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Neuro > Unit IV, week 2 > Flashcards

Unit IV, week 2 Flashcards

1
Q

General Anesthesia is a ___________ depression with progressive loss of function from ________ to ____________ levels within the CNS

A

DESCENDING depression: progressive loss of function from HIGHER (cognition, consciousness) to LOWER (respiratory control) levels within the CNS

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2
Q

Stages of general anesthesia (1-4)

A

Stage I =analgesia

Stage II = excitement, delirium

Stage III = surgical anesthesia

Stage IV = medullary paralysis
-Respiratory failure, vasomotor collapse and resulting circulatory failure lead to death within minutes

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3
Q

Time course of anesthesia (3)

A

1) Induction
2) Maintenance
3) Recovery

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4
Q

Induction

A

time between initiation of administration and attainment of surgical anesthesia (until stage III reached)

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5
Q

Maintenance

A

time during which surgical anesthesia is in effect (surgery)

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6
Q

Recovery

A

time following termination of administration, complete recovery of patient from anesthesia

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7
Q

Inhaled anesthetics enter _____________ in various membrane proteins (such as what?) –> what effects?

Is this specific binding?

A

hydrophobic pockets

such as GABA-A receptors

→ overall CNS depression

**Hydrophobic protein pockets within which volatile anesthetics bind are NOT specific binding sites

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8
Q

Rate an effective concentration of anesthetic is reached in brain depends on 5 factors:

A

1) Concentration of anesthetic in inspired air
2) Alveolar ventilation rate (Respiratory depression can prolong recovery time)
3) Pulmonary blood flow (cardiac output)
4) Blood:gas partition coefficient
5) Potency (oil:gas partition coefficient)

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9
Q

Uptake by blood from alveoli determined by…

how is rate of approach to stage III related to these two factors?

A

solubility of anesthetic in blood and cardiac output

rate of approach to stage III is INVERSELY PROPROTIONAL to pulmonary blood flow and solubility of anesthetic in blood

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10
Q

Solubility of General Anesthetic

How does solubility of GA in blood effect approach to equilibrium?

A

rate of rise in partial pressure ratio is faster for gas with low solubility

Highly soluble GA (halothane)→ slower approach to equilibrium because a larger amount must be dissolved in blood

Low-solubility GA (nitrous oxide) exhibits more rapid increase in partial pressure in blood

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11
Q

Faster pulmonary blood flow effects anesthetic uptake how?

A

Faster pulmonary blood flow → less time for anesthetic to diffuse into blood

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12
Q

Uptake from arterial blood to body tissues depends on (3)

A

1) anesthetic gas solubility in body tissues
2) tissue blood flow (Higher tissue blood flow = faster delivery)
3) partial pressure of anesthetic in blood/tissues

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13
Q

Tissue distribution of general anesthetics (3)

A

1) Vessel-rich groups: highly vascularized tissues (brain, heart, kidney, liver, endocrine glands) → high uptake
2) Muscle groups: muscle and skin → slower uptake, 2-4 hours

3) Fat group: very slow uptake due to high ability to dissolve anesthetic
Equally soluble in blood and lean tissues but more soluble in fatty tissue = large reservoir for anesthetic

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14
Q

Oil:gas partition coefficient vs. Blood:gas partition coefficient

A

Oil:gas partition coefficient = anesthetic potency
-Potency = 1/MAC (minimum alveolar concentration)

Blood:gas partition coefficient = anesthetic uptake and elimination kinetics

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15
Q

Metabolism and excretion of volatile anesthetics

A

Clearance of inhaled anesthetics primarily by lungs

Metabolism in liver of volatile anesthetics is not important in terminating anesthetic action BUT is important for adverse drug reactions and interactions

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16
Q

Xenon

A

not used clinically, equivalent potency to Nitrous oxide

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17
Q

Nitrous oxide

  • potency?
  • use?
  • onset?
  • contraindications (2)
A

low potency anesthetic, cannot reach surgical dose

Adjunctive agent due to analgesic and anxiolytic properties

Rapid onset

Contraindications: respiratory obstruction (COPD), pregnancy

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18
Q

Diethyl ether

A

no longer used
Flammable and explosive
Produces excessive respiratory tract excretions → choking patient
Good analgesic

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19
Q

Chloroform

A

no longer in common use

Can cause cardiac arrhythmias and hepatotoxicity

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20
Q

Halothane

A

was most widely used inhalational anesthetic until recently

Highly potent

Induction and recovery not prolonged (low blood:gas coefficient)

non explosive

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21
Q

Halothane negatives (4)

A

1) Not a good analgesic
2) Can easily produce respiratory and cardiovascular failure (arrhythmias)
3) Hepatotoxic (increased risk with repeated exposure)
4) Can trigger malignant hyperthermia

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22
Q

Malignant hyperthermia

A

Muscle rigidity, fever
TX = dantrolene (muscle relaxant), blocks Ca2+ release via ryanodine receptor

Can be triggered by halothane

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23
Q

Enflurane

-uses? (4)
negatives? (1)

A
  • Excellent analgesic
  • Fast induction and recovery
  • Good muscle relaxant
  • Less CV effects, less hepatotoxicity

Negatives: Can trigger seizures during induction/recovery

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24
Q

Isoflurane

A

most widely used inhalational anesthetic

  • More potent than enflurane
  • Minimal hepatotoxicity or renal toxicity
  • No seizure triggering
  • Rapid and smooth induction and recovery
  • Minimal CV depression
  • Good muscle relaxant

Negative: has pungent odor → can cause coughing

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25
Q

Desflurane

A
  • Low blood and fatty tissue solubility → faster recovery
  • Pungent odor
  • Not hepatotoxic

Contraindicated for malignant HTN patients

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26
Q

Sevoflurane

A

High potency, low blood:gas coefficient → rapid onset and recovery

Pleasant odor → can be used for induction

Chemically unstable → toxic to kidneys

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27
Q

Thiopental

  • mechanism?
  • onset?
  • use?
A

ultra-short acting barbiturate

Used for induction of general anesthesia

Rapid onset of action - LOC within 15-20 seconds, reawaken in 3-5 minutes

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28
Q

Propofol

  • mechanism?
  • use?
  • 2 benefits?
A

potentiates GABA-A receptor

Rapid onset induction anesthetic, fast recovery

Less nausea post-op
No involuntary movements

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29
Q

Etomidate

  • mechanism?
  • use?
  • benefit?
  • onset?
  • drawback?
A

potentiates GABA-A receptor

-Used for induction of general anesthesia

Larger safety margin - minimal depression of CV and respiratory function

LOC in seconds, recovery in 3 min

Can cause involuntary patient movements during induction

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30
Q

Ketamine

A

glutamate receptor antagonist, no action on GABA-A receptor

Catatonia, amnesia, analgesia

Potent bronchodilator

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31
Q

d-Tubocurarine

A

neuromuscular blocking agent (competitive ACh antagonist)

Relaxes skeletal muscle

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32
Q

Ondansetron

A

antiemetic

Postop nausea and vomiting

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33
Q

Glycopyrrolate

A

anticholinergic, given to combat HTN and bradycardia

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34
Q

Main mechanism of general anesthetics

A

Depress neuronal excitability in CNS via potentiation of GABA-A receptor activity

→ potentiate GABAergic IPSPs in CNS

→ greater inhibition of CNS and depression of neuronal excitability

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35
Q

Main brain regions involved in general anesthesia (3)

A

Hypothalamic nuclei involved in sleep

Reticular formation of brainstem → control of pain, alertness, sleep

Hippocampus → amnesia of post-op patients

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36
Q

Ideal characteristics of general anesthetics

A

rapid and smooth onset of action, rapid recovery from anesthesia upon termination of drug administration, and drug has wide margin for safe use

No drug has all these → use combination of drugs

**Specific drug combinations designed to take advantage of desirable properties of individual drugs while attenuating undesirable side effects

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37
Q

Identification of attentional dysfunction

A

Gold standard = good history and exam - screens supportive, but not sufficient

NOT a learning disorder, intellectual disability, or oppositional behavior

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38
Q

Types of ADHD (3)

A

1) Inattentive type
2) Hyperactive type
3) Combined type

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39
Q

Inattentive type

A

Frequently undiagnosed, more common in girls

Fails to give close attention to details, difficulty sustaining attention

Doesn’t appear to listen, struggles to follow instructions

Difficulty with organization, avoids tasks with lots of thinking

Loses things, easily distracted, forgetful

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40
Q

Hyperactive type

A

Diagnosed earlier (bothersome to others), frequently confused with oppositionality

Fidgets, squirms, difficulty remaining seated

Difficulty engaging in activities quietly, talks excessively

Blurts out answers before questions have been completed, interrupts others, difficulty waiting or taking turns

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41
Q

Combined type ADHD

A

meets criteria for both (6 symptoms from each category)

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42
Q

Functional impact of ADHD

A

Less likely to graduate from high school, get a higher education, and work in a professional environment.

More likely to use drugs/alcohol/tobacco and be incarcerated

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43
Q

Common comorbidities with ADHD

A

substance abuse, anxiety disorders, depression, learning disorders, oppositional behavior

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44
Q

Why is comorbidity so high with ADHD (5)

A

Underlying genetic vulnerability

Developmental changes

Psychological effects of having ADHD

Living with others who are irritated by the ADHD

Self-treating the problem

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45
Q

Treatment of ADHD (4)

A

1) Stimulants
2) Atomoxetine
3) Bupropion (Wellbutrin)
4) Alpha agnoists (guanfacine, clonidine)
- Mostly affect hyperactive symptoms

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46
Q

Stimulants used for treatment of ADHD (2 types)

A

standard of care

Amphetamines: Adderall, Vyvanse

Methylphenidates: Ritalin, Concerta

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47
Q

ADHD Long term

A

lifelong disorder that frequently requires chronic treatment

65% continue to have ADHD symptoms into adulthood

Hyperactivity tends to decrease with time

Inattentive symptoms, restlessness and impulsivity remain

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48
Q

Long term treatment of ADHD

A

Focus on quality of life, treatment can decrease burden on partner

May still need stimulants as adults

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49
Q

Epilepsy

A

tendency for recurrent seizures because of an underlying brain abnormality

disorder of recurrent spontaneous seizures

Generalized or partial

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50
Q

post ictal and during seizure

A

Postictal period: negative symptoms, loss of function in areas of brain involved
-Due to neuronal exhaustion or inhibitory inputs to that area

During seizure → positive symptoms

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51
Q

Signs of epileptic seizures

A

paroxysmal change in behavior or movement, or an alteration of consciousness

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52
Q

Focal (partial) seizures vs. Generalized seizures

A

Focal: begin in one area of cortex, remains localized or spreads

Generalized seizures: begins because cortex as a whole is hyper-irritable

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53
Q

Focal (partial) seizure with consciousness preserved

A

SIMPLE seizure

not effecting awareness or memory

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54
Q

Focal (partial) seizure with loss or impairment of consciousness

A

COMPLEX seizure

Partial onset followed by impairment of consciousness

affecting awareness or memory of events before, during, and immediately after the seizure and affecting behavior

Focal seizures can evolve (spread like a brush fire to “bigger seizure” including convulsive seizure)

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55
Q

Absence seizures

A

Generalized seizure

Involve widespread areas of cortex, but not all layers of neurons

Period of AMS unaccompanied by major motor manifestations

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56
Q

Partial complex seizures

A

followed by postictal state (most absence seizures are not)

Period of AMS unaccompanied by major motor manifestation

Often hard to distinguish from absence seizures

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57
Q

Seizures

A

episodic events which are unexpected and sudden resulting from abnormal and excessive activity of neurons

Involves electrical functions of brain

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58
Q

Intractable epilepsies

A

do not respond to trial of at least 3 anticonvulsants

30% of new onset seizure patients may develop intractable epilepsy

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59
Q

Febrile Seizures

A

Event in infancy/childhood occurring between 3 mos and 5 yrs, associated with fever but without evidence of intracranial infection or defined cause

Most common childhood seizure

No proof of occurrence with rise in fever

Usually within first 24hrs of illness

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60
Q

Simple vs. Complex febrile seizure

A

Simple: generalized, last 10-15 minutes, do not recur within 24 hrs

Complex: focal in nature, at onset, or during, longer than 10-15 min, recur in less than 24 hours

20-30% of febrile seizures are complex

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61
Q

What is the likelihood of future seizures after a febrile seizure?

A

25-40% will have recurrent febrile seizure

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62
Q

Future impact of febrile seizures on sleep, cognition, and risk of epilepsy

A

Cognition: almost all will have normal cognition, prolonged/complex than may have increased risk of cognitive problems

Sleep: tendency to have sleep problems, nightmares

Increased risk of epilepsy with complex seizure, neurological abnormality, or family history of afebrile seizures

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63
Q

Mechanisms of Seizure Pathophysiology (2 main ways neuronal membrane is made unstable)

A

unstable neuronal membrane (focal epileptogenesis → initiation)

1) Paroxysmal discharges can recruit and synchronize a large population of cortical neurons or neurons in thalamic region
2) Enhancement of excitatory neurotransmitters (primarily glutamate) or deficiency of inhibitory neurotransmitters (primarily GABA) can promote spread or propagation of abnormal activity as can metabolic causes.

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64
Q

Common causes of seizure: primary and secondary

A

Primary: hereditary or idiopathic causes

Secondary: mechanical (trauma, brain tumor), metabolic (hypoxia, hypoglycemia, hypocalcemia, alkalosis), withdrawal of CNS depressant drugs, toxins

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65
Q

Consequence of seizure

A

seizure activity → increased O2 demand of CNS → insufficient O2 supply → ischemia → brain damage (neuronal destruction)

Seizures beget seizures

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66
Q

3 drugs used to treat Grand mal (tonic clonic) seizures

A

valproate, lamotrigine, levetiracetam

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67
Q

Mechanism of grand mal seizure (4)

A

1) Loss of GABA inhibitory tone
2) Propagation due to decreased GABA tone over large area
3) Increased response to glutamate
4) Na+ channel excitation

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68
Q

Features of a grand mal (tonic clonic) seizure

A

loss of postural control, LOC, tonic phase (rigid extension of trunk and limbs), clonic phase (rhythmic contraction of arms and legs)

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69
Q

2 drugs used to treat a petit mal (absence) seizure

A

Ethosuximide, Valproate

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70
Q

Mechanism of petit mal (absence) seizure

A

inappropriate activation of low-threshold T-type Ca2+ channels

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71
Q

Features of petit mal (absence) seizure

A

normal muscle tone, impaired consciousness with staring spells (with/without eye blinks), function normal after seizure

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72
Q

Mechanism of partial seizures

A

involves initiation (Rather than propagation) → more difficult to treat

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73
Q

3 drugs used to treat partial seizures

A

carbamazepine, lamotrigine, levetiracetam

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74
Q

Treatment of status epilepticus (inpatient vs. outpatient)

A

BDZS → diazepam, lorazepam, midazolam

Inpatient → Fosphenytoin, Levetiracetam

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75
Q

Treatment of Atonic Myoclonic seizures (3 drugs)

A

Valproate, Levetiracetam, Lamotrigine

*same drugs that treat tonic clonic grand mal seizure!

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76
Q

Two goals of anticonvulsants

A

elevate seizure threshold (Stabilize membrane) and limit propagation (reduce synaptic transmission or nerve conduction)

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77
Q

Mechanism of action of anticonvulsant drugs (4)

A

1) Inhibition of sodium channel (VSSC)
2) Decrease T-type Ca2+ current
3) Inhibition of high-voltage activate Ca2+ channels (VSCC)
4) Enhance GABA action

78
Q

Anticonvulsant drugs: Inhibition of sodium channels

what does this accomplish?
5 drugs that do this

A

use dependent block that stops sustained high-frequency repetitive firing of APs that can initiate seizure formation

Drugs: Phenytoin (class IB antiarrhythmic), Carbamazepine, Lamotrigine, Topiramate, Valproic acid

79
Q

Anticonvulsant drugs: Decrease T-type Ca2+ current

what does this accomplish?
2 drugs that do this?

A

control oscillatory firing of thalamic neurons

Drugs: Ethosuximide (absence seizures), Valproic acid

80
Q

Each of these four drugs has a different mechanism to enhance GABA action. How?

1) Benzodiazepines and Phenobarbital
2) Vigabatrin
3) Tiagabine
4) Gabapentin

A

1) Benzodiazepines and Phenobarbital → facilitate GABA-Cl- channel opening
2) Vigabatrin → inhibit inactivation of GABA by GABA-transaminase
3) Tiagabine → block reuptake of GABA at synapse
4) Gabapentin → increase GABA levels in brain

81
Q

Valproate

Mechanism of action

A

VSSC block and T-type Ca2+ block

82
Q

Valproate

**Side effects (5)

A

GI complaints
hepatotoxicity**
weight gain common

CONTRAINDICATED IN PREGNANCY

DO NOT USE IN PATIENT UNDER 2 YEARS OLD

83
Q

Valproate

Use (3)

A

broad spectrum agent with efficacy against most seizure types

1) First line for generalized tonic-clonic seizures
2) Also very effective against absence seizures, BUT hepatotoxicity → use ethosuximide instead
3) Also can be used in mania

84
Q

Valproate

Drug interactions (3)

A

Alcohol/CNS depressants → additive effects

Anticonvulsants → inhibit metabolism of phenobarbital, phenytoin, lamotrigine, carbamazepine, ethosuximide

ASA/Warfarin → can inhibit platelet aggregation

85
Q

Lamotrigine

mechanism

A

binds to and disrupts function of SV2A

no one really knows!

86
Q

Lamotrigine

Side effects (4)

A

fatigue, somnolence, dizziness

**Minimal drug interactions, no CYP450 metabolism

87
Q

Lamotrigine

Use (1)

A

first line for generalized tonic-clonic seizures

88
Q

Ethosuximide

mechanism

A

T-type Ca2+ channel blocker

89
Q

Ethosuximide

side effects (4)

A

Metabolized (primarily hydroxylation) by CYP3A4→ DDIs with inducers or inhibitors possible

Gastric distress, headache, dizziness

90
Q

Ethosuximide

use (1)

A

drug of choice in absence (petit mal) seizures

91
Q

Carbamazepine

Mechanism

A

bind and block VSSC → suppress repetitive AP

92
Q

Carbamazepine

Use

A

partial seizures and generalized tonic-clonic

Inhibit peripheral sensitization in treatment of chronic pain (trigeminal neuralgia)

93
Q

Carbamazepine

Side effects (6)

A

1) P450 enzyme inducer**
2) Diplopia, ataxia, nausea-vomiting, drowsiness
3) Hyponatremia
4) Stevens-Johnson syndrome
5) Idiosyncratic blood dyscrasias (fatal cases of aplastic anemia, agranulocytosis), rare
6) Hepatotoxicity → monitor CBC, platelets, liver function

94
Q

Phenytoin

Mechanism

A

bind VSSC→ suppress repetitive AP

95
Q

Phenytoin

Side effects (5)

A

1) Strong P450 inducer**
2) Zero order rate of elimination
3) Nystagmus, ataxia, sedation (additive with other CNS depressants)
4) Rash, gingival hyperplasia, hirsutism
5) OD → death from respiratory/circulatory depression

96
Q

Phenytoin

Use (2)

A

no longer considered drug of first choice to to adverse effects

Partial seizures and generalized tonic-clonic seizures

97
Q

Phenobarbital

Mechanism

A

enhance GABA inhibition and antagonize glutamate excitation

98
Q

Phenobarbital

Side effects (3)

A

CYP450 enzyme inducer → significant DDIs

Sedative effect, interfere with learning

CONTRAINDICATED IN PREGNANCY (along with valproate)

99
Q

Phenobarbital

Use (3)

A

excessive sedation limits use to adjunctive role

Partial seizures and generalized tonic-clonic seizures

Neonatal status epilepticus

100
Q

Dorsolateral PFC

A

contributes to the representation, planning, and selection of goal-directed behaviors

101
Q

Input to DL PFC

A

somatosensory, visual and auditory cortical association areas (parietal, occipital, and temporal lobes)

Also involved in basal ganglia-thalamocortical circuit

102
Q

Output from DLPFC

A

premotor cortex and somatosensory association cortex

Also deep brainstem structures (superior colliculus, midbrain tegmentum, PAG)

103
Q

Lesion to DLPFC results in what symptoms?

A

Inability to employ intention (goals) to modulate attention (task at hand)

Perseveration: failure to switch attention appropriately

Environmental dependency: lack of internally generated goal direction → big requirement for environmental cues to accomplish a task

104
Q

Ventromedial PFC aka “orbitofrontal”

A

central role in assessing positive and negative valence of stimuli and (with dopaminergic VTA/nucleus accumbens input) computes potential gains/losses of potential actions

105
Q

Input to VM PFC

A

Somatosensory, visual, auditory assoc. areas (less than DLPFC)

Strong olfactory, gustatory, and visceral inputs

Amygdala and parahippocampal cortices

106
Q

Output from VM PFC

A

Cortical and subcortical regions of forebrain

Lateral and posterior hypothalamus → stress/autonomic centers

PAG, solitary nucleus tract, dorsal motor nucleus of vagus

107
Q

Lesion to VM PFC results in what symptoms

A

impair ability to estimate risk/reward of certain behaviors and impair suppression of excessively risky behaviors (esp. in context of social function)

Characteristic performance on Iowa Gambling Task

  • Continue to draw from “bad” decks even though they know they are losing
  • Don’t develop physiologic reaction to an impending punishment
  • Inadequate inhibition of aggression, sexual behavior, anxiety, and appetitive functions
108
Q

Anterior cingulate cortex

A

detects conflicts between current attention/behavior and desired results, promotes action towards goal (motivation)

109
Q

Anterior cingulate cortex input/output

A

Extensive reciprocal relationships with limbic and autonomic structures

Stimulation → autonomic and limbic responses (change HR, BP, respiration, vocalizations, and facial expressions)

110
Q

Lesion to Anterior Cingulate Cortex results in what symptoms?

A

syndrome of poor motivation, apathy, or lack of will

Abulia (lack of will), akinesia and mutism in some cases
Impaired attentional conflict and focused mental effort

Stroop test - active during the switching required to perform task

111
Q

Function of PFC

A

modulatory rather than transmissive

PFC guides activity flow along task-relevant pathways in more posterior and/or subcortical areas

112
Q

Bilateral hippocampal dysfunction –> ??

A

(patient HM)→ lose declarative or episodic memory as well as spatial memory

113
Q

Neurotransmitters involved in bottom up processing (2)

A

Acetylcholine: ACh released diffusely throughout cerebral cortex when something novel happens

Norepinephrine: projects diffusely throughout cortex, important for attention, learning, anxiety, and arousal

Both are important modulators for what our brains are tuned to

114
Q

Grid cells

A

cells of entorhinal cortex, principal input to hippocampus

Dynamic computation of self-position based on continuously updated info about position and direction

Send output to “place cells”

115
Q

Two main inputs to hippocampus

A

1) Entorhinal cortex

2) Septal nuclei

116
Q

Circuit of hippocampus:

1) Entorhinal cortex via _________ path –> _________
2) Dentate gyrus _________ cells send axons via _______ fibers to _______
3) _________ from CA3 neurons form __________ with other CA3 neurons and CA1 via ____________
4) _________ cells send projections to _______ field –> ____________ –> ___________ –> ____________

A

1) Entorhinal cortex via perforant path→ dentate gyrus
2) Dentate gyrus granule cells send axons via mossy fibers to CA3 field
3) Axon collaterals from CA3 neurons form auto-associations with other CA3 neurons and CA1 via Schaffer collaterals
4) → pyramidal cells send projection to CA1 field → subiculum (transition from 6 layered cortex to 3 layered hippocampus) → entorhinal cortex → cortical association areas

117
Q

Perforant path

A

entorhinal cortex → dentate gyrus and hippocampus

118
Q

Mossy fibers

A

granule cell axons that project to CA3

119
Q

Schaffer collaterals

A

axons from CA3 → CA1 neurons

120
Q

What role does synaptic plasticity play in the hippocampal circuit?

A

Synaptic plasticity in this circuit is crucial for forming memories and associations between places and actions, and associations between events

121
Q

Function of hippocampus (4)

A

1) Formation of declarative memories
2) Memory consolidation to neocortex
3) “Search engine” - search among deposited memories in neocortex
4) “GPS of brain” = spatial memory

122
Q

Place cells

A

firing of each cell indicates specific location in environment → space encoded in firing pattern of hippocampus

123
Q

Dentate gyrus

A

Contain granule cells and local circuit neurons (interneurons)

124
Q

Ammon’s Horn

A

Contain pyramidal cells and local circuit neurons (interneurons)

CA3 + CA2 + CA1 field

125
Q

CA3 field

A

next to dentate gyrus

CA3 neurons have recurrent collaterals to other CA3 cells → allows arbitrary associations between inputs from very different parts of cerebral cortex to be formed = Autoassociative memory

126
Q

CA2 field

A

follows CA3 field

127
Q

CA1 field

A

merges with subiculum

128
Q

Subiculum

A

transition zone between three layered hippocampus and 6 layered entorhinal cortex

129
Q

Sleep and memory consolidation

A

Hippocampus and neocortex interact during sleep → representations of recent experiences are transferred from hippocampus to neocortex via consolidation to form long-term memories

Hippocampus only has limited capacity storage of memories → teaches cortex about information when info is recalled → make memory hippocampus-independent

Hippocampus and cortical neurons synchronously active during sleep

130
Q

6 Layered cortex

A

Layer 4 = “inbox”, Layer 5/6 = “outbox”, Later 2/3 = interoffice mail

Layer 5 = motor output layer over entire cortex

Layer 4 contains granule cells

131
Q

Ascending pathway in cerebral cortex

A

= input into layer 4 from primary (first order) relay nucleus of thalamus

Bottom up attention: activity generated by sensory inputs, relayed through hierarchy of progressively more sophisticated processors

Driving in character - initiates activities

132
Q

Descending pathway in cerebral cortex

A

= feedback issuing from layers 5 and 6 and terminating in layers 6,5,1

Top down attention

Modulatory rather than driving in action - capable of modifying ascending activity, but not of initiating activity de novo

133
Q

Neural network models

A

assume that neural circuit function arises from activation of groups or ensembles of neurons

Ensembles generate emergent functional states that cannot be identified by studying one neuron at a time

Gene expression pattern reflects a state of the network

134
Q

EEG

A

measures electrical potential fluctuations at scalp surface

Fluctuations produced by temporal and spatial summation of electrical currents caused by relatively slow postsynaptic potentials (EPSPs and IPSPs) in cerebral cortex (may or may not lead to AP, represent fluctuations in resting potential)

135
Q

Pyramidal cells

A

(vertically oriented cells) sum the electrical potential changes in the cerebral cortex

136
Q

Distinct patterns of EEG

A

generated by simultaneous depolarization/ hyperpolarization of a large number of neurons → distinct continuous oscillations on EEG

137
Q

“Functional Connectivity”

A

maps of brain constructed based on synchrony observed in EEG, MEG, or fMRI signals

Connectivity is based on physiological synchrony, not anatomical connectivity

Alterations in structural and functional connectivity observed in wide variety of neurologic and psychiatric conditions

138
Q

Thalamic reticular nucleus

A

controls thalamocortical information flow = conductor entraining diverse cortical members in a concerted rhythm

Slow wave sleep, absence seizures, deep anesthesia → delta wave pattern representing temporary detachment of thalamic relay cells from sensory inputs

139
Q

Cholinergic input from brainstem

A

ACh depolarizes thalamic relay neurons → inhibit thalamic reticular nucleus → steady train of thalamic relay activity

ACh acts to open thalamocortical gate to sensory information → attention and arousal = conductor of a conductor

140
Q

Reticular formation of brainstem

A

stimulation → awaken from sleep

“Ascending reticular activating system”

141
Q

__________ learns drug and cues cause pleasure - may signal relief from craving

A

Amygdala

142
Q

Drug cues lead to ________ release in _______ –> trigger output to _______ and ________

A

DA release in nucleus acumbens

thalamus and cortex

143
Q

In absence of activity from _____________ system –> drug seeking initiated

A

reflective reward system

144
Q

Tolerance and ________ do not necessarily coexist, nor do addiction and ______________

A

dependence

physical dependence

145
Q

1) Increased dopamine release in the hypothalamus via the tuberoinfundibular pathway –> ?
2) Increased dopamine release in the nucleus accumbens via the mesolimbic pathway –> ?
3) Dopamine release in the striatum via the nigrostriatal pathway –> ?
4) Decreased dopamine release in the tegmentum via the mesocortical pathway –> ?

A

1) decreased prolactin release
2) Positive symptoms (Delusions, hallucinations, disordered thoughts)
3) movement
4) Negative symptoms (blunted affect, anhedonia, alogia, asociality)

146
Q

What’s the main difference between between typical and atypical antipsychotics?

A

Typical psychotics: Haloperidol, Chlorpromazine
-High D2 block, low 5HT2A block (more extrapyramidal side effects)

Atypical antipsychotics: Clozamine, Olanzapine, Quetiapine
-High 5HT2A block, low D2 block

147
Q

If you increase your dietary intake of salt what happens to your lithium levels?

A

decreased Li+ levels

148
Q

3 drugs to treat partial seizures

A

Carbamazepine
Levetiracetam
Lamotrigine

149
Q

3 drugs to treat Tonic-Clonic seizures

A

Valproate
Levetiracetam
Lamotrigine

150
Q

3 drugs to treat atonic myoclonic seizures

A

Valproate
Levetiracetam
Lamotrigine

151
Q

2 drugs to treat absence seizures

A

Ethosuximide

Valproate

152
Q

Ideal hypnotic

A

Rapidly induce sleep (absorption), duration sufficient to maintain sleep with no morning hangover (half-life)

No dependence/tolerance, no rebound insomnia with discontinued use

Normalize sleep without disturbing sleep

153
Q

BDZs and Barbs in treatment of insomnia:

mechanism

A

facilitate action of GABA at GABA-A receptor-chloride channel complex → membrane hyperpolarization, decreased neuronal excitability

BDZs → sleep and anxiolysis use

154
Q

BDZs and Barbs in treatment of insomnia:

Benefits

A

Useful for promoting sleep, and increasing duration of stage 2 sleep (maintenance of sleep state)

155
Q

BDZs and Barbs in treatment of insomnia:

Drawbacks (5)

A

1) Decreases delta-sleep = BAD
2) Decrease REM duration = BAD
3) Use for longer than 1 week → tolerance = BAD
4) Rebound insomnia with discontinued use
5) Day time sedation (“hangover”)

156
Q

NonREM stages of sleep

A

characterized by a reduction in physiological activity (70-75%)

Stage 1, stage 2, and slow wave sleep

157
Q

Stage 1 sleep

A

transition phase from being awake to falling asleep

EEG like wakefulness (a-rhythm)

Falling sensations, sudden muscle jerks

158
Q

Stage 2 sleep

A

light sleep, short fragmented thoughts

EEG slower with bursts of rapid waves

159
Q

Slow wave sleep

A

deepest level of sleep, most difficult to arouse a person, people groggy several minutes after awakening

EEG has very slow delta waves

Night terrors, nocturnal enuresis can occur

160
Q

REM sleep

A

active period of sleep with intense brain activity (25-30% of sleep)

EEG rapid and desynchronized (similar to waking state)

Rapid eye movements, decreased muscle tone, increased BP, pulse, and respirations

Most recallable dreams

161
Q

Z drugs

A

schedule 4 controlled substances (like benzos)

Drug names: Zolpidem (Ambien), Zaleplon, Eszopiclone (Lunesta)

Z-drugs → non benzos that bind GABA-chloride channels with a1 subunit ONLY (found in cortex) → sleep WITHOUT anxiolysis, reduced potential for dependence

162
Q

Zolpidem

A

effective for reducing sleep latency and nocturnal awakenings with an increase in total sleep time and efficiency

163
Q

Zaleplon

A

decreases time to sleep onset but not number of awakenings

Best suited for use as a sleep aid for middle-of-the-night awakenings

Short half life, eliminated by morning

164
Q

Eszopiclone

A

Longer half life

Safe long term use with no suggestion for development of tolerance or dependence

Help with sleep maintenance and onset

165
Q

Side effects of Z drugs

A

less than benzos

Drowsiness, amnesia, dizziness, headache, GI complaints

Next day psychomotor (driving) impairment

Complex sleep-related behaviors

Rebound effects and withdrawal/tolerance minimal but possible

166
Q

Use of Z drugs

A

first line agents for insomnia

Minimal effects on SWS and REM

167
Q

3 benzodiazepines that are used to treat insomnia

A

Triazolam
Temazepam
Flurazepam

168
Q

Side effects of benzos used for insomnia (5)

A

Fatal OD rare unless taken with other CNS depressants or alcohol

Daytime sedation and performance impairment

Anterograde amnesia

Rebound insomnia

Psychologic and physical dependence (Schedule 4 drug)

169
Q

Drugs used to treat insomnia that don’t act on GABA

A

Mirtazapine
Tricyclic antidepressants
Trazadone
Rameleteon/Melatonin

170
Q

Mitazapine

A

antidepressant known for sedative effects

Mechanism: block 5HT2 receptors and Histamine H1 receptors

171
Q

Tricyclic Antidepressants

A

amitriptyline

Mechanism: block reuptake of 5HT and NE, antagonist at histamine and muscarinic receptors

→ decrease REM and increase slow wave sleep

172
Q

Trazodone

mechanism and side effects (4)

A

Mechanism: complex effects on 5HT neurons
-Decrease REM sleep, increase slow wave sleep

Side effects:
Oversedation
Orthostasis
Dangerous in elderly
Priapism
173
Q

Ramelteon/Melatonin

mechanism, side effects, use

A

Mechanism: agonist at melatonin MT1 and MT2 receptors
Regulates circadian rhythms in suprachiasmatic nucleus

Side effects: dizziness, somnolence, fatigue

Use: chronic or transient insomnia characterized by difficulty with sleep onset

174
Q

Diphenhydramine

A

Mechanism: antihistamine H1 and muscarinic cholinergic antagonist

Use: NOT recommended for chronic use in adults or children

175
Q

Delirium

A

fluctuating confusion, inattention, misperceptions (illusions or hallucinations)

176
Q

Stupor

A

sleep-like state form which the patient can be aroused only by vigorous stimuli

177
Q

Coma

A

sleep-like state where the patient is unresponsive to external stimuli, and there are no sleep-wake cycles

Usually lasts no more than 4 weeks

GCS definition: GCS 8 or less
Patients in coma if they are unable to: follow commands, speak any recognizable words, open either eye

178
Q

Decerebrate (extension) posturing

A

UE extension with LE extension

Suggests lesion at upper brainstem

Prognosis worse in decerebrate than decorticate

179
Q

Decorticate (flexion) posturing

A

upper extremity flexion with lower extremity extension

Suggests lesion at hemispheres

180
Q

Vegetative state

A

where sleep-wake cycles are re-established but there is no sign of cognitive function

Eyes open spontaneously

No evidence of perception of the outside world or purposeful motor activity

Considered permanent if 1 month after acute onset, 3 months after anoxic injury, and 12 months after trauma

181
Q

Criteria for establishing brain death:

A

1) Unresponsive (GCS = 3)

2) Cerebrally modulated motor responses are absent during application of painful stimulus
- Spinal reflexes may be present
- Seizures or flexion/extension posturing may not

3) Brainstem reflexes are absent (pupils, corneals, oculocephalic, oculovestibular, cough, gag, respiratory effort/apnea test)

182
Q

4 other things that must be present for coma

A

Core body temp of 90F

Toxicology tests find no explanation for low neurological state

Adequate BP and pulse (SBP > 90, P>50)

No voluntary movements or response to pain

183
Q

Corneal blink reflex:

how do you do it, what CNs are involved?

What must not happen for brain death to be determined?

A

Touch cornea with tissue, there must be no blink response in either eye (CNs V and VII)

184
Q

Oculocephalic Reflex

how do you do it, what CNs are involved?

What must not happen for brain death to be determined?

A

rotate head quickly to one side and observe eyes

CNs VIII, III, IV, and VI)

There must be no eye movements of any kind

185
Q

Oculovestibular Reflex (Cold water calorics):

how do you do it, what CNs are involved?

What must not happen for brain death to be determined?

A

Flush each external auditory canal with 20 ml ice water x2 and observe

CNs VIII, III, IV, and VI

There must be no eye movements of any kind

186
Q

Cough reflex:

how do you do it, what CNs are involved?

What must not happen for brain death to be determined?

A

suction trachea at the carina

CN X

There must be no cough response

187
Q

Gag reflex:

how do you do it, what CNs are involved?

What must not happen for brain death to be determined?

A

tough oropharynx with Q-tip or suction

CNs IX and X

There must be no movement of the oral structures

188
Q

Raphe nucleus

Locus coeruleus

Nucleus basalis of Meynert

Substantia nigra

Release what NT?

A

Raphe nucleus –> 5HT

Locus coeruleus –> NE

Nucleus basalis of Meynert –> ACh

Substantia nigra –> Dopamine

189
Q

Minimally conscious state

A

eyes open spontaneously, sleep-wake cycles resume

Arousal level may be normal at times

Reproducible behavioral displays of perception comunication, or purposeful motor activity

190
Q

Consciousness

A

derives from activation of intralaminar nuclei of thalamus by the reticular activating system projecting from reticular formation of brainstem

191
Q

Unconsciousness

A

reflects diffuse or bilateral impairment of cerebral functions or failure of brainstem ascending reticular activating system or both

192
Q

Loss of Consciousness, Paralytic Coma

A

must be witnessed by observer

Eyes are closed in a sleep-like state

Unresponsive to external stimuli

Lasts seconds-minutes-hours-days-weeks (lasts less than one month)

Length of coma correlated with outcome

Neuro (8 decks)

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