3. Blood (2) Flashcards

1
Q

Haemostasis:

A

prevention of blood loss/stopping blood

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2
Q

If a vessel is severed, haemostasis is achieved by:

A
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3
Q
  • Rupture of vessel —-> wall of vessel contracts, sticks
    together
  • Contraction results from: (3)
A
  • nervous reflexes initiated by pain
  • local smooth muscle spasm (main factor)
  • local humoral factors from traumatized tissues and blood platelets (Thromboxane A2)
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4
Q
  • Smaller vessels: platelets mainly responsible for
    vasoconstriction by releasing _______ _____ and
    forming a “plug”
  • Spasm lasts several hours —-> time to form platelet plug and _____ clot.
A

Thromboxane
fibrin

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5
Q

What do they contain? (6)

A
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6
Q

What forms part of the platelet membrane? (3)

A
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7
Q

Dead platelets are removed by macrophages, particularly in the ______.

A

spleen

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8
Q

What is the process of the Formation of the platelet plug?

A
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9
Q

Platelets are also activated by: (4)

A
  • thromboxane A2
  • ADP
  • serotonin
  • thrombin
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10
Q

What are the features of activated platelets? (6)

A
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11
Q

What is on the surface of activated platelets? (2)

A
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12
Q

What are the platelet-limiting factors and anti-platelet
pharmaceuticals?

A
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13
Q

What are the multiple injuries of micro-vessels?

A
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14
Q

What is blood coagulation?

A

Blood coagulation = Secondary Haemostasis

  • Coagulation = transformation of blood from a liquid to a semi-solid, gel state = clot
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15
Q

What is blood coagulation initiated by? (3)

A
  • extravascular cells
  • platelets
  • damaged vessel walls
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16
Q

What is the ultimate effect of blood coagulation?

A

conversion of fibrinogen (soluble plasma
protein) to fibrin (insoluble fibres) = clot

Fibrin clot adheres to the damaged vessel
surface and platelet plug, traps blood cells,
fills the breach and blocks the vessel (~20
minutes).

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17
Q

What are the clotting factors?

A
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18
Q

All clotting factors, except tissue factor, are produced by the _____ and are present in the blood as inactive precursors (______)

A

liver
(zymogens)

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19
Q

When activated, factors IIa (thrombin), VIIa, IXa, Xa, XIa and XIIa are:

A

proteolytic enzymes that activate other clotting
factors, by cutting the proteins

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20
Q

Four factors, II, VII, IX and X, can only be produced if
______ ____ is available in the liver.

A

Vitamin K

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21
Q
  • Factor XIIIa is also an enzyme, but it _____-_____ fibrin.
A

cross-links

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22
Q

What is fibrinogen?

A

Fibrinogen (FI) is not an enzyme or a co-factor. When the
fibrinogen protein is cut by thrombin (FIIa) it becomes
insoluble and forms fibres, called fibrin, which is the clot.

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23
Q

Five clotting factors VIIa, IXa, Xa, XIa and XIIIa
require _____ as a cofactor. (Blocking ____ prevents
coagulation in blood collection tubes.)

A

Ca2+

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24
Q

Two protease clotting factors, IXa and Xa require
platelet _________ for full activity.

A

Phospholipid

25
* Three protease clotting factors VIIa, Xa and IXa require clotting “________” proteins.
“co-factor”
26
The cofactor proteins are, respectively, _____ ____ (TF, FIII ----> TF/FVIIa), FVa (FVa/FXa) and FVIIIa (FVIIIa/FIXa).
tissue factor
27
Clotting proteins are inactive in plasma to avoid ______________ clots and tissue factor is absent.
Spontaneous
28
What is the general coagulation sequence?
29
* 3 different coagulation pathways form fibrin, 1 physiological, 2 “biochemical”:
30
What is the process of cell-based coagulation? (3)
31
Fibrin Formation and Crosslinking: (4)
32
Once the clot is formed: (2)
33
Platelets secrete growth factors - Fibroblast cells grow around and into the clot - ______ tissue forms (1-2 weeks) - Fibroblasts become _______ cells - Clot is removed (_______) Clot Retraction and Fibroblast Invasion
Scar endothelial fibrinolysis
34
Fibrinolysis and Dissolution of the Clot:
35
Vessel injury ---> blood oozes out of the vessel. To stop this:
36
Biochemical (laboratory) measurement of clotting: Primary haemostasis: Secondary hemostasis: (3)
---> Bleeding time Extrinsic pathway ----> Prothrombin Time (PT) Intrinsic pathway ---> Partial Thromboplastin Time (PTT) also ---> Whole blood clotting time
37
Bleeding Time Test Measures Platelet Function:
38
Prothrombin Time (PT) test – Extrinsic Pathway, what must be added to the blood?
39
Explain the Prothrombin Time (PT) test – Extrinsic Pathway?
40
* Blood is collected into citrate or EDTA tube (to chelate Ca2+). Removal of Ca2+ prevents coagulation in blood collection tube. * Blood is _______ to separate the plasma. * Plasma is mixed with Ca2+, tissue factor and phospholipid. * Time to make a clot is measured ----> usual range = _________ * Tests function of factors VII, X, V, II & fibrinogen = _____ pathway. * ____ is often expressed as INR (international normalized ratio) or prothrombin ratio. * INR = (Patient’s PT/Normal PT) Normal INR = _____ Biochemical ________ Pathways
centrifuged 12-15s extrinsic pathway 0.8-1.2 Coagulation
41
What is the Partial Thromboplastin Time (PTT) test – Intrinsic Pathway?
Factor XII is a plasma protein that activates (cuts) itself after binding to negatively-charged surfaces and molecules, including * in vitro: glass, silica, kaolin etc. * in vivo: collagen, platelets, denatured proteins, nucleic acids, microbes FXIIa activates FXI and also stimulates inflammation.
42
What is the full intrinsic coagulation pathway?
43
* Blood is collected into _______ or EDTA tube (to chelate Ca2+) and centrifuged. * Plasma is mixed with phospholipid, Ca2+ and a factor _____ activator (kaolin, silica...) * Time to form a clot is measured - usual range is less than ____ seconds. * Tests function of factors XII, XI, IX, VIII, X, V, II = intrinsic pathway * These factors can also be activated by _______
citrate XII 39 inflammation
44
What is a whole blood clotting time test? (4)
45
What does the extrinsic and intrinsic pathway start with?
46
What are the Mechanisms of Anticoagulation?
1. Clots should not form in healthy/unbroken blood vessels. * 90% of thrombin is immobilised in the fibrin clot. 2. Endothelial cells inhibit coagulation by * Their smooth endothelial surface and glycocalix layer, which repel platelets and clotting factors * Stimulating vasodilation (prostacyclin and NO) * Stimulating fibrinolysis (secretes tPA) * Producing molecules that inhibit clotting factors, especially thrombin * Producing molecules that break down clotting factors
47
How does Thrombomodulin produce anti-coagulation?
48
How does Antithrombin & heparin produce anti-coagulation?
49
How does Tissue Factor Pathway Inhibitor (TFPI) produce anti-coagulation?
50
What are the therapeutic anticoagulants? (5)
51
Coagulation disorders: (2)
Hypercoagulability Hypocoagulability
52
Hypercoagulability (risk of thrombosis) * 3 main causes:
1. Haemodynamics 2. Vessel injury 3. Excess pro-coagulants vs anticoagulants
53
What are the Haemodynamics of Hypercoagulability? (3)
54
What are the vessel injuries associated with Hypercoagulability?
55
Hypercoagulability - Excess Pro-coagulants vs Anticoagulants: (4)
56
How does Hypocoagulability (bleeding risk) affect platelet cells?
57
How does Hypocoagulability affect the Extrinsic Pathway?
58
Vitamin K deficiency has a major disruptive effect on the extrinsic pathway because of its effect on factor VII, but also disrupts the intrinsic pathway to a lesser extent because it decreases production of factor IX, in addition to decreasing ___ and ________.
FX thrombin
59
How does Hypocoagulability affect the Intrinsic pathway? (2)