Drugs in Surgery Flashcards

1
Q

What two ways are general anaesthetics normally administered?

A

Intravenously (into the vein) and inhalational

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2
Q

What happens to the CNS when you use a general anasthetic?

A

Its functions are surpressed

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3
Q

hat 3 things does depression of CNS functions this lead to?

A

Supression of conciousness
Supression of pain
Surpression of SKELETAL muscle relflexes

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4
Q

What two bad side effects can general anathetics usually do?

A

Lower blood pressure

Affect respiration

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5
Q

What bad thing can rarely happen when using general anaesthetics?

A

Liver/kidney damage

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6
Q

What are the 10 things that make the ideal anaesthetic?

A
  1. Quick induction
  2. High potency
  3. Reversibility
  4. Good analgesic
  5. Causes amnesia
  6. Causes muscle relaxation
  7. Low or harmless metabolism
  8. Low toxicity
  9. No hangover
  10. Non-flammable
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7
Q

What does having a quick induction entail?

A

Having low solubility in the blood so the blood becomes saturated

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8
Q

What would give the general anaesthetic a high potency?

A

Having a high lipid solubility so less of the drug is needed to give a response

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9
Q

When it comes to reversibility; would intravenous or inhalational administration be more useful?

A

Inhalational as you have more control over it than you would intravenous

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10
Q

In order for a general anaesthetic to have low toxicity what three things would you want to avoid?

A
  1. Respiratory depression
  2. Cardiovascular depression
  3. Liver damage
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11
Q

What does no hangover from a general anasthetic mean?

A

Want the effects to wear off after the operation - no drowsiness or sickness

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12
Q

What does low or harmless metabolism entail?

A

We dont want that drug to be broken down into something harmful

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13
Q

What kind of molecules are involved in halational anaesthetics?

A

Small, unreactive molecules

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14
Q

What are two examples of small unreactive molecules used as inhalational anaesthetics

A

Halothane and nitric oxide

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15
Q

What sort of concentrations do these inhalational anaesthetics have to be adminstered at?

A

Very high concentrations

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16
Q

Why is halothane a good inhalational general anaesthetic?

A

It is potent, not irritant and volatile

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17
Q

Halothane and nitric oxide dont induce anasthesia; what do they do?

A

They maintain it

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18
Q

What is nitric oxide otherwise known as and what is it used in?

A

Laughing gas used in childbirth

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19
Q

Intravenous agents are very rapid; why is this?

A

Because of high cerebral blood flow

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20
Q

Intravenous agents have a very short duration; why is this?

A

They are quickly redistrubuted to other organs away from the CNS

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21
Q

With it high cerebral blood flow how long does it take for intravenous agents to take affect?

A

30 seconds

22
Q

What is thiopentone?

A

A intravenous general anasthetic

23
Q

Why is thipentone known as barbiturate?

A

It is derived from baribituric acid

24
Q

Why is thiopentone not a good general anasthetic?

A

It causes cardiovascular and respiratory depression and has a low therpeutic index

25
Q

What did thiopentone used to be used for and why is it not anymore?

A

Sleeping tablets and because it is fatal if overdosed

26
Q

What happens if you give one dose of thiopentone?

A

The subject stays asleep for about 5-10 minutes before the affect wears off

27
Q

Why does the effect of thiopentone wear off quickly after only one dose?

A

It rapidly distrubutes to other organs

28
Q

If you want a longer anathestia using thiopentone what do you have to do?

A

Repeat the dose so the metabolism is slow

29
Q

Intravenous agents are induction agents; what does this mean?

A

They are given to induce anathestia before other drugs are given to mentain it

30
Q

When can intravenous agents be used as the only drug?

A

During short procedures

31
Q

What areas of the brain are involved in GAs analgesic action?

A

Repression of reticular formation and the thalamus

32
Q

What area of the brain is involved in GAs amnesia action?

A

Repression of the hippocampus

33
Q

What area of the brain is involved in GAs unconsciousness action?

A

The reticular formation and the hippocampus

34
Q

What was the old theory of how general anaesthetics worked?

A

Lipid solubility theory

35
Q

What did the lipid solubility theory entail?

A

That the GAs interacted with hydrophobic structures which included those on the membrane and increased the fluidity of the membrane

36
Q

What is now the believed mechanism of how GAs work?

A

They act on GABA receptors

37
Q

What does the GAs acting on GABA receptors do?

A

Encourages the opening of chloride channels and chloride flooding into the neuron leads to hyperpolatisation and cell inhibition

38
Q

What is hyoscine?

A

A muscarnic receptor antagonist

39
Q

Why would hyoscine be used a premedication?

A

Because the parasympathic nervous systems stimulates the glands to secrete muscous so hyoscine would block this and dry up secretions

40
Q

Why would morphine be used as a premedication?

A

To prevent post operative pain

41
Q

What is lignocaine?

A

A local anasthetic

42
Q

How does lignocaine act as a loca anastethic?

A

It blocks sensory nerve conduction

43
Q

In order to relax voluntary muscles what receptors need to be targetted?

A

Nicotinic receptors

44
Q

What is tubocurraine?

A

A reversible competitve antagonist of acteylcholine

45
Q

Tubocurraine is non-depolarising; what does this mean?

A

It blocks the nictonic receptor so does not allow the influx of Na+ ions to cause depolarisation

46
Q

Is tubocurraine long or short acting?

A

Long

47
Q

How would you stop the effects of tubocurraine?

A

Inhibition of acteylcholineesterase so there is more ach to compete with the tubocurraine

48
Q

Suxamethonium is a depolarsing drug; what does this mean?

A

It doesnt block the cation channels like tubocurraine and they stay open leading to hyperpolarisation

49
Q

IS suxamethonium long or short acting?

A

Short

50
Q

Can suxamethonium be reversed with inhibition of acetylcholineesterate?

A

No

51
Q

What kind of drug is suxamethonium?

A

A nictonic receptor agonist