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Function Of Human Body > Mehta > Flashcards

Mehta Flashcards

0
Q

Heparane sulfate (HS)

A

An anticoagulant

Enhances activity of antithrombin

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1
Q

Prostaglandin PG12

A

An anticoagulant

Prevents platelet activation

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2
Q

Ecto ADPase (CD39)

A

An anticoagulant
Degrades ADP
Prevents platelet aggregation

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3
Q

Plasminogen Activator Inhibitor-1 (PAI-1)

A

Inhibits formation of plasmin
Anticoagulant
Opposes thrombus dissolution

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4
Q

Plasminogen Activator (TPA)

A

A protease
Converts plasminogen to plasmin
Dissolves clots

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5
Q

Thrombomodulin (TM)

A

An anticoagulant

Activates protein C to degrade factors V and VIII

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6
Q

Nitric Oxide (NO)

A

Relaxes smooth muscle cells to prevent platelet aggregation

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7
Q

Store and release Von Willbrand Factor (vWF)

A

Facilitates platelet aggregation

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8
Q

Thrombosis is due to abnormalities in:

A
  1. Blood flow or hemodynamics
  2. Blood vessel wall
  3. Blood constituents
  4. Genetic
  5. Acquired
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9
Q

Hemorrhage is due to abnormalities in:

A
  1. Synthesis or function of clotting and anti-clotting factors
  2. Generation and function of platelets
  3. Genetic diseases
  4. Acquired
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10
Q

Define thrombus.

A

Abnormal clot that develops in a blood vessel.

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11
Q

Define embolus.

A

A clot that flows freely in the blood.

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12
Q

Define infarct.

A

Necrotic tissue area formed due to obstruction of blood due to a thrombus or embolus.

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13
Q

Define hemostasis.

A

Hemostasis is prevention of blood loss upon injury to the blood vessel and reestablishment of blood flow.

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14
Q

List the 5 overlapping responses in the hemolytic cascade.

A
  1. Vasoconstriction: narrows the blood vessels
  2. Platelet adhesion and aggregation: lead to the formation of plug at the site of injury or disturbance
  3. Coagulation: converts plasma from a liquid to a gel. This forms the clot.
  4. Blood vessel repari: endothelial cells divide, fibroblasts migrate to the site of injury, collagen is synthesized and the vessel is healed.
  5. Clot dissolution: a series of biochemical events, resulting in the dissolution of the the clot/plug.
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15
Q

List and describe the classes of the clotting and anti-clotting factors

A
  1. Enzymes: circulate in inactive form, get activated to initiate clotting. Most are serine proteases.
  2. Cofactors: bind and stabilize clotting factors buy have no enzymatic activity.
  3. Control proteins: regulate coagulation and anti-coagulation.
  4. Substrates: Fibrinogen and fibrin
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16
Q

Hemophilia A

A

Factor VIII deficiency

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17
Q

Hemophilia B

A

Factor IX deficiency

18
Q

Hemophilia C

A

Factor XI deficiency

19
Q

Name the direct anti-clotting factor agents that are direct thrombin inhibitors.

A

These factors bind thrombin to inhibit activity.

  1. Hirudin
  2. Argatroban
  3. Melagatran
  4. Orgaran
20
Q

Name all direct anti-clotting factor agents that are indirect thrombin inhibitors.

A

These factors inhibit thrombin generation.

  1. ANTI-Xa antibodies
  2. TFP1
  3. Soluble thrombomodulin
21
Q

Name all the indirect anti-clotting factor agents that are ATIII dependent.

A

These factors will increase ATIII activity.

  1. Heparin
  2. Heparin fragments
22
Q

Name all the indirect anti-clotting factors that are Vitamin K antagonists.

A

These factors inhibit the synthesis of clotting factors. These are the most common drugs.

  1. Warfarin
  2. Coumarin
  3. Dicoumarol
23
Q

vWF

A

Facilitates platelet aggregation by binding to GP1b-IX-V.

Initiates adhesion of platelets to collagen and platelets to cell receptors.

24
Q

G-protein coupled receptors (GPCR)

A

Present on the platelet surface; binds PGI2, TXA2, Thrombin, and ATP.

25
Q

PGI2

A

Inhibits platelet aggregation and is coupled to receptor Cs (increases cAMP).

26
Q

TXA2

A

Induces platelet aggregation and is coupled to receptors Gq or Gi.

27
Q

ADP

A

Activates platelets by binding to 2 receptors, Gi or Gq and causes aggregation.

28
Q

Integrin alpha2beta1

A

Mediates adhesion of platelets to collagen on exposed vessel surfaces and strengthens and stabilizes the bonds.
It causes platelets to exocytose, releasing TXA2, ADP, and thrombin, thus causing platelet aggregation.

29
Q

Integrin alphaIIb-beta3

A

Mediates adhesion between platelets via fibrinogen.

Establishes cross-linking of integrins.

30
Q

Tissue factor (Factor III)

A

Initiates extrinsic pathway when it is exposed during injury or inflammation.
Is present on sub-endothelial tissues.

31
Q

Thrombin

A

A coagulation factor/protease that activates platelets and binds to GPCR (Gi or Gq).
Protease that cleaves fibrinogen into fibrin.

32
Q

Factor XIII.

A

Activated by trace thrombin and becomes part of the tenase complex.
Is a transglutaminase (NOT a serine protease).
Synthesized in the liver and circulates as a zymogen.
Crosslinks fibrin chains, strengthening the bonds.

33
Q

TPA

A

Plasminogen activator.
Protease that converts plasminogen to plasmin and dissolves clots (must be bound to fibrin to be activated).
Two types: tissue (TPA and UPA).

34
Q

Plasmin

A

Dissolves the clot (serine protease) by digesting cross-linked fibrin monomers.
Only has high affinity to TPA bound to fibrin, so only has affinity for clot.
Digests polymerized fibrin to produce D-dimers and E-fragments (the presence of D-dimers in circulation is used as a clinical test to rule out deep venous thromboses and pulmonary embolism).

35
Q

Gamma carboxylation clotting factors

A

Prothrombin, VII, IX, X, XI, XII and protein C and S

Mediated by Vitamin K

36
Q

Protein C

A

Class C anticoagulation factor
Degrades factors V and VIII
Inhibits the formation of prothrombinase, and hence the formation of thrombin.
Must have the cofactor protein S.

37
Q

NSAIDS

A

Block prostaglandin synthase (COX-1 and COX-2) in endothelial cells and platelets.
In platelets, they inhibit the production of TXA2 from PGH2, thus inhibiting aggregation of platelets.

38
Q

Hemophilia A

A

Factor VIII deficiency

39
Q

Hemophilia B

A

Factor IX deficiency.

Coagulation time is prolonged

40
Q

Hemophilia C

A

Factor XI deficiency.

Coagulation time is prolonged.

41
Q

Deep venous thrombosis.

A

Life threatening, severe clotting throughout the body.

Due to homozygous deletion of protein C.

42
Q

Name the three domains of serine proteases.

A
  1. GLA (gamma carboxylase acts on this)
  2. Kringle (regulatory role)
  3. Catalytic

Function Of Human Body (5 decks)

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