Week 4 Flashcards

1
Q

List four stimuli for platelet activation

A

Collagen
Thrombin
Thromboxane
ADP

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2
Q

What does aPTT stand for?

A

activated Partial Thromboplastin Time

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3
Q

What does aPTT mean clinically?

A

aPTT = the time for clot formation in citrated plasma after the addition of Ca2+, contact activator and phosphilipid to mimic the platelet membrane
I.e measures the function of the sample’s intrinsic pathway

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4
Q

What test would you use to measure the extrinsic pathway function of your sample?

A

Prothrombin time (time for clot formation of plasma after addition of Ca2+ and tissue factor)

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5
Q

What effect does giving low-dose aspirin therapy have, and avoid?

A

Inhibits platelet TXA2 formation, which inhibits aggregation of exposed platelets permanently
Cleared by liver, so largely avoid vasodilatory effects on blood vessels throughout the body

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6
Q

Name two drugs that aim to reduce coagulation by activating plasmin

A

Streptokinase

Alteplase

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7
Q

What are the three factors predisposing to thrombosis? Which is most important?

A
  1. Endothelial injury (most important)
  2. Abnormal haemodynamics e.g blood stasis or turbulence
  3. Hypercoaguability of blood
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8
Q

Name three things injured endothelial cells release that promotes thrombosis.

A
  1. vWF (platelet adhesion)
  2. Tissue factor (extrinsic pathway)
  3. Plasminogen-activator inhibitors (suppress plasmin production and thence fibrinolysis)
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9
Q

How does viral infection predipose to thrombosis?

A

Deposition of viral antigen-antibody complexes in BV walls > complement activation > membrane attack complex punches holes in endothelial cells, causing damage

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10
Q

How does blood turbulence predispose to thrombosis (2 things)?

A
  1. Creates counter currents of blood flow which create areas of blood stasis > thrombosis
  2. Increases activity of intravascular procoagulant cellular and enzymatic reactions that lead to blood coagulation
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11
Q

How does blood stasis predispose to thrombosis (3 things)?

A
  1. Stagnant blood becomes viscous and hypercoaguable
  2. Local endothelial cells may sustain hypoxic injury and release or express pro-coagulant molecules as a result
  3. Retards removal of procoagulant molecules and arrival of anticoagulant molecules from circulating blood
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12
Q

What does the presence of lines of Zahn signify?

A

That the thrombus was initially non-occlusive with continued blood flow over it

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13
Q

What three things influence the shape, size and colour of thrombi?

A

Age
Location (rate of blood flow)
Septic or not

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14
Q

Under what circumstances (specifically) might a pulmonary thromboembolus lodged in a medium sized artery cause pulmonary infarction?

A

Anything reducing O2 supply to the lung tissue itself so anemia, pneumonia, pre-exisiting fibrosis or oedema of lungs

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15
Q

At whay systolic BP range would you start to see clinical consequences of hypertension?

A

> 160-180 mmHg

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16
Q

What systolic BP value is considered hypotension? What about MAP?

A

Systolic < 80 mmHg

MAP < 60 mmHg

17
Q

What are the three major mechanisms of shock?

A

Hypovolemic
Cardiogenic
Distributive

18
Q

What are the four subsets of distributive shock?

A

Neurogenic
Anaphylactic
Heat stroke
Septic

19
Q

Define cardiac tamponade

A

The adverse consequences of rapid, excess fluid volume in the pericardial sac