Botulism, tetanus, and drug induced myopathies Flashcards
Clostidium botulinum?
gram positive rod that forms spores
after ingesting toxin/wound, nausea vomit dizziness, cranial palsy double vision swallowing difficult, respiratory paralysis
Neurotoxins with botulinum?
A, B and E in humans
prevents release of acetylcholine from the alpha-motor neuron, muscle cannot receive signal, flaccid paralysis
Heavy chain B/ light chain a?
B binds to the toxin to the specific types of axon terminals
A part is active, cleaves and released into cytoplasm
degrades snare protein
prevents neuro-secretory vesicles from docking/fusing with the nerve synapse plasma membrane and releasing their NT
Infant botulism?
floppy baby syndrome
baby’s immature immune system and inability to process toxin in intestinal tract
Symptoms
-general muscle fatigue, weak sucking, ptosis, inactivity, constipation
Diagnosis- from stool
Tetanus?
from release of toxin by Clostridium tetani
headache, jaw cramp, tightening, stiffness, seizures, high mortality
Clostridium tetani?
virulence factor- tetanospasmin
suppress release of GABA (inhibitory nt) signals are unopposed and constant stim to contract
Pathogenesis of clostridium tetani?
CNS (PNS, spinal cord, brainstem)
toxin is taken up into the nerve axon and transported across the synaptic junctions, until it reaches the CNS where it is bound by the heavy chain at the presynaptic junctions of the inhibitory motor nerve endings
Diagnose tetani?
gram pos motile rod with terminal spores
Treat tetani?
antitoxin, debride tissue, Penicillin
Prevention tetani?
DTaP
tetanus booster
Actue Alcohol induced myopathy?
longstand alcohol
men more common
nontraumatic rhabdomyolysis
dose related, damage muscle and usually recover
Chronic alcohol induced myopathy?
women more common
diffuse muscle atrophy
muscle pain usually absent
Cocaine induced myopathy?
usually for other problems, incidental
increase sympathetics, vasoconstrict skeletal muscle ischemia
Glucocorticoids induced myopathy?
common cause of drug induced
direct catabolic effects
affects intermediary metabolism that provides amino acids as a substrate for gluconeogenesis
may increase muscle degredation/atrophy
Lipid lowering drugs induced myopathy?
primarily the statins
myalgias to myostitis to overt rhabdomy