CHAPTER 1 - HEMOSTASIS PART 2 Flashcards

1
Q

retains the blood within the vascular system during periods of injury

A

(vasoconstriction)

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2
Q

localizes the reaction involved to the site of injury.

A

(platelet adhesion and aggregation)

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3
Q

repairs and re-establishes blood flow through the injured vessels.

A

(coagulation and fibrinolysis)

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4
Q

Three Hemostatic Components

A

1) Extravascular component
2) Vascular component
3) Intravascular component

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5
Q

Play a part in hemostasis by providing back pressure on the injured vessel through swelling and entrapment of escaped blood

A

Extravascular components

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6
Q

Extravascular components Depends on the:

A

bulk or amount of surrounding tissue

type of tissue

tone of the surrounding tissue (

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7
Q

Vascular components Depends on the:

A

Size of the blood vessels

Amount of smooth muscle within their wall

Integrity of the endothelial cell lining

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8
Q

Platelets and biochemicals in the plasma.

A

Intravascular components

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9
Q

Stages of Hemostasis

A

Primary Hemostasis
Secondary Hemostasis

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10
Q

Platelet Clot

A

Primary Hemostasis

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11
Q

Temporary

A

Primary Hemostasis

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12
Q

Fibrin Clot

A

Secondary Hemostasis

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13
Q

Permanent

A

Secondary Hemostasis

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14
Q

activated by desquamation of damaged endothelial cells from small tissue injuries

A

Primary Hemostasis

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15
Q

Activated by large injuries to the blood vessel, releasing tissue factor.

A

Secondary Hemostasis

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16
Q

Primary Hemostasis Steps involved:

A

a) Blood vessel constriction
b) Platelet function cascade
c) Product: Platelet plug formation

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17
Q

Secondary Hemostasis Steps involved:

A

a) Activation of coagulation proteins.
b) Stabilization of platelet plug.
c) Fibrinolysis.

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18
Q

Platelet function cascade

A
  1. Adhesion
  2. Activation
  3. Secretion
  4. Aggregation
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19
Q

Primary Hemostasis Characteristics:

A

Rapid, shortlived response.

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20
Q

Secondary Hemostasis Characteristics:

A

Delayed, long term

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21
Q

Regulation: Naturally occurring inhibitors block activated coagulation factors to avoid widespread coagulation.

A

Secondary Hemostasis

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22
Q

Primary Hemostasis Involves:

A

(1) Vasoconstriction
(2) Platelet function Cascade

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23
Q

Secondary Hemostasis Involves:

A

• activation of a series of plasma proteins in the coagulation system until fibrin clot formation

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24
Q

Activated by desquamation and small injuries to blood vessels

A

Primary Hemostasis

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25
Q

→ Procoagulant substances are exposed or released by damaged or activated endothelial cells

A

Primary Hemostasis

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26
Q

Activated by large injuries to blood vessels and surrounding tissues

A

Secondary Hemostasis

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27
Q

→ Tissue factor exposed on cell membranes

A

Secondary Hemostasis

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28
Q

Involves vascular intima and platelets

A

Primary Hemostasis

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29
Q

Involves platelets and coagulation system

A

Secondary Hemostasis

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30
Q
  • Slow breakdown & removal of fibrin clot as healing of the injured vessel occurs
A

Fibrinolysis

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31
Q

lumen becomes small to ctrl blood flow to prevent blood loss

A

vasoconstriction

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32
Q

During injury, substances like collagen factor will call/attract hemostatic substances.

A

platelet adhesion and aggregation

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33
Q

bv exposes substances to attract hemostatic components

A

platelet adhesion and aggregation

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34
Q

collagen activators etc w/in bv

A

platelet adhesion and aggregation

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35
Q

platelet travels

A

platelet adhesion and aggregation

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36
Q

complete occlusion (clog)

A

coagulation and fibrinolysis

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37
Q

sealing plt clog

A

coagulation and fibrinolysis

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38
Q

a. Repairs -

A

Coagulation

39
Q

b. Re-establish -

A

Fibrinolysis

40
Q
  • Sealer
A

Coagulation Factor

41
Q

Vasoconstriction during injury due to surrounding tissues that swells until maipit ang blood vessel.

A

Extravascular components

42
Q

(Fleshy part exerts more pressure unlike in the scalp)

A

bulk or amount of surrounding tissue

43
Q

(Skeletal tissue: more effective than loose connective tissue = more vasoconstriction = less bleeding)

A

type of tissue

44
Q

(“ Elasticity or Flexibility “ - lesser for varicose veins)

A

tone of the surrounding tissue

45
Q

Extravascular cells that participates –

A

a. Fibroblasts
b. Smooth muscle cells

46
Q
  • All are highly pro-coagulant
  • Temporary seals
A

a. Fibroblasts b. Smooth muscle cells

47
Q

Size of the blood vessels.
- Arteries – thicker & larger
- (?)– harder to seal
-(?) – easier to seal

A

Thicker

Thinner

48
Q

(does not easily clot; with strong pressure causing excessive bleeding; with many sm)

A

Arteries - larger and thicker

49
Q

(compare the walls of the arteries from that of the veins and capillaries)

A

Amount of smooth muscle within their wall

50
Q

have higher amount of SM

A

Arteries

51
Q
  • Platelet affects endothelial cell lining and make the cessel strong
A

Integrity of the endothelial cell lining

52
Q
  • arteries have thick walls, but can be a cause of death due to difficulty to seal (longer clotting)
A

Integrity of the endothelial cell lining

53
Q

: coagulation factor

A

Biochemicals

54
Q

Less important systems:

A

complement system (inflammation)
kinin system (bradykinin)
serine protease inhibitors

55
Q
  • controls heart beat during hemostais
A

kinin system (bradykinin)

56
Q

– regulate clotting, inhibits coagulation, fibrinoloysis; proteins from the liver

A

serine protease inhibitors

57
Q

endothelial lining shedding

A

desquamation

58
Q

tissue factors and collagen is released from the damaged endothelium

A

small tissue injuries

59
Q

Platelet function Cascade:

A

a. Platelet adhesion
b. Attraction
c. Secretion
d. Aggregation

60
Q

– change their shape

A

b. Attraction

61
Q

– secretes granules and these granules attracts more platelet.

A

c. Secretion

62
Q

Activation of coagulation - (?) (proenzyme ) inactivated enzymes

A

Zymogens

63
Q

Zymogens Example :

A

Fibrinogen – inactivated fibrin Factor 10 (inactivated) – Factor 9 (inactivated to Activated form

64
Q
  • assembly area for coagulation factors (in the cell membrane)
A

Platelet phospholipid

65
Q

Primary Hemostasis Ends with

A

(3) platelet plug formation

66
Q

: These substances work against the coagulation process, preventing blood coagulation.

A

ANTICOAGULANTS

67
Q

: initiates the process of fibrinolysis or blood clot degradation.

A

FIBRINOLYTIC

68
Q

: substances that keep the blood vessels from narrowing or contracting.

A

VASODILATOR

69
Q

Warfarin is an example of this.

A

ANTICOAGULANT

70
Q

It causes the blood vessel’s interior (lumen) to widen.

A

VASODILATOR

71
Q

: substances that tighten or shrink the blood vessels.

A

VASOCONSTRICTOR

72
Q

It causes the blood vessels’ lumen to be smaller.

A

VASOCONSTRICTOR

73
Q

: a substance that is necessary for the coagulation of blood to occur.

A

PROCOAGULANT

74
Q

These promote/stimulate coagulation, hence known as “hemostatic agents.”

A

PROCOAGULANT

75
Q

Examples of these are Tissue factor and FXa.

A

PROCOAGULANT

76
Q

• Stimulates vasodilation

A

Prostacyclin (PGIz)

77
Q

• Inhibits platelet activation

A

Prostacyclin (PGIz)

78
Q

Prostacyclin (PGIz)

A

Anticoagulant

79
Q

Heparan sulfate

A

Anticoagulant

80
Q

Thrombomoduli n (Endothelial protein C receptor)

A

Anticoagulant
Fibrinolytic

81
Q

Tissue factor pathway inhibitor (TFPI)

A

Anticoagulant

82
Q

Tissue plasminogen activator (tPA)

A

Fibrinolytic

83
Q

Reduces blood flow rate

A

Adenosine

84
Q

Adhesion molecules

A

Procoagulant

85
Q

von Willebrand factor (VWF) (Weibel-Palade bodies)

A

Procoagulant

86
Q

• Coats the endothelial cell surface and weakly enhances activity of antithrombin-III

A

Heparan sulfate

87
Q

• Endothelial surface receptor for thrombin (binds and inactivates thrombin)

A

Thrombomoduli n (Endothelial protein C receptor)

88
Q

• Enhances anticoagulant and fibrinolytic action of protein C

A

Thrombomoduli n (Endothelial protein C receptor)

89
Q

• Controls activation of the extrinsic pathway

A

Tissue factor pathway inhibitor (TFPI)

90
Q

• Stimulates vasodilation

A

Prostacylin
Adenosine

91
Q

• Required for platelet adhesion to site of vessel injury

A

von Willebrand factor (VWF) (Weibel-Palade bodies)

92
Q

• P-selectin; Intercellular adhesion molecules (ICAMs)

A

Adhesion molecules

93
Q

• Platelet endothelial cell adhesion molecules (PECAMs)

A

Adhesion molecules

94
Q
  • help cells stick to each other and to their surroundings.
A

• Platelet endothelial cell adhesion molecules (PECAMs)