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physiology > Blood: Haemostasis L3 > Flashcards

Blood: Haemostasis L3 Flashcards

1
Q

what is Haemostasis

A

the arrest of bleeding from a broken blood vessel
- capillaries, arterioles, venules

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2
Q

what are platelets

A

cellular elements of the blood
- they are fragments of large cells from bone marrow called megakaryocytes
- have no nucleus

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3
Q

what hormone regulated megakaryocytes and platelet production and where is it made

A

thrombopoietin
produced in liver and kidneys

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4
Q

describe thrombopoiesis
-platelet synthesis

A
  1. starts with hematopoietic stem cell
    - differentiate into megakaryoblasts
  2. megakaryoblasts follow myeloid line
    - develop into megakaryocytes by undergoing repeated mitotic cycles without ever actually dividing.
    - Megakaryocytes are massive cells with multiple copies of DNA
  3. thrombopoietin stimulates megakaryocyte to extend arm through bone marrow sinusoids into blood vessels
    - Break off as platelets
    Produce about 1011 a day
    1000-3000 platelets/megakaryocyte in its life span
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5
Q

describe the structure of platelets

A

Exterior coat – rich in glycoproteins (adhesion, aggregation and activation)
Tubular System - site of thromboxane A2 synthesis and release
Microtubules and microfilaments – maintain shape
Granules – alpha: contain clotting mediators including von Willebrand factor, factors V, VIII and fibrinogen;
delta (dense bodies): contain ADP, Ca++ and serotonin, required for platelet activation and clotting
mitochondria

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6
Q

where are platelets stored and when are they released

A

in the spleen (short life span- undergo apoptosis and phagocyted in liver and spleen)
released by contraction of the spleen activated by sympathetic nervous system

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7
Q

what are the 3 main steps in Haemostasis

A
  1. vascular spasm (contraction of vessel)
  2. formation of platelet plug
  3. blood coagulation
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8
Q

describe vascular spasm

A
  1. damage to vessel causing damaged cells and platelets to release potent vasoconstrictors such as serotonin and ADP at cut site
    - causes smooth muscle layer in vessel wall to constrict slowing flow of blood and limiting blood loss
  2. ends of endothelial layer pushed together by the spasm becoming sticky
    - adhere to each other
    - aided by platelets that stick to exposed collagen
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9
Q

describe formation of platelet plug

A
  1. platelet adhesion
    - platelets stick to each other using von Willebrand’s factors (plasma protein secreted by endothelial cells and platelets
  2. platelet activation
    - activation causes platelets to have irregular shape with many protruding pseudopodia
    - they are more sticky this way
    - Secrete things that cause them to stick together and attract more platelets
  3. plug is formed
    - seals the break in the lining
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10
Q

what is the function of the platelet plug

A
  1. seal break
  2. compaction/ strengthening
  3. further vasoconstriction
  4. stimulate clotting cascade
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11
Q

what is the role of Prostacyclin (PGI2) which is released by normal vessel lining

A

inhibits platelet aggregation
limits platelet plug to the damaged region of the vessel preventing it’s spread to normal, undamaged tissue.

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12
Q

describe Blood coagulation

A

aka blood clotting
-process changing liquid blood to a solid gel (clot or thrombus)
- Clot strengthens and supports the platelet plug

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13
Q

what is the final step in blood coagulation

A

fibrinogen (large soluble plasma protein) converted to fibrin (insoluble thread like molecule) which RBC get trapped in

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14
Q

what factors are involved in the final steps of blood clotting

A
  1. thrombin (IIa- active 2)
    - turn fibrinogen (factor 1) into fibrin monomers
  2. XIII (active 13) and calcium
    - turns fibrin monomer to fibrin polymer which forms the clot
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15
Q

what are the three pathways of blood clotting

A
  1. intrinsic
    - Initial stimulus is exposed collagen (through damage to the endothelium wall).
  2. extrinsic
    - Initial stimulus is blood contact with damaged tissue outside of the blood vessel that exposes tissue factor (also known as factor III; or tissue thromboplastin).
  3. common pathway
    - I and E join in the later stages of coagulation
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16
Q

describe intrinsic pathway

A
  1. blood vessel damaged
    - active XII (12) activates XII (11) which activates IX (9) which activates X (10) (active X is start of common pathway)
17
Q

describe extrinsic pathway

A
  1. damage to tissue outside blood vessel
    - exposes tissue factor III (3)
    - tissue factor III and active VII (thromboplastin) activates IX (9) which activates X
18
Q

give 2 examples of positive feedback in the pathways

A
  1. high levels of thrombin leads to more XI being activated
  2. high levels of active X causes more tissue factor III and VII (thromboplastin)
19
Q

what does Anti-thrombin do in the anti clotting system

A

inhibits clotting factors including thrombin

20
Q

what does Thrombomodulin do in the anti clotting system

A

binds to thrombin stopping its clotting effects and inactivates factors Va and VIIIa

21
Q

what does tissue factor pathway inhibitors do in the anti clotting system

A

bind to factor III/VIIa complex preventing it from activiating IX and X
binds directly to Xa

22
Q

what does Thrombin do in the anti clotting system

A

binds to its receptor stimulating production of prostaglandins (PGl), nitric oxide and ADP to inhibit further platelet aggregation

23
Q

what is Fibrinolysis

A

clot break down

24
Q

describe fibrinolysis

A

Aggregated platelets secrete platelet derived growth factor β (PDGF β) that recruits fibroblasts from the surrounding tissue.
Fibroblasts form scar tissue at the site of the damage.
Simultaneous with healing - clot is dissolved by a fibrinolytic enzyme called plasmin.

25
Q

what is plasmin activated by

A

tissue plasminogen activator (t-PA), secreted by endothelial cells.
t-PA needs to bind fibrin to become active, hence only works on clot.

26
Q

give summary of clotting factors

A

Clotting factors other than III, V, VIII and XIII are proteases that activate downstream factors
III, V and VIII are glycoproteins
XIII is a transglutaminase

27
Q

give 4 types of haemostasis disorders

A
  1. excessive or inadequate clotting
  2. acquired (something happens that changes physiology) or inherited
  3. defects of platelets
    - quantitative (thrombocytopaenia)
    - qualitative (thrombopathy)
  4. Deficiency or dysfunction of coagulation factors (coagulopathy)
28
Q

acquired disorders are more common than inherited
- give examples

A
  • renal disease – lack of thrombopoeitin
  • hepatic disease - lack of fibrinogen
  • vitamin K deficiency – needed for synthesis of clotting factors II, VII, IX and X (VK needed)
  • drug-induced disorders
    include effects on platelet activity
    e.g. aspirin and other non-steroidal anti-inflammatory drugs inhibit thromboxane A2 synthesis and secretion
29
Q

give examples of inherited disorders

A
  • Structural defects to vascular system.
  • Thrombotic disorder: an alteration to haemostasis that impairs capacity to combat clot formation
  • Quantitative (thrombocytopaenia) or qualitative (thrombopathy) defects of platelets
  • Deficiency or dysfunction of coagulation factors (coagulopathy)
30
Q

what is Haemorrhage

A

“Black and blue” marks caused by internal bleeding.

Due to degradation of haemoglobin to biliverdin, bilirubin and heamosiderin
- Come from break down of heam

Eventually removed by plasmin and phagocytosis

31
Q

Thrombosis - Excessive/unwanted clotting
what are consequences of thrombosis

A
  1. Thrombus – Blood clot within a vessel or the heart
  2. Embolus – detached mass able to travel in a vessel
    Solid, liquid or gas
  3. Embolism - the lodging of an embolus
  4. Thrombo-embolism – blockage by a thrombus
  5. Stenosis – abnormal narrowing of a passage in the body
32
Q

Virchow’s Triad describes three risk factors for thrombosis:
what are they

A
  1. Blood stasis e.g. deep vein thrombosis (DVT)
    - Blood not moving around body in normal way blood more likely to clot
  2. Changes in the vessel wall
    – injury, inflammation
  3. Thrombogenic changes in the blood – hypercoagulability (causes/risk factors include obesity, smoking, pregnancy, cancer, age; can be inherited)
33
Q

how does thrombosis effect blood flow
- Thromboembolism

A

Need to get to high percentage of blocking before it really affects blood flow

34
Q

what treatments are there for thrombosis

A

anticoagulant drugs
Warfarin: Most widely prescribed oral anticoagulant; inhibits vitamin K.
Heparin: endothelial cell–derived polysaccharide.
Given by injection (not absorbed through gut).
Activates antithrombin III (AT)

Used where the likelihood of forming clots is increased:
- atrial fibrillation (an irregular heart beat where blood can pool and clot in the heart) sits in heart- more likely to clot
- aortic valve replacement
- recent surgery
- autoimmune disease attacking fat and protein components of blood vessel walls

35
Q

what is Thrombocytopenia

A

quantitative platelet disorder that sees low platelet count
caused by
autoimmune disease
drug induced – inhibition of platelet synthesis (eg interferon, alcohol), immunologic destruction of platelets (eg ibuprofen, tamoxifen)
results in Easy bruising, petechial rash, mucous membrane bleeding or excessive bleeding after minor trauma
- Petechiae

36
Q

what is Thrombotic thrombocytopenic purpura

A

platelet disorder caused by formation of small clots in the circulation; results in low platelet numbers.
Spontaneous aggregation of platelets and initiation of the clotting cascade
Rare but serious disorder; can be congenital, an autoimmune disease or caused by toxins

37
Q

give 3 examples of inherited coagulopathies

A

1.von Willebrand’s Disease:
- Lack of von Willebrand factor ->. poor platelet aggregation. Common symptom: excessive gum bleeding. Autosomal dominant. Mild.
2. Haemophilia A:
- Deficiency in factor VIII. X-linked recessive disorder. Excessive bleeding
3. Haemophilia B:
- Deficiency in factor IX. Also known as ‘Christmas disease’. Less server
- both associated with excessive bleeding
- Severity depends on how much factor VIII or IX is present in blood.

Treatment: replacement of ‘missing’ clotting factor

physiology (10 decks)

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