Session 8 Flashcards

1
Q

Describe the three categories involved in Virchow’s triad.

A
  • Hypercoagulability: alterations in constitution of blood.
  • Haemodynamic changes: alterations in normal blood flow
  • Endothelial injury/dysfunction.
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2
Q

How does warfarin work?

A

Inhibits production of vitamin K dependent clotting factors (II, VI, IX, X). By preventing reduction of the oxidised vitamin K, hence it cannot be re-used to make more clotting factors.

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3
Q

Give two uses of warfarin.

A

DVT, PE, AF and for mechanical prosthetic heart valves.

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4
Q

Describe the PKs of warfarin.

A

Good GI absoption, slow onset of action and heavily protein-bound. Metbaolised via CYP450, and it is also able to cross the placenta.

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5
Q

How do you monitor levels of warfarin?

A

Via the International Normalised Ratio. This is the time taken for blood to clot compared for specific age and gender. High INR indicates poor clotting.

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6
Q

Between which INRs is warfarin used for DVT, PE or AF?

A

2.0-3.0

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7
Q

How can you reverse warfarin?

A

Administer vitamin K or fresh frozen plasma.

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8
Q

Give two drugs that potentiate warfarin.

A

Amiodarone, aspirin, cephalosporin antibiotics.

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9
Q

What is heparin?

A

An anti-coagulant that activates anti-thrombin III to inhibit thrombin and factor XI. Also affects factors IXa, XIa and XIIa.

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10
Q

Describe the role of unfractionated heparin.

A

Binds to anti-thrombin III and thrombin. Inactivates thrombin and factor Xa.

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11
Q

Describe the role of low-molecular weight heparin.

A

Binds to anti-thrombin III, inhibiting only factor Xa and has no effect on thrombin. No monitoring is usually required.

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12
Q

How is heparin administered?

A

Parenteral as poor GI absorption.

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13
Q

How is heparin monitored?

A

APTT test, which is the activated partial thromboplastin time and measures the efficacy of the coagulation pathways.

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14
Q

Give two indications of heparin.

A

Prevention of thrombo-embolism peri-operatively.
DVT, PE and AF, prior to warfarin.
Acute coronary syndromes.
Pregnancy, in place of warfarin.

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15
Q

Give two ADRs of heparin.

A

Bruising, thrombocytopenia, osteoporosis.

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16
Q

How do you reverse heparin therapy?

A

Protamine sulphate dissociates heparin from anti-thrombin III.

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17
Q

What are the two main thromboxane A2 inhibitors?

A
  • Aspirin prevents thromboxane A2 production, hence platelet aggregation.
  • Dipyridamole inhibits its production. Used to prevent strokes.
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18
Q

What is the role of plasmin?

A

Breaks down fibrin to form fibrin degredation products. Plasminogen is converted to plasmin by tPA or uPA.

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19
Q

What is streptokinase?

A

Derived from beta-haemolytic streptococci. Binds to plasminogen and induces a conformational change to plasmic, hence there becomes a surplus of plasmin.

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20
Q

Give two examples of recombinant tPAs.

A

Altepase, reteplase, tenecteplase.

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21
Q

Give the main conditions for which thrombolytics are used.

A

Acute MI, PE, major venous thrombosis.

22
Q

What is the window of opportunity fo thrombolytics for coronary occlusion compared to ischaemic stroke.

A

Coronary occulsion = within 12 hours.

Ischaemic stroke = within 3 hours.

23
Q

Give three contraindications to thrombolytic therapy.

A
History of haemorrhagic stroke
Active peptic ulcer
Recent trauma or surgery
CNS neoplasm
Aortic dissection
Uncontrolled hypertension
24
Q

Why are r-tPAs used clinically instead of streptokinase?

A

They can be administered repeatedly and more easily.

25
Q

Give an example of an IV anaesthetic.

A

Propofol, Barbiturates, Ketamine.

26
Q

Give an example of an inhaled anaesthetic.

A

Halothane, isoflurane, sevoflurane and desflurane.

27
Q

Give two reversible effects of anaesthesia.

A

Sedation, amnesia, muscular relaxation, reflex suppression, alalgesia.

28
Q

Name the four types of anaesthetic.

A

General, regional, local and dissociative.

29
Q

What are the differences between general and regional anaesthetic?

A

General: affects whole body to inhibit sensory, motor and sympathetic nerve transmission in the CNS.
Regional: renders large specific regions of the body insensate. Remains conscious. Transmission block between part of the body and the spinal cord.

30
Q

What is dissociative anaesthesia?

A

Uses ketamine to inhibit transmission of nerve impulses between higher and lower centres of the brain.

31
Q

What is MAC?

A

Minimum alveolar concentration. This is the end-tidal conc. of inhaled anaesthetic needed to eliminate movement in 50% of patients stimulated by a standardised incision.

32
Q

Give an example of something that would increase and decrease MAC.

A

Increase: hyperthermia, chronic alcohol abuse.
Decrease: increased age, hypothermia, pregnancy, sepsis, acute intoxication.

33
Q

Give two inhibitory ion channels affected by some anaesthetics.

A

1) GABA-A activated chloride channels. Increases sensitivity to GABA. Causes hyperpolarisation and decreases its excitability.
2) Glycine activated chloride channels. Increases sensitivity to Glycine. Also causes hyperpolarisation and reduced excitability.

34
Q

Give two excitatory ion channels affected by some anaesthetics.

A

1) Neural nicotinic ACh receptors: inhibition leads to reduced excitation.
2) NMDA receptors: anaesthetics reduce calcium current involved in modulation of synaptic responses. E.g. Ketamine.

35
Q

How are inhaled anaesthetics administered?

A

Titration to vaporise the fluranes. Anaesthetic agent is then mixed with a carrier of oxygen, air and often nitrous oxide. This is then fed to the respiratory system.

36
Q

What is the blood:gas coefficient?

A

The volume of gas in litres that can dissolve in one litre of blood.

37
Q

Describe inhibitory LGIC pharmacodynamics.

A

These drugs decrease the concentration of the EC50. Hence, a lower level of GABA/glycine is needed to produce the same effect.

38
Q

Describe excitatory LGIC pharmacodynamics.

A

EC50 stays unchanged. However, efficacy decreases. Theres reduced inward movement of excitatory currents.

39
Q

Give three examples of anaesthetic adjuvants.

A

Benzodiazepines, propofol, nitrous oxide, opioids, neuromuscular blockers.

40
Q

Describe the role of benzodiazepines.

A

Facilitate amnesia and anxiolysis, while causing sedation. Have an agnostic effect on GABA receptors.

41
Q

Describe the role of propofol.

A

IV sedative/hypnotic used for induction/maintenance of anaesthesia.

42
Q

Describe the role of neuromuscular blockers.

A

Abolish normal muscular reflexes that would dangerously interfere with surgery.

43
Q

Give an ADR of fluranes, nitrous oxide and propofol.

A

Fluranes: CVS and resp depression, arrythmias and hypotension.
Nitrous oxide: expansion of airway cavities.
Propofol: CVS and resp depression.

44
Q

What is noted in the pre-surgical review of a patient?

A

Age, BMI, medical and surgical history, current medication, fasting time and airway assessment.

45
Q

Name the three stages of anaesthesia.

A

Induction - propofol and inhalation agent delivered. Adjuvants also IV.
Maintenance - adjuvants kept in balance to maintain adequate anaesthetic depth.
Recovery - agents are withdrawn and physiological function is monitored closely.

46
Q

What are the four stages of anaesthetic depth?

A

1) Analgesia
2) Excitement
3) Surgical anaesthesia
4) Medullary paralysis.

47
Q

What is medullary paralysis?

A

Severe depression of the respiratory and vasomotor centres. Ventilation and circulation must be supported to prevent death.

48
Q

What takes place during stage 1?

A

Loss of pain sensation due to interference of spinothalamic tract.

49
Q

What takes place during stage 2?

A

Delirium and possibly combative behaviour. Irregular BP and respiration.

50
Q

What takes place during stage 3?

A

Gradual loss of muscle tone and reflexes as the CNS is depressed further.