Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Medicine > Behavioral Science > Flashcards

Behavioral Science Flashcards

1
Q

Quantative

A

Numbers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Qualitative

A

Words express data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Observational studies increasing strength ofevidence

A

Cross sectional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Best evidence

A

Meta analysis and systemic reviews

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Population vs sample

A

All in a common group, and subset o population usually made with random processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Null hypothesis

A

No true difference between the groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Alternative hypothesis

A

Will be a difference between the groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prospective, retrospective, ambidirectional

A

Outcome not known, outcome is known at start, look back then forward for additional occurrences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 key questions to see sting study design

A
  1. Allocating or forced intervention? This is interventional or observational
  2. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Case control

A

Disease vs no, look back on exposure

Rare disease. Low incidence/low prevelance/long latency. RETROSPECTIVE

OR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

A cohort study may not always do what

A

Describe how groups are allocated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Strength cohort

A

Low occurrence, association, multiple outcomes of one exposure, long induction/latent periods, temporality, less ethical issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cross sectional study

A

Prevelance study.

Study exposure and disease at the same time

Snapshot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Phase 0

A
  1. Small number
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Phase 1.

A

Safety/tolerance of doses
Small n

Short duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phase 2

A

Effectiveness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Phase 3

A

Superiority

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Stage 4

A

FDA approval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Simple interventional studies

A

Subjects randomly allocated once into a single treatment group
-no further randomizations into subtreatment groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factorial intervention

A

Subjects randomly allocated into an initial group, then further randomly-divided into a subgroup
-multiple randomizations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Parallel intervention

A

Subjects simultaneously yet exclusively managed in a single treatment

No switching groups after initial randomization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cross over

A

Subjects switched to other treatment group after initial treatment assignment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Consent

A

Agree to participatedbased on being informed given by mentally capable individuals of legal consent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Assent

A

Agreement to participate after informed, mentally capable individuals not able to give legal consent

Kids babies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Advantage to interventional

A

Cause precedes effect

Only designs used by FDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Incidence

A

New occurrences of an outcome/event/disease (included.added)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Prevelance

A

Existing occurrences of an outcome

Previously occurring plus new cases, collectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Calculate incidence

A

New cases/ppl at risk

Always subtract out those who are not at risk (already have disease/outcome or are immune)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

NNT NNH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

OR

A

A/C/B/D

Or

AD/BC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

RR OR HR 1.8

A

80% increased risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

1 RR OR HR

A

No difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

.25 RR OR HR

A

75% decreased risk/odds/hazard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When looking at the CI rations (RR/OR/HR) if both values are on the same side of 1 (equality0 it is always

A

Statistically significant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

ADHD meds

A

Stimulants and non stimulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Stimulants

A

Amphetamine, dextroamphetamie

Lisdexamfetamine

Methylphenidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Non stimulants ADHD

A

Atomoxetine
Guanfacine
Clonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Stimulants

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

D vs L isomers of AMP/MPH

A

D more CNS than L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Methylphenidate

A

Inhibit DA reuptake n inhibition of NT presynaptic reuptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MPH

A

Doesn’t stimulate release of NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

AE stimulants

A 
Dyspepsia/GI
HA
Decreased appetite
Insomnia
Anxiety/jitters
Irritability/aggression
Elevated BP/HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Rare bad AE stimulants

A

Priapism, seizures, sudden cardiac death-ALWAYS ASSESS FOR CARDIAC STRUCTURAL ABNORMALITIES
Stroke and MI
Chemical leukoderma-big white patch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Who not use stimulant in

A 
Anxiety/agitation
CV disease
Moderate or bad HTN
Glaucoma
Motor tics tourettes
Ineffectively treated bipolar / psychoses
Poorly controlled seizures
History of drug abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What r stimulants

A

CONTOLLED SUBSTANCE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the amphetamine based stimulants for ADHD

A

Dextroamphetamine

Amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

AE dextroamphetamine

A

HA, insomnia, circulation prob, decreased appetite, slowing of growth new psychotic problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Amphetamine ae

A

Mood changes, new or worse bipolar illness, aggressive behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How long those work

A

4-6 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Extended release amphetamine

A

8-12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are extended release

A

Dextroamphetamine, amphetamine, lisdexamfetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Non-ir forms

A

Adzenys X-RAY-ODT

Amphetamine d and l 50.50 ratio

No water necessary

For 6 and over

54
Q

Methylphenidate based stimulants

A

Dexmethylphenidate

55
Q

Methylphenidate

A

4-6 hrs

HA, insomnia, circulation problems, decreased appetite, slowing of growth new psychotic problems

56
Q

Sustained release methylphenidate

A

Methylphenidate

4-8 hrs

57
Q

AE extended release methylphenidate

A

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

58
Q

Non stimulant ADHD

A

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

59
Q

Non stimulants

A

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

60
Q

Non stimulants

A

Atomoxetine

61
Q

Duration atomoxetine

A

34 hrs
Cap form

-do not open capsules

62
Q

Interesting atomoxetine

A

Metabolized by CYP2D6

6 and older QD

63
Q

AE atomoxetine

A

Nervousness, sleep problems, fatigue, upset stomach, dizziness, dry mouth, in rare cases ,ay liver injury or suicide

64
Q

Antihtn for adhd

A

Clonidine

Guanfacine

65
Q

Clonidine

A

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

66
Q

Guanfacine and clonidine

A

A2 agonists
Do not crush, chew or break tabs
6 older
QD

Downward dose titration over 1 weeks for discontinuation

67
Q

Why downward titration for guanfacine and clonidine

A

Risk rebound HTN

68
Q

SedatI’ve

A

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

69
Q

Hypnotic

A 
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
70
Q

Why use sedative-hyponotics

A

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

71
Q

Benzodiazepines

A

Act on gaba a receptors

Sedation, hypnotic , muscle relaxation, anxiolytics and anticonvulsant

72
Q

Barbiturate

A

Gaba a

Cause widespread spectrum of effects: mild sedation to anesthesia

73
Q

Miscellaneous sedative-hypnotics

A

Act on multiple receptor systems : gaba a melatonin

Used as sleep aids, treatment of delirium, anxiety, seizures

74
Q

Benzodiazepines

A

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

75
Q

Treatment of anxiety states

A

 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

76
Q

Intermediate to long acting benzodiazepines

A

Diazepam, lorazepam, clonazepam

77
Q

Diazepam

A

20-80 hrs

High lipid solubility

Active metabolite

78
Q

Lorazepam

A

10-20 hours

Moderate lipid solubility

Not active

79
Q

Clonazepam

A

19-59 hours

Moderate lipid solubility
Not active

80
Q

Short to intermediate acting

A 
Alprozolam
Oxazepam
Temazepam
Midazolam
Triazolam

Not active

81
Q

Cumulative toxicity

A

Benzodiazepines with long half lives are more likely to cause cumulative effects with multiple doses

82
Q

Barbiturates

A

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,

83
Q

Ultra short barbituate

A

Thiopental used in anesthesia

84
Q

Short acting barbiturates

A

Secobarbital for insomnia

85
Q

Long acting barbituates

A

Phenobarbital for seizures

86
Q

Sedative hypnotics

A

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

87
Q

RA Elton

A

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

88
Q

New hypnotics (sleep aids

A

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

89
Q

Buspirone

A

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

90
Q

Alcohol use and health

A

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

91
Q

What is a drink

A

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).

92
Q

Excess drinking

A

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

93
Q

Pharm alcohol

A

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

94
Q

acute alcohol intoxication

A

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

95
Q

Chronic alcohol abuse

A

Acute withdrawal syndrome vs alcohol dependence

96
Q

Acute withdrawal syndrome

A

Can be life threatening
• Major pharmacological objective is to prevent
seizures, delirium, and arrhythmias,
electrolyte rebalancing, thiamine therapy • Benzodiazepines

97
Q

Alcohol dependence

A

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

98
Q

Treat acute alcohol withdrawal

A

Diazepam
Lorazepam
Oxazepam
Thiamine

99
Q

Drugs for prevention of alcohol abuse

A

Acamprosate
Disulfiram
Naltrexone

100
Q

Drugs for treatment of acute methanol or ethylene glycol poisoning

A

Ethanol

Fomepizole

101
Q

Naltrexone

A

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

102
Q

Acamprosate

A

• 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)

103
Q

Disulfram

A

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

104
Q

Who drinks methanol

A

Windshield washer fluid

Antifreeze

105
Q

Abstinence syndrome

A

The signs and symptoms that occur on withdrawal of a drug in a dependent person

106
Q

Addiction

A

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

107
Q

Controlled substsance

A

A drug known to have abuse liability that is listed on governmental schedules of controlled substances

108
Q

Dependence

A

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

109
Q

Designed 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 designed drugs

110
Q

Designer drug

A

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

111
Q

Tolerance

A

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

112
Q

Sensitization

A

Increase in response with repetition of the same dose of the drug(left shift in dose response curve)

113
Q

Withdrawal

A

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

114
Q

Schedule 1

A

No medical sue high addiction

115
Q

II

A

Medical use high potential

Amphetamines, methylphenidate, barbituates

116
Q

AmpheIII

A

Medical use moderate abuse

Barbituates, opoid agonists

117
Q

IV

A

Medical use low risk

Benzodiazepines, Colorado hydrate, mild stimulants,

118
Q

Most common abused prescription drugs

A

Diazepam, methylphenidate

119
Q

Amphetamine, methylphenidate, cocaine

A

Agitation HTN tachycardia, delusions, hallucinations

Withdraw-apathy, irritable, sleep, disoriented depresssed

120
Q

Barbituates benzodiazepines

A

Slurred speech drunken, dilated pupils,

Withdraw-anxiety, insomnia, delirium, tremors, seizures

121
Q

Heroin

A

Constricted pupils, clammy skin, n, drowsiness

Withdrawal-n, chills, cramps, lacrimation, rhinorrhea, yawning

122
Q

Drugs abused but not addictive

A 
LSD
Mescaline
Psilocybin
PCP
Ketamine
123
Q

Long term effects

A

• 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

124
Q

Drugs used to treat dependence

A 
 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
125
Q

Ache inhibitors

A

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

126
Q

Ache inhibitso

A

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

127
Q

Drug drug

A

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
Q

Dementia pharm

A

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
Q

Dementia pharm

A

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

130
Q

Memantine

A

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

131
Q

Thiamine in alcohol

A

Give it

Clin Medicine (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions