Neurology Flashcards
When should anti-epilpetics be started for seizures
Earlier start = better outcome for seizure control
- Identifiable structural lesion or hx of brain disease/ injury
- Acute repetitive seizures, Status epilipticus
- > 2 or more seizures in 6 months
- prolonged, severe, unusual post ictal periods
What are the good first line medications for seizures
1) Phenobarb, Imepitoin 2) bromide 3) Leviteracitam, zonisamide
What are good second line medications for Seizures
Phenobarb, bromide, levetiracitam
What is pahtophys of necrotizing menginiioencephalitits
Young middled aged pugs
multifocal asymmetrical necrosis in deep cebral cortex adjacent to white matter
What is the pathophys of necrotizing leucoencphalitits
Yorkies
asymmetrical malacic changes in cerebral white matter and thalmus
What is the pathophys of granulomatous ME
Any breed toy/terrier
idiopathic granulamatous inflammation
Perivascular accumulation of epithealoid macrophages and lymphocytes in the CNS
What are the effects of Mannitol on the brain
- Plasma expanding effect that reduces blood viscosity thus increased cerebral blood flow
- osmotic effect 15-30 minutes following admin when gradients are established causing decrease in brain water content
What are the negative effects of mannitol
Hypotension, electrolyte imbalances, Rebound ICH (increased cerebral blood flow), worsening cerebral edema free H2O diruesis
How does Hypternoic saline work to decreased ICP
Hypovolemia- restores circulating volume an maintains cerebral perfusion pressure
What are the drawbacks of administering hypertonic saline for ICP
Severe hypernatremia in dehydrated patients or suffering marked water loss
How does stress affect the body
immune suppression, GI disease, cutaneous disease, delayed wound healing, alteration s in pain receptors
What is the MOA of trazodone
Seritonin atangonist
No effect on seizure threshold
Minimally lowers CO
What is the MOA for dexmedetomidine for sedation
Alpha 2 agonist
blockade of alpha 2 receptor in locus coerulus inhibiting norepi release
Disinhibiting the aurosal usppression neurons in the area
What is the pathophys of SRMA and resultant CSF findings
Non supperative inflammatory lesions of the leptomeninges and vasculitis of mengial arteries
Responsive to steroids
Marked neutrophilic pleocytosis with hight TP
Where is CSF produced
choid plexus in the brain and to smaller extent the ependymal cells of the ventricular system
What are the functions of CSF
protect brain assisting with regulation of ICP, Medium for transport of metabolites, Neurohormones and neurotransmitters
What medications are reported to decrease CSF production?
Steroids, omeprazole, furosemide,
acetazolamide (carbon anhydrase inhibitior)
Define seizure
Sustained and uninhibited neuronal depolarization
What are the two types of spondylomyelopathy
Disk associated: Secondary to herniation : Dobermans
Osseus associated: Compression of cord due to osseus proliveration of the artericular process
What MOA advantages does IN midazolam have
Becomes lipid soluble as crosses the nasal mucosa
Some goes to systemic circiulation
Some will go straight to BBB bypasing the liver which enhances the activity
Define ICP
Pressure exerted by intracranial contents agains an inelastic cranial vault
What is the formulate of Cerebral perfusion pressure
CPP= MAP - ICP
What are 4 different ways to measure ICP
Intraventricular ICP Device- that is fluid coupled to transducer
Non-fluid coupled ICP tranducer with catehter tip miniature strain gauges
- Fiber optic linked
Transcranial doppler ultrasound of the basilar arteries through the Transforminal window
Define status epilepticus
Seizure activity lasts for more than 5 minutes or 2 or more seizures without recovery of consciousness
What is the pathophysiology of seizures
Ca influx due to sustained neuronal depolarization
Opening of voltage gated Na channels and influx of Na causing burst action potentials
Rapid repolarization then depolarization mediated by GABA receptor
GABA Receptor agonists have decreased efficacy with increasing seizure activity
What is the mechanism of drug resistance in seizures
Over expression of P-glycoprotien encoded by MDR-1 Gene
What are the systemic effects of phase 1 in status epilepticus?
Increase catecholamines and steroids
Hypertension, tachycardia, hyperglycemia, hyperthermia, ptyalism
Increase cerebral blood flow to meet O2 demand
Increase autonomic stimulation
Rhabdomyliss, hypotension, shock, NC Pulmonary edema, acute tubular necrosis
What are the systemic effects of phase 2 in status epilepticus?
Uncompensated after 30 minutes
cerebral vascular autoregulation fails and intracranial pressure increases
Hypoxia, hyperthermia, hypoglycemia, respiratory failure, acidosis, hyperkalemia, hyponatremia, uremia
What is the cushing’s reflex
MAP increased with increasing ICP to attempt to maintain cerebral perfusion pressure
Bradycardia often seen but won’t if hypovolemia
What is the MOA of benzodiazepines
Enhancement of pre and post synaptic GABA ergic transmission that is mediated by benzodiapine specific receptor
Increases distance between depolarization threshold and resting membrane potential
What are the drawbacks of benzodiazepines
Respiratory and CNS depression
Tachyphyalixis with prolonged use
Diazepam carried in propylene glycol
What is the MOA of phenobarbital
Binds sites on Gaba-regulated ion channels and AMPA recptor
Increases time Cl channel open enhanced hyperpolarization
Neuropeptided effects, and lowers body temperature
What are the draw backs of phenobarbital
IV use with benzos hyptension and cardiorespiratory depresseion
Hepatotoxicity; idiosyncratic blood dyscrasia, necrolytic dermatitis
Autoinducer of hepatic microsomal enzyems can progressively decrease elimination 1/2 life
What is the MOA of phenytoin/fosphenyton
Blockage of Na gated voltage channels:
Fosphenyton- prodrug of phenytoin with less severe side effects
What area the draw backs of phenytoin/fosphyenyton
Poor oral bioviability, short 1/2 life, and causes cardiac dysrrhythmia and hypotension
What is the MOA of levetiracetam
Binds to synaptic vesicle 2 A decreases release of neurotransmtor during high frequency bursts
Lack protien bidnings, not metabolized by liver, primarily renal excretion
What is the MOA of Propofol for seizure control?
Alkylphenol injectable anesthetic
GABA-A agonist- binds differently than benzos or barbituates
Reversibly inhibits NMDA receptors, Modulates Ca channels
What is the MOA of Zonisamide
Sulfonamide deravitive, biologically similar to serotonin
Inhibition of neuronal voltage gated Na and T type calcium channels
What are the draw backs of zonisamide
Ataxia, lethargy, vomiting, KCS
Heptatic metabolism
Higher dose needed when given with Pheno
How might a vagal maneuver reduce seizures
Ocular compression
Reduce cerebral extracellular glutamate concentrationes
What is an EEG
electroencephalograph
epileptiformactive = Non convulsive seizure
Can inform on foci
What is imepitonin MOA
Potentiates gabaergic inhibition by acting as a low affinity low efficacy partial agonist at the benzodiazepine site of GABA receptor
Not available in US
In traumatic spinal cord injury what results in decreased outcome regardless of time elapsed
Loss of deep pain perception
<12 % ambulate and non regained urinary / fecal continence
What is the pathophys of acute polyradiculoneuritis
Imnune mediated injury to peripheral myelin and axons
Ascending flaccid paresis over 3-10 days
What treatments have been shown to reduce recovery tine in polyradiculoneuritis
Plasmapharesis or IVIG
What is the pathophys of tick paralysis
Salivary neurotoxin secreted by tick into host while attached
Impairs ACh release at neuromuscular junction by blocking calcium influx at the terminal
Progressive ascending flacid paralysis
What is the treatment for tick paralysis
REmove the ticks
What is the pathophys of Botulism
Rapidly and IRREVERSIBLY binds to neuronal surface receptors on nerve terminals to prevent the synaptic release of ACh at the NMJ
What is the pathophys of myasthenia gravis
Aquired immune mediated disease where antibiodies are formed agains the nicotinic Ach receptor on the post-synaptic membrane of the NMJ
What is an inhouse test that may be performed for myasthenia gravis what is the definitive test
Positive response to Acetylcholinesterase inhibitor:
Edrophonium; Neostigmine
In fulminant may not get response because functional Ach receptors low
Compare and contrast the clinical signs with botulism, tick paralysis, acute polyradiculoneuritis, Fulminant MG, and tetanus
Acute Polyradiculoneuritis: Flacid ascending paresis/paralysis over 3-10 days. No CNS, autonomic
Tick Paralysis: Progressive ascending flacid paresis/paralysis over 1-3 days. No CNS, autonomic
Botulism: Flacid paralysis with CNS and autonomic signs common
MG- skeletal muscle weakness: tetraplegia with respiratory fatigue and CN dysfunction
Tetanus: Rigid paralysis with CN involvement
What is the MOA of edrophonium
Acetylcholinesterase inhibitor
What is the MOA of neostigmine
Acetylcholinesterase inhibitor
What is the MOA of pyridostigmine
Acetylcholinesterase inhibitor
What is the MOA of atracurium
Competitive antagonist of the Ach receptor
What is the treatment for fulminant MG
No steroids
TPE, IVIG
What are the types of injury with TBI
Primary- Immediately after direct impact
Secondary- delay injury minutes to weeks
MGCS Decreasing less survivial
What is the MOA of tetanus
Clostridium Tetani
Inhbitis neurotransmiter release
CN1
Olfactory: Loss of smell
CN2
Optic: Loss of vision
CN3
Oculomotor: abnormal eye movements
CN4
Troclear: Rotary nystagmus
CN5
Trigeminal: Absent facial senstation, masseter and temproal muscle atrophy
CN6
Abducens: retractor bulbi muscle and lateral rectus muscle
absent glob retraction and medial strabismus
CN 7
Facial: Lip facial trop, absent meannce/palpebral
CN8
Vestibulochia- vestibular
CN9
Glossopharyngeal: absent gag
CN10
Vagus: dysphagia
CN 11
Spinal accessory: Laryngeal paralysis, mega esophagus
CN 12
Hypoglossal: unilateral tongue atrophy/divieation
Dysphagia
List the precursor 1.___ of the molecule 2____, that stimulates the 3 ____ receptor resulting in the release of 4__________ ion to cause hyperpolaerization of the post synaptic neuron and inhibits seizure activity. The anticonvulsant 5. _______, is a ___________ receptor agaonsit
Glutamate GABA GABA-A Chloride Benzodiazpine, zonisamide GABA-A
Define vasogenic edema- brain
Disruption of BBB resulting in extravsation of fluid and intravascular protiens into the cerebral paryenchyma
Define Cytotoxic edema
Abnormal accumulation of fluid into brain cells and cell swelling
Cerebral ischemia and liver failure
