Neurologicall Pharmacology Flashcards

Question

What are DRA side effects

Answer 1

* Sedation * Hallucinations * Confusion * Nausea * Hypotension Older the patient 0 more likely to have pd. may have slight dementia or confusion. Dont want to onfoun

Answer 2

* Monoamine oxidase B * Metabolises dopamine * Predominates in dopamine containing regions in brain * MAOB inhibitors enhance dopamine

Answer 3

• Monoamine oxidase B inhibitors * Selegiline * Rasagaline

Answer 4

* Can be used alone * Prolong action of L-DOPA * Smooths out motor response * May be neuroprotective

Answer 5

• Catechol-O-methyl Transferase (COMT) Inhibitors • Entacapone – doesn’t cross BBB reduce peripheral breakdown of l-dopa No longer used: • Tolcapone – crosses BBB but main effect peripheral » Monitor liver function

Answer 6

• Reduce peripheral breakdown of L-DOPA to 3-O-methyldopa » 3-O-methyldopa competes with L-DOPA active transport into CNS • No therapeutic effect alone » Can use combination tablets COMT inhibitor and L-DOPA and peripheral dopa decarboxylase inhibitor - Stalevo • Have L-DOPA ‘sparing’ effect • Prolongs motor response to L-DOPA » Reduces symptoms of ‘wearing off’

Answer 7

Acetyl Choline may have antagonistic effects to dopamine * Trihexyphenidydyl * Orphenadrine * Procyclidine • Minor role in treatment of PD ``` These do not affect bradykinesia and rigidity bc those are dopamine effects. But t helps with tremor.but it makes pl confused. Less beneficial effects and too many side effects to have a major role. Tremor had less impact then stiffness and slowness. ```

Answer 8

Advantages • Treat tremor • Not acting via dopamine systems

Answer 9

Disadvantages ``` • No effect on bradykinesia • Side effects • Confusion • Drowsiness • Usual anticholinergic s/e ```

Answer 10

• Mechanism action uncertain – possibly * enhanced dopamine release * Anticholinergic NMDA inhibition * Poorly effective * Few side effects * Little effect on tremor

Answer 11

* Carried out stereotactically * Of value in highly selected cases * Dopamine responsive * Significant side effects with L-DOPA * No psychiatric illness * Controlled trials * Lesion * Thalamus for tremor * Globus Pallidus Interna for dyskinesias ``` • Deep brain stimulation • Subthalamic nucleus Dont destroy any brain tissue. Put an electrode into subthalamic nucleus. Have to be dopamine reposnisve but nto able to take l dopa ```

Answer 12

• Fluctuating, fatiguable, weakness skeletal muscle – Extraocular muscles – commonest presentation – Bulbar involvement – dysphagia, dysphonia, dysarthria – Limb weakness – proximal symmetric – Respiratory muscle involvemeng Double vision + ptosis and weakness common and possible slurring or speech/problem swallowing - indicates MG ``` O sensory involvement - post synaptic probelm. Extraoccula muscles and bulbar muscles (speech and swallowing) - pharynx and larynx — limb Double vision + ptosis and weakness common and possible ```

Answer 13

``` Exacerbate it • Aminoglycosides • Beta-blockers, CCBs, quinidine, procainamide • Chloroquine, penicillamine • Succinylcholine • Magnesium • ACE inhibitors ``` ``` What drugs are we not going to give them. Not contraindicated but we are not going to give these. Safest thing - tell them I theyre going to start a thug tell the gp that u have MG. doesnt mean u cant abhvae it but ight interfere ```

Answer 14

• Acute exacerbation – Myasthenic crisis • Overtreatment – Cholinergic crisis Muscles increasingly weak either secondary to myasthenia crisis but can also be overtreatment - give ache inhibitor - ach is metabolise by esterase - leave ach there so. If oevrtert. Depolarising block - caused by the treatment. Cant get cholinegic crisis if MG unless on a treatment that would cause it

Answer 15

• Acetylcholinesterase inhibitors

Answer 16

``` • Acetylcholinesterase inhibitors – Enhance neuromuscular transmission – Skeletal and smooth muscle – Excess dose can cause depolarising block – cholinergic crisis – Muscarinic side effects ``` Pyridostigmine - oral Neostigmine – oral and IV preparations (ITU) • Quicker action, duration up to 4 hours • Significant antimuscarinic side effect

Answer 17

``` • Prevents breakdown of ACh in NMJ • ACh more likely to engage with remaining receptors • Onset 30min; peak 60-120min; duration 3-6hr • Dose interval and timing crucial • Antimuscarinic side effect – – miosis and the SSLUDGE syndrome: » Salivation, » Sweating, » Lacrimation » Urinary incontinence » Diarrhea, » GI upset and hypermotility » Emesis) ```