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NEUR 321 > Midterm 2 Part 2 > Flashcards

Midterm 2 Part 2 Flashcards

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1
Q

Where are weak acids better absorbed?

A

stomach

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2
Q

Where are weak bases better absorbed?

A

intestine

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3
Q

bioassay

A

provides information on the pharmacological activity of new or chemically-undefined substances

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4
Q

pharmacodynamics

A

What the drug does to the body
Quantitative relationship between concentration and receptor interaction AND specific cellular response

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5
Q

Steeper quantal dose response curve means

A

lower variation in the population

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5
Q

Less steep, slow-rising quantal dose response curve means

A

higher variation in the population

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6
Q

Minimal effective dose, MED

A

Lowest dose that will produce the desired therapeutic respond

Makes up the lower part of the therapeutic window

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7
Q

Maximum tolerated dose (MTD)

A

highest dose that can be administered w/o adverse/toxic effects

Makes up the higher part of the therapeutic window

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8
Q

ED50

A

Effective dose in 50% of the concentration

Makes the lower part of the therapeutic index

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9
Q

TD50

A

toxic effect in 50% of the population at this dose

Makes up the upper part of the therapeutic index

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10
Q

Potency

A

A comparative expression of drug activity.
Does not indicate efficacy. Just because one drug is more potent, doesn’t mean it is more effective

Potency increases as EC50 decreases

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11
Q

What receptor is LSD an agonist for?

A

serotonin receptor. It is less potent than serotonin however.

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12
Q

Non-competitive antagonists

A

Bind to allosteric site rather than orthostatic site. Form a strong bond and thus slowly or does not dissociate from receptor –insurmountable because you can’t add more agonist to displace the antagonist. Emax decreases

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13
Q

Psychoactive drug

A

Drug that affects the CNS and alters behaviour including mood and cognition
Can be therapeutic or recreational

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14
Q

Tolerance

A

When repeated exposure to drugs decreases effectiveness of the drug. Lower response to a given dose of drug.
Need higher dose to get the same ‘desired’ effect

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15
Q

METABOLIC tolerance

A

body gets more efficient at elimination of the drug

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16
Q

cellular tolerance

A

target tissue has decrease sensitivity. The number of receptors is reduced or else they just become less sensitive

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17
Q

How are some ways the body will try to maintain homeostasis when on drugs?

A

If taking an agonist - body might try to reduce the receptors to reduce the response
If taking on antagonist - body might try to increase the number of receptors to increase the response

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18
Q

Learned tolerance

A

Adapt behaviour based off experience to compensate for the effects of the drug. Consciously or unconsciously you have learned how you respond to the drug.
Lowers the response

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19
Q

Cross tolerance

A

Tolerance of one drug can be transferred over to another drug within the same family. Therefore, you can exhibit tolerance for a drug that you have never taken before.

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20
Q

Drug sensitization

A

Intermittent exposure to a drug can lead to enhanced responses to subsequent exposure to the same dose.
Can last a long time and occur after a single use.

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21
Q

Amphetamines

A

Enhance the release of dopamine AND block re-uptake transporters of NE, 5-HT, and dopamine. 1

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22
Q

Caffeine

A

Is an antagonist that binds to caffeine receptors and prevents a response from occurring.
Caffeine tolerance - neurons synthesize more adenosine receptors - makes it so that more caffeine is required to block the additional receptors.
- SO when you stop drinking coffee and have many receptors - increased sensitivity to adenosine - sleepy

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23
Q

Nicotine

A

Binds and activates the nicotinic ACh receptor (Na+ flows in)
At low initial doses - acts as a stimulant
At high initial does - acts as a relaxant

Leads to release of dopamine
Rapid tolerance

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24
Acetylcholinesterase inhibitors
Used for treatment of Alzheimers and dementia
25
Benzodiazepines
AFFECT GABA receptor. They bind to the receptor and promote the influx of chorine ions into the cell. Therefore - they reduce the responsiveness of the cell. Used for anxiety, sleep, epilepsy They decrease sleep problems by decreasing neuronal activity
26
GABA receptor agonists
Benzodiazapines, alcohol, GABA
27
Alcohol
GABA receptor agonist. Promotes the influx of chloride ions Excessive usage can lead to nerve damage, cortical loss, and decreased neurogenesis
28
What happens if you have a poor diet and drink lots of alcohol?
Thiamine deficiency - Korsakoff's Syndrome
29
What is the main excitatory neuron in the forebrain and cerebellum?
Glutamate. Involved in learning and memory
30
Phencycladine
PCP; angel dust Hallucinogenic, cognitive impairment Act by blocking NMDA receptors (these receptors are essential for synaptic plasticity - learning/memory) Drug affecting glutamate
31
Ketamine
Dissociative anaesthetic. Low IV doses showing benefits for depression Act by blocking NMDA receptors (these receptors are essential for synaptic plasticity -learning/memory)q
32
Monoamine oxidase inhibitors (MAOI)
Inhibit the breakdown of 5HT in the presynaptic terminal so that more serotonin is available for release
33
5-HT receptor agonists
LSD, mescaline, ecstasy - all hallucinogenic
34
therapeutic lag
When a drug takes some time to make a noticeable difference in the body. Characteristic of some serotonin anti-depressants
35
SSRIs and tricyclics
Block transporter protein for the re-uptake of serotonin
36
LSD
partial agonist for serotonin receptor increase glutamate transmission in the frontal cortex Has rapid tolerance (down regulation of the serotonin receptor) Not considered toxic or addictive
37
Schizophrenia
Associated with excessive MESOLIMBIC dopaminergic activity Antipsychotics decrease dopaminergic related activity particularly in the frontal lobe Best treated with ATYPICAL NEUROLEPTICS
38
What meds are the best to treat Schizophrenia and why?
Atypical neuroleptics because these don't cause as many movement problems (from decreasing dopamine too much - Parkinson's symptom)
39
1st generation neurolyptics
anti-pschotics used originally to treat schizophrenia (decrease dopamine) They act as D2 antagonists (they prevent dopamine release from the presynaptic terminal- cause movement problems - with Parkinson's - don't get enough dopamine production and get movement problems.
40
ADHD
Used to treat with dopamine agonists Drug treatment involves preventing the reuptake of dopamine and or NE from the synapse - enhance activity at the synapse - better control attention and behaviour
41
How do cocaine and amphetamines act?
THey work in a similar fashion to ADHD treatment drugs --> block uptake of Dopamine and NE - increase activity - agonist
41
How do cocaine and amphetamines act?
THey work in a similar fashion to ADHD treatment drugs --> block uptake of Dopamine and NE - increase activity - agonist
42
Parkinson's disease
Disease associated with loss of neurons producing dopamine in the mesolimbic area. not enough dopamine production Treatment with L-Dopa is good but need to combine treatment with benserazide to prevent adverse effects in the body as there are dopaminergic neurons outside of the brain.
43
Benserazide
Inhibits DOPA decarboxylase. This is important when treating Parkinson's disease to lower adverse effects in the body. Given in combination with L-Dopa Cannot cross the BBB Prevents the formation of excessive dopamine in the body but still allowing formation of dopamine in the brain as it does not cross the BBB
44
Treatment for Parkinsons
L-Dopa and Benserazide
45
Opiates
Agonists to the opiate receptor (GPCR) Used for pain relief, medicinal and recreational use Can be converted into morphine, codeine, heroin Endogenous opioid receptor ligands: enkephalins, endorphins (can activate AC or an ion channel) Major drug abuse substance Can get tolerance or sensitiziation overdose risk Excessive stimulation
46
Endogenous opioid receptor agonist ligands
Enkephalins, endorphins
47
What is an antagonist for opiates?
naloxone
48
Cannabis
Contains 84 active incredients including THC and CBD Activate endocannabinoid receptors
49
What is the primary component of cannabis that causes psychoactive effects?
THC too much THC can lead to paranoia and hallucinations
50
Medicinal uses for cannabinoids?
Glaucoma, chronic pain, decreasing nausea
51
Cannabidiol
CBD - pure. CLinical use -Don't get hallucinations like with THC overusage May help with epilepsy and other things
52
Substance abuse
Drug use when a person relies on a drug and its use becomes a major component in their life
53
Addiction
Substance DEPENDANCE Escalating, compulsive, relapsing Disproportionate amount of time seeking, preparing and consuming the drug Interferes with everyday life Even if you want to stop, its very difficult to actually stop Want the drug, even if you don't like the drug
54
Escalation of drug consumption
increasing in dose and frequency of taking the drug. MORE THAN SIMPLY TOLERANCE transformation of drug abuser to drug addict
55
How does a drug addiction form?
Psychomotor activation - give an energized feeling Activation of the dopaminergic system either directly (cocaine) or indirectly (ventral tegmentum - nucleus accumbens) Drugs that block this reward pathway can help with addiction
56
Hedonia hypothesis
Addictions form due to pleasure? ie sex, food, sports, excitement - endorphins produced that give a high After the initial pleasures wear off - user is still wanting (craving) the drug
57
allomone
hormone released to attract other species
58
Protein hormones
String of amino acids. Water soluble Most bind to R on the cell membrane - often kinase-linked - activate second messenger pathways
59
Amine hormones
Based off of a single amino acid Tyrosine or tryptophan w/modified groups WAtersoluble Most bind to R on the cell membrane - often kinase-linked - activate second messenger pathways
60
Base AA for amino hormones?
Tyr Trp
61
Steroid hormones
based on a cholesterol molecule LIPID soluble Cholesterol is essential to make these hormones

NEUR 321 (6 decks)

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