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PHAR 100 > Module 3 - section 1 + 2 > Flashcards

Module 3 - section 1 + 2 Flashcards

1
Q

sedative hypnotic agents

A

they are CNS depressants

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2
Q

magnitude of CNS depressions

A

dose determines effects

low dose to high dose
- anti anxiety
- sedation
- hypnonis
- general anesthesia

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3
Q

mechanisms of sedative hypnotics

A

when a person is anxious or having difficulty sleeping the aim is to depress overall brain activity

decrease glutamate induced nerve firing by increasing inhibitory signalling in the brain

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4
Q

brain mechanisms without sedative hypnotics

A

brain activity involve excitatory neurons

neurons release the neurotransmitter glutamate

when excitatory inputs exceed inhibitory inputs the neurons fire

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5
Q

brain mechanisms with sedative hypnotics

A

inhibitory signals from GABA neurons increase

leads to decreased glutamate nerve firing

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6
Q

GABA

A

primary inhibitory neurotransmitter in the CNS

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7
Q

GABA signalling

A

GABA inhibits by binding to and selectively opening chloride channels

when open chloride ions flow into the postsynaptic neuron
- makes it harder to transmit incoming messages to other neurons
- depresses CNS neuronal signalling

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8
Q

GABA receptor subunit

A

has four transmembrane spanning regions

receptor is a pentamer, two alpha subunits, two beta and one gamma

when nothing bound its close

when bound channel opens

span the neuronal cell membrane

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9
Q

drugs binding to chloride channel

A

all modulate the chloride ion channel in brain and spinal cord

dif drugs bind to dif sites on the chloride channel
- increases synaptic inhibition

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10
Q

benzodiazepines

A

most widely prescribed drug

different types exist
- therapeutic effects and duration of action dif
- mechanisms of action the same

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11
Q

route of administration of benzodiazepines

A

usually taken as a capsule or tablet

some available for IV or intranasal

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12
Q

mechanism of action of benzodiazepines

A

activation of the benzodiazepine receptor increases the frequency of the opening of the chloride channel

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13
Q

therapeutic effects of benzodiazepines

A

relaxation, calmness and relief from anxiety or tension

can produce skeletal muscle relaxation and have anticonvulsant effects

some are effective hypnotics

can have minimal suppression of REM type sleep

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14
Q

lethality of benzodiazepines

A

most commonly involved in overdose

high therapeutic index

death occurs form
- ingestion of enormous doses
- rapid IV injection of large doses
- taken with other sedating drugs (alcohol)

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15
Q

antidote for benzodiazepines

A

flumazenil reverse its effects in the event of an overdose
- benzodiazepine receptor antagonist (blocks effects)

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16
Q

adverse effects of short term benzodiazepine use

A

CNS
drowsiness, lethargy, fatigue, impairment of thinking and memory (depends on targeted therapeutic effect)

lungs
respiratory depression flowing rapid IV administration

impair motor coordination and driving

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17
Q

adverse effects of long term benzodiazepine use

A

vary between individuals

some have no intoxication

some have symptoms of chronic sedative hypnotic intoxication
- impaired thinking
- poor memory and judgement
- disorientation
- incoordination
- slurred speech

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18
Q

benzodiazepine use in pregnant/chestfeeding ppl

A

cross the placenta and distribute into the fetus
- in first trimester risk of fetal abnormalities

secreted into milk exposing infant to therapeutic or toxic doses of the drug
- result in sedation or death

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19
Q

benzodiazepine in older adults

A

can produce cognitive dysfunction

metabolized slower in older adults
- leads to over sedation, falls and injury

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20
Q

benzodiazepine misuse potential

A

have weaker reinforcing properties than other drugs

inherent harmfulness is low

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21
Q

benzodiazepine tolerance

A

can develop to sedative effects, impairment of coordination, anxiolytic effects or the euphoric effects

magnitude of tolerance does not produce clinical concerns

high degree f cross tolerance occurs among benzodiazepine and other sedative hypnotic drugs

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22
Q

benzodiazepine withdrawal

A

mild distinct withdrawal can occur
- anxiety, headache, insomnia

chronic use withdrawal
- agitation, paranoia, seizures, delirium

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23
Q

benzodiazepine addiction

A

may develop in some but no all

depends on many factors
- genetics and environment

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24
Q

barbiturates

A

class of sedative hypnotic

order class of drugs
- replaced by safe more effective drugs

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25
route of administration of barbiturates
vary in administration, depends on what they are being used to treat epilepsy oral anesthesia IV
26
mechanisms of action of barbiturates
activation of barbiturate receptors increases the duration of opening of chloride channels demonstrate the full spectrum of dose dependent CNS depressions (magnitude of CNS depressions)
27
therapeutic use of barbiturates
low dose - tranquility and relaxation - sleep if the dose is sufficient clinical use (limited) - ultra short and short acting barbiturates used to induce anesthesia - long acting used as antiepileptics
28
lethality of barbiturates
low therapeutic index so replaced with newer and safer drugs lethality due to depression of respiration (especially when combined with alcohol) - is dose dependent - lethal dose varies between individuals antidote for barbiturate doesnt exist death can occur during withdrawals
29
adverse effects of short term barbiturate use
low dose - mild euphoria - reduced interest in surrounding dizziness and mild impairment of motor coordination pleasurable state of intoxication and euphoria as dose increases high dose - depress the cardiovascular system (slow heat, lower blood pressure)
30
adverse effect of long term barbiturate use
chronic inebriation - memory, judgement, thinking impaired exhibit hostility and mood swings - depression
31
barbiturate potential for misuse
should be avoided - potential for misuse equal or greater than alcohol effects give a significant degree of reinforcement inherent harmfulness is very high - risk of death from respiratory depression or withdrawal
32
barbiturate tolernace
can develop high degree of cross tolerance occurs between barbiturates and other sedatives
33
barbiturates withdrawal
occurs after discontinuation of chronic use initial symptoms - tremors, anxiety, weakness, insomnia, postural hypotension progressive symptoms - seizures - delirium - visual hallucinations - high body temperature must be withdrawn slowly under medical supervision
34
barbiturate addiction
can result from regular use or irrespective dose will crave the drug and have a feeling of panic craving persists long after use has stopped
35
zopiclone and zolpidem
benzodiazepine like drugs class of sedative hypnotics used to treat anxiety or difficulty sleeping bind to a subset of GABA receptors to causes sedation
36
zopiclone/zolpidem and benzodiazepine similarities and differences
zopiclone/zolpidem - advantage over benzodiazapines as a hypnotic - disturb sleep patterns (REM sleep) even less than benzodiazapines - more sedative effects as to compared to anxiolytic effects both should be used with caution in older adults
36
benzodiazepines effect on GABA
when bound to the chloride ion channel at the same time as GABA it increases the frequency of openings - enhance effects - increased CNS inhibition
37
zopiclone effect on GABA
same effect as benzodiazepine - bind at similar location
38
barbiturates effect on GABA
have separate distinct binding site compared to benzodiazepine dont enhance GABA bind to GABA receptor directly and open the chloride ion channel for an increased duration of time - increased CNS inhibition
39
buspirone
anxiolytic that doesn't act on GAB Receptor acts on serotonin receptor used in generalized anxiety states advantage over other drugs - no addictive effects
40
use of buspirone
used instead of benzodiazepine/benzo like drugs when the individual is already taking other CNS depressant drugs and there is a concern for addictive effects
41
alcohol (ethonal)
CNS depressant that slows down brain functioning and neural activity ethanol is the only type that can be safely consumed
42
absorption of alcohol
rapidly absorbed by stomach (20%) and upper small intestine (80%) absorbtion rate for a given dose is affected by - stomach emptying time/time to reach small intestine - ethanol concentration in the GI and the presence of food time from the last drink to the maximal blood alcohol concentration ranges from 30-90 mins
43
distribution of ethanol
distributed throughout the total body water readily gains access to the brain can readily transfer across the placenta and distribute throughout a developing fetus
44
metabolism of ethanol four steps
- alcohol dehydrogenase - MEOS - aldehyde dehydrogenase - acetate
45
alcohol dehydrogenase
ethanol is converted to acetaldehyde by alcohol dehydrogenase - rate limiting step (speed of conversion sets pace for the rest of metabolism)
46
microsomal ethanol oxidizing system (MEOS)
part of the cytochrome p450 system breaks down ethanol to acetaldehyde important at high doses when alcohol dehydrogenase is at full capacity (saturated)
47
aldehyde dehydrogenase
acetaldehyde converted to acetate by aldehyde dehydrogenase
48
acetate (acetic acid)
metabolized further by a number of tissues into CO2 and water
49
genetic variability in ethanol metabolism
variation in the gene that codes for alcohol dehydrogenase - some rapidly convert acetaldehyde (cause accumulation in body, considered protective since it causes unpleasant side effects, flushed face) aldehyde dehydrogenase has some genetic variability
50
rate of ethanol metabolism
occurs at a constant rate irrespective of the blood alcohol concentration - due to alcohol dehydrogenase becomes rate limiting or saturated - rate is about 120mg ethanol/kg body weight/hour
51
excretion of ethanol
over 95% eliminated by biotransformation (liver), 5% excreted i the breath, urine and sweat
52
metabolism men vs women
mainly occurs in liver in men some occurs in stomach, less in stomach of women
53
medical use of ethanol
very few uses - alcohol sponge applied topically to treat fever - skin disinfectant - antidote in the treatment of methanol (wood alcohol) poisoning - hard sanitizer
54
CNS effect of ethanol
CNS effects proportional to blood alcohol concentration
55
mechanism of action of alcohol
affects a large number of membrane proteins that participate in signalling pathways binds to chloride. ion channel and augmenting GABA mediated neuronal inhibition
56
alcohol and chloride ion channel
interaction of alcohol with the chloride ion channel on dopaminergic neurons in the reward areas of the brain - explain reinforcing effects of drug
57
effects of short term use of alcohol - cardiovascular
low dose - create vasodilation (flushing) of vessels to the skin, cause feeling of warmth high dose - depress cardiovascular system - alternation in the normal rhythm of the heart
58
effects of short term use of alcohol - stomach
low dose - increased gastric secretion high dose - irritate stomach lining (inflammation and erosion, gastritis) - vomiting and abdominal pain - ulcers may be aggravated, gastrointestinal bleed
59
effects of short term use of alcohol - liver
low dose - no significant adverse effects high dose - inhibit glucose production - with fasting can lead to hypoglycemia (low blood sugar)
60
adverse effects of short term high dose alcohol use
memory loss psychiatric effects (depression, irritability over sedation) overdose, respiratory depression, coma and death
61
adverse effects of chronic high dose alcohol use - CNS
neurological and mental disorders occur - alcoholic dementia (decrease in cognitive function affecting memory, judgement and thinking) alcohol damages axons of neurons within the brain - result in fewer connections between neurons
62
adverse effects of chronic high dose alcohol use - cardiovascular
lead to alcoholic cardiomyopathy (destruction of or poor health muscle) increased incidence of hypertension and strok
63
adverse effects of chronic high dose alcohol use - liver
leads to alcoholic liver disease (causes hospitalization and death) - early stages can be reversible with alcohol abstinence - late stages irreversible, liver functions severely impaired
64
effects of alcohol use during pregnancy
chronic use of high doses can produce teratogenic effects in the embryo/fetus can lead to fetal alcohol spectrum disorder abstinence during pregnancy recommended, no safe dose established
65
fetal alcohol spectrum disorder features
- short nose - flat midface - thin upper lip
66
alcohol and drug interactions types (list)
- alcohol use during drug therapy - chronic alcohol use before drug thearpy
67
alcohol use during drug therapy
effects of drugs and alcohol in the body at same time - CNS depressants + ethanol > addictive or synergistic effect of CNS depression - inhibition of metabolism of certain drugs (sedative hypnotics)
68
chronic alcohol use before drug therapy
only occurs if there is no co existing ethanol induced liver injury increases metabolizing enzyme activity in liver - increase metabolism of certain drugs (sedative hypnotics)
69
alcohol potential for misuse
moderate potential availability + social and legal acceptance contributes to misuse harmfulness is moderate
70
alcohol tolerance
tolerance to chronic consumption occurs develop tolerance to ethanol induced impairment of performance tasks when repeatedly performed under the influence
71
alcohol cross tolerance
occurs between - sedative hypnotics (higher dose needed) - general anesthetics (higher dose needed)
71
alcohol withdrawal
withdrawal produced compensatory excitation of CNS (arousal, stimulation) severe withdrawal can lead to delirium tremens (involved convulsions, coma and possible death)
72
alcohol addiction
compulsive desire to seek, obtain and drink ethanol most powerful factor in chronic use
73
drug used to treat AUD (name)
naltrexone and benzodiazepines
74
naltrexone treatment of AUD
it is an opioid antagonist diminishes craving for ethanol blacks activation of dopaminergic reward pathways in the brain
75
benzodiazepine treatment of AUD
have similar mechanisms of action, so suppressed withdrawal symptoms the dose use is gradually decreased over time

PHAR 100 (4 decks)

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