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Final Multisystems Pharmacology > Substance Abuse > Flashcards

Substance Abuse Flashcards

1
Q

Ok so starting off with the heavy stuff, let’s name the 1st two dopamine (DA) pathways from the ventral tegmental area (VTA) involved with reward

A

VTA–> nucleus accumbens

VTA–> prefrontal cortex

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2
Q

What’s the neural DA pathway from the substantia nigra? What is it associated with?

A

SN –> CPu
caudate/putamen)

A/w with habit and compulsions

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3
Q

What’s the neural NE pathway from the locus coeruleus (LC) and what is it associated with?

A

LC –> forebrain, cerebellum

A/w with arousal and attention

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4
Q

What’s the neural serotonin (5HT) pathway from the raphe nucleus and what is it associated with.

A

Raphe nuc –> forebrain, cerebellum

A/w mood and visual

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5
Q

On to the actual drugs. Starting with Opiates. Name 4 opiates

A
  1. Heroin
  2. Morphine
  3. Oxycodone
  4. Hydrocodone
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6
Q

What are the effects of opiates. Many many many options here.

A 
nausea
emesis
“foam cone”
euphoria (lasts~1hr), 
somnolence
sedation (lasts 2-4hrs)
dissociation
analgesia
resp depression
LOC
endocrine/immune disturbances
constipation
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7
Q

What is the mechanism of opioids

A
  1. 1’ target: Mu opioid-R
  2. 1’ effect: Gi/o receptor that when stimulated causes hyperpolarization.
    3: Result: disinhibition of DA release and euphoria.
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8
Q

What’s the most terrifying effect of opiates?

A

OD/Sudden Death: Profound respiratory depression, arrhythmia, cardiac arrest, severe pulmonary edema

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9
Q

What are the pulmonary effects of opiates?

A
  1. Pulmonary edema
  2. Septic embolism (from endocarditis)
  3. Lung abscess,
  4. Foreign body granulomas from Talc
  5. Opportunistic infections.

*Note, granulomas can be found elsewhere like spleen, liver and lymph nodes

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10
Q

Infections due to opiate use are likely to end up:

A
  1. Skin
  2. Heart valves (Right sided tricuspid - S. Aureus)
  3. Liver
  4. Lungs
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11
Q

What kind of skin shit happens when you take too many opiates?

A
  1. Cutaneous lesions from subQ injections

2. Hyperpigmentation over injection sites

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12
Q

What kind of kidney shit happens when you take too much opiate shit in your shit

A
  1. Amyloidosis from skin infections
  2. Segmental glomerulosclerosis
  3. Proteinuria
  4. Nephrotic syndrome
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13
Q

What will you see on labs when you have an opiate overdoser on your hands?

A

6-MAM

monoacetylmorphine

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14
Q

Talk me through the withdrawal process of opiates?

A

6-12h: lacrimation, rhinorrhea, yawning, sweating, goosebumps, anxiety

12-24h: restless sleep

16-96h: dilated pupils, goosebumps, tremor, weakness, anorexia, nausea, vomiting, intestinal spasms (cramps), diarrhea, muscle/back pain/spasms/jerks, CNS stimulation, depression, wt loss, acid-base change, dehydration, ketosis

Max sx at 48-72h; abate w/in 7-10d

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15
Q

What happens after detox of opiates?

A
  1. Relapse extremely common (80%)
  2. Craving for months-years
  3. Conditioned withdrawal syndrome – return to environment previously used shows features of withdrawal
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16
Q

What’s going on with drug tolerance?

A
  1. no change in opiate drug metabolism
  2. mu opioid receptor are desensitized (receptors are phosphorylated)
  3. NO/little reduction in # of receptors
  4. Signal transduction pathways are modified
  5. Gene expression altered
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17
Q

What’s going on with drug dependence?

A
  1. Compensatory changes are “unmasked” when drug is withdrawn aka there is withdrawal
  2. Withdrawal sx are often opposite to the acute drug effects
  3. Withdrawal is caused by giving a drug antagonist like naloxone or naltrexone for opiates
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18
Q

What is addiction?

A

Tolerance+Physical dependence+psychological dependance

May be considered a dz of maladapted learning

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19
Q

How do you treat a opiate addiction?

A
  1. Detox
  2. Maintenacne therapy

More detail in next cards

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20
Q

What does detox for opiate addiction look like

A
  1. Cold turkey – not recommended
  2. Methadone
  3. Clonidine: suppression of sx by α2 R activation (inhibits firing of locus ceruleus neurons)
  4. Antagonist-accelerated withdrawal: naltrexone-precipitated withdrawal induces rapid transition to non-dependent state
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21
Q

What’s the maintenance therapy like for opiate addiction?

A
  1. Heroin maintenance (not legal in US) – replace illegal w/legal heroin
  2. Methadone maintenance – dose increased progressively, blocks assoc of high w/heroin, maintained daily for months-years, decrease when stable, significantly dec relapse rate
  3. Antagonist or partial agonist – after detox give naltrexone to block effects of any self-administered opiate
  4. Buprenorphine – mixed agonist-antagonist – blocks opiate effects, but induces high by itself
  5. Buprenorphine/Naloxone (Suboxone) – naloxone has poor oral bioavailability, but if injected naloxone is activated
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22
Q

What is fentanyl

A

Short acting synthetic opiate

Used for anesthesia

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23
Q

What is the mechanism for benzodiazepines?

A

1’ target: Acts allosterically on GABA(a) receptors
1’ effect: potentiates GABA
Result: hyperpolarization, sedation, mild euphoria, DA release

24
Q

Where do we get cocaine from?

A

Extracted from coca leaves → water soluble powder. Mixed with Talcum powder or lactose. Snort or dissolve in water and inject.

25
Q

What’s crack? Say crack again. Crack.

A

Crack = crystallized cocaine → Heat (causes it to crackle hence the name) and inhale vapors → far more potent than cocaine but same effects

26
Q

What’s the mechanism of cocaine?

A

Blocks DAT, NET and SERT (DA, NE and 5HT transporters) → inc extracellular DA, NE, 5HT → “high”

27
Q

Are the withdrawal effects of cocaine just like nbd?

A

NO THEY SUCK: dysphoria, depression, hunger, craving

28
Q

What are the CV effects of cocaine?

A
  1. Increase in NE/Epi → Tachycardia, HTN, peripheral vasoconstriction.
  2. Enhances platelet aggregation and thrombus formation → Coronary artery vasoconstriction → Myocardial ischemia.
  3. Enhanced sympathomimetic activity + ion transport disruption (Na+, K+, Ca2+) → Lethal arrhythmias
  4. Development of dilated cardiomyopathy (doesn’t say why)
29
Q

What are the CNS effects of cocaine?

A

Blocks reuptake of Dopamine → euphoria and hyperpyrexia (very high fever due to dopaminergic pathways of body temperature control) and seizures

30
Q

What about cocaine use in pregger ladies? JUST LIKE NBD RIGHT?

A

Acute decreases in blood flow to placenta → Fetal hypoxia, degeneration of neural development and potentially spontaneous abortion

31
Q

What about your nose? Is your nose safe from cocaine?

A

NO NOTHING’s SAFE FROM COCAINE.

Perforation of nasal septum in snorters

32
Q

What happens when you OD on cocaine?

A
  1. tachycardia/arrhythmias, HTN
  2. MI
  3. hyperthermia
  4. seizures
  5. intracranial hemorrhage/stroke
  6. coma/death
33
Q

What are some of the chronic effects of cocaine?

A
  1. anxiety/depression,

2. hunger and weight gain

34
Q

What labs will be (+) for a cocaine user?

A

BE (benzoylecgonine, the major cocaine metabolite)

35
Q

What is the mechanism of amphetamines?

A

blocks VMAT (displaces DA from vesicles into neuron endplate) → inc extracellular DA, NE & 5HT → “high”

36
Q

What happens with chronic amphetamine use?

A

loss of stimulatory effects, depression, anxiety, hunger, weight gain

37
Q

What happens to your MAO receptors with chronic amphetamine use?

A

MAO R downregulated (less stimulation) & MAO vesicular stores depleted (less DA release)

38
Q

Now they went and OD’d on amphethamines. What’ll be going on with them now?

A
  1. tachycardia/arrhythmias, HTN
  2. MI
  3. hyperthermia,
  4. intracranial hemorrhage/stroke,
  5. psychotic episodes, 6. paranoia
  6. aggression
39
Q

What are the withdrawal effects of amphetamines?

A

dysphoria, drowsiness, irritability, depression, hunger, weight gain, craving

40
Q

What is the mechanism of MDMA (methylenedioxyamphetamine)

A

Mechanism: blocks SERT and DAT?–> inc extracellular 5HT → euphoria

41
Q

What are the effects of MDMA?

A

taken orally, effects last 3-6hrs –> inc HR/BP, alertness; dehydration, mild hallucinogen

42
Q

What are the effects at higher doses of MDMA?

A
  1. hyperthermia
  2. muscle brkdn=rhabdo, 3. kidney
  3. CV failure
  4. MI/stroke
  5. seizure
  6. neurotoxicity
  7. memory impairment
43
Q

What are these newish bath salt things?

A

synthetic canthinones

44
Q

What is the mechanism of nicotine?

A

activate nACHN receptors, esp in VTA, Nuc accumbens & caudate putamen (regions where DA is a critical neurotransmitter –> inc cation currents –> inc extracellular DA

45
Q

What happens with nicotine toxicity?

A

dysphoria; nicotine inc BP & HR , MI (green tobacco sickness).
Smoke can lead to CO poisoning, CV problems, lung/esophageal cancer

46
Q

What is a major byproduct of nicotine metabolism?

A

cotinine made by liver metabolism. Inactive.

47
Q

How do you treat a nicotine addiction?

A

nicotine patch/gum, bupropion/varenicline

48
Q

What’s the mechanism of caffeine?

A

Adenosine receptor antagonists at A1 and A2 receptors
A1: normally inhibits Gi and Go receptors→ antagonist increases Gi/o activity
A2: normally activates Gs: antagonism reduces Gs activity

49
Q

WEEEEEEED.

What’s the mechansim?

A

binds receptors CB1 and CB2 to dec neurotransmitter release. More specifically:

Gi and Go stimulated: inhibit Adenylyl Cyclase –> open K+ ch –> dec Ca2+ conductance → disinhibition of DA release and reduced transmitter release

50
Q

What are the sx of weed?

A

tachycardia, dry mouth, hunger, peripheral vasodilation, euphoria, audio/visual distortions, altered perception of time, garrulousness, relaxation/sedation, psychomotor impairment

51
Q

What are the sx at higher doses of marijuana?

A

confusion, delusions, hallucinations, anxiety, panic, paranoia

52
Q

What do CB1 receptors usually do and where do we find them?

A

Many CB1 receptors in brain (hippocampus, cortex nuc accumb, striatum)

Functions:

  1. retrograde signaling in hippocampus and cerebellum -> depression
  2. Extinction of fearful memories (amygdala)
  3. Regulation of appetite
  4. Control of pain
53
Q

What about the CB 2 receptors?

A

High [CB2 R] in immune cells: Immunomodulation

54
Q

What are some of the theraputic uses of marijuana?

A
  1. Tx nausea & vomiting in chemotherapy
  2. inc appetite in AIDS, chemo pts
  3. dec intra-ocular pressure in glaucoma (not 1st line)
  4. Pain relief
55
Q

What are some of the chronic sx of marijuana use?

A
  1. respiratory problems (smoke),
  2. immune suppression
  3. dec secretion of gonadotrophins & sex steroids (inhib spermatogenesis & placental function);
  4. antimotivational syndrome
  5. memory loss
  6. impairment of mental performance

Final Multisystems Pharmacology (3 decks)

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