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Coags Flashcards

1
Q

Intima factors

A

endothelial layer
vwf
tissue factor
prostacyclin
no

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2
Q

media factors

A

subendothelial layer
collagen
fibronectin

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3
Q

Undamaged endothelium does not express

A

Tissue factor or collagen

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4
Q

Endothelial cells modulate hemostasis by synthesizing and secreting:

A

Procoagulants (initiators of coagulation)
Anticoagulants (inhibitors of coagulation)
Fibrinolytics (to dissolve the clot)

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5
Q

Endothelial cells release mediators….

A

Vasoconstrictors
Vasodilators- NO

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6
Q

von Willebrand factor (vWF) do what….

A

Adherence of platelets to the subendothelial layer

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7
Q

Tissue factor does what

A

Activates the clotting cascade pathway when injury to the vessel occurs

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8
Q

Some of these mediators control blood flow by vasoconstriction

A

thromboxane A2, adenosine diphosphate [ADP])

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9
Q

control blood flow by vasodilation

A

nitric oxide, prostacyclin

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10
Q

Coagulation factors function

A

Coagulation

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11
Q

Collagen function

A

Tensile strength

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12
Q

Fibronectin function

A

Mediates cell adhesion

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13
Q

Thrombomodulin function

A

Regulates anticoagulation pathway

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14
Q

Antithrombin III function

A

Degrades factors XII, XI, X, IX, II

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15
Q

Tissue pathway factor inhibitor function

A

Inhibits tissue factor

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16
Q

Plasminogen function

A

Converts to plasmin

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17
Q

tPA function

A

Activates plasmin

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18
Q

Urokinase function

A

Activates plasmin

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19
Q

Vasoconstiction mediators

A

serotonin, Thromboxane A2
adenosine diphosphate

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20
Q

Nitric Oxide function

A

Vasodilates, promotes smooth muscle relaxation

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21
Q

Prostacyclin function

A

Vasodilates, inhibits aggregation, promotes smooth muscle relaxation

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22
Q

media collagen function

A

A potent and important stimulus for platelet attachment to the injured vessel wall

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23
Q

media fibronectin function

A

Facilitates the anchoring of fibrin during the formation of a hemostatic plug

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24
Q

Adventitia Controls blood flow by ….

A

influencing the vessel’s degree of contraction

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25
Q

The endothelial cells produce ….

A

nitric oxide and prostacyclin, which influence the adventitia

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26
Q

Nitric oxide’s ability to influence and promote smooth-muscle relaxation results in …..

A

vascular vasodilation

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27
Q

Once the vessel vasodilates, the increase in blood flow limits the activity of procoagulant mediators by…..

A

simply washing the procoagulant mediators away

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28
Q

Nitric Oxide Synthesis occurs where and how

A

This metabolic reaction occurs within the endothelial lining

Under the influence of nitric oxide synthetase (NOS), L-arginine is converted to nitric oxide
NO -> activates soluble guanylate cyclase, subsequently producing a second messenger, cyclic guanosine monophosphate, that causes muscle relaxation

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29
Q

Eicosanoids refered to as

A

Collectively referred to as prostanoids or eicosanoids
Prostacyclin
Leukotriene
Thromboxane

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30
Q

Prostacyclin is a …..

A

lipid molecule produced in the endothelial cells from prostaglandin
A powerful vasodilator, prostacyclin also interferes with platelet formation and aggregation

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31
Q

smm eicosanoids factors

A

prostaglandins
PGE2
PGF2

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32
Q

4 Phases of Hemostasis and Coagulation

A

Vascular phase (Vascular spasm)

Primary hemostasis (Formation of platelet plug)

Secondary hemostasis (Coagulation and formation of fibrin)

Fibrinolysis (Lysis of clot)

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33
Q

Vascular Phase

A

spasm/constrict of smm done by endothelins -> fibroblasts

Vasoconstriction “may” slow down or stop bleeding
Localized in injured area

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34
Q

Primary Hemostasis

A

happens after spaces -> attract plat -> plat plug

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35
Q

Initiates the phases of platelet formation….

A

Adherence
Activation
Aggregation

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36
Q

Where are plat located in the bv

A

they tend to be pushed aside, strategically positioned near the vessel-wall surface where they can then “react” in the event of injury

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37
Q

plat formation , life span’ concentration

A

They are formed in the bone marrow from megakaryocytes
Maintain a concentration count of approximately 150,000 to 300,000/mm3
1-2 weeks lifespan

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38
Q

plat cleared by….

A

Cleared by macrophages in the reticuloendothelial system and the spleen
Spleen sequesters up to 1/3 of the circulating PLT for later us

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39
Q

Glycoproteins responsibility

A

Adheres to injured endothelium, collagen and fibribogen
GpIb sticks/attaches PLT to vWF
GpIIb-IIIa complex links activated PLT together to form a plug

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40
Q

Gp2b, 3a inhibitor mediations

A

ranexa, integrelin

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41
Q

Phospholipids responsibility

A

Substrates to prostaglandin synthesis
Produce thromboxane A2 which activates PLT

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42
Q

Actin and myosin
responsibility

A

Contraction to form the PLT plug

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43
Q

Thrombosthenin responsibiilty

A

PLT contraction

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44
Q

ADP responsiblity

A

PLT activation and aggregation

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45
Q

Calcium responsbility

A

Plays a role in the coagulation cascade

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46
Q

Fibrin-stabilizing factor
responsbility

A

Cross links fibrin

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47
Q

Serotonin responsibility

A

Activates nearby PLT

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48
Q

Growth factor responsiblity

A

Repairs damaged vessel walls

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49
Q

Adherence

A

vWF mobilizes from within the endothelial cells and emerges from the endothelial lining
Glycoprotein Ib (GpIb) receptors emerge from the surface of the platelet
The purpose of GpIb is to attach to vWF and attract platelets to the endothelial lining
vWF makes platelets “sticky” and allows them to adhere to the site of injury

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50
Q

Activation

A

tissue factor ->conformational transformation-> activated
Structure swells and becomes oval and irregular
From the platelet surface, two other major glycoproteins, IIb and IIIa, project themselves outward
The purpose of the GpIIb-IIIa receptor complex is to link other activated platelets together in an effort to form a primary platelet plug
When this action is complete, the platelets seal and heal the site of injury within the blood vessel

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51
Q

Aggregation

A

As platelets undergo this metamorphosis, they release the alpha and dense granules, the contractile granules, thrombin, and many important mediators into the blood in an effort to promote procoagulant activity
These mediators are responsible for platelet aggregation to form a primary unstable clot
When injury is minute and less threatening, this primary plug is enough to maintain hemostasis
When the injury is large, activation of the coagulation clotting cascade is required for permanent repair to create and stabilize a secondary clot to cease bleeding

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52
Q

fibrin production requires….

A

all the clotting factors

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53
Q

single most important protein involved in clotting

A

fibrin

54
Q

fibrin formation

A

A series of enzymatic reactions (clotting cascade) that ultimately activate prothrombin to thrombin, the enzyme that converts soluble fibrinogen to fibrin

55
Q

factor 1

A

fibrinogen
liver

not vitmain k depednednt

56
Q

factor 2

A

prothrombin

liver

vit K dependendt

57
Q

factor 3

A

name; Tissue Factor or Thrombo-plastin

Source; Vascular wall and extracellular membrane; released from injured cells

58
Q

factor 4

A

name; Calcium

source; diet

59
Q

factor 5

A

name; Proaccelerin
source; Liver

not vitamin K dependent

60
Q

factor 7 name and source

A

name; Proconvertin
source; Liver

vit K dependent

61
Q

factor 7 name and source

A

name; Proconvertin
source; Liver

vit K dependent

62
Q

factor 8 C name and source

A

name; Antihemo-
philiac factor

source; liver

not vit K dependent

63
Q

factor VIII:vWF name and source

A

name; vonWillibrand’s Factor

source; vascular endothelial cells

64
Q

factor 9 name and source

A

name; christmas factor
source; liver and other tissue

vit K dependent

65
Q

factor 10 name and source

A

name; Stuart-Prower Factor

source liver

vitmain K depedneent

66
Q

factor 11 name and source

A

name; Plasma thromboplastin antecedent

source; Liver

67
Q

factor 12 name and source

A

name; Hageman Factor
souce; liver

68
Q

factor 13 name and source

A

name; Fibrin Stabi-
lizing factor

source; liver

69
Q

Liver factors that are vitamin k dependent

A

2,7,9,10

70
Q

Warfarin works on what pathways

A

extrinsic

71
Q

Extrinsic Pathway

A

Tissue factor release from sub-endothelium during trauma. Tissue factor activates the extrinsic pathway
Factor X activation; Tissue factor activates factor 7; 7 activates 10 in the presence of factor 4 (calcium)
Prothrombin activator and platelet phospholipids activate factor 2 (thrombin); Factor 5 accelerates the positive feedback mechanism (increase production of prothrombin activator)

Clot forms within 12 to 15 seconds
For 37 cents, you can purchase the extrinsic pathway

72
Q

Intrinsic Pathway

A

Slower process

12,11,9,8-> collagen -> factor 12-> 11 (activated by stilmulation of kinogen and accellerated by prekalcerin) -> factor 9 activation-> factor 9a -> factor 10 ……..

73
Q

Common Pathway

A

Prothrombin activator changes prothrombin (II) to thrombin (IIa)
Prothrombin changes fibrinogen to fibrin in the presence of calcium
Fibrin is added to the aggregated platelet plug.
Activated fibrin-stabilizing factor (XIIIa) cross-links fibrin-fibers to complete the clot
Clot is formed. Stays in place until vascular tissue is repaired.

74
Q

When is fibrinolysis activated

A

When the clotting cascade is activated, so is the process of fibrinolysis.

75
Q

labs and meds for intrinsic pathway

A

hepatin, ptt, act

76
Q

extricnsic pathway meds and labs

A

coumadin, pt, inr

77
Q

mechanism for fibrinolysis

A

release of tissue plasminogen activator (tPA) by damaged endothelial cells

78
Q

urokinase function

A

urokinase is produced and released by the kidneys as a means of prevent small clots getting lodged in the kidney tissue

79
Q

fibrinogenic factors

A

Kallikrien and neutrophil elastase

These circulating activators will then convert plasminogen to plasmin, which then breaks down fibrin

80
Q

circulating activators that convert plaminogen to plasmin

A

TPA & UPA

plasmin breaks down fibrin to fibrin degradation products (split products)

81
Q

PLT values

A

150,000 to 300,000/mm3

82
Q

Bleeding time values

A

3-10 min

83
Q

PT values

A

12-14 sec

84
Q

aPTT values

A

25-35 sec

85
Q

TT (Thombin time) value

A

30 secs

86
Q

ACT (activated clotting time) values

A

80-150 secs

87
Q

Fibrinogen values

A

> 150 mg/dl

88
Q

Most common hereditary bleeding disorders

A

vWF Disorder

89
Q

Diagnosis vWF Disease

A

PT and aPTT = normal
BT is prolonged
Hematologist to analyze labs

90
Q

Treatment for vWF Dz

A

Correct the deficiency of vWF
Using desmopressin
By the transfusion of the specific factor
Cryoprecipitate

91
Q

how does DDAVP work

A

A synthetic analogue of vasopressin and stimulates the release of vWF by endothelial cells

92
Q

DDAVP dose

A

intravenously at a dose of 0.3 µg/kg in 50 mL of normal saline over 15 to 20 minutes

93
Q

DDAVP time effect

A

effect in 30 minutes and lasts from 6 to 8 hours

When do we give to to them; give it when get to OR or before in preop , consider redosing during sx.

94
Q

The side effects of DDAVP

A

Headache, stupor, hypotension, tachycardia, hyponatremia, and water intoxic

95
Q

In order to decrease water intoxication, hyponatremia, and consequent seizures, the administration of water, orally or intravenously, should be restricted ______ after the use of the drug

A

4-6 hrs

96
Q

Cryoprecipitate risk

A

In common preparation, the cryoprecipitate is not submitted to viral attenuation and, therefore, poses an increased risk of infection

97
Q

if pt unresponsive to ddavp w/ vWF use…..

A

Cryoprecipitate

98
Q

Cryoprecipitate raises the fibrinogen levrl by….

A

1 unit raises the fibrinogen levels by 50 mg/dL

99
Q

what is Factor VIII concentrate and when do we give it

A

Factor VIII concentrate is prepared from the pool of plasma from a large number of donors

It undergoes viral attenuation

Contains F VIII and vWF

Given preoperatively and during surgery

100
Q

Anesthesia Consideration for clotting disorders

A

General anesthesia- avoid epidurals

Arterial puncture is not recommended

avoid IM

101
Q

Patients with coagulopathies undergoing neuroaxial block results in…..

A

increased risk of developing a hematoma and compression of neurological structures

102
Q

how does heparin work

A

Heparin inhibits thrombin (thrombin needed to convert fibrinogen to fibrin)

Heparin derives its anticoagulant effect by activating antithrombin III

103
Q

labs to monitor heparin

A

PTT and ACT

104
Q

reversal for heparin

A

Heparin’s anticoagulant effect is rapidly reversible by protamine (+ polypeptide forming a stable complex neutralizing heparin)

105
Q

LMWH vs UFH

A

LMWHs -effective at VTE prophylaxis compared to UFH (more specific)

LMWHs have a more predictable pharmacokinetic response, fewer effects on platelet function, and a reduced risk for heparin-induced thrombocytopenia (HIT)

Monitoring of LMWHs is not performed routinely

106
Q

Coumadin works by….

A

Interferes with hepatic synthesis of vitamin K–dependent coagulation factors: factors II, VII, IX, X

107
Q

reversal for coumadin and how long does it take

A

Vitamin K reverses coumadin anticoagulation - takes 6-8 hours to correct

108
Q

coumadin more rapid reversal option….

A

More rapid reversal - prothrombin complex concentrates, recombinant factor VIIa and FFP

109
Q

Fibrinolytics act by ….

A

converting plasminogen to plasmin, which in turn cleaves fibrin, thereby causing clot dissolution

110
Q

common fibrinolytic

A

Tissue plasminogen activator (tPA), streptokinase (SK), and urokinase (UK)

111
Q

Anti-Fibrinolytics works by

A

inhibits the conversion of plasminogen to plasmin

112
Q

medications that are Anti-Fibrinolytics

A

Antifibrinolytic agents–tranexamic acid, ε–aminocaproic acid, and aprotinin

113
Q

what is Disseminated Intravascular Coagulopathy

A

Systemic activation of the coagulation system simultaneously leads to thrombus formation and exhaustion of platelets and coagulation factors

114
Q

underlying disorders may precipitate DIC

A

trauma, amniotic fluid embolus, malignancy, sepsis, or incompatible blood transfusions

115
Q

DIC expected labs

A

Reductions in PLT,
prolongation PT, PTT, and thrombin time (TT),
elevated concentrations of soluble fibrin degradation products

116
Q

tx for DIC

A

blood component transfusions to replete coagulation factors and platelets consumed in the process

treat the cause

117
Q

what is contraindicated in DIC

A

Antifibrinolytic therapy

118
Q

what is Factor V Leiden

A

Factor V is a protein for normal clotting

When enough fibrin has been made, a substance called activated protein C inactivates factor V, helping stop the clot from growing any larger than necessary
Factor V Leiden is an abnormal version of factor V that is resistant to the action of activated protein C
Activated protein C cannot easily stop factor V Leiden from making more fibrin

Mutations in genes for factor V (factor V Leiden)

119
Q

Factor V Leiden is associated with

A

an increased risk of developing an episode of DVT (with or without a PE)

120
Q

when is screening for Factor V leiden

A

pregnancy

121
Q

Tx factor V leidan

A

Because of high risks of DVT and PE, patients are on anticoagulants….. + being pregnant

Common anticoagulation options include warfarin, unfractionated heparin, and LMWH

122
Q

Factor 5 Levidan in preganncy

A

First presentation of DVT, repeated missed abortions, and recurrent late fetal losses

123
Q

what is Heparin-induced Thrombocytopenia

A

HIT describes an autoimmune-mediated drug reaction occurring in as many as 5% of patients after exposure to unfractionated heparin or (rare cases) LMWH

124
Q

hallmark of findings of HIT

A

The hallmark of findings is a decrease in PLT < 100,000
Thrombocytopenia occurring 5 -14 days after initial therapy

125
Q

Hit results in….

A

platelet activation and potential for venous and arterial thromboses

126
Q

Evidence suggests that HIT is mediated by …..

A

immune complexes (composed of IgG antibody, platelet factor 4 [PF4], and heparin)

127
Q

Patients developing HIT during heparin therapy experience substantially increased risk for …..

A

thrombosis (absolute risk 30%-75%).

128
Q

TX for HIT

A

D/C heparin STAT (i.e., including unfractionated heparin, heparin-bonded catheters, heparin flushes, LMWH)

Alternative non-heparin anticoagulation must be administered concurrently

129
Q

Heparin is usually substituted for….. in HIT

A

a direct thrombin inhibitor (i.e., bivalirudin, lepirudin, argatroban)

130
Q

What is a synthetic factor Xa inhibitor

A

Fondaparinaux - to treat VTE. Off labelled use

131
Q

Typically, PF4/heparin immune complexes clear from the circulation within….

A

3 months

132
Q

If possible, patients experiencing HIT should avoid……

A

avoid future exposure to unfractionated heparin

HA (15 decks)

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