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Med School Year 2 Flash Cards > FOBS Exam II Pharm > Flashcards

FOBS Exam II Pharm Flashcards

1
Q

Drugs of ADHD

A 
Methylphenidate
Amphetamines
Lys-dexamphetamine
Pemoline
Atomoxetine
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2
Q

Amphetamines are CNS Stimulants that act to

How are they diff in adults and children?

A

enhance DA in the synapse, enhanced NE neurotransmission in the CNS
Adults - euphoria, insomnia, appetite suppression, and shift to paranoia
Children - calm hyperactive behavior

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3
Q

Mechanism of amphetamines

A

run the DA re uptake transporter (DAT) in reverse (synaptic concentration of DA are increased)

reverse the action of the re-uptake transporter at catecholamine synapses (NE and DA levels are elevated)

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4
Q

children with ADHD have a DAT that runs

A

in reverse - extrudes DA (ADHD sx)

so amphetamines cause them to start fxning to take up DA (slowing behavior)

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5
Q

Methylphenidate mechanism

A

facilitation of release of central DA and NE

mechanism in ADHD is unknown though

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6
Q

Methylphenidate metabolism

A

hepatic metabolism
2.5 h 1/2 life
dosing in the morning and during school hours
penetration to CNS is slower compared with cocaine or amphetamine (lower abuse potential)

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7
Q

Methylphenidate toxicity and contraindications (CI)

A

insomnia
anorexia
weight loss and growth retardation (long term therapy)
CI in HTN, glaucoma, anxiety, seizure disorder

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8
Q

Methylphenidate XL

A

Extended release

effects last 12-14 hours (dont need to give during school hours)

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9
Q

Methylphenidate transdermal patch

A

Slow onset - delayed 1 hr, good for kids who can’t swallow pills
Approximately 8 - 10 hr effect
Take off patch!!

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10
Q

Amphetamine Combinations

A

d-amphetamine saccharate
amphetamine aspartate
amphetamine sulfate
d-amphetamine sulfate

different salts contribute to more sustained effects because the salts have diff rates of going into solution in GI tract

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11
Q

Most likely to be abused ADHD formulation?

A

Amphetamine combination (adderall)

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12
Q

Lys-dexamfetamine

Children or adults?

A

Both children and adults - decreased the abuse potential of the d-amphetamine (bound to lysine that has to be split off in liver)

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13
Q

amphetamine side effects

A

insomnia, weight loss, emotional lability (adults - elated/out going to angry/withdrawn, emotions not seen so much in children)
High doses in adults can cause paranoia

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14
Q

Major problem with prescribing amphetamines

A

high abuse potential

Schedule II agents

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15
Q

Pemoline
Duration of action
Toxicity
Abuse

A

Equal to methylphenidate in effectiveness
Long duration of action
HEPATOTOXICITY
No abuse potential

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16
Q

Atomoxetine
Duration of action
Toxicity
Abuse

A

NE selective reuptake inhibitor
Non-stimulant, long acting
Anticholinergic effects - BPH males are not good candidates
Low abuse potential

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17
Q

BZD Agonists

A 
Diazepam
Alprazolam
Lorazepam
Oxazepam
Flurazepam
Triazolam
Estazolam
Temazepam
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18
Q

BZD antagonist

A

Flumazenil

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19
Q

BZD-1 Selective Binding Drugs

A

Eszopicolone
Zolpidem
Zaleplon

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20
Q

Sedative definition

A

diminish awareness
cause drowsiness
diminish motor activity

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21
Q

Hypnotic definition

A

promotes sleep and inhibits wakefulness

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22
Q

GABAa receptor complex effected by what anxiolytics/sedative-hypnotics

A

BZD
Barbiturates
Ethanol

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23
Q

Alpha unit binds
Alpha/beta junction binds
Gamma unit used for

A

GABA
BZD
Gamma unit present for BZD to modulate GABA

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24
Q

When GABA binds the channel opens to release

A

Cl- ions
Increased Cl- conductance inhibits neural firing
Decrease Cl- conductance excites neurons (seizures –> why local anestheics can cause seizures because they effect the small unmyelinated fibers first which GABA neurons are small unmyelinated)

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25
Q

BZD as an hypnotic
Problem with combining with other hypnotics?
Dependence?

A 
Efficacious hypnotic with fast onset
SAFE by themselves
When combined with sedative-hypnotics such as etoh or barb, lethality is enhanced 
Dependence is a serious problem 
Long half lives = hangover
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26
Q

BZD Overdose

A

Usually not a problem

If mixed with EtOH or opioids –> severe respiratory depression

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27
Q

Diazepam
Actions
Half life

A

anxiolytic, hypnotic, muscle relaxant, pre-anesthetic
blocks convulsions in EtOH or BZD withdrawal
Terminates status epilepticus (second to lorazepam which is more water soluble)
Long half life = 50+ hrs

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28
Q

Alprazolam
Actions
Side effects

A

Anxiolytic, hypnotic
Intermediate acting
Early morning awakening, tolerance/dependence if over-used, less sedative than other BZD

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29
Q

Lorazepam

A

Anxiolytic and hypnotic

DOC for status epilipticus - better water solubility

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30
Q

Oxazepam

Beneficial for people w/ this dz?

A

Anxiolytic and for sleep induction
Live dz patients and elderly because better pharmacokinetics (changes in Phase 1 metabolism)
Also seen in Temazpeam and Lorazepam

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31
Q

Drug interactions with BZDs

A

Additive: EtOH, BZDs, opioids, antipsychotics, TcA, antihistamines

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32
Q

BZD Abstinence Syndrome (withdrawal signs and sx)

A

Signs: tremor, seizures
Sx: anxiety, insomnia, nausea, malaise

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33
Q

BZD tolerance

A

More tolerance with sedative than anxiolytic
Many pts escalate the dose to treat anxiety or insomnia
Higher the dose, more frequent the dose, longer the dose is taken = greater the tolerance
Greater the physical dependence = nastier the withdrawal syndrome

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34
Q

BZD dependence problem with anxiety

A

Initial anxiety returns during withdrawal
Additional anxiety occurs because of withdrawal
= intolerable anxiety
Sx occur BEFORE signs of withdrawal

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35
Q

BZD Dependence

A

Cross dependence with other sedative hypnotics - EtOH and barbs
“Dependence of the sedative-hypnotic type”
Limit the # of pills in a prescription and counsel the pt

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36
Q

Shorter elimination 1/2 life drugs give what kind of s/sx of withdrawal

A

Nastier

Longer are less severe but more protracted (consider giving a long acting BZD if withdrawal s/sx seem to be intolerable)

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37
Q

Two problems with insomnia

A

getting to sleep

staying to sleep

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38
Q

BZD as sedative-hypnotics
Problem with long, short, intermediate acting?
Problem with all BZDs?

A

Effective
Hangover with long-acting BZDs
Rebound insomnia and anxiety in short acting
Early morning awakening in short/intermediate acting
Tolerance/dependence/withdrawal

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39
Q

Triazolam
1/2 life
SE

A

Short half life = 3-4 hours
No hangover
SE: rebound insomnia and other withdrawal signs with continued use (some even with 1 dose), amnesia, tolerance

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40
Q 
Zolpidem
Binds what?
As efficacious as BZD?
1/2 life?
Abuse?
Rebound insomnia?
A

Binds a subset of BZD receptors (BZD1) - not a BZD!!
Nearly as efficacious in producing sleep as a BZD but less anxiolytic, anticonvulsant, muscle relaxant
Short 1/2 life = 3-5 hrs (less hangover)
Abuse/dependence = lower than BZD
No rebound insomnia

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41
Q

Eszopiclone
Zolpidem
Zaleplon
All work on what receptor

A

Selectively to GABA receptors containing the alpha1 subunit (BZD1)

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42
Q

Zaleplon
Binds?
Use PRN for what?

A

Binds BZD1 receptors
Shorter half life than zolpidem = 1 hr
Used for before bedtime or awakening in the middle of the night (4+ hr remaining)

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43
Q

Eszopiclone

A

d-isomer of zopiclone, not a BZD but binds BZD1

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44
Q

Melatonin
Hormone from?
Used for?
CI in what?

A

Pineal gland hormone that regulates sleep/wake cycle
Useful for sleep problems related to jet lag, changing day/night working hours
Variable dose - can get OTC, no dependence problems
Depression is Contraindicated

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45
Q

Ramelteon
Binds?
Abuse?
Withdrawal?

A

Binds melatonin receptors (MT1 and MT2)
No dependence of abuse liability
No rebound insomnia or withdrawal

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46
Q

Can’t use Ramelteon with

A

Fluvoxamine - bc it binds CYP1A2 inhibiting its metabolism

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47
Q

Caution in administering any hypnotic to a pt with a hx of

A

Depression

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48
Q

Barbiturates

A

Pentobarbital
Secobarbital
Phenobarbital

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49
Q

Barbiturates Therapeutic Index

A

Poor

Phenobarbital for seizure control and the other two are supervised (hospital) as sleep agents (seco/pentobarbital)

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50
Q

BZD + Barbiturates

A

Profound CNS depression, anesthesia, coma
Respiratory depression
Abuse potential

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51
Q

BZD vs Barbiturates

A

Both facilitate GABA but neither bind GABA site directly
Barb directly increase Cl- flux at high doses
No dose of BZD ever directly affects Cl- flux

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52
Q

Other OTC Agents that aren’t melatonin as hypnotic

A

Antihistamine and block muscarinic receptors - limited dose range (if too high can be more sedative)
Less efficacious and tolerance occurs more rapidly

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53
Q

Drugs for Control of Appetite

A 
Low-efficacy CNS stimulants
Topiramate
Phetermine + Topirmate
Fluoxetine
Orlistat
Fenfluramine
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54
Q

Weight-control programs

A

EXERCISE
Restriction of energy intake (anorexiant medication)
Behavioral modification

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55
Q

Criteria for anorexiant medication

A

BMI > or equal to 30
OR
BMI > or equal to 27 with HTN, DM, hyperlipidemia

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56
Q

Amphetamine anorexiant MOA

A

Modification of NE and DA neurotransmission (reverse reuptake transporter)
Appetite-control areas of the hypothalamus - NE mechanism, DA in mesolimibic also of interest

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57
Q

What amphetamines can’t be prescribed for weight loss?

A

Schedule II agents

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58
Q

Therapeutic effects of amphetamine related anorexiants

A 
Decrease in appetite
Less interest in food
Less pleasure from eating
Increased satiety with eating
Decrease in total energy intake

ONLY LOW EFFICACY CNS STIMULANTS ARE PERMITTED (high efficacy would also give euphoria, and abuse potential)

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59
Q

Amphetamine related anorexiants effectiveness:

Tolerance?

A

Limited by tolerance (2-3 weeks)
Should discontinue before reaches tolerance
Weight loss then plateau (thereafter, weight gain is likely)

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60
Q

Amphetamine related anorexiants precautions

A

Unusual reactivity to sympathomimetics (amphetamine, epi, isoproternol, phenylephrine, pseudoephedrine, terbutaline)
Dental problems - reduce salivary flow –> exacerbating periodontal disease

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61
Q

Amphetamine related anorexiants side effects

A 
Insomnia (avoid 4-6 h before bed) 
Increased BP
Anxiety
Tremor
Potential for abuse (psychosis, dependence)
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62
Q

Amphetamine related anorexiants overdose

A

Arrhythmia, confusion, diarrhea, fever
Assaultive behavior, hallucinations (shift toward paranoid thinking, typically high dose of Schedule II)
Circulatory collapse, coma before DEATH

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63
Q

Amphetamine related anorexiants contraindications

A 
CVD
Glaucoma
HTN - moderate or severe
Hyperthyroid
Psychosis
Alcoholism
Hx of drug abuse/dependence
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64
Q

Amphetamine related anorexiants drug interactions

A

Thyroid hormones

MOAI

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65
Q

Amphetamine related anorexiants names, their classes and specific problems

A 
Benzphetamine (class III, CI in preg)
Diethylpropion (class IV, blood dyscrasias)
Phentermine (class IV, long acting/most precscribed)
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66
Q

Topiramate
Other uses
Untoward effects

A

Anticonvulsant

Dizziness, drowsiness, tiredness, attention/memory issues

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67
Q

Phentermine + Topiramate

A

Sympathomimetic + anti-seizure

Efficacy is good - over 1 yr pts lost weight on a monthly basis

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68
Q

Fluoxetine
Other use
How does it help with weight loss?
Tolerance?

A

SSRI - mood disorders
Appetite reduction - SATIETY
Tolerance develops within days or weeks

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69
Q

Orlistat
MOA?
SE?

A

Tetrahydrolipstatin - bonds and inhibits gastric and pancreatic lipases (prevents hydrolysis of triglycerides to absorable free FA)
Need to supplement fat-soluble nutrients
SE: flatulence, loose stools - esp after high fat meals

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70
Q

Herbal/Nutritional supplements that haven’t been shown effective

A

Hydroxy citric acid
Fat binding fiber
Ginkgo, Biloba, vitamin E

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71
Q

BZD + Barbiturates

A

Profound CNS depression, anesthesia, coma
Respiratory depression
Abuse potential

How well did you know this?
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72
Q

BZD vs Barbiturates

A

Both facilitate GABA but neither bind GABA site directly
Barb directly increase Cl- flux at high doses
No dose of BZD ever directly affects Cl- flux

How well did you know this?
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73
Q

Other OTC Agents that aren’t melatonin as hypnotic

A

Antihistamine and block muscarinic receptors - limited dose range (if too high can be more sedative)
Less efficacious and tolerance occurs more rapidly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Drugs for Control of Appetite

A 
Low-efficacy CNS stimulants
Topiramate
Phetermine + Topirmate
Fluoxetine
Orlistat
Fenfluramine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Weight-control programs

A

EXERCISE
Restriction of energy intake (anorexiant medication)
Behavioral modification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Criteria for anorexiant medication

A

BMI > or equal to 30
OR
BMI > or equal to 27 with HTN, DM, hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Amphetamine anorexiant MOA

A

Modification of NE and DA neurotransmission (reverse reuptake transporter)
Appetite-control areas of the hypothalamus - NE mechanism, DA in mesolimibic also of interest

How well did you know this?
1
Not at all
2
3
4
5
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78
Q

What amphetamines can’t be prescribed for weight loss?

A

Schedule II agents

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79
Q

Therapeutic effects of amphetamine related anorexiants

A 
Decrease in appetite
Less interest in food
Less pleasure from eating
Increased satiety with eating
Decrease in total energy intake

ONLY LOW EFFICACY CNS STIMULANTS ARE PERMITTED (high efficacy would also give euphoria, and abuse potential)

How well did you know this?
1
Not at all
2
3
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80
Q

Amphetamine related anorexiants effectiveness:

Tolerance?

A

Limited by tolerance (2-3 weeks)
Should discontinue before reaches tolerance
Weight loss then plateau (thereafter, weight gain is likely)

81
Q

Amphetamine related anorexiants precautions

A

Unusual reactivity to sympathomimetics (amphetamine, epi, isoproternol, phenylephrine, pseudoephedrine, terbutaline)
Dental problems - reduce salivary flow –> exacerbating periodontal disease

82
Q

Amphetamine related anorexiants side effects

A 
Insomnia (avoid 4-6 h before bed) 
Increased BP
Anxiety
Tremor
Potential for abuse (psychosis, dependence)
83
Q

Amphetamine related anorexiants overdose

A

Arrhythmia, confusion, diarrhea, fever
Assaultive behavior, hallucinations (shift toward paranoid thinking, typically high dose of Schedule II)
Circulatory collapse, coma before DEATH

84
Q

Amphetamine related anorexiants contraindications

A 
CVD
Glaucoma
HTN - moderate or severe
Hyperthyroid
Psychosis
Alcoholism
Hx of drug abuse/dependence
85
Q

Amphetamine related anorexiants drug interactions

A

Thyroid hormones

MOAI

86
Q

Amphetamine related anorexiants names, their classes and specific problems

A 
Benzphetamine (class III, CI in preg)
Diethylpropion (class IV, blood dyscrasias)
Phentermine (class IV, long acting/most precscribed)
87
Q

Topiramate
Other uses
Untoward effects

A

Anticonvulsant

Dizziness, drowsiness, tiredness, attention/memory issues

88
Q

Phentermine + Topiramate

A

Sympathomimetic + anti-seizure

Efficacy is good - over 1 yr pts lost weight on a monthly basis

89
Q

Fluoxetine
Other use
How does it help with weight loss?
Tolerance?

A

SSRI - mood disorders
Appetite reduction - SATIETY
Tolerance develops within days or weeks

90
Q

Orlistat
MOA?
SE?

A

Tetrahydrolipstatin - bonds and inhibits gastric and pancreatic lipases (prevents hydrolysis of triglycerides to absorable free FA)
Need to supplement fat-soluble nutrients
SE: flatulence, loose stools - esp after high fat meals

91
Q

Herbal/Nutritional supplements that haven’t been shown effective

A

Hydroxy citric acid
Fat binding fiber
Ginkgo, Biloba, vitamin E

92
Q 
Nicotine epidemiological factors
Education
Social
Mental Illness
Death rate
Dollars
Cancer
A

Lower education - no high school (37%)
Heavy drinkers (12.6%), illicit drugs (13.8%)
Mental illness 50% psych, 70% bipolar, 90% schizo
400,000 premature deaths in US each year
60% health care dollars
30% cancer deaths

93
Q

Nicotine MOA

1/2 life

A

Agonist at the nicotinic subtype of the ACh –> 25% from smoke enters blood and within 15 seconds into the brain
Half life = 2 hrs
DA reward system - binds to cell bodies in the VTA and the dopaminergic terminal of the nucleus accumbens
Stimulates the release of DA and glutamate

94
Q

Smokers are at reduced risk for

A

Parkinson’s
Alzheimer’s
Ulcerative colitis

95
Q

Stimulatory effects of nicotine

A

improved attention, learning, reaction time, problem solving ability
lifts mood, decreases tension, lessens depressive feelings

96
Q

Nicotine in cerebral blood flow

A

Short term - nicotine exposure increases the CBF without changing cerebral O2 metabolism
Long term - decreases the CBF, skeletal muscle relaxant

97
Q

Nicotine dependence

A

develops quickly due to VTA dopaminergic activity (same as cocaine and amphetamines)
positive reinforcement is the process by which certain consequences of a response increase –> how nicotine works

98
Q

Acute nicotine intoxication

A 
At least one of these:
Insomnia
Bizarre dreams
Lability of mood
Derealization
Interference with personal fxning
AND at least one of these:
Nausea/vomiting
Sweating
Tachycardia
Cardiac arrhythmias
99
Q

Nicotine Dependence syndrome

A

Three or more of for 1 month or w/i 12 month period:
1. a strong desire or sense on compulsion to take substance
2. impaired capacity to control substance taking (termination - longer period of time, onset - persistent desire, level of use - larger amnts)
3. physiological withdrawal when reduced/ceased
4. evidence of tolerance - increased amnts needed
5, preoccupation with substance use
6. persistent substance use despite clear evidence of harmful consequences

100
Q

Nicotine withdrawal
Onset
Sx

A

Develops with 2 hours and peaks within 24-48
Sx: craving, tension, anxiety, dysphoric mood, irritability, difficulty concentrating, drowsiness, trouble sleeping, decreased HR/BP, increase appetite, weight gain, malaise, decreased motor, increased muscle tension

101
Q

Overdose of Nicotine

A

60 mg fatal to adults (0.5 mg from common cigarette)
Signs: N/V, salivation, pallor, weakness, ab pain, diarrhea, dizzy, HA, increase BP/HR, tremor, cold sweats, inability to concentrate, confusion, sensory disturb, decreased REM, low birth weight in preg, increase risk of pulm HTN

102
Q

Tx of Nicotine addiction

A

Abstinence
First line: patch, gum, patch + gum
Second line: nasal spray, inhaler, medications

103
Q

Varenicline
Targets?
Length of tx?
SE?

A

Target nicotine dependence
Prescribed for 12 weeks
SE: N/V, gas, HA, insomnia, change in behavior, hostility, agitation, depressed mood, suicidal thought/action

104
Q

Bupropion

A

Smoking cessation drug
Safer than Varenicline
Contraindicated in eating disorder

105
Q

Behavioral therapy for nicotine

A 
discover high risk relapse situations
create aversion to smoking
self-monitoring of smoking behavior
competing coping responses
figure out how to perform common daily activities without smoking** and cope with dysphoria/weight gain
106
Q

Best tx for nicotine?

A

Combo of systemic nicotine admin and behavioral counseling (60% sustained abstinence rate)

107
Q

How can smoker women reduce risk of low birth weight babies?

A

Stop smoking before pregnancy or during first 3 to 4 months to reduce risk

108
Q

One drink =

A

14 g EtOH
1.5 oz 80 proof whiskey
12 oz beer
4 oz glass of wine

1-2 drinks produces a BEC of 0.025 g/dL or 0.025% or 0.25 mg%

109
Q

EtOH Pharmacokinetics
Peak BEC when?
Absorbed where?
Distribution?

A

Absorbed rapidly/completely
Peak BEC ~ 30 min (longer with food)
Small intestine primary site
Rapid, passes easily through membranes, distributes total body water, females have smaller volume of distribution = higher BEC

110
Q

EtOH metabolism and elimination

A

Small, predictable amounts excreted through lungs/urine/sweat (breathalyzer)
Metabolized by oxidation in liver
ZERO ORDER KINETICS

111
Q

Zero Order Metabolism of EtOH

A

Independent of concentration
Varies slightly with body weight/liver weight
7 to 10 g/hr

112
Q

Primary route of EtOH metabolism

A

EtOH –> acetaldhyde by Alcohol dehydrogenase that requires an NAD+ to NADH
(90 to 98% ingested EtOH)
Cytosol

113
Q

What may be responsible for HA in hangover?

A

Acetaldehyde

114
Q

Secondary route of EtOH metabolism

A

Ethanol –> Acetaldhyde by MEOS using NADP+ to NADPH
Microsomal EtOH Oxidizing System
Microsomes of smooth ER
When EtOH is high and NAD is inadequate

115
Q

Acetaldhyde metabolism

A

Acetaldhyde –> acetate via aldehyde dehydrogenase with NAD
Cytosol and mitochondria
Acetate –> acetyl CoA –> TCA
Chronic alcoholics have too much acetate –> acetoacetate –> ketosis

116
Q

EtOH induced metabolic disorders

A

Reduced gluconeogensis
Hypoglycemia
Ketoacidosis
Increase triglyceride synthesis from free FA

bc excess NADH and NADPH

117
Q

Acute EtOH of liver

A

Increased O2 utilization
Decreased gluconeogensis
Increased lactate production
Decreased oxidation of FA - increased fat accumulation (blocking blood flow in the liver causing cirrhosis)

118
Q

EtOH effects on Ion channels

A

Chloride - GABA gated is facilitated

Calcium - Glutamate gated is inhibited (NMDA)

119
Q

Acute EtOH on cardiovascular

A

Vasodilation - hypothermia producing effects of EtOH (smooth muscle relaxation by acetaldhyde, depression of vasomotor system in CNS)
Depression of myocardial contractility

120
Q

Acute EtOH on endocrine

A

Diuresis - inhibition of antidiuretic hormone release (all ADH release is prevented)

121
Q

BEC = 50 - 100 sx

A

Sedation
Subjective “high”
Increased time to react to stimuli
2-4 quick drinks

122
Q

BEC = 100 - 200 sx

A

Impaired motor fxn
Slurred speech
Ataxia

123
Q

BEC = 200 - 300 sx

A

Emesis

Stupor

124
Q

BEC = 300 - 400 sx

A

Coma

125
Q

BEC > 500 sx

A

Respiratory depression

Death

126
Q

Acute tolerance to EtOH

A

Intoxication more pronounced when BEC is rising than when falling
BEC rising –> brain DA in mesolimbic released –> stimulating
BEC falling –> drowsiness

127
Q

Acute/Chronic ETOH on CNS

A

Blackouts - anterograde amnesia
Fragmentation of sleep patterns - diminish REM sleep early
Relaxes muscles in pharynx - snoring, sleep apnea

128
Q

Management of acute alcohol intox

A

Prevent respiratory depression
Prevent aspiration of vomitus
GIVE THIAMINE before glucose (avoid Wernicke’s encephalopathy)
Glucose for hypoglycemia/ketosis
May need to tx electrolyte/phosphate levels

129
Q

How do you get Wernicke’s in acute alcohol intox?

A

Increased NADH favors the conversion of pyruvate to L-lactate instead of to glucose and if thiamine deficient and only given glucose –> lacticacidemia

130
Q

Chronic EtOH signs

A

Wernicke-Korsakoff, neuropathy, cerebeller degen
Myopathy
Hyperlipidemia/uricemia, anemia, thrombocytopenia
Isolated wrist drop
Gastritis, pancreatitis, malabsorption, malnutrition

131
Q

Chronic EtOH liver disease

A

Steatosis - reversible - 90%
Hepatits/fibrosis - 40%
Cirrhosis/failure - 15-30% (fibrous nodules and loss of normal structure of the liver tissue w/ fxnal decline; women > men; hep B/C to make worse)

132
Q

Chronic EtOH GI signs

A

pancreatitis - 3x higher than general public
gastritis
reversible SI injury - diarrhea, weigh loss, vit deficiencies
blood & plasma protein loss

133
Q

Chronic EtOH & cancer

A

Cancer - 10x increase carcinoma

134
Q

Chronic EtOH & heart

A

Cardio - dose/dependent HTN (~15% of all HTN is related to heavy alcohol consumption),
cardiomyopathy (dilated, ventricular hypertrophy/fibrosis)
arrhythmias
increased HDL cholesterol

135
Q

Chronic EtOH tolerance

A

Adaptive changes such that proteins, cells, tissues, organs, systems and individuals are less affected by EtOH
Increased MEOS
Attenuation of drug effect due to learning to cope with intoxication
Cross tolerance with other sedative-hypnotics

136
Q

Chronic EtOH dependence

A

Ethanol withdrawal syndrome

Craving and desire to avoid withdrawal

137
Q

EtOH withdrawal syndrome

A

Amount, rate and duration of alcohol consumption can affect severity
Repeated withdrawals - increase probability of more severe withdrawal
Sx: hyperexcitability, convulsions, toxic psychosis, delirium tremens

138
Q

Delirium Tremens

A

Relatively rare, but life threatening
Mental confusion with fluctating levels of consciousness
Tremor
Agitation
Autonomic over-activity (increase BP/P/R)

139
Q

Management of EtOH Withdrawal

A 
Thiamine
Glucose
Prevent seizures - diazepam/BZD
K, Mg, Phos
Psychosocial therapy, pharm

BZD substitute for EtOH with tapering (long acting BZD like diazepam, but use oxazepam/lorazepam for liver dz)

140
Q

When DT’s occur can you give BZD?

A

Little impact

141
Q

Wernicke-Korsakoff

A

Wernicke’s: confusional state associated with alcoholic thiamine deficiency - tx with thiamine
Korsakoff’s: long lasting memory impairment (confabulations)

142
Q

Fetal Alcohol Syndrome

A 
Epicanthal folds at corner of eye
Low nasal bridge
Short nose
Indistinct philtrum
Small head
Small eye opening
Small midface
Thin upper lip
Retarded body growth
Poor coordination
Minor joint anomalies
Heart/kidney defects
Greatest preventable form of MR
143
Q

Best treatment of alcoholism

A

AA

144
Q

Genetics of alcoholism

A

higher concordance for monozygotic

four fold increase risk in children of alcoholics

145
Q

Alcoholic Labs

A

Increase MCB

Increase liver enzymes (GGT and CDT)

146
Q

Naltrexone

A

Opioid antagonist (mu)
Reduces CRAVINGS
Can’t use in impaired liver or opioid pts

147
Q

Acamprosate

A

Treating abstinent alcoholics
Reduces CRAVING
Blocks NMDA and activates GABAa
Combo with naltrexone or conseling/psychosocial

148
Q

Disulfiram

A

Aversion therapy
Blocks aldehyde dehydrogenase
Acetaldehyde syndrome - N/V, flushing, HA, sweating, confusion

149
Q

EtOH as a therapeutic in what?

A

MeOH and Ethylene Glycol poisoning
Used with hemodialysis, emesis, gastric lavage, correction of acidosis, supportive care
Higher affinity for alcohol dehydrogenase - inhibit formation of toxic aldehydes

150
Q

Fomepizole

A

Inhibit the action of alcohol dehydrogenase to reduce synthesis and accumlation of toxic aldehydes
MeOH and ethylene glycol poisoning

151
Q

Psychostimulants

A

Cocaine
Amphetamines
Nicotine

152
Q

Hallucinogens

A

LSD, LSD-like
Phencyclidine
Ketamine
MDMA

153
Q

Most drugs of abuse increase ____ in ____

A

DA in nucleus accumbens

154
Q

Targets of drug abuse in the brain

A

Reward pathway
VTA, nucleus accumbens, prefrontal cortex
VTA connected to both - VTA release DA to NA and prefrontal cortex –> rewarding stimulus

155
Q

Differences in route of admin

A

Oral - slow absorption for most, ethanol is rapid
Sublingual: more rapid than oral, bittera alkaloid taste deters
Nasal: readily absorbed
Inhaled: allows drug to reach large absorbing surface - high concentration to brain quickly
IV: most direct route

156
Q

Termination of reinforcing effect is associated with

A

declining plasma concentration
abused drugs tend to have short t1/2 lives
continued drug taking to achieve reinforcing may lead to accum in plasma at toxic level

157
Q

Pharmacokinetic Tolerance

A

Changes in distribution or metabolism of a drug after repeated admin –> diminished concentration of drug at site of action

158
Q

Pharmacodynamic Tolerance

A

Adaptive changes in target tissue occur with repeated use so diminished reponse to the same concentration of drug (reduced receptor density, uncoupling of receptors to signal transduction, compensatory changes in systems mediating opposing effects)

159
Q

Learned Tolerance

A

Behavioral: skills developed through experience with drug

Conditioned tolerance: pairing of drug admin with a specific environmental cues related to drug taking

160
Q

Acute tolerance

A

rapid tolerance developing w/ repeated use on single occasion (cocaine)

161
Q

Cross tolerance

A

Tolerance conferred upon one or more other drugs as a result of repeated use of a given drug (drugs in same structural/mechanistic category)

162
Q

Sensitization

A

increase in response to a drug after repeated admin

163
Q

Cocaine

MOA

A

Reinforcing correlated with blocking DA transporter; also binds NE and 5HT transporters
Also local anesthetic action - convulsion effect in OD

164
Q

Cocaine

Targets

A

Reward pathway: VTA - NA (mesolimbic/cortical DA pathway)
Arousal: NE - Locus Ceruleus, dorsal bundle
Autonomic: NE in periphery (BP, arrhythmia)

165
Q

Cocaine
Sources
Forms

A

Coca plant Erythroxylon coca (peru, bolivia, coloumbia, argentina, brazil, ecuador)

Chewing leaf or powder (snorting, oral, IV, smoked = crack - less effect)

166
Q

Cocaine

Pharmocokinetics

A

1/2 life = 50 min
Toxicity by local anesthetic action
Fatality related to plasma concentration from binge abuse to maintain high

167
Q

Cocaine
Effects
Acute

A 
Euphoria
Arousal
Sense of psychic/physical well being
Self confidence
Improved vigilance/alertness
Increase HR/BP
Decrease appetite
Delays ejaculation
168
Q

Cocaine
Effects
Chronic

A 
Dysphoria
Stereotyped behavior
Anxiety
Sexual dysfxn: impotence
Hallucination: objects in periphery, voices, sensations of bugs crawling under skin
Paranoia
Hyperreflexia
Convulsions, coma, CV collapse
169
Q

Cocaine

Withdrawal

A

Dysphoria, depressed mood
Fatigue
Craving
Bradycardia

170
Q

Cocaine

Toxicity

A

Fatality MC with IV or smoking
Arrhythmias (NE/E at heart), seizures, coma, CV collapse
MC due to binge usage over several hours (toxic plasma levels)

171
Q

Cocaine

Interactions

A

Opioids

Alcohol - cocaethylene –> long 1/2 life, blocks DA transporter

172
Q

Cocaine

Tolerance

A

Occurs to euphoria during a run of use but not much carryover tolerance
Don’t really escalate dose across sessions

173
Q

Amphetamine

MOA

A

Reinforcing effects correlates best with presynaptic release of DA (reuptake transporter in reverse)

174
Q

Amphetamine

Neural Targets

A

Reward pathway: VTA –> NA (mesolimbic/cortical DA pathway)
Arousal systems (NE pathway –> Locus ceruleus/dorsal bundle)
Autonomic: not as profound as cocaine

175
Q

Amphetamine
Effects
Acute

A 
Alertness/anti-fatigue
Euphoria
Anorexia
Emotionality
Toxic psychosis with chronic use
176
Q

Amphetamine

Toxicity

A

Low acute toxicity
Paranoid psychosis and violence in high dose/prolonged used
Sympathetic arousal

177
Q

Amphetamine

Drugs

A

d-Amphetamine
methamphetamine - ice is smoked
methylphendiate - ritalin
phenmetrazine

178
Q

Military uses what for anti-fatigue?

A

Amphetamine

179
Q

Tx for Narcolepsy

A

Amphetamine but low abuse potential ones - modafanil and armodafanil

180
Q

Nicotine MOA/targets

A

Agonist at CNS/peripheral nicotinic sites
Activate VTA –> NA with DA pathway (less so than amphet/cocaine)
Onset with 7 seconds –> 10 puffs/cig
Stim and depressant –> more alert and less tension

181
Q

Indoleamien like hallucinogen

A

LSD (lysergic acid diethylamide)
DMT (dimethyltryptamine)
Psilocybin (mushrooms)

182
Q

Phenethylamine like hallucinogen

A

DOM (dimethoxymethylamphetamine)
MDMA derivatives
Mescaline

183
Q

MDA/MDMA

A

Methamphetamine analog
Modest stimulant/hallucinogen
Initial sedative/dysphoria

184
Q

Phencyclidine

MOA

A

PCP, angel dust, ozone, rocket fuel
Non-competitive blocker of NMDA receptors
Smoking, snorting, oral
Psychotomimetic effects with profound tolerance
12-24 hr 1/2 life

185
Q

Phencyclidine

Effects

A

Euphoria
Staggering
Disorientation
Paresthesia
Nystagmus
Slurred speech
Distortion of body image
Strength/power/invulernability/anger/rage
Depression/paranoia/hostility
Moderate dose - tachy, increase BP, mydriasis, xerostomia
High dose - analgesia, anesthsia, decreased BP/R, horizontal/vertical nystagmus

186
Q

Phencyclidine

OD

A

Anxiety, agitation, aggression, hallucination
Dysphoria, catatonia, muscle rigidity, convulsion
Tachy, sweating, salivation, lacrimation, HTN crisis

187
Q

Ketamine

MOA

A

Special K, vitamine K, cat valium
Dissociative anesthetic, non-competitive blocker of NMDA receptor
Power/liquid - snorted, smoked

188
Q

Ketamine

Effects

A

Disorientation
Sensory illusions
Hallucinations

189
Q

Marijuana

MOA

A

Dope, pot, grass, reefer, herb, ganja
Binding to cannabinoid receptors
Smoked, food, tea

190
Q

Marijuana

Uses

A 
delta-9-THC and dronabinol for
Glaucoma
Reduce N/V in chemo
Anorexia - weight loss in AIDS
Recreational
191
Q

Marijuana

Pharmacokinetics

A 
Rapid absorption following inhalation
Euphoria after 10-30 min for 3-4 hours
Accum in fatty tissue
Active and inactive metabolites
10-15% urinary excretion - up to 30 days
192
Q

Marijuana

Acute Effects

A 
Increased pulse
Decrease exercise tolerance
Reddening on conjunctiva
Euphoria/relaxation
Impaired memory/motor coord
Distorted time sense, hunger, dizzy
193
Q

Marijuana

Chronic Effects

A 
Bronchial - irritation, impaired fxn, cancer
Aggravation of angia
Ortho hypoTN
Decrease testosterone
Diminished intellect
Amotivational
194
Q

Marijuana

Dependence

A

Tolerance reported

Withdrawal: anorexia, N/V, diarrhea, irritability, restlessness, insomnia (after sudden stopping of prolonged use)

195
Q

Marijuana

Overdose

A

Euphoria, time space distortion, tachycardia, fever
Psychosis (hallucinations, depersonalization)
tx with haldol/diazepam for agitation and propranolol for CV

196
Q

Inhalants

A

glue, gasoline, nail polish
damage to neurons, kidney, liver
excitation followed by drowsiness, disinhibition, staggering, agitation

197
Q

Nitrates/Nitrites

A

Systemic vasodilators (amyl nitrate, butyl nitrite)
Abuse associated with enhancedment of sexual sensations
Toxicity: HA, peripheral pooling of blood, decrease myocardial flow

198
Q

GHB

A

alcohol like effects, anabolic steroid like effects, aphrodisiac
synergistic interaction with alcohol - coma like sedation (date rape)

199
Q

Flunitrazepam

A

Rapid onset BZD
Sedative-hypnotic
Amnestic effect - date rape

Med School Year 2 Flash Cards (18 decks)

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