neuro post midterm Flashcards
Atenolol
B1 adrenergic antagonist. Tx HTN
Salbutamol
B2 adrenergic agonist. Tx asthma (bronchodilator)
Atropine
Muscarinic antagonist. Mydriatic, reduction of drooling in Parkinson’s dz, antidote in poisoning with insecticide
Amyotropic lateral sclerosis (ALS)
Degeneration of anterior horn cells and V, VII, X, XII, parts of pyramidal tract, and primary motor area. Affects LMNs. Flaccid and spastic paralysis. Affects UEs. Decreased cough reflex -> aspiration pneumonia, respiratory insufficiency
Anterior spinal artery (ASA) syndrome
Flaccid paralysis, spastic paresis. Positive Babinski (UMN), lose pain and temp
Central medullary syndrome
I.e. syringomyelia d/t tumors. Lose pain and temp, get flaccid paralysis (no spastic paralysis). Common in cervical spine
Posterior parietal cortex
Brodmann 5+7, integrate sensory info for motor planning in concert w/premotor areas
Lateral corticospinal tract
Mainly flexor. Alpha and gamma. Cortical input. Mainly excitatory
Rubrospinal tract
Flexor. Alpha and gamma. Cortical input. Excitatory
Medullary/lateral reticulospinal tract
Flexor, bilateral innervation. Alpha and gamma via interneuron. Cortical input. Excitatory
Pontine/medial reticulospinal tract
Extensor. Gamma ONLY, via interneuron. Cortical input. Excitatory. Mostly involuntary
Lateral vestibulospinal tract
Extensor. Alpha ONLY, via interneuron. NO CORTICAL INPUT. Vestibular organ - excitatory. Cerebellum - inhibitory
Medial vestibulospinal tract
Extensor. Alpha ONLY. NO CORTICAL INPUT. Inhibition of alpha (glycine). Vestibular organ - excitatory. Cerebellum - inhibitory
Type I motor unit
Slow-twitch; low-tension; fatigue-resistant, aerobic; small motor neuron and axon
Type IIA motor unit
Fast; relatively fatigue-resistant; large tension; some aerobic; relatively large motor neurons
Type II B motor unit
Fast; fatigue-susceptible; large tension; anaerobic; large motor neurons
Dx and tx for myasthenia gravis
Dx - Tensilon test. Tx - azathioprine and corticosteroids - immunosuppressants
Myotonia congenita
Defect in gene encoding Cl- channels, can’t bring Em close to Ecl to recover from AP when K+ is accumulating in TTS -> spontaneous firing of muscles after nerve end stimulation. Prolonged relaxation phase
Ballismus
Due to lesions of subthalamic nucleus. Decreased excitation of GPi -> disinhibition of thalamus and cerebral cortex -> increased contralateral movement
Tardive dyskinesia
D/t antipsychotic drugs (dopamine receptor antagonists), can become permanent
Dopa-induced dyskinesia
Occurs in txt of Parkinson’s w/DOPA -> chorea
Drug-induced Parkinson’s disease
Antipsychotics, depletors of DA stores (ex reserpine), toxic contaminants (MPTP)
Striatal neuronal degeneration and Huntington’s disease
Destruction of striatal neurons expressing D2 receptors -> decreased thalamic inhibition -> increased cortical activity. HYPERKINESIS, CHOREA
Sydenham disease
Chorea d/t autoimmune ABs against striatum resulting from childhood rheumatic fever
Mech of L-DOPA and carbidopa
L-dopa -> increased dopamine synthesis in surviving SNc. Carbidopa -> decreased peripheral metabolism of L-DOPA. Txt w/L-DOPA and carbidopa becomes less effective over several years
Bromocriptine
Stimulates D2 receptors
Pergolide
Stimulates both D1 and D2 receptors
Amantadine
Antiviral drug, may benefit some manifestations of Parkinson’s (akinesia, rigidity) -> ma promote release of dopamine and/or block ACh receptors (also weakly blocks NMDA receptors). Psychiatric SE’s!
Selegiline (deprenyl)
Irreversibly binds MAO B -> may improve responses to or delay need for other therapies