Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BSMS 103 > Theme 3 - Haemostasis > Flashcards

Theme 3 - Haemostasis Flashcards

1
Q

what are the three main functions of endothelial cells?

A

increase surface area, control blood vessel size, prevent clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is extravasation?

A

when cells leave the blood and enter the tissue (injury)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is haemostasis?

A

a process that causes bleeding to stop by allowing clots to form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the response of endothelial cells when there is injury?

A

basement membrane is exposed and endo cells stop secreting factors that promote haemostasis and instead secrete von willebrand factor which promotes clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does von willebrand factor do?

A

promotes clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the three platelet based ways to repair blood vessels?

A

1) haemostatic plug - plats adhere, activate and aggregate
2) co-agulation - mesh work of protein fibre which acts as a barrier and also traps platelets (an enzyme cascade that requires part of the platelet membrane)
3) vasoconstriction (blood moves slower) - plats secrete vasoconstrictor and pro thrombotic molecules eg 5HT, ADP and thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is virchows triad?

A

platelet plug, co-agulation and vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which common lineage are platelets derived from?

A

common myeloid lineage (megakaryocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how many platelets can a megakaryocyte make in its lifetime?

A

4000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does plat count compare to RBC count?

A

40x less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the three steps in which plats are activated for haemostasis?

A

exocytosis of dense granules, change in shape (to irregular shape) and increased respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what the endothelium is breached what signals to the rest of the body that there has been an injury?

A

the exposed collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do platelets adhere to in injury?

A

the exposed collagens via proteins such as GPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do plats start to exocytose when preparing to activate?

A

dense granules filled with 5HT, ADP and calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

once platelets active they stick together - what molecule stimulates this?

A

ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which two drugs block ADP and therefore plat aggregation and coagulation?

A

prasugrel and popitugrel (P2Y inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what facilitates aggregation of plats?

A

fibrinogen and ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the mechanism of action of ADP?

A
  • usually inside the cell so when its outside the cell its a signalling molecule
  • platelets detect it via a P2Y receptor
  • this leads to flow of cations across the membrane
  • cation flow leads to exocytosis of dense granules and release of thomboxane A2
  • ADP activates dense granule release which also contain ADP - positive feedback loop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the three steps to a haemostatic plug formation?

A

1) plats adhere to exposed collagen
2) plats activate then exocytose dense granules with ADP, 5HT and Calcium
3) plats aggregate due to ADP and fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

which clotting factors aren’t enzymes?

A

factor 5 and factor 8 (they are co-enzymes needed for enzymes to function)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where does tissue factor normally sit?

A

in the basement membrane of the capillary so there is usually an endothelial cell between it and the clotting enzymes in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what causes conversion of fibrinogen to fibrin?

A

thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what factor is fibrin cross linked with to make the cross linked clot?

A

factor XIII (13)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are two anti coagulation factors used in the lab?

A

heparin and citrate

25
what heart condition can lead to clot formation?
atrial fibrillation - atria dont contract so blood sits around and clots then clots spread to body - stroke
26
what factors does serum lack?
fibrinogen, factor I, II V and VIII
27
what is factor 1?
fibrin (active form of fibrinogen which is made in the liver)
28
which pathway needs tissue factor as its initiator?
extrinsic pathway
29
which two factors are needed to activate thrombin?
Xa and V
30
what makes up intrinsic Xase?
factor 9a and 8a
31
what do factors Xa and Va make?
thrombinase which causes prothrombin to thrombin
32
summarise the common coagulation pathway
Xa and Va (thrombinase) cause prothrombin to thrombin (2a) which causes fibrinogen to fibrin (Ia) - fibrin joins with factor XIII to make the fibrin clot
33
what factors are in the thrombin group?
I, V and VIII
34
what three things increase the factors in the prothrombin group?
inflammation, pregnancy and the oral contraceptive pill
35
what factors are in the pro-thrombin group?
II, VII, IX, X
36
what do the pro-thrombin factors require for synthesis and activation?
vitamin K for synthesis and calcium for activation
37
what does vitamin K do for the pro thrombin factors?
post translational modification of gamma carboxylation
38
what is the main role of plasmin?
lyses fibrin therefore destroys clots (fibrinolytic)
39
what is the precursor of plasmin and where is it made?
plasminogen made in the liver
40
what is required for plasminogen to plasmin
tissue plasminogen activator (TPA) which is on the surface of endothelial cells when in tact
41
what is the function of protein C?
inhibits clot formation - by inactivating factor 5a and 8a | - also works with protein S (inhibits 5a)
42
what does anti thrombin III work with?
heparin
43
what does anti-thrombin III inhibit?
thrombin, factor Xa and factor IXa.
44
what does anti-thrombin deficiency result in and what can be used to treat it?
results in lots of clots and recombinant forms can be used to treat it
45
what does vitamin K deficiency result in?
clotting insuffiency
46
what are two causes of vitamin K deficiency?
GI disease (lack of absorption) or liver disease (lack of bile salts)
47
what drug inhibits vitamin K recycling and what can it be used for?
warfarin prevents recycling (not immediately) and can be used in patients that clot too much
48
what is the cause of haemophilia A?
congenital lack of factor VIII
49
how is haemophilia A characterised and how is it treated?
- X linked recessive - bleed a lot - into joints and muscles - usually only males are symptomatic - treat with purified factor 8
50
what factor is implicated in haemophilia B?
factor 9
51
what is the main function of anti-plat drugs and when are they used
block clot formation in arteries (anticoagulants have limited use here) - used in acute coronary syndromes
52
name two classes of anti-platelet drugs and how they work
- Aspirin - inhibits COX which blocks the formation of thromboxane A2 formation in plats - ADP inhibitors (prasugrel and clopidogrel) - P2Y receptor antagonist
53
what is the affect of aspirin on bleeding time and co-agulation time?
increases bleeding time but doesn't increase coagulation time (used for MI prophylaxis)
54
what do anti-coagulants do?
prevent clots in veins and the low pressure pulmonary circulation therefore prevent DVT and PE
55
what are three types of anticoagulants?
heparin, NOACS and warfarin
56
how does heparin work
inhibit coagulation with anti-thrombin III by inhibiting factor X
57
name two NOACs
dabigatran (inhibits thrombin) and rivoroxaban (inhibits factor X)
58
what do fibrinolytic drugs do and when are they used?
CLOT BUSTERS - break clots apart in arteries | - used in acute coronary syndromes and acute MI
59
name three fibrinolytic drugs
recombinant TPA (increases plasminogen to plasmin which lyses fibrin therefore breaks up clot), streptokinase and urokianasae

BSMS 103 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions