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A. Y5 PRESCRIBING > SESSION 6: OVERDOSES > Flashcards

SESSION 6: OVERDOSES Flashcards

1
Q

What drug is used to treat an ethylene glycol poisoning?

A

IV Fomepizole
(Historically alcohol was used which works by competing with ethylene glycol for alcohol dehydrogenase which limits the formation of toxic metabolites)

If this doesnt work haemodialysis is used

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2
Q

MOA of Fomepizole?

A

It inhibits alcohol dehydrogenase which usually catalyses the metabolism of ethylene glycol to its toxic metabolite

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3
Q

How do we monitor the beneficial efefcts of naloxone in the short term?

A

RR

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4
Q

Management of a TCA OD?

A

Oral activated charcoal can be used if they present within 1 hour
IV bicarbonate - used for hypotension, widening of the QRS interval >100 msec or a ventricular arrhythmia
other drugs can be used for arrhythmias (but not class 1 a/c or class 3 drugs as they can prolong depolarisation/QTc)

intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity

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5
Q

What can the QRS length in a TCA OD tell you about the risk?

A

Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

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6
Q

Most common SE of glucagon?

A

Nausea!!

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7
Q

Lithium monitoring rules?

A

Serum-lithium concentrations should be monitored 1 week after treatment initiation, and 1 week after each dose/formulation change, and then weekly until concentrations are stable
When serum-lithium concentrations are stable, monitor every 3 months for the first year, and every 6 months thereafter.
(Remember check conc 12 hours after drug given)

Thyroid and renal function checked every 6 months

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8
Q

Anticholinergic Toxidrome?

A

Tachycardia, hypertension
Hyperthermia
Decreased bowel sounds
Mydriasis
Decreased sweating

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9
Q

Cholinergic Toxidrome?

A

Miosis
Increased bowel sounds
Increased sweating

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10
Q

Opioid Toxidrome?

A

Bradycardia
Hypotension
Bradypnoea
Miosis
Decreased bowel sounds
Decreased sweating

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11
Q

Sympathomimetic Toxidrome?

A

Tachycardia
Hypertension
Tachypnoea
Hyperthermia
Mydriasis
Increased bowel sounds
Increased sweating

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12
Q

Sedative & hypnotics Toxidrome?
E.g. benzos, barbs, Z-drugs and antihistamines

A

Bradycardia
Hypotension
Bradypnoea
Hypothermia
Decreased bowel sounds
Decreased sweating

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13
Q

Where can you call id you need help 24/7 on a toxicology?

A

National poisons information service

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14
Q

Management of opioid OD?

A

400 micrograms IV/IM naloxone (remmeber very short half life!!)
If no response can be repeated multiple times at higher doses - check BNF

Be very careful about monitoring their airway!!

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15
Q

Most noticeable way benzo OD present differently to an opioid OD?

A

Benzos pt often complain of diplopia, have nystagmus and may have Mydriasis

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16
Q

Management of a benzo OD?

A

Flumazenil
The majority of ODs are managed with supportive care only though!! It is generally only used with severe (i.e. resp depression) or iatrogenic overdoses

In patients who are physically dependent on benzodiazepines, flumazenil can cause abrupt withdrawal by rapidly displacing benzos from their receptors = seizures.
Mixed OD Scenarios: In cases where benzodiazepines have been co-ingested with substances that lower the seizure threshold (e.g., TCAs, cocaine, or alcohol), the sudden removal of benzo-mediated sedation can unmask these pro-convulsant effects.

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17
Q

Symptoms of SSRI OD?

A

N&V
Agitation
Tremor
Nystagmus
Drowsy
Sinus tachycardia
Convulsions

Rarely severe poisoning can cause serotonin syndrome (altered mental status, neuromuscular hyperactivity, autonomic nervous system excitation)

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18
Q

Management of SSRI OD?

A

Activated charcoal if within 1 hour
If temp >39 they need rapid sedation and internal cooling with cold fluid lavage (if less severe you can use external cooling devices)
Supportive Tx e.g. fluids or convulsions can be treated with benzos
If very severe serotonin antagonists can be used e.g. cyproheptadine or chlorpromazine

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19
Q

Whats important to remmeber about administering sodium bicarbonate?

A

Should be given through a central line if undiluted as can cause tissue necrosis

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20
Q

MOA of sodium bicarbonate?

A

Systemic alkalizer - increases plasma HCO3-, buffers excess H+ and raises blood pH
Urinary alkalizer which increases the excretion of free HCO3- raising urine pH
Also acts as an antacid to neutralize/buffer stomach acid and increase pH of stomach contents

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21
Q

Features of aspirin OD?

A

May take up to 6-12 hours to manifest:
N&V, epigastric pain
Hyperventilation
Tinnitus, decreased hearing, vertigo
Agitation, confusion
Sweating/hyperthermia
Convulsions
If severe - coma

Hypokalaemia
Mixed respiratory alkalosis & metabolic acidosis with high anion gap (metabolic acidosis is a late sign!!!)

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22
Q

Tx of aspirin OD?

A

IV fluids may be needed
Seizures may need IV benzos
Intubation may be required if declining GCS
Activated charcoal if within 1 hour
Correct K+ levels before giving sodium bicarbonate! May interfere with alkalinisation of the urine
If plasma levels s>500mg/L consider sodium bicarbonate for urinary alkalisation
Pt may need cooling
If very severe may need haemodialysis

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23
Q

Features of a TCA OD?

A

Tachycardia & palpitations
Drowsy
Confusion
Hyperthermia
Dry skin
Dry mouth
Mydriasis
Urinary retention
Ataxia
Nystagmus
Hyperkalaemia
Hypertension
Metabolic acidosis
In recovery visual hallucinations, confusion and agitation can occur

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24
Q

ECG changes in TCA OD?

A

Widened QRS
Prolonged QTc

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25
Q

What % of TCA ODs are fatal and why?

A

70% because they are VERY cardiotoxic

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26
Q

Monitoring needed during TCA OD?

A

ECG monitoring for the first 24 hours!

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27
Q

Tx of TCA OD?

A

Supportive measures e.g. airway, benzos for seizures
Activated charcoal if within 1 hour
If QRS >120ms, arrhythmia or acidosis - sodium bicarbonate for serum alkalisation

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28
Q

Sx of alcohol toxicity?

A

Ataxia
Dysarthria
Nystagmus
Drowsiness -> coma
Hypotension
Acidosis
Hypoglycaemia
Aspiration of vomit!

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29
Q

Why does hypokalaemia cause digoxin toxicity?

A

digoxin normally binds to the ATPase pump on the same site as K+
When K+ is low → digoxin more easily bind to the ATPase pump → increased inhibitory effects

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30
Q

Precipitating factors for digoxin toxicity?

A

Most commonly hypokalaemia
Renal failure
Increasing age
MI
Low magnesium, high calcium/sodium, acidosis
Low albumin
Hypothermia
Hypothyroidism
Drugs that compete for secretion in DCT and so reduce excretion e.g. amiodarone, verapamil, diltiazem, spironolactone
Drugs that cause hypokalaemia e.g thiazides and loop diuretics

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31
Q

What are most fatalities from alcohol toxicity from?

A

Aspiration
Hypoglycaemia
Cardiac arrhythmias

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32
Q

Symptoms of digoxin OD?

A

generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia

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33
Q

Management of alcohol toxicity?

A

If hypoglycaemia give glucose
If withdrawal - long acting benzos e.g. chlordiazepoxide or lorazepam if liver cirrhosis
Thiamine supplements may be needed

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34
Q

Management of digoxin toxicity?

A

Digibind (digoxin antidote containing digoxin-specific antibody Fab fragments)
Also monitor K+ and correct any arrhythmias

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35
Q

Antidote for benzos?

A

Flumezanil

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36
Q

Antidote for insulin ?

A

Glucagon

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37
Q

Tx of an overdose of beta blockers?

A

Fluid resuscitation. Vasopressors and inotropes may be needed
IV glucagon if severe hypotension, HF or cardiogenic shock
Can consider IV sodium bicarbonate for metabolic acidosis
IV atropine sulfate for sy,ptmaic bradycardia (or a temp cardiac pacemaker)
Treat bronchospasm with neb bronchodilators and corticosteroids
If prolonged convulsions not responding to supportive Tx consider benzos

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38
Q

Antidote for iron salt OD?

A

Desferrioxamine mesilate (chelates iron)

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39
Q

Antidote for methanol or ethylene glycol?

A

Fomepizole or ethanol

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40
Q

Features of ethylene glycol toxicity?

A

Stage 1: confusion, slurred speech, dizziness (similar to alcohol)
Stage 2: metabolic acidosis with high anion gap and high osmolar gap. tachycardia & hypertension
Stage 3: AKI

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41
Q

Toxic mechanism of salicylate OD?

A

Salicylates irreversible block the COX-1 pathway and modify the COX-2 pathway resulting in a decrease in inflammation and platelet aggregation. It stimulates the respiratory centres causing hyperpnoea, noted as a respiratory alkalosis on a gas sample. Its other effect is uncoupling of the oxidative phosphorylation which results in in a build up of lactic acidosis and a resultant metabolic acidosis.

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42
Q

Monitoring of a pt with salicylate OD?

A

Plasma salicylate levels and repeat as absorption is slow so concentration may continue to rise for several hours
PH
Electrolytes - particuarly K+

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43
Q

Monitoring of a pt with salicylate OD?

A

Plasma salicylate levels and repeat as absorption is slow so concentration may continue to rise for several hours
PH
Electrolytes - particuarly K+

44
Q

Features of beta blocker OD?

A

Bradycardia
Hypotension
Syncope
Conduction abnormalities (prolonged QT may leas to VT eg. If pt has taken Sotalol or prolonged QRS in Propanolol)
HF
Drowsiness -> severe cases coma
Confusion
Convulsions
Hallucinations
Respiratory depression
Bronchospasm

45
Q

Management of stimulant drug poisoning e.g. cocaine or Ecstacy?

A

IV diazepam to control agitation or seizures
Cooling for hyperthermia
Manage bp changes and cardiac effects - may need specific Tx

46
Q

Organophosphate insecticide OD symptoms?

A

SLUD:
Salivation
lacrimation
urinary incontinence
Defecation/diarrhoea

CNS - anxiety, confusion, seizure, coma
Cardiovascular - hypotension, bradycardia
Miosis and muscle weakness/fasciculations

47
Q

Tx of organophosphate insecticide poisoning?

A

Move pt to fresh air, remove soiled clothing, wash contaminated skin
Frequent removal of bronchial secretions
IV atropine sulfate to reverse muscarinic effects of ACh - give until skin flushed, dry, Mydriasis and bradycardia disappears
Pralidoxime should be used in adjunct to atropine in mod/severe poisoning - continue until pt hasn’t needed atropine for 12 hours - improves muscle tone which is particuarly important for respiratory muscles

48
Q

Mechanism of organophosphate poisoning?

A

Organophosphates inhibit acetylcholinesterase (enzyme responsible for breaking down ACh at synapses) leading to up-regulation of cholinergic neurotransmission

49
Q

MOA of atropine and pralidoxime in organophosphate poisoning?

A

Atropine is a muscarinic antagonist so blocks ACh at muscarinic receptors
Pralidoxime is an acetylcholinesterase reactivator which binds to the organophosphate-enzyme complex and removes the organophosphate, restoring acetylcholinesterase activity

50
Q

When does ALT typically rise after paracetamol OD?

A

Typically 8-12 hours after significant ingestion
(So if a pt says they took it <8 hours ago but ALT is up from baseline likely untrue)

51
Q

Management of paracetamol OD if it’s <8 hours after ingestion?

A

Consider activated charcoal if within 1 hour
After 4 hours take plasma paracetamol level - use nomogram. If paracetamol level above treatment line OR evidence of acute liver injury then start acetylcysteiene infusion

52
Q

Whats the toxic dose for paracetamol OD?

A

150mg/kg

(If obese pt >110kg then use 110 as max weight rather than actual weight)

53
Q

Management of paracetamol OD if it’s 8-24 hours after ingestion?

A

If dose suspected >150mg/kg OR symptomatic OR any evidence of acute liver failure start acetylcysteine immediately whilst waiting for serum paracetamol levels

Discontinue acetylcysteine if plasm paracetamol is below Tx line and pt is asymptomatic, normal LFTs/serum creatinine/INR

If dose <150mg/kg and no signs of acute liver failure take serum levels and then consider Tx

54
Q

Management of paracetamol OD if it’s >24 hours after ingestion?

A

Take serum sample straight away
If pt is jaundiced, has hepatic tenderness, raised ALT, INR >1.3 or suspected >150mg/kg or serum paracetamil level is detectable -> start acetylcysteiene
Otherwise take serum levels and then consider Tx

55
Q

What is considered a staggered OD?

A

When not all drugs are taken within 1 hour

56
Q

Management of a staggered OD of paracetamol?

A

Commence IV acetylcysteien without delay to all pts!
Check serum levels 4 hours after last paracetamol ingestion

Consider stopping acetylcysteine if low risk of hepatotoxicity: paracetamol conc <10mg/L, normal ALT, INR <1.3 and asymptomatic

57
Q

What are the 2 acetylcysteine regimens in the UK?

A

Standard 21 hour regimen - 150mg/kg over 1 hour, 50mg/kg over 4 hours and then 100mg/kg over 16 hours
Modified 12 hour SNAP regimen - 100mg/kg over 2 hours and then 200mg/kg over 10 hours

(Remember the ceiling weight of 110kg!!)

58
Q

Dosing of acetylcysteiene in pregnancy?

A

The toxic dose of paracetamol ingested should be calculated using the patient’s pre-pregnancy body-weight and the acetylcysteine dose should be calculated using the patient’s actual pregnant body-weight

59
Q

Sx of anaphylactoid reaction to acetylcysteiene?

A

Nausea
Flushing
Urticaria
Tachycardia
Bronchospasm

(Unlike anaphylaxis its non-immune mediated so doesnt require prior sensitisation and can occur on first exposure. Sx are often mild/moderate i.e. less severe than true anaphylaxis. The reactions and often infusion-rate dependant)

60
Q

Tx of anaphylactoid reaction to acetylcysteiene?

A

Stop infusion
antihistamine or nebulised salbutamol
Restart infusion at slower rate

61
Q

Risk factors for increased chance of hepatotoxicity in paracetamol OD?

A

• pts taking liver enzyme inducing drugs
• Malnourished pts e.g. EDs or pts who have not eaten for a few days
• Chronic alcohol excess (acute may actually be protective!)

62
Q

What criteria do we use for ?liver transplantation aftr patracetamol OD/

A

Kings college hospital criteria

63
Q

What are the kings college hospital criteria for liver transplantation?

A

Arterial pH <7.3 24 hours after ingestion

OR all of the following:
◦ PT >100 seconds
◦ Creatinine >300
◦ Grade 3 or 4 encephalopathy

64
Q

How fast is acetylcysteiene given and why?

A

Over 1 hour
Used to be 15 minutes but slowing it down reduces the number of SE

65
Q

Sx of paracetamol OD?

A

Often asymptomatic
N&V
Abdominal pain
Jaundice
AKI
Metabolic acidosis
Hepatic encephalopathy
Coma
Bruising or systemic haemorrhage - coagulopathy secondary to impaired hepatic clotting factor production

66
Q

Adverse effects of NRT?

A

Dizziness
headache
hyperhidrosis
n&v
palpitations
skin reactions

67
Q

MOA varencicline?

A

Nicotinic receptor partial agonist

68
Q

Most important risk of varencicline?

A

May cause suicidal ideation

69
Q

CI for varencicline and bupropion?

A

Pregnancy and breast feeding
Bupropion also cannot be used in epilepsy!

70
Q

Main risk of bupropion?

A

1 in 1000 risk of seizure

71
Q

Therapeutic levels of aspirin?

A

0.7-2.2

72
Q

Why in overdose is aspirin absorption delayed?

A

salicylate-induced pylorospasm or the formation of pharmacobezoars

At therapeutic level aspirin is actually absorbed relatively quickly

73
Q

Outline metabolism of aspirin at therapeutic vs toxic levels?

A

Aspirin is metabolized to salicylic acid, its active form. This undergoes conjugation in the liver, primarily to form salicyluric acid (via glycination) and glucuronides, which are excreted in the urine. At therapeutic levels, this metabolic pathway is efficient and non-saturable.
The binding of salicylic acid to plasma proteins means only about 10% is “free” or pharmacologically active at therapeutic doses.

At toxic doses, the metabolic pathways, especially glycination, become saturated. So salicylate elimination shifts to being more dependent on renal excretion, which is a slower process. This reduced efficiency in elimination causes the half-life of salicylic acid to extend significantly, from the usual 2-4 hours to potentially 15-30 hours or more.
Additionally, free salicylate levels rise, leading to increased pharmacological and toxic effects.

74
Q

Why should you only intubate a pt with aspirin OD if absolutely necessary?

A

Intubation often causes a period of apnoea which would transiently worsen the acidosis and exacerbate CNS toxicity

75
Q

Outline pathophysiology of alcohol withdrawal?

A

Alcohol enhances the activity of GABA, the brain’s primary inhibitory neurotransmitter. This leads to sedative, anxiolytic, and CNS depressant effects.
Alcohol simultaneously inhibits NMDA glutamate receptors, which play a role in excitatory neurotransmission. This suppression further contributes to the depressant effects of alcohol.

With chronic use, the brain adapts by downregulating GABA_A receptors and upregulating NMDA receptors to maintain homeostasis in the presence of alcohol.

When alcohol intake suddenly stops, the enhanced GABAergic inhibition rapidly diminishes, and the previously inhibited NMDA glutamatergic system becomes overactive. This leads to CNS hyperexcitability, manifesting as: Tremors, anxiety, seizures & delirium tremens in severe cases

76
Q

Why do we give lorazepam instead of chlordiazepoxide for alcohol withdrawal in a pt with liver cirrhosis?

A

Lorazepam is metabolised through glucuronidation, which is less dependent on liver function. Safer as glucuronidation is preserved even in cirrhosis.

Chlordiazepoxide is etabolized in the liver via cytochrome P450 enzymes. It has active metabolites that are eliminated more slowly in liver disease, increasing the risk of drug accumulation and prolonged sedation.

77
Q

How do we determine the severity of alcohol dependance?

A

Number of daily units
AUDIT questionnaire - if suggests dependency then severity can be categorised using SADQ (Severity of Alcohol Dependence Questionnaire) or LDQ (Leeds Dependence Questionnaire)

78
Q

Causes of wernickes?

A

Most commonly - alcoholics
Rarer causes include persistent vomiting, stomach cancer, and dietary deficiency

Administering IV glucose to chronic alcoholics who are hypoglycemic can precipitate Wernicke’s encephalopathy if thiamine deficiency is present but not corrected beforehand

79
Q

Why can hypoglycaemia & administering glucose precipitate Wernickes in chronic alcoholics?

A

Thiamine is essential for glucose metabolism as it acts as a coenzyme in pathways e.g. Krebs cycle and pentose phosphate pathway.
When glucose is administered without replenishing thiamine, it increases the metabolic demand for thiamine, which can worsen the deficiency and precipitate Wernicke’s encephalopathy.

Do not give high dose glucose before vitamin replacement!

80
Q

What is pabrinex?

A

Thiamine B1
B2 - riboflavin
B3 - niacin
B6 - pyridoxine
Vit C
Glucose

81
Q

What actually kills you in a paracetamol OD?

A

Acute liver failure can lead to hepatic encephalopathy ans cerebral oedema - this can cause coning
(This is why its important to not wait until last minute to transfer the pt to liver transplant unit - movement, bright lights, sounds etc may precipitate coning in a pt with cerebral oedema)

82
Q

If giving a child activated charcoal what should you consider?

A

Giving it in a fruit juice/ice cream etc
Giving it with an antiemetic as it commonly causes N&V

83
Q

What is the 1 situation where you wont see metabolic compensation for a chronic respiratory acidosis?

A

Renal failure - HCO3- wont rise as compensation as the kidney cannot re-absorb it effectively

84
Q

What length of Tx is considered long term steroid therapy and therefor requires a steroid treatment card?

A

Anyone on steroids >3 weeks

85
Q

What monitoring do you need to do for long term nitrofurantoin?

A

LFTs
Pulmonary Sx - can cause acute and chronic pulmonary reactions - including fibrosis

86
Q

Indications to decrease the dose of fludrocortisone?

A

When supine BP is high
Hypokalaemia
HF
Acute/severe renal failure

87
Q

Why isnt fludrocortisone needed in an addisonian crisis?

A

At high doses hydrocortisone exerts glucocorticoid and mineralocorticoid actions

88
Q

Causes of addisonian crisis?

A

Sepsis/infections
Surgery
GI illness
Adrenal haemorrhage - Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
Steroid withdrawal

89
Q

Tx of addisonian crisis?

A

hydrocortisone 100 mg IM/IV
1L normal saline infused over 30-60 mins +/- dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

90
Q

Whilst on variable rate IV glucose infusion… what should you do if a pt has a hypo?

A

Stop IV insulin
Give 10% Dextrsoe 200ml or 20% 100ml
Restart VRII when BG >4mmol/L but at a reduced rate

91
Q

When to use a fixed vs variable rate insulin infusion?

A

VRII - use when erratic BGs e.g. perioperative and acute illness with high glucose variability (not DKA or HHS!!). Reduces the risk of hypoglycaemia but requires frequent monitoring!

FRII - consistent rate of insulin used in DKA, HHS or critical care - risk of hypoglycaemia if not combined with adequate glucose monitoring and adjustments

92
Q

Up to when can ulipristal be given as EC?

A

120 hours / 5 days

93
Q

Up to when can levonorgestrel be given as EC?

A

72 hours / 3 days

94
Q

Up to when can the copper coil be given as EC?

A

Within 5 days of UPSI or within 5 days of estimated date of ovulation (14 days before next menstrual cycle)

95
Q

MOA of ulipristal?

A

Selective progesterone receptor modulator
Delays/inhibits ovulation by suppressing the LH surge

96
Q

What is more effective uliprostal or levonorgestrel?

A

Ulipristal

97
Q

When can you restart the contraceptive pill after ulipristal or levonorgestrel?

A

Ulipristal - wait 5 days as it may reduce effectiveness. When you restart pill use condoms for 7 days if COCP or 2 days if POP
Levonorgestrel - can start either pill straight away with condoms for 7 days if COCP or 2 days if POP

98
Q

Common SE of ullipristal and levonorgestrel EC?

A

N&V
If you vomit within 3 hours of taking it you must take another dose

99
Q

CI for ulipristal?

A

Severe asthma controlled by oral glucocorticoids
Breast, cervical, ovarian, uterine cancer or undiagnosed vaginal bleeding
Cannot breastfeed for 1 week - pump & dump

100
Q

Dose of ulipristal?

A

30mg single dose

101
Q

Dose of levonorgestrel for EC?

A

1.5mg single dose
3mg if women >70kg or BMI >26
Double dose if taking a liver enzyme-inducing drug (giving IUD instead is the best option)

102
Q

MOA of levonorgestrel for EC?

A

Binds to progesterone and androgen receptors. Slows release of GnRH from hypothalamus which suppresses the LH surge
Inhibits and delays ovulation

103
Q

Main SE of levonorgestrel?

A

Common to disturb the menstrual cycle
N&V too / GI discomfort

104
Q

Most effective emergency contraception options?

A

Copper IUD

105
Q

What can you do if you need to give copper IUD as EC but the pt is high risk of PID?

A

Prophylactic antibiotics

106
Q

When does starting the COCP not need any additional contraception?

A

If the COCP is started within the first 5 days of the cycle! Otherwise you need 7 days of alternative contraception

A. Y5 PRESCRIBING (6 decks)

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