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sam oral > 43. diseases of neuromuscular junction. toxicosis, tetanus, botulism > Flashcards

43. diseases of neuromuscular junction. toxicosis, tetanus, botulism Flashcards

1
Q

NMJ disorders fifferentiation

A

presynaptic: decreased release of acetylcholine
postsynaptic: Ach receptor related
enymatic: Ach esterase inhibitors

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2
Q

list presynaptic diseases

A

LMN type deficits (hypotonia, hyporeflexia)

botulism

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3
Q

list postsynaptic diseases

A

exercise induced weakness

myasthenia gravis

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4
Q

list toxic diseases

A 
tetanus 
strychinine poisoning 
ivermectin poisoning 
lead toxicosis 
methaldehyde toxicosis 
pyrethrins 
ethylene glycol
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5
Q

what is presynaptic disease?

A

inability to release Ach from presynaptic channels
botulism
tick paralysis

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6
Q

botulism etiology

A

neurotoxin from C. botulinum
ingestion of preformed neurotoxin
botulinum toxin irreversibly cleaves a protein that docks Ach vesicles at presynaptic membrane

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7
Q

botulism clinical signs

A

acute paresis starting in hindlimbs
facial nerves can be involved - facial paralysis, dysphonia
autonomic signs: ileus, tachycardia, urinary retention, Megaoesophagus

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8
Q

botulism diagnosis

A

history, clinical signs, toxin analysis

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9
Q

botulism treatment

A

supportive: fluid, bladder expression, feeding tube
AB NOT indicated - toxin not bacteria

antitoxin - don’t work for toxin already in nerves, only circulating toxins

prognosis good, recovery after 2-4 weeks

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10
Q

postsynaptic disease

A

inability of postsynaptic membrane to react to Ach
congenital myasthenia gravis
aquired myasthenia gravis
organophosphate, carbamate toxicosis

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11
Q

myasthenia gravis acquired vs congenital

A

congenital: deficiency or abnormality of Ach receptors
aquired: antibodies produced against Ach receptors -> low number of functioning receptors

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12
Q

three forms of myasthenia gravis

A

fulminant
focal
generalized

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13
Q

generalized myasthenia gravis

A

normal at rest
exercise induced - get more and more tired, rest and get better
unknown background
can have concurrent autoimmune or endocrine disorder: hypo, hyperthyroidism

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14
Q

focal myasthenia gravis

A

weakness of one muscle group
laryngeal paralysis
megaesophagus

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15
Q

fulminant myasthenia gravis

A

no improvement at rest

generalized weakness

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16
Q

myasthenia gravis diagnosis

A 
tensilon test (anticholinesterase)-> weakness disapear for a moment 
determination of Ach receptor antibodies
17
Q

myasthenia gravis treatment

A

Ach esterase inhibitor: pyridostigmine bromide

sometimes immunosuppression

18
Q

exercise induced collapse of lab retrievers

A

similar to myasthenia gravis
exercise - overheat- fatigue, flaccid paralysis
genetic disorder
genetic test available

19
Q

organophosphate, carbamate toxication

A

insecticides, flea collars
inactivate Ach esterase - increased Ach - increased stimulation (tonic-clonic seizure, facial twitch)
vegetative overstimulation (muscarinic Ach receptors -> salivation, lacrimation

pralidoxime: resolution of nicotinic effect of Ach on skeletal muscle
Atropine: resolution of muscarinic signs

20
Q

tetanus etiology

A

cl. retain into anaerobic wound - neurotoxin production
toxin (tetanospasmin) enter blood stream, - > neuron->inhibitory interneurons => inhibit glycine and GABA release
LOSS of inhibition of motor neurons -> rigid paralysis

21
Q

tetanus - forms, incubation

A

local tetanus
general tetanus
incubation 1-2 weeks
progression until day 4-7

22
Q

tetanus signs

A

extensor rigidity - saw horse
ricis sardinosus - special grin expression (facial muscle spasm)
difficulty swallowing - salivation
stimuli further increase symptoms

23
Q

tetanus treatment

A

debridement of wound if found
AB: penicillin, metronidazole, tetracycline
antitoxin - can cause allergic reaction
muscle relaxants - acepromazine, diazepam
supportive care: feeding tube, empty bladder, turning
quiet environment

24
Q

strychinine poisoning

A

alkaloid from strychnine tree
glycin antagonist (glycin is inhibitory signal)
(in small dose it increase salivation and appetite-appetite stimulant)
rigid paralysis - saw horse
retraction of mouth, ears pulled back
hypersensitive to stimulation

25
Q

ivermectin poisoning

A

anti parasitic drug, MDR1 gene mutation dogs sensitive
GABA antagonist, bind to gaba receptor
salivation, vomiting ataxia, tremors
supportive treatment

26
Q

lead toxicosis etiology, clinical signs

A

ingesting lead
lead inhibit sulfhydryl groups of important metabolic enzymes
Gi signs, hematology change(microcytic, hypo chromic anemia)
lethargy, ataxia, seizure, blindness, anorexia

27
Q

lead toxicosis diagnosis, treatment

A

determination of lead levels in blood, urine, liver, kidney

1: remove lead source
2: calcium EDTA IV
3: sedative, anticonvulsant
4: diuretics
5: short acting GCC

28
Q

methaldehyde toxicosis

A

slug drug ;) decomposed to acetaldehyde in stomach
acetaldehyde and methaldehyde rapidly absorbed-> Elin signs appear fast
decrease conc of GABA, and serotonin
panting, salivation, trembling, seizures

29
Q

methaldehyde toxicosis therapy

A

no specific therapy

diazepam, methocarbamol for seizures, trembling

30
Q

pyrethrin toxicosis

A

aldehyde of chrysanthemum plant
used as insecticide
inhibit Ca/Mg-ATP-ase in nervous tissue (atpase helps muscle relaxation)

31
Q

pyrethrin toxicosis - who is sensitive

A 
cats are sensitive
low hepatic glucuronidase activity, slow metabolism -> toxicosis 
seizure, tremor 
supportive therapy 
good prognosis
32
Q

ethylene glycol toxicosis mechanism, clinical signs

A

ethylene glycol degraded to toxic metabolites

  • glycolaldehide, glyoxylic acid, oxalic acid, glycolic acid
    1. apathy, salivation, ataxia (like drunk)
    2. AKI
33
Q

ethylene glycol toxicosis, diagnosis treatment

A

US: halo sign on kidney due to oxalate crystals
urine: ca oxalate crystals
IV ethyl alcohol

sam oral (42 decks)

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