Coags- ChatGPT's Version (Exam IV, Mordecai) COPY Flashcards
What are the goals of hemostasis?
Limit blood loss, maintain blood flow, promote vessel repair.
What are the 2 stages of hemostasis?
Primary: Platelet plug
Secondary: Clotting factor activation → fibrin clot
What roles do endothelial cells play in clot prevention?
Repel platelets (negative charge)
Release prostacyclin & nitric oxide
Degrade ADP
Produce TFPI & tPA
Activate Protein C
What are the 3 phases of platelet response to injury?
Adhesion
Activation
Aggregation
What do platelet alpha granules and dense bodies contain?
Alpha: Fibrinogen, vWF, factor V/VIII
Dense bodies: ADP, calcium, serotonin, histamine
What are the 4 components needed for clotting complexes?
Substrate (inactive factor)
Enzyme (active factor)
Cofactor
Calcium
What triggers the extrinsic pathway?
Tissue Factor (TF) is exposed to blood stream
TF + VIIa → activates X and IX.
What is the main purpose of the intrinsic pathway?
Amplification of thrombin generation (not initiation).
What activates the intrinsic pathway?
Contact with negatively charged surfaces, such as:
- Exposed collagen in a damaged vessel wall
- Glass, dextran, or kaolin in lab tests (like aPTT)
- Platelet phospholipid membranes during in vivo coagulation
→ XIIa → XIa → IXa + VIIIa → Xa
What happens in the common pathway?
Xa + Va = prothrombinase → converts prothrombin (II) to thrombin (IIa) → converts fibrinogen (I) to fibrin (Ia) → XIIIa crosslinks fibrin
What is the most important step in regulating hemostasis?
Thrombin generation
What are the 4 major anticoagulant systems?
Fibrinolysis: TPA/urokinase → plasmin → breaks down fibrin.
TFPI: Inhibits TF–VIIa and Xa (extrinsic pathway)
Protein C system: Inhibits factors IIa, Va, VIIIa (common pathway)
SERPINs: Antithrombin inhibits IIa, IXa, Xa, XIa, XIIa (enhanced by heparin).
How does heparin work?
Binds antithrombin → accelerates inhibition of thrombin and factor Xa.
What does PT measure?
Extrinsic + common pathways (factors I, II, V, VII, X); used for warfarin monitoring.
Especially sensitive to which 2 factors?
What does aPTT measure?
Intrinsic + common pathways, especially sensitive to factors VIII & IX; used for heparin monitoring.
What does the Anti-Xa assay measure?
Functional effect of heparin, LMWH, or Xa inhibitors.
What is the ACT used for?
Point-of-care test for heparin responsiveness; used intraoperatively.
What tests assess global clot function?
TEG and ROTEM (viscoelastic testing).
What is the most common inherited bleeding disorder?
Von Willebrand disease (vWF deficiency).
What labs are abnormal in vWD?
aPTT may be prolonged (due to low factor VIII), PT and platelet count are usually normal.
What is the first-line treatment for mild vWD?
DDAVP (desmopressin) → increases vWF release.
What factor is deficient in Hemophilia A?
Factor VIII.
What factor is deficient in Hemophilia B?
Factor IX.
What is normal?
What lab is prolonged in hemophilia?
aPTT is prolonged; PT and platelet count are normal.
What are treatments for hemophilia?
Factor replacement, DDAVP (for mild A), and hematology consult pre-op.
7 of them
What are the most common medications that increase bleeding risk?
Heparin, warfarin, DOACs, beta-lactam antibiotics, SSRIs, NTG, nitroprusside.
Why must CRNAs understand anticoagulants?
To anticipate bleeding risk and know how to reverse each agent.
What clotting factors does the liver produce?
Factors V, VII, IX, X, XI, XII, proteins C/S, and antithrombin.
How does liver disease affect coagulation?
↓ clotting factor production, ↓ platelet function, ↓ clearance of pro/anti-coagulants → unstable balance.
Are PT/PTT reliable in liver disease?
Not entirely — they show low procoagulants but not anticoagulant levels
What tools guide transfusion in liver disease?
TEG or ROTEM (viscoelastic testing)
Why do CKD patients have bleeding risk?
Anemia (↓EPO) and platelet dysfunction due to uremia.
4 treatments listed
How is uremic platelet dysfunction treated?
- Dialysis
- cryoprecipitate
- DDAVP
- conjugated estrogens
What causes DIC?
Excess TF–VIIa activation → widespread clotting → depletion of clotting factors → bleeding.
5 triggers listed
Triggers of DIC?
- Trauma
- sepsis
- malignancy
- amniotic embolism
- incompatible transfusion
Labs in DIC?
- ↓ platelets
- ↑ PT/PTT/thrombin time
- ↑ fibrin degradation products
Management of DIC?
Treat underlying cause + blood products (FFP, cryo, platelets) as needed.
Linked to three things
What is trauma-induced coagulopathy (TIC)?
Acute coagulopathy in trauma, linked to:
- protein C activation
- platelet dysfunction
- auto-heparinization
What is auto-heparinization in trauma?
Severe trauma or shock leads to low blood flow to tissues causing:
→ Breakdown of glycocalyx (lining of vascular endothelium)
→ proteoglycan release (act as an endongenous form of heparin)
→ makes you bleed more.
What are the two most common inherited thrombophilias?
Factor V Leiden (resistant to Protein C)
Prothrombin gene mutation (↑ Prothrombin levels)
What is Antiphospholipid Syndrome?
Your immune system makes antibodies that attack parts of your own blood clotting system — specifically phospholipid-binding proteins.
→ recurrent thrombosis and pregnancy loss
→ requires lifelong anticoagulation.
What is Virchow’s Triad?
- Blood stasis
- endothelial injury
- hypercoagulability
How does Warfarin work?
Inhibits vitamin K-dependent factors: II, VII, IX, X, and proteins C & S.
What labs are used to monitor Warfarin?
PT/INR
How does Heparin work?
Binds antithrombin → inhibits thrombin (IIa) and Xa.
How is Heparin reversed?
Protamine (1 mg per 100units heparin)
Half Life vs Reversibility w/ protamine
What are LMWH & Fondaparinux differences?
LMWH: Longer half-life (in relation to heparin), partial reversal with protamine
Fondaparinux: Longest half-life, not reversible with protamine
Name the direct thrombin inhibitors (DTIs)
Argatroban, Bivalirudin, Dabigatran (Pradaxa)
Name the direct Xa inhibitors (DOACs)
- Rivaroxaban (Xarelto)
- Apixaban (Eliquis)
- Edoxaban (Savaysa)
Which DOAC has an antidote?
Dabigatran (Pradaxa) → Idarucizumab
What reverses Xa inhibitors?
Andexanet alfa
What’s the DOC for emergent Warfarin reversal?
Prothrombin Complex Concentrates (PCC)
How long before surgery should Warfarin be stopped?
5 days (bridge with heparin if high risk)
When to stop LMWH before surgery?
24 hours prior
When should ASA be stopped before surgery?
Low risk: stop 7–10 days prior
Moderate/High risk: often continued
How long should surgery be delayed after coronary stents?
Bare metal: 6 weeks
Drug-eluting: 6 months
What is the risk of neuraxial anesthesia with anticoagulants?
Must carefully time anticoagulants to prevent epidural hematoma — follow ASRA guidelines!
Where does Ca++ come into play?
Step-By-Step; Intrinsic Pathway
Exposure of a negatively charged substance to plasma, such as collagen in the endovascular lining
- Factor XII (12) is activated→ XIIa
- XIIa activates Factor XI (11) → XIa
- XIa activates Factor IX (9) → IXa
- IXa works with Factor VIIIa (8a), calcium, and phospholipids to activate…
- Factor X (10) → Xa
This is the key step that leads into the common pathway, where thrombin and fibrin form the final clot.
Where does Ca++ come into play?
Step-By-Step; Extrinsic Pathway
- Tissue Factor (TF) (also Factor III) is released from damaged tissue outside the vessel.
- Tissue Factor binds to Factor VII → activates it to VIIa
- The TF–VIIa complex (plus calcium) activates… Factor X → Xa
-You’re now in the common pathway just like the intrinsic side.
“3 + 7 = 10”
Tissue Factor (III) + Factor VII → activates X
Where does Ca++ come into play?
Step-By-Step; Common Pathway
- Factor X (10) is activated → Xa
- Xa teams up with:
-Factor V (5a)
-Calcium
-Phospholipids
-This combo forms the prothrombinase complex - Prothrombinase turns Prothrombin (Factor II) → Thrombin (IIa)
- Thrombin (IIa) then converts Fibrinogen (Factor I) → Fibrin (Ia)
- Fibrin strands form a meshwork to create a stable clot
- Finally, Factor XIII (13) cross-links the fibrin → making the clot strong and permanent
What is it?
What is the value for TEG-ACT?
- 80-140 sec
- Activated clotting time to initial fibrin formation
What is R-Time? What does it measure? Short/prolonged values?
What is the normal value for R time?
- 5.0 - 10.0 min
- Reaction time, initial clot formation (time for first fibrin strand to appear)
- Measures coagulation factor activity, specifically intrinsic pathway clotting factors
- Prolonged R-time: Hypocoagulable
- Short R-time: Hypercoagulable
What is K time? What does it measure? Short/long values mean?
What is the normal value for K time?
- 1-3 minutes
- “Kinetic” time; the speed at which the clot reaches a 20mm amplitude on the TEG tracing
- Measures the speed at which fibrin builds and cross-links–> directly reflects fibrinogen function
- Short K time –> hypercoagulable state (high fibrinogen, pregnancy). Corresponds w/ a large a-angle
- Long K time –> prolonged clot formation (anticoags, low fibrinogen). Corresponds w/ a short a-angle
What is it/what does it measure? Small or large A-angle?
What is the normal value for α angle?
Inversely related to what?
- 53 - 72°
- The α-angle represents the rate of clot formation and reflects fibrin cross-linking and fibrinogen function
- Slope of the curve = rate of clot formation
- Reflects fibrinogen + platelet interaction
- Low angle = slow clot formation → give cryo
- High angle = fast clot formation
Inversely related to K-time
What is it? What does it measure? High or low values mean what?
What is the normal value for MA?
- 50-70mm
- Maximum amplitude of teg tracing; shows peak of clot strength
- Measures platelet number and function
- High MA suggests increased clot strength
- Low MA indicates low fibrinogen or abnormal platelet function
What is it? What does it measure? High or low values?
What is the normal value for G value?
- 5.3-12.4 dynes/cm2
- measures the overall clot strength in numerical form
- Calculated from the MA (Maximum Amplitude)
- Higher G = stronger clot (hypercoagulable)
- Lower G = weaker clot (hypocoagulable)
💡 Easy interpretation:
G ↑ → blood clots too easily
G ↓ → blood is too thin / weak clot
What is it? What does it measure? High or low values?
What is the normal value for LY 30?
- 0-3%
- Percent of clot broken down 30 minutes after MA
- Measures fibrinolysis
- High LY30 = give TXA or antifibrinolytics
If TEG-ACT is > 140 what do we transfuse?
- FFP
If R time is > 10 what do we transfuse?
- FFP or prothrombin complex concentrate
If K time is > 3 what do we transfuse?
- Cryo because K time directly measures fibrinogen
If α angle < 53° what do we transfuse
- Cryo and platelets
If MA < 50 what do we transfuse?
Check fibrinogen and platelet mapping
FF low—> give cryo
Platelet mapping abnormal —> give platelets
If LY30 is >3% what do we transfuse?
TXA (Tranexamic Acid)
- R-Time
- K-time
- A-angle
- Maximum amplitude
- LY-30
- Shows time in minutes
- This side of the graph indicates coagulation
- This side indicates fibrinolysis
What is Factor I?
Fibrinogen – converted by thrombin into fibrin to form the clot mesh.
What is Factor II?
Prothrombin – converted by prothrombinase into thrombin (IIa).
What is Factor III?
Tissue Factor (TF) / Thromboplastin – triggers extrinsic pathway when exposed.
What is Factor IV?
Calcium (Ca²⁺) – required for multiple steps in both pathways.
What is Factor V?
Labile Factor – cofactor for Factor Xa in prothrombinase complex.
What is Factor VII?
Stable Factor / Proconvertin – forms complex with TF to activate Factor X (extrinsic).
What is Factor VIII?
Anti-hemophilic Factor A – cofactor for IXa in the intrinsic pathway.
Deficiency = Hemophilia A.
What is Factor IX?
Anti-hemophilic Factor B / Christmas Factor – activates X with VIIIa.
Deficiency = Hemophilia B.
What is Factor X?
Stuart-Prower Factor – activated by intrinsic or extrinsic tenase → initiates common pathway.
What is Factor XI?
Plasma Thromboplastin Antecedent (PTA) – activated by XIIa → activates IX.
What is Factor XII?
Hageman Factor – contact-activated by negative surfaces → starts intrinsic pathway.
What is Factor XIII?
Fibrin-stabilizing Factor – crosslinks fibrin to form a stable, insoluble clot.
