PHAR 100 > MODULE 3 > Flashcards

MODULE 3 Flashcards

(98 cards)

Study These Flashcards
1
Q

sedative-hypnotics dose magnitudes

A
  1. anti-anxiety
  2. sedation
  3. hypnosis
  4. general anesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

sedative hypnotics mechanism of action

A

increasing inhibitory signalling in the brain to decrease glutamate-induced nerve firing

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

brain without sedative hypnoics

A

excitatory neurons releases the neurotransmitter glutamate. neurons “fire” when the excitatory inputs exceed inhibitory inputs

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

brain with sedative hypnotics

A

inhibitory signals from GABA neurons increase with most sedative-hypnotics, resulting in decreased glutamate nerve firing

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

why does the influx in chloride ions cause CNS depression

A

when chloride ions flow into the postsynaptic neuron (because GABA binds to and opens chloride channels), it makes it harder for the postsynaptic neuron to transmit messages, depressing CNS neuronal signalling

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

benzodiazepines routes of administraton

A

usually taken by capsule but some can be intravenous or intranasal

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

benzodiazepine mechanism of action

A

increase frequency of the opening of the chloride channel

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

benzodiazepine therapeutic effects

A

relaxation, calmness, reducing anxiety, skeletal muscle relaxation, anticonvulsant effects

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

benzodiazepines and REM sleep

A

minimal suppression of REM sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

lethality of benzodiazepines

A

very high therapeutic index so wide margin of safety (deaths from overdose is rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

benzodiazepine antidote

A

flumazenil

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

what is flumazenil

A

benzodiazepine receptor antagonist that blocks the effects of benzodiazdepines

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

short-term use adverse effects of benzodiazepines

A
  • CNS: drowsiness, lethargy, fatigue, impairment of thinking and memory
  • breathing: respiratory depression following rapid intravenous administration
  • motor coordination and driving impaired
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

long-term use adverse effects of benzodiazepines

A

varies between individuals. some demonstrate symptoms of chronic intoxication like impaired thinking, poor memory and judgement, incoordination, slurred speech

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

pregnancy and benzos

A
  • benzos cross the placenta (fetal abnormalities in first trimester)
  • secreted into milk risking sedation or death of infants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

older adults and benzos

A

benzos can produce cognitive dysfunction and are metabolized flower leading to over-sedation, falls, and injury

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

benzo misuse potential

A

weaker reinforcing properties. inherent harmfulness is low because it does not depress respiration

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

benzo tolerance

A

can develop to sedative effects and impairment of coordination, anxiolytic, and euphoric effects

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

benzo withdrawal after therapeutic use

A

mild but distinct, anxiety, headache, insomnia

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

benzo withdrawal after chronic use

A

agitation, paranoia, seizures, delirium

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

benzo addiction

A

addiction develops for some not all. depends on genetics and environment

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

barbiturates routes of administration

A

depends what they are used for. for epilepsy its orally, for anesthesia its intavenously

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

barbiturates mechanism of action

A

increases the duration of the opening of chloride channel

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

barbiturates therapeutic use

A

tranquility and relaxation. induce sleep with sufficient dose. clinical uses limited; ultra short/short acting barbiturates can be used to induce anesthesia. long-acting used as antipileptics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
barbiturates lethality
- low therapeutic index - lethal due to respiratory depression (especially combined w alcohol)
26
barbiturates and REM sleep
they suppress REM sleep
27
barbiturates short-term use adverse effects
- low doses: mild euphoria and reduced interest in ones surroundings, dizzines and mild impairment in coordination, pleasurable state of intoxication and euphoria as dose is increased - high doses: depress cardiovascular system, slowing heart and lowering bp
28
barbiturates long-term use adverse effects
chronic inebriation. memory, judgement, and thinking all impaired
29
barbiturates misuse potential
equal or greater than alcohol. pleasurable effects give significant reinforcement. inherent harmfulness very high due to risk of death from respiratory depression
30
barbiturates tolerance
tolerance can develop. high degree of cross-tolerance occurs between barbiturates and other sedatives
31
barbiturates withdrawal
tremors, anxiety, weakness, insomnia, postural hypotension. may progress into seizures, delirium, visual hallucination, and high body temp
32
zopiclone and bezodiazepine-like drugs mechanism of action
bind to subset of GABA receptors and cause sedation
33
zopiclone and bezodiazepine-like drugs advantage over benzos
less disturbance of REM sleep. better hypnotic
34
zopiclone and bezodiazepine-like drugs effects
more sedative effects than anxiolytic effects
35
what receptor does buspirone act on
acts on serotonin receptor
36
when would buspirone be prescribed over benzos or benzo-like drugs
when individual is already taking other CNS depressant drugs
37
buspirone advantage
does not have additive effects with other sedative hypnotic drugs
38
when is buspirone used
generalized anxiety states
39
major reason for the extensive use and misuse of alcohol
ready availability and permissive attitudes of society
40
absorptions of alcohol
ethanol absorbed rapidly from stomach (20%) and upper small intestine (80%)
41
what is absorption rate of alcohol affected by
stomach emptying time (time required for alc to reach small intestine), ethanol concentration in the gastrointestinal tract and presence of food
42
alcohol distribution
distributes throughout total body water and readily gains access to brain. ethanol can also cross placenta
43
metabolism of alcohol
1. alcohol dehydrogenase converts ethanol to acetaldehyde 2. if high dose and alcohol dehydrogenase is at full capacity, MEOS break down ethanol to acetaldehyde 3. aldehyde dehydrogenase converts acetaldehyde to acetate 4. acetate is metabolized into carbon dioxide and water
44
excretion of alcahol
95% excreted in liver, remaining 5% excreted in breath, urine, and sweat
45
medical uses of ethanol
applied topically to treat fever, skin disinfectant, antidote in treatment of methanol poisoning, hand sanitizer
46
BAC 0.05-0.1% effect
sedation, subjective "high", slower reaction times
47
BAC 0.1-0.2% effect
impaired motor function, slurred speech, ataxia
48
BAC 0.2-0.3% effect
emesis, stupor
49
BAC >0.4% effect
respiratory depression, death
50
alcohol mechanism of action
binding to the chloride channel and augmenting GABA-mediated neuronal inhibition
51
what explains the reinforcing effects of alcohol
the interaction of alcohol with the chloride ion channels on dopaminergic neurons in the reward areas of the brain
52
cardiovascular effects of alcohol
low doses: vasodilation (flushing) of vessels to skin, resulting in feeling warm high doses: depress cardiovascular system, leading to abnormal heart rhythm
53
stomach effects of alcohol
low doses: increased gastric secretion high doses: irritate lining of stomach causing inflammation and erosion (gastritis) which causes vomiting and abdominal pain
54
short term high dose effects
memory loss, depression, irritability, over sedation, can lead to self-harm or act of violence, or overdose (respiratory depression, coma, death)
55
chronic high dose alcohol adverse effects on CNS
number of neurological and mental disorders such as alcoholic dementia. alcohol also damages axons of neurons within the brain, resulting in fewer connections between neurons
56
chronic high dose alcohol adverse effects on cardiovascular system
cardiomyopathy, increased incidence of hypertension and stroke
57
chronic high dose alcohol adverse effects on liver
liver disease. reversible in early stages
58
alcohol misuse potential
misuse is moderate due to reinforcing properties of ethanol and availability and social acceptance
59
alcohol inherent harmfulness
moderate. death can occur from high dose acute ethanol ingestion and chronic ingestion can have long term effects on health
60
alcohol tolerance
tolerance to ethanol-induced impairment of task if task if repeated
61
alcohol cross tolerance
1. sedative-hypnotics: higher dose of sedative hypnotics is required 2. general anesthetics: higher dose required
62
alcohol withdrawal
compensatory excitation of the CNS. in severe cases, delirium tremens may occur, which can involve convulsions, coma, and possibly death
63
drugs used to treat alcohol use disorder
naltrexone helps with cravings from blocking activation of dopaminergic pathways in the brain (decrease reinforcement), benzos manage withdrawal symptoms
64
most potent psychoactive agent in cannabis
THC
65
what is cannabis classified as
CNS depressant, euphoriant, and hallucinogen (only at high doses)
66
Cannabis mechanism of action
THC binds to type 1 cannabinoid receptors (CB1). CB1 inhibits release of excitatory neurotransmitters, explaining reduction of cognitive function and CNS depressant effects
67
CB1 receptors in cerebral cortex
mediate distortions of time, colour, sound, and taste, as well as decrease in cognitive function and concentration
68
CB1 receptors in the hippocampus
account for changes in memory and learning
69
why is THC not lethal
there's no CB1 receptors in the brain stem, so cannabinoids don't depress respiration
70
CB2 receptors
found only outside CNS. not involved in psychoactive effects but involved in inflamation
71
CB2 receptors on lymphocytes
responsible for immunosuppressive properties of THC
72
THC absorption
inhaled: rapid and action is immediate ingested: slow and incomplete. effect is less
73
THC distribution
throughout body especially to tissues w/ high blood perfusion, placenta. THC is highly lipid soluble and over time will be stored in adipose tissues
74
cannabis metabolism
slow metabolism. metabolites can be seen for weeks after stopping use
75
cannabis half-life
30 hours
76
short-term cannabis effects on CNS
relaxation and drowsiness, feeling of well being and euphoria, impaired motor coordination, increased appetite, pseudo-hallucinations
77
short-term cannabis effects on cardiovascular system
increased heart rate, increased bf to extremities, postural hypotension
78
short-term cannabis use on GI tract
increased appetite, dryness of mouth and throat
79
long-term cannabis use psychological effects
low dose: nothing high doses: amotivational syndrome, lack of concentration, loss of abstract thinking, loss of short-term memory
80
long-term cannabis use cardiovascular effects
reversible, increased hr potential problem for those with heart disease
81
long-term cannabis use fertility effects
males: decreased sperm count females: follicle stimulating hormone and luteinizing hormone to be reduces, and cycles can occur without ovulation
82
cannabis tolerance
tolerance occurs to psychoactive properties, cardiovascular system effects, and effects on impairment of performance and cognitive function
83
cannabis withdrawal
sleep disturbances, irritability, loss of appetite, nervousness, mild agitation, upset stomach, sweating
84
cannabis addiction
persistent cravings for drug, risk of addiction more evident for those who use cannabis to control psychological stress
85
what is an opioid
any natural or synthetic substance which exerts actions on body through binding to the opioid receptors
86
endogenous opioids
opioids made in body that bind to opioid receptors and exert analgesic effects
87
3 families of endogenous opioids
1. enkephalins 2. dynorphins 3. beta-endorphins
88
what do endogenous opioids affect
affect the perception of pain and the emotional responses to pain
89
natural opioids
morphine and codeine
90
morphine
binds directly to opioid receptors. used for severe pain and can cause euphoria
91
codeine
converted to morphine in the body by liver enzymes
92
semi-synthetic opioids
hydromorphone and diactylmorphine
93
hydromorphone
clinically used for analgesia and five time more potent than morphine
94
diacetylmorphine
used as part of injectable opioid agonist therapy to manage OUD
95
synthetic opioids
fentanyl and related compounds, loperamide, methadone
96
fentanyl and related compounds
100 times more potent than morephine and designed to treat pain. contribue to OUD crisis
97
loperamide
98
PHAR 100
flashcards
Decks in class (5)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions