final Flashcards

1
Q

4 Ways of identifying chemicals from plants

A

Extraction, purification, predictions, characterization

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2
Q

Caffeine metabolites

A

From CYP1A2. Theophylline (Inhibits PDE, increases cAMP which aids breathing), theobromine (dilates vessels, increases urine vol), parazanthine (increases blood glycerol/fatty acids from lipolysis)

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3
Q

Caffeine chemical nucleus

A

Purine(rgic)

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4
Q

Chlorogenic acids

A

Also found in coffee induces liver enzymes

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5
Q

Dihyrdocaffeic acid

A

also found in coffee, anti inflammatory from NO production

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6
Q

Kahweol and cafestol

A

Diterpenes found in coffee, induce anti stress genes, but elevate cholesterol

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7
Q

Caffeine

A

A methylxanthines which have a purine base nucleus

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8
Q

Caffeine beneficial effects

A

-Respiratory stimulation in infants
-bronchodilator (asthma)
-reduce cranial blood flow (migranines)

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9
Q

Methyl xanthine cellular drug actions

A

adenosine receptor (AR) antagonists and phosphodiesterase PDE antagonist (increasing cAMP). also Ca release and GABA receptors

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10
Q

Adenosine receptor

A

3 major types, 4 subtypes (A1, A2a, A2b, A3). A1 and A2a are the major roles in caffeine effects (presynaptic receptors limiting NT release)

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11
Q

A1 adenosine receptor

A

inhibits adenylyl cyclase (reduced cAMP) lowers NT release. therefore when caffeine an antagonist binds it increases NT release. found in reward and in hippocampus A

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12
Q

A2a adenosine receptor

A

activates adenylyl cyclase (increased cAMP) increases NT release. when Caffine an antagonist binds decreased NT release. found in DA rich regions on GABA neurons

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13
Q

Extensive pairs

A

At rest receptors form a raft that can change signalling when activated. A1-D1, 2A2a+2D2, A1+A2a

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14
Q

Acute caffeine effects

A

stimulant, mild compared to cocaine. though increased urination. increase NE, Glu, DA. constriction of cranial vessels can treat headaches. Activates kidneys (increase urine and prevents water/salt reabsorption). can increase intracellular [Ca] increasing work capacity

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15
Q

Caffeine wakefulness effect

A

intracellular adenosine from ATP use builds up which stimulates A2a receptors triggering GABA release. Caffeine stops the binding and inhibits A2a

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16
Q

Caffeine long term effects

A

-Reduces risk of Parkinson’s
-if slow metabolizer of caffeine due to CYP1A2 (mutations) increased heart attack risk
-osteroporosis, from increases calcium elimination
-panic attacks
-could be antidepressants
-aids learning and memory

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17
Q

Caffeine tolerance/withdrawal

A

quick tolerance to cardiovascular, respiratory and sleep effects.
headache, fatigue, low energy, thirst when withdrawing

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18
Q

Nootropic

A

cognitive enhancer
-Taurine (red bull), anxiolytic
-L-theanine
-herbs (like ginkgo blob and ginseng)
-Nicotine
-Ritalin
-amphetamines (adderall)
-(-afinil family) modafinil, adrafinil, armodafinil

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19
Q

e-cigs

A

juice contains glycerin or PG. severe effects from additives
-Diacetyl (butter flavour), obliterates lungs
-Vit E acetate, allergic reactions
-creates ROS damges immune system
-5-8X higher dose than cig

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20
Q

Hookahs

A

water cools smoke so less irritating. uses Shisha (flavoured tobacco)
- produces lots of CO gas
-increases lung disease, oral too
lS

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21
Q

Smoke

A

particles of nicotine, water, tar, PAHs, benzoapyrene, metals. and gas, CO, CO2, NO, ammonia, nitrates, alcohols. form an aerosol. can have first, second and third hand inhalation

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22
Q

Nicotine plant

A

alkaloid causes addiction, competitive ACH receptor agonist. lives as free base and protects plants from pests

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23
Q

Nicotine absorption

A

inhalation
-control pH to increase free base for better absorption
-burning creates ~4000 chemicals
-1 cig is 8mg but delivers 0.5-2mg (10-70% bioaval)
oral
-3-4x greater absorption, just slower rate. but lasts much longer at high dose

liver, kidney, spleen, lung get largest amounts as most is found in blood

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24
Q

Nicotine metabolism

A

Half life=2 hours.
CYP2A6, CYP2B6 generate cotinine
monooxygenases also process small amounts

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25
Nicotine acute effects
sympathomimetic effects. effects ACH, DA, GABA, Glu NTs binds and activates nAChRs (high dose leads to inactivation, biphasic) -acetaldehyde from burning may inhibit monoamine oxidases to boost NT levels Adverse effects -stimulates vomiting centre -headaches, nausea, ANS disruption -seizures, hypotension, respiratory depression
26
Nicotine reward
Increased Glu, DA release activation and release of GABA. but desensitized quickly so really shuts off GABA
27
nicotinic ACH receptors in brain
heteropentameric, alpha and beta subunits (9 alpha, 3 beta). a Na and Ca channel. -will inactivate if continuously bound like nicotine does -alpha 6, modulates locomotor effects (non rewarding) -alpha 7, glutamate release (reward) (not inactivated) -beta 2 knock out stops all reward -alpha 4, beta 2 antagonists block reward (on Da terminal in Mac) (governs GABA release so when desensitized disinhibited)
28
Nicotine dependance
if within 30min of waking up you have craving you're addicted (happens within days)
29
Nicotine long term effects
benzopyrene initiated cancer (from smoke) nicotine only enhances growth once cancer is there does not directly cause it (inhibits alpha 7 which prevents apoptosis) -accelerated skin age -sexual dysfunction stressed vasculature from NO release
30
smoking and pregnancy
constriction of umbilical arteries, can increase addiction risk for infant higher risk of miscarriage or still birth
31
quiting smoking
-only 6% actually quit has 3 day hump for nicotine clearance -bupropion, antidepressant nAChR antagonist to block channel, DAT NET inhibition -varenicline, partial nAChR agonist
32
sedative
relieve anxiety, cause relaxation, mild CNS depressants. overall these are calming agents
33
hypnotics
cause drowsiness and sleep (sleeping agents)
34
Z-Drugs
orexin antagonists, melatonin agonists, anti-histamines
35
Difference between sedatives and hypnotics
sedatives are more lipophilic with faster onset within the class there is also characterization on length of action. -long acting are anticonvulsants, muscle relaxants and anxiolytics short acting are pre anesthetic sedatives or insomnia treatments
36
Barbiturates
An activator of GABA by enhancing affinity and increasing duration of opening. binds between alpha and beta subunits
37
Benzodiazepines
allosteric modulators of GABA increasing the frequency of channel opening. Bind between alpha and Gamma subunits. also less lipophilic than barbers. also don't effect breathing as there are no receptors there
38
Sedative metabolism
CYP450 system. producing some active metabolites (chlordiazepoxide, diazepam, midazolam)
39
Sedative acute effects
reduce muscle tone, impair coordination and increase sleep but not good sleep. can prevent the consolidation of short term memories (alpha containing receptors)
40
Flumazenil
Sedative overdose treatment a GABA antagonist. more like to OD on barbiturates
41
Sedative tolerance
subunit shifting. happens at different rates -anxiolytic 3-4 months -no respiratory depression -up to 40x original dose benzodiazepines produce tolerance fast and common
42
Sedative withdrawal
worse for short acting drugs due to hyperexciability -insomnia, anxiety
43
Sedative dependance and abuse
both physical and mental, barbiturates are more addictive but still low in comparison
44
sedative reward
disinhibition of DA interneurons from increases GABA release
45
gamma hydroxybutyric acid
GABAb receptor agonist, it is precursor of GABA, Glu and Gly. similar to alcohol inebriation when taken. -low dose just binds to and releases Glu -and high dose binds GABAb lead to low respiration, coma and death
46
Cannabis vs cig smoke
probably worse as there is no filter. Increases irritation
47
2-arachidonoylglycerol (2-AG)
endogenous cannabinoid
48
arachidonoyl ethanol amide (AEA)
endogenous cannabinoid
49
CB1
expressed in CNS, eyes, pancreas liver pretty much everywhere. also blocks pain
50
CB2
immune cells, spleen and tonsils
51
Endocannabioids
are retrograde signallers to turn off NT release of other NTs. also like cannabis have many downstream effects (pleiotropic)
52
cannabis tolerance
metabolic, cellular and behavioural
53
cannabis withdraw
burn-out leading to lethargy, but not too bad
54
Cannabis dependance
slight psychological not too addictive relatively
55
cannabis adverse effects
vomiting from complex 5-HT signals in some people it reduces 5-HT leading to anti emetic activity high THC can impair learning, memory from hippocamal effects on LTP -psychosis
56
cannabis long term effects
increased cough, miscarriage, low sex hormones
57
Vaping
can deliver de-carbed chemicals without burning and you can control temp`
58
Cannabis reward
Via CB1-mediated inhibition of GABA release leading to disinhibition of VTA->NAc neurons (presynaptic on axon)
59
Cannabis blood shot eyes
noradrenaline narrows blood vessels and AEA dilates them causing blood to enter
60
Cannabis olfactory effects
caused by an inhibition via CB1 receptors on GLU neurons that stimulate the GABA receptors on the olfactory neuron's (mitral cells). this hyper sanitizes them and make you want to eat. this stimulates centrifugal GLU in MOB