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Drugs & Behaviour > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

What is a CNS depressant?

A

Reduces CNS response to outside signals - whether generated internally or externally to the body

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2
Q

Depressants are also known as:

A

Sedatives, anaesthetics, tranquilizers, relaxants, anxiolytics, hypnotics, anticonvulsants

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3
Q

How do we measure blood alcohol levels in the body?

A

BAC: mg of alcohol/100ml of blood
BAC of 80mg/ml = 0.08%

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4
Q

Why do people tend to eat less while drinking?

A

Alcohol is a food - releases energy

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5
Q

How long does it take to metabolize a single drink?

A

About an hour

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6
Q

T/F: absorption is slower on an empty stomach

A

False

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7
Q

Where does first pass metabolism occur when alcohol is administered the most common way?

A

Stomach

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8
Q

T/F: Males metabolize alcohol faster

A

True

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9
Q

Which chemical facilitates the passage of alcohol through the stomach?

A

Increased CO2

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10
Q

Alcohol distribution depends on:

A

Body size & composition (fat levels as alcohol is distributed in body water)

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11
Q

How much alcohol is metabolized in the liver?

A

85-90%

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12
Q

How much alcohol is metabolized in extra-hepatic sites (i.e., the stomach)

A

10-15%

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13
Q

How much alcohol is excreted unchanged?

A

5% through anywhere with glands (sweat, lungs)

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14
Q

What is the metabolic pathway for alcohol?

A

Broken down by alcohol dehydrogenase -> forms acetaldehyde -> broken down by acetaldehyde dehydrogenase -> forms acetic acid -> broken down with oxidation reaction -> produces CO2 + H2O + energy

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15
Q

What are 3 non-specific effects of alcohol

A
  • Disturbs the relationship of protein in membrane
  • Interacts with polar heads of phospholipids
  • Alters lipid composition
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16
Q

What are 4 specific effects of alcohol?

A
  • Acts as NT binding site
  • Modifies gating system inside channel
  • Stimulates Gs which are linked to adenylyl cyclase
  • Direct interaction with channel protein
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17
Q

What receptor is affected by both alcohol and glutamate

A

NMDA (they block Ca2+ & Na+ from entering cell)

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18
Q

What is the chronic effect of alcohol on the NMDA receptor?

A

Upregulation (pharmacodynamic tolerance)

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19
Q

In a chronic drinker, the glutamate:

A

Moves to be able to function with alcohol in the system

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20
Q

Alcohol _______ GABA(a) receptor transmission

A

Enhances

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21
Q

What is the effect of alcohol on Cl- in chronic and acute use?

A

Decrease in conductance; influx of Cl-

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22
Q

How is DA affected by alcohol?

A

Indirectly. When GABA neuron in VTA releasing inhibitory substance, more GABA is released, exciting DA neurons

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23
Q

How does alcohol affect serotonin & acetylcholine

A
  • Increased depolarization
  • Increased hyperexcitability
  • When withdrawn, behaviour may seem like mania or psychosis
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24
Q

What are 3 things barbituates are used for?

A
  • Treatment of anxiety and insomnia
  • Anticonvulsant
  • Surgical anesthesia
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25
Q

Drugs ending in -barbital, -butal, or -tal are_______

A

Barbituates

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26
Q

What is the most common way to administer barbituates?

A

Water-soluble salt preparation

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27
Q

What is the issue with barbituates?

A

Most have a very narrow therapeutic index (very easy to OD)

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28
Q

What are 4 classic barbituates

A

Secobarbital (seconyl); amobarbital (amytal); thiopental (pentothal); pentobarbital (nembutal)

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29
Q

This barbituate is also known as truth serum

A

Thiopental (pentothal)

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30
Q

Why were Benzodiazepines invented?

A

To have a larger therapeutic window than barbituates, people were ODing too easily

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31
Q

This drug, “Mothers little helper”, invented in 1963 is when housewives became drug addicts

A

Valium

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32
Q

Rohypnol (flunitrazepam) is more commonly known as:

A

Roofies

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33
Q

Gamma-Hydroxybutyrate (GHB) works well because of it’s similar structure to ____

A

GABA

34
Q

GHB was created as a ______ and used to treat ______but was taken off the market due to _______

A

Sedative/anaesthetic; cataplexy associated with narcolepsy; it’s use as a date-rape drug

35
Q

What are symptoms of too much endogenous GHB?

A

brain damage, seizures, loss of muscular control, profound intellectual delay

36
Q

What is an inhalant?

A

Volatile solvents (aerosols, gases)

37
Q

What are behavioural effects of inhalants?

A

Intoxication and light anaesthesia

38
Q

How do inhalants work?

A

Physiochemical processes in cell membranes (non-specific) & by acting as GABA and glutamate agonists

39
Q

Cocaine and amphetamine are examples of what class of drugs?

A

Psychostimulants

40
Q

Psychostimulants have the ability to affect _______ transmitters.

A

Monoamine

41
Q

T/F: Modfications to psychostimulant drug structure is common.

A

True in amphetamines

42
Q

The cocaine molecule:

A

Is odd, doesn’t look like any biological molecules or amphetamines, weird structure blocks reuptake site

43
Q

What are some common forms of cocaine?

A

Coca leaves (used in Bolivia), crystallized salt (cocaine hydrochloride - snorting & IVs; often mixed with baby formula), Freebase (alkaline solution and organic solvent - prepare for smoking), crack (heated with baking soda and dried - smokable, affordable)

44
Q

IV administration of cocaine or smoking, which one lasts longer?

A

Smoking - lasts roughly 4 hours, IV lasts 2

45
Q

How is cocaine metabolized?

A

Enzymes in plasma and liver

46
Q

What is the primary metabolite for cocaine?

A

Benzoylecgonine (tested for in urine)

46
Q

What metabolite is present when cocaine is mixed with alcohol?

A

Cocaethylene

47
Q

When applied topically, procaine, novocaine, etc.:

A

Block volatge-dependent Na+ channels (topical creams for pain relief)

48
Q

What are some mild-moderate effects of psychostimulant use?

A
  • Mood amplification (both euphoria and dysphoria)
  • Heightened energy
  • Sleep disturbance, insomnia
  • Motor excitement, restlessness
  • Talkativeness, pressure of speech
  • Hyperactive ideation
  • Increased sexual interest
  • Anger, verbal aggression
  • Mild to moderate anorexia
  • Inflated self-esteem
49
Q

What are effects of abusing psychostimulants?

A
  • Irritability, hostility, anxiety, fear, withdrawal
  • Extreme energy or exhaustion
  • Total insomnia
  • Compuslive motor sterotypies
  • Rambling, incoherent speech
  • Decreased sexual interest
  • Possibility for extreme violence
  • Delusions of grandiosity
  • Total anorexia
50
Q

What are some side effects of cocaine use?

A

Expensive, mimicks activation of sympathetic nervous system (increased heart rate, blood pressure, glucose utilization), alters plasticity, tremors, loss of motor coordination, seizures

51
Q

What does cocaine toxicity look like?

A

Heart attack (big ones, disproportionate to age), stroke (usually hemorrhagic), permanent brain damage. Related to vascular insufficiency and decreased blood flow due to vasoconstriction

52
Q

What amphetamine was readily available in health food stores until a few years ago?

A

Ephedra

53
Q

This drug is known as the original amphetamine, and used as an inhaler for asthma

A

Benzedrine

54
Q

What is an amphetamine (AMPH)?

A
  • All related someway to monoamine alkaloid phenethylamine (naturally ocurring trace nutrient)
  • Similar to phenylalanine (precursor to tyrosine, found in meat and milk)
55
Q

A toxic build up of phenylalanine due to deficient or absent enzyme is called: (acronym)

A

PKU

56
Q

What is different about MDMA compared to AMPH?

A
  • Double methylation
  • Does not work on DA or NE
  • Classified as hallucinogen
57
Q

What is the average half life of AMPH?

A

7-30 hours depending on urinary pH

58
Q

AMPHs are one of the only classes that are able to:

A

Have a direct action on DA transmitters to cause a conformational change that reverses the direction of transmitter flow (as well as blocking re-uptake of released DA)

59
Q

What system does MDMA most effect?

A

5-HT (serotonin); hardly any effects on catecholamines

60
Q

Why is MDMA deadly?

A

Raises body temp so much that brains/organs cook from inside

61
Q

What are behavioural effects of MDMA?

A
  • Doesn’t produce whole profile of effects as amphetamine
  • In addition to stimulant effects, produces entactogenic effects that arise from selective affinity for 5-HT neurons
62
Q

MDMA side effects and toxicity result from:

A
  • Hyperthermia leading to febrile seizure (can cause brain damage)
  • Lack of O2/CO2 exchange (hyperventilation)
  • Dehydration
  • Hypovolemia (sweating, vomiting, diarrhea, menstruation = imbalance of electrolytes = can lead to water toxicity)
63
Q

What is the unifying property of the general stimulants?

A

Transmitter is not one of the monoamines (nicotine works on ACh); do not cause psychomotor effects

64
Q

The half-life of nicotine is about ___ hours, leading to morning loading to achieve ______

A

2; steady-state levels

65
Q

What are some common routes of nicotine administration?

A

Cigarette, nasal spray, patch, chewing gum

66
Q

Most nicotine is metbolized in the _______ by enzyme _______

A

liver; CYP2A6

67
Q

Nicotine _______ muscle tone in skeletal muscles, and ______ tone in smooth muscle sites

A

Decreases; increases

68
Q

What are some physiological effects of nicotine?

A
  • Cardiovascular effects (increase heart rate, blood pressure)
  • Decrease in urination, changes to urinary pH
  • Release of EPI in PNS causing general arousal of CNS
  • Increased respiration
  • Release of DA and NE in multiple brain regions
  • Interacts in a complex fashion with serotonin system
69
Q

What are some behavioural effects of nicotine?

A

Increase in arousal, concentration, vigilance, working memory

70
Q

What happens when nicotine (not smoked) is given to rat mothers?

A

Babies are smarter, have better memory

71
Q

What are nicotine withdrawal symptoms?

A
  • Decreased heart rate
  • Increased eating (weight gain)
  • Depression
  • Inability to concentrate/pull thoughts
  • Sleep disruption & increased awakening
  • Anxiety, anger, agression, nervousness, fear, headaches, dizziness, tremors, nausea
72
Q

T/F: Caffeine changes blood flow, and is good for headaches

A

True

73
Q

What is the half life of caffeine?

A

2.5-4.5 hours

74
Q

Caffeine is metabolized in the liver by:

A

CYP1A2

75
Q

Caffeine molecule can be broken into _______ (84%), _______ (12%) & _______ (4%)

A

paraxanthine, theobromine, theophylline

76
Q

Caffeine is an antagonist for which receptors?

A

Adenosine

77
Q

What are some acute physiological effects of caffeine?

A
  • Increased blood pressure, heart rate, respiration
  • Vasconstriction in periphery
  • Increase in EPI
  • Increase in urination
  • Decrease in smooth muscle tone
78
Q

What are some acute behavioural effects of caffeine?

A
  • Increase in arousal, concentration, vigilance, working memory, reaction time, cognitive performance
  • Assists in pain relief
  • Tolerance, dependence and sensitization
79
Q

What are withdrawal effects of caffeine?

A
  • Loss of concentration
  • Headache, irritability, fatigue, mild mood depression
  • Rebound effects of compensatory increases in adenosine in multiple systems
80
Q

What are side effects and toxicty of caffeine?

A
  • Caffeinism (caused by excess caffeine)
  • Heart palpitations, heart arrythmia, insomnia, diarrhea (aggressive), restlessness, anxiety, involuntary contractions of limbs, tremors, seizures, psychotic behaviour

Drugs & Behaviour (3 decks)

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