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SL12100 Health and Disease Y1 > Lecture 16- blood clotting > Flashcards

Lecture 16- blood clotting Flashcards

1
Q

Thrombopoietin role

A

regulates platelet production

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2
Q

erythropoietin role

A

regulates red blood cell production

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3
Q

Megakaryote role

A

platelet production

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4
Q

Platelet

A

cell fragment- not a true cell, They do contain granules.

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5
Q

List blood vessels

A

vein  venule  capillary  arteriole  artery.

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6
Q

Describe arteries

A
  • carry oxygenated blood around the body and back to the heart
  • High blood pressure.
  • Thick walls. Many layers of smooth muscle and connective tissue and elastic fibres.
  • Narrow lumen- high blood pressure.
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7
Q

Describe capillaries

A

one cell thick, reduced rate of blood flow through the capillaries for sufficient exchange.

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8
Q

Describe veins

A
  • carry deoxygenated blood to the lungs from the heart. Low blood pressure.
  • wide lumen- thin walls- few elastic layers and few layers of smooth muscle and connective tissue
    -low blood pressure.
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9
Q

what is a bruise ?

A

blood loss from capillaries near to the surface of skin

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10
Q

What is a haematoma?

A

accumulation in the blood in the tissues as a result of bleeding from any vessel type- it is not always visible.

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11
Q

Blood loss would be greatest from which blood vessel and why?

A

greatest from an artery- higher blood pressure and blood flow. It is the most dangerous.

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12
Q

Why is it good to raise limb when bleeding?

A

lowers blood pressure, slow blood flow through the tissue, less blood is lost.

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13
Q

What is the immediate response to a damaged vessel? Why shouldn’t this be done for too long?

A

Immediate response of a damaged vessel is to constrict- the two opposing endothelial surfaces can temporarily glue together. However, this shouldn’t be done for too long- prolonged constriction of vessels can lead to damage to downstream organs and potentially organ failure.

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14
Q

Haemostasis is broken down into two parts. Describe.

A

primary haemostasis- platelet plug formation
secondary- blood clotting mechanism to transform and stabilize the weak platelet plug into a clot by fibrin network.

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15
Q

Describe the stages of platelet plug formation- primary haemostasis.

A
  1. Damage of endothelial cells exposes the subendothelial layers consisting of connective tissues- collagen fibres
  2. Platelets bind to the collagen fibres by a protein called vWF – the von Willebrand factor
  3. Platelet activation: binding causes the release of ADP and serotonin from their granules resulting in further platelet activation and causes a change in shape and surface protein expression
  4. Platelet aggregation: These changes cause platelets to adhere to each other to form a plug
  5. Adhesion of the platelets induces them to synthesise and release thromboxane A2 (from arachidonic acid) enhances the platelet activation and aggregation stages. Thromboxane A2 also causes contraction of vascular smooth muscle- vasoconstriction whilst the platelet plug is forming.
  6. Fibrinogen also has a crucial role in platelet aggregation. Fibrinogen forms bridges between aggregating platelets. Receptors- binding sites- for fibrinogen on the platelet plasma membrane become exposed and activated during activation.
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16
Q

Describe contraction and where it occurs during primary haemostasis.

A

Platelets contain high concentration of actin and myosin which are stimulated to interact in aggregated platelets. The actin and myosin cause contraction of the plug- cause compression and strengthening of the plug. They bind it tightly together.

Smooth muscle in vessels also contracts, as we know, due to thromboxane A2 and other chemicals released from the platelet’s granules.

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17
Q

Once started, why does the platelet plug not continuously expand?

A

Healthy, undamaged endothelial cells synthesize and release prostacyclin (PGI2) and nitric oxide
- PGI2 = inhibitor of platelet aggregation.
- Nitric oxide inhibits adhesion, activation and aggregation. Nitric oxide is a vasodilator- works against thromboxane A2 which is causing vasoconstriction.

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18
Q

Define clotting

A

the transformation of blood into a solid gel- a clot/thrombus- consisting mainly of fibrin polymers.

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19
Q

Other name for a clot

A

thrombus

20
Q

Where does clotting occur?

A

around the platelet plug- it reinforces platelet plug and solidifies the blood.

21
Q

Like platelet aggregation, how is clotting initiated?

A

clotting is initiated when a vessel is damaged and endothelium is disrupted, allowing blood to come in contact with underlying tissues (subendothelial collagen).

A cascade of chemical activations is triggered.

22
Q

During clotting, in the cascade of chemical reactions, at each step what occurs?

A

an inactive plasma protein is converted to become an active enzyme/cofactor activating the next step- generating the next enzyme in the sequence

23
Q

What is the key step in clotting cascade?

A

activation of prothrombin to thrombin

24
Q

What does thrombin convert?

A

converts fibrinogen into fibrin molecules.

25
Q

Role of fibrin

A

Fibrin bind together to form a mesh of fibrin- a network

26
Q

What can get trapped in fibrin meshwork/ What is the essential component?

A

Many erythrocytes and other cells are trapped in the fibrin meshwork, but the essential component is fibrin.

27
Q

Why are activated platelets essential for clot formation? As well as being activated in primary haemostasis, how else are platelets activated?

A

many cascade reactions take place on the surface of the platelets. Platelets are activated in the platelet plug stage, but in addition, thrombin stimulates platelet activation.

28
Q

The specific part of the clotting cascade when prothrombin is converted to thrombin, occurs via two pathways. Name.

A

intrinsic and extrinsic.

29
Q

Everything needed for the intrinsic pathway to occur comes from…

A

the blood

30
Q

What is needed for extrinsic pathway to occur?

A

cellular element outside the blood

31
Q

The intrinsic pathway is triggered after….

A

the extrinsic pathway.

32
Q

Describe extrinsic pathway. How is it a form of positive feedback?

A

initiated by tissue factors- not a plasma protein- located on the outside of the plasma membrane of cells found in sub endothelial tissue (which are exposed when vessels are damaged). When the subendothelial cells are exposed to blood, tissue factors are activated.
These initiate the pathway.
Normal pathway to activate clotting in the body.
Generates small amount of thrombin. Thrombin then feeds back onto the intrinsic pathway to activate components and generate more thrombin- positive feedback

33
Q

Describe the intrinsic pathway. Just name a couple of the key cofactors.

A

The vessel becomes damaged and XII- an essential cofactor, plasma protein in the blood- is activated by contact with collagen.

Many cofactors are activated throughout the pathway. one of them- FVIII is essential - its absence actually causes haemophilia.

34
Q

role of the liver in terms of clotting.

A
  • Site of the production of clotting factors
  • Produces bile salts required for the absorption of vitamin K- vitamin K is needed to produce prothrombin.
  • This is why patients with liver disease have bleeding problems.
35
Q

Thrombin is an enzyme which catalyses…How?

A

conversion of fibrinogen to fibrin.

activating factor V

36
Q

Thrombin activates platelets. Describe how.

A

The thrombin binds to a receptor on the surface of platelets called the protease activated receptor.

37
Q

Give four anti-clotting mechanism.

A
  • PGI2 and NO are anticlotting factors- they inhibit platelet activation
  • Endothelial cells production of tissue factor inhibitor.
  • Thrombin binds to endothelial cell receptor thrombomodulin to activate protein C which inactivates FV and VIII- in other words, it switches off its own pathway.
  • Plasma protein- antithrombin inactivates thrombin and other clotting factors.
38
Q

How does the fibrin clot dissolve?

A
  • Plasminogen activators activate the conversion of plasminogen to plasmin
  • Plasmin converts fibrin to soluble fibrin fragments
39
Q

disorders caused by damage to endothelium

A

myocardial infarction, atherosclerosis

40
Q

disorders caused by clots

A

DVT, pulmonary embolism

41
Q

What is haemophilia?

A

can’t clot- lack of clotting facotrs.

42
Q

Aspirin

A
  • pain killer
  • blood thinner- anticlotting agent
43
Q

Heparin

A

anticoagulant

44
Q

Warfarin

A

anticoagulant, blocks vitamin K

45
Q

Recombinant

A

dissolve clots already formed in the body.

SL12100 Health and Disease Y1 (18 decks)

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