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Y2 LCRS 1 - Pharm, Endo, Reproduction > PHARM; Lecture 13, 14 and 15 - Drugs of Abuse I, II and Alcohol > Flashcards

PHARM; Lecture 13, 14 and 15 - Drugs of Abuse I, II and Alcohol Flashcards

1
Q

Why are drugs of abuse used?

A

For euphoria -> cell bodies in the ventral tegmental area which project into nucleus accumbens, releasing DA to induce a euphoric high

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2
Q

What are the methods of admin of drugs of abuse?

A

Intra-nasal (Mucous membranes of nasal sinuses, slow absorption), oral (GIT, v. slow), inhalation (Small airways and alveoli = rapid), IV (veins, rapid)

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3
Q

What are the classes of drugs of abuse?

A

Narcotics (opiates - heroin), depressant (alcohol, benzodiazepines, barbiturates), stimulants (cocaine, amphetamine, caffeine, methamphetamine), misc. (cannabis, ecstasy)

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4
Q

What is cannabis?

A
  • From the cannabis sativa plant;
  • cannabinoids being the main compound (delta-9 THC is the main compound)
  • main part of plant are the trichomes on the plant.
  • Main aim of new versions of cannabis are to increase levels of delta-9 THC (seem to increase -ve consequences)
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5
Q

What are the methods of admin of cannabis?

A

Oral - 5-15% (delayed onset/slow absorption with 1st pass metabolism); inhalation - 25-35% to be absorbed in blood stream

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6
Q

Once in the blood stream, what occurs to cannabis?

A
  • VERY lipid soluble
  • Diffuses to highly perfused tissues first and slow accumulation in not well perfused tissues
  • slowly accumulated in poorly perfused fatty tissues, with ratio 10^4 fatty tissue : 1 plasma, which will slowly release back into the plasma.
  • Distributes also to the brain and sits in the brain tissues for a long time, with prolonged effect as it isn’t clearing from the tissues
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7
Q

What occurs to cannabis when broken down?

A

In the liver - a more potent cannabinoid is formed (11-OH-THC) from the cannabinoid; In the GIT (65%), most of it goes into the bile (to be excreted) so it is recycled in the enterohepatic circulation; excreted 25% via urine. Poor correlation between plasma cannabinoid concentration and degree of intoxication

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8
Q

How long after smoking a cannabis cigarette will the effects persist in the body? 5 hours 12 hours 7 days 30 days 10 years

A

30 days

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9
Q

What are the receptors that cannabis acts on?

A
  • CB1
    • hippocampus
    • cerebellum
    • cerebral cortex
    • basal ganglia.
  • CB2 - on immune cells.
  • Acts on adenylate cyclase to inhibit it (hence depressant).
  • Body’s cannabinoid = endogenous anandamide
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10
Q

What is the pharmacodynamics of euphoria?

A
  • GABA maintains the pathway inhibited to prevent constant euphoria.
  • Cannabis depresses the GABA inhibition, inhibiting the inhibition, to increase firing of VTA so NAcc releases more DA
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11
Q

What are the functions of cannabis?

A
  • Euphoria,
  • paranoia/schizophrenia,
  • hunger,
  • immunosuppressant,
  • memory loss (limbic regions with amnestic effects with decreased BDNF),
  • psychomotor performance (cerebral cortex),
  • tachy/vasodilation (red eyes via vanilloid receptor),
  • medulla (low CB1 receptor expression so it is very difficult to OD on cannabis so no decrease to cardioresp centre in medulla)
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12
Q

What does the Anterior cingulate cortex do and what occurs to it with cannabis?

A
  • Involved with performance monitoring with behavioural adjustment in order to avoid losses
  • hypoactivity in cannabis users;
  • can increase psychosis and schizophrenia
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13
Q

What is the effect of cannabis on food intake?

A
  • Positive effect on orexigenic neurones in lateral hypothalamus
  1. presynaptic inhibition of GABA increases MCH activity;
  2. inceased orexin production
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14
Q

How does cannabis cause immunosuppression?

A
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15
Q

What are the medical uses of cannabis?

A
  • Increased regulation of CB receptors;
  • MS/pain/stroke = regulatory;
  • fertility = in males with upregulation of CB1 receptors interferes with sperm production;
  • and in obesity there is an upregulation of CB1
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16
Q

What are the functions of the drugs that affect the CB receptors?

A
  • Dronabinol/nabilone used as anti-emetic for cancer patients;
  • sativex as analgesic for MS;
  • rimonobant used for obesity as downregulates hunger but now withdrawn as instances of suicide associated
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17
Q

What is the t1/2 of cannabis and the elimination method?

A

t1/2= 7d; elimination = synth into 11OH THC - 65% in gut, urine 25%

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18
Q

What is cocaine and the different forms?

A

Plant derived (erythroxylum coca).

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19
Q

How do you admin cocaine?

A

Oral isn’t a good admin method

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20
Q

How do you metabolise cocaine?

A
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21
Q

How do cocaine pharmacokinetics contribute to the addictive potential of the drug?

A

Short elimination time means that it’s effects are short lived so want constant admin; also quick method of admin makes it more likely to be admin

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22
Q

What are the functions of cocaine?

A
  • Local anaesthetic,
  • reuptake inhibition,
  • euphoria -> mild-moderate effects are positive/reinforcing effects and severe effects are negative/stereotypical effects;
  • cardiovascular, MI
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23
Q

How does cocaine act as a local anaesthetic?

A

High dose -> blocks Na channels

24
Q

How does cocaine act as a reuptake inhibitor?

A
  • Blocks uptake systems so more DA in the synapse
  • doesn’t affect affinity/efficacy,
  • but increase DA in synapse,
  • so more present to try to bind to the receptor to outcompete
25
Q

How does cocaine cause euphoria?

A

Blocks DA transporter in the NAcc to increase DA in synapse which is released

26
Q

How does cocaine cause MI/cardiovascular problems?

A
  • With dose increasing as you go down;
  • Releases endothelin-1 which increases vasoconstriction;
  • CNS effects -> vasoconstriction and hyperpyrexia (caused by increase ANS activation) which can affect epilepsy
27
Q

What is nicotine?

A
  • From plant;
  • present in cigarettes;
  • tar droplets deposited in lung and nicotine diffuses through that into the alveoli.
  • Nicotine in particulate side
28
Q

How is nicotine admin?

A

Cigarettes are acidic and nicotine is alkaline, so is ionised in cig smoke, but then diffuses across the alveoli as the membrane is so thin.

29
Q

How is nicotine metabolised?

A

Met by cytochrome P450 in liver (70-80%) into cotinine. T1/2= 1-4h Eliminated via urine

30
Q

Where does nicotine act?

A

Acts on ANS nAChR

31
Q

What are the functions of nicotine?

A

Euphoria, cardiovascular effects, metabolic effects, protective against neurodegenerative disorders

32
Q

How does nicotine cause euphoria?

A

Increases firing rate of VTA so increases DA release from NAcc

33
Q

What CV effects does nicotine cause?

A

No effect on lungs but increases CV disease risk but are long developing (unlike cocaine)

34
Q

How does nicotine affect metabolism?

A

Increases metabolic rate and decreases appetite

35
Q

How does nicotine affect neurodegenerative disorders?

A

Protection against development of: Parkinson’s (increases CYP in brain so decreases neurotoxins). Alzheimer’s (decreases beta-amyloid toxicity and amyloid precursor protein)

36
Q

Does caffeine affect euphoria?

A

Caffeine is adenosine receptor antagonist so blocks inhibitory effects of adenosine, so increases DA release

37
Q

What is a safe dose of alcohol?

A

Men/Women =< 14 u/wk.

Binge drinking > 8u in one sitting

38
Q

How you administer alcohol?

A

Oral -> 20% absorbed from stomach, 80% absorbed from intestines. Speed of onset is proportional to gastric emptying so full stomach = slower absorption

39
Q

How is alcohol metabolised?

A

90% is metabolised. 85% in liver -> mostly by alcohol DHase (75%) and mixed function oxidase (25%) which form acetaldehyde. In chronic alcoholism, mixed function oxidase is increased, so you become more tolerant. 15% in stomach (<50% capacity in females). Aldehyde DHase metabolises acetaldehyde into acetic acid

40
Q

How can metabolism of alcohol be saturated?

A

By giving a high dose at once, rather than all at once - first pass metabolism

41
Q

What is the difference in distribution between women and men?

A
  • Women have higher fat levels so less water content, meaning that alcohol is less dilute in the blood
  • less body water and less alcohol DHase in the stomach in women
42
Q

What is a problem that can occur with aldehyde DHase?

A

Asian flush = polymorphism in the enzyme; also Disulfiram acts as an alcohol aversion therapy as it causes build up of acetaldehyde, increasing bad effects

43
Q

What is the pharmacological potency of alcohol?

A

LOW -> less than nicotine and cocaine; this means that due to it having a non-selective target it can act on many targets with low potency, as it doesn’t activate/block targets

44
Q

What are the acute effects of alcohol?

A

Depressant effect, slight euphoria, CNS effects, CVS effects, polyuria

45
Q

How does alcohol cause a depressant effect on the CNS?

A
  • Low dose -> with slight CNS agitation sometimes, can be difficult to see where it works as CNS is functionally complex and ethanol has low potency/selectivity.
  • Dependent on:
46
Q

What are the targets that alcohol influences?

A

Increases GABAa function via pre/post synaptic function (allopregnenlone increased in presynaptic region, enhancing GABAa function which increases Cl influx post synaptically); binds to NMDA receptors via allosteric site, reducing firing rate of that receptor; decreases Ca influx via Ca channels so decrease release of NT

47
Q

How does alcohol cause a euphoric effect?

A

Via the same pathway as opiates

48
Q

Which parts of the CNS does alcohol affect?

A
49
Q

Which CV effects does alcohol cause?

A
  • Cutaneous vasodilation (decreases Ca entry, increases Prostaglandin);
  • centrally mediated HR as alcohol prevents baroreceptor control of HR, so increased HR
50
Q

How does alcohol increase diuresis?

A

Prevents VP secretion, so prevents reabsorption of water, increasing need to go to toilet

51
Q

What are the chronic CNS effects with alcohol?

A
  • WKS: chronic alcoholics gain most calories from alcohol,
  • so don’t gain enough thiamine in the diet.
  • If energy metabolism is disturbed for long enough then it goes from
    • reversible (Wernicke’s Ecephalopathy)
    • to irreversible (Korsakoff’s psychosis)
52
Q

What are the chronic liver effects from alcohol?

A
  • NAD+ is being used up by alcohol metabolism (chronic alcohol),
  • so kreb’s cycle is impaired (pyruvate met, TCA -> instead: pyruvate to lactate, ACoA to ketones,
  • causing build up of TAG in the liver causing fatty liver, which causes an inflammatory stimulus,
  • Inflammatory free radicals are released causing release of cytokines
  • causing inflammation (IL-6 and TNFa),
  • causing hepatitis (which can still be reversible) but if it continues long enough
  • cirrhosis occurs (fibroblasts inflitrate the liver, deposite fibrous tissue, active liver tissue decreases, increases fibroblasts and decreases hepatocyte regeneration)
  • Liver cannot manage met demands of body if it gets bad enough, so liver transplant/treatment needed
53
Q

What are the beneficial effects of alcohol?

A
  • LOW DOSES ->
    • decreased mortality from coronary artery disease,
    • increases HDL,
    • increases tPA levels
    • decreases platelet aggregation
54
Q

How does alcohol affect the GIT?

A

Acetaldehyde is always present in stomach lining in chronic alcoholics which damage mucosa and can be carcinogenic (increase in stomach cancer in alcoholics)

55
Q

What are some endocrine effects of chronic alcohol?

A

Increase ACTH secretion (alcohol stimulated so Cushing’s like syndrome) and decrease testosterone secretion (feminine characteristics)

56
Q

How are the hangover effects caused?

A

Nausea is most profound when reaching blood alcohol conc of 0.

Rebound excitation occurs when reaching conc of 0.

Best cure: sleep it off until rebound effects have dissipated.

Y2 LCRS 1 - Pharm, Endo, Reproduction (19 decks)

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