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Neurology > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

3 transmitters with ascending regulation of thalamus

A

NE, ACh, and 5HT

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2
Q

NE on Thalamus

A

Release from LC causes fight/flight

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3
Q

ACh on Thalamus

A

Release from Reticular Activating System causes awakening

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4
Q

5HT on Thalamus

A

Release from Raphe Nuclei causes sleep and wakefullness

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5
Q

Two drugs that inhibit T-type Ca channels

A

Valproate and Ethosuximide

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6
Q

Declarative Memory

A

recalling events/facts with temporal and spatial components

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7
Q

Where is declarative memory formed?

A

Hippocampus

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8
Q

Procedural Memory

A

learning motor skills

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9
Q

Where is procedural memory formed?

A

Cerebellum, Striatum, frontal cortex

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10
Q

Short Term Memory

A

Seconds, sensory input, sensory cortex

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11
Q

Working Memory

A

Minutes, frontal lobes (executive function region)

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12
Q

Long Term Memory

A

Days+, stored in neocortex, different types in different places

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13
Q

Which Hippocampal Fibers are important for associative memory?

A

CA3

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14
Q

Describe Condition Flavor Aversion

A

Novel food causes cholinergic activation in the forebrain. ACh is released in insular cortex (taste response) and NMDAs are phosphorylated. IF amygdala receives vagal input of malaise while NMDAs are phosphorylated, stimulation of the insular cortex from amygdala produces conditioned flavor aversion.

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15
Q

Criteria for SCZ

A

2+ symptoms for 1+ month each, total of 6 months

- Delusions, hallucinations, disorganized speech, catatonic behavior, negative symptoms

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16
Q

SCZ prevalence

A

1% of general population

10% with 1st degree relative

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17
Q

Typical SCZ onset

A

Late Adolescence - Early Adulthood

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18
Q

How to generally think of SCZ

A

Sensory gating disorder and difficulty processing short term memory
All caused by NT imbalances

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19
Q

DA theory of SCZ

A

Increased mesolimbic system of VTA onto NA, increasing reward pathway and causing positive smptoms
Decreased mesocortical of VTA to PFC (executive functioning in DLPFC) and from SN to basal ganglia for motor control causing negative symptoms

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20
Q

What causes positive symptoms of SCZ?

A

Mesolimbic Hyperactivity

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21
Q

What causes negative symptoms of SCZ?

A

Mesocortical Hypoactivity

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22
Q

Glutamate model of SCZ

A

Similar to DA but w/ NMDA effects.
NMDA antagonism chronically increases DA in NA and reduces DA in PFC. Suggests glutamate hypoactivity might cause both positive and negative symptoms

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23
Q

Association Cortex in SCZ:

A

all cortical areas other than primary sensory (includes DLPFC), atrophy in SCZ w/ abnormal blood flow, physiological inefficiency

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24
Q

Medial Temporal and Hippo in SCZ

A

MTL is needed for sensory integration and attaching limbic value, atrophied in SCZ.
Hippo has reduction of pyramidals, increased flow during positive symptoms

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25
Q

Thalamus in SCZ

A

atrophy in SCZ, reduced sensory filtering

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26
Q

Basal Ganglia in SCZ

A

caudate atrophy, reduced integration of cortical inputs

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27
Q

Final common pathway of drug-reward reinforcement?

A

VTA releasing DA onto NA

This integrates emotional response to motor

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28
Q

Addiction potential is proportional to…..

A

DA release in NA

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29
Q

3 parts of reflective reward system

A

All in PFC:
OFC (impulses)
VMPFC (emotions)
DLPFC (analysis)

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30
Q

Pharmocokinetics of Drug Addiction

A

Faster rate of onset: inhalation > IV > mucous membranes > oral
Shorter Half Lives: frequent use, more withdrawal
Genetics: ex ADH in Asians

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31
Q

Catecholamie Hypothesis in Depression

A

Increasing NE and 5HT reduces depression

BUT: effects take 2-3 weeks……

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32
Q

High potency typical anti-psychotic effects

A

Extrapyramidal side effects

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33
Q

Low potency typical anti-psychotic effects

A

No extrapyramidal but higher concentrations produce anti-muscarinic effects

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34
Q

Atypical anti-psych side effects

A

Agranulocytosis, weight gain, cholesterol, diabetes

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35
Q

4 main brain dopamine pathways

A

Mesolimbic (hyperactivity = positive SCZ)
Mesocortical (hypoactivity = negative SCZ)
Nigrostriatal (coordinated/planned movement, PD)
Tuberoinfundibular (hypothalamic, prolactin inhibition)

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36
Q

Disability worldwide form neuropsych and mood disorders

A

50% is neuropsych; half of neuropsych are mood disorders

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37
Q

What percent of depressed patients are treated?

A

50% are treated, 20% adequately

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38
Q

Depression Diagnosis

A

Sad mood AND 5+ of SIGECAPS for 2+weeks

- Sleep, Interest, Guilt, Energy, Concentration, Anhedonia, Psychomotor changes, SI

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39
Q

Bipolar Diagnosis

A

distinct period of elevated/irritable/expansive mood AND persistent goal directed activity for 1 week AND 3+ of DIGFAST
- Distractibility, Insomnia, Grandiosity, Flight of ideas, Activity, Speech, Thoughtlessness

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40
Q

Atypical Depression

A

mood reactive, leaden paralysis, increased weight gain and hypersomnia

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41
Q

Pyschotic Depression

A

auditory hallucinations, nihilistic delusions

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42
Q

Melancholic Depression

A

Worse in morning, anorexia, weight loss, guilt

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43
Q

Bipolar I vs II

A

I: depression and mania
II: major depression + hypomania

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44
Q

Depression recurrence?

A

50% after 1
60-70% after 2 episodes
90% after 3+

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45
Q

Other causes of mood symptoms

A

Mood disorder, medical illness, drugs, side effects, baseline personality

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46
Q

Are depression or bipolar chemical imbalances?

A

No, neural circuitry issues

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47
Q

Which is more heritable? Depression or Bipolar?

A

Bipolar, x10 RR

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48
Q

Neuroendocrine dysfunction in depression?

A

high hypothalamus stimulation for ACH release, high cortisol damages hippocampus (inhibitory of symptoms) and does not impact amygdala (excitatory)

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49
Q

Possible Bipolar etiology

A

Too much amygdala, not enough DLPFC

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50
Q

Possible MOA of anti-depressants

A

increased BDNF, replacing hippocamus

51
Q

Response rate to anti-depressants?

A

2/3

52
Q

Suicide Facts (COD, ages, genders, etc.)

A

11th COD, 2nd among 20-30s.
Genders: Male > Female, Females attempt 2-3x more
2/3 saw PCP w/in last month

53
Q

Which anti-depressant has immediate effects?

A

Katamine, but has 1-2 week tolerance

54
Q

4 domains for personality disorder

A

2+ of:

Cognition, affectivity, interpersonal functioning, impulse control

55
Q

When does a personality style become a disorder

A

When it deviates markedly from culture, becomes inflexible, impairs social functioning, and is stable for long duration

56
Q

ETOH absorption

A

GI tract, particularly small intestine, peak concentration reduced by 30% w/ meal

57
Q

Distribution of ETOH

A

all body water, high blood flow faster than low blood flow (fat). CNS effects in 5 minutes, peak in 15-60

58
Q

ETOH metablism

A

zero order by liver (7-10g/hr)

59
Q

NADH and alcohol metabolism

A

Loss of NAD can cause acidosis, hypomagnesemia (convulsions), hyperuricemia, high acetyl CoA (fatty liver), hypoglycemia

60
Q

What increases NADH to NAD?

A

Fructose, but causes diarrhea

61
Q

Why does alcohol stimulate initially?

A

GABA neurons depressed first

62
Q

Why no ETOH in epilepsy?

A

anti-convulsant by nature but rebound increases seizure liklihood

63
Q

ETOH and sleep

A

somnolece but decreases REM sleep

64
Q

ETOH and liver

A

reversible damage of increased fatty acids
irreversible when replaced by collagen in cirrhosis
- congestion, ascites, esophagela varices, clotting factors

65
Q

ETOH and GI

A

Irritation, ulceration w/ aspirin, pancreatitis from increased secretions

66
Q

ETOH and heart

A

vasodilation (HTN in heavy drinkers), protective at low doses (J curve)

67
Q

ETOH and kidney

A

Diuresis from reduced ADH secretion (only when BAC is actively rising)

68
Q

Withdrawal stages (EtOH)

A

6-48: seizures, agitation, anxiety, insomnia
12-48: hallucinations
48-96: delerium tremens (no seizure risk)

69
Q

ETOH withdrawal treatment

A

benzos to prevent hyperexcitability, alpha2 agonists to reduce autonomic hyperactivity

70
Q

ETOH intoxication treatment

A

Supportive: IVF, glucose, thiamine, electrolytes

71
Q

Drugs for Alcoholism (3)

A

Disulfiram
Naltrexone
Acamprosate

72
Q

Drugs for Opioid Disorders (3)

A

Methadone
Buprenorphine
Naltrexone

73
Q

Nicotine disorder meds (3)

A

NRT (20mg/pack), rash and tachy
Buproprion: nAChR agonist, DA reuptake inhibitor
Varenicline: A4B2 agonist, black box SI and Dep

74
Q

What determines GA potency?

A

oil:water coefficient

75
Q

GA MOA?

A

Binding in pockets of GABAa receptors

76
Q

General structure of GAs

A

No consistent structural motifs

77
Q

Other targets of GAs

A

brainstem chloride Rs, nAChRs, background K channels

78
Q

Major sits of GA action

A

Hypothalamus (sleep), Reticular Formation (pain, sleep), and Hippocampus (short term memory)

79
Q

4 stages of anesthesia

A

I: analgesia
II: excitement, delerium
III: surgical anesthesia (muscle relaxation and respiratory depression increase through phase)
IV: medullary paralysis

80
Q

What symptoms to watch for before stage IV GA?

A

dilated pupils and diaphragmatic breathing

81
Q

Uptake factors for GAs

A 
Lung factors: ventilation rate
Solubility in blood
Pulmonary blood flow
Solubility in tissue (tissue:blood coefficient)
Tissue blood flow
partial pressures in blood/tissues
82
Q

Potency vs solubility

A 
Potency = oil:water
Solubility = blood:gas (uptake)
83
Q

Major route of elimination of GAs

A

Lungs: function of CA and respiration, liver is negligible, fat reservoirs are important

84
Q

Xenon

A

Noble gas, similar to N2O, not used

85
Q

Nitrous Oxide (MAC, uses, etc)

A

Only gas agent used

MAC 105%, must be used in combo for balanced anesthesia, rapid onset and recovery

86
Q

N2O Weird Stuff (3)

A

Concentration Effect: Uptake faster than predicted as 1L/min inspired volumes rapidly enter blood and pull more with it.

Diffusion Hypoxia: Large volume leaving blood dilutes alveolar O2

Second gas effect: high concentration of N2O uptake pulls any combo anesthetic with it faster too

87
Q

N2O contraindications

A

obstructive disease and pregnancy

88
Q

Diethyl Ether

A

Liquid, complete anesthetic (all stages), flammable so no longer used
Respiratory secretions might choke patient
Slow induction and recovery (high blood:gas)

89
Q

Chloroform

A

Not used, cardiac arrhythmia risk, hepatotoxic

90
Q

Halothane

A

Highly potent, low blood:gas, poor analgesic.
High respiratory/cardio failure potential
Liver damage, potentially from immune reponse
Can cause malignant hyperthermia

91
Q

What do you give for malignant hyperthermia?

A

Danrolene

92
Q

Enflurane

A

Good analgesic, good muscle relaxant
USE FOR MAINTENANCE
can trigger seizures, less toxic than halothane

93
Q

Isoflurane

A

More potent than enflurane, little hepato/renal toxicity
NO SEIZURES
Pungent odor can cause coughing
MOST WIDELY USED INHALANT

94
Q

Desflurane

A

New, minimal solubility, also pungent, can be complete anesthetic, needs special vaporizer

95
Q

Sevoflurane

A

High potency, low blood-gas, pleasant odor

RENAL TOXIC

96
Q

Thiopental

A

short acting barbituate, GABAa potentiation

Common for induction

97
Q

Propofol

A

GABAa potentiation, rapid onset and fast recovery

98
Q

Etomidate

A

No analgesia, induction, larger safety margin than theopental

99
Q

Ketamine

A

NMDA antagonist, potent bronchodilator

100
Q

Adjuvants (5 categories)

A

D-tubocurarine (neuromuscular blocker, non-depolarizing, don’t cross BBB)
Anxiolytics (Benzos and Barbs)
Analgesics (opioids)
Antiemetics (odansetron)
Anticholinergics (hypotension and bradycardia treatment, glycopyrrolate)

101
Q

What part of the brain atrophies in MS?

A

Corpus Collosum

102
Q

3 types of ADHD

A

Inattentive, Hyperactive, Combined

103
Q

Which type of ADHD is most common in girls?

A

Inattentive

104
Q

Major comorbities with ADHD? (5)

A 
Substance Abuse
Anxiety Disorders
Depression
Learning Disorders
Oppositional Behavior
105
Q

Prevalence of ADHD

A

3-8% in kids

106
Q

Gender of ADHD

A

Male > Female (gender bias based on type?)

107
Q

ADHD diagnostic criteria

A

6+ symptoms of 1 or both disorder types, before age of 12, present in 2+ settings

108
Q

2 types of ADHD stimulant medications

A

Amphetamines and Methylphenidates

109
Q

Are stimulants effective?

A

80-90% reduction in symptom burden

110
Q

What percentage of ADHD persist into adulthood?

A

65%

111
Q

Which ADHD types decrease with time?

A

Hyperactivity

112
Q

Why are psych co-morbidities high? (5)

A 
Genetics
Developmental influences of ADHD
Psychiatric effects 
Living Situation
Self Treating
113
Q

Prevalence of epilepsy and etiology

A

0.7%; 50% unknown cause

114
Q

Differentiating complex partial and absence seizures?

A

Complex partial are followed by post-ictal

115
Q

What percent of epilepsy is intractable?

A

36%

47% respond to 1st med, +13% to 2nd, +4% to 3rd

116
Q

Most common childhood seizure?

A

Febrile, 2-4%

117
Q

What percent of febrile seizures are complex?

A

20-30%

118
Q

Risk factor for recurrent febrile seizures (6)

A 
Age <1 year
Family history
Low grade fever at onset
brief fever
complex seizure
day care
119
Q

DLPFC Lesion Symptoms

A

Perseveration and environmental dependency

120
Q

VMPFC Lesion Symptoms

A

Iowa Gambling Task issue, lack of inhibition.

Overall an inability to estimate risk/reward behavior

121
Q

Anterior Cingulate Cortex Lesion Symptoms

A

Lack of will; issues with mental effort

122
Q

Granular vs Agranular cortex

A 
Granular = input (primary sensory)
Agranular = output
123
Q

Frequency of EEG rhythms

A

Beta > Alpha > Theta > Delta

Neurology (5 decks)

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