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Brain and Behavior > Week 10 (Test 4) > Flashcards

Week 10 (Test 4) Flashcards

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1
Q

What mechanisms can be used by AED’s to reduce excessive excitation?

A

A. Prevent repetitive action potential propagation of seizure discharges by inactivation of voltage-gated sodium channels B. Reduce excessive presynaptic glutamate release –binding to presynaptic Ca2+ channels at the a2d subunit – binding to presynaptic vesicle SV2A protein C. Block AMPA glutamate receptors

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2
Q

What mechanisms can be used by AED’s to increase inhibition?

A

A. Increase GABA-mediated neurotransmission 1. Enhancing post-synaptic GABA-A Receptor function 2. Increasing GABA synthesis 3. Reducing GABA breakdown B. Activate inhibitory potassium channels

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3
Q

Side effects of Sodium Channel AEDs:

A
  • Double vision (diplopia), jerky eye movements (nystagmus) -Coordination problems (ataxia) and dizziness (vertigo)
  • Sleepiness, lethargy, cognitive slowing

These problems are dose-dependent and reversible

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4
Q

Describe the metabolism of Phenytoin.

A

–95% hepatic, by a cytochrome P450 enzyme (CYP2C9)
–elimination is first order (concentration-dependent) until P450 enzymes saturated, then
–slows to zero-order – fixed amount metabolized per hour
•a small increase in dose can result in very high drug levels

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5
Q

What’s the mechanism of action of Phenytoin?

A

•Sodium channel inactivation

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6
Q

What are the long term adverse effects of Phenytoin?

A

gingival hyperplasia

osteopenia

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7
Q

What’s the mechanism of action of Carbamazepine?

A

Sodium channel inactivation

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8
Q

What are the long term adverse effects of Carbamazepine?

A

–aplastic anemia (rare)
–rash
–hyponatremia (low sodium)

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9
Q

What’s the mechanism of action of Valproic Acid (Depakote)?

A

•Sodium Channel inactivation

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10
Q

a good choice if you can’t tell whether the patient has a focal or generalized seizure disorder

A

Valproic Acid (Depakote)

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11
Q

What are the common adverse effects of Valproic acid (Depakote)?

A

–“fat, shaky, bald, yellow”
•weight gain (fat)
•Tremor (shaky)
•hair loss (bald)
•jaundice (yellow)

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12
Q

What is a very common side effect of Lamotrigine?

A

rash

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13
Q

What’s the mechanism of action of Topiramate (Topamax)?

A

sodium channel inactivation

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14
Q

What are the adverse effects we need to know for Topiramate (Topamax)?

A

–confusion/psychosis (“dopamax”)

–Renal stones (avoid in pts w/ history of renal stones)

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15
Q

What’s the mechanism of action of Gabapentin?

A

decreases presynaptic glutamate release by binding to a2d subunit of the voltage gated calcium channel

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16
Q

What’s the mechanism of action of Levatiracetam (Keppra) ?

A

–Binds to SV2A synaptic vesicle protein
•inhibits excessive neurotransmitter release

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17
Q

What are the adverse effects of Levatiracetam (Keppra)?

A

–Somnolence (sleepiness), ataxia, weakness (rare)
Irritability/personality change

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18
Q

What’s the mechanism of action of Perampanel (Fycompa)?

A

•Non-competitive AMPA glutamate receptor antagonist
–Only AED with this mechanism

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19
Q

What’s an important side effect of Perampanel (Fycompa)?

A

–risk of serious neuropsychiatric events: Violent thoughts or threatening behavior including homicidal ideation

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20
Q

What’s the mechanism of action of Phenobarbital?

A

–Enhances GABAa receptor currents
–also sodium channel inactivation

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21
Q

What are the adverse effects of phenobarbital ?

A

–sedation, cognitive slowing, dizziness, mood change
–paradoxical hyperactivity in kids

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22
Q

What’s the mechanism of action of Ezogabine?

A

–Activates voltage gated K+ channel
–Leads to hyperpolarization, decreased excitability

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23
Q

What are the adverse effects of Ezogabine?

A

–Urinary Retention
–Vision and skin problems
•Turns skin blue! (rare)

24
Q

What is unique about the pharmacokinetics of Carbamazepine?

A

–Autoinduces cytochrome P450
•Increases expression of the same isozymes that metabolize it
•Start with low dose and increase gradually over 2-3 weeks.

25
Q

What is the only use for the AED Ethosuximide?

A

•only against generalized absence

if generalized absence and + GTC or other type–> give valproic acid

26
Q

What’s the mechanism of action of Ethosuximide?

A

–Inhibits “T” Ca++ channels in thalamus

27
Q

Which AEDs are associated with neural tube defects?

A

•Valproic acid and carbamazepine associated with neural tube defects

28
Q

Describe focal seizures

A

Focal seizures are conceptualized as originating at some point within networks limited to one hemisphere (how you can stay conscious)

29
Q

Describe generalied seizures.

A

Generalized seizures are conceptualized as originating at some point within and rapidly engaging bilaterally distributed networks

30
Q

Describe West syndrome

A
  • Flexion or extension spasms
  • 60-70% have lifelong epilepsy
  • Hypsarrhythmia pattern on EEG
31
Q

Think this syndrome when a young patient has mutiple types of seizure

A

Lennox-Gastaut Syndrome

32
Q

What is the main metabolite of nicotine that is measured in the blood?

A

Cotinine

33
Q

What’s the mechanism of action of Varenicline (Chantix)?

A

Partial agonist at α4β2 nicotine receptors

34
Q

What’s the mechanism of action of Buproprione (Wellbutrin)?

A

Dopamine reuptake inhibitor & Nicotine antagonist

35
Q

Who do you not give Buproprion to?

A

Don’t give buproprion to people who have eating disorders. Will mess up electrolyte balance and can cause seizure

36
Q

How do you define binge drinking?

A
  • Women, 4 or more drinks during a single occasion.
  • Men, 5 or more drinks during a single occasion.
37
Q

How do you define heavy drinking?

A
  • Women, more than 1 drink per day on average.
  • Men, more than 2 drinks per day on average.
38
Q
  • Result of thiamine deficiency in alcoholism
  • Atrophy of mamillary bodies & regions of thalamus
A

Wernicke Encephalopathy

39
Q

What are the triad of symptoms seen in patients with Wernicke Encephalophathy ?

A
  • Confusion
  • Nystagmus, opthalmoplegia, anisocora, sluggish pupillary reflexes
  • Ataxia
40
Q
  • results from mother consuming alcohol her pregnancy
  • mental retardation is common (44% have an IQ <79)
  • wide-set eyes
  • short palpebral fissure
  • short and broad-bridged nose
  • hypoplastic philtrum
  • thinned upper lip
  • flattened midface
A

Fetal alcohol syndrome

41
Q

Which biomarker can be used to distinguish heavy drinking?

A

CDT - carbohydrate-deficient transferrin

42
Q

How do you treat Withdrawal from: ALCOHOL,

BENZODIAZEPINES,

BARBITURATES?

A

benzodiazepines

43
Q

What are the FDA approved pharmacological treatments for alcohol dependence?

A

Disulfiram

Naltrexone

Acamprosate

44
Q

What’s the mechanism of action of Disulfiram?

A

inhibits aldehyde dehydrogenase which allows acetaldehyde to build up and cause adverse effects

45
Q

Opioids cause miosis except _____.

A

Meperidine

46
Q

What’s the opioid overdose/toxicity triad?

A
  • miotic pupils
  • abnormal mental status
  • respiratory depression (<12/min)
47
Q

What medication do you give for opioid intoxication/overdose?

A

naloxone (pure opioid antagonist)

48
Q

In ______, you see CNS noradrenergic hyperactivity in the Locus ceruleus.

A

opioid withdrawal syndrome

49
Q

What are your two drug choices for opioid maintenance treatment?

A

–Methadone
–Buprenorphine

50
Q

What is the gold standard for opioid maintenance treatment in pregnant women?

A

methadone

51
Q

What are the most common physician abused drugs?

A
  • alcohol (number 1)
  • opioids (highly associated with mortality )
52
Q

What are the 3 D’s you see with impaired physicians (or any other addict for that matter)?

A
  • Delusional
  • Denial
  • Defiance
53
Q

What do you need to see in a patient to have the Clinical Determination of Brain Death ?

A
  • absent brainstem reflexes
  • apnea
  • flaccid limbs
54
Q

KORSAKOFF’S PSYCHOSIS symptoms triad consists of what?

A
  • Amnesia
  • Confabulation
  • Hallucinations
55
Q

may play an important role in the storage or retrieval of past, autobiographical memories.

A

anterolateral temporal lobes

56
Q
A

Brain and Behavior (11 decks)

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