Hemostasis & coagulation Flashcards

(51 cards)

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
How does heparin work?
It binds to antithrombin 3, which inhibits thrombin.
26
What does streptokinase do?
Breaks down clot... It activates plasmin that'll break down the clot
27
Which type of vessel does thrombosis usually occur in & why?
.
28
What is the main reason of why u get a thrombis in a vein?
Usually problem with the blood comstuents rather than the vessle itself.
29
What is virchofs triad?
.
30
what r the natural anticoagulants of our body?
-protein C -protein S -anti-thrombin
31
describe The production of thrombin and fibrin
,
32
Explain the tests in a coagulation screen
j
33
when can u get bleeding disorders?
when there is a problem in the -vessel wall -coagulation factors -platelets
34
what r 2 types of coagulation factor disorders? (2)
-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
function of Vit K?
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
what can cause acquired Hemophilia?
hemophilila is excessive bleeding -liver disease (clothing factors r made there) -vit K deficiency! -DIC\> can consume coagulation factors
37
in coagulation factor disorders, what determines the severity of the disease?
it depends on the amount of the COAGULATION FACTOR present
38
which of the hemophilias is most rare?
hemophilia B
39
what is deficient in haemophilia A & B
Intrinsic pathway defect Hemophilila A=factor 8 Hemophilila B= Factor 9
40
what is epistaxis?
nose bleed
41
What is the medical term for a low platelet count?
Thrombocytopenia
42
Do you think a platelet transfusion would be an effective treatment in someone with ITP?
No, Because they will be destroyed immediately so its pointless. Autoimmune antibodies will destroy them
43
What is Trousseau’s syndrome? Why does it occur?
Increase risk of developing thrombosis, if you have malignant cancer.
44
why is DVT asymptomatic in many people?
We can develop alternative channels in our veins so thats why swelling sometimes doesn't appear. (More collatrels in the veins).
45
if the process of **vasoconstriction** in haemostasis is not enough to stop bleeding, then what is its purpose?
its enugh to decrease the pressure downstream.
46
What stimulates platelets "aggregation"
47
What type of necrosis will be seen microscopically in the heart?
Coagulative
48
What is warfarin’s mechanism of action?
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
The main natural anticoagulants are (3). If a person lacks any of these proteins they will experience repeated episodes of \_\_\_\_\_\_\_
**antithrombin III, protein C, protein S** **thrombosis**
50
2 examples of causes of thrombocytopenia is Sequestration & Dilutional of platelets, explain how this happens
***Sequestration*** – in an enlarged spleen (hypersplenism) ***Dilutional*** – due to massive blood transfusions (blood stored for more than 24 hours does not contain platelets).
51
This is the most common inherited bleeding disorder. name me
VWF disease