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Phsyiology 210 > BLOOD 3 > Flashcards

BLOOD 3 Flashcards

1
Q

“Pro-hemostatic” or

“Pro-coagulant” factors

A

(prevent blood loss)

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2
Q

“Anti-hemostatic” or

“Anti-coagulant” factors

A

(Keep blood fluid)

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3
Q

Key steps of hemostasis

A
  1. Vasoconstriction
  2. Primary hemostasis
  3. Secondary hemostasis
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4
Q

Primary hemostasis

A

platelet plug formation (“white thrombus”)

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5
Q

Secondary hemostasis

A

blood clotting or blood coagulation (“red thrombus”)

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6
Q

Where do platelets come from?

A

in the BM from cells called megakaryocytes

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7
Q

Strucure of platelets contain :

A
  • Alpha granules

- Dense granules

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8
Q

Do platelets have a nucleus?

A

No,

  • no DNA
  • short lived
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9
Q

Alpha granules contain relatively large molecules:

A 
– Adhesion molecules such
as von Willebrand factor
(vWF) 
– Growth factors 
– Clotting factors 
– Cytokines
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10
Q

Dense granules contain relatively small molecules

A
  • ADP and ATP
  • 5 hydroxytryptamine (5HT) or serotonin
  • Ca++
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11
Q

Platelet plug formation (primary hemostasis)

A
  1. ADHESION of platelets
    – they stick to damaged vessel wall
  2. ACTIVATION of platelets
    – they change shape, express various receptors and secrete various substances
  3. AGGREGATION of platelets
    – they stick to each other and form a plug
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12
Q

Activated platelets affect:

A
  • 5HT
  • TXA2
  • ADP
  • PL
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13
Q

Why does platelet plug not continuously expand?

A

adjacent endothelial cells are a source of chemical signals that influence platelet aggregation and alter blood flow and clot formation at the affected site.

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14
Q

Effects of Arachidonic acid metabolites

A

Disturbance in cell memb. —> Memb. Phospholipids —>
Arachidonic acid:
—> lipoxygenase pathway (inflammation)
—> cyclooxygenase pathway (hemostasis)

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15
Q

Effect of Aspirin on Hemostasis

A

Low aspirin, favours COX 1 is inhibited and COX 2 is inhibited I totally, but is then replenished because endothelial cells are nucleated, which forms prostacyclin which prevents blood clotting

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16
Q

COX 1 is in the _______ and COX 2 is in the ________

A

Platelets. Endothelial cells

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17
Q

COX 1

A

Thromboxane A2

  • vasoconstriction
  • increased platelet aggregation
  • “PRO-hemostatic effect”
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18
Q

COX 2

A

Prostacyclin

  • vasoconstriction
  • decreased platelet aggregation
  • “ANTI-hemostatic effect”
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19
Q

Secondary Hemostasis occurs following a

A

platelet plug formation

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20
Q

Secondary hemostasis involves

A
  • a cascade of enzyme (clotting factors) activation
  • Activation of enzymes occur by proteolytic cleavage
  • Formation of gel-like fibrin clot
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21
Q

Clotting/coagulation factors

are

A

plasma proteins

22
Q

Where are plasma proteins made

A

Liver

23
Q

What does the synthesis of plasma proteins (clotting/ coagulation factors) require?

A

Vitamin K

24
Q

Factors 1-4 (I-IV)

A

I : fibrinogen
II : Prothrombin
III : tissue factor
IV : calcium

25
Q

Factors 5 and 12 (V and VII) are both

A

Cofactors

26
Q

Activation of thrombin

A
  • intrinsic pathway —> (
  • extrinsic pathway —> (

)—> “Common activated factor” —> Prothrombin —> Thrombin

27
Q

Traditional/Classical mechanism of blood clotting

A

Intrinsic extrinsic pathways meet up at one point. 3 pathways intrinsic, extrinsic, and common pathway. Know the sequence of activation in both pathways. Know how they are related and how they form a clot.

28
Q

A deficiency in the factors _________ cause severe bleeding

A
  • VII (7)
  • VIII (9)
  • XI (11) (moderate bleeding)
29
Q

A deficiency in factor XII causes

A

No bleeding problem in vivo; failure to clot in vitro

30
Q

Vivo =

Vitro =

A 
Vivo = inside body 
Vitro = outside body
31
Q

Blood from a healthy normal individual can clot when placed in a glass test tube ?

A

YES

32
Q

Blood will have a delayed clot formation in a

A

silicone-coated test tube.

33
Q

Physiological mechanism of blood clotting in vivo

A
  • Activation of the extrinsic and intrinsic pathways happen in a sequential manner
  • Initiation happens at extrinsic pathway,
    small amounts of thrombin amplify the
    intrinsic pathway to form a large clot
  • Note where V and VIII works in the pathway
34
Q

Amplification of clotting protein activity by

A

thrombin

35
Q

Wh at does Thrombin do in the clotting pathway?

A
  1. Activation of platelets
  2. Conversion of soluble fibrinogen to insoluble fibrin
  3. Activation of several other clotting factors
    (factor V, VIII,XI, and XIII)
  4. Activation of “protein C” (anticoagulant activity)
36
Q

Hemophilia B: X-linked recessive gene

A
  • Deficiency of factor IX
  • Less common than Hemophilia A (Factor 8)
  • Expressed in males
  • No treatment available
37
Q

Regulation of blood clotting

A
  1. Prevention of clot formation where and when it is not required
    – Role of various anticoagulants
  2. Breakdown of clot as tissue repair occurs
    – Role of fibrinolytic system
38
Q

Role of various anticoagulants

A

Prevention of clot formation where and

when it is not required

39
Q

Role of fibrinolytic system

A

Breakdown of clot as tissue repair occurs

40
Q

Prevention of clot formation: natural anticoagulants and wat they inhibit/change

A
  • TFPI (inhibit X a and VII a)
  • antithrombin 3 (inhibit thrombin)
  • thrombomodulin (changes thrombin)
  • protein C and S (inhibit V a and VIII a)
41
Q

When thrombin is bound to thrombodulin, it has

A

PRO-coagulant activity

  • increases platelet activation and fibrin formation
42
Q

When thrombin is NOT bound to thrombodulin, it has

A

ANTI-coagulant activity

43
Q

Actions of thrombin as an anticoagulant

A 
Normal endothelial cells —-> 
Thrombomodulin —> 
Thrombin —> 
Protein C —> 
Activated protein C 
-> factor VIIIa
-> factor Va
44
Q

Prevention of clot formation: “Clinical Anticoagulants”

A
  • Calcium chelators (eg. Na citrate) (vitro): removed ionized Ca++
  • Heparin (vitro and vivo): increases effects of antithrombin 3
  • antagonists of vitamin K (vivo): inhibits synthesis of II, VII, IX, and X in liver
45
Q

Fibrinolysis is the

A

Breakdown of Fibrin Clot

46
Q

Breakdown of Fibrin Clot: Fibrinolysis

A

We have many enzymes, but here were just mentioning one of the model enzymes, plasminogen activators, that converts inactive plasminogen to an active plasmin. For this activation to take place, it has to be in contact with the fibrin clot.

47
Q

Fibrinolysis

A 
• Natural Plasminogen
activator
– tissue plasminogen activator 
– released from endothelial cells 
– release increased by exercise

• Clinical clot busters or thrombolytic drugs
– used to treat patients with heart attacks
– eg., tenectaplase

48
Q

Failure of hemostatic mechanisms when they ARE required

A
  1. problems with platelets
    a) not enough platelets (thrombocytopenia)
    b) abnormal platelet function (eg., deficiency of vWF)
  2. problems with clotting factors
    a) hereditary deficiencies (eg.hemophilias)
    b) acquired deficiencies (eg. due to vit K deficiency)
49
Q

Formation of blood clot when

they are NOT required

A
  1. Hereditary disorders: deficiency in anticoagulants and fibronoyltic factors
  2. Acquired disorders: decreased/sluggish blood flow, damage to the blood vessel wall
50
Q

Abnormal hemostasis when this fine balance is broken

A
  • Excessive bleeding Hemorrhage

- Thrombosis may lead to stroke, heart attack

Phsyiology 210 (18 decks)

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