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Pathological Processes > 7. Haemostasis > Flashcards

7. Haemostasis Flashcards

1
Q

What is clotting?

A

Process whereby blood becomes a solid mass when it makes contact with connective tissue

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2
Q

What are the 3 streps of haemostasis?

A

Vasoconstriction (if artery that is damaged).
Primary haemostatic plug of platelets forms, sticking to injured vessel and connective tissue outside it.
Secondary haemostatic plug forms as fibrin filaments stabilise the friable platelet plug into a blood clot.

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3
Q

What 4 things activate platelets?

A

Collagen surfaces.
ADP released by activated platelets and injured RBCs.
Thromboxane A2 released by activated platelets.
Thrombin, an enzyme that cleaves circulating fibrinogen into fibrin.

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4
Q

What happens to platelets when they are activated?

A

Stick to exposed subendothelium (specifically to Von Willebrand factor which is concentrated on the subendothelial basement membrane).
Aggregate.
Swell and change shape to sticky, spiny spheres.
Secrete factors from platelet granules that help plug to grow and aid clotting.

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5
Q

How does aspirin work to reduce blood clotting?

A

Irreversibly inactivated cyclooxygense, an enzyme responsible for production of thromboxane A2, so decreases platelet aggregation.

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6
Q

What vitamin is required for synthesis of clotting factors and the anticoagulants protein C and S?

A

Vitamin K

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7
Q

Does thrombin circulate in the blood in an active form?

A

No, else blood would be solid. Is activated by clotting factors I to XIII.

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8
Q

Name 2 co-factors for the enzymes in the blood clotting pathway

A

Phospholipids

Calcium

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9
Q

What is the intrinsic pathway of clotting?

A

Involved factors all of which are contained within the blood. Triggered by a negatively charged surface eg subendothelium. No vessel needs to be broken for it to occur.

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10
Q

What is the extrinsic pathway of blood clotting?

A

Triggered by thromboplastin, a tissue factor, which is present outside of the blood and released from damaged cells adjacent to the area of haemorrhage.

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11
Q

What happens in the vascular wall in haemostasis?

A

Arterial media contracts.
Subendothelium traps platelets.
Endothelial balances clotting and opposing clotting by secreting von Willebrand factor and thromboplastin that favour clotting, and tissue plasminogen activator and thrombomodulin that oppose clotting.

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12
Q

Name 3 factors that oppose clotting

A

Dilution of clotting factors by blood flow.
Natural anticoagulants - antithrombin III, protein C and S, oppose formation of fibrin.
Fibrin degradation products - eg tissue plasminogen activator.

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13
Q

Whah happens to a clot as the platelets in the clot die?

A

Cling to the fibrin, pull by their actin-myosin filaments causing clot retraction, pulling together the sides of small wounds and toughening the clot by squeezing out fluid.

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14
Q

What is fibrinolysis?

A

The process by which a blood clot in dissolved after the hole in the vessel has been repaired.

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15
Q

What breaks down a blood clot in fibrinolysis?

A

Macrophages.

Plasmin - enzyme responsible for fibrinolysis.

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16
Q

What is the inactive precursor that plasmin circulates as? Where is it made?

A

Plasminogen

Liver

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17
Q

Name 3 plasminogen activators, and there they are secreted from

A

Tissue plasminogen activator - secreted by vascular endothelium.
Urokinase - found in urine.
Streptokinase - obtained from streptococci and not normally found in the body.

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18
Q

Why should a patient only be given streptokinase once as a therapeutic method of dissolving thrombi and thromboemboli?

A

Is antigenic

19
Q

Where does bleeding commonly occur from as a side effect of giving tissue plasminogen activator as a therapy for dissolving thrombi and thromboemboli?

A

Gums, nose, brain

20
Q

What increases the activity of tissue plasminogen factor?

A

Fibrin, so clotting cascade sets off fibrinolysis

21
Q

What is fibrin broken down into in fibrinolysis? Therefore give an example of when they are increased

A

Fibrin degradation products (FDP) eg D-dimer.

Increased in conditions where there is thrombosis, eg disseminated intravascular coagulation, DVT, PE

22
Q

What happens to fibrinolytic activity after surgery?

A

Drops and remains low for 7-10 days

23
Q

What happens once a clot becomes organised?

A

Replaced by granulation tissue and then a scar

24
Q

What part of haemostasis is impaired in haemophilia?

A

Normal platelets, but cannot produce adequate amounts of fibrin due to deficiency in a clotting factor. So secondary haemostatic plug cannot form.

25
Q

What clotting factor is affected in haemophilia A? How does this affect the disease severity?

A

Factor VIII, decreased amount or decreased activity. Severity of disease depends on by what amount the amount or activity of the factor is decreased.

26
Q

What type of genetic inheritance are haemophilia A and B?

A

X-linked recessive

27
Q

What is normal and abnormal on a blood test in patients with haemophilia?

A

Normal - platelet count, bleeding time (measure of platelet activity), PT.
Abnormal - prolonged APTT (measure of intrinsic pathway), low factor VIII assay in haemophilia A.

28
Q

What clotting factor is affected in haemophilia B?

A

Factor IX deficiency

29
Q

What do patients with haemophilia usually present with?

A

Easy bruising.
Haemorrhage after trauma and surgery.
Spontaneous haemorrhage in joints, leading to joint deformities.

30
Q

How would you treat haemophilia?

A

Infusion of recombinant factor VIII or IX

31
Q

What happens in von Willebrand disease?

A

Deficiency or abnormality in von Willebrand factor.
Assists in platelet plug formation by attracting circulating platelets to sites of vessel damage (so therefore harder for primary haemostatic plug to form) and stabilises factor VIII protecting it from premature destruction (so decreased thrombin activation to convert fibrinogen to fibrin).

32
Q

What is thrombocytopenia?

A

A low platelet count of less that 100 x 10^9/L

33
Q

With a platelet count lower than what does spontaneous bleeding occur?

A

Less than 20 x 10^9/L

34
Q

What is seen on a blood test in patients with thrombocytopenia?

A

Normal - PT and APTT (as assess clotting cascade).

Abnormal - prolonged bleeding time, decreased platelet count.

35
Q

Where is spontaneous bleeding seen from in patients with thrombocytopenia? How does the bleeding appear?

A

Small vessels in places such as skin, GI tracts, GU tracts, sometimes intracerebral bleeding.
Appears as petechiae.

36
Q

Give 4 causes of thrombocytopenia and an example of a reason for each

A

Decreased platelet production - eg bone marrow malignancy, drugs, infections (eg HIV), B12 and folate deficiency.
Decreased platelet survival - eg immune destruction, non-immune destruction (eg disseminated intravascular coagulation).
Sequestration - hypersplenism (enlarged spleen).
Dilutional - massive blood transfusions.

37
Q

What is disseminated intravascular coagulation?

A

Thrombohaemorrhagic disorder occurring as a secondary complication in a variety of conditions.

38
Q

What happens in disseminated intravascular coagulation?

A

An activator of clotting gets into the blood, microthrombi form throughout circulation. Consumes platelets, fibrin, coagulation factors, activated fibrinolysis, so may then haemorrhage.

39
Q

Give 4 conditions which disseminated intravascular coagulation can occur secondary to

A

Sepsis - gram negative bacteria produce endotoxin which activated clotting.
Severe trauma - especially to brain as contains large amounts of thromboplastin (triggers extrinsic clotting pathway).
Extensive burns.
Complications of childbirth - eg amniotic fluid embolism, retained dead foetus.
Malignancy.
Snake bite.

40
Q

What needs treating in disseminated intravascular coagulation?

A

The underlying cause

41
Q

Give 4 conditions/symptoms that disseminated intravascular coagulation can cause

A

Microvascular thrombosis leads to neurological impairment, gangrene of skin, renal failure, respiratory distress, GI ulceration.
Haemorrhage leads to intracerebral bleeding, petechiae, haematuria, epistaxis, GI bleeds.
Anaemia - as RBCs traumatised as squeeze past micro-thrombi.

42
Q

What can be measured in the blood in disseminated intravascular coagulation?

A

Fibrin degradation produces eg D-dimers, as fibrinolytic system is activated

43
Q

What are thrombophilias?

A

Inherited or acquired defects of haemostasis, resulting in predisposition to thrombis, eg DVT.

44
Q

Give two examples of thrombophilias

A

Factor V Leiden - abnormal permanently activated factor V.

Antithrombin deficiency - as normally as anticoagulant.

Pathological Processes (14 decks)

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