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Mar: Sem 2 - Health Assessment > Coagulation (final) > Flashcards

Coagulation (final) Flashcards

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1
Q

Describe Hemostasis

A

Normal hemostasis is a balance btw clot generation, thrombus formation, andcounter-regulatory mechanisms that inhibit uncontrolled thrombogenesis or premature thrombus degradation

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2
Q

3 Goals of Hemostasis

A

to limit blood loss from vascular injury
maintain intravascular blood flow
promote revascularization after thrombosis

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3
Q

What are the 2 stages of Hemostasis?
Describe each…

A

Primary: Immediateplatelet deposition at the endovascular injury site
Leads to the initial platelet plug formation
Only adequate for minor injury
Secondary: clotting factors activated
Stabilized clot formed and secured with crosslinked fibrin

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4
Q

What is the Vascular Endothelial Role?

A

Vascular endothelial cells have antiplatelet, anticoagulant, and profibrinolytic effects that inhibit clot formation

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5
Q

Describe the anti-clotting mechanisms of endothelial cells

A

-are negatively charged to repel platelets
-produce platelet inhibitors such as prostacyclin and nitric oxide
-excrete adenosine diphosphatase, which degrades -adenosine diphosphate (ADP), a platelet activator
-increase protein C, an anticoagulant
-produce Tissue Factor Pathway Inhibitor (TFPI), inhibiting factor Xa & TF-VIIa complex
-Synthesize tissue plasminogen activator (t-PA)

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6
Q

____ play a critical role in hemostasis and are derived from ____

A

Platelets and megakaryocytes

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7
Q

Nonactivated platelets circulate as ____ with a lifespan of ____

A

discoid anuclear cells and 8-12 days

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8
Q

normally, ~ ____ of platelets are consumed to ____ with ____ new platelets formed daily

A

10%
support vascular integrity
1.2-1.5 X10^11

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9
Q

2 important things about the platelet membrane

A

1) contains numerous receptors
2) has a surface canicular system, which increases membrane surface area

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10
Q

Describe the process of platelets undrgoing hemostasis

A

Damage to endothelium exposes the underlying extracellular matrix (ECM), which contains collagen, von Willebrands factor, and other platelet-adhesive glycoproteins
Upon exposure to ECM, platelets undergo 3 phases of alteration:
-adhesion
-activation
-aggregation

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11
Q

Describe Adhesion of platelets

A

Adhesion: occurs upon exposure to ECM proteins

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12
Q

Describe activation of platelets
What are 2 types of storage granules in platelets?

A

Activation: stimulated when platelet interacts w/collagen & tissue factor (TF), causing the release of granular contents
Plts contain 2 types of storage granules: alpha granules and dense bodies
-Alpha granules: contain fibrinogen, factors V & VIII, vWF, Plt-derived growth factor & more
-Dense bodies: contain ADP, ATP, calcium, serotonin, histamine, epinephrine

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13
Q

Describe aggregation of platelets

A

Aggregation: occurs when the granular contents are released, which recruit and activate additional platelets, propagating plasma-mediated coagulation. Activated glycoprotein IIb/IIIa receptors on plt surface bind fibrinogen, promoting fibrin crosslinking

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14
Q

Each stage of the platelet cascade requires what?

A

Assembly of membrane-bound activation tenase-cmplexes

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15
Q

Each tenase complex is composed of

A

1) a substrate (inactive precursor)
2) an enzyme (activated coagulation factor)
3) 3) a cofactor (accelerator or catalyst)
4) 4) calcium

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16
Q

Describe the intrensic pathway

A

Beginning w/XIIa, it was initially thought to occur only in response to endovascular contact with negatively-charged substances (glass, dextran)

Current understanding is the intrinsic pathway plays a more minor role in theinitiation of hemostasis, and is more an amplification system to propagate thrombin generation initiated by the extrinsic pathway

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17
Q

Describe the extrensic pathway

A

The Extrinsic pathway is the initiation phase of plasma-mediated hemostasis
Begins endothelial injury, exposing TF to the plasma
TF forms an active complex with VIIa (TF/VIIa complex)
TF/VIIa complex binds to and activates factor X, converting it to Xa
TF/VIIa complex also activates IX→ IXa in the intrinsic pathway
IXaand calcium convert factor X to Xa (intrinsic pathway)
Factor Xa begins the final common pathway

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18
Q

Describe the intrinsic pathway hemostasis initiation

A

Upon contact with a negatively charged surface, factor XII becomes activated
Factor XIIa converts XI to XIa
(IXa + VIIIa +plt-membrane phospholipid + Ca++) converts factor X to Xa
Xa initiates the final common pathway

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19
Q

Describe intrinsic pathway propogation

A

Activated Thrombin (IIa) activates factors V, VII, VIII and XI to amplify extrinsic thrombin generation
This process activates the platelets, leading to propagation of the FCP(final common pathway)

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20
Q

Describe the common pathway

A

Factor X becomes Xa and binds with Va to form “prothrombinase complex”
Prothrombinase complex rapidly converts prothrombin (II) into thrombin (IIa)
Thrombin attaches to the platelets and converts fibrinogen (I) to fibrin (Ia)
Fibrin molecules crosslink to form a mesh that stabilizes the clot
Thrombin cleaves fibrinopeptides A & B from fibrinogen to generate fibrin monomers, which polymerize into fibrin strands to form basic clot
Finally, factor XIIIa crosslinks the fibrin strands to stabilize and make an insoluble clot, resistant to fibrinolytic degradation

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21
Q

Vascular injury exposes ____, initiating ____ pathway. ____ pathway further amplifies thrombin and fibrin generation. Platelets adhere to ____, become activated and ____ additional platelets

A

TF
extrensic
intrinsic
collagen
recruit

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22
Q

What is the key step to regulating hemostasis?

A

Thrombin generation

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23
Q

What does the common pathway depict?

A

Thrombin generation and firbin formation
*both intrinsic and extrinsic tenase-complexes facilitate the formation of the prothrominase complexes

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24
Q

What is the function of prothrombinase complex?

A

Converts PT (II) into thrombin (IIa)

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25
What are the 4 major Coagulation counter mechanisms?
Fibrinolysis tissue factor pathway inhibitor (TFPI) protein C system Serine Protease inhibitors (SERPINs) | Slide 19
26
Describe fibrinolysis
endovascular TPA & urokinase convert plasminogen to plasmin Plasmin breaks down clots enzymatically, and degrades factors V & VIII | Slide 19
27
Describe TFPI
forms complex w/Xa that inhibits TF/7a complex, along with Xa; Downregulating the extrinsic pathway | Slide 19
28
Describe the protein C system
inhibits factors 2 (II), 5a (Va) & 8a (VIIIa) | Slide 19
29
What are the SERPINs?
Antithrombin (AT) inhibits thrombin, factors 9a (IXa), 10a (Xa), 11a (XIa), 12a (XIIa) Heparin binds to AT, causing a conformational change that accelerates AT activity Heparin cofactor II inhibits thrombin alone | Slide 19
30
Preoperative assessment factors for coagulation
1) identify and correct hemostatic disorders 2) bleeding hx is more effective predictor of bleeding 3) inquire: frequent epistaxis, bleeding gums, easy bruising? 4) hx of excess bleeding with procedures or blood transfusion? 5) family hx 6) use of blood thinners (ASA, NSAID, Vit E, Ginko, Ginger, Garlic supp 7) coexisting disease (renal, liver, thyroid, bone marrow) | Slide 20
31
If a bleeding disorder is suspected in the preop assessment, what are the standard first-line labs?
PT, aPTT | Slide 20
32
Common bleeding disorders
Von Willebrand's Hemophilia Drug-induced bleeding Liver disease Chronic renal disease Disseminated Intravascular Coagulation Trauma-induced coagulopathy | Slide 21
33
What is the most common inherited bleeding disorder? What percent of the population is affected?
Von Willebrand's- effects 1% of the population | Slide 22
34
Describe the MOA of a deficiency in vWF
Deficiency in vWF, causing defective plt adhesion/aggregation vWF plays critical role in plt adhesion & prevents degradation of factor 8 (VIII) | Slide 22
35
In vWF, are routine labs helpful? how will labs look? Which tests are more beneficial?
No normal: platelets and PT, prolonged: aPTT d/t deficiency in factor 8 better tests: vWF level, vWF plt-binding activity, factor 8 level, plt function assay | Slide 22
36
What treatment is vWF responsive to?
DDAVP in mild cases (it increases vWF) | Slide 22
37
for patients with vWF, intraoperative bleeding may require administration of what?
vWF, and factor 8 concentrates | Slide 22
38
What are the 2 types of Hemophilia? is this inherited or not?
A: factor 8 (VIII) deficiency; occurs in 1 in 5,000 B: factor 9 (IX) deficiency; occurs in 1 in 30,000 2/3 of cases are inherited, 1/3 present as new mutation w/o family hx | Slide 23
39
How does hemophlia commonly present?
in childhood as spontaneous hemorrhage involving joints and muscles | Slide 23
40
Labs in hemophilia
Normal PT, plts, bleeding time PTT is prolonged | Slide 23
41
In patients with bleeding disorders, especially hemophilia, who should be consulted?
Hematology | Slide 23
42
What may be indicated pre-operatively for patients with hemophilia?
DDAVP and factors 8 and/or 9 | Slide 23
43
What is the most significant cause of intraoperative bleeding?
Anticoagulant medications Heparin Warfarin Direct Oral Anticoags (DOAC Beta lactam ABx Nitroprusside NTG NO SSRI | Slide 24
44
What are common supplements that increase the risk of bleeding?
Cayenne, Garlic, Ginger, Ginkgo Biloba, grapseed oil, st johns wart, Turmeric, Vitamin E Good Grief Girls, St. John's Grape's Turned Very Crimson | Slide 24
45
When should common herbal supplements be stopped prior to surgery?
| Slide 24
46
The ____ is the primary source of which factors?
* Liver * 1,2,5,7, 9, 10, 11, 12 (I, II, V, VII, IX, X, XI, XII) along with proteins C & S, and antithrombin | Slide 25
47
How can liver disease lead to hemostatic issues?
Impaired synthesis of coagulation factors Quantitative and qualitative platelet dysfunction Impaired clearance of clotting and fibrinolytic proteins | Slide 25
48
Lab findings in liver disease
-Prolonged PT and PTT ***lab values only reflect the lack of pro-coagulation factors, NOT accounting for concurrent lack of anti-coagulation factors TEG and ROTEM are valuable guidelines | Slide 25
49
Chronic liver patents often display a ________ ________ as well as ________ amount of ________ production What should we still consider with these patients?
rebalanced hemostasis, sufficient, thrmobin although rebalanced, they are very susceptible to disruption in coagulation | Slide 25
50
CKD patients have baseline ______ d/t what 2 things?
Anemia! -lack of erythropoietin -platelet dysfunction | Slide 26
51
what 2 things can shorten bleeding times in CKD?
dialysis and correction of anemia | Slide 26
52
Tx of platelet dysfunction includes
Cryoprecipitate (rich in vWF) DDAVP Conjugated estrogens given pre-operatively x 5 days  | Slide 26
53
What is DIC
Disseminated Intravascular Coagulation Pathological hemostatic response to TF/7a complex causing excessive activation of the extrinsic pathway, which overwhelms the anticoagulant mechanisms and generates intravascular thrombin Coagulation factors & platelets become depleted during widespread microvascular thrombotic activity, causing multi-organ dysfunction | Slide 27
54
DIC may be precipitated by
trauma, amniotic fluid embolus, malignancy, sepsis, or incompatible blood transfusion | slide 27
55
Lab findings in DIC
↓Plts, prolonged PT/PTT/Thrombin time,↑soluble fibrin & fibrin degradation products | Slide 27
56
How to manage DIC
correct underlying condition, administration of appropriate blood products | Slide 27
57
What is trauma induced coagulopathy?
Independent acute coagulopathy seen in trauma pts, which is thought to be related to activated protein C decreasing thrombin generation -Hypoperfusion: driving factor for protein C activation -The endethelial glycocalyx, which contains proteoglycans, degrades. Proteoglycan-shedding results in "auto-heparinization" Platelet dysfunction contributes to the increased bleeding | Slide 28
58
What is a common cuase of trauma-related death?
Uncontrolled hemorrhage | Slide 28
59
Why do coagulopathies occur?
acidosis, hypothermia, and/or hemodilution | Slide 28
60
What are the most common inherited prothrombotic diseases caused by?
A mutation in factor V or PT | Slide 27
61
___________ mutation leads to _____________ resistance. What popualtion is this present in?
Factor V Leiden mutation, activated protein C ***present in 5% caucasion population | Slide 29
62
___________ mutation causes _______ Concentration, leading to _____________
Prothrombin, increased PT, hypercoagulation | Slide 29
63
What is Thrombophilia? How does is manifest?
Inherited or acquired predisposition for thrombotic events Manifests as venous thrombosis Highly susceptible to Virchow's triad | Slide 29
64
What is Virchow's Triad?
Blood stasis, endothelial injury, hypercoagulability | Slide 29
65
what is anti-phospholipid syndrome? Characterized by?
autoimmune disorder w/antibodies against the phospholipid-binding proteins in the coagulation system. Characterized by recurrent thrombosis and pregnancy loss Often require life-long anticoagulants | Slide 30
66
What are other common prothrombotic states?
Oral contraceptives, pregnancy, immobility, infection, surgery & trauma greatly increase the risk of thrombosis in these populations | Slide 30
67
HIT is a mild to moderate ____ associated with ____
thrombocytopenia heparin | Slide 31
68
When does HIT occur?
5-14 days after heparin treatment | Slide 31
69
HIT results in a ____ count reduction as well as activation of the ____ platelets and potential thrombosis
platelet remaining | Slide 31
70
autoimmune-mediated response occurring in up to ____ pts receiving heparin
5% | Slide 31
71
If pt has received a prior heparin dose, thrombocytopenia or thrombosis may occur within ____ day of subsequent dose
1 | Slide 31
72
Which patients are at higher risk of HIT? What type of heparin carries a greater risk of HIT?
women, pts receiving high heparin doses such as w/CPB unfractionated | Slide 31
73
If HIT is suspected what needs to happen? What is contraindicated?
D/C heparin, convert to alternative anticoag Warfarin: contraindicated b/c it decreasse Protein C and S synthesis | Slide 31
74
How is HIT diagnosis confirmed?
HIT antibody testing
75
When are antibodies from HIT typically cleared from the circulation?
3 months | Slide 31
76
To find PT, ____ is mixed with ____ and the number of seconds is measured until a clot forms
Plasma and TF | Slide 32
77
What does PT assess? What does it reflect? What is it used to monitor?
Assesses integrity of extrinsic & common pathways.  Reflects deficiencies in factors 1, 2, 5, 7, 10 (II, V VII, X) Used to monitor vit K antagonists s/a Warfarin  --->(factors 2, 7 & 10  are vit K dependent) | Slide 32
78
aPTT measures seconds until clot forms after mixing ____ with ____, ____, and ____ of the intrinsic pathway
plasma phospholipid Ca activator | Slide 32
79
aPTT assesses what? which factors is it more sensitive to? aPTT is used to measure the effect of ____
Assesses integrity of intrinsic and common pathways More sensitive to deficiencies in factor 8 & 9 (VIII, IX) than others May be used to measure effect of Heparin | Slide 32
80
anti-factor Xa activity assay is also known as what? ____ is combined wth ____ and an ____ substrate that releases a colorimetric signal after factor ____ is cleaved
Factor Xa inhibition test plasma Xa artificial Xa | Slide 33
81
Anti-factor Xa activity assay provides functional assessment of ____'s anticoagulant effect can also be used to assess effect of ____, ____, and factor ____ inhibitors
Heparin's LMWH, fondaparinux, factor Xa | Slide 33
82
Platelet count is a standard component of ____ testing Normal plt count? Is POC testing available?
coagulation greater than 100,000plts/microliter yes | Slide 33
83
Activated clotting time: variation of ____ blood clotting time, with the additiona of ____ activator to accelerate clotting time
whole clotting | Slide 33
84
ACT addresses which pathway? What is it used to measure? what is normal? IS POC analyzation available?
both intrinsic and extrensic responsiveness to heparin 107 +/- 13 seconds Yes | Slide 33
85
Heparin Concentration Measurement: ____-concentration is the most popular POC method to determine perioperative heparin concentration
Protamine | Slide 34
86
With heparin concentration measurement: 1mg protamine will inhibit ____ heparin as increasing amounts of protamine are added to heparinezed blood, time to clot ____ until protamine concentration>heparin concentration it estimates plasma ____concentration
1mg decreases heparin | Slide 34
87
____ Coagulation Tests: Measures all aspects of clot formation from early fibrin generation to clot retraction & fibrinolysis. Coagulation diagrams generated.
Viscoelastic | Slide 34
88
Viscoelastic Coagulation Tests: allows for more precise ____ ____ administration Examples: ____ and ____
blood product TEG (thromboelastogram) ROTEM (rotational thromboelastrometry) | Slide 34
89
Picture of a TEG
| Slide 35
90
____ Inhibit platelet aggregation and/or adhesion What are the 3 main classes?
Anti-platelet agents cyclooxygenase inhibitors P2Y12 receptor antagonists platelet GIIb/IIIa R antagonists | Slide 36
91
Cyclooxygenase Inhibitors: Block ____ from forming ____, which is important in plt aggregation what are 2 examples and how long do their anti-plt effects last?
cox1 TxA₂ ASA, 7-10 days after d/c NSAID's 3 days | Slide 36
92
P2Y12 receptor antagonists: Inhibit ____→preventing ____ expression What are 3 ex's and how long do their anti-plt affects last?
P2Y12-R GIIb/IIIa clopidogrel: 7days after d/c ticlodipine: 14-21 days after d/c ticagerelor & cangrelor <24h activity | Slide 36
93
Platelet GIIb/IIIa R antagonists: prevent ____ & ____ from binding to GIIb/IIIa-R Examples?
vWF Fibrinogen Abciximab, Eptifibatide, Tirofiban | Slide 36
94
Vitamin K antagonists: Inhibit synthesis of Vit-K dependent factors...which are?
2, 7, 9, 10, Protein C & S | Slide 37
95
What is the most common vitamin K antagonist? its the DOC for ____ and ____ It has a long half life of ____, can take ____ days to reach therapeutic INR of ____ usually requires ____ until therapeutic effect achieved Frequent lab monitoring required such as ____ and ____ Reversable with ____
warfarin afib and valve replacements 40h, 3-4d 2-3 heparin PT and INR vitamin K | Slide 37
96
Heparin: Binds to antithrombin→ ____ inhibits soluble thrombin and Xa What are 3 examples?
directly unfractionated heparin LMWH Fondaparinux | Slide 38
97
Unfractionated Heparin ____ HL, given IV Fully reversable w/____ Close monitoring required
short protamine | Slide 38
98
LMWH  ____HL, dosed BID SQ No coag testing needed Protamine only ____ effective
Longer partially | Slide 38
99
Fondaparinux Much ____ HL ( ____-____hrs), dosed once/day Protamine ____ effective
Longer (17-21hrs) not | Slide 38
100
direct ____ inhibitors: bind/block ____ in both soluble and fibrin-bound states What are some examples?
thrombin, thrombin (hehe) hirudin, argatroban, bivalirudin, and dabigatran (pradaxa) | Slide 39
101
Hirudin is naturally found in ____
Leeches | Slide 39
102
Argatroban: synthetic, reversibly binds to thrombin. HL 45 min. Monitored intraop w/____ or ____
PTT or ACT | Slide 39
103
____ is a synthetic direct thrombin inhibitor with the shortest HL of DTI's It is the DOC for ____ impairment
Bivalirudin renal or liver | Slide 39
104
Dabigatran is the ____ DOAC It is approved for ____ prevention and non-valvular ____
1st CVA and afib | Slide 39
105
What is DOAC
Direct Oral Anti-coagulants | Slide 40
106
DOAC's are a newer class introduced over the last ____ years have ____ pharmacokinetics/dynamics ____ drug interactions dosed ____ w/o lab monitoring efficacy is similar to ____ but much shorter ____ fewer ____ events, ____, and lower mortality than warfarin
10 predictable fewer daily warfarin, half life embolic events, intracranial hemorrhage | Slide 40
107
Direct thrombin inhibitor that is a DOAC: ____ Direct Xa inhibitors that is a DOAC: ____, ____, and ____
Dabigatran (Pradaxa) Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa) | Slide 40
108
thrombolytics are used to ____ blood clots can be given ____ or directly into ____ most are ____ ____ that convert plasminogen to plasmin, which breaks down fibrinogen to fibrin
dissolve IV, site of blockage serine proteases | Slide 41
109
What are 2 categories or thrombolytics? examples of each?
Fibrin-Specific: Alteplase (tPA), Reteplase, Tenecteplase Non-Fibrin-Specific: Streptokinase * not widely used d/t allergic reactions | Slide 41
110
Surgery is contraindicated within ____ days of thrombolytic treatment
10 | Slide 41
111
Absolute and relative contraindications for thrombolytics
| Slide 42
112
procoagulants are used to ____ blood loss What are the 2 classes?
mitigates anti-fibrinolytics factor replacements | Slide 43
113
antifibrinolytics have 2 subclasses: ____ and ____
Lysine analogues SERPIN | Slide 43
114
Lysin analogues: ____ and ____ MOA?
Epsilon-amino-caproic acid (EACA) & Tranexamic Acid (TXA) Binds & inhibits plasminogen from binding to fibrin→impairing fibrinolysis | Slide 43
115
What are the factor replacements (4)? and how does each one work?
Recombinant VIIa (RfVIIa): ↑’s thrombin generation via intrinsic & extrinsic paths Prothrombin Complex Concentrate (PCC): contain vitamin-K factors Fibrinogen Concentrate: derived from pooled plasma. Standard concentration. Cryoprecipitate & FFP: Cheaper & contain more coag factors, but less specific composition Remember:Factor Replacements R Put Forth Carefully | Slide 43
116
pre-op guidelines: warfarin low risk patients should d/c ____ prior to surgery and restart ____ post-op high risk patients should stop ____ prior and bridge w/ ____ or ____
5d, 12-24hrs post op 5d, UFH or LMWH | Slide 44
117
Pre-op guidelines: heparin UFH dc ____ prior to surgery and resumed ( ____ ) greater than or equal to 12 hours post op LMWH should be dc'd ____hr prior to surgery and resumed ____ postop
4-6hr, no bolus 24hrs prior, 24h postop | Slide 44
118
Pre-op guidelines: ASA (not as defined) mod/high risk: ____ low risk: stop ____ prior to surgery
continue 7-10d | Slide 44
119
pts post-coronary stent placement bare-metal stents--> delay elective surgery ____ after placement drug-eluding stents--> delay active surgery ____ after placement
6 weeks 6 months | Slide 44
120
Neuraxial anesthesia on anti-coags
| Slide 45
121
warfarin reversal may be required for excessive ____ or ____ what is the DOC for emergent coumadin reversal (even though HL is short)? Concurrent ____ required to restore carboxylation of vit-k dep factors by the liver for more sustained correction
bleeding, emergent surgery PCC: prothrombin complex concentrates vit k | Slide 46
122
What is the reversal for direct thrombin inhibitors? Half life is ____
no reversal half life is relatively short | Slide 46
123
We just said direct thrombin inhibitors do not have a reversal, but there is 1 exception! which drug has a reversal and what is the reversal?
dabigatran (pradaxa)-->antidote: idarucizumab | Slide 46
124
DOAC factor Xa inhibitors may be reversed by ____ which is a derivative of Xa
Andexanet | Slide 46
125
Which labs are required to monitor for each drug and possible reversal for each | Pic
| Slide 47
126
What are the names of each Factor?
I: fibrinogen II: prothrombin III: tissue thromboplastin (tissue factor, TF) IV: Ca ions V: labile factor VII: stabile factor VIII: antihemophillic factor IX: plasma thromboplastin component X: stewart prower factor XI: plasma thromboplastin antecedent XII: hageman factor XIII: fibrin stabilizing factor | Slide 10

Mar: Sem 2 - Health Assessment (32 decks)

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