Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiorespiratory 2 > Haemostasis Basics > Flashcards

Haemostasis Basics Flashcards

1
Q

what type of feedback system is blood coagulation

A

positive feedback

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

Define haemostatsis

A

Haemostatsis is defined as the cessation of bleeding at a vascular injury site via the formation of a thrombus

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

what is the two primary components of a thrombus

A
  • platelet plug

- fibrin clot

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

describe what a platelet plug is

A
  • this is when the circulating platelets form a physical plus by adhering to the injury site and each other
  • aggregation of platelets is termed primary haemostats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the difference between primary and secondary haemostatsis

A
  • primary haemostatsis is the platelet plug

- secondary haemostats is the fibrin clot

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

describe what a fibrin clot is

A
  • activation of coagulation factor proteases results in a protease thrombin
  • thrombin is essential for the production of fibrin monomers
  • these are cross linked and form a meshwork around the platelet plug
  • this is termed secondary haemostasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the structure of platelets

A
  • NOT CELLS, little bags of cytoplasm shed from megakaryocytic
  • no nuclei
  • 1-4um in diameter
  • each megakaryocyte can produce over 1000 platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how long can platelets survive for

A
  • there are about 1-2 platelets per 20 RBC

- survive 8.5-10 days and have a half life of 4 days

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

what regulates platelet production

A
  • Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced in the kidneys and liver.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a low platelet count called

what is a high platelet count called

A

thrombocytopenia

thrombocytosis

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

Describe how the platelet plug forms (primary haemostasis)

A
  • damaged endothelium
  • this means that collagen underneath the endothelium is exposed to the blood
  • Von willebrand factor (VWF) binds to the exposed collagen
  • platelets then bind to the VWF via the platelet GP1b receptors (platelets can also bind directly to the collagen via Gp1a and Gp6 receptors but this is very weak)
  • the VWF has formed a bridge between the collagen and platelets, this is called platelet adherence
  • the adherent platelets express the GP2b/3a receptor
  • GP2b/3a receptors bind to fibrinogen which binds more platelets to form a meshwork this is called platelet aggregation
  • the binding of platelets cause the platelets to become activated
  • they change shape and become spiky and entailed together
  • they release ADP and thromboxane A2 (TXA2) and serotonin (5-HT) from granules, this is called the platelet release reaction
  • ADP & TXA2 attract more platelets to the site which aggregate to form a platelet plug.
  • 5-HT acts on local smooth muscle to increases local vasoconstriction.
  • The spiky platelets in turn release cytokines which attract even more platelets and so a positive feedback system operates until a plug large enough to stop the bleeding is formed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what normally prevents platelet adhesion

A
  • the endothelium which is intact continuously releases nitric oxide and prostacyclin (PG12) this prevents platelet adhesion
  • this also happens adjacent to the damage endothelium to prevent the platelet plug from separating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is van willebrand factor

A
  • it is a glycoprotein that circulates in the blood and binds to the exposed collagen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what receptors do the platelets bind to when creating the platelet plug

A
  • platelets then bind to the VWF via platelet GP1b receptors.
  • Platelets can also bind directly to collagen via Gp1a and Gp6 receptors: However without VWF the binding is very weak and the platelets are easily dislodged).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is platelet adherence

A
  • when the platelets bind to the VWF via platelet GP1b receptors
  • this means that the VWF has formed a bridge between the collagen and platelets this is called platelet adherence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

where is Von williebrand factor stored

A

stored in the endothelial cells, inside granules called Weibel–Palade bodies (WPBs)

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

what substances are released in the platelet release reaction

A
  • They release adenosine diphosphate (ADP), thromboxane A2 (TXA2) and serotonin (5-HT) from granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what does ADP and TXA2 do in the platelet plug

A
  • ADP & TXA2 attract more platelets to the site which aggregate to form a platelet plug.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does 5HT do in the platelet plug

A

5-HT acts on local smooth muscle to increases local vasoconstriction which reduces the local blood flow

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

where is VWF made

A

liver

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

what determines the bleeding time

A
  • the formation of the platelet plug determines the bleeding time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how long does it take for bleeding to stop

A

normally stops within 1-9 minutes but may be longer in children (1-13 minutes) and tends to take slightly longer in females than in males

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

what does the bleeding time test involve (test for platelet function)

A
  • A lancet or scalpel blade is used to make a shallow incision 1 millimeter deep on the underside of the forearm.
  • The time from when the incision is made until all bleeding has stopped is measured and is called the bleeding time
  • Normal values fall between 3 – 10 minutes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the three pathways in the fibrin clot

A
  • extrinsic pathway
  • intrinsic pathway
  • common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the steps in the extrinsic pathway

A
  • Factor VII is exposed to tissue factor (III) when the blood vessel is injured
  • the tissue factor (III) converts factor VII to VIIa
  • VIIa then reacts with calcium and factor X in the blood to form factor Xa
26
Q

what is the clinical test for extrinsic and common pathway

A

PT

27
Q

what type of protein is factor VII

A

plasma protein

28
Q

where is tissue factor (III) found

A
  • it is intracellular in the endothelium and smooth muscle
29
Q

what are the substances called that convert factor X to Xa called

A

The enzymes and calcium which convert factor X to Xa are sometimes called the tenase complex

30
Q

Describe the steps of the common pathway

A
  • Xa and calcium from the extrinsic pathway cause prothrombin to be converted to thrombin
  • thrombin turns fibrinogen to fibrin
  • thrombin also creates a bit of XIII
  • XIII turns into XIIIa
  • XIIIa stabilises the fibrin into a stable clot
31
Q

what does a stable clot consist of

A
  • matrix of fibrin
  • platelets
  • trapped erythrocytes
32
Q

What causes amplification of thrombin formation

A
  • the extrinsic pathway produces a small amount of thrombin by forming a small amount of Xa
  • The initially formed thrombin converts three other factors – V VIII, XI into their active forms Va VIIIa Xia
  • Xia then converts factor IX to IXa
  • VIIIA and Isa increases conversion of X to Xa
  • Va increases effective of the increased Xa
33
Q

Describe the steps of the intrinsic factor

A
  • Factor XII is converted into XIIa
  • XI is converted to XIa by XIIa
  • IX is converted into Isa by XIa and calcium
  • then IXa and calcium is used to convert X to Xa
34
Q

when is the intrinsic factor activated

A
  • it activates clotting when the blood is stagnant
  • often happens in the atria or leg veins (deep vein thrombosis)
    -
35
Q

what is the clinical test for the intrinsic pathway and common pathway

A

is APPT (activated partial prothrombin time) – sometimes called surface activation pathway, the surface of the slide which is polar activates this surface

36
Q

what test is used for assessing platelet function

A

bleeding time

37
Q

What is the INR

A
  • number derived from the prothrombin time
  • it is used to assess the coagulability of blood in patients taking warfarin or heparin as they are at risk of abnormal clot formation such as deep vein thrombosis or pulmonary emboli
38
Q

What is the ideal INR value

A
  • in patients on warfarin or heparin 2-3 (not more than 3) is aimed for
  • INR healthy range is 0.8-1.2
39
Q

what are two types of haemophilia

A

Haemophilia A

Haemophillia B

40
Q

what is the difference between haemophilia A and haemophilia B

A
  • Hameophilia A is caused by a deficiency of factor VIII. It reduces the effectiveness of the positive feedback loop forming thrombin
  • Haemophilla B is caused by a deficiency of factor IX
41
Q

What are the two substances involved in getting rid of clots

A
  • antithrombin III

- plasmin

42
Q

Describe how clots are removed

A
  • Plasmin circulates in the blood in the form of an inactive precursor plasminogen. Plasminogen binds to platelet plugs as they form, and gets incorporated into the final clot. Plasminogen is held in its inactive form by alpha-2 antiplasmin which circulates in high concentration in the plasma
  • When the tissue is healed the plasminogen becomes plasmin this happens by tissue plasminogen activator (tPA)
  • this causes fibrinogen to be proteolysis and turned to fibrin
43
Q

what type of protein is antithrombin III

A
  • plasma protein
44
Q

what is the dominant form of antithrombin found in the blood plasma

A

α-antithrombin is the dominant form of antithrombin found in blood plasma.

45
Q

what does tPA do

A
  • Tissue plasminogen activator (tPA) is released from normal endothelial cells. It catalyses conversion of plasminogen to plasmin
  • One of its functions is to prevent a clot extending too far along a blood vessel into healthy tissue.
46
Q

name a product of fibrin breakdown

A

D-dimer

47
Q

why is D dimer important

A

Measurement of D-Dimer levels is an important test performed in patients with suspected thrombotic disorders (eg DVT).
- it is an indication that thrombosis is not present

48
Q

what other factors also catalyse plasminogen to plasmin

A

urokinase plasminogen activator, kallikrein, and factor XIIa

49
Q

what factors is vitamin K important for

A

requires for full effectiveness of Factors VII, IX and X of the coagulation cascade.

50
Q

what does vitamin K do

A

Vitamin K modifies the proteins to allow them to bind calcium ions.

51
Q

what are the two main forms of vitamin K

A

Vitamin K1 and vitamin K2.

52
Q

where are two main forms of vitamin K found

A
  • Vitamin K1 is found in highest amounts in green leafy vegetables because it is directly involved in photosynthesis.
  • Animals can convert it to vitamin K2.
  • Bacteria in the gut flora can also convert K1 into vitamin K2
53
Q

what are the risk factors for vitamin K deficiency

A
  • Liver disease,
  • poor diet (no green vegetables)
  • poor absorption, antibiotics
  • Deficiency of vitamin K seen as increased INR and may result in unstable clots. It may also be a factor in osteoporosis
54
Q

what is used in treatment for overdose of the anticoagulant drug warfarin and rat poisoning

A

Vitamin K

55
Q

what are the two classic anticoagulants

A

heparin

warfarin

56
Q

what does heparin do

A

Heparin binds to and massively increases the activity of anti-thrombin
Activated AT inhibits thrombin and factor Xa

57
Q

how is heparin given

A

Must be given parenterally (i.v. or subcutaneous) as not absorbed through gut

Short half-life (one hour) so give continuously or regularly

Effective instantly

58
Q

what does warfarin effect

A
  • Warfarin interferes with the hepatic synthesis of vitamin K–dependent coagulation factors especially Factors VII, IX and X.
  • It also competes with sites on these factors that bind vitamin K reducing their effectiveness
59
Q

name the modern anticoagulants

A

Direct acting anticoagulatns DOACs

60
Q

name some direct acting anticoagulants DOACs

A
  • These agents include a direct thrombin inhibitor(dabigatran)
  • factor Xa inhibitors (eg rivaroxaban, apixaban and edoxaban).
61
Q

describe the positives and negatives for DOACs

A

Positives

  • less serious side effects than traditional anticoagulants
  • a rapid onset action and relatively short half-lives, therefore more effective
  • don’t need monitoring like warfarin

negative

  • more expensive and needed for kidney problem patients
  • is no antidote for the factor Xa inhibitors, so it is difficult to stop their effects in the body in cases of emergency

Cardiorespiratory 2 (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions