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B2 > Haemostasis & Haematopoeisis > Flashcards

Haemostasis & Haematopoeisis Flashcards

1
Q

Haemostasis =

What’re its 3 components?

A

A series of regulatory processes that culminate in the formation of a blood clot to limit bleeding from an injured vessel
3 components: platelets, vascular wall and coagulation cascade

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2
Q

Haemorrhage =

A

Extravasation of blood into extravascular spaces

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3
Q

What’s the role of the endothelium and platelets in haemostasis?

A

Endothelium: has antiplatelet, anticoagulant and fibrinolytic properties to act as a barrier expressing factors which limit clotting to site of injury (prevent thrombosis)

Platelets: form the initial haemostatic plug, providing a surface for recognition of coagulation factors

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4
Q

What’re the 3 ways platelets form the initial plug and recruit coagulation factors?

A

Adhesion to ECM at sites of vascular injury
Activation by secretion of granules
Aggregation of platelets

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5
Q

What’s the coagulation cascade?

A

Two pathways extrinsic and intrinsic lead to final common pathway of FXa + FVa + Ca2+>prothrombin>thrombin>fibrinogen>fibrin which stabilises the clot

Intrinsic: FXIIa>FXIa>FIXa>FVIIIa> FXIa + FVIIIa + Ca2+

Extrinsic: TF>FVIIa> TF + FVIIa + Ca2+

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6
Q

What are the 3 stages of haemostasis?

A

1: Vasoconstriction - minimises blood loss and activated by endothelin release and neurogenic reflex
2: Primary haemostasis - initial platelet plug formed as vWF expressed on endothelial cells to recruit platelets, change platelet shape to enhance platelet-platelet interactions by secretory granules released
3: Secondary haemostasis - platelet plug consolidation by TF expression on subendothelial cells which binds to and activates factor VII and thrombin to initiate coagulation cascade. Thrombin cleaves circulating fribinogen to fibrin.

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7
Q

What drugs interfere with the coagulation cascade?

A

Heparin - binds to antithrombin III to inactivate thrombin and FXa

Warfarin - affects metabolism of vitamin K therefore affecting production of prothrombin, factors VII, X, IX

New oral anticoagulant: Dabigatran, reversible inhibitor of Thrombin

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8
Q

Step 4: clot stabilisation, resorption and role of fibrinolytic system

A

Fibrin and platelet aggregates undergo contraction to form permanent plug
Counterregulatory mechanisms limit clot to site of injury
Involves fibrinolytic system: inactive circulating plasminogen converted to plasmin which breaks down fibrin to reduce size of clot and contribute to later dissolution

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9
Q

How is coagulation controlled? Why is it important?

A

Needs to be restricted to the site of injury
Fibrinolytic cascade
Requires negatively charged surface (platelets)
Anticoagulation factors are expressed on adjacent intact endothelium
Circulating inhibitors eg antithrombin III
Dilution

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10
Q

Thrombosis =

A

Formation of a sold mass of blood products in a vessel lumen (thrombus)
Pathological process leading to vascular occlusion/ischaemia/infarct

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11
Q

What is Virchow’s triad? What are its 3 features?

A

Predisposition to thrombosis

Endothelial injury, abnormal blood flow, hypercoagulability

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12
Q

What are the fates of thrombi?

A

Propagation
Embolisation
Resolution/dissolution
Organisation

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13
Q

Embolism =

A

A detached intravascular solid/liquid/gas that is carried by the blood to a site distant from origin

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14
Q

What are common embolisation sites?

A

Lower extremities - limb ischaemia
CNS - stroke
Intestines - bowel ischaemia
Kidney/spleen - may be asymptomatic

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15
Q

Infarction =

A

Area of ischaemic necrosis caused by inadequate blood supply

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16
Q

What’s haematopoiesis?

A

The production of all types of mature blood cells

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17
Q

What causes megaloblastic anaemia?

A

Folic acid (vitamin B9) and cobalamin (vitamin B12) deficiency

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18
Q

What causes pernicious anaemia?

A

Intrinsic factor deficiency (maybe by autoimmune destruction of parietal cells) meaning reduced vitamin B12 absorption in the terminal ileum

19
Q

What’s the composition of blood? Plasma?

A

Cells + plasma = blood

Plasma: h20, small organic compounds, electrolytes, proteins (globulins, albumin, fibrinogen)

20
Q

Where are haematopoietic stem cells located? How do they give rise to cell lineages?

A

Bone marrow

Stem cells proliferate -> differentiate -> mature

21
Q

What are the 5 different types of stem cell in order of their potency?

A

Totipotent - any cell type
Pluripotent - any cell type of the embryo
Multipotent - several related cell types
Oligopotent - small number of very closely related cells
Unipotent - can produce more of the identical cell type

22
Q

What are the 2 common progenitor cells from a multipoint haematopoietic stem cell that starts the 2 lineages?

A

Common myeloid progenitor -> erythrocytes, thrombocytes, granulocytes, macrophages

Common lymphoid progenitor -> lymphocytes

23
Q

Outline Erythropoiesis, including what’s needed for it

A

Proerythroblast -> erythroblast -> reticulocyte -> erythrocyte

Controlled by EPO, requires Iron, folic acid and vitamin B12

24
Q

What are the 4 changes in erythrocyte maturation?

A

Acquisition of biconcave disc shape
Loss of organelles, including nucleus
Decrease in cell size
Haemoglobin production

25
Q

What’s the point of the biconcave disc shape of erythrocytes?

A

Maximises surface area
Minimises distance from surface
Increases flexibility
Simple internal structure, simplified metabolism, structural proteins maintain shape

26
Q

What 2 things does DNA synthesis require?

A 
Folic acid
Vitamin B12 (and intrinsic factor for absorption)
27
Q

What does haemoglobin synthesis require?

A

a and B globin chains

Haem (containing iron), vitamin B6 + Fe2+

28
Q

Where are folic acid and vitamin B12 absorbed?

A

Folic acid - duodenum and jejunum

B12 - terminal ileum

29
Q

What are inherited disorders of haem synthesis called?

A

Porphyrias

30
Q

Once iron is absorbed, where is it stored? What regulates iron absorption and how?

A

Bone marrow to make haem
Remainder stored in liver and spleen

Regulated by Hepcidin - released by liver when iron levels are raised so it decreases Ferroportin activity on the basolateral membrane of intestinal epithelial cells to inhibit absorption

31
Q

How are types of anaemia classified?

A

Microcytic hypochromic

Normocytic normochromic

Macrocytic

32
Q

What are types of leukocytes?

A

Granulocytes: neutrophils, eosinophils, basophils
Monocytes
Lymphocytes

33
Q

What are some white cell count disorders?

A

Leukocytosis - high WCC
Leukopenia - low WCC
Neutrophillia - acute bacterial infections
Eosinophillia - allergic disorders eg asthma
Lymphocytosis - viral infections

34
Q

Outline thrombopoiesis

A

Megakaryoblast -> Promegakaryoblast -> Megakaryocyte -> Thrombocytes (platelets)

35
Q

What are 2 platelet count disorders?

A

Thrombocytosis - high platelet count

Thrombocytopenia - low platelet count (reduced production or increased destruction)

36
Q

Role of Erythropoietin?

A

Released by fibroblasts in the kidneys in response to hypoxia to stimulate erythropoiesis in bone marrow
Binds to specific receptors on proerythroblasts to stimulate cell survival

37
Q

Role of Thrombopoietin?

A

Produced in the liver to stimulate differentiation of megakaryocytes and thrombocytes

38
Q

What 3 things does haemostasis allow?

A

Prevention of haemorrhage
Blood to be in fluid state in normal vessels
Formation of localised haemostatic clot at sites of vascular injury

39
Q

Outline blood vessel histology

A

Intima: endothelium, basement membrane, connective tissue, internal elastic lamina
Media: circumferentially arranged smooth muscle
Adventitia: connective tissue containing vascular and neural supply

40
Q

Which coagulation factors are dependent on vitamin K?

A

VII
IX
X
Prothrombin

41
Q

Outline the intrinsic pathway

A

Measured as partial thromboplastin time (PTT)
Initiated when FXII comes into contact with negatively charged surface (activated platelet)

FXIIa -> FXIa -> FIXa -> FVIIIa

FIXa + FVIIIa + Ca2+ activate final common pathway (FX)

42
Q

Outline the extrinsic pathway

A

Measured as prothrombin time (PT)
Initiated by tissue factor

TF activates FVII -> FVIIa + Ca2+ activates final common pathway (FX)

43
Q

What’s the final common pathway in the coagulation cascade?

A

FXa + FVa + Ca2+ = Prothrombinase complex for conversion of Prothrombin -> Thrombin

Thrombin converts Fibrinogen -> Fibrin

Fibrin monomers polymerise to form insoluble network around primary platelet plug
Clot further stabilised by FXIIIa forming strong cross links

44
Q

What’s the difference between unfractionated and low molecular weight Heparin?

A

Unfractionated: inactivates both FXa and Thrombin
LMWH: primarily inactivates FXa

B2 (21 decks)

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