  4. Bone Marrow Disorders
81
Q

What are standard first-line labs if a bleeding disorder is suspected?

A

PT, aPTT
*address both extrinsic & intrinsic pathways

82
Q

What is the most common inherited bleeding disorder?

A

Von Willebrand’s Disease

83
Q

What does a deficiency in vWF cause?

What does vWF play a critical role in?

A
  • defective platelet adhesion/aggregation
  • plays a role in plt adhesion & prevents degradation of factor VIII
84
Q

vWF

Are routine coag labs helpful?

What better tests are there?

A
  • No - plts & PT normal. aPTT might be prolonged d/o Factor VIII
  • vWF level
  • vWF plt binding activity
  • Factor VIII level
  • plt function assay
85
Q

vWF

Treatment (mild & intra-op bleeding)

A
  • mild: DDAVP - increases vWF
  • bleeding: vWF & Factor VIII
86
Q

Hemophilia A

What is the factor deficiency?

Incidence?

A
  • factor VIII deficiency
  • 1:5,000
87
Q

Hemophilia B

What factor deficiency?

Incidence?

A

IX
1:30,000

88
Q

Hemophilia

What amount is genetic?

What amount is a new mutation w/o family Hx?

A
  • 2/3 genetic
  • 1/3 new mutation w/ no family Hx
89
Q

Hemophilia

When does it present and how?

A
  • in childhood as spontaneous hemorrhage involving joints & muscles
90
Q

Hemophilia Labs

A
  • normal PT, Plts, & bleeding time
  • PTT normally prolonged
91
Q

Hemophilia

Who ya gonna consult pre-op?

What drugs/Factors may be indicated before surgery?

A
  1. Hematology
  2. DDAVP/Factor VIII or IX
92
Q

What meds are the most significant cause of intraoperative bleeding?

A

Anticoagulants duhhhh

93
Q

What 8 drugs can lead to bleeding?

A
  1. Heparin
  2. Warfarin
  3. Direct Oral Anticoagulants
  4. Beta-lactam Abx
  5. Nitroprusside
  6. NTG
  7. NO
  8. SSRIs
94
Q

What 8 supplements/herbals can cause bleeding?

A
  1. Cayenne
  2. Garlic
  3. Ginger
  4. Gingko Bilboa
  5. Grapeseed Oil
  6. St. John’s Wort
  7. Tumeric
  8. Vitamin E
95
Q

What factors come from the Liver?

A
  • I
  • II
  • V
  • VII
  • IX
  • X
  • XI
  • XII
  • protein C & S, antithrombin
96
Q

What does liver disease lead to? (3 things)

A
  • complex, multifactorial hemostatic issues
    1. impaired synthesis of coagulation factors
    2. quantitative and qualitative platelet dysfunction
    3. impaired clearance of clotting and fibrinolytic proteins
97
Q

Liver Disease

What do lab findings show?

what do these labs account for?

What do they not account for?

A
  • prolonged PT & possible prolonged PTT
  • they reflect lack of pro-coagulation factors
  • don’t account for concurrent lack of anticoagulation factors
98
Q

Liver Disease

Chronic liver pts displace a ________ ________. They also have sufficient amounts of ________ production.

But, they are still susceptible to disruption in ________.

A
  1. rebalanced hemostasis
  2. thrombin
  3. coagulation

** they are compensated but not optimized **

99
Q

What are valuable guides for Liver Disease pts?

What do these labs tell you?

A
  • TEG, ROTEM
  • tell you what they are lacking/what blood products they need

Health Assessment - Autumn (6 decks)

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