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NSB > Block 3 > Flashcards

Block 3 Flashcards

1
Q
A

Precentral gyrus

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2
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Precentral sulcus

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3
Q
A

Red: Superior frontal gyrus

Blue: Middle frontal gyrus

Orange: Inferior frontal gyrus (A,B,C)

A) Par opercularis

B) Pars triangularis

C) Pars obitalis

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4
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Orbitofrontal cortex:

Red: orbital gyri

Blue: gyrus rectus

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5
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A

Red: Postcentral Gyrus

Yellow: intraparietal sulcus

Purple: superior parietal lobe

Orange/green: lateral sulcus

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6
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Inferior parietal lobe:

Red: supramarginal gyrus

Blue: angular gyrus

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7
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A

Red: superior temporal gyrus

Green: middle temporal gyrus

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8
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Temporal Lobe:

Blue: Inferior temporal gyrus

Red: Occipitotemporal gyrus

Green: parahippocampal gyrus

Orange: uncus (part of parahippocampal gyrus)

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9
Q
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Occipital Lobe:

Red: parietooccipital sulcus

Blue: Cuneus gyrus

Green: Lingual gyrus

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10
Q
A

Red: occipital gyri

Green: preoccipital notch

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11
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Visual processing streams:

Red arrow: “Where?”, analysis of motions and spatial relations

Blue arrow: “What?”, analysis of form and color

Occiput regions: Brodmann’s area’s 17 (yellow), 18 (green), and 19 (blue), corresponding to 1’, 2’, and 3’ centers

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12
Q
A

Cingulate gyrus; contains cingulum, the associational fibers that connect the cingulate gyrus with the parahippocampal gyrus

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13
Q
A

Language areas:

Red area = Broca’s area

Blue area = Wernicke’s area

Connected by superior longitidunal (arcuate) fasciculus , associational fibers

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14
Q
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Orange arrow points to the uncinate fasciculus, associational fibers interconnecting limbic areas (i.e. septal and uncus).

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15
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Superior and Inferior occipitofrontal fasciculi; associational fibers interconecting visual areas with association cortices of frontal cortex.

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16
Q
A

Corpus callosum (yellow); a commissure interconnecting most of cerebral cortex, except portions of temporal lobes

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17
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Corpus Callosum;

A) Genu (connects frontal hemispheres)

B) Body

C) Splenium (connects occipital hemipsheres)

D) Rostrum

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18
Q
A

Anterior commissure; interconnects portions of the temporal lobes, lies anterior to hypothalamus and dorsal to optic chiasm

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19
Q
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Posterior commissure; really part of the brainstem, crossing over of pretectal neurons involved in pupillary (consensual) light reflexes, located ventral to pinneal gland

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20
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A

Red: olfactory bulb

Orange: gyrus rectus

Blue: olfactory tract

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21
Q
A

Red: orbital gyrus

Orange: Uncus

Blue: parahippocampul gyrus

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22
Q
A

Red: Cingulate gyrus (mood, personality)

Green: corpus callosum

Blue: fornix

Purple: parahippocampal gyrus

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23
Q
A

Red line over the Uncus

deep to the uncus lies the amygdala (anteriorly, pink arrow) and hippocampus (posteriorly, green arrow)

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24
Q
A

Red arrow: Amygdala, which is located in same coronal plane as the Basal ganglia (blue arrows)

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25
Q
A

Amygdala (pink arrow) the center for experiencing fear, anxiety, and rage. Has many inputs/outputs including ventral basal ganglia, mediodorsal nucleus of thalamus, orbital and medial prefrontal cortex.

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26
Q
A

Red: hippocampal formation, located in same coronal plane as the thalamus (green arrow), in the medial temporal lobe.

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27
Q
A

Nucleus Accumbens: area of the basal ganglia involved in emotion, reward, and addictive behaviors; this region helps in choosing the appropriate emotional response to a given situation.

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28
Q
A

Cross section of midbrain:

Yellow = ventral tegmental area, sends dopaminergic inputs to the Nucleus accumbens; centrally this is associated with rewards and addiction

Red = median raphe nucleus

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29
Q
A

Mammillary bodies (contain mammillary nuclei); considered part of the hypothalamus.

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30
Q
A

Diencephalic regions of the Limbic System:

Red= anterior thalamic nucleus; receives input from mammillary nuclei and projects to cingulate gyrus

Pink= Medial dorsal nucleus of thalamus; receives input from cortex, amygdala (orange ball below mammillary nucleus), ventral pallidum (n. accumbens), and projects to orbital frontal cortex and medial frontal cortex

Orange= mammillary nucleus (part of hypothalamus)

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31
Q

First line drug tx for partial seizures

A

carbamazepine and phenytoin

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32
Q

First line tx for generalized seizures

A

ethosuximide (for pure absence epilepsy)

valproate a traditional med for generalized sz but bad SE profile (fatal hepatoxicity and NT defects), so lamotrigine an alternative.

Drugs specific for partial-sz may make generalized sz’s WORSE (carbamazepine, gabapentin, tiagabine).

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33
Q

MOA for antiepileptic drugs

A

1) Na+ ch. blockers
2) Ca2+ influx blockers
3) Glutamate antagonists
4) GABA potentiators

34
Q

Sodium Channel Blockers for epilepsy

A

Phenytoin, carbamazepine, valproate, lamotrigine, topirimate, Zonisamide

“Val Pro-ate, so she took Phen-phen to metabolize carbs to fit in her lamo top”

Causes use-dependent block of vg-Na+ channels, reducing sustained high rates of repetitive firing by neurons, may block glutamate release (via presynaptic Na+ ch), prevent spread of sz discharges

35
Q

Ca+ influx blockers, antiepileptic

A

**-Ethosuximide **blocks rhythmic firing bursts in thalamic neurons seen in absence sz

-Gabapentin: inhibits Ca2+ ch, also a GABA analog

- trimethadone and valproate also reduce Ca2+ currents

36
Q

Glutamate antagonists, antiepileptic drugs

A

NMDA receptor antagonists (effective but toxic)

Felbamate (blocks strychnine-insensitive glycine site on NMDA receptor, causes aplastic anemia)

Perampanel: blocks glutamate (AMPA) receptor

Lamotrigine may selectively reduce synaptic release of glutamate

Leviteracetam: may modulate glutamate release

37
Q

GABA potentiators, antiepileptics

A

1) Increase affinity of GABA f_or GABAa receptor:_ barbituates (phenobarbital, primidone), benzodiazepines (clonazepam, diazepam, lorazepam, clorazepate),
2) Inhibition of GABA transaminase (slows breakdown of GABA): vigabatrin, valproate
3) GABA agonist: progabide, pregabalin, gabapentin, clobazam
4) Inhibition of GABA transporter: tiagabine

38
Q

Describe the dose-dependent elimination kinetics of phenytoin

A

Phenytoin does not have linear elimination kinetics! It has linear kinetics at low doses, but then increases to zero order kinetics at high doses; thus at high doses can rapidly accumulate in blood (become toxic)

39
Q

Which antiepileptic drugs are inducers of hepatic enzymes?

A

CYP450 inducers: phenytoin, carbamazepine, phenobarbital, primidone, topiramate, oxcarbazepine

40
Q

What antiepileptic drug(s) are inhibitors of hepatic enzymes?

What effect do inducers/inhibitors of hepatic enzymes have on other medications?

A

CYP450 inhibitor: valproate

Inhibitors/Inducers can affect many meds including AED’s, anticoagulants, and antibiotics. Can lower efficiacy of hormonal contraceptives.

41
Q

Treatment of epilepsy in pregnancy

A

Safest AED: lamotrigine

Most teratogenic AED: valproate (phenobarbital #2)

42
Q

Phenytoin

A

Na+ ch inactivator, narrow spectrum (PS, PC, 2’ gen sz), also used to tx chronic pain, and cardiac arrhythmia, zero order kinetics

SE’s: gingival hypertrophy, may worsen myoclonic and absence sz

43
Q

Valproate

A

Na+ ch inactivator, inhib of GABA transaminase, 1st line tx for GTC sz, also tx focal and gen. absence sz’s (broad MOA), also used to tx chronic pain , SE’s include weight gain, tremor, PCOS, and hyperammonemia

44
Q

Phenobarbital/primidone

A

increases GABA action, narrow spectrum (PS, PC, 2’ gen sz)

SE’s: sedation, tolerance, dependence, induction of CYP450, cardiorespiratory depression

45
Q

Carbamazepine

A

Na+ ch inactivator, narrow spectrum (PS, PC, 2’ gen sz), may worsen juvenile myoclonic epilepsy, also used to tx chronic pain

Blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of CYP450, SIADH, Stevens-Johnson syndromes

46
Q

Felbamate

A

a glutamate blocker, potentially lethal side effects are aplastic anemia and acute hepatic failure

47
Q

Common adverse effects of AEDs

A

dizziness, fatigue, blurry vision, diplopia, unsteadiness, cognitive issues, mood affects

rarely: Stevens-Johnson syndrome

48
Q

General PK parameters of AED’s

A

Essentially complete absorption for all AED’s except gabapentin

AED’s bind to proteins in varying degrees, so total and free fractions of meds can vary significantly (potential for toxicity) so important to monitor serum levels

Most AED’s are metabolized by liver and eliminated by kidneys

Most AED’s follow linear kinetics (exception: phenytoin)

49
Q

What drugs could you use to tx partial complex sz if unresponsive to phenytoin?

A

Pretty much anything except ethosuximide or benzo’s, first line tx for partial complex sz is carbamazepine

50
Q

What is the first line tx for status epilepticus?

A

status epilepticus is 5+ min of continuous clinical/electrographic sz activity or recurrent sz activity without return to baseline between sz’s.

1st line tx is lorazepam (or diazepam or clonazepam) within 5-10 minutes or emerging SE; at 10-30 minutes out could tx with valproate or phenytoin. If refractory or 30-60 minutes out, tx with **midazolam **or pentobarbital.

51
Q

Cholinesterase inhibitors

A

decreases breakdown of ACh in synaptic cleft, increases cognitive fxn, but doesn’t slow progression of dz; SE’s: N/V/D for all

- Donepezil (Aricept) prototypical agent, may cause insomnia

  • tacrine
  • rivistigmine: may cause HA’s
  • galantamine
52
Q

Memantine

A

aka Namenda

NMDA antagonist used to tx dementia, tx excitotoxicity, non-cholinergic so can be used with AChE inhibitor, neuroprotective but can cause hallucinations, also dizziness and confusion.

53
Q

What are the different classes of mood agents?

A

TCA’s, SSRI’s, MAOI’s, SNRI’s, 5HT2 antagonists, monocycle/unicyclic, and others

54
Q

Serotonin syndrome

A

potential SE of any drug that increases 5HT (MAOI, SSRI, SNRI, TCA)—causes hyperthermia, confusion, myoclonus, CV instability, flushing, diarrhea, sz’s. Tx with cyproheptadine (5HT2 receptor antagonist).

55
Q

Tricycle antidrepressants (TCA)

A

Imipramine and Despiramine

  • poorly tolerated, very sedating, and can be lethal in OD, so not used very much now
  • SE’s include anticholinergic effects (tachycardia, urinary retention, dry mouth), alpha1-blocking effects (orthostasis), prolonged QT, sexual side-effects, discontinuation syndrome.
  • “Tri-C’s: Convulsion, Coma, Cardiotoxicity”
  • tx with NaHCO3 to prevent arrhythmia.
56
Q

MAOI’s

A

Phenelzine, Isocarboxazidmare, Tranylcypromine, selegiline

“MAO Takes Pride In Shanghai”

  • irreversible action, slows down monoamine metabolism thereby increasing DA, 5HT, and NE
  • risk of hypertensive crisis when eating foods with high levels of tyramine.
  • Drug interactions with SSRI’s and TCA’s. Causes CNS stim with meperidine.
  • Also cause orthostasis, weight gain, sexual side effects, and confusion.
57
Q

SSRI’s

A

Fluoxetine (mildly activating, long half-life), Citalopram (sedating), Paroxetine, Fluvoxamine, Escitalopram

  • inhibit 5HT transporter;
  • 1st line tx for depression; cheap, well-tolerated, broad spectrum of use
  • SE’s include increase gut motility, decrease sexual fxn, HA, weight gain, discontinuation syndrome
58
Q

SNRI’s

A

Venlafaxine (risk of HTN at high doses), desvenlafaxine, duloxetine (risk of hepatotoxicity), Milnacipran

  • target 5HT and NE transporters (not receptors)
  • used as 2nd line tx for depression, also tx chronic pain
  • SE’s same as SSRI’s plus, HTN, CNS stim.
59
Q

5HT2 antagonists

A

no great evidence, but used a lot to tx sleep/depression; SE’s include GI and sedation

        **Trazodone**: used to tx insomnia, non-addictive, risk of priapism (“traza**bone**”)

Nefazodone: risk of hepatotoxicity

60
Q

Bupropion

A

aka Wellbutrin, a unicyclic antidepressant, resembles amphetamine in structure, stimulating, works on NE and DA; no sexual side effects

61
Q

Mirtazapine

A

antidepressant; tetracyclic, and sedating, causes weight gain, no sexual side effects

62
Q

Lithium

A

MOA possibly related to inhib of phosphoinositol cascade, used to stabilize mood in BPD, “LMNOP= Lithium SE’s: Movement (tremor), Nephrogenic DI, hypOthyroidism, Pregnancy problems

63
Q

Valproic Acid (valproate)

A

AED, also used to tx bipolar disorder

64
Q

Benzodiazepines

A

Any drug ending in “-zepam” or “-zolam”

Triazolam (Halcion)

flurazepam (Dalmane)

temazepam (Restoril)

diazepam (Valium)

alprazolam (Xanax)

chlordiazepoxide (Librium)

lorazepam (Ativan)

clonazepam (Klonopin)

midazolam (Versed)

  • All benzos potentiate GABA by increasing freq. of Cl- ch opening
  • Decrease REM sleep
  • older antiepileptic drug
  • Most have long t ½ and active metabolites, except “ATOM” (alprazolam, triazolam, oxazepam, and midazolam)
  • SE’s: dependence, see additive CNS depression w/ EtOH, less resp depression/coma than barbituates
65
Q

flumazenil

A

txs benzo OD, a competitive antagonist at GABA bz receptor

66
Q

buspirone (BuSpar)

A

non benzo anxiolytic, stimulates 5HT receptors, non-addictive, not sedating, no interaction w/ EtOH

67
Q

zoldipem (Ambien)

A

non benzo anxiolytic used tx insomnia, activates GABA receptor via BZ1 subtype

68
Q

Typical Antipsychotics

A

“Haloperidol + -azines,”

  • all block D2 receptors which increases cAMP
  • toxicities include tardive dyskinesia, constipation, dry mouth, hypotension, sedation, prolonged QT, and neuroleptic malignant syndrome
  • “NMS think FEVER: fever, encephalopathy, vitals unstable, enzymes increase, rigidity of muscles”

Haloperidol (Haldol)—high potency, can administer PO, IV, or IM

thioridazine

fluphenazine

trifluoperazine (Stelazine)

chlorpromazine (Thorazine)—low potency

69
Q

Atypical Antipsychotics

A

unknown MOA, but varied effects on 5HT2, DA, alpha and H1 receptors; in general has fewer extrapyramidal effects (tardive dyskinesia) and fewer anticholinergic SE’s, though all can cause prolonged QT

“It’s atypical for old closets to quietly risper from A to Z.”

Clozapine (Clozaril)–weight gain, agranulocytosis (need to check CBC’s weekly)

ziprasidone (Geodon)

olanzapine (Zyprexa)—weight gain

quetiapine (Seroquel)

risperidone (Risperdal)—increase prolactin leading to lactation, gynecomastia, irregular menses and infertility

aripiprazole (Abilify)

70
Q

Lamotrigine

A

AED; blocks vg-Na+ ch, tx focal, GTC, and gen. absence szs (broad MOA), safest AED to use in pregnancy

71
Q

Gabapentin

A

inhibits Ca2+ ch, also GABA analog, txs focal szs, also used to tx chronic pain

72
Q

Topirimate

A

blocks Na+ ch, increase GABA action, glutamate (NMDA) receptor blocker, tx PC, PS, and GTC sz (broad MOA), SE include nephrolithiasis, weight loss

73
Q

Tiagabine

A

GABA reuptake inhibitor, tx’s PC and PS sz

74
Q

Zonisamide

A

Na+ ch blocker, tx partial sz, broad MOA, SE’s include nephrolithiasis and weight loss

75
Q

Oxcarbazepine

A

narrow spectrum AED; txs PS, PC, 2’ gen sz

76
Q

Leviteracetam

A

unknown MOA, may modulate GABA and glutamate release, broad MOA, tx focal and GTC sz, can cause mood disturbances and other psych effects

77
Q

Pregabalin

A

AED, possible GABA activity, also used to tx chronic pain

78
Q

Lacosamide

A

narrow spectrum AED: tx PS, PC, 2’ gen sz

79
Q

Rufinamide

A

AED used in Lennox-Gastaut syndrome (sx’tic gen epilepsy)

80
Q

Clobazam

A

GABA receptor agonist used to tx szs

81
Q

Ezogabine

A

AED that activate v-g K+ ch

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