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Apex > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What are the 4 steps of hemostasis?

A
  1. Vascular spasm
  2. Formation of platelet plug
  3. Coagulation and fibrin formation (secondary hemostasis)
  4. Fibrinolysis when the clot is no longer needed
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2
Q

What is collagen?

A

Procoagulant

Tensile strength

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3
Q

What is wVf?

A

Procoagulant

Platelet adhesion

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4
Q

What is fibronectin?

A

Procoagulant

Cell adhesion

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5
Q

What is protein C?

A

Anticoagulant

Degrades factor 5 and 8

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6
Q

What is protein S?

A

Anticoagulant

Cofactor for C

(S’ing that C “sucking that cock”)

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7
Q

What is antithrombin?

A

Anticoagulant

Inactivates 2a (thrombin) and factors 9, 10, 11, and 12

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8
Q

What is tissue pathway factor inhibitor?

A

Anticoagulant

Inhibits tissue factor

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9
Q

What is thrombomodulin?

A

Anticoagulant

Regulates naturally occurring anticoagulants

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10
Q

What is plasminogen?

A

Precursor to plasmin

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11
Q

What is tPA?

A

Activates plasmin

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12
Q

What is urokinase?

A

Fibrinolytic

Activates plasmin

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13
Q

What is alpha-antiplasmin?

A

Antifibrinolytic

Inactivates tPA/urokinase

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14
Q

What is plasminogen activator inhibitor?

A

Antifibrinolytic

Inhibits plasmin

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15
Q

What are the three vasoactive mediators that cause vasoCONSTRICTION?

A

Thromboxane A2
ADP
Serotonin

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16
Q

What are the two vasoactive mediators that cause vasodilation?

A

Prostacyclin
Nitric oxide

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17
Q

What do platelets lack?

A

Nucleus!

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18
Q

Where are platelets produced?

A

Bone marrow

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19
Q

What are some components for clot formation that are on the outside of the platelet?

A

Gylcoproteins ( repelled by healthy endothelium) ~ adhere to damaged endothelium

Phospholipids (substrate for prostaglandin synthesis) produce thromboxane A2~ activates platelets

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20
Q

What are some components inside the platelet that are part of clot formation?

A

Actin and myosin (help platelet contract for plug)

Thrombosthenin (assist with platelet contraction)

ADP (platelet activation)

Calcium (factor 4)

Fibrin-stabilizing factor (crosslinks fibrin)

Serotonin (activates other platelets)

Growth factor (helps repair damaged walls)

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21
Q

Platelet adhesion is associated with what?

A

von Willebrand

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22
Q

Platelet activation and adhesion is associated with what?

A

ADP and thromboxane A2

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23
Q

What two functions does vasospasm serve?

A

Reduces blood loss
Helps procoagulants remain in the affect area

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24
Q

What factor does von Willebrand factor bind to?

A

GpIb

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25
Q

What does the GpII receptor do?

A

Links activated platelets to each other to form the platelet plug

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26
Q

What are the 3 steps required to produce a platelet plug?

A

Adhesion
Activation
Aggregation

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27
Q

What is the final common pathway in the coagulation cascade?

A

Thrombin activation (2a)

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28
Q

When is the extrinsic pathway activated?

A

When Coagulation is initiated outside of the intravascular space

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29
Q

When is the intrinsic pathway activated?

A

Coagulation is initiates inside of the intravascular space

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30
Q

What is the intrinsic pathway?

A

12 > 11 > 9 (+8) > 10 (+5) > 2 > 1

It’s “IN a line” so it’s “INtrinsic”

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31
Q

Which lab value is for the intrinsic pathway?

A

PTT (intrinsic is longer just like PTT is longer)

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32
Q

What is the extrinsic pathway?

A

Tissue factor (3) > 7 (4+ ~ calcium) > 10 (+5) > 2 > 1

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33
Q

What lab value correlated with the extrinsic pathway?

A

PT (shorter than PTT~ just like the intrinsic pathway)

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34
Q

Which anticoagulant inhibits the EXtrinsic pathway?

A

WARFARIN

The extrinsic pathway looks like a little gun ~ you use guns in WAR

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35
Q

How is the extrinsic pathway activated?

A

When you have a gun (as in the extrinsic pathway ~ you need a trigger finger)

Trigger finger ~ TF ~ tissue factor

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36
Q

What factors are dependent on vitamin K?

A

Just remember 1972

10, 9, 7, and 2

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37
Q

What factors are in the common final pathway?

A

Remember they are all part of the money system.

10$, 5$, 2$, and 1$

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38
Q

How fast is the extrinsic pathway?

A

Fast! 15 seconds (think PT value)

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39
Q

What is the first factor to become deficient in patients with liver failure?

A

Factor 7! It has a very short half life

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40
Q

Which factor is missing in hemophilia A?

A

Factor 8

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41
Q

How fast is the intrinsic pathway?

A

Slow! Up to 6 minutes

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42
Q

What is activated fibrin-stabilizing factor?

A

13a

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43
Q

Where is plasminogen synthesized?

A

Liver

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44
Q

What is plasmin?

A

Proteolytic enzyme that degrades fibrin to fibrin degradation products

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45
Q

What are fibrin degradation products measured by?

A

D-diner

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46
Q

What three phases does the coagulation cascade consist of?

A
  1. Initiation: (tissue factor is expressed)
  2. Amplification: (platelets and cofactors lay groundwork for large scale production)
  3. Propagation: (large quantities of thrombin are produced)
47
Q

What type of feedback mechanism does the coagulation cascade express?

A

Positive!

48
Q

What is the BEST predictor of bleeding during surgery?

A

History and physical

49
Q

What does the PTT measure?

A

Value: 30ish seconds
Measures: Intrinsic and common pathway

Unfractionated heparin

50
Q

What does PT measure?

A

Value: 13ish
Measures: extrinsic pathway and final
Med: warfarin

51
Q

What is INR?

A

Value: 1ish
Standardization if the PT. Patients PT/standard mean
Med: warfarin target ~ 2-3x control

52
Q

What is activated clotting time? (ACT)

A

Value: 90-120
Guides heparin dosing ~ should be measured before heparin, 3 mins after, and 30 mins following

> 400 for CPB

53
Q

What platelet count increases surgical bleeding risk? What count increases spontaneous bleeding?

A

< 50,000 surgical
< 20,000 for spontaneous

54
Q

What does bleeding time measure?

A

Platelet function
Value: 2-10 mins

55
Q

What does a D-Dimer measure?

A

Fibrinolysis (fibrin degradation products)
If Fibrinolysis is increased ~ likely a clot somewhere

Normal < 500

**think DDP ~ DIC, DVT, and PE

56
Q

What is a thromboelastogram? (TEG)

A

Real time visualization of disorders of coagulation and Fibrinolysis

57
Q

What is the R time in the TEG?

A

Time to begin clot formation
Think coagulation factors ~ FFP

58
Q

What is the K time on the TEG?

A

Time until clot has achieved strength
**think fibrinogen ~ cryo

59
Q

What is the alpha angle on the TEG?

A

Speed of fibrin accumulation
**fibrinogen ~ Cryo

60
Q

What is the maximum amplitude (MA) on the TEG?

A

Measures clot strength
**(platelets) ~ platelets and DDAVP

61
Q

What is the amplitude at minutes after maximum amplitude (A60)

A

Determines Fibrinolysis
**excessive Fibrinolysis ~ TXA/Amicar

62
Q

What does heparin inhibit?

A

***Intrinsic and final common pathways

Binds antithrombin and accelerates it’s ability.

63
Q

Is heparin positively or negatively charge?

A

Negative!!

64
Q

Does heparin cross the placenta?

A

No! It’s large and is SAFE during pregnancy

65
Q

What is the standard dosing for heparin in cardiac surgery patients?

A

Cardiac surgery: 300-400 U/kg
VTE prophylaxis: 5,000 U SC
Active VTE: 5,000 U IV ~ 1250 U/hr
Acute MI: 5,000 IV ~ 100U/hr

66
Q

What is protamine derived from?

A

Salmon sperm

67
Q

What charge does protamine have?

A

Protamine is POSITIVE

68
Q

What is the dose of protamine?

A

1 unit of protamine for every 100 units of heparin

69
Q

What are the 3 main side effects of protamine?

A

Hypotension (histamine release)
Pulmonary HTN: (TxA2 and serotonin release)
Allergic reaction: previous sensitization to NPH, vasectomy and/or fish allergy

70
Q

What total factors does Warfarin inhibit?

A

1972 ** and C and S

71
Q

What are antidotes to vitamin K?

A

FFP and vitamin K

(In an emergency ~ warfarin should be reversed with FFP, factor 7a or prothrombin complex)

72
Q

What can impair fat absorption and the production of vitamin K?

A

Malabsorptive disorders and decreased bile production

73
Q

What are some risk factors for vitamin K deficiency?

A

Poor diet
Abx therapy (requires bacteria to manufacture)
Malabsorption
Hepatocellular dx
Neonates must receive vitamin K IM (no bacteria yet)

74
Q

What is the risk associated with IV phytonadione (vitamin K)?

A

Life threatening anaphylaxis

75
Q

What is clopidogrel?

A

ADP receptor antagonist

76
Q

What is abciximab?

A

GpIIb/IIIa receptor antagonist

77
Q

What is warfarin?

A

Vitamin K antagonist

78
Q

What is Enoxaparin?

A

Antithrombin cofactor

79
Q

What are the ADP receptors inhibitors? How long should you hold?

A

Ass: “girls/grel don’t like it is in the ass”
Dick: only wait 7ish days for a dick apt, except for ticlopidine
Pussy: Plavix (clopidogrel) is the main one

80
Q

What are the GpIIb/IIIa receptor antagonists?

A

“Fib and fab(mab) hit the G[pll]b”

Abciximab (3 days)
Eptifibatide (1 day)
Tirofiban (1 day)

81
Q

What are the COX inhibitors (non specific)?

A

ASA (7 days)
NSAIDS (1-2 days)

82
Q

What are the COX 2 inhibitors?

A

Rofecoxib (none)
Celecoxib (none)

83
Q

What are the anticoagulants? (Heparins) how long should you hold?

A

Unfractionated: 6 hours
Low molecular heparin (parin): 1-2 days

84
Q

What are the anticoagulants? (Thrombin inhibitors) how long should you hold?

A

Argatroban (4-6 hours)
Bivalirudin (2-3 hrs)

85
Q

What is the factor for factor 10 inhibitors?

A

Fondaparinux (4 days)

86
Q

What are the factors for the vitamin K anticoagulants?

A

Warfarin (hold for 3 days)

87
Q

Which medication inhibits protein C and plasmin?

A

Aprotinin

88
Q

Which medication stimulates factor 8 and vWF release?

A

DDAVP

89
Q

What are the three types of von Willebrand?

A

Type 1: mild ~ reduction in the amount
Type 2: vWF doesn’t work well
Type 3: severe reduction in the amount

90
Q

Which type of vWF is DDAVP good for?

A

TYPE 1

91
Q

What two factors does vWF affect?

A

Bleeding time (affect platelets)
And PTT (affects the intrinsic pathway because of factor 8)

92
Q

What is the dose of Desopressin?

A

0.3 mcg/kg IV

93
Q

Which two blood products can be used for all three type of vWF?

A

FFP and cryo

94
Q

What is the first line agent for a patient with type 3 vWF?

A

Purified 8-vWF

95
Q

Which lab value is prolonged with Hemophilia A and hemophilia B?

A

PTT ( hemophilia a ~ deficient factor 8 and hemophilia B ~ deficient factor 9 are part of the INTRINSIC pathway)

96
Q

What is considered the “last ditch” treatment for bleeding without an identifiable cause?

A

Recombinant Factor 7

97
Q

What is DIC?

A

Disseminated Intravascular Coagulation ~ disorganized clotting and Fibrinolysis

98
Q

How are lab values affected in DIC?

A

Increased PT/PTT
Increased D-Dimer
Decreased fibrinogen
Decreased platelets

99
Q

What are some signs of DIC?

A

Ecchymosis
Petechiae
Mucosal bleeding
Bleeding at IV sites

100
Q

What are the 3 type of patients at HIGHEST risk for DIC?

A

Sepsis ~ highest (gram negative)
Obstetric ~ preeclampsia, placental abrupt
Malignancy: leukemia, lymphoma

101
Q

What is the definite treatment for DIC?

A

Reversing the underline cause

Otherwise treatment is supportive!
IV fluids, FFP, platelets, cryo, IV heparin

102
Q

What is contraindicated in a patient with type 2 HIT? What should he used instead?

A

Heparin is contraindicated

Bivirudin is a direct thrombin inhibitor

103
Q

What are some traits of HIT type 1?

A

Heparin induced platelet aggregation
Occurs with LARGE heparin dose
1-4 days after administration
Platelets < 100,000
Morbidity: min
Tx: resolves spontaneously

104
Q

What are some traits of Type 2 HIT?

A

If you get hit twice, it’s BAD

Anti platelet antibodies ~ form immune complexes

Occurs after ANY heparin dose

Platelets < 50,000

Hypercoagulable state causes high risk of death or amputation

Heparin MUST be discontinued.

105
Q

What is factor 5 Leiden mutation?

A

Causes a resistance to the anticoagulant effect of protein C

Lifelong anticoagulation is unwarranted

106
Q

What four factors are inhibited by antithrombin?

A

9, 10, 11, 12

107
Q

What is sickle cell disease?

A

Inherited disorder that affects erythrocytes

108
Q

In sickle cell dx, what is substitution in the RBC?

A

Valine is substituted for glutamic acid (that is what is on the beta chain in sickle cells)
**this happens on the BETA chain

Ultimately alters RBC geometry

109
Q

What are the triggers to avoid in sickle cell crisis?

A

Pain
Hypothermia
Hypoxemia
Acidosis
Dehydration

110
Q

What are the main complications of sickle cell?

A

Vaso-occlusive: impaired tissue perfusion > ischemic injury (most common)

Acute chest: thrombosis, embolism and infection > common in kids > new lung infiltrates and AT LEAST ONE [cough, cp, Dyspnea, wheezing]

Sequestration crisis: spleen removes RBCs faster than bone marrow produces >anemia

Aplastic crisis: bone marrow suppression > anemia (usually with viral infections)

111
Q

What resp disorder occurring in 50% of sickle cell patients?

A

Asthma

112
Q

What is sickle cell trait?

A

Heterozygous sickle cell disease

DO NOT advance to crisis unless hypoxic!!!

113
Q

For the ABO system, what is O traits?

A

RBC antigen: O
Plasma antibodies: anti-B; Anti-A
Compatibility: O

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