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BIOCHEM Unit 2 > Lecture 10 Hemo1Platelet Coag > Flashcards

Lecture 10 Hemo1Platelet Coag Flashcards

(58 cards)

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1
Q

Hemostasis

A

1st step in
wound healing: stop bleeding
from injured blood vessels

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2
Q

What is the opposite of Hemostasis?

A

Hemorrhage

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3
Q

What are the three processes involved in hemostasis?

A

Primary, Secondary, Fibrinolysis

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4
Q

What is Primary Hemostasis?

A

Formation of Platelet Plug

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5
Q

What is Secondary Hemostasis?

A

Maintaning the plug through the crosslinking of fibrin

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6
Q

What is Fibrinolysis?

A

After the injury is repaired, the clot is dissolved.

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7
Q

Dysregulation of Hemostasis can cause what?

A

Bleeding and Thrombosis

Bleeding: Inability to form proper clot

Thrombosis: Excessive clotting

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8
Q

Platelets

A

Platelets are fragments of membrane
from cells known as megakaryocytes.

Platelets shed from
megakaryocytes

Platelets do not have a nucleus

Lifespan approx 10 days

150,000 – 400,000
platelets per 1 μl blood

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9
Q

Thrombocytopenia

A

platelet deficiency

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10
Q

Thrombocytosis

A

excess platelets

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11
Q

Platelets and
Endothelial Cells

A

Both have net negative
surface charges which cause repulsion

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12
Q

Endothelial Cells

A

Secrete numerous
components that inhibit
activation of platelets, because you dont want it to clot the healthy stuff, only clot when injured.

Healthy endothelial cells prevent
the blood from clotting abnormally

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13
Q

After Injury, what happens?

A

Formation of Platelet Plug

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14
Q

Steps involved in the formation of platelet plug after injury

A

The platelet/endothelial cell barrier is gone, platelets come in contact with sub-endothelium

Interaction of platelets with sub-endothelium begins a series of events in platelets

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15
Q

Platelet Response to Injury in 3 Mechanisms

A
  1. Adhesion: Binding of Platelets to exposed sub endothelium
  2. Activation: Change in Platelet shape and release of stored molecules
  3. Aggregation: Platelets link with the help of fibrinogen
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16
Q

Three Important receptors on platelets involved in formation of plug

A
  1. GpIIb/IIIa: binds fibrinogen
  2. GpVI: binds collagen
  3. GpIb-IX-V: binds vWF
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17
Q

Adhesion

A

Forward movement of platelets stopped by binding to components of sub-endothelium.

Platelet receptors bind exposed collagen and von Willebrand Factor (vWF) in the subendothelium.

GpVI binds collagen

GpIb-IX-V binds vWF

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18
Q

Activation

A

Change in platelet
shape and release of stored molecules

Activated platelet sees increase in surface area important for 2nd Hemostasis.

Degranulation of
platelets releases
molecules.

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19
Q

What molecules are released by activated platelets?

A
  • ADP
  • Serotonin
  • Fibrinogen
  • Ca2+
  • Thromboxane A2 (TXA2)

Platelets contain secretory molecules
stored within intracellular vesicles

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20
Q

What is the importance of Serotonin and thromboxane A2 (TXA2) during the Activation Phase?

A

Serotonin and TXA2
cause contraction of
smooth muscle cells which cause Vasoconstriction.

Which then:
Helps minimize blood
loss following injury

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21
Q

What is the importance of Ca2+ during the Activation Phase?

A

Increase in extracellular Ca2+ will help to activate secondary hemostasis

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22
Q

What is the importance of ADP and TXA2 during the Activation Phase?

A

ADP and TXA2 are released from platelets and act on receptors on platelet (autocrine signaling).

Then,
Activated ADP and TXA2
receptors cause increase
in cytosolic Ca2+ levels.

Finally,
Increased intracellular
Ca2+ activates the
receptor GpIIb/IIIa.

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23
Q

What is the importance of Fibrinogen during the Activation Phase?

A
  1. Activated platelets release fibrinogen.
  2. Released fibrinogen binds to
    activated GpIIb/IIIa receptors.
  3. Important for
    platelet aggregation
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24
Q

Aggregation

Study These Flashcards
A

Formation of platelet plug

ADP and TXA2 activate GpIIb/IIIa.

Activation of GpIIb/IIIa allows
binding of fibrinogen between platelets.

Platelet plug must be stabilized by the process of secondary hemostasis.

25
What are diseases involved in Primary Hemostasis?
1. Bernard-Soulier Disease Defect in GpIb-IX-V (binds vWF) 2. Glanzmann Thrombastenia Defect in GpIIb/IIIa
26
Bernard-Soulier Disease
Defect in GpIb-IX-V (binds vWF) Causes reduced platelet adhesion to sites of injury due to lack of vWF binding
27
Glanzmann Thrombastenia
Defect in GpIIb/IIIa Platelets cannot bind fibrinogen, reduces aggregation of platelets, platelets do not form a plug
28
Von Willebrand Disease (VWD)
Normal vWF, GpIb-IX-V binds vWF. Deficiency in production or Mutation means GpIb-IX-V cannot bind vWF. Which then means, Platelets cannot properly adhere at sites of injuries. Clinical Signs: Bleeding and Bruising Complications
29
Secondary Hemostasis
Production and crosslinking of fibrin Conversion of fibrinogen to fibrin that becomes crosslinked to stabilize the platelet plug This is accomplished through activation of “coagulation factors”
30
What helps accomplish Secondary Hemostasis and Fibrin Production?
Activation of Coagulation Factors
31
Active vs Inactive Coagulation Factor
Coagulation factors referred to as “Factors” designated by Roman Numerals often preceded by an “F” Addition of “a” for “active” form FVIIa active. FVII Inactive
32
Where are CoAg factors synthesized and secreted into?
Many coagulation factors synthesized by liver and secreted into blood. Others may be produced by cells in subendothelium or released from platelets.
33
Coagulation Cascades
1. Coagulation factors exist in an inactive form and must be activated 2. Many coagulation factors exist in a “cascade” where activation of one factor activates the next factor.
34
What is the site for activation of some coagulation factors?
Surface of platelets
35
What happens to the platelets in the activation of CoAg factors?
Change in shape of activated platelets INCREASES surface area
36
Role of Scramblase
Activated by Increased cytosolic Ca2+ Then, Moves phosphatidyl serine (negatively charged) from inner to outer surface Finally, Scramblase increases amount of phosphatidyl serine on surface of platelet which then increases Negative charge
37
What facilitates activation of coagulation factors?
Phosphatidylserine on platelet surfaces facilitates activation of coagulation factors. Phosphatidyl serine acts as a scaffold for the activation of coagulation factors on the surface of the platelet membrane.
38
γ-(gamma) carboxylation
Some coagulation factors require γ-(gamma) carboxylation to become activated γ-carboxylation results in negative charges
39
What do CoAg factors with γ-carboxylation require?
Coagulation factors with γ-carboxylation require extracellular Ca2+ to interact with the negatively charged platelet surface.
40
Extracellular Ca2+
Extracellular Ca2+ allows CoAg factors with γ-carboxylation to be brought to the platelet surface for activation Mechanism: 1. Surface of membrane negatively charged due to phosphatidylserine (PS) 2. Coagulation Factor with γ-carboxylation and plasma membrane of activated platelet 3. Ca2+ forms a bridge between negative charges.
41
Vitamin K
Required cofactor for γ-carboxylation
42
γ-glutamyl-carboxylase
Vitamin K dependent enzyme
43
Vitamin K Defficiency
Risk of bleeding when vitamin K is deficient in diet due to lack of proper γ-carboxylation of coagulation factors
44
Three Coagulation Pathways (KNOW THESE THREE)
Intrinsic: Amplifies response, initiated in the blood Extrinsic: Initiates response at site of injury Common: From Factor X to Crosslinked Fibrin
45
Extrinsic Pathway
Initiates at Injury Site Involves FVII, TF FVII: circulates in the blood TF embedded into subendothelium Damage to blood vessel exposes FVII to TF. FVII is activated by binding exposed TF at site of injury
46
FVII and TF steps leading to Factor X
1. Vascular injury exposes TF to FVII in the blood 2. Binding of FVII to TF leads to activation (FVIIa) 3. TF/FVIIa complex activates Factor X
47
Common Pathway
Involves FX, FV, Thrombin, FXIII 1. Activated Factor X associates with Factor V causing conversion of prothrombin to thrombin 2. Thrombin activates FXIII. 3. FXIIIa crosslinks fibrin
48
Thrombin and FXIIIa
Both needed to form the final, strengthened clot. 1. Thrombin is needed to convert fibrinogen to fibrin 2. FXIIIa crosslinks the fibrin, strengthening the clot.
49
Intrinsic pathway
Involves XI, FIX, FVIII NOTE: The Intrinsic Pathway needs to be stimulated by components of the Extrinsic AND Common Pathways
50
Intrinsic Pathway Mechanisms
1. Activates FX which will “amplify” the coagulation response 2. FIXa and FVIIIa complex activates FX amplifying the production of crosslinked fibrin 3. Amplifies response by activating more FX FVIIIa.
51
Intrinsic pathway relation to other pathways
Stimulated by components of the extrinsic and common pathways 1. Thrombin (Common pathway) activates FVIII and FXI 2. F/FVII (Extrinsic pathway) provides additional stimulation for activation of FIX Activation of the extrinsic and common pathways leads to activation of the intrinsic.
52
Hemophelia Secondary Hemostasis Disease
Defects in intrinsic pathway caused by deficiencies in specific factors production of crosslinked fibrin is impaired Factor VIII, Factor IX, Factor XI
53
Final Product of Common Pathway
Crosslinked Fibrin
54
Types of Hemophelia
A B and C Factor deficiencies for different types of hemophilia Each type involves insufficient levels of an intrinsic pathway coagulation factor
55
Hemophelia Treatment
1. Injections of missing factor 2. Transfusions containing coagulation factors
56
Liver Failure Secondary Hemostasis Disease
Liver damage/failure will cause bleeding due to lack of synthesis of coagulation factors. Dec 2nd Hemo, Inc Bleeding Risk
57
Evaluation of coagulation activity
Blood sample mixed with phospholipid and Ca2+ and then Extrinsic or Intrinsic pathway is stimulated Pt Test: Extrinsic PTT Test: Intrinsic Increased time required to form clot in either test means a defect/deficiency in that pathway
58
Products that help to facilitate hemostasis in times of emergency
Microfibrillar collagen: causes platelets to activate Fibrin glue: production of fibrin QuikClot: activate intrinsic pathway

BIOCHEM Unit 2 (2 decks)

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