Hematology Flashcards

1
Q

Extrinsic pathway activation

A

“TF pathway”

  • Starts with injury outside the vessel wall
  • Organ trauma, crush injury
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2
Q

Extrinsic pathway factors

A

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

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3
Q

Intrinsic pathway activation

A
  • Damage to blood vessels

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

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4
Q

Factor IV

A

Calcium

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5
Q

Intrinsic pathway factors

A

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”

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6
Q

Thrombin (in coagulation pathways)

A

Assists in activating V, VIII, I, XIII

  • Influences platelet recruitment
  • Activates adequate fibrin to clot
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7
Q

Common pathway

A

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”

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8
Q

Factors dependent on vitamin K

A

II, VII, IX, X

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9
Q

Cell based coagulation theory phases

A

Initiation
Amplification
Propagation

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10
Q

Factor II vs IIa

A

II: Prothrombin
IIa: Thrombin

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11
Q

Factor III

A

Tissue Factor

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12
Q

Factor I vs Ia

A

I: Fibrinogen
Ia: Fibrin

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13
Q

Cell-based theory initiation phase

A
  • 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
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14
Q

Cell-based theory amplification phase

A
  • 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
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15
Q

Cell-based theory propagation phase

A
  • 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
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16
Q

Fibrinolytic system

A
  • 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
17
Q

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

A
TEG (thromboelastogram)
Indicates:
-Clot strength
-Platelet number and function 
-Intrinsic pathway defects
-Thrombin formation
-Rate of fibrinolysis
18
Q

Life span of donated platelet

A

4-5 days

19
Q

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

A

Fibrinogen, factors I, VIII, VWF, XIII

1 unit increases fibrinogen by 50mg/dL

20
Q

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)

A

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