Brainscape's Knowledge GenomeTM

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


See full index

PHAR 100 > PHAR 100 - Module 3 > Flashcards

PHAR 100 - Module 3 Flashcards

1
Q

sedative-hypnotics and anxiolytics

A
  • are CNS depressants

- decrease glutamate-induced nerve firing

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

GABA signalling

A
  • primary inhibitory neurotransmitter in the CNS
  • causes inhibition by binding to and selectively opening chloride channels, resulting in hyperpolarization of the post-synaptic membrane of a neuron
  • overall effect is that it is harder for the post-synaptic neuron to transmit incoming messages to other neurons, depressing overall CNS neuronal signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

drugs that bind to the chloride channel

A
  • most sedative-hypnotics:
  • modulate the chloride ion channel in the brain and spinal cord
  • result is an increase in synaptic inhibition and thus a dampening of neuronal responses
  • in essence, they enhance the inhibitory effect of GABA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

benzodiazepines mechanism of action

A
  • activation of the benzodiazepine receptor increases the frequency of the opening of the chloride channel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

benzodiazepine routes of admin

A

capsule, tablet or IV

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

benzodiazepine lethality

A
  • commonly involved in overdoses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

benzodiazepine pharmacological processes

A
  • very high therapeutic index

- some members of this group are effective hypnotics

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

benzodiazepine short-term use

A
  • CNS → relaxation, calmness, anxiety relief
  • lung → respiratory depression
  • motor coordination → can impair motor coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

benzodiazepine long-term use

A
  • impaired thinking, poor memory
  • disorientation
  • slurred speech
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

benzodiazepine abuse potential

A
  • low abuse liability
  • low inherent harmfulness
  • margin of safety is high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

benzodiazepine dependence

A
  • tolerance → can develop to sedative effects; high degree of cross-tolerance occurs among other sedative-hypnotics
  • dependence → low for short term use
  • addiction → may develop for some
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

barbiturates

A
  • potent CNS depressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

barbiturates mechanism of action

A

activation of the barbiturate receptor increases the duration of the opening of the chloride channel

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

barbiturates pharmacology

A
  • possess a low therapeutic index
  • suppress REM sleep
  • depress respiratory system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

barbiturates short-term effects

A
  • mild euphoria
  • dizziness
  • sleep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

barbiturates long-term effects

A

chronic inebriation

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

barbiturates abuse potential

A
  • abuse liability is equal to or greater than alcohol

- inherent harmfulness is high due to risk of death from respiratory depression

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

barbiturates dependence

A
  • tolerance → can develop to sleep induction and mood effects
  • dependence → a withdrawal syndrome occurs (tremors, anxiety, insomnia, seizures, hallucinations)
  • addiction → can result from regular use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

flumazenil

A
  • a benzodiazepine receptor antagonist that blocks the effect of benzodiazepines
  • can be used as an antidote to benzodiazepine overdose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

zolpidem

A
  • bind to a subset of the GABA receptors, causing sedation

- disturb sleep less than benzodiazepines

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

buspirone

A
  • acts at the serotonin receptor
  • used in generalized anxiety states
  • doesn’t have an addictive effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

gamma-hydroxybutyric acid (GHB)

A
  • an agonist at a subset of GABA receptors, causing sedation and anesthesia
  • implicated as a date-rape drug
23
Q

ADME of alcohol → absorption

A
  • overall rate for a given dose of ethanol is affected by: stomach-emptying time and ethanol concentration in GI tract and presence of food
24
Q

ADME of alcohol → distribution

A

distributes throughout the total body water and readily gains access to the brain

25
Q

ADME of alcohol → metabolism

A
  • ethanol is converted to acetaldehyde by alcohol dehydrogenase (ADH)
  • genetic variants in the gene that codes for ADH exist
  • a 2nd pathway of ethanol metabolism is the microsomal ethanol oxidizing system (MEOS), which is part of the cytochrome P450 system
  • the MEOS contributes to the removal of a dose of ethanol, especially at high doses
  • acetaldehyde is then converted to acetate by aldehyde dehydrogenase (ALDH)
  • acetate is further metabolized by a number of tissues into CO2 and water
  • constant amount of alcohol is metabolized each hour
  • ADH is rate-limiting
26
Q

alcohol CNS effects

A
  • CNS depressant
27
Q

alcohol mechanism of action

A
  • affects a large number of membrane proteins that particpate in signalling pathway
  • augments GABA-mediated neuronal inhibition
28
Q

alcohol non-CNS effects

A
  • short-term (1-3 drinks) → vasodilation of skin vessels, increases gastric secretion
  • short-term (5+ drinks) → depress cardiovascular system, irritation of stomach lining, inhibit glucose production
  • adverse effects → blackouts, psychiatric effects, drinking and driving, violence
29
Q

alcohol effects of chronic high dose

A
  • CNS → alcohol dementia
  • cardiovascular system → alcohol cardio myopathy
  • liver → fatty liver, alcohol hepatits, cirrhosis
30
Q

alcohol abuse potential

A
  • significant reinforcing properties

- dependence liability is moderate

31
Q

alcohol tolerance

A
  • tolerance to chronic use of ethanol does occur

- cross-tolerance can occur between ethanol and sedative-hypnotics and general anesthetics

32
Q

alcohol dependence

A

withdrawal from ethanol produces excitability of the NCS

33
Q

drugs used to treat alcoholism

A
  • disulfriam → inhibits hepatic aldehyde dehydrogenase, and results in aldehyde concentration if the person drinks ethanol
  • naltrexone → opioid antagonist, diminishes craving for ethanol
  • acomprosate → effects mang receptor systems
34
Q

cannabis mechanism of action

A
  • THC binds to receptors, located in the brain and spinal cord called type 1 cannabinoid receptors (CB1)
  • anandaminde was determined to be an endogenous ligand for CB receptors
35
Q

cannabinoid receptors

A
  • 2 types of CB receptors exist
  • a large number of CB receptors are in the brain
  • THC is not a very effective agonist
36
Q

cannabis pharmacokinetics

A
  • THC is slowly metabolized

- inhalation is complete and fast

37
Q

cannabis short-term use effects

A
  • CNS → relaxation, drowsiness, euphoria, impaired judgement
  • cardiovascular → increased HR and blood flow to extremities
  • GI → increased appetite
  • other effects → reduction in sex drive in males, can disrupt ovarian cycle
  • cannabis and impaired driving → motor coordination impaired
38
Q

cannabis long-term effects

A
  • psychological → loss of short-term memory, lack of concentration, “amotivational syndrome”
  • cardiovascular → usually reversible
  • respiratory → asthma, lung cancer, COPD
  • fertility → can decrease sperm count, FH and LH are reduced
39
Q

medical uses of cannabis

A
  • hard to separate beneficial effects from psychotropic effects
  • can help with nausea, appeitite, neuropathic pain
40
Q

cannabis abuse potential

A
  • dependence liability is low to moderate

- inherent harmfulness is also low

41
Q

cannabis dependence

A
  • dependene → can occur with high-dose use
  • tolerance → occurs to psychoactive properties and to impairment of performance and cognitive function
  • addiction → develops with regular use
42
Q

opiate

A

any drug derived from opium (ex: morphine, cocaine)

43
Q

opioid

A
  • any natural or synthetic substance which exerts actions on the body that are similar to those induced by morphine and that are antagonized by the drug naloxone
  • include: opiates, substances structurally related to morphine
44
Q

Mu opioid receptor

A
  • mediate analgesia and are responsible for morphine-mediated depression of respiration in the brain stem
45
Q

kappa opioid receptor

A

involved in analgesia, dysphoria, and miosis

46
Q

delta opioid receptor

A
  • involved in analgesia at the level of the spinal cord and brain
  • may also modulate the emotional response to opioids
47
Q

opioids mechanism of action

A
  • morphine and other opioids block pain pathways in the spinal cord and brain
  • exerted through activation of Mu opioid receptors
    1. reduced presynaptic release of chemical transmitters that are mobilized by pain impulse
    2. blockade of postsynaptic effect of these transmitters
    3. activation of descending inhibitory pathways to block pain input
    4. reduced emotional reaction to pain by acting on the limbic area of the brain
48
Q

opioids effects of short-term use

A
  • analgesia → reduce intensity of pain
  • sedation and hypnosis
  • suppression of cough centre
  • respiratory depression → Mu and delta opioid receptors
  • endocrine effects → reduction in testosterone, estrogens and progesterone
  • miosis - constriction of pupils
  • HR and thermoregulation → irregular HR, low body temp
  • decreased GI mobility
49
Q

opioids long-term effects

A
  • physiological deterioration

- psychological impairment

50
Q

opioids therapeutic uses

A
  • relief of severe pain
  • treatment of diaherrea
  • suppression of cough
51
Q

opioid abuse potential

A
  • powerful euphoric and analgesic effects

- moderate inherent harmfulness`

52
Q

oxycodone

A
  • recently made as a tamper-resistant tablet
53
Q

opioid dependence

A
  • tolerance → occurs to most pharmacological effects
  • dependence → pronounced withdrawal syndrome can occur, not life-threatening
  • addiction → euphoric actions are powerful reinforcers
54
Q

treatment of opioid use disorder

A
  • buprenorphine/naloxone →long-acting synthetic opioid that acts as a partial mu opioid receptor agonist; prevents withdrawal syndromes, decreased euphoria; combined with naloxone to deter people from abusing it
  • methadone → synthetic opioid that is effective following oral administration

PHAR 100 (6 decks)

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