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
What did thiopentone used to be used for and why is it not anymore?
Sleeping tablets and because it is fatal if overdosed
26
What happens if you give one dose of thiopentone?
The subject stays asleep for about 5-10 minutes before the affect wears off
27
Why does the effect of thiopentone wear off quickly after only one dose?
It rapidly distrubutes to other organs
28
If you want a longer anathestia using thiopentone what do you have to do?
Repeat the dose so the metabolism is slow
29
Intravenous agents are induction agents; what does this mean?
They are given to induce anathestia before other drugs are given to mentain it
30
When can intravenous agents be used as the only drug?
During short procedures
31
What areas of the brain are involved in GAs analgesic action?
Repression of reticular formation and the thalamus
32
What area of the brain is involved in GAs amnesia action?
Repression of the hippocampus
33
What area of the brain is involved in GAs unconsciousness action?
The reticular formation and the hippocampus
34
What was the old theory of how general anaesthetics worked?
Lipid solubility theory
35
What did the lipid solubility theory entail?
That the GAs interacted with hydrophobic structures which included those on the membrane and increased the fluidity of the membrane
36
What is now the believed mechanism of how GAs work?
They act on GABA receptors
37
What does the GAs acting on GABA receptors do?
Encourages the opening of chloride channels and chloride flooding into the neuron leads to hyperpolatisation and cell inhibition
38
What is hyoscine?
A muscarnic receptor antagonist
39
Why would hyoscine be used a premedication?
Because the parasympathic nervous systems stimulates the glands to secrete muscous so hyoscine would block this and dry up secretions
40
Why would morphine be used as a premedication?
To prevent post operative pain
41
What is lignocaine?
A local anasthetic
42
How does lignocaine act as a loca anastethic?
It blocks sensory nerve conduction
43
In order to relax voluntary muscles what receptors need to be targetted?
Nicotinic receptors
44
What is tubocurraine?
A reversible competitve antagonist of acteylcholine
45
Tubocurraine is non-depolarising; what does this mean?
It blocks the nictonic receptor so does not allow the influx of Na+ ions to cause depolarisation
46
Is tubocurraine long or short acting?
Long
47
How would you stop the effects of tubocurraine?
Inhibition of acteylcholineesterase so there is more ach to compete with the tubocurraine
48
Suxamethonium is a depolarsing drug; what does this mean?
It doesnt block the cation channels like tubocurraine and they stay open leading to hyperpolarisation
49
IS suxamethonium long or short acting?
Short
50
Can suxamethonium be reversed with inhibition of acetylcholineesterate?
No
51
What kind of drug is suxamethonium?
A nictonic receptor agonist