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BIOCHEM Unit 2 > Lecture 10 Hemo1Platelet Coag > Flashcards

Lecture 10 Hemo1Platelet Coag Flashcards

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

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
Q

What are diseases involved in Primary Hemostasis?

A
  1. Bernard-Soulier Disease
    Defect in GpIb-IX-V (binds vWF)
  2. Glanzmann Thrombastenia
    Defect in GpIIb/IIIa
26
Q

Bernard-Soulier Disease

A

Defect in GpIb-IX-V (binds vWF)

Causes reduced platelet adhesion to sites of injury due to lack of vWF binding

27
Q

Glanzmann Thrombastenia

A

Defect in GpIIb/IIIa

Platelets cannot bind fibrinogen,
reduces aggregation of platelets,
platelets do not form a plug

28
Q

Von Willebrand Disease (VWD)

A

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
Q

Secondary Hemostasis

A

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
Q

What helps accomplish Secondary Hemostasis and Fibrin Production?

A

Activation of Coagulation Factors

31
Q

Active vs Inactive Coagulation Factor

A

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
Q

Where are CoAg factors synthesized and secreted into?

A

Many coagulation factors
synthesized by liver and
secreted into blood.

Others may be produced by cells in
subendothelium or
released from platelets.

33
Q

Coagulation Cascades

A
  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
Q

What is the site for activation of some coagulation factors?

A

Surface of platelets

35
Q

What happens to the platelets in the activation of CoAg factors?

A

Change in shape of activated
platelets INCREASES surface area

36
Q

Role of Scramblase

A

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
Q

What facilitates activation of coagulation factors?

A

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
Q

γ-(gamma) carboxylation

A

Some coagulation factors require γ-(gamma) carboxylation to become activated

γ-carboxylation
results in negative charges

39
Q

What do CoAg factors with γ-carboxylation require?

A

Coagulation factors with
γ-carboxylation require extracellular
Ca2+ to interact with the negatively
charged platelet surface.

40
Q

Extracellular Ca2+

A

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)

  1. Coagulation Factor
    with γ-carboxylation and plasma membrane of activated platelet
  2. Ca2+ forms a bridge between negative charges.
41
Q

Vitamin K

A

Required cofactor for γ-carboxylation

42
Q

γ-glutamyl-carboxylase

A

Vitamin K dependent enzyme

43
Q

Vitamin K Defficiency

A

Risk of bleeding when vitamin K
is deficient in diet due to lack of
proper γ-carboxylation of
coagulation factors

44
Q

Three Coagulation Pathways (KNOW THESE THREE)

A

Intrinsic:
Amplifies response, initiated in the blood

Extrinsic:
Initiates response at site of injury

Common:
From Factor X to Crosslinked Fibrin

45
Q

Extrinsic Pathway

A

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
Q

FVII and TF steps leading to Factor X

A
  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
Q

Common Pathway

A

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
Q

Thrombin and
FXIIIa

A

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
Q

Intrinsic pathway

A

Involves XI, FIX, FVIII

NOTE: The Intrinsic Pathway
needs to be stimulated by
components of the Extrinsic
AND Common Pathways

50
Q

Intrinsic Pathway Mechanisms

A
  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
Q

Intrinsic pathway relation to other pathways

A

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
Q

Hemophelia
Secondary Hemostasis Disease

A

Defects in intrinsic pathway caused by deficiencies in specific factors

production of
crosslinked fibrin is impaired

Factor VIII, Factor IX, Factor XI

53
Q

Final Product of Common Pathway

A

Crosslinked Fibrin

54
Q

Types of Hemophelia

A

A B and C

Factor deficiencies
for different types of hemophilia

Each type involves insufficient
levels of an intrinsic pathway
coagulation factor

55
Q

Hemophelia Treatment

A
  1. Injections of missing
    factor
  2. Transfusions containing
    coagulation factors
56
Q

Liver Failure
Secondary Hemostasis Disease

A

Liver damage/failure will cause bleeding due to lack of synthesis of coagulation factors.

Dec 2nd Hemo, Inc Bleeding Risk

57
Q

Evaluation of coagulation activity

A

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
Q

Products that help to facilitate hemostasis in times of emergency

A

Microfibrillar collagen: causes
platelets to activate

Fibrin glue: production of fibrin

QuikClot: activate
intrinsic pathway

BIOCHEM Unit 2 (2 decks)

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