Midterm Review Flashcards

1
Q

Describe the metabolism of alcohol. What enzymes are involved?

A

Alcohol diffuses easily across all membranes and is thus completely absorbed by the GI tract in the stomach and upper intestine.

95% of alcohol is metabolized by the enzyme alcohol dehydrogenase (ADH) and the other 5% is excreted through the lungs

85% is metabolized in the liver and 15% is metabolized by first-pass metabolism

Max metabolism is 170g/24hours or 7-8g (10mL)/1hr

  1. ADH converts alcohol to acetaldehyde.
  2. Acetaldehyde dehydrogenase (ALDH) converts acetaldehyde to acetic acid.
  3. Acetic acid is broken down into carbon dioxide and water
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2
Q

How long does it take for an adult to metabolize the alcohol in a 1oz glass of 80 proof whiskey? A 4oz glass of wine? A 12oz bottle of beer? and a pint of 7% microbrew?

A

1 hour

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3
Q

Is a man safe to drive if he is 200lbs and has had 6 drinks in 4 hours?

A

BAC of 200lbs man after 6 drinks = .11

Alcohol burned up after 4 hours = .060
0.11 - 0.60 = 0.05

He is not safe to drive as he is over the legal limit

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4
Q

Is the claim ‘men can handle their alcohol better!” true?

A

For the majority, yes.

Women have a lower level of ADH and thus less or broken down and more alcohol gets into the blood stream

Men typically have a greater ratio of muscle to fat which means they have a larger vascular compartment and thus more blood = more dilution

Women have higher body fat which concentrates alcohol is plasma

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5
Q

What are the pharmacodynamics of alcohol (GABA and Glu)?

A

Alcohol has been shown to affect the Glutamate and GABA systems and the intracellular transduction process

Alcohol depresses the responsiveness of the NMDA glutamate receptor - an excitatory receptor

Alcohol binds to the GABAA receptor, resulting in increased inhibition (reducing panic and anxiety)

  • GABA inhibition induces opioid release which triggers DA in the reward system
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6
Q

Is the stimulation people feel from drinking alcohol pharmacological or psychological?

A

Psychological - alcohol is a depressant

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7
Q

What are the pharmacodynamics in chronic alcohol users?

A

Chronic exposure leads to:

  • Upregulation of NMDA receptors - Acamprosate interacts with these NMDA receptors to reduce neuronal hyper excitability (seizures, nerve damage and loss)
  • An antagonistic effect on 5-HT increasing its activity (remaining in the cleft) - impulsivity and dependence
  • Formation of NT anandamide which activated the cannabinoid receptor, causing down-regulation and hyperactive activation (cravings)
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8
Q

What are the pharmacological effects of alcohol?

A
  • Graded (worsens with increase of dose) reversible depression of behaviour and cognition
  • Depression of respiration
  • Additive effects with other sedative-hypnotic compounds
  • Reduction of circulation function (dilates blood vessels)
  • Increased risk for coronary artery disease and drugs
  • Increase of HD-lipoprotein and HD-choleseterol (good fat and cholesterol)
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9
Q

What are the psychological effects of alcohol?

A
  • Activates GABA system to reduce anxiety
  • Activates DA system so impulse control is reduced and aggression is increased
  • Depressed Glutamate system causing impaired cognitive function, alcohol myopia (short sightedness), and cognitive and attentional deficits
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10
Q

What are the different types of tolerance?

A

Metabolic tolerance - body’s ability to adapt to alcohol

Tissue/functional tolerance

Homeostatic tolerance - environmental cues

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11
Q

What are some side effects of alcohol use?

A

Acute use: clouded sensorium, impaired judgement, anterograde amnesia

High/chronic use: delusions, hallucinations, unconscious

Physical effects: liver damage, dementia (nerve damage), Wenicke Korsakoff syndrome, digestive problems, cancer

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12
Q

Describe some of the fetal effects of alcohol. Is there a ‘safe’ level of drinking during pregnancy?

A

There is no safe limit. Alcohol exposure can cause FAS or alcohol related neurodevelopment disorder (ARND)

FAS is marked by CNS dysfunction, retardation, body growth deficiency, FAS facial/body features

Facial features: microencephaly, palperbral tissue (short opening of eye), epicanthal folds, mid face (flat), low nasal bridge, philtrium (flat upper lip(, micrognathia (small jaw), railroad track ears)

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13
Q

Summarize some of the drugs used in treating alcoholism

A

Alcohol ingestion decreases Glutamate and increases GABA. Alcohol rebound/withdrawl increases glutamate and decreases GABA

  • Benzos treat withdrawal by increasing GABA
  • Antipsychotics alleviate delirium, haullucinosis, and seizures
  • Anticonvulsants treat alcohol dependency
  • Drugs used to maintain abstinence: antabuse, naltrexone, acamprosate,DA drugs (wellbutrin), 5-HT drugs
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14
Q

What differences does Type A and Type B have on alcohol use?

A

Type A are later onset drinkers and Type B drinkers start at a younger age

Alcohol treatment is more difficult with Type B personalities as they started younger.

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15
Q

What is a BrAC?

A

Breath alcohol concentration

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16
Q

If a BAC ratio is .08BAC/..02BrAC what is their BAC is their BrAC is .03

A

X BAC .08 BAC
——— = ————–
.03 BrAC .02 BrAC

x = (.08 BAC)(.03 BrAC)
—————————–
.02 BrAC

x = 0.12

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17
Q

What is the reaction that occurs in a brethalyzer?

A

Potassium Dichromate is the reactive agent that changes colour

Sulfuric acid is what is measured in the breath

Silver nitrate is the catalyst that speeds up the reaction without parking

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18
Q

A rapid change of air temperature can impact a breathalyzer reading

True or False

A

True - requires frequent calibration

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19
Q

Holding your breath will decrease you BAC levels

True or False

A

False - in concentrated it

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20
Q

Running will decrease your BAC levels

True or False

A

True - it decreases the amount of air to expel

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21
Q

Rinsing with mouthwash will increase your BAC

True or False

A

True - it creates false positives because there is alcohol in it

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22
Q

Describe the mechanism action of bentos and how it differs from that of barbiturates

A

Barbituates and benzos are both GABA receptor agonists.

Barbiturates bind to the GABAA receptor and result in an increased duration of the opening of the cl- channel. They also act as an NMDA receptor antagonist, blocking glutamate transmission (blocking excitation)

Benzos bind to an adjacent GABA binding site and cause a 3-dimensional conformation change that increases the affinity (binding) of GABA, increasing the inhibitory action resulting in an influx of Cl- ions hyperpolarizng the postsynaptic neuron depressing excitability

Since barbiturates do not require the presence of GABA they are more toxic

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23
Q

At what point is someone considered to be demented?

A

When they have 5 out of 12 components altered.

  1. Sensorium - orientation to time and place
  2. Affect - feelings
  3. Mental content (knowledge)
  4. Impaired intellectual function
  5. Impaired insight and judgement
24
Q

What are some pharmacological effects of barbiturates?

A
  • Low degree of selectivity
  • Suppression of REM
  • impaired cognition
  • Similar to alcohol effects
  • high doses cause general depression and sleep. When mixed with alcohol can affect respiration and cause lethal overdose
25
Q

Why are babituates rarely used?

A
  • They are lethal in overdose
  • They have a very narrow therapeutic range
  • Large potential for tolerance, dependence, abuse
  • Dangerous drug interactions
26
Q

How does a nonbarbituate differ from a barbiturate?

A

Same effects but different chemical structures

Nonbarbiturates: Soma, Quaalude, Paraldehyde

27
Q

Define synergistic

A

Worse together than apart

Creates a combined effect greater than the sum of their separate parts

28
Q

Why was GHB such a popular date rape drug?

A
  • Depresses the CNS before causing body to be unresponsiveness
  • It is liquid and rapidly absorbed - onset occurred 30-75 min after ingestion, allowing time to leave the bar
  • It is rapidly metabolized (30 min half life)
  • There is low urine detectability so easy to get away with
29
Q

What is the site of action of benzos?

A

Limbis system (hippocampus and fornix)

30
Q

Which 3 main brain structures does Benzos affect?

A

Amygdala, Orbitofrontal cortex, and insula

These decrease anxiety, panic and behavioural response to fear

31
Q

What happens when you metabolize a benzo?

A

Depending on the drug your body either metabolizes it immediately to an inactive metabolite and excretes it

OR

Creates an active metabolite that needs to be further metabolizes

When looking at blood concentration you will see a decrease in the drug but an increase in the active metabolite

32
Q

Elderly individuals handle benzos better than young individuals.

True or False

A

False.

Elderly people have difficulty metabolizing long-acting BZ and their metabolites. It can cause significant cognitive dysfunction

33
Q

What are the pharmacological effects of BZs?

A
  • Anxiolytic activity at amygdala, orbitofrontal cortex, insular
  • Mental confusion & amnesia - cerebral cortex and hippocampus
  • Behavioural rewarding effects - ventral tegmenjtum & nucleus accumbent
34
Q

List some clinical uses of benzos

A
  • Short-term treatment of stress related anxiety and insomnia
  • long term treatment of depression
  • effective of producing anterograde amnesia
35
Q

Combining benzos with CBT increases treatment effectiveness

A

False - it interferes with cognitive therapy

36
Q

Discuss some advantages and disadvantages or Benzos

A

A: rapid onset, anxiolytics, low-level side effects, good patient acceptance

D: impaired psychomotor performance, impaired learning and cognition, reduced alertness, paradoxical agitation, potential for dependence and abuse

37
Q

Are benzos teratogenic?

A

Yes.

If BZ use is near birth it can cause infant dependence or floppy-infant syndrome (low muscle tone)

38
Q

What are some treatment options for BZ overdose?

A

Flumazenil is a GABA-A receptor agonist which binds to the receptor but has no intrinsic affect - blocking the BZ interaction and assisting with potential overdose

39
Q

What is the difference between benzos and ‘Z-drugs’?

A

Z drugs are 2nd generation anxiolytics (nonbenzos) that have a greater sedative affect than anxiolytics and are therefore used for sleep disorders

They have less motor and neuropsychological impairment, less dependence, withdrawal, and abuse potential

40
Q

Compare Zolpidem and Zaleplon

A

Zolpidem and Zaleplon are both agonists of the GABA1A receptor that are used as a hypnotic agent to treat sleep disorders.

Zaleplon has a very short half life and only 30% reaches blood plasma

41
Q

What are the most common anaesthetic drugs ?

A

They are potent CNS depressants that crease unconsciousness and are used in medical settings

They are administer through inhalation or injection

Inhalation: nitrous oxide, isoflurane, halothane

Injectable: Pentothal, Brevital, Dioprovan, Amidate

42
Q

Discuss the history of cocaine

A

Cocaine’s active ingredient was first isolated 1860. It is a crystalline topaane alkaloid. It is derived from the coca plant in south america.

It was thought to be the cure all drug in the late 1800’s but then called the ‘third scrooge’

43
Q

How is cocaine metabolized?

A

Cocaine’s half life is approx 50 min. The major metabolite is benzoylecgonine which can be detected in the body for up to 2 weeks after last dose

When interacting with alcohol it produces cocaethylene which blocks presynaptic DA reuptake transporter making it more toxic

44
Q

Snorted cocaine gets to the brain quicker through the right nostril.

True or false.

A

False.

Cocaine is snorted absorbed in the mucous membrane, sent to the heart, then the lungs for oxygen, back to the heart and then to the brain

Cocaine that is smoked goes from the lungs to the heart to the brain and therefore is faster

45
Q

What are the pharmacological characteristics of cocaine?

A
  • potent local anesthetic
  • Vasoconstrictor
  • psychostimulant
46
Q

Describe the mechanism of cocaine

A

Cocaine potentiates synaptic action of DA, NE, and 5-HT

DA change occurs in nucleus accumbens with activated the DA reward system

The DA transporter is blocked by cocaine which means DA is not being taken back into the presynaptic cell

47
Q

What are the effects cocaine has on an individual?

A

Short-term low dose:
- increased alterness, hyperactivity, euphoria, enhanced self-consciousness, poor appetite and sleep

Moderate dose:
- progressive loss of coordination, rebound depression, seizures, nasal-septal perforations, cerebrally ischemia

Long term high-dose:
- anxiety, paranoia, hyperactivity, aggression, toxic paranoia psychosis, cereal ischemia

48
Q

What is the treatment for cocaine?

A

There is no accepted treatment.

However, there are aversive agents which can make you feel sick after taking it, DA agents to increase DA levels, and anti-craving agents

49
Q

Is cocaine teratogenic ?

A

Yes. It concentrates in the fetus and cause cause spontaneous abortion, low birth weight, decreased head circumference, and withdrawal symptoms in the infant

50
Q

What are amphetamines?

A

Amphetamines are also called sympthamimetic agents because they mimic the actions of adrenaline

They used to be used to treat fatigue but are now used to treat ADHD

They cause vasoconstriction, hypertension, and tachycardia

51
Q

What is the mechanism for amphetamines?

A

They increase presynaptic DA release and block the DA reuptake transporter

Since more DA is in the cleft for longer it has pronounced effects

52
Q

What are the effects of amphetamines?

A

Low lose:
- increased BP, increased HR, relaxed bronchial muscle, euphoria

Moderate dose:
- stimulation of respiration, tremors & restlessness, insomnia, aviation, De nono anxiety disorders

Chronic use:
- repetitive acts, outburst of aggression, paranoia, severe anorexia

53
Q

What does ICE stand for?

A

Methamphetamine also known as ‘speed’ or ‘ice’

54
Q

What is Meth used for?

A

It is an effective treatment of ADHD that is very rapidly absorbed

It can produce long-term neurotoxicity and severe physical addiction

55
Q

Severe decline in physical appearance is related to cocaine addictions

A

False. It is related to methamphetamines