Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Lecture week 4 > Drug Overdose > Flashcards

Drug Overdose Flashcards

1
Q

What happens to the Paracetamol when is taken at a normal dose?

A

It gets conjugated

*conjugates are harmless - filtered out by the kidney and completely safe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens when normal paracetamol metabolic pathways become saturated?

A

Normal pathways (safe pathways): 1) glucuronyl transferase 2) phenolsulphotranseferase

When normal pathways get saturated (overwhelmed by OD)-> 3rd pathway activated (it is called N-acetyl-p-benzoquinoneimine) -> NAPQI produced -> it destroys hepatocytes in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does the body get rid of NAPQI?

A

It combines with Glutathione -> that conjugates NAPQI and gets rid of it (by removing it from the body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do we give in paracetamol OD/ what’s the physiological princple?

A

We want to increase Glutathione dose -> so we can conjugate NAPQI (harmful metabolites of paracetamol in OD)

For that purpose we give N-acetylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the timeframe to give N-acetylcysteine after paracetamol OD?

A

within 4 hours from OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do the inducers do?

A

Induced cytochrome P450 -> more metabolism -> other drugs (that are metabolized) are less effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cytochrome P450 inducers

A

CRAP GPS

  • *C**arbemazepines
  • *R**ifampicin
  • *A**lcohol (chronic)
  • *P**henytoin
  • *G**riseofulvin (anti-fungal)
  • *P**henobarbitone
  • *S**ulphonylureas / St John’s Wort (alternative remedy for depression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cytochrome P450 inhibitors

A

SICKFACES.COM

  • *S**odium valproate
  • *I**soniazid
  • *C**imetidine
  • *K**etoconazole
  • *F**luconazole
  • *A**lcohol (acute - binge drinking)
  • *C**hloramphenicol
  • *E**rythromycin
  • *S**ulfonamides
  • *C**iprofloxacin
  • *O**meprazole
  • *M**etronidazole

*grapefruit juice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do cytochrome p450 inhibitors do?

A

Cytochrome p450 inhibitors -> inhibit liver metabolism -> other drugs are less metabolised -> toxicity (overdose/accumulation may occur)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the connection between the inducer of cytP450 and paracetamol OD?

A

As more liver CytP450 activity -> more activation of pathway that produce NAPQI = more dangerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment protocol for paracetamol

(to treat or not to treat)

A

Drug paracetamol level is taken 4 hours after the OD -> to check what blood Paracetamol level is

If it is above the line -> treat with NAC (N-acetylcysteine)

If the blood level of Paracetamol is below -> then do not treat *at that point perhaps enough glutathione to metabolise paracetamol + side effects of having NAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Side effects of NAC treatment

A

NAC = N-acetylcysteine

  • nausea/ vomiting
  • bronchospasm
  • anaphylactoid reation* - rash (in about 20% of people)

*anaphylactoid reaction is anaphylaxis - like picture but not mediated by IgE but by direct release of inflammatory mediators from mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Do we treat paracetamol OD if we do not know when a person took OD, confusion about where the levels of Paracetamol fall on the ‘treatment line’?

A

If there is confusion - we treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What groups of the patients are at high risk of toxic effects of Paracetamol?

A

High risk of toxic effects of Paracetamol = due to low glutathione stores

  • alcoholics
  • immunosuppressed
  • malnourished
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Best investigations for a person coming with Paracetamol OD

A
  • Paracetamol level
  • LFT -> to check liver function and bilirubin
  • INR -> to make sure clotting is not affected (synthetic function)
  • U&Es -> to ensure that there is no multi-organ failure
  • glucose -> if pt has low GCS/mental state - to role out that cause of pt state
  • ABG -> always to do with a patient with low GCS
  • metabolic flap test -> to check if encephalopathy has happened
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Paracetamol OD management

if taken <1 hour ago

A

Activated Charcoal

MoA: it is going to the stomach and absorbs paracetamol particles

*but effective only if a drug is in the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Main treatment for Paracetamol OD

  • how much / when
  • what do we do
A

NAC (N-acetylcysteine)

  • take blood (levels of Paracetamol) -> give NAC
  • 3 x bags of NAC over 21 hours
  • repeat bloods afterwards

* to check if they are in ‘safe zone’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s a ‘safe zone’ following NAC treatment?

A

After treatment with NAC -> we check the bloods

‘safe zone’ is:

  • INR <1.3

- ALT <2 X upper limit abnormal

Then, they are likely to recover - not dangerous state for the liver

*if not within ‘safe zone’ limit -> give more NAC over 16 hours and keep patient for another day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do we need to do before discharging a patient with Paracetamol OD?

A

We need to arrange psychological review (mental health team)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the last resort in the treatment of Paracetamol OD?

A

Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What criteria are used to determine who should be referred for an immediate liver transplant?

A

King’s criteria

to determine who should receive a liver transplant after acute or chronic paracetamol induced severe liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the most important King’s College criteria for liver transplant

A
  • pH <7.3 or lactate >3.5 after fluids -> indicates metabolic acidosis due to liver failure

OR all 3 of:

  • INR >6.5
  • Creatinine >300 -> renal dysfunction
  • hepatic encephalopathy - grade III or IV -> low GCS and liver flap

*All these are signs of severe liver damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Common examples of benzodiazepines

A
  • Diazepam
  • Lorazepam
  • Midazolam
  • Zopiclone
  • Flunitrazepam / Rohypnol
24
Q

Uses of benzodiazepines

A
  • anxiolytic
  • sedative
  • hypnotic
  • anticonvulsant
  • muscle relaxant
25
Q

What is the clinical picture of benzodiazepine OD?

A
  • confusion
  • retrograde amnesia
  • low GCS
  • altered mental state
  • altered balance
26
Q

Investigations in benzodiazepines OD

A
  • glucose
  • ABG
  • U&E
  • FBC
  • urine toxicity -> to role out other drugs OD (the person would be unconscious so no Hx provided)
  • ECG
27
Q

Is there a risk to life in benzodiazepine OD?

A

No risk to life as their breathing of heart rhythm would not be affected (although low GCS)

28
Q

Management of benzodiazepine OD

A
  • support airway and respiration (if low)
  • watch and wait for GCS to recover
  • Flumazenil - competitive antagonist
29
Q

Flumazenil

  • MoA
A

Flumazenil

*antidote for benzodiazepine OD

MoA: selective GABA-A antagonist (competative inhibitor)

30
Q

Side effects of Flumazenil

A

Side effect:

  • promote seizures (that may be resistant as we cannot treat it with benzodiazepines - due to already OD on them) - so often just ‘watch and wait’ approach
  • arrhythmias
31
Q

Common Tricyclic anti-depressants

A
  • Amitriptyline
  • Imipramine
  • Nortriptyline
  • Doxepin
  • Clomipramine
32
Q

What is side effect of TCAs?

A

Anticholinergic

Result: less PNS -> more SNS activity

Examples:

  • dilated pupils
  • tachycardia
  • dry mouth
  • urinary retention
  • blocks alpha1 adrenal receptors in blood vessels -> lower blood pressure as vasoconstriction is blocked -> more vasodilatation
  • coma
  • fast sodium channels in the heart are blocked -> arrythmais

- seizures -> due to GABA antagonist

33
Q

Signs of TCAs OD on ECG

A

ECG with TCAs OD

  • tachycardia
  • R axis deviation (lead I and aVF - ‘returning/reaching’)
  • widen QRS
34
Q

Investigations in TCAs OD

A
  • ECG

- ABG

- glucose

  • U&E
  • FBC
  • urine toxicology
35
Q

Management of TCAs OD

A

TCAs OD:

  • ECG (signs of TCAs OD)
  • activated charcoal if presented <2 hours
  • sodium bicarbonate -> if ECG changes (to increase the bioavailability of sodium, as sodium channel blocked) + buffer against seizures and acts against acidosis
  • fluids -> for hypertension
  • seizures treatment -> benzodiazepines (NOT PHENYTOIN! )
36
Q

What drug and why is contraindicated in the treatment of TCAs OD induced seizures?

A

Phenytoin is contraindicated

This is because it acts as Na+ channel blocker and in TCAs OD we have already blocked Na+ channels -> risk of arrhythmias would be increased

37
Q

Would haemodialysis work in management of TCAs OD?

A

No, as TCAs are protein bound

38
Q

Example (1) of typical antipsychotic

A

Haloperidol

39
Q

Examples (4) of atypical antipsychotics

A
  • Clozapine
  • Olanzapine
  • Quetiapine
  • Risperidone
40
Q

Uses of anti-psychotics

A
  • schizophrenia
  • bipolar
  • dementia
41
Q

What are effects of anti-psychotic drugs?

A

Anticholinergic

  • dry mouth
  • increased HR
  • low BP (as no vasoconstriction -> vasodilation)
  • dilated pupils
  • serotonin blocked -> low GCS
  • arrhytmias and seizures -> as block of Na+ channels
42
Q

How to differentiate anti-psychotics OD from TCAs?

A

Anti-psychotic meds also block dopamine-2 receptors -> involuntary movements are not blocked

Involuntary movements: pseudoparkinsonism, acute dystonia, tardive dyskinesia

43
Q

Investigations for anti-psychotic OD

A
  • ECG

- ABG

- glucose

  • urine toxicology
  • INR
  • U+E
  • FBC
  • INR
44
Q

Neuroleptic Malignant Syndrome

  • what is this?
  • clinical presentation
A

A possible outcome of anti-psychotic OD -> neuroleptic malignant syndrome

Clinical presentation:

  • hyperthermia -> temp keeps going up
  • autonomic dysfunction -> sympathetic effects are out of control (pupils dilated all the time, BP keeps going down)
  • muscle rigidity -> uncontrolled muscle contraction -> leads to rhabdomyolysis
  • reduced GCS
45
Q

How do we test for Neuroleptic Malignant Syndrome

A
  • check the urine -> will be red due to muscle breakdown (myoglobin)
  • CK levels -> creatinine raised of thousands
46
Q

Management of Neuroleptic Malignant Syndrome

A

Mx of Neuroleptic Malignant Syndrome

  • stop anti-psychotics
  • rapid cooling and anti-pyretic (Ice packs, cold fluids and paracetamol)
  • IV fluids
  • drugs (Dantrolene, Bromocriptine, Benzodiazepine, Procyclidine)
  • haemodialysis -> to get rid of myoglobin
47
Q

Drugs used in Rx of Neuroleptic Malignant Syndrome (4)

A

Dantrolene -> muscle relaxant

Bromocriptine -> D2 antagonist (to reverse effects of anti-psychotics)

Procyclidine -> anti - muscarinic (help with muscle rigidity)

Benzodiazepine -> muscle relaxants

48
Q

Opioids examples

A
  • codeine
  • morphine
  • tramadol
  • fentanyl
  • buproprione
  • methodone
49
Q

Side effects of morphine/ opioids

A
  • nausea a vomiting
  • abdominal pain -> due to constipation
  • low GCS
  • respiratory depression (in OD)
  • marked pupil constriction (in OD)
50
Q

Investigations in opioid OD

A
  • ABG

- glucose

  • urine toxicology
  • U&E
  • FBC
  • ECG
51
Q

Management of opioid OD

A
  • support airway and respiration (ABCD)
  • monitor GCS
  • charcoal if OD <2 hours (if can be taken orally)
  • Naloxone IV
52
Q

What do we need to know about dosing of Naloxone?

A

Naloxone IV has a rapid onset of action but also very short half-life -> needs repeated dosing

53
Q

Opiate withdrawal symptoms

A

Naloxone may induce opioids withdrawal symptoms:

‘everything is running’ - fluid out

  • muscle aches
  • insomnia
  • runny nose
  • fever
  • abdominal cramps
  • diarrhoea
  • vomiting
  • tachycardia
54
Q

The antidote to iron OD

A

Deferoxamine IV - chelating agent (to absorb and excrete iron molecules)

55
Q

Antidote for anti-freeze (glycol) poisoning

A

Glycol / anti-freeze poisoning

Antidote: alcohol -> Ethanol IV or Fomepizole

Alcohol is a competitive antagonist

56
Q

Symptoms of Carbon Monoxide poisoning

A
  • headache
  • nausea
  • dizziness
  • collapse
  • breathlessness - but sats are 100% (as CO misinterpreted as O2 by sats probe); with ABG CO2 will be very low
  • loss of consciousness
57
Q

Management of CO poisoning

A

Carbon Monoxide poisoning Mx:

  • hyperbaric O2 chamber (to get rid of CO and allow O2 to bind to RBCs again)

Lecture week 4 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions