Unit 4 Flashcards
(123 cards)
1
Q
3 transmitters with ascending regulation of thalamus
A
NE, ACh, and 5HT
2
Q
NE on Thalamus
A
Release from LC causes fight/flight
3
Q
ACh on Thalamus
A
Release from Reticular Activating System causes awakening
4
Q
5HT on Thalamus
A
Release from Raphe Nuclei causes sleep and wakefullness
5
Q
Two drugs that inhibit T-type Ca channels
A
Valproate and Ethosuximide
6
Q
Declarative Memory
A
recalling events/facts with temporal and spatial components
7
Q
Where is declarative memory formed?
A
Hippocampus
8
Q
Procedural Memory
A
learning motor skills
9
Q
Where is procedural memory formed?
A
Cerebellum, Striatum, frontal cortex
10
Q
Short Term Memory
A
Seconds, sensory input, sensory cortex
11
Q
Working Memory
A
Minutes, frontal lobes (executive function region)
12
Q
Long Term Memory
A
Days+, stored in neocortex, different types in different places
13
Q
Which Hippocampal Fibers are important for associative memory?
A
CA3
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.
15
Q
Criteria for SCZ
A
2+ symptoms for 1+ month each, total of 6 months
- Delusions, hallucinations, disorganized speech, catatonic behavior, negative symptoms
16
Q
SCZ prevalence
A
1% of general population
10% with 1st degree relative
17
Q
Typical SCZ onset
A
Late Adolescence - Early Adulthood
18
Q
How to generally think of SCZ
A
Sensory gating disorder and difficulty processing short term memory
All caused by NT imbalances
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
20
Q
What causes positive symptoms of SCZ?
A
Mesolimbic Hyperactivity
21
Q
What causes negative symptoms of SCZ?
A
Mesocortical Hypoactivity
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
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
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
25
Thalamus in SCZ
atrophy in SCZ, reduced sensory filtering
26
Basal Ganglia in SCZ
caudate atrophy, reduced integration of cortical inputs
27
Final common pathway of drug-reward reinforcement?
VTA releasing DA onto NA
| This integrates emotional response to motor
28
Addiction potential is proportional to.....
DA release in NA
29
3 parts of reflective reward system
All in PFC:
OFC (impulses)
VMPFC (emotions)
DLPFC (analysis)
30
Pharmocokinetics of Drug Addiction
Faster rate of onset: inhalation > IV > mucous membranes > oral
Shorter Half Lives: frequent use, more withdrawal
Genetics: ex ADH in Asians
31
Catecholamie Hypothesis in Depression
Increasing NE and 5HT reduces depression
| BUT: effects take 2-3 weeks......
32
High potency typical anti-psychotic effects
Extrapyramidal side effects
33
Low potency typical anti-psychotic effects
No extrapyramidal but higher concentrations produce anti-muscarinic effects
34
Atypical anti-psych side effects
Agranulocytosis, weight gain, cholesterol, diabetes
35
4 main brain dopamine pathways
Mesolimbic (hyperactivity = positive SCZ)
Mesocortical (hypoactivity = negative SCZ)
Nigrostriatal (coordinated/planned movement, PD)
Tuberoinfundibular (hypothalamic, prolactin inhibition)
36
Disability worldwide form neuropsych and mood disorders
50% is neuropsych; half of neuropsych are mood disorders
37
What percent of depressed patients are treated?
50% are treated, 20% adequately
38
Depression Diagnosis
Sad mood AND 5+ of SIGECAPS for 2+weeks
| - Sleep, Interest, Guilt, Energy, Concentration, Anhedonia, Psychomotor changes, SI
39
Bipolar Diagnosis
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
40
Atypical Depression
mood reactive, leaden paralysis, increased weight gain and hypersomnia
41
Pyschotic Depression
auditory hallucinations, nihilistic delusions
42
Melancholic Depression
Worse in morning, anorexia, weight loss, guilt
43
Bipolar I vs II
I: depression and mania
II: major depression + hypomania
44
Depression recurrence?
50% after 1
60-70% after 2 episodes
90% after 3+
45
Other causes of mood symptoms
Mood disorder, medical illness, drugs, side effects, baseline personality
46
Are depression or bipolar chemical imbalances?
No, neural circuitry issues
47
Which is more heritable? Depression or Bipolar?
Bipolar, x10 RR
48
Neuroendocrine dysfunction in depression?
high hypothalamus stimulation for ACH release, high cortisol damages hippocampus (inhibitory of symptoms) and does not impact amygdala (excitatory)
49
Possible Bipolar etiology
Too much amygdala, not enough DLPFC
50
Possible MOA of anti-depressants
increased BDNF, replacing hippocamus
51
Response rate to anti-depressants?
2/3
52
Suicide Facts (COD, ages, genders, etc.)
11th COD, 2nd among 20-30s.
Genders: Male > Female, Females attempt 2-3x more
2/3 saw PCP w/in last month
53
Which anti-depressant has immediate effects?
Katamine, but has 1-2 week tolerance
54
4 domains for personality disorder
2+ of:
| Cognition, affectivity, interpersonal functioning, impulse control
55
When does a personality style become a disorder
When it deviates markedly from culture, becomes inflexible, impairs social functioning, and is stable for long duration
56
ETOH absorption
GI tract, particularly small intestine, peak concentration reduced by 30% w/ meal
57
Distribution of ETOH
all body water, high blood flow faster than low blood flow (fat). CNS effects in 5 minutes, peak in 15-60
58
ETOH metablism
zero order by liver (7-10g/hr)
59
NADH and alcohol metabolism
Loss of NAD can cause acidosis, hypomagnesemia (convulsions), hyperuricemia, high acetyl CoA (fatty liver), hypoglycemia
60
What increases NADH to NAD?
Fructose, but causes diarrhea
61
Why does alcohol stimulate initially?
GABA neurons depressed first
62
Why no ETOH in epilepsy?
anti-convulsant by nature but rebound increases seizure liklihood
63
ETOH and sleep
somnolece but decreases REM sleep
64
ETOH and liver
reversible damage of increased fatty acids
irreversible when replaced by collagen in cirrhosis
- congestion, ascites, esophagela varices, clotting factors
65
ETOH and GI
Irritation, ulceration w/ aspirin, pancreatitis from increased secretions
66
ETOH and heart
vasodilation (HTN in heavy drinkers), protective at low doses (J curve)
67
ETOH and kidney
Diuresis from reduced ADH secretion (only when BAC is actively rising)
68
Withdrawal stages (EtOH)
6-48: seizures, agitation, anxiety, insomnia
12-48: hallucinations
48-96: delerium tremens (no seizure risk)
69
ETOH withdrawal treatment
benzos to prevent hyperexcitability, alpha2 agonists to reduce autonomic hyperactivity
70
ETOH intoxication treatment
Supportive: IVF, glucose, thiamine, electrolytes
71
Drugs for Alcoholism (3)
Disulfiram
Naltrexone
Acamprosate
72
Drugs for Opioid Disorders (3)
Methadone
Buprenorphine
Naltrexone
73
Nicotine disorder meds (3)
NRT (20mg/pack), rash and tachy
Buproprion: nAChR agonist, DA reuptake inhibitor
Varenicline: A4B2 agonist, black box SI and Dep
74
What determines GA potency?
oil:water coefficient
75
GA MOA?
Binding in pockets of GABAa receptors
76
General structure of GAs
No consistent structural motifs
77
Other targets of GAs
brainstem chloride Rs, nAChRs, background K channels
78
Major sits of GA action
Hypothalamus (sleep), Reticular Formation (pain, sleep), and Hippocampus (short term memory)
79
4 stages of anesthesia
I: analgesia
II: excitement, delerium
III: surgical anesthesia (muscle relaxation and respiratory depression increase through phase)
IV: medullary paralysis
80
What symptoms to watch for before stage IV GA?
dilated pupils and diaphragmatic breathing
81
Uptake factors for GAs
```
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
Potency vs solubility
```
Potency = oil:water
Solubility = blood:gas (uptake)
```
83
Major route of elimination of GAs
Lungs: function of CA and respiration, liver is negligible, fat reservoirs are important
84
Xenon
Noble gas, similar to N2O, not used
85
Nitrous Oxide (MAC, uses, etc)
Only gas agent used
| MAC 105%, must be used in combo for balanced anesthesia, rapid onset and recovery
86
N2O Weird Stuff (3)
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
N2O contraindications
obstructive disease and pregnancy
88
Diethyl Ether
Liquid, complete anesthetic (all stages), flammable so no longer used
Respiratory secretions might choke patient
Slow induction and recovery (high blood:gas)
89
Chloroform
Not used, cardiac arrhythmia risk, hepatotoxic
90
Halothane
Highly potent, low blood:gas, poor analgesic.
High respiratory/cardio failure potential
Liver damage, potentially from immune reponse
Can cause malignant hyperthermia
91
What do you give for malignant hyperthermia?
Danrolene
92
Enflurane
Good analgesic, good muscle relaxant
USE FOR MAINTENANCE
can trigger seizures, less toxic than halothane
93
Isoflurane
More potent than enflurane, little hepato/renal toxicity
NO SEIZURES
Pungent odor can cause coughing
MOST WIDELY USED INHALANT
94
Desflurane
New, minimal solubility, also pungent, can be complete anesthetic, needs special vaporizer
95
Sevoflurane
High potency, low blood-gas, pleasant odor
| RENAL TOXIC
96
Thiopental
short acting barbituate, GABAa potentiation
| Common for induction
97
Propofol
GABAa potentiation, rapid onset and fast recovery
98
Etomidate
No analgesia, induction, larger safety margin than theopental
99
Ketamine
NMDA antagonist, potent bronchodilator
100
Adjuvants (5 categories)
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
What part of the brain atrophies in MS?
Corpus Collosum
102
3 types of ADHD
Inattentive, Hyperactive, Combined
103
Which type of ADHD is most common in girls?
Inattentive
104
Major comorbities with ADHD? (5)
```
Substance Abuse
Anxiety Disorders
Depression
Learning Disorders
Oppositional Behavior
```
105
Prevalence of ADHD
3-8% in kids
106
Gender of ADHD
Male > Female (gender bias based on type?)
107
ADHD diagnostic criteria
6+ symptoms of 1 or both disorder types, before age of 12, present in 2+ settings
108
2 types of ADHD stimulant medications
Amphetamines and Methylphenidates
109
Are stimulants effective?
80-90% reduction in symptom burden
110
What percentage of ADHD persist into adulthood?
65%
111
Which ADHD types decrease with time?
Hyperactivity
112
Why are psych co-morbidities high? (5)
```
Genetics
Developmental influences of ADHD
Psychiatric effects
Living Situation
Self Treating
```
113
Prevalence of epilepsy and etiology
0.7%; 50% unknown cause
114
Differentiating complex partial and absence seizures?
Complex partial are followed by post-ictal
115
What percent of epilepsy is intractable?
36%
| 47% respond to 1st med, +13% to 2nd, +4% to 3rd
116
Most common childhood seizure?
Febrile, 2-4%
117
What percent of febrile seizures are complex?
20-30%
118
Risk factor for recurrent febrile seizures (6)
```
Age <1 year
Family history
Low grade fever at onset
brief fever
complex seizure
day care
```
119
DLPFC Lesion Symptoms
Perseveration and environmental dependency
120
VMPFC Lesion Symptoms
Iowa Gambling Task issue, lack of inhibition.
| Overall an inability to estimate risk/reward behavior
121
Anterior Cingulate Cortex Lesion Symptoms
Lack of will; issues with mental effort
122
Granular vs Agranular cortex
```
Granular = input (primary sensory)
Agranular = output
```
123
Frequency of EEG rhythms
Beta > Alpha > Theta > Delta
