Flashcards in neuro midterm Deck (21):
Toxin from cobra snake venom that binds irreversibly to ACh binding sites
Txt for myasthenia gravis
Neostigmine - inhibits AChE in cleft -> larger ACh concentration -> prolonged duration of ACh action at end plate.
Given with atropine, an antagonist of ACh's effects on the cardiovascular system
Blocks K+ channels, prolongs duration of impulses = enhanced entry of Ca2+ ions into motor nerve endings -> increased release of ACh (alters quantal release).
Alternative to neostigmine for tx'ing Lambert-Eaton syndrome
Exotoxin with protease component that enters nerve endings of peripheral nerves, transported by retrograde axial transport to cell bodies, carried into spinal cord via ventral roots and leaving motor neuron cell bodies, entering inhibitory interneurons where it prevents normal release of inhibitory transmitter by breaking down synaptobrevin irreversibly.
Normal regulation of reflex arcs is disturbed leading to hyperreflexia -> abolition of reciprocal innervation with both agonist and antagonist muscles experiencing stimulation -> spasms that spread to arms, trunks, and legs, interference with respiration.
Tx: use neuromuscular blocking agents with assisted ventilation
Blocks glycine receptors in the CNS, spasms, convulsions, and interference with breathing
Degrades synaptobrevin (SNARE) and prevents docking for vesicle fusion/exocytosis. Prevents ACh binding irreversibly. Sx's: several hours after ingestion - double vision, difficulty swallowing, dry mouth, difficulty speaking. Then greater muscular weakness of limbs and respiratory muscles (life-threatening). Assisted pulmonary ventilation may be necessary.
Microinjection of botulinum toxin can tx dystonias
Toxin in venoms of some snakes that binds irreversibly to actin and possibly other cytoskeletal components in cholinergic nerve endings, blocks ACh release. Resulting paralysis can be fatal if subject is not ventilated
Toxin of black widow spider. Promotes fusion of cholinergic vesicles by binding to the neurexin/synaptotagmin complex. Induces such a massive release of vesicular ACh that motor nerve terminals become severely depleted of synaptic vesicles. Periods of irregular muscle spasm followed by flaccid paralysis. May need ventilation.
Sarin and tabun
Nerve gases. Covalently bind irreversibly to AChE and prolong ACh-induced depolarization. Cause death by polarizing respiratory muscles.
Snail toxin. Irreversibly binds to voltage-gated Ca2+ channels in nerve terminal membrane -> impaired Ca2+ entry, low probability of exocytotic release of ACh -> flaccid paralysis
Neomycin and streptomycin
Aminoglycoside antibiotics. Inhibit exocytosis of ACh at motor nerve terminals by blocking presynaptic Ca2+ channels. Neomycin is more effective than streptomycin and the effects of both are reversed competitively by raising extracellular Ca2+. (Both abx can also block postsynaptic nAChRs when present at high concentrations). Alter quantal release
Dopamine receptor antagonists. Block hallucinations (including L-DOPA hallucinations) and delusions
Dopamine receptor agonist. Alleviate signs of Parkinson's disease
Mimics effects of ACh. Agonist for muscarinic receptors of the parasympathetic nervous system. Tx glaucoma
Autoimmune disease affecting exocrine glands, esp salivary and lacrimal glands due to dysfunction of M3 muscarinic receptor. CD4+ T cells infiltrate into lacrimal and salivary glands leading to dry Wes and dry mouth
Unilateral lesion in CNS pathway (hypothalamus -> spinal cord -> superior cervical ganglion -> ciliary nerve). Lack of NE (pre- or postganglionic). Cocaine test (slowly inhibits re-uptake of NE).
Usually affects only one side of the face - drooping eyelid, decreases pupil size, decreased sweating on affected side of face
High # neutrophils/leukocytes. High protein. Low glucose
High lymphocytes. High protein. Normal glucose
Normal cell number. Increased IgG, changes in T cells depending on dz activity. Normal protein and glucose
<10 mononuclear leukocytes. Protein >50