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PHYSIO B1 > HAEMOSTASIS > Flashcards

HAEMOSTASIS Flashcards

1
Q

define Haemostasis

A

process of arrest of bleeding while maintaining blood in a fluid state within the vascular system.

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2
Q

what are the 2 stages of haemostasis

A

notes

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3
Q

platelet formation

A

notes

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4
Q

describe platelets( MCQ)

A
  • Nucleus absent
  • Cell membrane : glycoproteins, phospholipids, canalicular system, receptors,
    precursors of various substances.
  • Cytoplasm :
    a. ER & golgi apparatus: synthesize enzymes, store Ca.
    b. Mitochondria: ATP & ADP
    c. Contractile proteins: actin, myosin, thrombosthenin
    d. Other proteins present in the cytoplasm are fibrin stabilizing factor, platelet-derived growth factor, Von Willebrand factor.
    e. Granules : clotting factors and platelet-derived growth factor (PDGF).
    f. Enzymes: adenosine triphosphatase and the enzyme necessary for the synthesis of prostaglandins
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5
Q

Properties of platelets 3A

A
  1. Adhesiveness : when in contact with any wet surface or rough surface, these are activated and stick to the surface.
    * for adhesiveness- collagen, thrombin, ADP, thromboxane A2, calcium ions and von Willebrand factor.
  2. Aggregation- they stick to each other.
    * due to ADP and thromboxane A2.
  3. Agglutination. Clumping together
    * due to the actions of fibrinogen and GpIIb-IIIa.
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6
Q

Describe the functions of platelets.

A
  1. Haemostasis
    2.clot formation: formation of the intrinsic prothrombin activator
  2. Role in clot retraction: Contraction of contractile proteins
  3. Role in repair of injured blood vessels: The PDGF - repair of endothelium and other structures of damaged blood vessels.
  4. Role in defence mechanism: Phagocytosis of carbon particles, viruses and immune complexes.
  5. Transport and storage function: The 5HT is stored in the platelets and transported to the site of injury where it is released.
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7
Q

Normal Count and Variations

A

150,000 -450,000 platelets per microliter of blood. Thrombocytopenia: platelet count less than 150,000 /μl)
* platelet count below 50,000/ μl of blood is called critical count. Thrombocytosis: platelet count > 450,000 platelets/ μl

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8
Q

List the various clotting factors.

A

1- fibrinogen
2- prothrombin
3- thromboplastin
4- calcium
5- labile factor
7-stable factor
8- antihaemophilic factor A
9- christmas factor
10- stuart power factor
11-plasma thromboplastin anticedent
12- hagman factor
13-fibrin stabilising factor

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9
Q

Temporary Haemostatic Plug Formation

Platelets Adhesion
Secretion
Aggregation

A

Endothelial injury and exposure of collagen and (vWF)
|
Platelet adhesions and activation
|
Secretion of (ADP), thromboxane A2 (TXA2), and platelet-activating factor (PAF)
|
Recruitment of additional platelets (aggregation)
|
Hemostatic plug.

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10
Q

Mechanism of blood coagulation

A

1.Rupture of the vessel or damage to the blood itself
2.Complex cascade of chemical reactions -blood coagulation factors.
3.Prothrombin activator.
4.Prothrombin into thrombin.
5.Fibrinogen into fibrin fibers
6.Clot formation

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11
Q

common pathway

A

notes

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12
Q

Intrinsic pathway for initiating blood clotting.

A

n

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13
Q

Extrinsic pathway for initiating blood clotting.

A

n

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14
Q

Mechanism of fibrin stabilization.

A

n

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15
Q

Calcium:

A

Activation of clotting factor II, VII, IX, and X.
Absence of calcium- clotting does not occur

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16
Q

Vitamin K :

A

For the synthesis of following factors. * Coagulant like prothrombin,
* Factors VII, IX and X, and
* Circulatory anticoagulant protein
* Gastrointestinal disease - vit K is not absorbed
* Deficiency of vitamin K, prothrombin time and blood clotting time is prolonged.

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17
Q

Blood clot retraction

A

n

18
Q

Serum =

A

plasma – clotting factors

19
Q

Fibrinolysis

A

n

20
Q

Plasminogen activator

A
  • Tissue plasminogen activator (tPA)
    -Predominates under most conditions
  • Urokinase plasminogen activator (uPA)
  • Released in inflammatory conditions -Extravascular fibrinolysis
  • Converts plasminogen into plasmin
21
Q

Plasmin

A
  • Breaks fibrin into fibrin degradation products –clot dissolution
  • Degrades fibrin at healthy sites –Prevents unnecessary clot formation * Non-Specific: degrades fibrinogen, prothrombin, factor V, VIII & XII
  • Excessive activity- Depletes above clotting factors- hypocoagulability
22
Q

Regulation of fibrinolysis in
Healthy vessels

A
  • Plasminogen activator inhibitor
  • PAI-1 -Released from endothelium- predominant
  • PAI-2 - Released from placenta – mainly during pregnancy
  • Inhibit plasminogen activator- plasmin is not generated.

α2 – Antiplasmin
* Released from liver and kidney
* Inhibit excess plasmin

23
Q

Regulation of fibrinolysis in clot

A

Fibrin
* Potentiates plasminogen activator – plasmin is generated
* Occupies active site of plasmin- α2 – Antiplasmin cannot inhibit plasmin

24
Q

Why blood does not clot in circulation? (5)

A
  1. smoothness of the endothelial cell surface
    -prevents contact activation of the intrinsic clotting system
  2. Glycocalyx on endothelium-repels clotting factors and platelets
  3. Thrombomodulin - binds thrombin –slows the clotting process by removing thrombin and activates a plasma protein, protein C, that acts as an anticoagulant by inactivating activated factors V and VIII.
    4.Endothelial cells secrete
    * Prostacyclin
    * NO
    -inhibts platelet aggregation, vasodilation
  4. Natural anticoagulants: heparin, antithrombin-III
25
Q

Thrombosis definition

A

Pathological conditions that can cause intravascular clotting.
* The intravascular clotting is called thrombosis and the clot so formed is called thrombus.

26
Q

Predisposing factors and effects of thrombosis

A

Virchow’s triad
Endothelial injury.
Alterations in flow of blood
Hypercoagulability of blood

effects:
Ischaemia and infarction.
Thromboembolism – Pulmonary and cerebral

27
Q

Anticoagulants

A
  • Anticoagulants refer to the substances which delay or prevent the process of coagulation of blood.
    In vitro
  • Substances which sequester calcium, e.g. sodium citrate or oxalate, sodium edetate (EDTA).
    In vivo
  • Antagonizing clotting factors (e.g. heparin),
  • By destruction of the key substance fibrinogen
  • By inhibiting the synthesis of factors II, VII, IX and X (vitamin-K antagonists).
28
Q

Endogenous anticoagulants/ Circulatory anticoagulants

A

present inside the blood naturally
* Heparin,
* Antithrombin III,
* Protein-C.

29
Q

Exogenous anticoagulants: administered from outside or are used in vitro

A
  • Heparin,
  • Calciumsequesters,
  • Vitamin K antagonist
  • Defibrination substances
30
Q

Heparin

A

-Natural, Polysaccharide with sulphate group.
-Secreted by Basophils and mast cells.
-location: luminal surface of vascular endothelium
Mechanism:
* Prevents activation of prothrombin to thrombin
* Facilitates antithrombin III- deactivate 9,10,11,12

31
Q

Antithrombin III

A

Present in plasma and vascular endothelium
Along with Heparin deactivate Thrombin,9,10,11,12

32
Q

Protein C

A

n

33
Q

Calcium sequesters or decalcifying agents

A

Two types
1. Substances which form insoluble salts with calcium: E. g. sodium citrate and sodium oxalate
2. Calcium chelators which bind calcium: E.g. Ethylene diamine tetraacetic acid (EDTA)

34
Q

Vitamin K antagonists.

A

Mechanism:
occupy vitamin K receptor sites in the liver and hinder its activity.
Inhibit synthesis of vitamin K-dependent factors- 7,9,10
coumarin derivatives : e.g. dicoumarol, warfarin, phenindione.

35
Q

Defibrination substances.

A

Mechanism: Destruction of fibrinogen.
Malaysian pit viper venom: vivo acts as an anticoagulant by causing defibrination and also by stimulating fibrinolytic system.
In vitro, it has a direct anticoagulant effect on fibrinogen by forming imperfect fibrin polymer.
Arvin or Ancord.

36
Q

Haemophilia

A
  • Haemophilia A: deficiency of factor VIII (8)
  • classic hemophilia : 85%
  • Haemophilia B :deficiency of factor IX.
  • 15 %
  • (X) chromosome - Recessive in their inheritance.
  • Affects men
  • Women are carriers
  • Rare in women
  • Mutation causes 1/3rd cases with no family history
  • Treatment: Injection of factor VIII or IX.
37
Q

Factor VIII

A

Large component- Von Willebrand disease
Small component- Classic Haemophilia

38
Q

Thrombocytopenic purpura

A

Thrombocytopenia: presence of very low numbers of platelets in the circulating blood.
* tendency to bleed from small venules or capillaries.
* small punctate hemorrhages -petechiae, red or purplish blotches

39
Q

major causes of thrombocytopenia purpura

A
  1. Decreased platelet production in the bone marrow due to infections or sepsis, nutrient
    deficiencies, or myelodysplastic disorders.
  2. Peripheral platelet destruction by antibodies.
  3. sequestration (pooling) of platelets in the spleen, especially in individuals with portal hypertension and excessively splenomegaly.
  4. Consumption of platelets in thrombi.
  5. Dilution of the blood from fluid resuscitation or massive transfusion
    * Idiopathic thrombocytopenia- specific antibodies have formed and react against the platelets to destroy them.
40
Q

Thrombocytopenic purpura Treatment

A

-fresh whole blood transfusions with large numbers of platelets
- splenectomy

41
Q

Blood Coagulation Tests

A

The prothrombin time indicates the concentration of prothrombin in the blood.
* Blood removed from the patient is immediately oxalated- prothrombin cannot change into thrombin.
* Large excess of calcium ion and tissue factor is quickly mixed with the oxalated blood.
* The excess calcium nullifies the effect of the oxalate, and the tissue factor activates the prothrombin to thrombin reaction by means of the extrinsic clotting pathway.
* The time required for coagulation to take place is known as the prothrombin time.

PHYSIO B1 (19 decks)

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