Brainscape's Knowledge GenomeTM

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


See full index

Y3 Lecture week IV > 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)

Y3 Lecture week IV (18 decks)

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