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Structure & Function 4 > Haemostasis - Platelets > Flashcards

Haemostasis - Platelets Flashcards

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1
Q

what is haemostaiss?

A

this is a physiological process which stops the bleeding at the site of vascular injury

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2
Q

what does haemostasis do?

A

refers to process in which blood coagulation is initiated and terminated in a tightly controlled fashion

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3
Q

what happens when the ‘vessel’ is healed/remodelled?

A

clot dissolution (removal)

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4
Q

haemostasis happens whilst still maintaining?

A

blood flow elsewhere in the circulation

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5
Q

Haemostasis is a defence mechanism that does what?

A

it preserves the integrity of the vascular system

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6
Q

what are the 5 key players in haemostasis?

A

blood vessels
platelets
coagulation factors
coagulation inhibitors
fibrinolytic factors

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7
Q

what is the first step of haemostasis?

A

vasoconstriction - restricts blood flow in and to the damaged vessel

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8
Q

what is the second step of haemostasis?

A

platelets aggregate and form a platelet plug
termed as ‘Primary haemostasis’

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9
Q

what is the third step of haemostasis?

A

coagulation cascade activated to facilitate thrombin generation
this proteolyzes soluble fibrinogen to yield insoluble fibrin
referred to as ‘Secondary haemostasis’

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10
Q

what is the fourth step of haemostasis?

A

fibrinolysis - removal of the clot in a controlled fashion

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11
Q

why is haemostasis important?

A

essential to preserve the high pressure of vascular system
response must be rapid but regulated to prevent blood loss and also stop inappropriate clot formation - localised to maintain flow elsewhere
inappropriate coagulation could block vessels
restriction of blood flow
o2 starvation
cell death - brain, heart, other organs, limbs

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12
Q

haemostasis has an important role in?

A

in preventing microbes from gaining access to the circulation - link to innate immune system

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13
Q

pathological condition and risks associated with haemostasis?

A

haemophilia
DVTs
pulmonary embolism
surgical interventions - blood loss and fluid replacement causing a dilution of coagulation factors
liver disease
leukaemias

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14
Q

how is haemostasis so speedy?

A

platelets are circulating in blood in high numbers
ready to be activated at the site of injury and undergo rapid amplification of activation
coagulation proteins (made in liver) circulate/stored as inactive precursors (zymogens)
ALL COMPONENTS READY TO GO IN CIRCULATION

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15
Q

why is haemostasis localised?

A

platelets use receptors to sense proteins that are only exposed during vascular injury
collagens in ECM
Von Willebran Factor (VWF) in blood can then bind collagen and bridge the platelet to the ECM

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16
Q

platelets in avian species are different to other platelets, why?

A

platelets in avian species have a nucleus but platelets are anucleate in other species

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17
Q

lifespan of platelets?

A

up to 10 days species dependent

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18
Q

platelets?

A

cell fragments produced by bone marrow

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19
Q

production of platelets regulated by?

A

by the hormone thrombopoietin that is made by the liver and kidney

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20
Q

what disease may reduce platelet numbers?

A

liver disease

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21
Q

what is thrombocytopenia?

A

platelet deficiency

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22
Q

normal ranges of platelet numbers?

A

*Humans 150-400 x 109/L
*Most animal species 200-500 x 109/L
*Rodents at least 900 x 109/L

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23
Q

what are platelets sometimes called and give an example of when?

A

thrombocytes
e.g. in avian species

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24
Q

size of platelets?

A

2-4 micrometres diameter, varies between species

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25
describe resting platelets?
discoid in shape stain dark w/ visible red to pink granules do not adhere to healthy vessel wall or aggregate w/ each other vessel wall also releases factors that keep platelets inactive e.g. prostacyxlin extremely sensitive to activation - hard to maintain storage
26
thrombus formation needs to be?
rapid localised stable - doesn't have chunks embolising coordinated - rapid activation of platelets and coagulation to give stabilising fibrin
27
fibrin generation?
fibrin forms a mesh at the injury site to stabilise the thrombus formed as the endpoint of the coagulation pathway
28
when is the coagulation pathway activated?
during primary haemostasis
29
where are coagulation complexes formed?
on the negatively charged platelet membrane surfaces - a complex series of protein-protein interactions - lead to generation of thrombin from prothrombin - blood/platelet-derived soluble fibrinogen cleaved to fibrin by thrombin (secondary haemostasis)
30
VWF?
very large protein
31
size of VWF?
forms multimers of 80 subunits >20,000 kDa
32
where is VWF present?
present in plasma, platelet granules, storage granules in endothelial cells (Weilbel Palade bodies) and also bound to some ECM proteins)
33
describe VWF in resting conditions?
VWF is globular and does not bind to platelets
34
what can cause VWF to unfold? and what does this expose?
high shear stress or collagen binding causes VWF to unfold which exposes platelets binding sites
35
von willerband disease reported in which animals?
cats (rarer), rabbits, cattle, horses and pigs
36
von willerband disease in dogs?
most common inherited platelet defect in dogs
37
what is Von Willerbrand disease caused by?
Caused by defective VWF production
38
type 1 von willerband disease?
most common clinically mild/moderate, low VWF concentration, normal multimer formation
39
type 2 von willerband disease?
clinically moderate/severe, low VWF, loss of high MW multimers
40
DIC?
disseminated intravascular coagulation always secondary to a primary disorder sepsis is a massive cause
41
what does DIC do?
lots of tiny clots throughout circulation sequesters all platelets lack of coagulation factors so you get bleeding and thrombosis at same time no way to stop bleeding but also need to remove clots
42
type 3 von willerband disease?
clinically severe total absence of VWF
43
which is the less common type of von willerbrand disease?
autosomal recessive
44
which is the more common version of von willerbrand disease?
autosomal dominant with incomplete penetrance
45
treating von willerbrand disease?
no cure but can be treated
46
in which dog breeds is von willerbrand disease relatively common in?
Doberman Pinschers, German Shepherds, Golden Retrievers, Miniature Schnauzers, Pembroke Welsh Corgis, Shetland Sheepdogs, Basset Hounds, Scottish Terriers, Standard Poodles, and Standard Manchester Terrier
47
what is a thrombosis?
an inappropriate clot formation in vessels without vascular injury leads to: myocardial infarction and stroke
48
what is an arterial thrombosis?
atherosclerosis plaque rupture or immune stimulus
49
what is a venous thrombosis?
a DVT
50
how does cancer lead to a thrombosis?
hyperactivation of platelets, weak blood vessels, involvement of coagulation factors
51
if thrombosis results in sepsis, what can this lead to?
DIC disseminated intravascular coagulation
52
thrombosis can also lead to? an example is COVID
can lead to viral activation
53
what are the primary disorders that DIC can be secondary to?
sepsis, cancers, pancreatitis, heartworm disease, toxoplasmosis, gastric dilation-volvulus, immune conditions - immuen mediated haemolytic anaemia or thrombocytopenia, snake/insect bites, heat stroke, septic peritonitis
54
what does DIC result in?
in systematic microvascular thrombosis, ischaemia and organ failure
55
what happens in DIC?
small clots use up platelets and coagulation factors causing serious bleeding
56
what does VWF act like and in order to do what?
acts like a fishing line 'snagging' passing platelets
57
haemostasis is a balancing act - what does haemostasis need to be in order to keep it balanced?
sensitive, rapid, localised, stable, coordinated, controlled
58
59
describe how haemostasis can be in balance?
procoagulant forces and anticoagulant forces are level with each other
60
what happens to the haemostasis balance when we are bleeding?
There is a haemostasis disbalance anticoagulant forces are stronger than procoagulant forces the anticoagulant forces outweigh the procoagulant forces
61
describe the haemostasis balance when there is a thrombosis?
Haemostasis disbalance the procoagulant forces outweigh the anticoagulant forces
62
unsettling the haemostasis balance will cause what?
it will either result in inappropriate clotting (thrombosis)
63
what does VWF stand for?
Von Willerbrand Factor
64
rapid -
thrombus appears in seconds
65
localised -
limited to injury and compacts so no occlusion
66
stable -
doesn't have lots of chunks embolising
67
coordinated -
rapid activation of platelets and coagulation to give stabilising fibrin
68
Describe platelet activation - 1?
platelets have adhesion receptors on their surface receptors recognise components of ECM incl. GPCR, Integrins, Glycoproteins/Ig superfamily Initial interactions (between receptors and ECM) mediated through collagen and VWF Binding of platelets to ECM starts activation through signalling cascades Activation causes granule secretion
69
Describe platelet activation - 2?
Granule contents support further platelet activation Granular fibrinogen supports platelet aggregation Granular P-selectin supports interaction between platelets + WBC Platelets change shape and spread over wound Changes in phospholipid composition Exposure of PS gives a negatively charged surface Charged surface promotes the assembly of coagulation cascades leads to thrombin generation thrombin cleaves fibrinogen to fibrin fibrin stabilises the clot
70
what two molecules help when granule contents support further platelet activation?
ADP and VWF
71
what does PS stand for?
phosphatidylserine
72
what does PS do?
exposure of PS gives a negatively charged surface
73
many severe diseases involve thrombocytopenia - what are these diseases?
infections neoplasia (cancers) immune disorders pancreatitis drugs e.g. chemotherapy or antibiotics
74
signs of thrombocytopenia?
nosebleeds, gum bleeds, bleeding under the skin
75
thrombocytopenia can affect both?
both cats and dogs
76
what is hereditary macrothrombocytopenia?
it is a benign inherited giant platelet disorder
77
who does hereditary macrothrombocytopenia affect?
affects 50% Cavalier King Charles Spaniels
78
what do platelets use receptors for?
to sense proteins that are only exposed during vascular injury
79
what proteins do platelets sense with their receptors?
collagens found in the extracellular matrix and Von Willebrand Factor (VWF) in blood can then bind collagen and bridge the platelet the ECM
80
activated, adhered platelets expose what?
they expose a surface that is procoagulant
81
exposure of a procoagulant surface allows what?
allows assembly of coagulation complexes leads to local generation of thrombin receptor for this activation normally anatomically sequestered from blood (TF)
82
meaning of ECM?
extracellular matrix
83
unperturbed meaning?
unphased - not unsettled
84
what does unperturbed endothelium present?
it presents an anticoagulant response to prevent inappropriate activation of coagulation
85
what does an anticoagulant response limit?
limits the spread of the clot (thrombus) beyond the injury site to prevent vessel occlusion
86

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