Behavioral Science Flashcards
(131 cards)
1
Q
Quantative
A
Numbers
2
Q
Qualitative
A
Words express data
3
Q
Observational studies increasing strength ofevidence
A
Cross sectional
4
Q
Best evidence
A
Meta analysis and systemic reviews
5
Q
Population vs sample
A
All in a common group, and subset o population usually made with random processes
6
Q
Null hypothesis
A
No true difference between the groups
7
Q
Alternative hypothesis
A
Will be a difference between the groups
8
Q
Prospective, retrospective, ambidirectional
A
Outcome not known, outcome is known at start, look back then forward for additional occurrences
9
Q
2 key questions to see sting study design
A
- Allocating or forced intervention? This is interventional or observational
- For observational studies, how were groups organized
By disease-case control/nested case control
Be exposure-cohort
Together with common factor-cohort
Data collected across large pop-cross sectional
10
Q
Case control
A
Disease vs no, look back on exposure
Rare disease. Low incidence/low prevelance/long latency. RETROSPECTIVE
OR
11
Q
Nested case control
A
Case control study Derived out of or conducted after a prospective previous study type
Used to evaluate other exposures
12
Q
A cohort study may not always do what
A
Describe how groups are allocated
13
Q
Strength cohort
A
Low occurrence, association, multiple outcomes of one exposure, long induction/latent periods, temporality, less ethical issues
14
Q
Cross sectional study
A
Prevelance study.
Study exposure and disease at the same time
Snapshot
15
Q
Phase 0
A
- Small number
16
Q
Phase 1.
A
Safety/tolerance of doses
Small n
Short duration
17
Q
Phase 2
A
Effectiveness
18
Q
Phase 3
A
Superiority
19
Q
Stage 4
A
FDA approval
20
Q
Simple interventional studies
A
Subjects randomly allocated once into a single treatment group
-no further randomizations into subtreatment groups
21
Q
Factorial intervention
A
Subjects randomly allocated into an initial group, then further randomly-divided into a subgroup
-multiple randomizations
22
Q
Parallel intervention
A
Subjects simultaneously yet exclusively managed in a single treatment
No switching groups after initial randomization
23
Q
Cross over
A
Subjects switched to other treatment group after initial treatment assignment
24
Q
Consent
A
Agree to participatedbased on being informed given by mentally capable individuals of legal consent
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Assent
Agreement to participate after informed, mentally capable individuals not able to give legal consent
Kids babies
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Advantage to interventional
Cause precedes effect
Only designs used by FDA
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Incidence
New occurrences of an outcome/event/disease (included.added)
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Prevelance
Existing occurrences of an outcome
Previously occurring plus new cases, collectively
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Calculate incidence
New cases/ppl at risk
Always subtract out those who are not at risk (already have disease/outcome or are immune)
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NNT NNH
patients needed to be treated to receive the stated benefit/harm
1/ARR
Take the difference in risks between 2 groups and place that difference in decimal form in the denominator below the value of 1
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OR
A/C/B/D
Or
AD/BC
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RR OR HR 1.8
80% increased risk
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1 RR OR HR
No difference
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.25 RR OR HR
75% decreased risk/odds/hazard
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When looking at the CI rations (RR/OR/HR) if both values are on the same side of 1 (equality0 it is always
Statistically significant
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ADHD meds
Stimulants and non stimulants
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Stimulants
Amphetamine, dextroamphetamie
Lisdexamfetamine
Methylphenidate
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Non stimulants ADHD
Atomoxetine
Guanfacine
Clonidine
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Stimulants
Enhance NT transmission by serving as direct and indirect non catecholamines sympathomimetics
Block presynaptic reuptake, interference with vesicular monoamine transporter VMAT, increase NT release (NE then DA then serotonin)
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D vs L isomers of AMP/MPH
D more CNS than L
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Methylphenidate
Inhibit DA reuptake n inhibition of NT presynaptic reuptake
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MPH
Doesn’t stimulate release of NT
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AE stimulants
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Dyspepsia/GI
HA
Decreased appetite
Insomnia
Anxiety/jitters
Irritability/aggression
Elevated BP/HR
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Rare bad AE stimulants
Priapism, seizures, sudden cardiac death-ALWAYS ASSESS FOR CARDIAC STRUCTURAL ABNORMALITIES
Stroke and MI
Chemical leukoderma-big white patch
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Who not use stimulant in
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Anxiety/agitation
CV disease
Moderate or bad HTN
Glaucoma
Motor tics tourettes
Ineffectively treated bipolar / psychoses
Poorly controlled seizures
History of drug abuse
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What r stimulants
CONTOLLED SUBSTANCE
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What are the amphetamine based stimulants for ADHD
Dextroamphetamine
Amphetamine
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AE dextroamphetamine
HA, insomnia, circulation prob, decreased appetite, slowing of growth new psychotic problems
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Amphetamine ae
Mood changes, new or worse bipolar illness, aggressive behavior
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How long those work
4-6 hr
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Extended release amphetamine
8-12 hours
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What are extended release
Dextroamphetamine, amphetamine, lisdexamfetamine
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Non-ir forms
Adzenys X-RAY-ODT
Amphetamine d and l 50.50 ratio
No water necessary
For 6 and over
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Methylphenidate based stimulants
Dexmethylphenidate
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Methylphenidate
4-6 hrs
HA, insomnia, circulation problems, decreased appetite, slowing of growth new psychotic problems
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Sustained release methylphenidate
Methylphenidate
| 4-8 hrs
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AE extended release methylphenidate
HA, insomnia, circulation problems, decreased appetite, slowing of growth new psychotic problems, nervousness, dizziness, diarrhea, constipation, increased tics, stroke, mi, increase BP HT, worse bipolar illness, runny nose, dry mouth, ABUSE
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Non stimulant ADHD
Exact pharmacological effects uncertain
Enhance NT transmission by inhibiting NE-pre synaptic reuptake (atomoxetine)
Agonists of CNS adrenergic receptors (guanfacine/clonidine)
-modulates noradrenergic tone in PFC by enhanced noradrenergic input from locus cureruleus and direct postsynaptic stimulation of a2 receptors located on dendritic spines of cortical pyramidal cells, thereby directly promoting functional connectivity of PFC networks
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Non stimulants
1-4 weeks to set n
Useful for patients intolerant to stimulate
-effect size not as large as with stimulants
Non schedules , refills and samples for a year
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Non stimulants
Atomoxetine
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Duration atomoxetine
34 hrs
Cap form
-do not open capsules
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Interesting atomoxetine
Metabolized by CYP2D6
| 6 and older QD
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AE atomoxetine
Nervousness, sleep problems, fatigue, upset stomach, dizziness, dry mouth, in rare cases ,ay liver injury or suicide
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Antihtn for adhd
Clonidine
| Guanfacine
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Clonidine
Tab 12-24 hours
Fatigue, drowsiness, dizziness, dry mouth, decreased appetite, constipation, irritability, low bp, abrupt discontinuation may lead to elevated levels of nervousness anxiety and bo
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Guanfacine and clonidine
A2 agonists
Do not crush, chew or break tabs
6 older
QD
Downward dose titration over 1 weeks for discontinuation
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Why downward titration for guanfacine and clonidine
Risk rebound HTN
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SedatI’ve
drug that decreases CNS activity, moderates excitement, and calms the recipient
•Anxiolytic
•Sedation is a side effect of many drugs that are not general CNS depressants
(e.g., antidepressants, antihistamines, neuroleptics/antipsychotics) •Fast-acting compared to SSRIs
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Hypnotic
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a drug that produces drowsiness and facilitates the onset and maintenanceof sleepandfromwhichtherecipientcanbearousedeasily
Hypnotic effects involve more pronounced depression of the CNS, which can be achieved with many drugs (not all) in this class by increasing th
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Why use sedative-hyponotics
For relief of anxiety
For insomnia
For sedation /amnesia before and during medical/dental and surgical procedures For treatment of epilepsy and seizure states
As a component of balanced anesthesia (IV admin)
For control of EtOH and other Sedative-Hypnotic withdrawal states
For muscle relaxation in specific neuromuscular disorders
As diagnostic aids or for treatment in
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Benzodiazepines
Act on gaba a receptors
Sedation, hypnotic , muscle relaxation, anxiolytics and anticonvulsant
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Barbiturate
Gaba a
Cause widespread spectrum of effects: mild sedation to anesthesia
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Miscellaneous sedative-hypnotics
Act on multiple receptor systems : gaba a melatonin
Used as sleep aids, treatment of delirium, anxiety, seizures
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Benzodiazepines
Widely distributed throughout the body: CNS, placenta, breast-milk
Hepatic metabolism and excretion via kidney •CYP3A4 (phase I) and glucuronidation (phase II) •Elimination half-lives vary (2-100 hours) •Cumulative toxicity
MOA: binds to the GABAA receptor and enhances GABA’s effects (shifts dose response curve to the left)
•↑ chloride influx, ↑ hyperpolarization, ↓ number of action potentials (CNS depression)
Risk of dependence and tolerance
Examples: diazepam (Valium), alprazolam (Xanax), lorazepam
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Treatment of anxiety states
Benzodiazepines are sometimes used to treat anxiety •Alprazolam, diazepam, clonazepam, lorazepam, others
Advantages
•High therapeutic index, antagonist available for overdose (flumazenil),
low risk of drug-drug interactions, minimal effect on cardiovascular or autonomic function
Disadvantages
•Risk of dependence, depression of CNS function, amnestic effects,
CNS depression when combined with other drugs (ethanol) Newer antidepressants are sometimes preferred SSRI
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Intermediate to long acting benzodiazepines
Diazepam, lorazepam, clonazepam
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Diazepam
20-80 hrs
High lipid solubility
Active metabolite
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Lorazepam
10-20 hours
Moderate lipid solubility
Not active
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Clonazepam
19-59 hours
Moderate lipid solubility
Not active
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Short to intermediate acting
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Alprozolam
Oxazepam
Temazepam
Midazolam
Triazolam
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Not active
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Cumulative toxicity
Benzodiazepines with long half lives are more likely to cause cumulative effects with multiple doses
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Barbiturates
ly distributed throughout the body: CNS, placenta, breast-milk
Hepatic metabolism and excretion via kidney
•Exception: 20-30% phenobarbital excreted unchanged •Elimination half-lives long and can lead to cumulative toxicity •Can induce CYP450 enzymes
MOA: binds to the GABAA receptor increases the duration of GABA-gated channel openings
•↑ chloride influx, ↑ hyperpolarization, ↓ number of action potentials (CNS depression) Risk of dependence and tolerance
Examples: phenobarbital, amobarbital,
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Ultra short barbituate
Thiopental used in anesthesia
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Short acting barbiturates
Secobarbital for insomnia
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Long acting barbituates
Phenobarbital for seizures
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Sedative hypnotics
enzodiazepines are used but cause daytime sedation and patients may develop anterograde amnesia and tolerance
•Zolpidem, Zaleplon, and Eszopiclone
•Highly effective, rapid onset and with minimal hangover effects
•Zolpidem in biphasic release formulation for sustained sleep maintenance •Eszopiclone has a longer ha
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RA Elton
MOA: agonist at MT1 and MT2 melatonin receptors
•Oral bioavailability less than 2% due to first-pass metabolism
•Metabolized by CYP1A2; avoid coadministration with CYP1A2 substrates/inhibitors (e.g.,
fluvoxamine, an SSRI and CYP1A2 inhibitor)
•Adverse effects include dizziness, somnolence, fatigue, and endocrine changes (decreases in
testosterone and increases in prolactin
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New hypnotics (sleep aids
Sedative-Hypnotics
Ramelteon
Treatment of Insomnia
•Benzodiazepines are used but cause daytime sedation and patients may develop anterograde amnesia and tolerance
•Zolpidem, Zaleplon, and Eszopiclone
•Highly effective, rapid onset and with minimal hangover effects
•Zolpidem in biphasic release formulation for sustained sleep maintenance •Eszopiclone has a longer half-life
•MOA: agonist at MT1 and MT2 melatonin receptors
•Oral bioavailability less than 2% due to first-pass metabolism
•Metabolized by CYP1A2; avoid coadministration with CYP1A2 substrates/inhibitors (e.g.,
fluvoxamine, an SSRI and CYP1A2 inhibitor)
•Adverse effects include dizziness, somnolence, fatigue, and endocrine changes (decreases in
testosterone and increases in prolactin)
Newer Hypnotics (Sleep Aids)
Hepatic metabolism and excretion via kidney
•P450 metabolism (CYP3A4)
•Relatively short half-lives (<6 hours), useful as hypnotics rather than sedatives
MOA: binds to GABAA receptors that contain the α1-subunit
•↑ chloride influx, ↑ hyperpolarization, ↓ number of action potentials (CNS depression)
•Only approved for treatment of sleep disorders
•No anxiolytic, anesthetic, anticonvulsant, muscle relaxing, respiratory, or cardiovascular effects
Examples: eszopiclone (Lunesta), zolpidem (Ambien), zaleplon
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Buspirone
Buspirone
•Approved for the treatment of generalized anxiety disorder
•Anxiolytic effects may take more than a week to become established (less effective in acute panic disorders)
•Does not cause sedation, hypnotic, euphoric, anticonvulsant, or muscle relaxant effects
•Extensive metabolism by CYP3A4
•Exact MOA unknown; effects may be mediated by a variety of CNS receptor systems including serotonergic, dopaminergic, cholinergic, and noradrenergic (α-adrenergic
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Alcohol use and health
Drinking too much can harm your health.
• Excessive alcohol use led to approximately 88,000 deaths
and 2.5 million years of potential life lost (YPLL) each
year in the United States from 2006 – 2010,
• Shortening the lives of those who died by an average of 30
years
• Excessive drinking was responsible for 1 in 10 deaths
among working-age adults aged 20-64 years.
• The economic costs of excessive alcohol consumption in
2010 were estimated at $249 billion, or $2.0
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What is a drink
contains 0.6 ounces (14.0 grams or 1.2 tablespoons) of pure alcohol. Generally, this amount of pure alcohol is found in
Excessive drinking includes binge drinking, heavy drinking, and any drinking by pregnant women or people younger than age 21.
12-ounces of beer (5% alcohol content). 8-ounces of malt liquor (7% alcohol content). 5-ounces of wine (12% alcohol content).
Binge drinking, the most common form of excessive drinking, is defined as consuming
1.5-ounces of 80-proof (40% alcohol content) distilled spirits or liquor (e.g., gin, rum, vodka, whiskey).
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Excess drinking
Excessive drinking includes binge drinking, heavy drinking, and any drinking by pregnant women or people younger than age 21.
12-ounces of beer (5% alcohol content). 8-ounces of malt liquor (7% alcohol content). 5-ounces of wine (12% alcohol content).
Binge drinking, the most common form of excessive drinking, is defined as consuming
1.5-ounces of 80-proof (40% alcohol content) distilled spirits or liquor (e.g., gin, rum, vodka, whiskey).
Heavy drinking is defined as consuming For women, 8 or more drinks per week.
For men, 15 or more drinks per week.
For women, 4 or more drinks during a single occasion.
For men, 5 or more drinks during a single occasion.
Most people who drink excessively are not alcoholics or alcohol
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Pharm alcohol
thanol undergoes extensive first-pass metabolism by gastric and liver alcohol
dehydrogenase (ADH)
• Metabolism of ethanol follows zero-order kinetics (rate of biotransformation is
independent of time and concentration of ethanol; enzymes are almost
immediately saturated)
• The typical 70-kg adult can metabolize 7-10 g of alcohol per hour, which is
equivalent to approximately one drink (variables include gender, % body fat, weight, empty vs. full stomach, tolerance, polymorphism
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acute alcohol intoxication
Clinical Pharmacology
Acute alcohol intoxication
•Monitor respiratory depression and aspiration of vomitus
•Glucose can treat metabolic alterations such as hypoglycemia and ketosis •Thiamine to protect against Wernicke-Korsakoff syndrome
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Chronic alcohol abuse
Acute withdrawal syndrome vs alcohol dependence
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Acute withdrawal syndrome
Can be life threatening
• Major pharmacological objective is to prevent
seizures, delirium, and arrhythmias,
electrolyte rebalancing, thiamine therapy • Benzodiazepines
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Alcohol dependence
Alcohol dependence
• Psychosocial therapy serves as the primary treatment for alcohol dependence • Often depression or anxiety disorders coexist with alcoholism and therapeutic
intervention for these other psychiatric problems decreases the rat
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Treat acute alcohol withdrawal
Diazepam
Lorazepam
Oxazepam
Thiamine
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Drugs for prevention of alcohol abuse
Acamprosate
Disulfiram
Naltrexone
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Drugs for treatment of acute methanol or ethylene glycol poisoning
Ethanol
| Fomepizole
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Naltrexone
Approved for the treatment of alcohol and opiate dependence
• MOA: μ opioid receptor antagonist (long-acting)
• Reduces the craving for alcohol and the rate of relapse to either drinking or alcohol
dependence for the short term (12 weeks)
• Individuals physically dependent on alcohol and opioids must be opioid-free before
initiating therapy because naltrexone precipitates an acute withdrawa
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Acamprosate
• MOA: weak NMDA-receptor antagonist and GABAA receptor agonist (also affects
serotonergic, noradrenergic, and dopaminergic systems)
• Reduces short-term and long-term relapse rates (more than 6 months)
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Disulfram
OA: irreversibly inhibits aldehyde dehydrogenase and causes extreme discomfort in patients who drink alcoholic beverages (flushing, throbbing headache, nausea, vomiting, sweating, hypotension, confusion due to the accumulation of aldehyde)
Hangovers
• Should not be administered with any medications that contain alcohol (cough syrups, cold preparations, mouthwashes)
• PATIENTS MUST BE HIGHLY motivated
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Who drinks methanol
Windshield washer fluid
| Antifreeze
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Abstinence syndrome
The signs and symptoms that occur on withdrawal of a drug in a dependent person
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Addiction
Compulsive drug dusing behavior in which the person uses the drug for personal satisfaction often int he face of known risk to health; formerly termed psychological dependence
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Controlled substsance
A drug known to have abuse liability that is listed on governmental schedules of controlled substances
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Dependence
te characterized by signs and symptoms, frequently the opposite of those caused by a drug, when it is withdrawn from chronic use or when the dose is abruptly lowered; formerly termed physical or physiologic dependence
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Designed drug
synthetic derivative of a drug, with slightly modified structure but no major change in pharmacodynamic action. Circumvention of the Schedules of Controlled Drugs is a motivation for the illicit synthesis of designed drugs
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Designer drug
a synthetic derivative of a drug, with slightly modified structure but no major change in pharmacodynamic action. Circumvention of the Schedules of Controlled Drugs is a motivation for the illicit synthesis of designe
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Tolerance
Tolerance:
DRUGS OF ABUSE
A decreased response to a drug, necessitating larger doses to achieve the same effect. This can result from increased disposition of the drug (metabolic tolerance), an ability to compensate for the effects of a drug (behavioral tolerance), or changes in receptor or effector systems involved in drug actions (functi
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Sensitization
Increase in response with repetition of the same dose of the drug(left shift in dose response curve)
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Withdrawal
Adaptive changesthat become fully apparent once drug exposure is terminated ; generally due to readaption of the cns to the absence of the drug dependence
Withdrawal is the evidence of physical dependence
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Schedule 1
No medical sue high addiction
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II
Medical use high potential
Amphetamines, methylphenidate, barbituates
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AmpheIII
Medical use moderate abuse
| Barbituates, opoid agonists
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IV
Medical use low risk
Benzodiazepines, Colorado hydrate, mild stimulants,
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Most common abused prescription drugs
Diazepam, methylphenidate
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Amphetamine, methylphenidate, cocaine
Agitation HTN tachycardia, delusions, hallucinations
| Withdraw-apathy, irritable, sleep, disoriented depresssed
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Barbituates benzodiazepines
Slurred speech drunken, dilated pupils,
Withdraw-anxiety, insomnia, delirium, tremors, seizures
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Heroin
Constricted pupils, clammy skin, n, drowsiness
| Withdrawal-n, chills, cramps, lacrimation, rhinorrhea, yawning
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Drugs abused but not addictive
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LSD
Mescaline
Psilocybin
PCP
Ketamine
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Long term effects
• Although considered nonaddictive, consistent use can have long‐term effects
• PCP may lead to irreversible schizophrenia‐like psychosis
• LSD can cause flashbacks of altered perception years after
consumption
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Drugs used to treat dependence
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Opioid receptor antagonist • Naloxone (Narcan)
• Naltrexone
Miscellaneous agents
Synthetic opioid • Methadone
Dronabinol, nabilone
Ketamine
Bupropion (Wellbutrin, Zyban)
Nicotine (Nicorette, Nicoderm CQ,
Partial μ-opioid receptor agonist • Buprenorphine
Nicotinic receptor partial agonist • Varenicline (Chantix)
others)
Benzodiazepines • Oxazepam
• Lorazepam
NMDA receptor antagonist
• Acamprosate
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Ache inhibitors
PHARMACODYNAMICS OF AChE INHIBITORS
A.Mechanism of action: Inhibition of AChE B. Duration of action
i) Alcohols bind weakly and reversibly resulting in short duration of action (2-10 minutes).
ii) Carbamic acid esters bind reversibly but with longer duration of action compared to alcohols (30 minutes to 8-hour duration of action)
iii)Organophosphates bind covalently and reversal of binding requires rapid administration of pralidoxime to regenerate the activity of AChE
C. Organ system effects
i) Depending on the site of action, AChE inhibitors have the ability to: (1)Stimulate mAChRs at autonomic effector organs (2)Stimulate, followed by depression or paralysis, all autonomic
ganglia and skeletal muscle (nAChRs
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Ache inhibitso
he major therapeutic uses of agents that stimulate AChRs (direct acting or indirect acting) are for diseases of the eye (glaucoma, accommodative esotropia), the GI and urinary tracts (postoperative atony, neurogenic bladder), the NMJ (myasthenia gravis, curare-induced neuromuscular paralysis), the heart (rarely for certain atrial arrhythmias), and Alzheimer disease
Dementia
Patients with progressive dementia of the Alzheimer type have a deficiency of intact cholinergic
• Tacrine was approved in 1993, but due to the high incidence of hepatotoxicity newer agents are preferred (donepezil, rivastigmine, galantamine, physostigmine
• Patients with dementia associated with Parkinson disease also benefit from AChE inhibitors
Although evidence of benefit is statistically significant, the amount of benefit is modest and does not prevent disease
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Drug drug
DRUG-DRUG INTERACTIONS
Nondepolarizing neuromuscular blocking agents: AChE inhibitors diminish NMJ blockade
i) Exception: mivacurium (metabolized by plasma AChE), AChE inhibitors prolong blockade
Succinylcholine: AChE inhibitors will enhance phase 1 block and antagonize phase 2 block
Cholinergic agonists (direct-acting): AChE inhibitors enhance effects of cholinergic agonists
Beta-blockers: AChE inhibitors may enhance the bradycardi
128
Dementia pharm
The dominant initial signs of AChE intoxication are those of mAChR stimulation:
• With poisoning from lipid-soluble agents, CNS involvement follows rapidly (confusion, ataxia, generalized convulsions, coma, and respiratory paralysis)
miosis, salivation, sweating, bronchial constriction, vomiting, loose stools, and diarrhea
• The route of administration dictate which symptoms are noted initially
(1)After ingestion, GI symptoms occur earliest (2)Percutaneous absorption results in early
• Time of death after a single acute exposure may range 5 minutes to 24 hours and is caused primarily by respiratory failure.
symptoms of localized sweating and muscle
129
Dementia pharm
Dementia Pharmacology
Atropine in combination with maintenance of vital signs (respiration) and decontamination
Atropine is ineffective against the peripheral neuromuscular stimulation (nAChRs)
• Cholinesterase reactivators (pralidoxime) are capable of regenerating active AChE enzyme by removal of the phosphorous group from the active site of the enzyme
To regenerate AChE at the NMJ, cholinesterase regenerators can be administered
• Restores the response to stimulation of the motor nerve within minutes
Toxicology/Treatment
Cholinesterase Regenerators
• Must be given soon after AChE inhibitor exposure
• Atropine, pralidoxime, and a benzodiazepine
(anticonvulsant) are typically combi
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Memantine
Memantine
Dementia Pharmacology
• Glutamate, the primary excitatory amino acid in the CNS, may contribute to the pathogenesis of Alzheimer's disease (AD) by overstimulating various glutamate receptors leading to excitotoxicity and neuronal cell death
• MOA: antagonist of the N-methyl-D-aspartate (NMDA) type of glutamate receptors
• Under normal physiologic conditions, the (unstimulated) NMDA receptor ion channel is blocked by magnesium ions, which are displaced after agonist- induced depolarization
• Memantine binds to the intra-pore magnesium site, but with longer dwell time, and thus functions as an effective receptor blocker only under conditions of excessive stimulation (does not affect normal neurotransmission)
• Adverse event rates similar to placebo; fewer side effects than cholinergic medications
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Thiamine in alcohol
Give it
