Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FIMC > Toxiciology > Flashcards

Toxiciology Flashcards

1
Q

What are the features of salicylate poisoning? (6)

A
  1. Increased RR
  2. Tinnitus
  3. Deafness
  4. Sweating
  5. Vasodilation
  6. Acid base disturbance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What metabolic disturbance do adults presenting with salicylate poisoning predominates?

A

Reps alkalosis > metabolic acidoses

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

What metabolic disturbance do children presenting with salicylate poisoning predominates?

A

Metabolic acidosis > resp alkalosis

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

What is mild salicylate poisoning and how should it be managed?

A
  1. < 300mg/L
  2. Asymp and normal VBG then home at 6 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is moderate salicylate poisoning and how should it be managed?

A
  1. 300-700mg/L
  2. Urinary alkalization - PH 7.5-8.5 using sodium bicarbonate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is severe salicylate poisoning?

A
  1. CNS features, acidosis or > 700mg/L
  2. Consider HD and I+V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pathophysiology of paracetamol poisoning?

A

Metabolite of paracetamol (NAPQI) binds glutathione in the liver and causes hepatic necrosis when glutathione stores are depleted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the features of TCA OD in conscious patients? (7)

A

Anti-cholinergic toxidrome

  1. Tachycardia
  2. Dry skin
  3. Dry mouth
  4. Dilated pupils
  5. Urinary retention
  6. Ataxia
  7. Jerky limb movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What signs do unconscious patients developed following TCA OD? (7)

A
  1. Divergent squint
  2. Hypertonia
  3. Hyper-reflexia
  4. Myoclonus
  5. Upgoing plantars

If comatose - areflexia and muscle facciditiy

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

What ECG changes will be seen in TCA OD and which is the most sensitive?

A
  1. Increased QRS (most sensitive)
  2. Increased PR
  3. Tachy
  4. P waves can be lost in T - looks like VT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the tx for TCA overdose? (5)

A
  1. If under 1 hour activated charcoal
  2. 50-100ml 8.4% bicarbonate
  3. Aim PH 7.5-7.55 (excessive is fatal) and normal QRS
  4. Avoid routine use anti-arrhythmics
  5. Severe consider glucagon or intralipid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the antidote to benzo OD?

A

Flumazenil

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

How long does flumezanil last?

A

1 hour

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

What are the risks of using flumazenil and when is it particularly high risk?

A

Can lead to convulsions and arrhythmias

With concurrent TCA OD - can lead to arrest

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

What signs/symptoms feature in haloperidol + chlorpromazine (and related drugs) OD?

A

Oculogyric crisis
Muscle spasms - torticollis/opisthotonus (body arched back)
- eye deviate upwards
- can have autonomic dysfunction
- can be painful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What ECG changes will you see in haloeridol/chlorpromazine/similar drugs in OD? (2)

A
  1. Increased QRS
  2. Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for haloperiol/chlorpromazine OD? (3)

A
  1. Proycylidine
  2. Diazepam
  3. Bicarbonate if QRS >120ms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the features of lithium toxicity? (6)

A
  1. n/v
  2. diarrhoea
  3. confusion
  4. ataxia
  5. increased tone
  6. clonus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment for lithium toxicity?

A

Supportive
Dialysis

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

What are the effects of sulfanylurea overdose?

A
  1. Low glucose
  2. Low potassium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the treatment for sulfanylurea overdose?

A

Octreotide

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

What are the features of unique to propanolol OD? (2)

A
  1. Bronchospasm in asthmatics
  2. Hypoglycaemia in children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does sotalol OD cause in particular?

A

Torsades des pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the treatments of beta blocker OD without severe hypotension?

A
  1. Consider activated charcoal
  2. Atropine may work (pacing probably not)
  3. Glucagon 5-10mg IV (anticipate vomiting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In severe beta-blocker OD with low BP what are 3 treatment options?

A
  1. High dose Insulin Euglycaemic Therapy (HIET)
  2. Intralipid
  3. Ionotropes/vasopressors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the features of CCB OD? (6)

A
  1. Bradycardia
  2. AV block
  3. Profound vasolidation
  4. Metabolic acidosis
  5. Hyperkalaemia
  6. Hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the treatment for CCB OD? (3)

A
  1. Consider activated charcoal
  2. Atropine +/- pacing
  3. Calcium chloride 10% over 10 mins and consider repeating up to x 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the treatment options for severe CCB OD? (4)

A
  1. Glucagon
  2. Intralipid
  3. HIET
  4. Vasopressors/ionotropes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the features of digoxin toxicity? (4)

A
  1. Xanthopisa- yellow flashes/discolouration
  2. Hyperkalaemia
  3. Brady, increased PR/QRS
  4. Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the treatment for digoxin toxicity? (3)

A
  1. Digiblind/Digifab
  2. Insulin/dex for increased K+ (rapid decrease with Digibind)
  3. Atropine/pacing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the biochemical changes in acute methanol poisoning? (3)

A
  1. Acidosis
  2. Hypergylcaemia
  3. Raised amylase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are survivors of methanol poisoning at risk of? (2)

A
  1. Blindness
  2. Parkinsonian features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the treatment for methanol poisoning? (4)

A

Ethanol
Fomepizole
Folinic acid
Bicarbonate if acidotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the early (<12 hours) features of ethylene glycol poisoning?

A

Appear drunk, no smell alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the late features of ethylene glycol poisoning? (6)

A
  1. CCF
  2. Acidosis
  3. Tachy/arrhythmias
  4. Hypocalcaemia (can be profound)
  5. Acute tubular necrosis
  6. CN palsies`
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the treatment options for ethylene glycol poisoning? (5)

A
  1. Fomepizole
  2. Ethanol
  3. Sodium bicarbonate for acidosis
  4. Calcium chloride only if seizures or QTc >500 as can lead to calcium oxolate stones
  5. HD + I+V
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What can occur in petrol ingestion?

A

Can be fine but aspiration lead to severe pneumonitis requiring steroids + resp support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the pathophysiology of organophosphate poisoning?

A

Inhibit cholinesterases which leads to build up of acetylcholine at nerve endings (cholinergic affect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the features of organophosphate poisoning (cholinergic toxidrome)? (8)

A

S- alivation
L - acrimation
U - rination
D - efecation
G - I upset
E - mesis
M - iosis
M - muscle twitching

Bradycardia, paralysis and resp failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the treatment for organophosphate poisoning and what is its mechanism

A

Atropine - blocks affect of acetylcholine at muscarinic receptors
Eases smooth muscle constriction and dries up secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the atropine dose in organophosphate poisoning?

A

2mg IV adult
0.02mg/kg children
Every 5 mins double dose until atropinisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the mechanism of pralidoxime?

A

Reactivate acetylcholinesterase inhibited by organophosphates allowing metabolisation of acetylcholine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What can lead to cyanide poisoning? (3)

A
  1. Polyurethane burning
  2. Fruit kernels
  3. Finger polish remover
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the features of cyanide poisoning? (4)

A
  1. Metabolic acidosis
  2. Seizures
  3. Pulmonary oedema
  4. Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the initial management of cyanide poisoning? (2)

A
  1. Remove clothes
  2. Wash exposed skinW
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the antidote for severe cyanide poisoning and what is the risk of giving it?

A
  1. Dicobalt edetate - Kelocyanor
  2. If no cyanide can be fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the treatments for mild cyanide poisoning? (2)

A
  1. Sodium thiosulphate
  2. Sodium nitrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the best treatment for inhaled cyanide poisoning?

A

5g hyroxycobalamin IV (Cyanokit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the max dose of lidocaine?

A

3mg/kg
max 200mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the maximum dose of lidocaine with adrenaline?

A

7mg/kg
max 500mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the maximum dose of bupivicaine?

A

2mg/kg
150mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the management of LA toxicity including dose?

A

Intralipid

1.1.5mg/kg bolus and 15mg/kg/hr infusion
5 mins no response:
2. 2nd bolus and increase infusion to 30mg/kg/hr
3.Continue to 3rd and 4th bolus which is maximum

In arrest may need 1 hour for intralipid to take effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How are hydrofluric burns managed? (4)

A
  1. Irrigate normal saline ++
  2. Calcium gluconate gel
  3. Tx low Ca2+
  4. In arrest - 60ml x 10% calcium chloride
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What drugs can cause methaemoglobinaemia?(7)

A

sulphonamides (abx, prefix sulf-)
chloroquine
dapsone
prilocaine
metoclopramide
nitrites (nitroglycerin, NO, sodium nitroprusside)
benzene derivatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the features of methaemoglobinaemia?

A

1.cyanosis
2. symptoms and signs of decreased oxygen delivery e.g. chest pain, dyspnea, altered metal state, end organ damage
3. SpO2 reading 85-90%
4. blood samples typically have a chocolate brown hue
5. Normal PaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the treatment for methaemoglobinaemia?

A

Methylene blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the triad of symptoms in serotonin syndrome?

A
  1. Change in mental staus
  2. Autonomic hyperactivity
  3. Neuromuscular manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the 3 major and 5 minor symptoms suggestive of neuroleptic malignant syndrome?

A

Major
1. Fever
2. Rigidity
3. Elevated CK

Minor
1. Tachycardia
2. Abnormal arterial pressure
3. Altered consciousness
4. Diaphoresis
5. Leucocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe an anticholinergic toxidrome (8)

A
  1. Altered mental status, confusion, restlessness, seizures, coma

Symptoms resulting from peripheral muscarinic receptor blockade:
2. Impaired sweat gland function
3. Dry mouth
4. Dry axillae
5. Mydriasis
6. Tachycardia
7. Flushing
8. Urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

In cases of serotonin syndrome where other management options have failed, what is the treatment?

A

Cryoheptadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the tx options for NMS? (2)

A
  1. Bromocriptine (first line)
  2. Dantrolene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the commonly used drugs in ED that might cause methaemaglobinaemia? (4)

A
  1. Metoclopramide
  2. Nitrites (including ‘poppers’ and GTN)
  3. Local anaesthetics
  4. Abx including dapsone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What level of methaemagobinaemia should be treated? (2)

A
  1. > 30% methaemaglobin
  2. Any evidence of tissue hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

If initial management of beta blocker OD with low BP doesn’t success (i.e. glucagon) what does toxbase suggest as second line?

A

HIET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How is the toxicity of something calculated?

A

From the Lethal Dose 50 (LD50) = concentration required to kill 50% of exposed individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How do cholinergic drugs act?

A

Class of medication that increase/mimic activity of acetylcholine and lead to parasympathetic activity increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Name anticholingergic medication? (7)

A
  1. Tricyclic antidepressants (amitryptyline)
  2. oxybutynin
  3. olanzepine
  4. quetiapine
  5. clozapine
  6. chlorpromazine
  7. prochlorperazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What type of toxidrome does Sarin gas cause?

A

Cholinergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Over what level does acute radiation syndrome?

A

> 0.5 Sv (Sievert)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the paeds ‘one pill killers?’ (8)

A
  1. Beta blockers
  2. Calcium channel blockers
  3. TCAs
  4. Amphetamines
  5. Opiates
  6. Sulfonyureas
  7. Theophylline
  8. Chloroquines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

When should we not offer PEP to a patient who has unprotected sex with a patient who is HIV positive?

A

If partner has been on ART > 6 months and has had an undetectable viral load in last 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

When should PEP be offered routinely (4)

A

If unknown or detectable vial load and:
1. Receptive anal sex
2. Receptive vaginal sex
3. Occupational exposure
4. Needle sharing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

When should PEP be considered? (2)

A

Unknown or detectable viral and:
1. Insertive vaginal sex
2. Insertive anal sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

When is PEP not recommended? (2)

A
  1. Sex/splash/injection in high risk group but not known HIV
  2. Human bite in HIV positive
75
Q

What PEP should be offered?

A

Tenovir + emtricitabne (Truvada) combination and raltegravir OD for 28 days

76
Q

When should PEP be started?

A

ASAP (ideally <24hours)

77
Q

After what period is PEP not effective?

A

> 72 hours

78
Q

What is a tetanus prone wound? (5)

A
  1. Puncture wounds occurring in contaminated enviroment
  2. Wounds with foreign body
  3. Compound #s
  4. Wounds/burns with sepsis
  5. Certain animal bites
79
Q

What are high risk tetanus prone wounds? (3)

A
  1. Heavy contamination with soil containing spores
  2. Wounds/burns with significant devitalised tissues
  3. Wounds/burns requiring surgery that are delayed over 6 hours
80
Q

What is full tetanus immunisation? (3)

A
  1. > 11 year priming course and last dose < 10 years ago
  2. 5-11 years and priming course pre-school booster
  3. < 5 years and priming course
81
Q

What is partial tetanus immunisation? (2)

A
  1. Over 11 years, priming course but last dose >10 years
  2. 5-11 years with priming course but no pre-school booster
82
Q

If fully immunised against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound

83
Q

If partially immune against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound

A

1.Nil
2. Vaccine dose
3. Vaccine and TIG

84
Q

If no immunisation against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound

A
  1. Vaccine
  2. Vaccine and TIG
  3. Vaccine and TIG
85
Q

What dose of TIG should be given in tetanus? (4)

A
  1. 250 IU IM
  2. 500 IU IM if :
    - heavy contamination
    - burns
    - > 24 hours

NB do not given vaccine and TIG at same site

86
Q

What is a clean wound re: tetanus risk?

A

< 6 hours
non-penetrating

87
Q

What level of TCA overdose is considered life threatening?

88
Q

What causes the ECG changes associated with TCA overdose?

A

Sodium channel blockade

89
Q

What ECG change in TCA OD is predictive of:
1. seizures
2. arrhythmia

A
  1. QRS > 100ms
  2. QRS >160ms
90
Q

What should be used to target sodium bicarbonate treatment for TCA OD? (2)

A
  1. Narrow QRS
  2. PH 7.5-7.55
91
Q

What is the mechanism behind malignant hyperpyrexia?

A
  • genetic abnormality of the ryanodine receptor and excitation-contraction coupling in the skeletal muscle when exposed to certain triggers
92
Q

What does malignant hyperpyrexia lead to?

A
  • continuous release of calcium into muscle cell
  • leads to a huge increase in metabolic demand, hypercalcaemia, continuous muscle contraction and rigidity
  • increaesed metabolic demand leads to consistent increase ETC02, tachycardia and pyrexia.
  • ultimately leads to MOF/DIC
93
Q

How should malignant hyperpyrexia be treated? (4)

A
  1. Stop/remove trigger
  2. Dantrolene (ryanodine receptor antagonist) 2.5mg/kg and repeated at 1mg/kg until ETC02 <6KPa and temp <38.5
  3. Active cooling to <38.5 degrees C
  4. Acidosis- hyperventilate to normal pC02 and add sodium bicarbonate if PH remains < 7.2
94
Q

What is the toxic dose of paracetamol?

A

10g or >200mg/kg

95
Q

What dose of paracetamol is considered safe?

A

75mg/kg (therapeutic excess)

96
Q

What is the maximum weight to be used when calculating NAC dose?

97
Q

How common are anaphylactoid reactions with NAC tx?

98
Q

What is intralipid made up of? (4)

A
  1. Soya oil
  2. Egg
  3. Phospholipids
  4. Glycerol
99
Q

What can be used as an adjunct to managing digoxin toxicity?

A

Magnesium sulphate

Natural antagonist of digoxin. Low magnesium can lead to significant affects even with relatively small OD

100
Q

How is arsenic poisoning managed?

A

Succimer or dimercaprol

Both metal chelating agents that treat mercury/lead/gold poisoning

101
Q

How should life threatening acute hypercalcaemia be managed?

A

IV pamidronate

102
Q

What is the mechanism of action of Paraquat poisoning?

A

Generates reactive oxygen species (ROS) and induces oxidative stress, leading to cell damage and death.

This mechanism primarily targets the alveolar cells in the lungs, which can result in severe pulmonary injury.

103
Q

How is Paraquat poisoning managed?

A
  1. Mild hypoxia tolerated 85-88%
  2. Anti-oxidants e.g NAC
  3. Supportive care
104
Q

What is the mechanism of action of cocaine?

A

Sodium channel blocker and inhibits noradrenaline and serotonin reuptake

105
Q

What are the sympathominetic effects from the sodium channel blockade of cocaine?

A
  1. Hypethermia
  2. Hypertension
  3. Cardiac conduction abnormalities
  4. Vasconstriction - IHD/SAH
106
Q

What are the 4 families of viruses that cause VHF?

A
  1. Arenavirus
  2. Filovirus
  3. Bunyavirus
  4. Flavivirus
107
Q

How are VHF transmitted?

A

Percutaneous/mucosal contact with bodily fluids

108
Q

What is the incubation period of VHF?

109
Q

What are some of the more common notifiable diseases? (9)

A
  1. Meningitis/encephalitis
  2. Covid
  3. Invasive group A step
  4. MMR
  5. Botulism
  6. Cholera
  7. Rabies
  8. SARS
  9. VHF
110
Q

How does cement cause injury?

A

Caustic injury and liquefactive necrosis

When it reacts with water cement powder produces highly alkali calcium hydroxide (PH >12)

111
Q

What does dry cement cause in terms of injury? (2)

A
  1. If powder reacts with sweat/resp secretions causs topical burns
  2. Can cause silicosis
112
Q

Describe the local and systemic mechanism for hydrofluoric burns?

A

Local:
- H+ and F- ions cause direct local tissue damage
- F- ions highly lipophilic and absorbed into the deep layers of the dermis and cause liquefactive necrosis. This causes a release of intracellular myoglobin, urate and K+

Systemic:
- F- also absorbed systemically resulting in systemic fluorosis (main mechanism of toxicity)
- F- chelate calcium and magnesium leading to profound hypocalcaemia/magnesia.
- Hypocalcaemia leads to Na+/K+ ATPase inhibition, negative ionotropy and QTc prolongation and increased permeability to K+ leading to hyperkalaemia
- Hypomagnesia can lead to polymorphic VT and seizures

113
Q

What are the dermal signs of HF burns?

A

Grey and sloughy
Patients can report deep pain but not have any dermal evidence

114
Q

What can ingested HF lead to?

A

Cardiac arrest within 30 mins to 6 hours

115
Q

Describe how phosphorous causes:
1. Local burns
2. Respiratory issues
3. Systemic toxicity

A
  1. Lipophilic and causes deep subcutaneous burns like HF acid
  2. Burning white phosphorous leads to phosphorous pentoxide smoke that is a respiratory irritant
  3. Presents in 3 phases:
    - non specific abdo pain and diarrhoea
    - then asymp
    - haemolysis, hypocalcaemia and MOF
116
Q

What is the treatment for phosphorous toxicity?

A

Supportive

117
Q

What do phosphorous burns appear like?

A

Yellow appearance and smell of garlic

118
Q

What is unique about the smell of hydrogen sulphide?

A
  1. Smells rotten eggs
  2. Proportion of population can’t smell it
  3. Smell diminishes at high concentrations.
119
Q

What is the priority when managing hydrogen sulphide poisoning? (2)

A
  1. Remove from source
  2. High flow 02
120
Q

What are the effects of hydrogen sulphide poisoning at:

  1. low
  2. high concentrations?
A
  1. Irritate the eyes and respiratory tract, resulting in sore throat, cough, and dyspnoea.
  2. Bronchospasm, Methaemoglobinaemia, respiratory paralysis, cyanosis, convulsions, coma, cardiac arrhythmias, and death within minutes.
121
Q

What is the appearance and odour of chlorine gas?

A

Green/yellow appearance

Bleach like odour

122
Q

Where will chlorine gas accumulate when mixed with air?

A

Low areas as it is heavier than air

123
Q

What are the local and systemic affects of chlorine?

A
  1. Local = irritant and corrosive. Causes sloughing of the pulmonary mucosa 3-5 days after inhalation causing metabolic alkalosis and respiratory acidosis
  2. None (according to book, not sure this is the case)
124
Q

What concentrations of chlorine are needed to cause:
1. acute symptoms
2. fatality

A
  1. > 15 parts per million (ppm)
  2. 430ppm for 30 mins
125
Q

How do button batteries cause damage to patients?

A
  • Saliva and oesophageal tissue allow current to flow between the positive and negative poles of the battery in an electrolytic reaction.
  • Sodium hydroxide that forms at the negative pole is a strong alkali and causes chemical burns
126
Q

What chemical causes burns in button batteries?

A

Sodium hydroxide (Strong alkali)

127
Q

What time frame can button batteries cause symptoms?

A

From 2 hours after ingestion up to 28 days (Even after removed)

128
Q

What are the risk factors for injury with regards to button batteries? (5)

A
  1. Oesophageal location (and above
  2. size (lower risk if <12mm, higher if >20mm),
  3. prolonged mucosal contact
  4. younger age (<6 years)
  5. coingestion with magnets
129
Q

What is the initial investigation of choice for button battery ingestion

A

AP + lateral neck/chest/abdo XR

130
Q

Whilst waiting for surgical removal of battery what other intervention can be attempted if:
1. > 1year
2. Any age

A

If ingestion occurred LESS than 12 hours ago;

  1. > 1 year give 10 mls honey every 10 mins (max 6 doses)

OR

  1. Any age give 1g sucralfate oral suspension every 10 mins
    (max 3 doses)
131
Q

What is the management for button batteries:
1. above clavicle
2. below diapragm

A
  1. Time critical surgical emergency
  2. D/w surgical team - likely follow up xr 24-48 hours
132
Q

How do organophosphates act?

A

Inhibit acetycholinesterase which breaks down acetylcholine leading to increased parasympathetic activation/CNS affects and progressive paralysis

133
Q

What is SLUDGEM used for and what does is mean?

A

Signs/symptoms of organophosphate poisoning/ cholinergic toxidrome

Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
Miosis

134
Q

What other signs/symptoms will nerve agent poisoning cause aside from SLUDGEM? (6)

A

Bronchospasm
Bradycardia
Sweating
Progressive paralysis of res muscles
Coma
Death

135
Q

What is the pathophysiology of organophosphate poisoning?

A

Inhibit cholinesterases which leads to build up of acetylcholine at nerve endings

136
Q

What are the features of organophosphate poisoning? (8)

A

S- alivation
L - acrimation
U - rination
D - efecation
G - I upset
E - mesis
M - iosis
M - muscle twitching

Bradycardia, paralysis and resp failure

137
Q

What is the treatment for organophosphate poisoning and what is its mechanism

A

Atropine - blocks affect of acetylcholine at muscarinic receptors
Eases smooth muscle constriction and dries up secretions

138
Q

What is the atropine dose in organophosphate poisoning?

A

2mg- IV adult
0.02mg/kg (20mcg/kg) children
Every 5 mins double dose until atropinisation

139
Q

What is the mechanism of pralidoxime?

A

Reactivate acetylcholinesterase inhibited by organophosphates allowing metabolisation of acetylcholine.

140
Q

What can lead to cyanide poisoning? (3)

A
  1. Polyurethane burning
  2. Fruit kernels
  3. Finger polish remover
141
Q

What are the features of cyanide poisoning? (4)

A
  1. Metabolic acidosis
  2. Seizures
  3. Pulmonary oedema
  4. Arrhythmias
142
Q

What is the antidote for severe cyanide poisoning and what is the risk of giving it?

A
  1. Dicobalt edetate - Kelocyanor
  2. If no cyanide can be fatal
143
Q

What are the treatments for mild cyanide poisoning? (2)

A
  1. Sodium thiosulphate
  2. Sodium nitrate
144
Q

What is the best treatment for inhaled cyanide poisoning?

A

5g hyroxycobalamin IV (Cyanokit)

145
Q

How do vesicants (Mustard, Lewisite) cause injury?

A

Damage DNA leading to cell death in exposed tissue

146
Q

How should vesicant (Mustard, Lewisite) poisonings be managed?

A

Decontamination
Supportive treatment

147
Q

How do pulmonary agents (Chlorine/Phosgene) cause damage?

A

Damage cell membranes in respiratory tract + lungs leading to airway irritation + oedema.

Severe = death

148
Q

Which substances does the BTS guidelines state specifically that oxygen may be harmful in?

A

Paraquat
Bleomycin

149
Q

What are the target SATs in paraquat and bleomycin poisoning and why?

A

85-88%

Oxygen maybe harmful

150
Q

How does methane exposure lead to hypoxia?

A

Simple asphyxiant

  • only harmful in enclosed space with no ventilation
  • Displaces oxygen and leads to oxygen poor enviroment
  • can also causes pneumonititis (rare)
151
Q

What is GHB?

A

Gamma-Hydroxybutyrate

Precursor metabolite of GABA

152
Q

What is the relationship between alcohol and GHB?

A

GHB requires alcohol dehydrogenase to metabolise it. Therefore, if taken with alcohol can delay/inhibit onset

153
Q

What is the classic presentation of GHB?

A

Fluctuating from GCS 3 to very agitated and difficult to manage. CNS and respiratory depression.

154
Q

What is the pathophysiology of cyanide poisoning?

A
  • Binds to ferric ion (Fe3+) of cytochrome oxidase & inhibits oxidative metabolism which causes lactic acidosis.
  • Biogenic amines also released which result in pulmonary & coronary vasoconstriction.
155
Q

What is the pathophysiology of Yew Tree poisoning?

A
  • Most potent alkaloid in Yew Trees (Taxus baccata) is a Taxine B
  • Causes dose-dependent blockade of calcium and sodium channels in cardiac myocytes
  • QRS prolongation, decreased myocardial contractility and prolonged atrioventricular conduction time.
156
Q

What are the effects of Yew Tree poisoning?

A
  • QRS prolongation, decreased myocardial contractility and prolonged atrioventricular conduction time
  • broad complex tachyarrhythmias difficult to shock
  • bradycardia
157
Q

What is the management of Yew Tree Poisoning?

A

No specific tx:

  1. Activated charcoal
  2. Management of arrhythmias
  3. Pacing
158
Q

What is the clinical course of iron poisoning? (7)

A

Initial d/v / abdopain/ GI bleed

Symptoms settle 6-12 hours but then at 24-48hours can present with:
- shock
- hypoglycaemia
- jaundice
- metabolic acidosis
- hepatic failure
- renal failure
- bowel infarction

159
Q

What is not indicated in Fe poisoining?

A

Activated charcoal

160
Q

What investigations maybe useful in Fe poisoning?

A
  1. XR as tablets radio-opaque
    Can consider bowel irrigation
161
Q

What is the treatment for iron poisoning?

A

Desferrioxamine

162
Q

What can desferrioxamine cause?

A

Anapx
hypotension
ARDS

163
Q

If giving desferrioxamine before Fe level back what confirms it was appropriate?

A

Iron-desferrioxamine complex causes orange/red urine

164
Q

In paracetamol level what level is:
1. Safe
2. Needs bloods but not NAC empirically
3. Needs NAC
4. Likely to be toxic

A
  1. <75mg/kg
  2. <150mg/kg
  3. > 150mg/kg
  4. > 200mg/kg
165
Q

What are 2 types of rat poison used?

A
  1. Arsenic (historical)
  2. Vit K antagonists
166
Q

What is the treatment for ‘super warfarin) rat poisons?

A
  1. Activated charcoal
  2. Vit K IV
167
Q

What is considered highly toxic and relatively harmless in terms of LD50?

A

Extremely toxic = <5mg/kg
Relatively harmless = >15mg/kg

168
Q

Describe the nicotinic/muscarinic affects NA poisoning?

A

Cholinergic toxidrome effects both nicotinic and muscarinic receptors. Atropine predominantly affects muscarinic.

Nicotonic receptors = HTN/tachycardia/mydriasis (dilation)

Muscarinic = brady/hypotension/meiosis (constriction)

169
Q

With regards to Lewisite:
1. What type of agent is it?
2. What is the smell?
3. How does it present differently to mustard gas?

A
  1. Vesicant (blister) agent containing arsenic
  2. Odor of geraniums but can cause burning pain to the respiratory tract at a concentration that has no odor.
  3. Pain and tissue destruction immediate and will more obvious than with Mustard
170
Q

What are the two main blistering (vesicant) chemical warfare agents?

A
  1. Mustards
  2. Arsenic containing Lewisite
171
Q

What is the antidote to Lewisite?

A

Dimercaprol 3mg/kg IM

172
Q

Describe the characteristics of Sulphur mustard (HD) (5)

A
  1. Reacts chemically with bleach
  2. Combustible
  3. Products of combustion toxic
  4. Vaporises at room temperature, increases in moist environment
  5. Lipophilic
173
Q

How can sulphur mustard be removed from skin?

A

Warm detergent solution

174
Q

If contaminated with liquid sulphur mustard, what should be ensured?

A

Remove within minutes and if some residual noted later also remove as it will off-gas vapour

175
Q

What are the systemic complications of sulphur mustard poisoning?

A

Crude alkylating agent which can damage DNA and result in suppression of bone marrow, sepsis and death.

176
Q

What is the smell of sulphur mustard and why is this relevant clinically?

A

Garlic or mustard

Olfactory threshold below that which toxicity occurs and therefore is an early warning to exposure

177
Q

Describe the characteristic of Chlorine gas (2)

A
  1. 2.5 x heavier than air
  2. Gas at room temperature
178
Q

What are the clinical features of chlorine gas toxicity? (4)

A
  1. Mild - mucous membrane irritation
  2. Bronchospasm
  3. Acute lung injury / ARDS
  4. Skin/eye irritation in high concentration and burns in very high
179
Q

How does chlorine gas cause damage?

A

Partially dissolves in water to form hydrochloric acie and hypochlorous acid - deposits onto mucous membranes/skin/airways.

180
Q

How should chlorine toxicity exposure be managed? (3)

A
  1. Inhalational injury - oxygen, bronchodilators
  2. Irrigate to skin PH >4.5
  3. Ocular irrigation until normal PH
181
Q

What are the 3 types of nerve agent?

A
  1. G agents - invented in Germany 1930s. Sarin, soman and tabun
  2. V agents (VX + VG)
  3. Novichocks ‘newcomer’
182
Q

Once ‘atropinisation’ achieved, what rate should the infusion be set at?

A

20% of the total dose that achieved atropinisation /hr

183
Q

How should Sarin/soman/tabun/VX and VG be managed?

A

As per organophosphates e.g. atropine/praloxidime/seizure control

184
Q

When is HIV PEP most effective?

FIMC (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions