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Psych > Midterm > Flashcards

Midterm Flashcards

1
Q

What is epidemiology

A

Pubic health basic science that studies the distribution an determinants of health related states or events in specific populations to control dz and illness and promote health

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2
Q

What are the epidemiological assumptions

A

Disease occurrence is not random, investigation of diff populations can identify associations and causal/preventative factors, making comparisons is cornerstone of systematic dz assessment

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3
Q

What is descriptive epi

A

Frequencies of dz occurnce and patterns of dz (who/where/when)

Used to know if a location or group is experiencing dz more frequently than usual for that group or than other locations

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4
Q

What are the diff kinds of surveillance systems

A
  • passive: relies on healthcare system to reporting diseases
  • active: public health officials go to communities to search for new dz
  • syndromic: looks for pre-denied signs and sx of patients related to diseases
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5
Q

What is outbreak

A

Epidemic limited to localized increase in occurrence of dz; interchanged with cluster

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6
Q

What is epidemic

A

Occurrence of dz in excess of normal expectancy

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7
Q

What is analytic epi

A

Looks at the causes of dz and tries to fix it

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8
Q

What is incidence

A

New occurrences/those at risk

Those NOT at risk = those already with the dz or are immune

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9
Q

What is prevalence

A

Existing and new cases/people in population

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10
Q

What is incidence rate

A

Number of new cases/person-time of people at risk

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11
Q

What is risk

A

Probability of an outcome in a specific group

Probability of outcome in exposed: A/A+B

Probability of outcome in nonexposed: C/C+D

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12
Q

What is absolute risk reduction aka attributable risk

A

Subtract diff in risk btw the 2 groups; AR defines risk diff of outcome attributable to exposure diff btw groups

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13
Q

What is the relative risk reduction

A

Absolute risk reduction/Risk of those unexposed

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14
Q

What is the number needed to treat/harm

A

1/absolute risk reduction

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15
Q

What is a risk ratio

A

Aka relative risk; risk of outcome in exposed/risk of outcome in non-exposed

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16
Q

What are odds

A

Frequent of an outcome occurring vs not occuring in a specific group

In cases: A/C
In controls: B/D

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17
Q

What is an odds ratio

A

Odds of exposure in diseased or outcome/odds of exposure in non-diseased or non-outcome

(AxD)/(BxC)

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18
Q

What are the projections from the VTA to NA

A

Dopaminergic -> released onto NA -> inhibits NA activity = pleasure

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19
Q

What activates VTA

A

Prefrontal cortex (EAA), other tegmental nuclei (Ach or EAA), lateral hypothalamic nucleus (orexin - food)

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20
Q

What are the projections from NA to PFC

A

GABAergic -> inhibits PFC; activation of NA inhibits or prevents pleasure

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21
Q

What activates NA

A

Hippocampus, amygdala, PFC - EAA

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22
Q

What are the projections from NA to VTA

A

GABAergic; also releases dynorphin as cotransmitter -> binds kappa opioid receptors and activates CREB; suppresses further DA release from VTA

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23
Q

What is the dopamine hypothesis of reward

A

Dependence producing drugs activate Mesolimbic DA system releasing DA; reward can also be induced via DA independent mechanisms (opioid pathway)

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24
Q

What do opioids activate

A

VTA; endogenous and exogenous; also activates locus cerouleus and periaqueductal gray

Ex: ethanol activates opioid inputs on the VTA

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25
Q

How do opioids increase DA in the VTA

A

Disinhibition of GABAergic neurons through mu receptors; allows increased dopamine in NA

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26
Q

What does the VTA to prelimbic cortex do

A

Promotes attention toward cues that are good predictors of an outcome relative to other rewards

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27
Q

What does the VTA to amygdala do

A

Cues that inconsistently predict an outcome; uncertain predictors

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28
Q

What does VTA to orbitofrontal Cortex do

A

Promotes attention toward cues that are particularly noticeable even if they are inconsistent predictors

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29
Q

What is the mechanism of long term potentiation

A

Increased phosphorylation of AMPA receptors and insertion of additional AMPA receptors into post-synaptic membrane - eventually activation of calcium-calmodulin-CREB mechanism

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30
Q

What is CREB

A

Camp response element binding protein targeting CRE; within NA, target is dynorphin; in locus cerulus, mediates physical dependency; shorter acting (days) and returns to normal after drug cessation

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31
Q

What is FosB and AP-1

A

Upregulated by stress and drugs of bush; upregulates expression of EAA receptor (AMPA/NMDA), elements of cll signal transduction pathways, factors promoting drug seeking, motivation, locomotion; long term*

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32
Q

What is the role of NFkB in reward

A

Induced within NA nad promotes growth of dendritic spines; increased drug rearward; thought to correlate with addiction and depression; interacts with FosB

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33
Q

What is physical dependence due to physiologically

A

Excessive nor adrenergic output from locus ceruleus;due to CREB dependent upregulation of target genes in LC

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34
Q

What is the diff in conditioning btw drugs and natural rewards

A

Natural rewards cease phasic firing of DA in VTA when event concludes; drugs continue increasing DA release

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35
Q

What is a conditioned response in terms of drugs

A

Cues such as being in a room that you do drugs in

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36
Q

What are drug-associated cues

A

Being around people you do drugs with or drug paraphernalia; elicits symp activation and reward circuits

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37
Q

What are the benzodiazepines

A

Alprazolam, chloridiazepoxie, clonazepam chlorezepate, diazepam, flurazepam, lorazepam, midazolam, oxazepam, triazolam

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38
Q

What drug is a benzodiazepine antagonist

A

Flumazenil

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39
Q

What are the barbiturates

A

Amobarbital, butabarbital, pentobarbital, phenobarbital, secobarbital, thiopental

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40
Q

What are the newer sedative hypnotic drugs

A

Buspirone, chloral hydrate, eszopiclone, hydroxyzine, meprobamate, paraldehyde, ramelteon, zaleplon, zolpidem

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41
Q

What are the drugs for treatment of acute alcohol withdrawal syndrome

A

Diazepam, lorazepam, oxazepam, thiamine

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42
Q

What are the drugs used to prevent alcohol abuse

A

Acamprosate, disulfiram, naltrexone

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43
Q

What are the drugs used for treatment of methanol/ethylene glycol poisoning

A

Ethanol, fomepizole

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44
Q

What are the drugs used to treat dependence and addiction

A
  • opioid receptor antagonist: naloxone, naltrexone
  • synthetic opioid: methadone
  • partial mu agonist: buprenorphine
  • nicotinic receptor partial agonist: varenicline
  • benzo: oxazepam, lorazepam
  • NMDA antagonist: acamprosate
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45
Q

What are the duration of action of each of the benzo

A

Short: triazolam
Intermediate: alprazolam
Long: flurazepam

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46
Q

What are the durations of action of each of the barbiturates

A
  • ultra short: thiopental
  • short: secobarbital
  • long: phenobarbital
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47
Q

What is the diff btw sedative and hypnotic

A

Sedative decreases CNS activity, and calms recipient

Hypnotic produces drowsiness and facilitates onset of sleep

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48
Q

What do sedative hypnotics work on

A

GABAa receptors

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49
Q

What are the features of benzo

A

Crosses BBB, placenta and breast milk; hepatic metabolism (CYP3A4) and renal excretion; cumulative toxicity; enhances chloride influx -> hyperpolarization; risk of dependence and tolerance

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50
Q

What are the advantages and disadvantages of benzo

A
  • Advantages: high therapeutic index, antagonist available,

- disadvantages: risk of dependence, depression of CNS, CNS depression when combined with ethanol*

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51
Q

Which benzo has the fastest onset of action

A

Diazepam (alprazolm is second); longest half life

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52
Q

Which benzo has the slowest onset

A

Oxazepam; shortest half life

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53
Q

Which benzos are intermediate onset of action

A

Lorazepam, clonazepam

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54
Q

Which benzos are most likely to cause cumulative effects with multiple doses

A

Those with long half lives

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55
Q

What are the overall features of barbiturates

A

Crosses BBB, placenta, breast milk; cumulative toxicity; inducers of CYP450; MOA: binds to GABAa and increases duration of GABAa openings; risk of dependence

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56
Q

What are the indictions for diff barbiturates

A

Thiopental: anesthesia
Secobarbital: insomnia
Phenobarbital: seizures

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57
Q

What can be used to treat insomnia

A
  • sedative-hypnotics: benzos cause daytime sleepiness; zolpidem, zaleplon and eszopiclone - min hangover effects
  • Ramelteon: agonist at melatonin receptors; dont give with CYP1A2 inhibitors (fluvoxamine - SSRI); dizziness, fatigue, endocrine changes
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58
Q

What are the features of the newer sleepaids

A

Shorter half lives; bind GABAa with alpha subunit; no anxiolytic, anesthetic, anticonvulsant, muscle relaxing, resp or CV effects

Ex: eszopiclone, zolpidem, zaleplon

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59
Q

What is buspirone

A

Treats generalized anxiety disorder; anxiolytic effects take more than a week* - not used for acute panic disorders; does not cause sedation or euphoria; metabolized by CYP3A4; unknown MOA

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60
Q

What is one drink

A

12 oz of beer, 8 oz of malt liquor, 5 oz of wine, 1.5 oz of 80 proof liquor

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61
Q

What is excessive drinking

A

Binge drinking: 4 for women or 5 for men on single occasion

Heavy drinking: for women 8 or more per week; men 15 or more per week

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62
Q

How is alcohol metabolized

A

Alcohol -> acetaldehyde via alcohola DH -> acetic acid via acetaldehyde DH -> carbon dioxide and water via oxygen

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63
Q

What kinetics is alcohol metabolized through

A

Zero order; t1/2 increases with dose

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64
Q

What is naltrexone used for in terms of alcohol

A

Reduces craving for alcohol; must be alcohol and opioid free before starting treatment

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65
Q

What is acamprosate

A

NMDA antagonist and GABAa agonist; reduces short and long term relapses

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66
Q

What is disulfiram

A

Irreversibly inhibits aldehyde DH and causes extreme discomfort in patients who rink alcohol; do not administer with any meds that contain alcohol

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67
Q

What is a schedule I drug

A

High addiction potential; flunitrazepam, heroin, LSD, mescaline, PCP, MDA, MDMA, STP

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68
Q

What are schedule II drugs

A

Amphetamines, cocaine, methylphenidate, short acting barbiturates, strong opioids

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69
Q

What are schedule III drugs

A

Anabolic steroids, barbiturates, dronbinol, ketamine, moderate opioid agonists

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70
Q

What are schedule IV drugs

A

Benzo, chloral hydrate, mild stimulates, most hypnotics, weak opioids

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71
Q

What are the effects of alcohol use

A

Normal pupil size, normal convergence, normal temp, high pulse, high BP

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72
Q

What are signs of tobacco use

A

Normal pupils, convergence and temp, high BP and pulse

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73
Q

What are signs of marijuana use

A

Dilated pupils, lack of convergence, normal temp, high BP and pulse; slower time estimation; eyelid tumors

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74
Q

What are the signs if inhalant use

A

Not detectable by drug test; normal pupils, lack of convergence; varied temp, high BP an pulse; faster time estimation; nausea, HA, disoriented

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75
Q

What are the signs of stimulant use

A

Dilated pupils, normal convergence, higher temp, BP and pulse; faster time estimation; jittery, talkative, runny nose or dry mouth

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76
Q

What are the signs of depressant use

A

Normal pupil size, lack of convergence, Normal temp; lower BP and pulse; slower time estimation

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77
Q

What are the signs of hallucinogen use

A

Dilated pupils, normal convergence; higher temp, BP and pulse; slower movement; spacey, hallucinations, paranoia, memory loss, uncoordinated

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78
Q

What are the signs of narcotic use

A

Constricted pupils, normal convergence; lower temp, BP and pulse; slower movement; sleepiness, droopy eyelids, soft low voice

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79
Q

What are the signs of PCP use

A

Normal pupils, lack of convergence; higher Temp, BP and pulse; faster movement; confused, aggressive, sweaty, repetitive

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80
Q

What are the OD effects of amphetamines, methylphenidate and cocaine

A

Agitation, HTN, tach, delusions, hallucinations, hyperthermia, seizures, death

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81
Q

What are the OD effects of barbiturates, benzo, ethanol

A

Slurred speech, dilated pupils, weak and rapid pulse, clammy skin, shallow respiration, coma, death

Withdrawal: anxiety, insomnia, tremors, seizures

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82
Q

What are the OD effects of heroin

A

Constricted pupils, clammy skin, nausea, drowsiness, resp depression, coma death

Withdrawal: nausea, chills, cramps, lacrimation, rhinorrhea, yawning, hyperpnea, tremo

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83
Q

What drugs of abuse are not necessarily additive

A

LSD, mescaline, psilocybin, phencyclidine (PCP), Ketamine

Long term effects: PCP - schizophrenia like psychosis; LSD - flashbacks of altered perception years after consumption

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84
Q

What drugs are approved for use in patients with dementia

A

Donepezil, galantamine, rivastigmine

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85
Q

What is memantine

A

Antagonist of N-methyl-D-aspartame NDMA type of glutamate receptor; binds to magnesium site with longer action and functions as receptor blocker only under conditions of excessive stimulation; used for dementia

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86
Q

What are the stimulant vs non-stimulant ADHD meds

A
  • stimulants: amphetamine, dextroamphetamine, lisdexamfetamine (prodrug), methylphenidate, dexmethylphenidate
  • non-stimulants: atomoxetine, guanfacine, clonidine
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87
Q

How do stimulants for ADHD work

A

Block presynaptic reuptake, interfere with vesicular monoamine transporter (VMAT) and increase NT release (NE, then DA then 5HT)

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88
Q

What is methylphenidate main activity

A

Inhibition of DA reuptake and inhibition of NT pre-synaptic reuptake - doesn’t stimulate NT release

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89
Q

What are the side effects of stimulants

A

ab pain, HA, decreased appetite, insomnia, reduced growth progression, anxiety, irritability, elevated BP/HR

RARE: priapism, seizures, sudden cardiac death - always assess for cardiac structural abnormaltieis, stroke and MI in adults, chemical leukoderma with daytrana patch

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90
Q

What are the formulation abbreviations

A

Immediate release(IR), extended release (ER), long acting (LA), controlled delivery (CD), oral disintegrating tablet (ODT)

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91
Q

What cautions should you take when administering stimulates

A

Consider if patient has glaucoma, HTN, Tourette’s, bipolar, seizures, history of drug abuse

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92
Q

What is the onset of activity of stimulants

A

Usually within 24 hours; controlled substances - *1 month supply only, no refills, no samples

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93
Q

What are the immediate release amphetamine based stimulants

A
  • dextroamphetamine (Adderall): duration 4-6 hours; tablet
  • dextroamphetamine sulfate (ProCentra): 4-6 hours; liquid
  • amphetamine sulfate (Evekeo): 4-6 hours; capsule
  • dextroamphetamine (Zenzidi): 4-6 hours; tablet
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94
Q

What are the extended release amphetamine based stimulants

A
  • dextroamphetamine Adderrall XR: 8-12 hours; capsule
  • Dextroamphetamine (Dexedrine): capsule
  • amphetamine (dyanavel): 13 hours; liquid
  • lisdexamfetamine (Vyvanse): 10-12 hours; capsule
  • amphetamine (Mydayis)mixed salts): 16. Hours; capsule
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95
Q

What is adzenys XR-ODT

A

3:1 ratio of d-amphetamine and l-amphatamine; 50% IR and 50% XR; no water necessary approved for ages 6 and older qd dosing

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96
Q

What are the immediate release methylphenidate based stimulants

A
  • dexmethylphenidate (focalin): 4-6 hours; tablet
  • methylphenidate (methylin): 3-4 liquid
  • methylphenidate (Ritalin): 3-4 tablet
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97
Q

What are the sustained release methylphenidate based stimulants

A
  • methylphenidate(Ritalin SR): 4-8 hours tablet

- methamphetamine (Desoxyn): 4-8 hours tablet

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98
Q

What are the extended release methylphenidate based stimulants

A
  • methylphenidate (Aptensio): 12 hours capsule
  • methylphenidate HCL (concerta): 10-12 hours tablet
  • methylphenidate ER ODT (contempla): 12 hours tablet
  • methylphenidate transdermal (daytrana): 10-12 hrs transdermal patch
  • dexmethylphenidate HCl (focalin):6-10 hrs capsule
  • methylphenidate HCl (metadate): 8-10 hours capsule
  • methylphenidate HCl (Quillichew): 8 hours chewable tablet
  • methylphenidate (quillivant): 8-12 hrs liquid.
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99
Q

What is the effect of non-stimulant drugs for ADHD

A

Inhibition of NE pre-synaptic reuptake (atomoxetine); agonists of CNS alpha 2a receptors (guanfacine and clonidine) -modulate tone by enhanced input from locus ceruleus and direct postsynaptic stimulation of alpha 2a receptors on dendritic spins of cortical pyramidal cells promoting functional connectivity of PFC

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100
Q

What is the duration of onset for non-stimulants

A

1-4 weeks; useful for patient intolerant of stimulants; non scheduled

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101
Q

What are the features of atomoxetine

A

aka strattera ER; 24 hours; capsule; can lead to liver injury or suicidal thoughts; do not open capsules; met by CP2D6; approved for 6 and over; qd dosing

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102
Q

What are the features of the antiHTN non-stimulants for ADHD

A

Both are ER, 12-24 hours; tablet

*do not crush, chew or break tablets, 6 and up, qd dosing; downward titration upon discontinuation - rebound HTN

103
Q

What is the limbic system involved in

A

Emotional behavior, motivational drives

104
Q

What is the hypothalamus involved in

A

Emotional experience phys response to emotion

105
Q

What part of the limbic system deals with olfaction

A

Olfactory areas (paraolfactory)

106
Q

What is the thalamus function in limbic system

A

Anterior nucleus is part of papez circuit

107
Q

What emotion is the parahippocampal region linked to

A

Surprise

108
Q

What is the cingulate cortex role in limbic system

A

After-discharge - still angry after event

109
Q

What pathways do sensory inputs travel through to create fear

A
  • direct thalamo-amygdaloid pathway to lateral nucleus of amygdala: rapid response
  • indirect thalamo-cortico-amygdaloid pathway to lateral nucleus of amygdala: later responses
110
Q

What does the lateral nucleus of the amygdala do

A

Integrates inputs of fear (ie: sound and electrical shock)

111
Q

Where is the information of fear sent after lateral nucleus

A

Basal and intercalated nuclei for additional processing then to central nucleus of amygdala which decides what responses are required and relays this info to hypothalamus

112
Q

What does anger require

A

Dopamine acting at D2 receptors

113
Q

What parts of the brain are required for inhibition of anger

A

Neocortex, ventromedial hypothalamic nuclei, septal nuclei

114
Q

What part of the brain is involved in sadness

A

Lower sector of anterior cingulate cortex, strongly activated when recalling sad events

115
Q

What part of the brain is involved in disgust

A

Insular cortex and putamen; damage (Huntington’s) abolishes this

116
Q

What part of the anterior cingulate cortex is important in emotion

A

Ventral

117
Q

What is the role of the cortex in emotion

A

Integration of visceral, attentional and emotional input; regulation of affect, monitors or detects conflict btw functional state (right now) and nw into - relays info to PFC

118
Q

What are the divisions of the PFC

A
  • dorsolateral: receives input from motor areas, cingulate cortex
  • ventromedial: receives input from amygdala, hippocampus, temporal visual association cortex, dorsolateral PFC
119
Q

What does the orbitofrontal cortex do

A

Reward processing; link new stimulus to a primary reward

120
Q

What does the ventromedial PFC do

A

Integrations of bodily signals; “gut feeling” - decision when logical analysis is unable to help

121
Q

What makes up the mediational system for language

A

Areas in temporal, parietal and frontal association areas - relays info to language implementation system from the conceptual system

122
Q

What is the conceptual system for language

A

Broadly distributed set of structures that provides concepts underlying our language; ex: noun mediation area receives input from ventral visual pathway and provides us with names of things

123
Q

Where does a second language learned after language acquisition phase activate

A

Adjacent region of Brocas

124
Q

What are the components of social cognition

A

Emotional comprehension and theory of mind

125
Q

What is social cognition

A

Ability to infer emotional state from observable info

126
Q

What part of the brain are faces stored

A

Superior temporal sulcus and fusiform gyrus

127
Q

What areas bring in the emotional component to social cognition

A

Anterior cingulate cortex, PFC, amygdala

128
Q

What part of the brain focuses our eyes on the “triangle” of the face

A

Amygdala

129
Q

What part of the brain identifies the motor action of emotional recognition

A

Posterior mirror neuron system

130
Q

What part of the brain identifies the goal of the action in emotional response

A

Anterior mirror neuron system (ie: why the person is making an angry face)

131
Q

Where is the circuit for imitating behavior

A

Interacts with limbic structures via insula

132
Q

What is prosody

A

Study of tune and rhythm of speech and how these features contribute to meaning

133
Q

What is involved in perception of prosody

A

primary auditory cortex is required for basics of sound processing including identity of pitch, loudness, etc; that info is sent to right posterior superior temporal sulcus where we begin to piece together the meaning of the pitch etc; then sent to frontal cortex where we decide the judgment of emotional stimulus

134
Q

What is theory of mind

A

Ability to understand the mental states of others

135
Q

What is the core pathway of the theory of mind

A

Amygdala and connections to medial temporal lobes (memory) and orbitofrontal areas (sensory and emotional processing)

136
Q

What is the accessory pathway of theory of mind

A

Language - serves as scaffold;; becomes less important as ages

137
Q

What part of the brain evaluates the evidence available in making decisions

A

Stimulus encoding system; orbitofrontal cortex, ventromedial PFC, striatum

138
Q

What part of the brain learns and encodes subjective value of results in decision making as well as error detection

A

Action selection system - anterior cingulate cortex

139
Q

What predicts the expected reward in decision making

A

Basal ganglia, amygdala, insular cortex (social emotion) intraparietal cortex (somatosensory processing and planning/intent)

140
Q

What part of the brain is involved in explicit decision making (known risk)

A

Stimulus encoding system

141
Q

What part of the brain is involving in ambiguous risk

A

Expected reward system and eventually on action selection system

142
Q

what study designs have an increasing strength of evidence

A
  • interventional: phase 0-phase 4 (strongest)
  • observational: cross sectional -> case control -> cohort (strongest)

Interventional is strongest overall

143
Q

What is internal vs external validity

A

Internal: were study methods appropriate
External: does this apply to general public

144
Q

What are case-control studies useful for

A

Studying rare dz; generates odds of exposure and odds ratio

145
Q

What is study group allocations vs group definition

A

Allocation: based on exposure
Definition: group with commonality

146
Q

What is a cohort study useful for

A

Rare exposure; generates risk of disease and risk ratio; useful for assessing multiple outcomes of one exposure; can be ambidirectional; good for long induction/latent periods; able to represent temporality (prospective)

147
Q

Are cohort studies prospective or retrospective

A

Both

148
Q

What kind of study is a cross sectional study

A

Prevalence; no regard to exposure or disease/outcome

149
Q

What is pre-clinical part of interventional study

A

Prior to human investigation bench or animal research

150
Q

What is phase 0 of an interventional study

A

Assesses drug target actions and pharmacokinetics in non-therapeutic non-diagnostic doses - first in human use; healthy or diseased patients; N<20; very short duration

151
Q

What is phase 1 of an interventional study

A

Assesses safety/tolerance and pharmacokinetics of 1 or more dosages; healthy or diseased volunteers; small N (20-80); short duration days to weeks

152
Q

What is phase 2 of an interventional study

A

Assesses effectiveness*; diseased volunteers - may have narrow inclusion criteria; larger N (few to several hundred) short to medium duration few weeks - few months

153
Q

What is phase 3 of interventional study

A

Assesses effectiveness; diseased patients; may expand inclusion criteria and comparison groups; can test superiority, noninferiority, equivalency; larger N (several hundred to few thousand); longer duration; few months to a year

154
Q

What is phase 4 of interventional study

A

Post FDA approval; assesses long term safety, effectiveness and risk/benefits; diseased patient expand use criteria; larger population (few hundred to tens of thousands); longer durations months to several years

155
Q

What is a simple interventional study design

A

Subjects randomly allocated once into single treatment group; no further randomization

156
Q

What is factorial interventional study design

A

Subjects randomly allocated into initial group then further randomly divided into sub group

*useful in testing multiple hypotheses at same time - increases sample size requirement

157
Q

What is a parallel interventional study design

A

Subjects simultaneously yet exclusively managed in a single treatment group; *no switching groups after initial randomization

158
Q

What is a cross over aka self control interventional study

A

Subjects forcibly switched to other treatment group after initial treatment assignment

*allows for btwn and within group comparison; need wash out or lead in

159
Q

What is random vs non random group allocation

A
  • random: subjects have equal probability of being assigned to group; random number generator programs
  • non-random: odd/even days; every other patient; first 20 treated
160
Q

What are forms of randomization

A
  • simple: equal probability for allocation into one of the groups
  • blocked: ensures balance within each intervention group
  • stratified: ensures balance within known confounding variables
161
Q

What are the aspects of the Belmont report

A
  • respect for persons: research voluntary and autonomous
  • beneficence: risks justified by benefits
  • justice: risks and benefits equally distributed
162
Q

What is the diff btw consent an assent

A
  • consent: agreement to participate given by mentally capable individuals of legal consenting age
  • assent: agreement given by mentally capable individuals not able o give legal consent (children/adolescents)
163
Q

What is an open label study

A

Unmasked, unblinded

164
Q

What is a lead-in phase (aka run in )

A

Subjects given a placebo for initial pre-study time frame to determine new baseline of dz; can also study protocol compliance

165
Q

What are the levels of IRB review

A
  • full board: used for all interventional trials; more than low-to min risk
  • expedited: low-to-minimal risk; no patient identifiers
  • exempt: chart review or existing samples/data with no patient identifiers, no risk, environmental studies
166
Q

What is equipoise

A

Confidence that intervention/treatment may be worthwhile in order to use it in humans

167
Q

What is the data and safety monitoring board

A

Semi-independent committee not involved with conduct of study but reviews data as study progresses to assess for undue risk or benefit; can stop study early; pre-determined review periods

168
Q

How do you manage drop outs/lost to follow patients in interventional studies

A
  • include them: intent to treat; use last known assessment or baseline assessment or baseline assessment for all evaluations
  • exclude them: per protocol aka efficacy analysis; must meet pre-established level of compliance/participation to be included
169
Q

What does intent to teat vs per protocol restful in

A
  • intent to treat: preserves randomization, baseline characteristics and group balance, controls for cofounders, maintains statistical power
  • per-protocol: biases estimates of effect (over-estimates), can limit generalizability
170
Q

What are the advantages of interventional trials

A

Cause precedes effect- can demonstration causation only designs used by FDA for approval process

171
Q

What are the disadvantages of interventional trials

A

Cost, complexity, time, ethical considerations, generalizability

172
Q

What is addiction

A

Chronic dz of brain reward, motivation, memory and related circuitry

173
Q

What is the addictophrenia model

A

Developed for assessment of dz risk and severity

174
Q

What is type I alcoholism

A

Affects both men and women; requires presence of genetic and environmental predisposition, commences later in life after years of heavy drinking and can be either mild or severe

175
Q

What is type II alcoholism

A

Affects mainly sons of male alcoholics; influenced only weakly by environmental factors; beings during adolescence or early adulthood; moderate severity and usually assoc with criminal behavior

176
Q

What is addictophrenia type I

A

Genetic hx of addictive disorder; predominantly alcohol; genetic hx of diagnosable mood disorder; higher incidence of comorbid mood disorder

177
Q

What is addictophrenia type II

A

Genetic hx of addictive disorder - mixed substance abuse and non-substance related addictive disorders; genetic hx of personality disorder or criminal behavior; higher incidence of criminal behavior, risk taking, and gambling

178
Q

What is addictophrenia type III

A

Genetic hx of addictive disorder - not a prerequisite but increases vulnerability significant hx of trauma (predominantly alc and benzo use)

179
Q

What is addictophrenia type IV

A

Genetic hx of addictive disorder - not prerequisite but increases vulnerability; chronic use of high dose drugs known to cause severe physical dependency; highly associated with presence of severe psychosocial stressors

180
Q

What is substance use disorder

A

Using larger amounts for longer time than intended, persistent desire or unsuccessful attempts to cut down or control use, great deal of time obtaining, using or recovering, craving, fail to fulfill major roles, persistent social or interpersonal problems

181
Q

What substances usually do not have withdrawal

A

PCP, inhalants, hallucinogens

182
Q

What is the severity of substance abuse disorder depend on

A
  • mild: 2-3 symptoms
  • moderate: 4-5
  • Severe: 6 or more
183
Q

What are the substance use disorder specifiers

A
  • in early remission: no criteria for >3 months but <12 months, except for craving
  • in sustained remission: no criteria for >12 months except craving
  • in controlled environment: access to substance restricted
184
Q

What are substance induced mental disorders

A

Develops during or within 1 month of substance intoxication or withdrawal or taking a medication and the involved substance is capable of producing mental disorder

185
Q

What does the clinical presentation of intoxication depend on

A

Substance, dose, route of administration, duration, individual degree of tolerance, time since last dose, person’s expectations of substance effect

186
Q

What is pharmacokinetic vs pharmacodynamic neuroadaptation

A
  • pharmacokinetic: adaptation of metabolizing system

- pharmacodynamic: ability of CNS to function despite high blood levels

187
Q

What are your options for where to treat drug abuse

A
  • hospital: drug OD, risk of severe withdrawal, medical comorbidities, requires restricted access to drugs, psychiatric illness with suicidal ideation
  • residential treatment unit: on intensive medical/psych monitoring needs, requires restricted environment, partial hospitalization
  • outpatient: no risk of med/psych morbidity and highly motivated patient
188
Q

What are the components of alcohol withdrawal

A
  • early: anxiety, irritability, tremor, HA, insomnia, nausea, HTN, hyperthermia, hyperactive reflexes
  • seizures: generally an 24-48 hours; most often grand mal
  • withdrawal delirium btw 48-72 hours; altered mental status, hallucinations, marked autonomic instability, life threatening
189
Q

What is delirium tremens

A

Most severe manifestation of alcohol withdrawal; 3-10 days following last drink; agitation, global confusion, disorientation, hallucinations, fever, HTN, diaphoresis, autonomic hyperactivity

Loss of GABA stimulation causes reduction in chloride influx and lack of NMDA inhibition

190
Q

What is CIWA

A

Clinical institute withdrawal assessment; assigns numerical values to orientation, N/V, tremor, sweating, anxiety, agitation, tactile/auditory/visual disturbances and HA; VS checked but not recorded; score >10 indicates more severe withdrawal

191
Q

What is the treatment for alcohol withdrawal

A

Benzo, anticonvulsants (carbamazepine or valproic acid)

192
Q

What should you check when giving naltrexone or acamprosate

A
  • naltrexone: LFT

- acamprosate: kidney

193
Q

What benzo/barbiturates would be more addicting

A

Lipophilic and shorter acting

194
Q

What is benzo withdrawal

A

Anxiety, irritability, insomnia, fatigue, HA, tremor, sweating, poor concentration; sx worsen at end of taper; convert short elimination to longer half life then taper;

195
Q

What benzos are the only ones not affected by hepatic insufficiency

A

Oxazepam, temazepan, lorazepam

196
Q

What are the sx of opioid intoxication

A

Pinpoint pupils, sedation, constipation, bradycardia, hypotension, decreased respiration

197
Q

What are the sx of opioid withdrawal

A

Not life threatening; dilated pupils, lacrimation, goosebumps, N/V/D, myalgias, dysphoria

198
Q

How do you treat opioid withdrawal

A

Anti-emetic, antacid, antidiarrheal, muscle relaxant (methocarbmol), NSAIDs, clonidine, and BZD

199
Q

What meds can be used for opiate use disorder

A

Methadone, naltrexone, buprenorphine

200
Q

What are the features of methadone maintenance

A

Only availed through medication assisted treatment program; oral solution only; high risk*; can be deadly with benzo - QTC prolongation *cyp3A4

201
Q

What should you do if a methadone maintenance patient needs pain meds

A

Verify dosage of methadone; correct methadone dosage continued while patient is hospitalized; use another opioid but not cyp3A4 substrate (NO BENZO)

202
Q

What is buprenorphine

A

Partial mu agonist with ceiling effect; physician needs to be certified ASAM; helpful for highly motivated people

203
Q

What are the sx of chronic intoxication of stimulants

A

Affective blunting, fatigue, sadness, social withdrawal, hypotension, bradycardia, muscle weakness, psychosis*

204
Q

What are sx of withdrawal from stimulants

A

Severe and suicidal depression

205
Q

What are the possible effects of Cocaine use

A

CVA MI, rhabdo with compartment syndrome, psychosis; prevent reuptake of DA

206
Q

What are the treatments options of stimulant use disorder

A

Narcotics anonymous; no meds approved

207
Q

What does chronic use of amphetamines result in

A

Neurotoxicity; can be fatal in Brugada syndrome; can cause permanent amphetamine psychosis; inhibits reuptake of DA, NE, SE

208
Q

What are the drug interactions of tobacco

A

Induces CYP1A2; watch with olanzapine - causes release of DA in nucleus accumbens; rapid tolerance; withdrawal - dysphoria, anxiety, decreased concentration increased appetite

209
Q

What meds are used for tobacco use disorders

A

Bupropion, varenicline

210
Q

What are the hallucinogens

A
  • natural: peyote cactus (mescaline), shrooms (psilocybin)
  • synthetic: LSD
  • DMT (dimethyltrypatmine): smoked, snuffed, IV
  • STP: oral
  • MDMA: ecstasy - oral
211
Q

What are the features of MDMA

A

Enhanced empathy, personal insight, euphoria, increased energy; 3-6 hours intoxication - illusions, hyperacusis, sensitivity of touch, taste, smell, tearfulness, euphoria, panic, paranoias; tolerance develops quickly and unpleasant side effects with continued use (teeth grinding) so dependence less likely

212
Q

What are the short term problems with MDMA use

A

Tachycardia, sweating, muscle spasms, extremely high temp - can progress to rhabdo, renal failure, seizures, DIC, death

213
Q

What is the neuroadaptation of MDMA

A

Affects serotonin, primarily 5HT2 receptor agonist; psychosis; serotonin neural injury assoc with panic anxiety, flashbacks, psychosis, cognitive change

214
Q

What are the features of cannabis intoxication

A

Increased appetite and thirst, sensations clearer, increased confidence, increased libido, severe panic attacks, transient depresssion, tachycardia, dry mouth, slowed reaction time

215
Q

What is the neuroadaptation of cannabis

A

CB1/2 agonists -> GPCR -> inhibits calcium influx -> decreased uptake of GABA and DA

216
Q

What are the negatives to cannabis

A

Adolescent males who use regularly have a 7fold increased risk of psychosis; frequently worsens comorbid psych problems; withdrawal: insomnia, anxiety, poor appetite, depression

217
Q

What is phenacyclidine (PCP)

A

Angel dust; dissociative anesthetic; similar to ketamine; intoxication: severe dissociative reactions - paranoid delusions and hallucinations can become very violent with decreased awareness of pain; cerebellar symptoms *nystagmus - horizontal and vertical; with severe OD - mute, catatonic, muscle rigidity, HTN, hyperthermia, rhabdo, seizures, coma

218
Q

What is the treatment for PCP abuse

A

Antipsychotic drugs, BZD, low stimulation environment, acidity urine if severe toxicity

219
Q

What is the neuroadaptation of PCP

A

Opiate receptor effects; allosteric modulator of NMDA receptor; no tolerance or withdrawal

220
Q

What subtype of ADHD do females most commonly present with

A

Inattentive subtype

221
Q

What is Tourette’s syndrome triad

A

Motor and vocal tics that are chronic (> 1 year); associated with OCD that do not always meet full criteria and disturbances of attention that do not always meet ADHD criteria

*boys more likely to have ADHD and tics - girls more likely to have OCD

222
Q

What can tics be exacerbated by

A

The stimulants used to treat ADHD

223
Q

What mental health issue was linked to the most suicides i the 5-14 year old age group

A

ADHD

224
Q

What are the parts of executive functioning

A

Ability to assess a situation, prioritize what is relevant, filter out extraneous info, make a plan, execute plan, assess effect of action in a fluid manner

225
Q

What is ADHD due to

A

Deficiency of dopamine and NE

226
Q

What is the region that is dysfunctional in ADHD

A

Dorsal anterior midcingulate gyrus

227
Q

What regions have a decreased activation in patients with ADHD in inhibition tasks

A
  • right inferior PFC extending to insula
  • supplementary motor area
  • cognitive division of anterior cingulate cortex
  • left caudate extending into putamen and insula and right mid thalamus
228
Q

What regions have a decreased activity in patients with ADHD during attention tasks

A
  • right dorsolateral PFC
  • left putamen and globules pallidus
  • right posterior thalamus and caudate tail extending to posterior insula
  • right inferior parietal lobe
  • precuneus and superior temporal lobe
229
Q

What regions have increased activity in patients with ADHD during attention tasks

A
  • left cuneus

- right cerebelllum

230
Q

What are the diagnostic criteria for ADHD

A

Need 6 or more sx; in people older than 17 need at least 5 sx

231
Q

What is the inattentive type of ADHD

A

Fails to give close attention to details or makes careless mistakes, has difficulty sustaining attention, does not appear to listen, struggles to follow through on instructions, has difficulty with organization, avoids or dislikes tasks requiring a lot of thinking, loses things, is easily distracted, is forgetful in daily activities

232
Q

What is the hyperactive type of ADHD

A

Fidgets with hands or feet or squirms in chair, difficulty remaining seated, runs about or climbs excessively (children) restless (adults), difficulty engaging in activities quietly, acts as if driven by a motor, talks excessively, blurts out answers before questions have been completed, difficulty waiting or taking turns

233
Q

What developmental hx should you ask for ADHD

A

Difficulties during pregnancy; reaching milestones, sick as a child

234
Q

What medical hx should you ask for ADHD

A

Accidents, loss of consciousness, seizures, trauma, surgery, cardiac ab

235
Q

What family hx should you ask for ADHD

A

Hx of psych disorder, cardiac ab, substance abuse

236
Q

What is TOVA

A

Test of variables of attention: measures reaction time, can be used in all ages, shorter test for young kids

237
Q

What is conners continuous performance test

A

Same as TOVA but for older than 8; administration time is 15 min

238
Q

What is the treatment for ADHD

A

Cutting back on yelling, criticism and other harsh parenting approaches;

  • for ages 4-5: parent and teacher administered behavior therapy is first line; then give methylphenidate if doesn’t work (still has moderate - severe sx)
  • for 6-11: FDA approved meds for ADHD (stimulants) with parentteacher behavior therapy
  • 12-18 same as above
239
Q

What can bupropion increase the risk for

A

Seizure

240
Q

What does atomoxetine do

A

Inhibits NE reuptake; can cause QT prolongation

241
Q

Who is modafinil used in

A

Adults with ADHD; binds to dopamine transporter ad inhibits DA reuptake; assoc with Steven Johnson, anxiety, mania, hallucinations, and suicidal ideation

242
Q

What is the main diff btw methylphenidate and amphetamine

A
  • methylphenidate: pure reuptake inhibitor or catecholamines, esp DA
  • amphetamine: reuptake inhibitor of catecholamines and also releases catecholamines
243
Q

What are the advantages of methylphenidate

A

Better CPT response, better with comorobid Tourette’s, better with visuo-motor disorder, less anorexia, less sleep delay

244
Q

What are the advantages of amphetamine

A

More consistent response day to day, higher proportion of patients with good/excellent response, better with comorbid conduct disorder, less depression/apathy, fewer stomachaches, may be better with high IQ

245
Q

What emotion is the anterior cingulate cortex responsible for

A

Sadness

246
Q

What is the ventral anterior cingulate cortex used for

A

Integration of sensory and emotional processing, controlling emotion (poker face vs crying), new info that has the power to change how I’m feeling (confluent detection)

247
Q

What is team based care

A

Provision of health services by at lest 2 health providers who work collaboratively with patients and their caregivers to the extent preferred by each patient

248
Q

What are the parts of patient centered medical home

A
  • comprehensive care
  • patient-centered
  • coordinated care
  • accessible services
  • quality and safety
249
Q

What are the benefits of integrated care

A

Improved patient experience and outcome, decreased healthcare expenditures, improved access to care, improved provider satisfaction, cultural competence

250
Q

What is the triple aim

A

Improving patient experience of care, improving health of populations, reducing per capita cost of health care

251
Q

What does a fully integrated care team look like

A

Shared treatment space, shared provision and medical records, full collaboration, team huddles, treatment plans shared and mutually supported, scope of problems targeted

252
Q

What functions can a BHC provide to assist physicians

A

Assessment, education, brief intervention, referral, warm hand offs, chronic illness, mental health disorders, prevention, quality improvement and quality assurance, pain management, substance misuse, improved communication btw provider and patient

253
Q

What are the stages of motivational interviewing

A
  • precontemplation
  • contemplation
  • determination
  • action
  • maintenance
  • recurrence

Psych (2 decks)

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