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MDTI 1 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

With the exception of what 2 factors, are the roman numerals involved in the clotting cascade proteases? Describe these 2 factors.

A
  • V and VIII
  • they are scaffold proteins that assemble multiprotein complexes that greatly accelerate clotting reactions; they are cleaved by thrombin and become more efficient in their ability too accelerate their reactions.
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2
Q

What do VIIIa and Va convert?

A
  • VIIIa: X to Xa

- Va: prothrombin to thrombin

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3
Q

T/F: missing contact factors (intrinsic pathway) causes bleeding.

A

-False

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4
Q

Do Hemophiliacs have shorter, longer, or normal PT time?

A
  • normal

- PT tests extrinsic pathway which is IXa and VIIIa independent

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5
Q

How to warfarin work?

A
  • it blocks the recycling of Vit K and depletes its levels in the liver
  • blocks vitamin K epoxide reductase
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6
Q

What accumulates when you take coumadin (warfarin)?

A

Vitamin K Epoxide

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7
Q

Why are the Gla residues biologically important?

A

-they promote the association of factors II, VII, IX, and X with the phospholipid bilayer–classically on the platelet surface, which promote clotting by flipping negatively charged phospholipids such as PS from the inner leaflet of the lipid bilayer to the outer leaflet when the platelets are activated

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8
Q

What are the 4 coordinated processes of hemostasis? Very general.

A
  • Fibrin deposition and platelet plug (hemostatic plug)

- anticoagulant and fibrin lysis (limit and remove hemostatic plug)

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9
Q

Hemostasis vs. thrombosis

A

Hemostasis: process that spontaneously arrests blood flow from vessels due to injury, etc
Thrombosis: pathologic process in which 1 or more components of the normal hemostatic mechanism is activated in wrong place @ wrong time

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10
Q

What is the end result of the coagulation pathway?

A
  • generate thrombin and produce fibrin in response to injury

- complex cascade to produce limited thrombin quickly and locally at site of vascular injury

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11
Q

Where does thrombin generation occur? And why is this beneficial?

A
  • Occurs on cell surfaces (2D), not in space (3D)

- this accelerates its generation

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12
Q

What is TFPI and what does it do? How can clotting still occur with TFPI present?

A
  • Tissue Factor Pathway Inhibitor
  • shuts down TF/VIIa/Xa complex
  • TF and VIIa have a second target, IX to form IXa that can cleave X with the help of VIIIa, Ca2+, and phospholipids from platelets
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13
Q

What activates V and VIII?

A

Thrombin; one example of a positive feedback loop
-thrombin is generated by help of activated VIIIa and Va, and once is produced can activate VIII and V even more to generate even more thrombin

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14
Q

What are 2 things that activate XI?

A
  • thrombin

- intrinsic “contact factor” pathway

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15
Q

What is blood from patients undergoing PT and aPTT tests treated with and why?

A

-citrate: a Ca2+ chelator so as to prevent coagulation which needs Ca2+ at steps along the pathway

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16
Q

What is the PT test? What does it test? What must be added in this test?

A
  • Prothrombin Time: measure time from TF input to fibrin polymer output; usually 10-12 seconds
  • measures the extrinsic/TF pathway: VIIa, V, X, II, fibrinogen
  • added citrate-treated plasma, Ca2+, Tissue factor, and p’lipids
17
Q

What does the aPTT test measure? What is added for this test?

A
  • Tests intrinsic/contact pathway; normally 28-35 seconds
  • add citrate-treated plasma, phospholipids, Ca2+, and a negatively charged surface to activate contact factors; NO TF ADDED
18
Q

3 things that can increase aPTT? What can you do to dissociate between these 3 possible explanations if a long aPTT is achieved?

A
  1. inherited deficiencies of 1 or more clotting factors; Hemophilia A or B (bleeding)
  2. Acquired deficiencies of multiple clotting factors (Vit K deficiency and liver disease-bleeding)
  3. Inhibitors: antibodies NOT causing bleeding (LAC); antibodies causing bleeding against certain factors, drugs like heparin (bleeding)
    - need to know if its due to factor deficiency or inhibitor, so 1:1 mix with normal plasma with clotting factors. If normal aPTT it is due to factor deficiency and you should perform factor assays. If still long aPTT, it is due to dominant negative inhibitor and you should check for LAC, factor inhibitor antibodies, and other meds they may be on like heparin
19
Q

Where are most clotting factors made and what are the exceptions?

A
  • most made in hepatocytes
  • VIII is made in liver, but not in hepatocytes
  • vWF is made in megakaryocytes and endothelial cells
20
Q

What factors are Vitamin K dependent? What role does Vitamin K serve? What other proteins involved in hemostatis require Vitamin K as well for their synthesis?

A
  • II, VII, IX, X
  • cofactor for posttranslational carboxylation conversion of select glutamate residues to Gla residues that helps these 4 factors adhere to cell surfaces better
  • Anticoagulant proteins C, Z, and S
21
Q

Give 3 endogenous regulators of coagulation

A
  1. TFPI: shuts down TF/VIIa/X complex
  2. Anti-thombin: serine protease inhibitor (serpin); binds Xa and IIa and inhibits clotting- risk of thrombosis in its absence
  3. Protein C pathway: thrombin-bound thrombomodulin (on endothelial cells) cleaves and activates PC which with PS, cleaves and inactivates Va and VIIIa, slowing thrombin production; Negative feedback loop
22
Q

How does heparin work?

A

-binds antithrombin and makes it a more potent inhibitor of Xa and IIa

23
Q

What enzyme is responsible for fibrinolysis? Describe the process and what byproduct signifies this process is occurring?

A
  • plasmin: protease that degrades fibrin/clot; formed by t-PA from plasminogen
  • thrombin converts fibrinogen to fibrin, XIII cross-links fibrin, plasmin cleaves fibrin into fragments, and if crosslinked fragments, called D-dimers
  • D-dimers:crosslinked fragments of polymerized fibrin; useful clot marker and elevated in patients with DIC and thrombosis
24
Q

Name 2 inhibitors of the fibrinolytic cascade.

A
  • PAI-1: inhibits t-PA from forming plasmin from plasminogen

- alpha2-antiplasmin inhibits plasmin from cleaving fibrin

MDTI 1 (12 decks)

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