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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
Q

What is the pathophysiology of seizures

A

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

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26
Q

What is the mechanism of drug resistance in seizures

A

Over expression of P-glycoprotien encoded by MDR-1 Gene

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27
Q

What are the systemic effects of phase 1 in status epilepticus?

A

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

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28
Q

What are the systemic effects of phase 2 in status epilepticus?

A

Uncompensated after 30 minutes
cerebral vascular autoregulation fails and intracranial pressure increases
Hypoxia, hyperthermia, hypoglycemia, respiratory failure, acidosis, hyperkalemia, hyponatremia, uremia

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29
Q

What is the cushing’s reflex

A

MAP increased with increasing ICP to attempt to maintain cerebral perfusion pressure
Bradycardia often seen but won’t if hypovolemia

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30
Q

What is the MOA of benzodiazepines

A

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
Q

What are the drawbacks of benzodiazepines

A

Respiratory and CNS depression
Tachyphyalixis with prolonged use
Diazepam carried in propylene glycol

32
Q

What is the MOA of phenobarbital

A

Binds sites on Gaba-regulated ion channels and AMPA recptor
Increases time Cl channel open enhanced hyperpolarization
Neuropeptided effects, and lowers body temperature

33
Q

What are the draw backs of phenobarbital

A

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
Q

What is the MOA of phenytoin/fosphenyton

A

Blockage of Na gated voltage channels:

Fosphenyton- prodrug of phenytoin with less severe side effects

35
Q

What area the draw backs of phenytoin/fosphyenyton

A

Poor oral bioviability, short 1/2 life, and causes cardiac dysrrhythmia and hypotension

36
Q

What is the MOA of levetiracetam

A

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
Q

What is the MOA of Propofol for seizure control?

A

Alkylphenol injectable anesthetic
GABA-A agonist- binds differently than benzos or barbituates
Reversibly inhibits NMDA receptors, Modulates Ca channels

38
Q

What is the MOA of Zonisamide

A

Sulfonamide deravitive, biologically similar to serotonin

Inhibition of neuronal voltage gated Na and T type calcium channels

39
Q

What are the draw backs of zonisamide

A

Ataxia, lethargy, vomiting, KCS
Heptatic metabolism
Higher dose needed when given with Pheno

40
Q

How might a vagal maneuver reduce seizures

A

Ocular compression

Reduce cerebral extracellular glutamate concentrationes

41
Q

What is an EEG

A

electroencephalograph
epileptiformactive = Non convulsive seizure
Can inform on foci

42
Q

What is imepitonin MOA

A

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
Q

In traumatic spinal cord injury what results in decreased outcome regardless of time elapsed

A

Loss of deep pain perception

<12 % ambulate and non regained urinary / fecal continence

44
Q

What is the pathophys of acute polyradiculoneuritis

A

Imnune mediated injury to peripheral myelin and axons

Ascending flaccid paresis over 3-10 days

45
Q

What treatments have been shown to reduce recovery tine in polyradiculoneuritis

A

Plasmapharesis or IVIG

46
Q

What is the pathophys of tick paralysis

A

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
Q

What is the treatment for tick paralysis

A

REmove the ticks

48
Q

What is the pathophys of Botulism

A

Rapidly and IRREVERSIBLY binds to neuronal surface receptors on nerve terminals to prevent the synaptic release of ACh at the NMJ

49
Q

What is the pathophys of myasthenia gravis

A

Aquired immune mediated disease where antibiodies are formed agains the nicotinic Ach receptor on the post-synaptic membrane of the NMJ

50
Q

What is an inhouse test that may be performed for myasthenia gravis what is the definitive test

A

Positive response to Acetylcholinesterase inhibitor:
Edrophonium; Neostigmine
In fulminant may not get response because functional Ach receptors low

51
Q

Compare and contrast the clinical signs with botulism, tick paralysis, acute polyradiculoneuritis, Fulminant MG, and tetanus

A

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
Q

What is the MOA of edrophonium

A

Acetylcholinesterase inhibitor

53
Q

What is the MOA of neostigmine

A

Acetylcholinesterase inhibitor

54
Q

What is the MOA of pyridostigmine

A

Acetylcholinesterase inhibitor

55
Q

What is the MOA of atracurium

A

Competitive antagonist of the Ach receptor

56
Q

What is the treatment for fulminant MG

A

No steroids

TPE, IVIG

57
Q

What are the types of injury with TBI

A

Primary- Immediately after direct impact
Secondary- delay injury minutes to weeks
MGCS Decreasing less survivial

58
Q

What is the MOA of tetanus

A

Clostridium Tetani

Inhbitis neurotransmiter release

59
Q

CN1

A

Olfactory: Loss of smell

60
Q

CN2

A

Optic: Loss of vision

61
Q

CN3

A

Oculomotor: abnormal eye movements

62
Q

CN4

A

Troclear: Rotary nystagmus

63
Q

CN5

A

Trigeminal: Absent facial senstation, masseter and temproal muscle atrophy

64
Q

CN6

A

Abducens: retractor bulbi muscle and lateral rectus muscle

absent glob retraction and medial strabismus

65
Q

CN 7

A

Facial: Lip facial trop, absent meannce/palpebral

66
Q

CN8

A

Vestibulochia- vestibular

67
Q

CN9

A

Glossopharyngeal: absent gag

68
Q

CN10

A

Vagus: dysphagia

69
Q

CN 11

A

Spinal accessory: Laryngeal paralysis, mega esophagus

70
Q

CN 12

A

Hypoglossal: unilateral tongue atrophy/divieation

Dysphagia

71
Q

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

A 
Glutamate
GABA
GABA-A
Chloride
Benzodiazpine, zonisamide
GABA-A
72
Q

Define vasogenic edema- brain

A

Disruption of BBB resulting in extravsation of fluid and intravascular protiens into the cerebral paryenchyma

73
Q

Define Cytotoxic edema

A

Abnormal accumulation of fluid into brain cells and cell swelling
Cerebral ischemia and liver failure

Board Review 2020 (37 decks)

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