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Clinical 2 (Sam) > 9 - Coagulation Disorders > Flashcards

9 - Coagulation Disorders Flashcards

1
Q

Describe the Virchow triad in thrombosis

A

Thrombosis can be caused by 3 things:

  • Endothelial injury (ex. car accident)
  • Abnormal blood flow
  • Hypercoagulability
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2
Q

When you expose ______ to blood it will induce clotting.

A

collagen

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3
Q

Describe the intrinsic pathway

A

-exposure of collagen basement membrane
-contact activation
F12 -> F12a
F11 -> F11a
F9 -> F9a + F8C
F10 -> F10a

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4
Q

Describe the extrinsic pathway

A

-tissue injury
-tissue thromboplastin (tissue factor)
F7 -> F7a
F10 -> F10a

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5
Q

Describe the common pathway

A

F10 -> F10a
(through F5a) F2 -> F2a
F2 = prothrombin
F2a = thrombin

F2a converts F1(fibrin) -> soluble fibrin

F2a is converted to F13, converted to F13a, which converts soluble fibrin to insoluble fibrin strands

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6
Q

In the presence of a clot, plasminogen is converted to _____

A

plasmin

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7
Q

Describe how vasoconstriction can cause a clot

A
  • vasoconstriction endothelial adhesion
  • stasis of blood flow
  • platelets
  • adhesion
  • release reaction
  • releases ADP, TXA2, Aggregation
  • vWF
  • platelet thrombus
  • retracted fibrin thrombus “fibrin clot”
  • soluble fibrin fragments (FDPs)
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8
Q

What is the only factor not generated by the liver?

A

Factor 8

*it is generated by endothelial wall

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9
Q

How does aspirin work?

A

inhibits COX enzymes
-platelets cannot regenerate and so it takes about a week to until new platelets are made

*in the blood vessel wall, COX is also inhibited which means PGI is inhibited.
PGI is prostacyclin which is a platelet anti-aggregator and vasodilator
**these can regenerate very quickly therefore will turn into PGI which is good bc it’s an anti-aggregator and vasodilator

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10
Q

What are examples of aDP receptor blockers?

A

clopidogrel, ticagrelor, prasugrel

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11
Q

What are some factors that predispose someone to bleeding?

A
  • open vessel
  • pro-clotting factor deficiencies
  • platelet defects
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12
Q

In the absence of ______ we don’t clot

A

calcium

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13
Q

What is PT?

A

prothrombin time

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14
Q

What is INR?

A

international normalized ratio

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15
Q

What is PT or INR?

A

A test based on the time for detection of clot formation in a test tube of the patients’ plasma after the addition of thromboplastin and calcium.

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16
Q

Interpretation of PT/INR:

If it takes more than ___ seconds it is suggestive of a defective extrinsic and common pathway

A

12

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17
Q

INR test is sensitive to reductions in which factors?

A

2, 7, 10

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18
Q

What factors does warfarin reduce the synthesis of?

A

2, 7, 9, 10

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19
Q

Factor _ is very sensitive to warfarin

A

7

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20
Q

When administering warfarin, we need at least _____ hours for coverage of both pathways so we need to administer another agent.

A

48-72

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21
Q

The INR or PT is not altered by thrombocytopenia or defective platelets but it prolonged when the ______ level is low

A

fibrinogen

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22
Q

T or F: ASA or NSAID’s affect the INR

A

FALSE - they do not alter it

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23
Q

What is the antagonist for warfarin?

A

vitamin K

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24
Q

Out of factors 7, 9, 10, and 2, which has the shortest half life?

A

7

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25
Q

What is the formula for INR?

A

INR = {PT/PTc}^ISI

PT = patient's prothrombin time
Pic = mean prothrombin time for your lab control
ISI = international sensitivity index
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26
Q

What is the normal INR range?

A

0.9 - 1.1

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27
Q

White thrombi = _____ thrombi

A

arterial

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28
Q

Describe a white thrombi

A

Arterial thrombi - primarily made up of platelets but also fibrin and WBCs

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29
Q

Red thrombi = ______ thrombi

A

venous

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30
Q

Describe a red thrombi

A

Venous thrombi - primarily fibrin and RBC’s and a small platelet plug

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31
Q

ASA plays no role in the treatment of prevention of _______ thrombi

A

venous

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32
Q

White or Red:

Has more platelets (therefore can be treated and prevented with ASA)

A

White

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33
Q

Give some examples of procoagulants

A
  • tissue thomboplastins
  • exposed collagen
  • activated factors
  • thromboxane A2
  • von Willebrand’s factor
  • factor 8 coagulant material
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34
Q

Give some examples of anticoagulants

A
  • Protein C & Protein S
  • factor defiiencies
  • antithrombin (AT)
  • prostacyclin
  • heparin
  • tPA
  • plasmin
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35
Q

Describe Type A Hemophilia

A
  • deficiency of Factor 8-C
  • normal Factor 8 - vWF
  • “Classical Hemophilia”
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36
Q

Describe Type B Hemophilia

A
  • deficiency of Factor 9

- “Christmas Disease”

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37
Q

Describe von Willebrand’s Disease

A
  • diminished factor 8-vWF

- normal factor 8-C material

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38
Q

What is DIC?

A

Disseminated Intravascular Coagulation:

  • simultaneous clotting & bleeding
  • commonly seen with severe sepsis or postpartum women
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39
Q

Why does severe liver disease cause bleeding or clotting?

A

Because all factors (except 8) are made by the liver.

  • Causes decreased synthesis of Factors 1-13 (except 8)
  • DIC may also occur
  • NOTE: there is also a decrease in synthesis of AT, plasminogen, and alpha 2-antiplasmin

THEY COULD EITHER BLEED OR CLOT

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40
Q

__________ = platelet count < 100,000

A

Thrombocytopenia

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41
Q

What could cause thrombocytopenia?

A
  • a decrease in bone marrow production

- increased peripheral (i.e. circulating blood) destruction

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42
Q

What are a few known thrombogenic risk factors? (i.e. risk factors that would increase your risk for clotting)

A
  • obesity
  • age > 40
  • malignancy
  • immobilization
  • major surgery
  • AMI (acute MI)
  • multiple trauma
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43
Q

What type of deficiency results in heparin not working?

A

anti thrombin 3

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44
Q

How does unfractionated heparin (UF) work?

A

binds with AT and neutralizes activated forms of factors 2, 9, 10, 11, 12

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45
Q

How do low molecular weight heparins (LMWH) work?

A

binds with AT and neutralizes activated forms of factor 10 (some 2a)

46
Q

Give a few examples of LMWH

A
  • enoxaparin
  • dalteparin
  • tinzaparin
47
Q

How does warfarin work?

A

Impairs the synthesis of clotting factors 2, 7, 9, and 10 (vitamin K dependent clotting factors)
**REMEMBER - works on factor 7 initially

  • warfarin also depletes the synthesis of protein C, a physiological anticoagulant (theoretically increasing clotting initially)
  • this is why warfarin is never given alone for the first few days
48
Q

How do ASA/NSAIDs work?

A

Inhibit TXA2 synthesis decreasing platelet aggregability

49
Q

How does TNKase (tenecteplase) work?

A

Increased fibrinolysis; converting plasminogen to plasmin (called a thrombolytic)

50
Q

How does DDAVP (desmopressin) work?

A

Increased release of factor 8-vWF and thus enhancing platelet aggregabililty …. thus a “pro platelet aggregation effect”

51
Q

How do Bivalrudin & Argatroban work?

A

Factor 2a (thrombin) inhibitors

52
Q

How does Dabigatran work?

A 
Factor 2a (thrombin) inhibitor 
(DOAC)
53
Q

DOAC

A

direct oral anticoagulant

54
Q

How does Rivaroxaban work?

A

Factor 10a inhibitor (DOAC)

55
Q

How does Fondaparinux work?

A

Factor 10a inhibitor

56
Q

How does Apixaban work?

A

Factor 10a inhibitor (DOAC)

57
Q

**If it has an ‘x’ in the generic name, it inhibits factor ___.

58
Q

Describe DVT (deep vein thrombosis)

A
  • unilateral, warm, swollen, painful leg
  • usually starts in the calf (distal DVT)
  • may progress, moving up the thigh (proximal DVT)
  • positive Homan’s sign (pain upon dorsiflexion of the foot)
59
Q

Describe PE (pulmonary embolism)

A
  • generic symptoms (tachypnea, chest pain, dyspnea, tachycardia)
  • commonly found in patients with recent history of a DVT chest X-ray findings, EKG, and blood gases may appear normal
  • these tests are performed to rule out other causes of the symptomatology
    ex. pneumonia, pneumothorax, AMI, aortic dissection, or PUD
60
Q

What does Atrial fibrillation result in?

A

stasis of blood within the atria, often resulting in atrial thrombus formation (mural thrombus)

61
Q

What does A. Fib increase the risk of?

A

cerebral embolization

62
Q

CHADS2 or CHA2DS2-VASc:

Score of 0 = ?

A

ASA 81 mg daily alone

63
Q

CHADS2 or CHA2DS2-VASc:

Score of 1 = ?

A

ASA OR a DOAC or warfarin (targeting INR of 2-3)

64
Q

CHADS2 or CHA2DS2-VASc:

Score of > 2 = ?

A

a DOAC or warfarin (targeting INR of 2-3)

65
Q

When are DOAC’s recommended?

A

for all forms of non-valvular atrial fibrillation

66
Q

What are forms of valvular a. fib?

A
  • mitral regurgitation
  • aortic stenosis
  • aortic regurgitation
67
Q

Do not use DOAC in ?

A
  • mitral stenosis

- prosthetic valve disease

68
Q

Patients with prosthetic heart valves are at an increased risk of ??

A

developing valvular thromboembolism (TE)

69
Q

Embolization is greater with _____ than bioprosthetic valves.

A

mechanical

70
Q

What are types of mechanical valves?

A

bileaflet or tilting disc

71
Q

Describe the pharmacotherapy for mechanical valves in aortic position.

A

Warfarin INR target of 2.5 (2-3) is recommended for valves in aortic position (AVR) and NO risk factors for TE. If they have risk factors then 3.0 (2.5-3.5)

72
Q

Describe the pharmacotherapy for mechanical valves in mitral position.

A

Warfarin INR target of 3.0 (2.5 - 3.5) is recommended for valve in mitral position (MVR)

73
Q

What should we add to the pharmacotherapy for pts with mechanical valves?

A

Add ASA 75-100 mg to all with mechanical valves

74
Q

Bioprosthetic valves are generally at lower risk for systemic ________.

A

embolization

75
Q

Should pts with bioprosthetic valves get ASA 75 - 100 mg as well?

A

yes - this is reasonable

76
Q

What is the target INR for pts on warfarin with bioprosthetic valves?

A

For the first 3 up to 6 months after bioprosthetic valve surgery (MVR or AVR) warfarin INR of 2.5 (2-3)

77
Q

What is the dose for heparin?

A

80 units/kg IV load
THEN
18 units/kg/hr IV

78
Q

Describe some goals/monitoring with heparin

A
  • Heparin provides for an immediate anticoagulant effect
  • Check aPTT’s q6h initially and adjust heparin infusion to maintain aPTT within desired range as early as possible (within 24 hours)
  • Check platelet count daily
  • Start warfarin on day 1 at 5mg for at least 2 days
  • Adjust subsequent doses according to INR goal
  • Stop heparin after at least 5 days of combined therapy and when INR is great than target for at least 2 consecutive days
79
Q

What are the parameters for monitoring therapy for UFH, LMWH or warfarin

A

aPTT, INR, Hgb, PLTS & clinical signs of bleeding at least daily

80
Q

What are clinical signs of bleeding?

A
  • melena (dark, tarry stools)
  • hematuria (blood in urine)
  • ecchymosis (discolouration of skin from bleeding underneath)
  • hematemesis (vomiting blood)
  • hemoptysis (coughing up blood)
  • epitaxis (nose bleed)
81
Q

What is the lab goal range for aPTT’s?

A

59 - 99 seconds

82
Q

High INR = ?

A

risk of bleeding

83
Q

Low INR = ?

A

risk of clotting

84
Q

What is the recommended pharmacotherapy of DVT & PE?

A
  • UFH or LMWH and start on warfarin at the same time.
  • UFH or LMWH is usually discontinued after 5 days, provided that the INR has been therapeutic range (i.e. INR > 2 for at least 24 hours)
85
Q

What type of patients should heparin be continued longer in? (10 days)

A

patients with massive pulmonary embolism or iliofemoral vein thrombosis

86
Q

For ______ VTE, continue warfarin for 3 months maintaining INR target of 2.5 (2-3).

87
Q

For idiopathic or unprovoked VTE, therapy is recommended for ??

A

> 3 months (up to 2.5 years)

*continue warfarin indefinitely if patient has risk factors (ex. malignancy, AT deficiency, etc.)

88
Q

If a pt has had a clot recurrence despite anticoagulation, what is the protocol?

A

continue warfarin indefinitely but at an increased intensity of INR target of 3.0 (2.5 - 3.5)

89
Q

How does LMWH (enoxaparin, dalteparin) work?

A

inhibits factors Xa and 2a

90
Q

Who should LMWH be avoided in?

A

its with CrCl < 30

91
Q

Dabigatran (Pradaxa) is ___& really excreted

92
Q

Antidote for heparin?

93
Q

Antidote for warfarin?

94
Q

What is FFP?

A

fresh frozen plasma (provides you with clotting factors to replace all the clotting factors that were consumed)

95
Q

What is rFVIIa?

A

recombinant factor VIIa

96
Q

What is 4-PCC?

A

4 factor prothrombin complex concentrates (also referred to as Octaplex)

97
Q

What is Idarucizumab?

A

a new monoclonal antibody fragment specifically targeted at dabigatran

98
Q

How early before surgeries should warfarin be stopped?

99
Q

If a patient is renally impaired can they get normal doses of warfarin?

100
Q

What options do we have for reversing warfarin?

A
  • vitamin K
  • FFP
  • rFVIIa
  • 4-PCC
101
Q

Is dialysis an option to remove warfarin in an overdose?

102
Q

What is dabigatran indicated for?

A

preventing stroke with A. fibrillation

103
Q

Full effects of dabigatran take?

104
Q

When do you need to stop dabigatran before surgeries?

A

1-2 days before

105
Q

If a patient is renally impaired can they get normal doses of dabigatran?

A

No. Dabigatran is contraindicated in patients with ClCr < 30

106
Q

What options do we have for reversal of Dabigatran?

A
  • hemodialysis
  • rFVIIa
  • no role for FFP bc dabigatran provides anticoagulation by inhibition not by clotting factor depletion
  • 4-PCC (Octaplex) NOT effective

-Idarucizumab 5 grams = 1st line reversal agent for Dabigatran

107
Q

What is Rivaroxaban/Apixaban used for?

A

the prevention of stroke with atrial fibrillation

108
Q

How early before surgeries do you need to stop Rivaroxaban/Apixaban ?

109
Q

Can you use normal doses of Rivaroxaban/Apixaban in the renally impaired

A

NO. Use is contraindicated if Clcr < 30

110
Q

Options for reversing Rivaroxaban/Apixaban ?

A

4-PCC (Octaplex)

  • dialysis NOT effective
  • no role for FFP bc these agents provide anticoagulation by inhibitor, not by clotting factor depletion
111
Q

What is a Caval Interruption - Greenfield Filter?

A

A mechanical device placed in the inferior vena cava to filter emboli origination from the lower extremities (i.e. proximal vein thrombosis)

Possible indications:

  • a contraindication to anticoagulant therapy (eg. bleeding PUD)
  • recurrent PE despite adequate anticoagulation
112
Q

How often are people monitoring their INR?

A

they will be undergoing weekly or biweekly monitoring of their blood INR values with their clinic visits, in order to ensure adequate warfarin anticoagulation

Clinical 2 (Sam) (18 decks)

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