Hemostasis, Hemophilia, Vit K Flashcards

1
Q

tertiary hemostasis

A

-aka blood coagulation

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2
Q

intrinsic pathway

A

-aka contact activation pathway
-initiated from the blood itself after exposure of
the blood to collagen from a traumatized blood vessel

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3
Q

extrinsic pathway

A
  • aka tissue activation pathway
  • more important
  • started by tissue injury and release of tissue factor, III
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4
Q

common pathway

A

-fibrinogen -> fibrin (via thrombin)

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5
Q

thrombin

A
  • acts on fibrinogen to create fibrin monomer which can interact with other fibrin monomers to form fibrin fibers
  • 4 molecules reomoved from fibrinogen -> fibrin
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6
Q

fibrinogen

A

-fibrin precursor (needs peptides removed to make fibrin monomer)

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7
Q

hemophilia A

A
  • inherited coagulation disorder, intrinsic pathway
  • cofactor VIII -> less Xa formed -> less thrombin
  • treatment: missing factor VIII (recombinant factors) or blood transfusions
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8
Q

hemophilia B

A
  • inherited coagulation disorder, intrinsic pathwat
  • cofactor IX -> less Xa formed -> less thrombin
  • -treatment: missing factor IX (recombinant factors) or blood transfusions
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9
Q

anticoagulants

A
  • Agents that decrease Ca2+
  • coumains (vit K antagonists)
  • heparin and derivatives
  • antithrombin-like agents (bind to thrombin, medicinal leeches = hirudin, bivalirudin)
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10
Q

tissue plasminogen activator

A
  • activating plasminogen activator to plasmin (Plasmin can be effective in dissolving intravascular clots)
  • Within 3 hours it can improve recovery odds of: pulmonary ebolism, myocardial infarction, stroke
  • risk of hemorrhage
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11
Q

hemostasis

A

prevention of blood loss

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12
Q

vit K

A
  • a co-factor in the production of an unusual amino acid, γ-carboxyglutamate (gla)
  • Gla residues are part of Vitamin K-dependent proteins (VKDP)
  • Addition of Gla residues confers on these proteins their capacity to bind to phospholipid surfaces in the presence of Ca2+
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13
Q

proteases

A
  • endopeptidases
  • exist in zymogen/inactive form
  • synthesized in liver (except III, tissue factor and some VIII, antihemophylic globulin)
  • present in low concentrations (except pro-thrombin, II = 1microM, and fibrinogen, I = 10microM)
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14
Q

protease cofactors

A

-also require activation

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15
Q

coagulation factors

A

-generally serine proteases

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16
Q

tissue factor

A

-a combination of phospholipids and lipoproteins released from damaged tissue that act as a proteolytic enzyme

17
Q

HMWK

A
  • High Molecular Weight Kininogen
  • bound to prekallikrein and factor XII
  • attracked to negatively charged surfaces such as injured blood vessel
18
Q

IXa-VIIIa-phospholipid-Ca2+ complex

A
  • aka tenase
  • activate X to Xa
  • where extrinsic and intrinsic pathways collaborate to start common pathway
19
Q

VKDP

A

Vitamin K-dependent proteins
– Intrinsic pathway: Factors IX
– Extrinsic pathway: Factor VII
– Common pathway: Factor II = Prothrombin and factor X
– Anti-coagulation factors: Protein C and Protein S

20
Q

vit K deficiency

A

-inefficient coagulation and bleeding

21
Q

vit K depletors

A
  • Warfarin/Coumadin, Dicoumarol
  • inhibit production and recycling of vit K
  • prescribed for elderly at risk for thrombosis for prolonged anticoagulant treatment
22
Q

heparin sulfate

A
  • facilitates the interaction of antithrombin with thrombin
  • > inhibits prothrombin conversion to thrombin
  • > inhibits thrombin action on fibrinogen
23
Q

vWF

A

-Von Willebrand Factor