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Health Assessment > Coags > Flashcards

Coags Flashcards

1
Q

what is normal hemostasis

A

a balance between clot generation, thrombus formation, and counter-regulatory mechanisms that inhibit uncontrolled thrombogenesis or premature thrombus degradation

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2
Q

what are the 3 goals of hemostasis

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

what are the 2 stages of hemostasis

A

primary hemostasis and secondary hemostasis

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4
Q

what is primary hemostasis

A

immediate platelet deposition at hte endovascualr injury site
* leads to the intial platelet plug

only adequate for minor injury

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5
Q

what is secondary hemostasis

A

clotting actors activated
stabilized clot formed and secured with crosslinked fibrin

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6
Q

what is a characteristic of vascular endothelial cells

A

they have antiplatelet, anticoagulant, and profibrinolytic effects that inhibit clot formation

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7
Q

anti-clotting mechanisms of the endothelial cell

is the enothelial cell negative or positively charged

A

negatively charged to repel platelets

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8
Q

anti-clotting mechanisms of the endothelial cell

what is produced by the endothelial cell

A

prodcue platelet inhibtors such as prostacylin and nitric oxide

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9
Q

what is released by vascular endothelial cells and what does it do

A

excrete adenosine diposphotase, which degreades adenosine diphosphate (ADP) a platelet activator

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10
Q

what anticoagulant is increased through the endothelial cells

A

increase protein C, an anticoagulant,

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11
Q

the endothelial cell produces tissue factor pathway inhibitor (TFPI) which inhibits what

A

factor Xa and TF-VIIa complex

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12
Q

what is synthesized by the endothelial cells

A

tissue plasminogen activator (t-PA)

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13
Q

platelets play a critical role in hemostasis, where are they derived from

A

bone- marrow megakarocytes

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14
Q

what is the lifespan of non-activated platelets

A

nonactivated platelets circulate as discoid anuclear cells with a lifespan of 8 to 12 years

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15
Q

approximately 10% of platelets are consumeed to support vascular integrity how many platelets are formed daily

A

1.2-1.5 x 10^11 formed daily

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16
Q

damage to the endothelium exposed the underlying

A

extracellular matrix (ECM)

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17
Q

the extracellular matrix contains

A

collagen, vWF, and other platelet adhesive glycoproteins

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18
Q

upon exposure to ECM platelets undergo what 3 phases of alteration

bonus: what stage of hemostasis is this

A

adhesion, activation, aggregation

primary heomstasis
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19
Q

when does adhesion occur

A

when exposed to ECM proteins

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20
Q

activation of platelets happens when the platelets are stimulated and interacts with

A

collagen and tissue factor (TF) causing the release of granular contents

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21
Q

platelets contain 2 type of storage granules what are they

A

alpha granules and dense bodies

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22
Q

alpha granules contain what

A

fibrinogen, factors V and VIII, vWF, plt-derived growth factor and more

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23
Q

what do the dense bodies contain

A

ADP, ATP, calcium, serotonin, histmaine, and epinphrine

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24
Q

aggregation occurs when

A

the granular contents are released, which recruits and activates additional platelets, propagating plasma-mediated coagulation

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25
Q

activated glycoprotein 2B/3A on the platelet surface bind what

A

fibrinogen, promoting fibrin crosslinking

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26
Q

each stage of the cascade requires assembly of the membrane activation tenase complexes
what is each complex composed of

A

a substrate (inactive precursor)
an ezyme (activated coagulation factor)
a cofactor (accelerator or catalyst)
calcium

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27
Q

Clotting Factors

Factor I is also called

A

fibrinogen

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28
Q
A
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29
Q

Factor II is also called

A

prothrombin

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30
Q

Factor III is also called

A

tissue thomboplastin

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31
Q

Factor IV is also called

A

calcium ions

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32
Q

Factor V is also called

A

labile factor

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33
Q

Factor VII is also called

A

stable factor

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34
Q

Factor VIII is also called

A

antihemophilic factor

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35
Q

Factor IX is also called

A

christmas factor, plasma thomboplastic component (PTC)

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36
Q

Factor X is also called

A

stuart-prower factor

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37
Q

Factor XI is also called

A

plasma thromboplastin antecedent (PTA)

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38
Q

Factor XII is also called

A

hageman factor

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39
Q

Factor XIII is also called

A

fibrin stabilizing factor

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40
Q

extrinisc pathway is the intiation of

A

plasma mediated hemostasis

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41
Q

what begins the extrinsic pathway

A

endothelial injury, exposing TF to plasma

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42
Q

what is the extrinisc pathway

A

TF forms an active complex VIIa (TF/VIIa complex)
TF/VIIa complex binds to and activates factor X converting it to Xa
TF/VIIa complex also activates IX to IXa in the the intrinsic pathway

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43
Q

what is needed to convert Factor X to Xa

A

IXa and calcium

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44
Q

what begins the final common pathway

A

factor Xa

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45
Q

what begins the intrinsic pathway

A

XIIa

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46
Q

most thrombotic events follow ______ pathway; however lab-coag studies rely on ____ pathway to activate the cascade

A

extrinsic ; intrinsic

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47
Q

the intrinsic pathway plays a ____ role in the initiation of hemostasis, and is more an ______ _______ system to progoate thombin generation intiated by the extrinisic pathway

A

minor; amplification system

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48
Q
A
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49
Q

upon contact with a ______ charged surface, factor ______ is activated

A

negatively charged ; factor XII

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50
Q

factor XIIa converts

A

XI to XIa

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51
Q

what converts factor X to Xa

A

XIa + VIIIa + platelet membrane phospholipid + Calcium

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52
Q

activated thrombin IIa activates which factors to amplify extrinisc thombin generation

A

V, VIII, XII

this process activates platelets leading to the propogation of the FCP

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53
Q

Factor X becomes Xa and binds with what to form prothrombinase complex

A

Va

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54
Q

p

prothrombinase complex rapidly converts

A

prothrombin (II) into thrombin (IIa)

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55
Q

thrombin attaches to platelets and converts

A

fibrinogen (I) to fibrin (Ia)

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56
Q

fibrin molecules _____ to form a mesh that stabilizes the clot

A

crosslink

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57
Q

whats happening

A

Vascular injury exposes TF, initiating extrinsic pathway. Intrinsic pathway further amplifies thrombin & fibrin generation. Platelets adhere to collagen, become activated, and recruit additional platelets.

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58
Q

thrombin cleaves fibrinopeptides A & B from fibringogen to generate fibrin monomers, which does what

A

polymerize into fibrin strands to form basic clot

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59
Q

what factor cross links the fibrin strands to stabilize and make the clot insoluble, resitant to fibrinolytic degradation

A

XIIIa

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60
Q

T/F only the intrinsic tenase complex factilitates the fromation of prothrominase complexes

A

false both intrinsic and extrinsic tenase complexes factilitate the formation of prothrombinase complexes

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61
Q

fibrinolysis

A

endocvascular TPA and urokinase
convert plasminogen to plasmin

62
Q

what does plasmin break down clots ____, and degrades which factors

A

ezymatically; degrading Factors V and VIII

63
Q

TFPI forms complex with which factor and inhibits what

A

forms complex with Xa that inhibits TF/7a complex, along with Xa

downregulating the extrinisic pathway

64
Q

protein C system inhibits which factors

A

Factor II, Va, VIIIa

65
Q

serine protease inhibitors (SERPINs)

A

AT3- inhibits thrombin, Factors 9a, 10a, 11a, 12a
heparin - binds to AT causing a conformational change that accelerates AT
Heparin Co-factor II - inhibits thombin alone

66
Q

if you suspect bleeding disorder preop what are the first line lab

A

PT, aPTT

67
Q

what Rx meds/ herbal supplements increase bleeding risk

A

ASA, NSAIDs, Vitamin E, Ginko, Ginger, Garlic supplements

68
Q

what coexisting disease are at risk for bleeding

A

renal, liver, thryoid, and bone marrow disorders

69
Q

list the common bleeding disorders (7)

A

Von Willebrand’s
Hemophilia
Drug-induced bleeding
Liver disease
Chronic renal disease
Disseminated Intravascular Coagulation
Trauma-induced coagulopathy

70
Q

1.

von Willebrand’s Disease

A

deficiency in vWF, causing defective platelet adhesion/aggregation

71
Q

vWF plats a critical role in

A

platelet adhesion and prevents degradation of factor VIII (8)

72
Q

why might routine coagulation labs not be helpful with von willebrand’s disease? what would be a better test to order

A

platelets and PT will be normal
aPTT may be prolonged depending on level of factor 8
better test: vWF level, vWF platelet bidning activity, Factor 8 level, platelet function assay

73
Q

mild vWD often responsive to

A

DDAVP which increases vWF

intraop bleeding may require administration of Factor 8/vWF concentrates

74
Q

difference between Hemophilia A and Hemophilia B

A

A- factor 8 deficiency
B- factor 9 deficiency

2/3 genetically inherited; 1/3 new mutation without family hx

75
Q

when does hemophilia present itself

A

in childhood as spontanoeus hemorrahe involving joints and muscles

76
Q

labs of hemophiliac

A

normal PT, plts, bleeding time
PTT normally prolonged

77
Q

Preop considerations in hemophilia

A

hematologist preop
DDAVP, Factor 8 and/or 9 may be indicated before surgey

78
Q

drug induced bleeding

A

Heparin
Warfarin
Direct Oral Anticoags (DOACs)
Beta-Lactam Abx
Nitroprusside
NTG
NO
SSRIs

79
Q

the liver is the primary source of which factors

A

5,7,9,10,11,12 as well as protein C & S, and antithombin

80
Q

liver disease leads to complex, multifactorial hemostatic issues such as

A

impaired synthesis of coagulation factors
quantitiative and qualitivat platelet dysfunction
impaired clearance of clotting and fibrinolytic proteins

81
Q

coags of pt with liver disease

A

prolonged PT and possible prolonged PTT

TEG & ROTEM are valuable guides

82
Q

CKD have a baseline anemia due to

A

lack of erythopoietin
platelet dysfunction due to uremic environment

83
Q

what can shorten bleeding times in CKD patietns

A

dialysis and correction of anemia

84
Q

treatment of platelet dysfunction in CKD includes

A

cryo
DDAVP
conjugated estrogen (give preop x 5days)

85
Q

what is Disseminated Intravascular Coagulation

A

pathological hemostatic response to TF/7a complex causing excessive activation of the extrinisc pathway which overwhelms the anticoagulant mechanism and generates intravasculat thrombin

86
Q

T/F in DIC: Coagulation factors & platelets become depleted during widespread microvascular thrombotic activity, causing multi-organ dysfunction

A

true!

87
Q

what can precipitate DIC

A

trauma, amniotic fluid emobolus, malignancy, sepsis, or incompatible blood transfusion

88
Q

labs of DIC

A

decreased platelets, prolonged PT/PTT/ thrombin time, increased soluble fibirn and fibrin degradation products

89
Q

management of DIC

A

treat cause, give appropriate blood products

90
Q

what is trauma-induced coagulopathy

A

independent acute coagulopathy seen in trauma patietns; thought to be related to activated protein C decreasing thombin generation

91
Q

coagulopathies occur to what 3 things

A

acidosis, hypothermia, and/or hemodilution

92
Q

whats the common cause of trauma related death

A

uncontrolled hemorrhage

93
Q

in trauma induced coagulopathies what is the driving factor for protein C activation

A

hypoperfusion

94
Q

endothelial glycocalyx, which contains proteoglycans degrades resulting in

A

auto-heparinization

95
Q

most common prothrombotic states are caused by a mutation where

A

factor V or Prothrombin

96
Q

Factor V Leiden Mutation leads to

A

activated protein C resistance

97
Q

prothrombin mutation causes

A

increased PT concentration, leading to hypercoagulation

98
Q

thrombophilia

A

inherited or aquired prediposition for thrombotic events

generally manifests as venous thrombosis

highly susceptible to virchows triad

99
Q

antiphospholipid syndrome

A

autoimmune disorder with antibodies against the phospholipid binding proteins in the coag system
characterized by recurrent thrombosis and pregnancy loss
often require life long anticoags

100
Q

in patients with thrombotic state disorders what can increase the risk of thrombosis in these patients

A

oral contraceptives, pregnancy, immobility, infection, surgery, trauma

101
Q

what is HIT (heparin-induced thrombocytopenia) and when does it occur after initiating heparin therapy

A

mild-moderate thrombocytopenia associated with heparin
occurs 5-14 days after heparin therapy

102
Q

HIT results in

A

platelet count reduction as well as activation of the remaining platelets and potential thrombosis

103
Q

risk factors for HIT

A

women, patietnt receiving high heparin doses such as with cardiopulmonary bypass

UFH greater risk than LMWH

104
Q

if HIT is suspected what should you do

A

DC heaprin convert to direct anticoagulant
wafarin CI bc it decreases protein C and protein S synthesis

105
Q

HIT is diagnosed with what
how long do the antibodies last in circualtion

A

diagnosed with HIT antibody test
antibodies cleared from circulation in 3 months

106
Q

PT assess integrity of extrinsic and common pathways and can reflect deficiences in what factors

A

1,2,5,7,10

used to monitor vitamin K antagonist warfarin (2,7,10 are v.K dependent)

107
Q

aPTT assess the integrity of intrinsic and common pathways and can reflect deficencies in which factors

A

Factor 8 and 9
may be used to measure effect of heparin

108
Q

which lab am I?
I measure the seconds until clot forms after mixing plasma w/phospholipid, Ca², and an activator of the intrinsic pathway

A

Activated Partial Thromboplastin Time (aPTT)

109
Q

What lab am I?
I measure the time until a clot forms after plasma is mixed w/TF

A

prothrombin time (PT)

110
Q

antifactor Xa activity assay provides assessment of which antiacoagulant effect

A

heparin’s anticoagulant effect
can also be used to assess effect of LMWH, fondaparinux, factor Xa inhbitors

111
Q

normal plt count

A

greater than 100K/microliter

112
Q

activated clotting time (ACT) measures which pathways?
what is the normal ACT value

A

addresses the intrinsic and common pathways
normal = 107 +/- 13 seconds

measures responsiveness to heparin

113
Q

1 mg of protamine will inhibit how much heparin (in mg)

increasing protamine will cause the clot time to decrease until protamine concentration > heparin concentration

A

1mg

114
Q

TEG :)

A

on the TXWes Reference Guide for alpha angle < 53 it has give cryo -/+ platelets

115
Q

3 main classes of antiplatelet drugs

A

Cyclooxygenase Inhibitors
P2Y12 receptor antagonists
Platelet GIIb/IIIa R antagonists

116
Q

moa of Cyclooxygenase Inhibitors

A

Block COX 1 from forming TxA₂, which is important in plt aggregation

ASA: anti-plt effects x 7-10 days after d/c
NSAIDS: anti-plt effect x 3 days

117
Q

P2Y12 receptor antagonists MOA

A

Inhibit P2Y12-R→preventing GIIb/IIIa expression
Clopidogrel: anti-plt effects x 7 days after d/c
Ticlopidine: anti-plt effects x 14-21 days after d/c
Ticagrelor & Cangrelor: Short-acting, <24h activity

118
Q

Platelet GIIb/IIIa receptor antagonists MOA

A

prevent vWF & fibrinogen from binding to GIIb/IIIa-R
Abciximab, Eptifibatide, Tirofiban

119
Q

anticoagulant drug

Vitamin K antagonist (wafarin)

A
  • inhibit synthesis of factors 2,7,9,10, protein C & S
  • DOC for valvular Afib & valve-replacements
  • Long half life (40h), can take 3-4 days to reach therapeutic INR (2-3)
  • Usually requires heparin until therapeutic effect achieved
  • Frequent lab monitoring required (PT/INR)
  • Reversable w/Vitamin K
120
Q

UFH

A

Short 1/2 life, given IV
Fully reversable w/Protamine
Close monitoring required

121
Q

1.

LMWH

A

Longer 1/2 life, dosed BID SQ
No coag testing needed
Protamine only partially effective

122
Q

Fondaparinux

A

Much longer HL (17-21h), dosed once/day
Protamine not effective

123
Q

direct thrombin inhibtors MOA

A

bind/block thrombin in both soluble and fibrin bound states

124
Q

direct thrombin inhibitors

A

Hirudin: naturally found in leeches
Argatroban: synthetic, reversibly binds to thrombin. HL 45 min.
Monitored intraop w/PTT or ACT
Bivalirudin: synthetic, shortest HL of DTI’s
DOC for renal or liver impairment
Dabigatran (Pradaxa): 1st DOAC
DTI approved for CVA prevention and non-valvular A-fib

125
Q

direct oral anticoagulants

A

Direct Thrombin Inhibitor-Dabigatran (Pradaxa)
**Direct Xa Inhibitors: **Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa)

Predictable PK/PD
Fewer drug interactions
Dosed daily w/o lab monitoring
Efficacy similar to Warfarin, but much shorter HL
Fewer embolic events, intracranial hemorrhages, and lower mortality than warfarin

126
Q

thrombolytics

A

used to dissolve blood clots
Most are Serine Proteases that convert plasminogen to plasmin, which breaks down fibrinogen to fibrin

127
Q

how long is surgery CI with use of thrombolytic therapy

A

10 days

128
Q

the 2 categories of thrombolytics are

A

Fibrin-Specific: Altepase (tPA), Reteplase, Tenecteplase
Non-Fibrin-Specific: Streptokinase * not widely used d/t allergic reactions

129
Q

absolute contraindications to thrombolytics (6)

A

vascular lesions
uncontrolled HTN (>185/>110)
recent cranial surgery or trauma
brain tumor
ischemic stroke <3 months prior
active bleeding

130
Q

relative contraindications to thrombolytics

A

ischemic stroke > 3 months
active peptic ulcer
current use of anticoagulant
pregnacy
prolonged/traumatic CPR < 3 weeks prior
major surgery < 3 weeks prior

131
Q

procoagulants are used to mitigate blood loss; which 2 classes are there

A

Antifibrinolytics:
Lysine analogues: Epsilon-amino-caproic acid (EACA) & Tranexamic Acid (TXA)
SERPIN: Aprotinin (removed from market d/t renal & cardio toxicity)
Factor Replacements
Recombinant VIIa (RfVIIa): ↑’s thrombin generation via intrinsic & extrinsic paths
Prothrombin Complex Concentrate (PCC): contain vitamin-K factors
Fibrinogen Concentrate: derived from pooled plasma.
Cryoprecipitate & FFP

132
Q

lysine analogues MOA

A

bind and inhibit plasminogen from binding to fibrin impairing fibrinolysis

133
Q

post coronary stent placement guidelines:

A

Bare-metal stents→ delay elective surgery 6 weeks after placement
Drug-eluding stents→ delay elective surgery 6 months after placement

134
Q

preop ASA guidelines

A

mod/high rx pts- current recommendation is to continue ASA
low rx pts- stop 7-10 days prior to surgery

135
Q

preop heparin guidelines

A

UFH should be d/c’d 4-6h prior to surgery & resumed (no bolus) ≥12h postop
LWMH should be d/c’d 24h prior to surgery & resumed 24h postop

136
Q

wafarin preop guidelines

A

**low rx pts **should d/c 5 days prior to surgery & restart 12-24h postop
high rx pts should stop 5 days prior & bridge w/UFH or LMWH

137
Q

neuraxial anesthesia and anticaogs

A

top 6 rows most common

138
Q

emergent reversal for wafarin

A

Prothrombin complex concntrates: DOC for emergent coumadin reversal (short 1/2 life)

concurrent Vitamin K required to restore carboxylation of Vitamin K dependent factors by the liver for more sustained correction

139
Q

emergent reversal of direct thrombin inhibitors

A

no reversal, however most direct thrombin inhibitors have a relativelt short half life

The DOAC Dabigatran (Pradaxa) does have an antidote –Idarucizumab

140
Q

Factor Xa inhibitors emergent reversal

A

Andexanet, a derivative of factor Xa

141
Q

anotha one..

A

know this one!

142
Q

how long should garlic be DC’d before surgery

A

7-10 days

143
Q

T/F st.johns wort will increase bleeding times

A

false, increased clotting risk

144
Q

what herbal supplements increased bleeding time (7)

A

cayenne
garlic
ginger
ginkgo bibloa
grapseed oil
tumeric
vitamin E

145
Q

heparin MOA

A

binds to antithrombin and directly inhibits soluble thrombin and Xa

146
Q

direct thrombin inhibitors

A

bind/block thrombin in both soluble and fibrin bound states

147
Q

NSAIDs/ASA neuraxial guidelines

A

no restrictions for catheter placement or removal

148
Q

BID Heparin SQ and neuraxial considerations

A

no restrictions for catheter placement or removal

149
Q

TID SQ Heparin and neuraxial anesthesia

A

at least 4 hours between last dose and catheter placement and removal
at least 2 hours after catheter placement and resuming drug, and removal of catheter and next dose

150
Q

Lovenox QD and neuraxial

A

Health Assessment (16 decks)

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