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PMCOL 305 > final > Flashcards

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
Q

Nicotine acute effects

A

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
Q

Nicotine reward

A

Increased Glu, DA release
activation and release of GABA. but desensitized quickly so really shuts off GABA

27
Q

nicotinic ACH receptors in brain

A

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
Q

Nicotine dependance

A

if within 30min of waking up you have craving you’re addicted (happens within days)

29
Q

Nicotine long term effects

A

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
Q

smoking and pregnancy

A

constriction of umbilical arteries, can increase addiction risk for infant
higher risk of miscarriage or still birth

31
Q

quiting smoking

A

-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
Q

sedative

A

relieve anxiety, cause relaxation, mild CNS depressants. overall these are calming agents

33
Q

hypnotics

A

cause drowsiness and sleep (sleeping agents)

34
Q

Z-Drugs

A

orexin antagonists, melatonin agonists, anti-histamines

35
Q

Difference between sedatives and hypnotics

A

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
Q

Barbiturates

A

An activator of GABA by enhancing affinity and increasing duration of opening. binds between alpha and beta subunits

37
Q

Benzodiazepines

A

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
Q

Sedative metabolism

A

CYP450 system. producing some active metabolites (chlordiazepoxide, diazepam, midazolam)

39
Q

Sedative acute effects

A

reduce muscle tone, impair coordination and increase sleep but not good sleep. can prevent the consolidation of short term memories (alpha containing receptors)

40
Q

Flumazenil

A

Sedative overdose treatment a GABA antagonist. more like to OD on barbiturates

41
Q

Sedative tolerance

A

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
Q

Sedative withdrawal

A

worse for short acting drugs due to hyperexciability
-insomnia, anxiety

43
Q

Sedative dependance and abuse

A

both physical and mental, barbiturates are more addictive but still low in comparison

44
Q

sedative reward

A

disinhibition of DA interneurons from increases GABA release

45
Q

gamma hydroxybutyric acid

A

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
Q

Cannabis vs cig smoke

A

probably worse as there is no filter. Increases irritation

47
Q

2-arachidonoylglycerol (2-AG)

A

endogenous cannabinoid

48
Q

arachidonoyl ethanol amide (AEA)

A

endogenous cannabinoid

49
Q

CB1

A

expressed in CNS, eyes, pancreas liver pretty much everywhere. also blocks pain

50
Q

CB2

A

immune cells, spleen and tonsils

51
Q

Endocannabioids

A

are retrograde signallers to turn off NT release of other NTs. also like cannabis have many downstream effects (pleiotropic)

52
Q

cannabis tolerance

A

metabolic, cellular and behavioural

53
Q

cannabis withdraw

A

burn-out leading to lethargy, but not too bad

54
Q

Cannabis dependance

A

slight psychological not too addictive relatively

55
Q

cannabis adverse effects

A

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
Q

cannabis long term effects

A

increased cough, miscarriage, low sex hormones

57
Q

Vaping

A

can deliver de-carbed chemicals without burning and you can control temp`

58
Q

Cannabis reward

A

Via CB1-mediated inhibition of GABA release leading to disinhibition of VTA->NAc neurons (presynaptic on axon)

59
Q

Cannabis blood shot eyes

A

noradrenaline narrows blood vessels and AEA dilates them causing blood to enter

60
Q

Cannabis olfactory effects

A

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

PMCOL 305 (3 decks)

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