Haematolgy 3 Flashcards

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1
Q

What is haemostasis

A

➢The mechanism for dealing with bleeding and clotting
➢Haemostasis comes from the Greek - heme meaning blood and stasis to halt

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2
Q

Why and what happens during normal haemostasis

A
  1. Maintain the fluidity of circulating blood
  2. Limit and arrest bleeding following injury by formation of a blood clot whilst at the same time maintaining blood flow through the damaged vessel
  3. Removal of a blood clot upon completion of wound healing
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3
Q

Sequence of haemostasis

A

1) the endothelium/blood vessel Wall is destroyed
2)platelets cause coagulation
3)coagulation factors

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4
Q

Platelets in haemostasis

A

-anuclear
-circulate for 7-10 days
-each days 100 billion is produced from megakaryocytes to maintain Normal count

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5
Q

Role of platelets

A

➢Their primary physiological role is in blood clotting
➢Detect damaged vessel endothelium ➢Accumulate at the site of the vessel injury ➢initiate blood clotting to block the circulatory leak

➢They are involved in ALL stages of haemostasis ➢Primary haemostatic plug (platelet to platelet interactions)
➢Secondary haemostatic plug (platelet – coagulation protein interactions)
➢Involved in tissue injury, inflammation and wound healing by attracting and binding leukocytes

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6
Q

Megakaryocytes

A

-Largest (50-100μm) and rarest cells in BM
-Polyploidal (More than one nucleus)
-Unique to mammals
-Can produce ~3000 platelets (compared to 2 daughter cells in other lineages)
-Platelet formation is far more complicated than the production of white cells

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7
Q

Platelet production

A

Phase I
-Megakaryocyte maturation(need to be big to have enough protein)
→ Endomitosis (DNA replication without cell division)
→Cytoplasm enlargement (cytoskeletal proteins and platelet granules)
Phase II
-Platelet generation
→ Mature megakaryocytes extend long branching processes (proplatelets)
→ Organelles and granules are transported to proplatelets
→ Driven by the cytoskeleton
They migrate to blood vessels in bone Marrow
Stimulated by thrombopoietin tpo

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8
Q

Processes that occur in a healthy blood vessel to prevent coagulation

A

-nitric oxide ptrostacyclin prevents platelets from being active as well as stops them from sticking

-continuous barrier of endothelium which prevents platelets sticking to collagen

-natural anticoagulants such as anti thrombotic which stops unwanted coaugulation

-platelets are not active

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9
Q

What happens when a blood vessel becomes damaged (platelet activation)

A

-Platelets become active
-Endothelium is damaged to platelets stick to collagen and to Von willebrand factor(vwf) at site of blood vessel damage(it forms a bridge between collagen and platelets sticking, stick to vwf first then collagen)
-Platelets become activated, change shape, release granules and aggregate
-prothrombotic factors

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10
Q

What is haemostasis and what does is require

A

-Fast series of reactions for stoppage of bleeding
-Requires clotting factors, and substances released by platelets andinjured tissues

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11
Q

3 steps of haemostasis

A
  1. Constriction of blood vessels (vasoconstriction)
  2. Platelet plug formation
  3. Coagulation (blood clotting)
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12
Q

HAEMOSTASIS: VASOCONSTRICTION

A

➢Direct injury to vascular smooth muscle
➢Chemicals released by endothelial cells and platelets
➢Pain reflexes

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13
Q

SECONDARY HAEMOSTASIS: COAGULATION

A

12 factors
Castcasereaction
Fibrinogen,prothrombin
Tissue factor

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14
Q

Blood coagulation cascade

A

Vessel injury-tissue factor-blood coagulation cascade -thrombin-fibrin(net,sits over blood cloth,stabilising clotting-stable haemostatic plug

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15
Q

Coagulation pathways

A

Consists of two distinct pathways:
-the extrinsic (tissue factor pathway)
-the intrinsic pathway
X marks the spot and is the common factor

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16
Q

Clot stabilisation

A

➢Soluble fibrinogen converted to insoluble fibrin
➢Stabilises platelet clot

17
Q

FIBRINOLYSIS(removal of cloths when we don’t need them)

A

-Two mechanisms limit clot size
>Swift removal and dilution of clotting factors >inhibition of activated clotting factors
-Fibrinolysis breakdown of clots
>Removes clots after healing
>Begins within two days; continues for several

18
Q

DISORDERS OF HAEMOSTASIS

A
  1. Thromboembolic disorders: undesirable clot formation
  2. Bleeding disorders: abnormalities that prevent normal clot formation
19
Q

Thrombus

A

-clot that develops and persists in unbroken blood vessel
–May block circulation leading to tissue death
–Deep venous thrombosis (DVT) and pulmonary embolism

20
Q

Embolus

A

thrombus freely floating in bloodstream
Formed somewhere else ans a small piece fractured

21
Q

Embolism

A

The fracture get stuck somewhere else

22
Q

Risk factors of thromboembolic conditions

A

atherosclerosis, inflammation, slowly flowing blood or blood stasis from immobility

23
Q

Antithromboric drugs

A

-Aspirin= Cyclooxygenase inhibitor, that blocks thromboxane A2 synthesis and inhibits platelet aggregation(arteries )
-heparin = Anticoagulant used clinically for pre- and postoperative cardiac care(venous)
-Warfarin= for those prone to atrial fibrillation, interferes with action of vitamin k (its an antagonist)(rat poison),used in old patients
-Apixaban, Rivaroxaban= Factor X Inhibitors (DOACs (direct oral anticoagulants)/NOACs (novel oral anticoagulants)

24
Q

Bleeding disorders

A

➢Thrombocytopenia - deficient number of circulating platelets ➢Haemophilia includes several similar hereditary bleeding
disorders
➢Haemophilia A: most common type (77% of all cases); factor VIII deficiency ➢Haemophilia B: factor IX deficiency
➢Haemophilia C: mild type; factor XI deficiency
➢Von Willebrand’s Disease most common inherited bleeding disorder