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PHAR 100 > Module 3 > Flashcards

Module 3 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
Q

route of administration of barbiturates

A

vary in administration, depends on what they are being used to treat

epilepsy oral

anesthesia IV

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26
Q

mechanisms of action of barbiturates

A

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)

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27
Q

therapeutic use of barbiturates

A

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
Q

lethality of barbiturates

A

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
Q

adverse effects of short term barbiturate use

A

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
Q

adverse effect of long term barbiturate use

A

chronic inebriation
- memory, judgement, thinking impaired

exhibit hostility and mood swings
- depression

31
Q

barbiturate potential for misuse

A

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
Q

barbiturate tolernace

A

can develop

high degree of cross tolerance occurs between barbiturates and other sedatives

33
Q

barbiturates withdrawal

A

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
Q

barbiturate addiction

A

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
Q

zopiclone and zolpidem

A

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
Q

zopiclone/zolpidem and benzodiazepine similarities and differences

A

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
Q

benzodiazepines effect on GABA

A

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
Q

zopiclone effect on GABA

A

same effect as benzodiazepine
- bind at similar location

38
Q

barbiturates effect on GABA

A

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
Q

buspirone

A

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
Q

use of buspirone

A

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
Q

alcohol (ethonal)

A

CNS depressant that slows down brain functioning and neural activity

ethanol is the only type that can be safely consumed

42
Q

absorption of alcohol

A

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
Q

distribution of ethanol

A

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
Q

metabolism of ethanol four steps

A
  • alcohol dehydrogenase
  • MEOS
  • aldehyde dehydrogenase
  • acetate
45
Q

alcohol dehydrogenase

A

ethanol is converted to acetaldehyde by alcohol dehydrogenase
- rate limiting step (speed of conversion sets pace for the rest of metabolism)

46
Q

microsomal ethanol oxidizing system (MEOS)

A

part of the cytochrome p450 system

breaks down ethanol to acetaldehyde

important at high doses when alcohol dehydrogenase is at full capacity (saturated)

47
Q

aldehyde dehydrogenase

A

acetaldehyde converted to acetate by aldehyde dehydrogenase

48
Q

acetate (acetic acid)

A

metabolized further by a number of tissues into CO2 and water

49
Q

genetic variability in ethanol metabolism

A

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
Q

rate of ethanol metabolism

A

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
Q

excretion of ethanol

A

over 95% eliminated by biotransformation (liver), 5% excreted i the breath, urine and sweat

52
Q

metabolism men vs women

A

mainly occurs in liver

in men some occurs in stomach, less in stomach of women

53
Q

medical use of ethanol

A

very few uses
- alcohol sponge applied topically to treat fever
- skin disinfectant
- antidote in the treatment of methanol (wood alcohol) poisoning
- hard sanitizer

54
Q

CNS effect of ethanol

A

CNS effects proportional to blood alcohol concentration

55
Q

mechanism of action of alcohol

A

affects a large number of membrane proteins that participate in signalling pathways

binds to chloride. ion channel and augmenting GABA mediated neuronal inhibition

56
Q

alcohol and chloride ion channel

A

interaction of alcohol with the chloride ion channel on dopaminergic neurons in the reward areas of the brain
- explain reinforcing effects of drug

57
Q

effects of short term use of alcohol - cardiovascular

A

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
Q

effects of short term use of alcohol - stomach

A

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
Q

effects of short term use of alcohol - liver

A

low dose
- no significant adverse effects

high dose
- inhibit glucose production
- with fasting can lead to hypoglycemia (low blood sugar)

60
Q

adverse effects of short term high dose alcohol use

A

memory loss

psychiatric effects (depression, irritability over sedation)

overdose, respiratory depression, coma and death

61
Q

adverse effects of chronic high dose alcohol use - CNS

A

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
Q

adverse effects of chronic high dose alcohol use - cardiovascular

A

lead to alcoholic cardiomyopathy (destruction of or poor health muscle)

increased incidence of hypertension and strok

63
Q

adverse effects of chronic high dose alcohol use - liver

A

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
Q
A

PHAR 100 (3 decks)

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