Hematology

Question 1

Extrinsic pathway activation

Answer 1

“TF pathway”

• Starts with injury outside the vessel wall
• Organ trauma, crush injury

Question 2

Extrinsic pathway factors

Answer 2

III, VII
Inhibited eventually to activate more by TF pathway inhibitor
“You can buy the extrinsic pathway for 37 cents”

Question 3

Intrinsic pathway activation

Answer 3

• Damage to blood vessels

- Initiated by high molecular weight kininogen (HMWK) and activation of XII

Question 4

Factor IV

Answer 4

Calcium

Question 5

Intrinsic pathway factors

Answer 5

Initiated by HMWK and aXII with help of IV (calcium)
-XII, XI, IX, VIII
“You can’t get the intrinsic pathway for $12, but you can get it for $11.98”

Question 6

Thrombin (in coagulation pathways)

Answer 6

Assists in activating V, VIII, I, XIII

• Influences platelet recruitment
• Activates adequate fibrin to clot

Question 7

Common pathway

Answer 7

aX activated II with help from V and Ca2+
-IIa (thrombin) -> I (fibrinogen) to Ia (fibrin)
-XIII secures platelet plus with Ia
“You can get the common pathway at the five (V) and dime (10) for $1 or $2 on the 13th of every month”

Question 8

Factors dependent on vitamin K

Answer 8

II, VII, IX, X

Question 9

Cell based coagulation theory phases

Answer 9

Initiation
Amplification
Propagation

Question 10

Factor II vs IIa

Answer 10

II: Prothrombin
IIa: Thrombin

Question 11

Factor III

Answer 11

Tissue Factor

Question 12

Factor I vs Ia

Answer 12

I: Fibrinogen
Ia: Fibrin

Question 13

Cell-based theory initiation phase

Answer 13

• Endothelial surface is injured
• TF exposed
• Endothelial surface is less repellant to platelets
• Sub endothelial anticoagulation is down regulated
• Platelets are recruited, VII -> VIIa
• Intrinsic and common pathways activated -> Xa and IXa
• Factors X and V form complex to generate a small amount of thrombin for clot (TF pathway inhibitor limits the amount of TF)
• IX attaches to activated platelet -> VIIIa -> Xa, more thrombin is produced
• Injury perpetuates, TF is expressed, platelets mobilize to injury site

Question 14

Cell-based theory amplification phase

Answer 14

• Thrombin generation gains momentum and acceleration
• Thrombin activated V, VIII, IX
• XIa assists in generating more IX on platelet surface
• vWF promotes platelet aggregation with Gp1b
• Platelet surface (GpIIb-IIIa) facilitates aggregation

Question 15

Cell-based theory propagation phase

Answer 15

• All coagulation factors are actively influencing one another, promoting coagulation, activating prothrombin -> larger bursts of thrombin
• Enough thrombin needs to be present to convert fibrinogen to fibrin to form a stable secondary hemostatic plug

Question 16

Fibrinolytic system

Answer 16

• Increased blood flow at an injury site washes away ADP and TX-A2 (procoagulants)
• Thrombin changes to act as an anticoagulant
• TFPI stops TF
• Proteins C and S inhibit III, V, VIII
• Antithrombin III inhibits thrombin by sequestering XII, XI, IX, and X (takes factors from clotting cascade out)
• Regulated by plasma proteins
• Plasminogen in clot -> TPA turns into plasmin -> degrades fibrin

Question 17

Best lab test for bleeding time/tool to guide blood therapy

Answer 17

TEG (thromboelastogram)
Indicates:
-Clot strength
-Platelet number and function 
-Intrinsic pathway defects
-Thrombin formation
-Rate of fibrinolysis

Question 18

Life span of donated platelet

Answer 18

4-5 days

Question 19

Clotting factors in transfused cryoprecipitate (and how much 1 unit increases your fibrinogen)

Answer 19

Fibrinogen, factors I, VIII, VWF, XIII

1 unit increases fibrinogen by 50mg/dL

Question 20

Course length for Plavix after bare-metal stents vs drug eluding stents (when elective surgery should be postponed, and what to do if surgery can’t be postponed)

Answer 20

Bare-metal stent: 4-6 weeks
Drug-eluding stent: 12 months
If surgery can’t be postponed, Plavix should be stopped and aspirin should be continued periop, Plavix should be restarted ASAP postop