Recreational Drugs Flashcards

(37 cards)

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
Describe the pain pathway and where opioids exert their action
Cortical neurones activate PAG (midbrain) which activate nucelus raphe magnus (medulla) which inhibit spinothalamic tracts Opioids activate PAG
26
Why do opioids lead to respiratory depression and bradycardia
Respiratory depression - opioids reduce the medullas sensitivity to O2 Bradycardia - stimulate vagal activity
27
What is the antidote to opioid toxicity
Naloxone 2mg IV
28
Talk through some symptomatic management options for recreational drug toxicities
``` 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
What are some specific risks associated with amphetamine use
Chest pain | Extremely high BP leading to cerebral bleeds
30
Systems that cocaine affects
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
What is the MOA of cocaine
Blocks pre-synaptic uptake of noradrenaline and dopamine so more at receptors leading to increased catecholamine release
32
How is cocaine induced chest pain managed
Benzodiazepines to reduced HR, BP and agitation Aspirin to prevent thrombus Nitrates eg GTN to reverse coronary vasoconstriction Labetalol or verapamil for HTN
33
Sympathomimetic toxidrome and examples
Raised HR, RR, BP, temperature Sweat Pupils dilate Bowels loud Cocaine, amphetamines, mephedrone, ecstasy, MDMA, LSD
34
Anticholinergic toxidrome and examples
Increased HR, BP, temperature Pupils dilate No sweating Loud bowel sounds Atropine
35
Cholinergic toxidrome and examples
Constricted pupils Sweating Loud bowel sounds Mushrooms
36
Opioid toxidrome and examples
Reduced HR, RR, BP, temp Pinpoint pupils Reduced bowel sounds Morphine, heroin, tramadol, fentanyl, methadone
37
Sedative-hypnotic toxidrome and examples
Reduced HR, BP, RR, temp No change in pupils or bowel sounds Benzodiazepines, barbituates, ketamine, GHB