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Board Review 2020 > Neurology > Flashcards

Neurology Flashcards

1
Q

When should anti-epilpetics be started for seizures

A

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
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2
Q

What are the good first line medications for seizures

A

1) Phenobarb, Imepitoin 2) bromide 3) Leviteracitam, zonisamide

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3
Q

What are good second line medications for Seizures

A

Phenobarb, bromide, levetiracitam

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4
Q

What is pahtophys of necrotizing menginiioencephalitits

A

Young middled aged pugs

multifocal asymmetrical necrosis in deep cebral cortex adjacent to white matter

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5
Q

What is the pathophys of necrotizing leucoencphalitits

A

Yorkies

asymmetrical malacic changes in cerebral white matter and thalmus

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6
Q

What is the pathophys of granulomatous ME

A

Any breed toy/terrier
idiopathic granulamatous inflammation
Perivascular accumulation of epithealoid macrophages and lymphocytes in the CNS

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7
Q

What are the effects of Mannitol on the brain

A
  • 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
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8
Q

What are the negative effects of mannitol

A

Hypotension, electrolyte imbalances, Rebound ICH (increased cerebral blood flow), worsening cerebral edema free H2O diruesis

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9
Q

How does Hypternoic saline work to decreased ICP

A

Hypovolemia- restores circulating volume an maintains cerebral perfusion pressure

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10
Q

What are the drawbacks of administering hypertonic saline for ICP

A

Severe hypernatremia in dehydrated patients or suffering marked water loss

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11
Q

How does stress affect the body

A

immune suppression, GI disease, cutaneous disease, delayed wound healing, alteration s in pain receptors

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12
Q

What is the MOA of trazodone

A

Seritonin atangonist
No effect on seizure threshold
Minimally lowers CO

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13
Q

What is the MOA for dexmedetomidine for sedation

A

Alpha 2 agonist
blockade of alpha 2 receptor in locus coerulus inhibiting norepi release
Disinhibiting the aurosal usppression neurons in the area

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14
Q

What is the pathophys of SRMA and resultant CSF findings

A

Non supperative inflammatory lesions of the leptomeninges and vasculitis of mengial arteries
Responsive to steroids
Marked neutrophilic pleocytosis with hight TP

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15
Q

Where is CSF produced

A

choid plexus in the brain and to smaller extent the ependymal cells of the ventricular system

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16
Q

What are the functions of CSF

A

protect brain assisting with regulation of ICP, Medium for transport of metabolites, Neurohormones and neurotransmitters

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17
Q

What medications are reported to decrease CSF production?

A

Steroids, omeprazole, furosemide,

acetazolamide (carbon anhydrase inhibitior)

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18
Q

Define seizure

A

Sustained and uninhibited neuronal depolarization

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19
Q

What are the two types of spondylomyelopathy

A

Disk associated: Secondary to herniation : Dobermans

Osseus associated: Compression of cord due to osseus proliveration of the artericular process

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20
Q

What MOA advantages does IN midazolam have

A

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

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21
Q

Define ICP

A

Pressure exerted by intracranial contents agains an inelastic cranial vault

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22
Q

What is the formulate of Cerebral perfusion pressure

A

CPP= MAP - ICP

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23
Q

What are 4 different ways to measure ICP

A

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

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24
Q

Define status epilepticus

A

Seizure activity lasts for more than 5 minutes or 2 or more seizures without recovery of consciousness

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25
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
26
What is the mechanism of drug resistance in seizures
Over expression of P-glycoprotien encoded by MDR-1 Gene
27
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
28
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
29
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
30
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
31
What are the drawbacks of benzodiazepines
Respiratory and CNS depression Tachyphyalixis with prolonged use Diazepam carried in propylene glycol
32
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
33
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
34
What is the MOA of phenytoin/fosphenyton
Blockage of Na gated voltage channels: | Fosphenyton- prodrug of phenytoin with less severe side effects
35
What area the draw backs of phenytoin/fosphyenyton
Poor oral bioviability, short 1/2 life, and causes cardiac dysrrhythmia and hypotension
36
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
37
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
38
What is the MOA of Zonisamide
Sulfonamide deravitive, biologically similar to serotonin | Inhibition of neuronal voltage gated Na and T type calcium channels
39
What are the draw backs of zonisamide
Ataxia, lethargy, vomiting, KCS Heptatic metabolism Higher dose needed when given with Pheno
40
How might a vagal maneuver reduce seizures
Ocular compression | Reduce cerebral extracellular glutamate concentrationes
41
What is an EEG
electroencephalograph epileptiformactive = Non convulsive seizure Can inform on foci
42
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
43
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
44
What is the pathophys of acute polyradiculoneuritis
Imnune mediated injury to peripheral myelin and axons | Ascending flaccid paresis over 3-10 days
45
What treatments have been shown to reduce recovery tine in polyradiculoneuritis
Plasmapharesis or IVIG
46
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
47
What is the treatment for tick paralysis
REmove the ticks
48
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
49
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
50
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
51
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
52
What is the MOA of edrophonium
Acetylcholinesterase inhibitor
53
What is the MOA of neostigmine
Acetylcholinesterase inhibitor
54
What is the MOA of pyridostigmine
Acetylcholinesterase inhibitor
55
What is the MOA of atracurium
Competitive antagonist of the Ach receptor
56
What is the treatment for fulminant MG
No steroids | TPE, IVIG
57
What are the types of injury with TBI
Primary- Immediately after direct impact Secondary- delay injury minutes to weeks MGCS Decreasing less survivial
58
What is the MOA of tetanus
Clostridium Tetani | Inhbitis neurotransmiter release
59
CN1
Olfactory: Loss of smell
60
CN2
Optic: Loss of vision
61
CN3
Oculomotor: abnormal eye movements
62
CN4
Troclear: Rotary nystagmus
63
CN5
Trigeminal: Absent facial senstation, masseter and temproal muscle atrophy
64
CN6
Abducens: retractor bulbi muscle and lateral rectus muscle | absent glob retraction and medial strabismus
65
CN 7
Facial: Lip facial trop, absent meannce/palpebral
66
CN8
Vestibulochia- vestibular
67
CN9
Glossopharyngeal: absent gag
68
CN10
Vagus: dysphagia
69
CN 11
Spinal accessory: Laryngeal paralysis, mega esophagus
70
CN 12
Hypoglossal: unilateral tongue atrophy/divieation | Dysphagia
71
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 ```
72
Define vasogenic edema- brain
Disruption of BBB resulting in extravsation of fluid and intravascular protiens into the cerebral paryenchyma
73
Define Cytotoxic edema
Abnormal accumulation of fluid into brain cells and cell swelling Cerebral ischemia and liver failure

Board Review 2020 (37 decks)

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