Nervous system durgs Flashcards Preview

pharmacology > Nervous system durgs > Flashcards

Flashcards in Nervous system durgs Deck (16):
1

Route of administration for non depolarising blockers?

poor absorption orally (highly polar) - administer IV

2

Example of a non-depolarising blocker?

tubocurarine

3

Example of a non-depolarising blocker?

rocuronium

4

Characteristics of depolarising blockers

- 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

5

What is pyridostigmine?

reversible anticholinesterase

6

clinical uses of irreversible anticholinesterases?

glaucoma, long-lasting
*deadly in small doses

7

Presentation of anti cholinesterase poisoning?

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

8

treatment of anticholinesterase poisoning

- 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

9

presentation of myasthenia gravis

- 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

10

Drug treatment of myasthenia gravis

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

11

clinical uses of irreversible anticholinesterases?

glaucoma, long-lasting
*deadly in small doses

12

Presentation of anti cholinesterase poisoning?

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

13

treatment of anticholinesterase poisoning

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

14

presentation of myasthenia gravis

- 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

15

Drug treatment of myasthenia gravis

Anti cholinesterase to increase [ACh]

16

Characteristics of non-depolarising blockers

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