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PHAR 100 > module 3 > Flashcards

module 3 Flashcards

1
Q

what is the general mechanism of sedative hypnotics

A

an increase in the GABA neurons which will decrease glutamate firing

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2
Q

explain GABA signalling

A

GABA can open select chloride channels which will release chloride ions which will make it harder for post synaptic neurons to transmit incoming signals , diminishing CNS signalling

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3
Q

explain the binding of sedative hypnotics to chloride

A
  • modulate ion channel in brain or spinal chord , however each different drug will bind to a different site on the chloride channel –> enhance inhibitory effect of GABA
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4
Q

therapeutic effects of Benzodiazepines

A

relaxation , calmness, relief of anxiety and tension , decrease in REM type sleep, relation of skeletal muscles , some can be effective hypnotics

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5
Q

administration of benzodiazepines

A

taken as a tablet or capsule however could be intravenous

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6
Q

mechanism of action of benzodiazepines

A

increase the frequency of opening of chloride channel

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7
Q

how are benzodiazepines lethal ?

A

commonly involved in overdose, death can occur when large amounts are used or when taken with other sedation drugs

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8
Q

what is the antidote for benzodiazepines ?

A

flumazenil which is a receptor antagonist which will block the effects of benzodiazepine , can be used to reverse the effects (overdose )

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9
Q

short term adverse effects of benzodiazepines

A

CNS - fatigue, impairment of thinking and memory
LUNGS- respiratory depression
MOTOR COORDINATION- moderate doses can impair driving and motor coordination , will get worse as dose gets larger

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10
Q

Adverse long term use of benzodiazepines

A

varies with the individual, others will demonstrate symptoms of chronic sedative - hypnotic intoxication ( impaired thinking, disorientation , poor memory

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11
Q

benzodiazepines and pregnancy

A

result in fetal abnormalities if administered within the first trimester - also found in breast milk, could result in infant death

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12
Q

elderly and benzodiazepines

A

can produce cognitive dysfunction in older adults , are metabolized more slowly and cold result in over sedation

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13
Q

potential for misuse with benzodiazepines

A

have weaker reinforcing properties , with low harmfulness ( won’t lead to death on its own )

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14
Q

tolerance to benzodiazepines

A

can develop for the sedative effects and impairment coordination , level of tolerance is very low. ( cross tolerance can occur with other sedative drugs )

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15
Q

short and long term withdrawal of benzodiazepines

A

with therapeutic use, there is mild withdrawal symptoms ( headache ), chronic use , there are worse symptoms, such as paranoia, agitation and seizures

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16
Q

addiction to benzodiazepines

A

can occur however depends on environmental factors and genetics

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17
Q

Barbiturates

A

class of sedative hypnotics that are grouped by their duration of effect , long, short or ultra short. Barbituric acid is the base

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18
Q

Mechanism of barbiturates

A

increases the duration of of the opening of the chloride channel

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19
Q

low doses of barbiturates cause

A

tranquility and relaxation , and possibly induce sleep

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20
Q

short and ultra short barbiturates can be used for

A

induce anaesthesia

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21
Q

barbiturates have been replaced because ?

A

low therapeutic index and possibly could cause death ( depression of respiration , especially with alcohol, dose depend on person and there is no antidote

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22
Q

effects of short term barbiturate use

A
  • mild euphoria, dizziness, mild impairment of motor coordination,
    high doses, depresses cardiovascular system , slowing heart and blood pressure
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23
Q

long term effects of barbiturate use

A

chronic inebriation - impaired memory , judgement, and thinking

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24
Q

adverse effects of barbiturates

A

suppress the REM sleep

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25
Q

potential for misuse of barbiturates

A

should be avoided as it is the same as alcohol

- sometimes are injected to obtain rush effect—> very dangerous

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26
Q

tolerance of barbiturates

A

high degree of cross tolerance between other sedatives

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27
Q

withdrawal of barbiturates and symptoms

A

will occur after chronic use , symptoms include, seizures, delirium, high body temperature and hallucinations
postural hypotension is also seen

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28
Q

addiction of barbiturates

A

can result from regular use no matter the dose . people may panic if cannot get supply , and craving is common

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29
Q

zopiclone and zolpidem

A

benzodiazepine like drugs that bind to a subset of the GABA receptors and cause sedation

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30
Q

advantage of zopiclone

A

disturb sleep patterns less than traditional benzodiazepine
- they have more sedative effects compared to anxiolytic effects

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31
Q

Buspirone

A

anxiolytic that acts on serotonin receptor instead of GABA and can be prescribed when the patient is already taking a CNS depressant –> doesn’t have additive effects

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32
Q

where is alcohol absorbed ?

A

20% in the stomach and 80%in the upper small intestine

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33
Q

what affects the absorption of alcohol

A
  • stomach emptying time and ethanol concentration in the GI tract and the presence of food
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34
Q

What are the 4 steps of alcohol metabolism

A

alcohol dehydrogenase, meos, aldehyde dehydrogenase and aldehyde dehydrogenase

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35
Q

what is alcohol dehydrogenase ?

A

the enzyme which is used to convert ethanol to acetaldehyde , is known as the rate limiting step

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36
Q

What is MEOS and what does it do ?

A

microsomal ethanol oxidizing system which is part of cytochrome p450 system
- contributes to the metabolism of ethanol , breaking it down to acetaldehyde when alcohol dehydrogenase is running at full capacity

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37
Q

acetaldehyde is converted to ?

A

acetate by the enzyme aldehyde dehydrogenase (ALDH)

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38
Q

Acetate is then metabolized to

A

CO2 and water by otters tissues

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39
Q

how do genetic variants contribute to ethanol metabolism ?

A

some ppl rapidly convert alcohol to acetaldehyde causing it to accumulate in the body ( protects agains alcoholism )

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40
Q

what is the rate of ethanol metabolism

A

occurs at a constant rate, irrespective of the blood alcohol concentration —> ADH becomes saturated at 20 mg per 100 ml of blood

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41
Q

body rate of ethanol metabolism is

A

120mg ethanol/ kg body weight / hour

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42
Q

how is alcohol excreted ?

A

95% of ethanol is eliminated via the liver, while the 5% is eliminated through breath, urine and sweat

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43
Q

alcohol is metabolized through

A

mainly the liver but some can happen in the stomach

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44
Q

build up of acetaldehyde causes

A
  • nausea, vomiting, flushed face, dizziness
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45
Q

medical uses of alcohol

A

can be used as a skin disinfectant, as an antidote the treatment of methanol poisoning and also as a hand sanitizer and topically to treat fever

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46
Q

what will take place with a BAC of 0.1- 0.2 %?

A

impaired motor function , slurred speech, ataxia

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47
Q

what will take place with a BAC of 0.2-0.3%

A

emesis, stupor

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48
Q

what will take place at a BAC of 0.3- 0,4 %?

A

coma

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49
Q

BAC greater than 0.4%?

A

Death and respiratory depression

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50
Q

what is the main mechanism of alcohol ?

A

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

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51
Q

alcohol interacts with ?

A

chloride ion channels in dopaminergic neurons in reward centres of brain ( could explain reinforcement )

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52
Q

Low doses and High doses of alcohol on cardiovascular system

A

LD - can create vasodilation of vessels which contributes to warmth feeling
HD- can lead to cardio depression which could alter the rhythm of the heart

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53
Q

Low dose and high dose of alcohol effect on stomach

A

LD- increase in gastric secretion

HD- will irritate the lining of the stomach and case immflamtion and gastritis , which causes vomiting

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54
Q

Low dose and High dose of alcohol on the liver

A

LD- does not have significant effects on the liver

HD- binge drinking will inhibit glucose production and can lead to hypoglycaemia

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55
Q

adverse effects of binge drinking include :

A

Memory loss , psychiatric effects ( depression irritability , and over sedation ) and overdose

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56
Q

adverse effects of chronic high dose alcohol consumption in the CNS include

A

neurological disorders such as alcoholic dementia, as alcohol can damage axons in the brain and will effect memory , judgement and thinking

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57
Q

Cardiovascular effects of chronic high dose alcohol consumption

A
  • leads to alcoholic cardiomyopathy ( destruction of heart muscle ) and an increased incidence of hypertension and stroke
58
Q

Liver and chronic high dose alcohol consumption

A
  • leads to alcoholic lever disease which is irreversible at later stages and severely impairs liver function
59
Q

chronic high dose alcohol and pregnancy effects

A

will manifest postnatally as fetal alcohol spectrum disorder (FASD)

60
Q

features of FASD

A

flat mid face, short nose, the upper lip , short palpebral fissure, indistinct phillirum

61
Q

what happens when alcohol is used in drug therapy

A

will have an additive or synergistic effect of CNS depression
- inhibition of metabolism of certain drugs ( sedative- hypnotics

62
Q

what happens when there is chronic alcohol use before drug therapy ?

A

increases the activity of metabolizing enzymes in the liver resulting in increased metabolism

63
Q

potential to misuse ethanol

A

has moderate misuse use potential due to its reinforcing properties. high availability contributes to possible misuse

64
Q

inherent harmfulness of alcohol

A

moderate , ethanol is less harmful than methanol

65
Q

tolerance to alcohol

A

can occur with chronic consumption

66
Q

cross tolerance can occur with alcohol and

A

sedative - hypnotics –> higher dose would be needed to achieve therapeutic effect and general anesthetics –>a higher dose of anaesthetic would be needed for someone who developed tolerance to alcohol

67
Q

withdrawal of alcohol

A

produces compensatory excitation of the CNS ( arousal stimulation ) with severe cases of withdrawal delirium tremens may occur which includes coma, tremors and possible death

68
Q

addiction of alcohol

A

very powerful when there is chronic use of alcohol contributing to SUD

69
Q

why is diazepam which is a benzodiazepine used to treat alcohol withdrawal symptoms

A

due to the similar mechanism of action to alcohol which is sued to suppress symptoms

70
Q

what drug is used to treat

A

Naltrexone which is an opioid antagonist in which it diminishes the craving of ethanol and helps in abstinence and blocks the activation of dopaminergic reward pathways

71
Q

cannabis contains

A

cannabis sativa, sativa and has 60 compounds known as cannabinoids ( THC is the most psychoactive agent)

72
Q

pharmacological classification of cannabis

A

is a CNS depressant , euphoriant and hallucinogen

73
Q

how is cannabis administered ?

A

it isa dried plant that is smoked or inhaled, extracts contain cannabinoids in oil that can be vaped or taken orally

74
Q

Mechanism of a action of cannabis

A

binds to receptor in brain and spinal cord known as type 1 cannabinoid receptors (CB1)

75
Q

Anandaminde and cannabis

A

is an endogenous ligand for CB receptors involved in learning and memory , when receptor is activated, it inhibits the release of excitatory neurotransmitters ( explains reduction of cognitive function with THC

76
Q

anandamide is considered a

A

retrograde transmitter, meaning it is released from postsynaptic neuron and influences pre synaptic neuron and will bind to CB1 receptor, and inhibiting release of excitatory neurotransmitters

77
Q

where are CB1 receptors located in Brain ?

A

CB1 receptors in cerebral cortex - mediate distortions of time and color and cognitive function
CB1 receptors in hippocampus - account for changes in memory and learning

78
Q

CB2 receptors are found ?

A

outside of the CNS and are not involved in the psychoactive effects of THC

79
Q

binding of THC to CB2 in lymphocytes is responsible for

A

immunosuppressive properties of THC

80
Q

absorption of THC

A

Once inhaled, effects are almost immediate, if ingested, there is a 30 to 60 minute delay and and absorption is slow and incomplete

81
Q

THC distributes where in the body ?

A

everywhere , however is higher in tissues with high blood perfusion ( lung , heart, brain and liver ) is highly lipid soluble and will be stored in adipose tissue over time

82
Q

THC is metabolized ?

A

very slowly and will remain in the body weeks after use

83
Q

THC excretion?

A

has a half life of around 30 hours but to remove from adipose tissues may take longer

84
Q

short term use of THC and the CNS

A

Relaxation and drowsiness , feeling of well being an euphoria, impaired motor coordination, and increased appetite

85
Q

with higher doses what can occur ?

A

pseudo- hallucinations where the person knows it is not real and running together of senses and impaired judgement

86
Q

cardiovascular system and short term effects of THC

A

increased heart rate, increased blood flow to extremities and postural hypotension ( low blood pressure when standing or sitting )

87
Q

GI tract and short term THC usage

A

increased appetite and dryness of mouth and throat

88
Q

other possible shrort term effects of cannabis

A

reduction in sex drive for males ( decrease in testosterone), disruption of the ovarian cycle and hangover feelings

89
Q

while driving, THC can impair ?

A

motor coordination, tracking, perception and vigilance

90
Q

psychological effects of long term cannabis use

A

at a high dose, there can be short term memory loss, lack of concentration, loss of abstract thinking. Amotivational syndrome is associated with long term use can possibly have permenent structural changes in the brain with long term use

91
Q

cardiovascular effects and long term use of THC

A

Some changes in blood pressure are seen as well increase in heart rate however are not serious and are reversible. could be an issue with heart disease

92
Q

respiratory effects of long term use of THC

A

incidence of lung cancer and COPD are increased with long term use . can be damaging due to the high amount of carcinogens found in the cannabis smoke and the smoke is held in the lungs for longer causing more damage from higher absorption of tars

93
Q

long term use of THC and fertility

A

can lead to decreased sperm count and FSH and LH will be reduced in which a cycle can occur without egg release , in pregnancy THC can readily cross the placenta causing possible delays in development

94
Q

vaping and E cigarettes can cause ?

A

EVALI a unique disease entity the results in lung injury

95
Q

medical use of cannabis needs to ?

A

separate the beneficial effects ( analgesia) from the psychotropic effects

96
Q

when can cannabis be prescribed ?

A

not an approved heath Canada therapeutic but, can be used to treat a variety of symptoms that have not response to traditional treatment

97
Q

misuse potential of cannabis ?

A

considered low to moderate as euphoria and reinforcement are lower compared to other drugs

98
Q

tolerance of cannabis can occur for

A

the psychoactive properties of THC , the effects on the cardiovascular system and the impairment of cognitive function

99
Q

withdrawal and cannabis

A

can occur with high dose long term use and can be characterized by sleep disturbances, irritability, nervousness , loss of appetite and sweating

100
Q

addiction and cannabis

A
  • develops as a persistent craving of a drug , risk is more evident in those that use it to control psychological stress
101
Q

Opioids are found

A

within the opium poppy plant and clinically produces morphine and codeine

102
Q

opioids can be

A

a natural or synthetic substance that will bind to opioid receptors

103
Q

endogenous opioids are

A

opioids that are made in the body that bind to opioid receptors and exert analgesic effects . the 3 families are enkephalins, dynorphins and beta endorphins
- are able to affect perception of pain and the emotional response and could influence mood and are associated with reward pathways

104
Q

The natural opioids are

A

morphine and codeine

105
Q

Morphine binds directly to

A

opioid receptors and is used clinically to treat severe and chronic pain and can cause euphoria ( is 10x more potent than codeine )

106
Q

codeine gets transformed into

A

morphine in the body by liver enzymes ( Tylenol is a combo of codeine and acetaminophen and caffeine )

107
Q

semi synthetic opioids

A

altered versions of morphine to chemically give other pharmacological properties

108
Q

hydromorphone

A

semisynthetic opioid that is used for analgesia and is 5x more potent than morphine

109
Q

diacetylmorphine

A

aka heroin is a semi synthetic and is used as part of injectable opioid agonist therapy (iOAT) to manage OUD , 2- 5x more potent than morphine

110
Q

synthetic opioids

A

not derived from morphine but are chemically synthesized to bind to opioid receptor

111
Q

fentanyl and other related compound

A

100x more potent than morphine and was designed to treat acute chronic pain

112
Q

loperamide

A

over the counter drug that is used to treat diahrrea ( uses a common side effect of opioids which is constipation , does not cause euphoria and is metabolized quickly in the intestine

113
Q

methadone

A

Is used for analgesia and can be used in treatment of OUD as it can prevent withdrawal symptoms but will not cause euphoria

114
Q

where are opioid receptors found ?

A

in both the central an peripheral nervous system and also in the GI tract

115
Q

Mu opioid receptor

A

found in brain and spinal cord and mediate analgesia and are responsible for morphine mediated depression in brain stem –> often involved in the misuse of opioids

116
Q

kappa opioid receptors

A

involved in analgesia, dysphoria and miosis (pinpoint pupils)

117
Q

Delta opioid receptors

A

involved in analgesia in the spinal cord and brain and may modulate emotional responses to opioids

118
Q

mechanism of action of opioid

A

will block pain pathways in spinal cord and brain through the activation of mu receptors

119
Q

how do opioids reduce pain signalling

A

prevent pain signals from traveling by reducing neurotransmitter release from presynaptic neurons and reducing the effect on post synaptic neurons

120
Q

opioids reduce emotional reaction through

A

modulation of the limbic system

121
Q

Analgesia and opioids

A

a short term effect which produces indifference to pain reducing both the reaction and intensity of the pain , respiratory depression is the limiting factor

122
Q

sedation and hypnosis and opioids

A

all opioid analgesics produce sedations but will not be as intense as cos depressants

123
Q

suppression of cough centre and opioids

A

short term effect in which relief or prevention of cough

124
Q

respiratory depression and opioids

A

a short term effect which surpasses the respiratory centre of the brain stem , respiratory drive of co2 is reduced mediated by mu and delta receptors , can cause death or overdose

125
Q

short term endocrine effects and opioids

A

reduced release of testosterone , estrogen and progesterone and drop in libido for men reduce the release of sex hormones from hypothalamus

126
Q

miosis and opioids

A

causes the constriction of pupils

127
Q

body temperature/ heart rate and opioids

A

heart rate will be irregular with high dose of opioids and the skin will be cold and clammy

128
Q

decreased motility

A

constipation is an adverse effect of short term opioid use

129
Q

what are the 3 therapeutic uses of opioids

A

treatment of severe pain, treatment of diarrhea and cough suppression

130
Q

misuse potential for opioids

A

have powerful euphoric effects which means there is a larger potential for misuse

131
Q

inherent harmfulness of opioids

A

low moderate dose: not very high for morphine

high doses : can be life threatening

132
Q

injection risk of opioids

A

higher risk of developing abcesses and injections ( heart valve ), using contaminated needles could spread AIDS or hepatitis

133
Q

what happens with opioid overdose

A

takes place when there is profound respiratory depression , treatment includes opioid antagonist naloxone

134
Q

tolerance of opioids

A

occurs with most pharmacological effects aside from constriction of pupils and the constipation, tolerance will be reversed a few days after usage stops

135
Q

cross tolerance of opioids

A

occurs between all opioid analgesics where they act on the same receptor( tolerance to morphine will result in a tolerance to methadone )

136
Q

withdrawal and opioids

A

pronounced withdrawal syndrome occurs after opioid discontinuation and symptoms include restlessness, anxiety, sweating, chills, increased respiratory rate , cramping and diahrrea

137
Q

opioids addiction

A

pronounced craving for opioid can develop due to powerful euphoria

138
Q

opioid in pregnancy

A

increased risk of premature delivery and low birth rate , at birth, baby will experience abrupt termination of opioid exposure which will lead to irritability, sleep disturbances poor feeding and seizures

139
Q

pharmacological treatment of OUD and opioids

A

buprenorphine/ naloxone long acting synthetic opioid which binds to mu and provide enough agonist to prevent withdrawal symptoms but has decreased euphoria and sedating effects . In Canada the 2 are administered together

140
Q

what is methadone ?

A

used for treatment of OUD and is a synthetic opioid that is effective in oral administration and is long lasting , potential of misuse is low and removes possible risks of injections . can lead to less euphoria due to the slow effects of taking it orally

PHAR 100 (3 decks)

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