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PHM BSc - Applied Science > Recreational Drugs > Flashcards

Recreational Drugs Flashcards

1
Q

How would serotonin syndrome present

A

Hypertonia, hypereflexia and clonus
Mental state changes
Autonomic instability inc hyperthermia, sweating, raised HR, mydriasis

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2
Q

What recreational drugs can cause serotonin syndrome

A

Ecstasy, LSD, amphetamines

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3
Q

How would you differentiate serotonin syndrome and NMS

A

Serotonin syndrome is quicker onset and reflexes are swift

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4
Q

How is serotonin syndrome managed

A

Cooling
Benzo’s for agitation
Propofol for rigidity
Cyproheptadine can be given in severe cases

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5
Q

What is ABD characterised by

A

Mentally - aggressive, violent, struggling, psychotic

Hyperadrenergic - raised temp, sweating, raised HR and RR

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6
Q

What is the typical ABD patient

A

Acute toxicity on top of long term cocaine use

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7
Q

What are the factors leading to death in ABD

A

Lactic acidosis, increased O2 demand (which may not be met if restrained etc), risk of arrythmias

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8
Q

How should ABD be managed

A

Don’t restrain them, ventilate them at the rate they were breathing at, sedation, IV fluids, temperature control

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9
Q

What are your options for sedation in ABD

A

Benzodiazepines
Good - familiarity, safe
Bad - resp depression, unpredictable dose-response relationship
Ketamine
Good - rapid, predictable, wide therapeutic range
Bad - inhibit catecholamine uptake so worse sympathomimetic effects
Haloperidol
Good - dopamine antagonist
Bad - need ECG, prolong QT, reduced seizure threshold

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10
Q

How would you reserve Benzodiazepines

A

Flumazenil - GABA antagonist (competitive inhibitor)

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11
Q

What are the risks of giving Flumazenil

A

Lowers seizure threshold

Cardiac arrhythmia

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12
Q

What is the mechanism of action of Benzodiazepines

A

Increase the affinity of GABAa receptors for GABA= Cl- influx = hyerpolarised cell

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13
Q

How do benzodiazepines differ from barbiturates

A

They have less action in the brainstem meaning there is less respiratory depression

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14
Q

What is spice

A

It’s a synthetic canabinoid

Full agonist at the canabinoid receptor so more potent

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15
Q

How would someone who has taken spice present

A 
Catatonic state
Hallucinogenic
Increased temp and HR
Respiratory depression
Risk of MI and seizures
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16
Q

How would you treat someone who has taken spice

A

Respiratory depression - Naloxone
Agitation - diazepam
Can give Rimonabant (inverse agonist of CB1 receptor)

17
Q

What is the mechanism of action of ketamine

A

NMDA antagonist

18
Q

What effects does Ketamine have

A

Increased HR, BP, temp and sweat
Respiratory depression
Long term: ulcerative cystitis

19
Q

How does NOS exert its effects

A

Anxiolytic - GABA agonist
Euphoric - NMDA antagonist leading to dopaminergic neurone activation and dopamine release
Analgesic - opioid receptor (mu) agonist

20
Q

What is a long term consequence of NOS

A

B12 deficiency which can lead to subacute combined degeneration of the spinal cord

21
Q

What are poppers

A

Alkyl nitrates

22
Q

What do poppers do to your HR and BP

A

Raised HR

Decreased BP - lightheaded

23
Q

What is the danger of swallowing poppers and how can this be reversed

A

Leads to methylglobinaemia (Fe2 —> Fe3) leading to Hb having no oxygen carrying capacity
Give methylene blue and oxygen

24
Q

What is the mechanism of action of opioids

A

They bind to opioid receptors
Pre-synaptic: close VGCC leading to reduced intracellular Ca and therefore reduced release of neurotransmitter
Post-synaptic: Open K channels leading to K efflux and a hyperpolarized neurone less sensitive to excitatory inputs

25
Q

Describe the pain pathway and where opioids exert their action

A

Cortical neurones activate PAG (midbrain) which activate nucelus raphe magnus (medulla) which inhibit spinothalamic tracts
Opioids activate PAG

26
Q

Why do opioids lead to respiratory depression and bradycardia

A

Respiratory depression - opioids reduce the medullas sensitivity to O2
Bradycardia - stimulate vagal activity

27
Q

What is the antidote to opioid toxicity

A

Naloxone 2mg IV

28
Q

Talk through some symptomatic management options for recreational drug toxicities

A 
Temperature - cool blankets, cool IV fluids, correct muscle rigidity
Acidotic - sodium bicarbonate
Raised potassium - glucose and insulin
Raised HR - B blocker
Raised BP - B blocker or verapamil
Seizures - lorazepam
29
Q

What are some specific risks associated with amphetamine use

A

Chest pain

Extremely high BP leading to cerebral bleeds

30
Q

Systems that cocaine affects

A

Mental state: insomnia, agitated, delusions
Neuro: seizures, aneurysm rupture, haemorrhage
Pulmonary: oedema, pneumothorax, septal perforation, fibrosis
Vascular: thrombosis and infarcts literally everywhere (mesenteric ischaemia, renal infarcts, DVT, stroke)
Cardiac: Chest pain, MI, coronary artery vasospasm, atherosclerosis, arrythmias, chronic HTN, aortic dissection

31
Q

What is the MOA of cocaine

A

Blocks pre-synaptic uptake of noradrenaline and dopamine so more at receptors leading to increased catecholamine release

32
Q

How is cocaine induced chest pain managed

A

Benzodiazepines to reduced HR, BP and agitation
Aspirin to prevent thrombus
Nitrates eg GTN to reverse coronary vasoconstriction
Labetalol or verapamil for HTN

33
Q

Sympathomimetic toxidrome and examples

A

Raised HR, RR, BP, temperature
Sweat
Pupils dilate
Bowels loud

Cocaine, amphetamines, mephedrone, ecstasy, MDMA, LSD

34
Q

Anticholinergic toxidrome and examples

A

Increased HR, BP, temperature
Pupils dilate
No sweating
Loud bowel sounds

Atropine

35
Q

Cholinergic toxidrome and examples

A

Constricted pupils
Sweating
Loud bowel sounds

Mushrooms

36
Q

Opioid toxidrome and examples

A

Reduced HR, RR, BP, temp
Pinpoint pupils
Reduced bowel sounds

Morphine, heroin, tramadol, fentanyl, methadone

37
Q

Sedative-hypnotic toxidrome and examples

A

Reduced HR, BP, RR, temp
No change in pupils or bowel sounds

Benzodiazepines, barbituates, ketamine, GHB

PHM BSc - Applied Science (12 decks)

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