Anaesthetic Drugs

Question 1

Name 3 weak opiods.

Answer 1

1. Fentanyl
2. Remifentanil
3. Alfentanil

Question 2

Drugs used for amnesia - induction agents.

Answer 2

1. Propofol - slow onset, reduces HR & BP, good for PONV, any general op.
2. Thiopentone - fast onset, reduces BP not HR, RSI, brain protective.
3. Ketamine - slow onset, increase HR & BP, good for bronchospasm + analgesia.
4. Etomidate - slow onset, organ protective, cardiac surgery, high PONV.

Question 3

Drugs used for akinesia.

Answer 3

1. Suxamethonium - DEPOLARISING.

2. Atracurium, mivacurium, vecuronium, rocuronium.

Question 4

Name 3 inhalation agents - keep px asleep

Answer 4

1. Sevoflurane - sweet smelling.
2. Desflurane - low lipid solubility, rapid onset and offset, used in long operations.
3. Isoflurane - least effect on organ blood flow.

Question 5

What are induction agents and give 4 examples?

Answer 5

IV drugs that cause a rapid loss of consciousness - used to induce amnesia quickly before giving maintenance drugs.

1. Propofol, Thiopentone, Ketamine, Etomidate.

Question 6

Propofol

1. Positives
2. Negatives

Answer 6

1. Excellent suppression of airwarys, reduces PONV, quick acting = 30 seconds.
2. Decreases HR + BP, painful on injection (‘stings’), involuntary movements.

Question 7

Thiopentone

1. What class of drug?
2. What is it used mostly for?
3. Positives
4. Negatives

Answer 7

1. Barbiturate
2. Rapid sequence induction.
3. Faster acting than propofol, also an anti-epileptic, protects the brain.
4. Decreases BP + raises HR, risk of bronchospasm, rash, contraindicated in porphyria.

Question 8

Ketamine

1. Positives
2. Negatives

Answer 8

1. Slow onset = 90 secs, increases HR + BP, bronchodilation.

2. PONV, ‘emergence phenomenon’ = vivid dreams and hallucinations.

Question 9

Etomidate

1. Positives
2. Negatives

Answer 9

1. Haemodynamic stability, lowest incidence of hypersensitivity reaction.
2. Pain on injection, spontaneous movements, adreno-cortical suppression, high incidence PONV.

Question 10

What are inhalation agents, name 4 and what are their MAC?

Answer 10

Drugs used to maintain amnesia.

Sevoflurane = 2%
Desoflurane = 6%

Isoflurane = 1.15%
Enflurane = 1.6%
Nitrous oxide = 104%

Question 11

What is ‘MAC’

Answer 11

Minimum alveolar concentration = the minimum alveolar concentration required to prevent a reaction to surgical stimulus, in 50% of px.

Question 12

What are the 2 different types of neuromuscular blockers?

Answer 12

1. Depolarising and non-polarising.

Question 13

1. What is the only depolarising type of neuromuscular blocker?
2. What is its method of action.

Answer 13

1. Suxamethonium

2. Non-competitive inhibitor of ACh - not rapidly hydrolysed by AChE.

Question 14

What is ‘suxamethonium apnoea’?

Answer 14

Rare condition (1:1000). Homozygotes lack enzyme to metabolise, typically takes 3-24 hours to wear off = must be intubated + monitored until it wears off.

Question 15

Name these non-polarising neuromuscular blockers:

1. Short acting
2. Medium acting
3. Long acting

Answer 15

1. Mivacurium + Atracurium (15 mins).
2. Rocuronium (40 mins).
3. Pancuronium (60 mins).

Question 16

What can be used to reverse non-depolarising, neuromuscular blockers?

Answer 16

1. Glycopyrolate (antimuscarinic) = reduces secretions, bradycardia, bronchospasm.
2. Neostigmine = blocks AChE, allows Ach in junction to accumulate, stimulates muscarinic receptors + parasympathetic nervous system (= bradycardia).

Question 17

Name 3 inotropic agents?

Answer 17

1. Ephedrine - acts on adrenergic receptors (alpha cells) + causes vasoconstriction = raises HR + contractility.

Question 18

What are local anaesthetics?

Answer 18

Drugs that locally prevent the transmission of the nerve impulse in the region in which it is applied WITHOUT affecting consciousness.

Question 19

Describe the sequence of pharmacological and clinical events when a dose of suxamethonium is given? What are the important side effects?

Answer 19

1. Suxamethonium molecules enter the neuromuscular junction and non-competitively binds to the post synaptic (nicotinic) receptors on the motor end plate on the muscle membrane.
2. Muscle fasciculation occurs as muscle membrane is depolarised.
3. Followed by paralysis as suxamethonium molecules remain bound to the post-synaptic (nicotinic) receptors = keeping muscle membrane depolarised.
4. Recovery occurs spontaneously - Suxamethonium is hydrolysed by the enzyme: plasma pseudo-cholinesterase.
5. Normal neuromuscular transmission is restored after 4-6 mins.

Side effects:

• increased IOP
• muscular pain
• histamine release
• prolonged apnoea in px with plasma pseudo-cholinesterase deficiency.
• significant rise in serum potassium
• malignant hyperthermia

Question 20

How do NSAIDs work? What are the relative and absolute contraindications to their use?

Answer 20

1. They inhibit the enzyme cyclo-oxygenase (COX) - this prevents the synthesis of inflammatory mediators (prostaglandins, prostacyclins, thromboxane A2) from arachidonic acids. Inhibition of COX-1 = unwanted effects, COX-2 = desired therapeutic effects.
2. Relative contraindications = high risk of bleeding, hepatic dysfunction, bleeding disorders, elderly >65, pregnancy, asthma.

ABSOLUTE contraindications = renal dysfunction, hyperkalaemia, HF, severe hepatic dysfunction, hx of GI bleeding, aspirin-induced asthma.

Question 21

1. What factors increase the risk of PONV?
2. How can these be stratified to identify px risk of PONV and guide prophylaxis?
3. Describe the drugs and doses used to treat PONV

Answer 21

1. Female sex, non-smoker, hx of PONV or motion sickness, post-operative opioids.
2. Apfel score - 1 point for each of the above. 0-1
   = low risk, don’t require routine antiemetics, 2+ = high risk, should receive combo therapy of antiemetics.
3. Cyclizine - 50 mg IM or IV,
   Ondansetron (5HT3 antagonist) - 4-8 mg orally or IV, Dexamethasone (corticosteroid) - 4-8 mg IV

Question 22

Describe the central effects of opioids. How can they be reversed?

Answer 22

Analgesia, sedation, euphoria, N+V, pupillary constriction, respiratory depression.

Reversed using naloxone - antagonist action at all opioid receptors.

Question 23

1. Describe how a nerve impulse is transmitted.
2. How do local anaesthetic drugs affect this?
3. How much lidocaine is contained in 15ml of a 0.75% solution?
4. What is the maximum safe dose, with and without adrenaline?

Answer 23

1. Significant stimulus opens sodium channels (Na rushes IN).

Depolarisation occurs = cell membrane potentials increases from -70 mV to +20 mV = action potential.

Voltage- gated sodium channels open - propagating the action potential along the nerve.

Membrane is rapidly repolarised by loss of K+ from within the cell and by actively pumping OUT sodium in exchange for K+.

2. LA blocks sodium channels from within nerve cell, preventing entry of sodium and therefore depolarisation - no action potential can be initiated or propagated along nerve.
3. Conc (%) x volume (ml) x 10
   = 0.75 x 15 x 10 = 112.5 mg
4. 3mg (max 200mg) without adrenaline
   6mg (max 500mg) with adrenaline.

Question 24

When using an IV drug to induce anaesthesia:

1. Propofol causes hypotension and respiratory depression?
2. Propofol is cumulative after repeated doses?
3. Thiopentone causes involuntary movement and hiccups?
4. Ketamine is antanalgesic?

Answer 24

1. T - also Thiopentone
2. F - why it can be used as an infusion for TIVA (total IV anaesthesia.
3. F - Etomidate causes involuntary movements and hiccups.
4. F - profound analgesia!

Question 25

Suxamethonium:

1. Is a non-depolarising neuromuscular blocking drug?
2. Has a rapid onset and short duration of action?
3. Can be reversed with neostigmine?
4. May cause hypokalaemia?

Answer 25

1. F - only DEPOLARIZING
2. T - hence why used in RSI
3. F - cannot be reversed. This occurs on its own after metabolism by pseudocholinesterase.
4. F - may cause HYPERKALAEMIA

Question 26

With respect to local anaesthetic drugs:

1. They are only active in the unionised form?
2. When used for regional anaesthesia, sensory block precedes motor block.
3. Lidocaine is less toxic than bupivacaine.
4. The maximum safe dose of lidocaine is 6-7mg/kg?

Answer 26

1. F - enters the nerves unionised but the IONISED form is what blocks sodium channels.
2. T - small diameter (sensory nerves) are blocked before large diameter (motor nerves).
3. T - bupivacaine = cardiotoxic.
4. F - max safe dose with adrenaline is 6-7mg/kg. on its own = 3mg/kg.

Question 27

Morphine:

1. Is more effective against visceral pain than pain after trauma?
2. When given IV has a peak effect in <5 mins?
3. Is a schedule 3 drug?
4. Causes pupillary dilation?

Answer 27

1. T - NSAIDs are more effective for bone and soft tissue injuries.
2. F - peak effect occurs between 5-10 mins.
3. F - schedule 2
4. F - mitosis (constriction) due to its action on Edinger-Westphal nucleus.

Question 28

When using inhalational anaesthesia:

1. An adequate depth of anaesthesia for surgery can be achieved reliably using NO alone?
2. The MAC is a measure of anaesthetic potency?
3. Speed of onset is faster with drugs that are more soluble in the blood?
4. The most suitable drug for an inhalational induction of anaesthesia is isoflurane?

Answer 28

1. F - NO is not very potent.
2. T - allows comparison of the alveolar concentrations of various anaesthetic drugs.
3. F - more soluble the drug, the more readily it dissolves in the blood = takes longer for partial pressure of drug to rise to a level which causes anaesthesia. (Basically doesn’t stay in the blood long enough to cause anaesthetic effect).
4. F - isoflurane is irritant to airways in high conc. = salivation and coughing. It is also relatively soluble in blood = slow onset.

(Insoluble in blood = faster onset).