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High-Yield Brain and Behavior Part II > Week 6 > Flashcards

Week 6 Flashcards

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1
Q

General anesthesia (balance)

A

balance btw hypnosis, analgesia (autonomic, somatic), and areflexia.

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2
Q

Modern inhaled anesthetics

A

Fluorinated ether derivatives

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3
Q

clinically relevant differences between inhaled anesthetics

A

potency, solubility, pungency, cost

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4
Q

distribution, elimination of inhaled anesthetics

A

uptake into blood and distributed 1) VRG (brain, liver, kidney) 2) fat 3) muscle. eliminated by ventilation (almost no metabolic breakdown)

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5
Q

solubility of inhaled anesthetics

A

low blood solubility = less potent, faster onset/offset, less accumulation in tissue/fat

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6
Q

MAC inhaled anesthetics

A

minimum alveolar concentration at which 50% patients will not move in response to surgical incision (hypnosis more important now)

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7
Q

MOA inhaled anesthetics

A

promiscuous binders allosterically and competitively. GABA-A.

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8
Q

Respiratory effects inhaled anesthetics

A

bronchodilation, inc rate, dec tidal volume, dec reflexes to maintain oxygenation/ventilation

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9
Q

CV effects inhaled anesthetics

A

Decrease blood pressure, redistribute blood from core to periphery. Impair autonomic reflexes, impaired contractile strength of heart.

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10
Q

pharmacokinetics of IV anesthetics

A

Redistribution terminates drug effect–not elimination! order of peaks: Plasma–>VRG–>muscle–>fat

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11
Q

Context-sensitive half time

A

longer you infuse a drug, the longer it takes to eliminate. Very fat-soluble drugs never get to steady state.

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12
Q

Propofol (mechanism, onset, use, metabolism, contraindications)

A

potentiates GABA (no effect on pain!), fast onset/offset, used for induction, TIVA, ICU sedation, partially metabolized in extrahepatic tissues. Redistribution > elimination! Egg allergy.

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13
Q

Etomidate (use, MOA, adverse effects)

A

induction drug of choice for hemodynamically compromised patients, potentiates GABA, causes adrenocortical suppression = reduced ability to compensate for shock!

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14
Q

Thiopental (general properties, contraindications)

A

similar to propofol, contraindicated in porhpyria

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15
Q

CV effects of IV anesthetics

A

hypotension!

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16
Q

Ketamine (autonomic effects, anesthetic advantages, disadvantages)

A

sympathetic stimulation, potent analgesic, causes dissociative anesthesia and dysphoria, no IV access required.

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17
Q

MOA local anesthetics

A

Cross membrane, bind intracellularly to Na+ channels in open and inactivated states. Acid reduces ability to cross membrane

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18
Q

amide local anesthetics

A

two “i”s in generic name. metabolized in hepatocytes, greater toxicity

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19
Q

ester local anesthetics

A

one “i” in generic name, metabolized in plasma to PABA (potential allergen), less toxic, OTC meds are esters.

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20
Q

pharmacology local anesthetics (solubility, pKa)

A

greater lipid solubility –> more potent, longer duration. Lower pKa–> more un-ionized–> more rapid onset.

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21
Q

toxicity and Tx of local anesthetics

A

tongue numbness, lightheadedness –> visual disturbance –> muscle twitching –> unconsciousness –> convulsion –> coma –> respiratory arrest. Ventricular arrhythmias. Intralipids given to absorb LA. Hyperventilate to generate acidosis

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22
Q

S vs R isomer local anesthetics

A

S preferred – reduced cardiotoxicity

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23
Q

Multi-Axial biopsychosocial model

A

I: clinical disorder (pervasive across all social interaction)
II: personality disorders, mental retardation, maladaptive personality features, defense mechanisms
III: general medical conditions
IV: psychosocial and environmental problems
V: global assessment of functioning

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24
Q

Organizational vs activational effects of gonadal hormones (and examples)

A 
organizational = development, fetal exposure, considered permanent (eg high CAH in girls leads to "masculinization"). 
Activational = re-exposure later in development, transient and super-imposed on organizational effects
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25
Q

sex hormone effects on NTs

A

estrogen is pro-5HT. progesterone acts on GABA

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26
Q

attachment behavior

A

behavior that promotes proximity to or contact with person(s) to whom an individual is attached

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27
Q

neurobiology of attachment (voles)

A

oxytocin mediates partner attachment/preference as well as mother-child attachment

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28
Q

Stages of normal infant attachment

A 
Indiscriminate sociability (2 mos)
Attachments in the making -- differentiating caregivers, developing internal representation. (2-7mos)
Clear Cut Attachment -- Still Face test. Stranger/Separation anxiety (7-24mos)
Goal Oriented Partnerships (>24 mos)
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29
Q

Healthy vs disturbed attachement cycle

A

Healthy: Need–> Cry –> Response –> Trust
Disturbed: Need–> Cry–> No Response –> Rage

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30
Q

Reactive attachment disorder (definition, subtypes, consequences, treatment)

A

Absence of the ability to be genuinely affectionate toward others.
Inhibited type: Fearful and restricted in caregiver interest
Disinhibited type: indiscriminate interest, shallow relationships
Consequences: poor mental and emotional health, social difficulties, substance abuse, adolescent problems, abusive behavior, cruelty, superficiality.
Interventions: support groups, relationship therapy

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31
Q

Temperament

A

in-born differences in reactivity (response to environment) and self-regulation (processes modulating reactivity) vis-a-vis emotion, motor activity, attention.

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32
Q

Key dynamic mediating link between temperament and developmental outcomes

A

“Goodness of fit”(!)

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33
Q

Neurobiology of vulnerability

A

short allele of SERT (5-HTT) conferred greater vulnerability to stressful events/poor rearing (rhesus and human). Exaggerated cortisol levels, MDD

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34
Q

stress diathesis model of psychopathology

A

inborn vulnerability x stress –> outcome

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35
Q

Stress and mothering in rats

A

Good moms have more GCRs in hippocampus, lower stress response. Offspring of bad moms are more promiscuous, more aggressive, reach puberty earlier (makes sense evolutionarily).

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36
Q

HPA axis and early experience

A

Stress–> CRH, AVP increase –> cognitive and affective disorders

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37
Q

psychological trauma

A

dysregulated neuropsychological functioning in response to experience (subjective experience more important than objective)

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38
Q

Symptoms of traumatic response in children

A

memory problems, poor concentration, anxiety, impulsiveness, aches, inc HR, obesity, sleep disturbance, procrastination, fighting, sexualized behaviors.

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39
Q

public health of trauma

A

higher ACE scores –> heart disease, cancer, lung disease, liver disease, early pregnancy, eating disorder, MDD, smoking, drugs

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40
Q

Treatment approach to childhood trauma

A

build resilience

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41
Q

Growth routes during adolescence

A

Continuous: tends to be more resilient
Surgent: uneven, usually not clinically significant
Tumultuous: turmoil, frequent crises, intense emotion. Most clinically significant: susceptible to acting out, getting overwhelmed.

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42
Q

CNS maturation during adolescence

A

linear increases in white matter, inverted- U in gray matter (arborization, pruning). Different lobes peak at different times. Frontal last!

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43
Q

Health risks in adolescence

A

risk taking: injury/accidents, sex, alcohol, dugs. Abuse, homelessness. Depression, suicide, truancy.

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44
Q

Neuroscience of adolescent risk-taking

A

dopamine remodling (increased sensitivity) without increase in self-regulation. Heightened attention to social stimuli (greater influence of peers).

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45
Q

Psychoanalytic view of personality

A

personality is primary pattern of ego defenses

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46
Q

Humanistic view of personality

A

personality influenced by conscious, subjective perception. Maslow’s hierarchy

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47
Q

Social cognitive view of personality

A

conscious thought greatly influence action. reciprocal determinism of behavior, environment, person. Most critical belief is self-efficacy! (virtuous vs vicious cycles)

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48
Q

Trait theory of personality

A

focuses on individual differences (surface traits, source traits).

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49
Q

“Big Five” for trait theory

A

Extraversion, neuroticism (stable-unstable), conscientiousness (dependable, undependable), agreeableness, openness to experience

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50
Q

Biosocial theory of personality

A

NTs and environment mutually influence each other –> personality

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51
Q

General features of personality disorder

A

Enduring, cross-context, lead to impairment or distress. Lack of insight, ego syntonic, difficult to treat.

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52
Q

Personality disorder cluster A

A

“weird” odd/eccentric. Paranoid (Accusatory)–pervasive distrust, projection, anger; Schizoid (Aloof)–voluntary social withdrawal, few friends, no humor; Schizotypal (Awkward)–eccentric, odd beliefs, neologisms, not psychotic.

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53
Q

Personality disorder cluster B

A

“Wild” Dramatic, erratic. Antisocial–disregard for norms, persuasive, shallow, “slick” type, poorly-socialized type. Borderline–instability of relationships, self-image, frantic to avoid abandonment, extreme closeness/distance. Histrionic–excessive emotionality, attention seeking, flamboyant, flirtatious, seductive; Narcissistic – Grandiosity, need for admiration, self centered, entitlement

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54
Q

Personality disorder cluster C

A

“Worried”: Avoidant (Cowardly)–hypersensitive to rejection, inhibited, inadequate, desires relationships (vs shizoid)l OCPD (Compulsive)–orderliness, perfection, control, not emotionally expressive, distrusts emotion in others, ego-syntonic (vs OCD); Dependent (Clingy) – submissive, need to be taken care of, sensitive to disapproval, low confidence.

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55
Q

Diagnostic criteria for ADHD

A

6+ maladaptive attention Sx; 6+ hyperactivity-impulsivity Sx; onset before age 7; impairment in >1 setting; not explained by another disorder

56
Q

Systems of attention

A

Posterior: orient and engage (wake up and smell the coffee). NE
Anterior: Decreases responsively to novel stimuli (executive). DA from VTA –> PFC

57
Q

Gene x Environment in ADHD

A

DRD4, DAT alleles confer risk. When combined with smoking, odds increase a LOT

58
Q

Neuro deficits in ADHD

A

smaller, less developed PFC, Basal Ganglia, Cerebellum, ant cingulate. 3 year lag in development, but typically reached by 16. DA and NE dysregulation

59
Q

assessment for ADHD

A

comprehensive, thorough, developmental approach

60
Q

Treatment approach for ADHD

A

need moderate catecholamine levels (inverted U–fatigued-alert-stressed). 2 prongs: Executive function and Motivation (need constant reinforcement). Skills-based approach. Multi-modal.

61
Q

Amphetamine (adderall) for ADHD

A

broad mechanism: prevents reuptake, increases vesicular release. NE, 5HT also respond.

62
Q

Methylphenidate (Ritalin) for ADHD

A

Many formulations. Narrow mechanism: binds DAT and inhibits re-uptake. Slow!

63
Q

Developmental Milestone themes

A

Gross motor: Head to Toe
Fine motor: flexor to extensor
Language: receptive to expressive
Social/emotional: me to you

64
Q

6months milestones

A

crawling (hip, core, arms). Caregiver preference, consonant stringing.

65
Q

1 yr milestones

A

walking, crawling, climbing, several single words

66
Q

2 yr milestones

A

playing, drawing, 2/4 speech understandable. Parallel play

67
Q

3 yr milestones

A

4-5 word phrases, 3/4 understandable. Transitioning to cooperative play. magical thinking

68
Q

4 yr milestones

A

training wheels. 4/4 understandable. games, cooperative play. imaginary vs real.

69
Q

Erikson’s psychosocial stages

A

infancy: sense of self, toddler: sense of self-control. preschool: sense of self-confidence. School age: sense of achievement. Adolescent: sense of identity. Young adult: sense of connectedness, support. Middle adult: sense of completeness. Late Life: sense of fulfillment.

70
Q

Non-prescription stimulant use in college

A

Common, associated with decline in performance

71
Q

Mania

A

Distinct period >7 days of impulsivity, high energy, tangentiality, distractibility, decreased sleep, poor judgment

72
Q

Bipolar vs schizoaffective

A

Bipolar has episodes of mood alone (+/- psychosis). Schizo has psychosis alone (if + mood = schizoaffective

73
Q

BPD heritability, course, outcome

A

highly heritable, often mis-diagnosed for 10 yrs, very disabling, poor outcomes (suicide, relapse).

74
Q

BPD Tx

A

Tx changes over time, several weeks needed to assess. need to optimize. Combination therapy is standards. Anti-depressants may worsen disease course!

75
Q

5-HT function in brain

A

MODULATES responses: mood, homeostasis, sex, nociception, behavior

76
Q

5-HT synthesis

A

Tryptophan is hydroxylated (RLS–Tph1 in periphery, Tph2 in brain), then decarboxylated (AADC)

77
Q

important 5HTRs in brain

A

5HTR1 and 5HTR2. 5HTR3 promotes vomiting

78
Q

Clinical strategies for modulating 5HT

A

Depression: SSRIs, MAOIs
Anxiety: 5HT1 agonist, SSRIs
Obesity: 5HT2 agonist
Vomiting: 5HT3 antagonist

79
Q

Tricyclic antidepressants

A

inhibit both SERT and NET

80
Q

Serotonin Syndrome

A

Overactivation of central serotonin receptors. Abdominal pain, diarrhea, sweating, fever, tachycardia, altered mental state. Occurs when switching among SSRIs or to other drug classes (MAOIs)

81
Q

Catecholamine synthesis

A 
Tyrosine --> Dopa by TH (RLS!)
Dopa --> Dopamine by LAAD
DA --> NE by Dopamine B Hydroxylase
NE --> E by PNMT
negative feedback!
82
Q

Gs

A

Increased cAMP

83
Q

Gi

A

decreased cAMP

84
Q

Gq

A

increased Ca++

85
Q

Types of adrenergic receptors

A

a1 (Gq)=stimulating
a2 (Gi) = inhibitory
b1, b2 (Gs) = stimulating

86
Q

Termination of catecholamine signaling

A

Reuptake1 (SERT): high affinity, low capacity
Metabolic transformation (MAOs, others)
Reuptake 2: extra-synaptic: low affinity, high capacity

87
Q

MAO isozymes

A

MAO-A: 5HT, NE, Tryptamine (depression)

MAO-B: DA, tryptamine (Parkinson’s?)

88
Q

Carbidopa

A

Inhibits peripheral LAAD

89
Q

reserpine

A

blocks VMAT DA uptake (HTN, snake bites, causes depression)

90
Q

Bretylium, Guanethidine

A

inhibit NE release, anti-HTN and VFib

91
Q

bromocriptine

A

selective D2 agonist (Parkinson’s)

92
Q

Cocaine and imipramine (tricyclic) MOA

A

NET inhibitors

93
Q

Ultradian pulsality of GCs

A

Peak in morning. Prednisone/depression flattens!

94
Q

U-shaped curve of GC activity

A

Adaptive: memory, immune cell trafficking, gluconeogenesis up. immune cell production, osteoblast activity down.
—> pathological: repro function, memory, growth down. Diabetes, muscle wasting, abdominal fat, osteoperosis, infection risk

95
Q

addiction and HPA

A

addictive behaviors relieve HPA activity, withdrawal activates

96
Q

HPA axis

A

hypothal—> CRF –> pituitary –> ACTH –>GCs, catechols –>neg feedback

97
Q

CRF effects on brain

A

found throughout. increased arousal, fear, sympathetic response, decreased appetite, repro

98
Q

Early life experiences and depression

A

High contact –> lower stress response, more GR in hippocampus (more sensitive to feedback?). Epigenetic phenomenon. Bad mothers have increased methylation of GR promoter

99
Q

Common MOA of antipsychotics

A

Block D2 receptor. Works on positive Sx, not so great on neg Sx

100
Q

Side-effects on antipsychotics

A

Parkinsonian mvmt disorders, acute dystonic reaction. Gynecomastia/galactorrhea. Lower seizure threshold, QTc prolongation

101
Q

First generation antipsychotics

A

High potency: less antihistamine, antiadrenergic, anticholinergic effects
Low potency: more off-target side effects.
Antihistamine: SEDATION, weight gain
Anticholinergic: Delirium, blurry vision, constipation
Antiadrenergic: orthostasis, arrythmias

102
Q

Second generation antipsychotics (properties, relative to 1st, side effects)

A

“Atypicals”
in addition to D2 blockate, block 5-HT2R. Good for bipolar disorder.
Not more effective, but better tolerated than 1st gen.
Side effects: Weight gain, metabolic syndrome. Clozapine: agranulocytosis

103
Q

aripiprazole (abilify)

A

atypical-atypical: partial DA agonist in parts of the brain. Can make psychosis worse in some people

104
Q

Clozapine

A

Atypical antipsychosic. Risk for

105
Q

Common mechanism of all antidepressants

A

increase monoamines: NE, 5-HT, DA.

Can also be used to treat anxiety!

106
Q

MAOIs side-effects

A

reduced metabolism of tyramine from food –> hypertensive crisis.
Also may unmask suicidality in short-term

107
Q

TCA adverse effect

A

overdose: torsade de pointe

108
Q

SSRIs side-effects

A

safest of the anti-depressants. libido, insomnia. May unmask suicidality in the short-term

109
Q

Potential MOAs of lithium/mood stabilizers

A

stabilize membrane potential? Enhance monamine function?

110
Q

Sedating effects of benzos

A

GABA-A increase. NB: treating Sx, not disorder

111
Q

Benzos with lesser hepatic burden

A

lorazepam, oxazepam, temazepam

112
Q

addiction potential of benzos

A

Fast onset, short duration (e.g. Xanex) has highest addiction potential

113
Q

Two strategies for medicating dementia

A

ACE inhibition, NMDA blockade

114
Q

Absorption of alcohol

A

Rapid, small intestine. Accelerated by CO2, concentration, habituality. Rate predicts BAL

115
Q

Distribution of alcohol

A

Vdist ~ total body water (.5-.7L/kg). Vdiff predicts BAL

116
Q

Metabolism of alcohol (enzymes, kinetics)

A

10% excreted, 90% metabolized. ADH, MEOS (when ADH saturated, byproducts are toxins). ALDH: inhibited by disulfuram. ADH: first order (t1/2~1hr). MEOS: zero-order (8g/hr)

117
Q

unit of alcohol

A

12g

118
Q

alcohol effect on drug metabolism

A

chronic: tolerance. CYP inc, met dec. Occasional: competitive inhibition, met dec.

119
Q

adverse alcohol effects

A

cardiomyopathy, triglycerides, liver failure, reduction and poor function of hematopoiesis and immune system,
lower sleep quality, malignancy, sexual dysfunction, fetal alcohol syndrome. All impacts are dose-dependent

120
Q

Alcohol Abuse Criteria

A

Maladaptive patter of alcohol use leading to significant impairment or distress

121
Q

Alcohol Dependence criteria

A

3+ Sx including tolerance, withdrawal, using more than intended, impairment, use despite consequences, unsuccessfully cutting down. When tolerance or abuse, is dependence with physiological dependence

122
Q

Stages of treatment

A

Identification, detox, rehab, aftercare

123
Q

Alcohol withdrawal (Sx, Tx)

A

Tremor, insomnia, anxiety, sweating, seizures, DTs

Tx: benzos, beta-blockers, anticonvulsants

124
Q

Alcohol relapse prevention Rx

A

Naltrexone (opiod antag), acamprosate (GABA antag), topiramate (anticonvulsant) OK

125
Q

methadone

A

full opiod agonist used for detox. Potential for abuse. Oral, long-acting, cheap. No injection risk. Stable levels (unlike highs/troughs of heroin)

126
Q

Buprenorphine

A

partial opiod agonist used for detox. Difficult to overdose on. Lower level of physical dependence.

127
Q

Naloxone

A

Opiod antagonist. used for relapse prevention. Few side effects. Depot injection

128
Q

Fatal Withdrawals

A

alcohol, benzos, NOT opiates

129
Q

opiate withdrawal

A

not fatal, just sucks

BUT relapse can kill you–> decreased tolerance!

130
Q

General types of alleles predisposing to addiction

A

1) increase euphoria/reward (GABA-A risk allele)

2) decrease experience of adverse effects (alpha-5 Neuronal AChR)

131
Q

Opiod neuroanatomy, action

A 
mu-spinal and supra-spinal
Delta: Spinal (Dorsal horn)
euphoria: VTA DA neurons
Respiratory depression: brainstem
Anti-tussive: brainstem (d-isomers eg dextromethorphan lack euphoria!)
132
Q

Suboxone

A

buprenorphine-naloxone prevents injection

133
Q

A118G opiod allele

A

increases euphoria experienced. Effectively blocked by naltrexone.

134
Q

Depression and medical illness

A

Mortality (not just suicide)
increased prevalence of depression among medically ill (depression associated with getting disease and worse outcomes)
Bidirectional relationship between depression and medical illness

135
Q

Depression and cardiovascular mortality mechanisms

A

Behavioral and lifestyle
Platelet activation
decreases heart rate variability
increased inflammatory response

High-Yield Brain and Behavior Part II (6 decks)

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