Thrombosis Flashcards

1
Q

List 4 Characteristics of abnormal bleeding

A

•Bleeding that is:

–‘Spontaneous’

–Out of proportion to the trauma/injury

–Unduly prolonged

–Restarts after appearing to stop

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2
Q
A
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3
Q

Defects of Primary Haemostasis (platelet plug formation)

List 3 examples of Deficiencies or Defects that can lead to problems of primary haemostatsis and list a common example for each one?

A
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4
Q

When Blood vessels are damaged they are exposed to two things.

Name them?

What happens if you don’t habe Von Williebrand Factor?

A

When the blood vessel is damaged the blood is exposed to two things it is not normally exposed to: collagen and tissue factor one the surface of cells ( subendothelial tissue and leukocytes).

Both are triggers for haemostasis- one for primary and one for secondary

If you don’t have the Von Williebrand factor you have failure of primary haemostasis, the platelets just sail on by (one or two bind to collagen)

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5
Q

Defects of primary haemostasis: pattern of bleeding

List 7 patterns of bleeding for a disease which causes a defect in primary haemostasis?

A
  • Immediate
  • Easy bruising
  • Nosebleeds (prolonged: >20 mins)
  • Gum bleeding (prolonged)
  • Menorrhagia (anaemia)
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
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6
Q

Summarise secondary haemostasis?

A

Stabilisation of the plug with fibrin

blood coagulation

Stops blood loss

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7
Q

What is the role of fibrin?

With hameophillia the person has …………., ……. ………… ………….. and …………….., so ………………. haemostasis goes okay but they can’t make that …………… to stabalise it and bind it together.

A

Haemostasis: Fibrin clot stabalise a platelet plug.

Fibrin makes the platelet plug very solid and prevents it from breaking apart and thrombin is needed for this

With hameophillia the person has collagen, von williebrand factor and platelets, so primary haemostasis goes okay but they can’t make that mesh to stabalise it and bind it together.

So in medium sized vessels it falls apart

In small vessels it is okay

In big vessels it will blead.

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8
Q

What causes a defect in secondary haemostasis?

Take note of the examples

A

Dilution- people are given red blood cells in hospitals if they have had a bleed, not plasma which contains the clotting factors.

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9
Q

What is *DIC = disseminated intravascular coagulation?

A

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body blocking small blood vessels.

Tissue factors triggers coagulationand normally it is kept outside the blood vessels.

In some pathologcal situations you express tissue factors inside the blood on monocytes, nuetrophils, and maybe endothelial cells. This happens during inflammatory responses: sepsis.

It uses all the coagulation factors up.

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10
Q

Defects of secondary haemostasis: pattern of bleeding

List 7

A
  • Often delayed (after primary haemostasis)
  • Prolonged
  • Deeper: joints and muscles
  • Not from small cuts (primary haemostasis ok)
  • Nosebleeds rare
  • Bleeding after trauma/surgery
  • After i/m injections
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11
Q

What is the most common cause of Defects of clot stability: excess fibrinolysis

A

Unbalanced haemostasis: anticoagulant excess

•Usually due to therapeutic administration:

–Eg heparin or thrombin and Xa inhibitors

Mostly doctors fault- Therapuetic

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12
Q

What is the role of von williebrand factor in primary haemostasis?

a) None, it is important in secondary haemostasis
b) it helps capture platelets onto collagen
c) It promotes vasoconstriction via smooth muscle cells
d) It promotes fibrin formation
e) it prevents tissue and joimt laxity

A

b

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13
Q

A bleeding time test is performed on a patient with Haemophilia A by making a small blade incision on his forearm. The likely outcome is:

a) A normal result: bleeding stops after <10 min
b) Pathological response
c) Prolonged bleeding without a break
d) Delayed but prolonged bleeding with periods of arrest
e) Healing with excessive bruising

A

a

Primary haemostasis okay.

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14
Q

Thrombosis

A
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15
Q

Besides location, what is a difference between arterial and venous thrombi?

A

Venous thrombi- blood factors are majors player in venous thrmobus

Arterial Thrombi- mostly to do with the arterial wall

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16
Q

What are the effects of thrombosis?

Name 2 broad effects

A

Obstructed flow of blood

–Artery – myocardial infarction, stroke, limb ischaemia

–Vein – pain and swelling

Embolism

–Venous emboli, to lungs (pulmonary embolus)

–Arterial emboli, usually from heart, may cause stroke or limb ischaemia

17
Q
A
18
Q

List 4 Consequences of thrombo-embolism

A
19
Q

Why do (some) people get thrombosis?

A
  • Genetic constitution
  • Effect of age and previous events, illnesses, medication
  • Acute stimulus

Virchovs triad

  • Stasis
  • Endothelial damage
  • Hypercoagubility
  • blood -dominant in venous thrombosis
  • vessel wall -dominant in arterial thrombosis
  • flow -complex, contributes to both
20
Q

What will increase your risk of thrombosis in your blood?

list risk factors to do with your blood

A
21
Q

Increased risk of thrombosis::flow

Reduced flow (stasis) increases the

risk of venous thrombosis.

list some reason for why you may have stasis of blood?

A

e.g.: surgery

fracture

long haul flight

bed rest

22
Q

Increased risk of thrombosis: “thrombophilia”

List 4 clinical and one lab

A

•Clinical:

–Thrombosis at young age

–‘idiopathic thrombosis’

–Multiple thromboses

–Thrombosis whilst anticoagulated

•Laboratory

–Identifiable cause of increased risk

•AT deficiency, Factor V Leiden, global measures of coagulation activity.

23
Q

Combined risks for thrombosis

Numerous conditions will alter blood coagulation, vessel wall and/or flow to precipitate thrombosis or make it more likely. Eg:

list 4

A

–Pregnancy

–Malignancy

–Surgery

–Inflammatory response

24
Q

•Provide a rough estimate of its prevalence thrombosis

A

Venous thrombosis, comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), occurs with an incidence of approximately 1 per 1000 annually in adult populations (1)

25
Q

Therapy and venous thrombosis

List 2 types of treatment

preventative

Therapuetic

A
  • Treatment: to lyse clot
  • eg tPA (high risk of bleeding)

• Treatment: to limit recurrence/extension/emboli

  • Increase anticoagulant activity
  • e.g: heparin (immediate acting, parenteral)
  • Lower procoagulant factors
  • e.g.: warfarin (oral, slow acting for long term therapy)
  • Inhibit procoagulant factors– direct inhibitors
  • Rivaroxaban (Xa), Apixaban (Xa), Dabigatran (IIa)
26
Q

A low plasma level of antithrombin is likely to result in:

a) Spontaneous Haemorrhage
b) Prolonged vleeding after surgery
c) Myocardial Infarction
d) An increased of post operative thrombosis
e) Herapin hypersenitivity

A

d

it is an anticoagulant factor

Factor mostly in venous disease

27
Q

The increased risk of thombosis associated with the COCP is likely to be a result of :

Combined Oral Contraceptive Pill -COCP

a) Factor 5 Leiden
b) Reduced concentration protein S
c) Reduced concentration of PAI-1
d) Reduced endothelial activation
e) Prolomged contact aactivation

A

b

28
Q
A