Nervous system durgs

Question 1

Route of administration for non depolarising blockers?

Answer 1

poor absorption orally (highly polar) - administer IV

Question 2

Example of a non-depolarising blocker?

Answer 2

tubocurarine

Question 3

Example of a non-depolarising blocker?

Answer 3

rocuronium

Question 4

Characteristics of depolarising blockers

Answer 4

• stimulate nicotinic receptors (initial muscle fasciculation)
• action potentiated by increasing [ACh]
• produced by high doses of nicotinic agonists
• act at muscle end plate to prevent cycles of depolarisation and repolarisation which are required for sustained muscle contraction
• inactive Na+ channel/receptors unresponsive to ACh

Question 5

What is pyridostigmine?

Answer 5

reversible anticholinesterase

Question 6

clinical uses of irreversible anticholinesterases?

Answer 6

glaucoma, long-lasting

*deadly in small doses

Question 7

Presentation of anti cholinesterase poisoning?

Answer 7

• symptoms of parasympathetic overactivity
• sweating, increased salivation, bradycardia (hypotension)
• skeletal muscle fasciculation and then NM blockades
• respiratory failure

Question 8

treatment of anticholinesterase poisoning

Answer 8

• atropine to block muscarinic actions of ACh
• use the cholinesterase reactivate (pralidoxime) to treat organophosphate pesticides *enzyme can’t be reactivated after a few hours
• artificial ventilation if necessary

Question 9

presentation of myasthenia gravis

Answer 9

• autoimmune disease affecting NM transmission
• reduced population of N receptors of muscle end plate due to antibodies binding to N receptors so AP only activated in small number of muscle fibres

Question 10

Drug treatment of myasthenia gravis

Answer 10

• Anticholinesterase to increase [ACh]
• ACh (will be broken down by pseudocholinesterase in the blood) + atropine to block unwanted muscarinic effects + corticosteroids or immunosuppressants

Question 11

clinical uses of irreversible anticholinesterases?

Answer 11

glaucoma, long-lasting

*deadly in small doses

Question 12

Presentation of anti cholinesterase poisoning?

Answer 12

• symptoms of parasympathetic overactivity
• sweating, increased salivation, bradycardia (hypotension)
• skeletal muscle fasciculation and then NM blockades
• respiratory failure

Question 13

treatment of anticholinesterase poisoning

Answer 13

atropine to block muscarinic actions of ACh
use the cholinesterase reactivate (pralidoxime) to treat organophosphate pesticides *enzyme can’t be reactivated after a few hours
artificial ventilation if necessary

Question 14

presentation of myasthenia gravis

Answer 14

• autoimmune disease affecting NM transmission
• reduced population of N receptors of muscle end plate due to antibodies binding to N receptors so AP only activated in small number of muscle fibres

Question 15

Drug treatment of myasthenia gravis

Answer 15

Anti cholinesterase to increase [ACh]

Question 16

Characteristics of non-depolarising blockers

Answer 16

competitive antagonists at nicotinic receptors
action overcome by increasing [ACh] e.g. anticholinesterases
no initial stimulant action
not absorbed orally, give IV
do not pass blood brain barrier/placenta