Hemostasis & coagulation Flashcards

1
Q

What r the mediating factors in hematosis?

A

VwF

Fibrinogen

Collagen

ADP

Thromboxane/ arachidonic acid

Thrombin

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2
Q

What is the clotting cascade?

A

Is an amplificatin system of activating precurser proteins to generate thrombin!

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3
Q

Where r coagulation factors made?

A

In the liver

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4
Q

Describe the intrinsic and extrinsic pathways

A

Notes

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5
Q

What is the role of thrombin?

A

Cleaves fibringien to form FIBRIN>> to form a clot

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6
Q

What is the function of Von Willebrand Factor?

A

~Allows platlets to stick on the vessel wall, and aggregate ~It also carries and protects factor 8

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7
Q

What initiates activation of clotting factors?

A

The exposure of collagen and TF

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8
Q

Hoe and why does fibrinolysis occurs?

A

Plasminogen activator breaks down plasminogen into plasmin,

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9
Q

Define heamostasis

A

Process of preventeing or stopping bleeding is case of trauma or disease while maintaing blood in its fluid state

OR

stopping of hemmorheage

Heme> blood

Stasis> halt

halting of blood.

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10
Q

What r the 3 major steps of hemostasis explain each? and timing of each

A

1) vasoconstriction> not enough to stop bleeding ;(
2) primary hemostatic plug of platelets
3) secondary hemostatic plug & blood coagulation> fibrin clot forms which stabilises the temporary platelet plug into a stable clot

(Secondary> stable clot)

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11
Q

What follows hemostasis?

A

Fibrinolysis>> breaks the clot

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12
Q

What happens if hemostasis is disturbed?

A

Patients can bleed excessivly

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13
Q

What is thrombosis?

A

Solid mass formation made from the constituents of the blood with the circulatory system, during LIFE (mu nafs clotting) Can occur in veins, arteries, THROMBIS AND CLOT R DIFFERENT THINGS

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14
Q

Why does thrombois occur?

A

VESSEL WALL ABNORMAILTY -atheroma >> mostly in artery -direct i jury -inflammation

BLOOD FLOW ABNORMAL -stagnation ex (DVT) -turbulence

BLOOD COMPONENT GONE WRONG -ppl who smoke >> stivky blood -Post partum>> area of placenta -Post operation>> ur lying down too much (u can get stagnation)

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15
Q

How does thrombi look like?

A

.

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16
Q

what r some types of embolism?

A

-air -amniotic fluid -nitrogen -medical equipment -tumour cells

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17
Q

what is the function of thromboxin A2?

A

-platelet aggregator -vasoconstrictor

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18
Q

how does aspirin work?

A

aspirin inhibits cyclooxygenase, which usually converts Arachidonic acid into Thromboxin !2 which is a platelet aggregator and vasoconstrictor.

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19
Q

describe platelet adhesion, activation,

A

DAMAGE>> dying endothelail cells cry, release sticky molecule “ von Willebrand factor” which has a dual function, it’ll bind to underlying exposed collagen and to platelets (via its Gp1b) . So platelets adhere to collagen via VWF.

VWF activate the recepters on the platelets (Gp1b), these recepters give signals to the platelets to do 2 things:

1) release their granules>> SAC (seritonin, ADP, Ca2) ADP=attracts more platelets & helps platelts adhere to epithelium ( platelts r so sensitive to them)
2) they will break down Phopholipase into A.A into THROBOXAINE A2!>>> which causes platelets aggregation and Vasoconstrictor

Aggregation> fibrinogen will bind to GpIIb/IIIa recepters and link platelets!

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20
Q

What is stoppimg blood from clotting during normal times?

A

Healthy endothealial cells release NO, PGI2, Normal heparin-like molecules r floating in the bloodstream.

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21
Q

Where do VWF come from? What things r exposed when the endothelail cells r damaged

A

Theyre stored in endothelails cell When endothealial cell r damaged, we get exposure of VWF, collagen, TF

22
Q

What di platlets release when activsted?

A

SAC,

TXA2>

ADP>> gunna feedback on platelets and cause them to change shape and expose recepters (gp2/3) this is important cuz its gunna allow fibrinogen to binf to platlelets.

23
Q

What is the point of the coagulation cascade?

A

To turn the unstable clot into a stable clot Fibrinogen >>> fibrin

24
Q

What is role of Vk? Why should we inject it into newborn babies?

A

It carboxylates the Gla domains on prothrombin, this gives it a negactive CHARGE that attracts calcium to bind to it and lets it bind to the endothelial cell

25
Q

How does heparin work?

A

It binds to antithrombin 3, which inhibits thrombin.

26
Q

What does streptokinase do?

A

Breaks down clot… It activates plasmin that’ll break down the clot

27
Q

Which type of vessel does thrombosis usually occur in & why?

28
Q

What is the main reason of why u get a thrombis in a vein?

A

Usually problem with the blood comstuents rather than the vessle itself.

29
Q

What is virchofs triad?

30
Q

what r the natural anticoagulants of our body?

A

-protein C -protein S -anti-thrombin

31
Q

describe The production of thrombin and fibrin

32
Q

Explain the tests in a coagulation screen

33
Q

when can u get bleeding disorders?

A

when there is a problem in the -vessel wall -coagulation factors -platelets

34
Q

what r 2 types of coagulation factor disorders? (2)

A

-Congenital Hemophilia A > factor 8 Hemophilia B > factor 9 -Acquired liver disease (can cause a reduction in the coagulation factors) vit k deficiency those who r on anticoagulants (ex warfarin> inhibits Vit K)

35
Q

function of Vit K?

A

it carboxylates the GLA domains on prothrombin! (- charge) this will attract Ca2+ to bind to it Calcium acts like a bridge btw the platelets (at site of wound) and prothrombin, holding everything in place!

36
Q

what can cause acquired Hemophilia?

A

hemophilila is excessive bleeding -liver disease (clothing factors r made there) -vit K deficiency! -DIC> can consume coagulation factors

37
Q

in coagulation factor disorders, what determines the severity of the disease?

A

it depends on the amount of the COAGULATION FACTOR present

38
Q

which of the hemophilias is most rare?

A

hemophilia B

39
Q

what is deficient in haemophilia A & B

A

Intrinsic pathway defect Hemophilila A=factor 8 Hemophilila B= Factor 9

40
Q

what is epistaxis?

A

nose bleed

41
Q

What is the medical term for a low platelet count?

A

Thrombocytopenia

42
Q

Do you think a platelet transfusion would be an effective treatment in someone with ITP?

A

No, Because they will be destroyed immediately so its pointless. Autoimmune antibodies will destroy them

43
Q

What is Trousseau’s syndrome? Why does it occur?

A

Increase risk of developing thrombosis, if you have malignant cancer.

44
Q

why is DVT asymptomatic in many people?

A

We can develop alternative channels in our veins so thats why swelling sometimes doesn’t appear. (More collatrels in the veins).

45
Q

if the process of vasoconstriction in haemostasis is not enough to stop bleeding, then what is its purpose?

A

its enugh to decrease the pressure downstream.

46
Q

What stimulates platelets “aggregation”

47
Q

What type of necrosis will be seen microscopically in the heart?

A

Coagulative

48
Q

What is warfarin’s mechanism of action?

A

Inhibits synthesis of vitamin K dependent factors (2, 7, 9 and 10), and to a lesser degree the natural anticoagulants protein C and S

49
Q

The main natural anticoagulants are (3).

If a person lacks any of these proteins they will experience repeated episodes of _______

A

antithrombin III, protein C, protein S

thrombosis

50
Q

2 examples of causes of thrombocytopenia is

Sequestration & Dilutional of platelets, explain how this happens

A

Sequestration – in an enlarged spleen (hypersplenism)

Dilutional – due to massive blood transfusions (blood stored for more than 24 hours does not contain platelets).

51
Q

This is the most common inherited bleeding disorder.

name me

A

VWF disease