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
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2
Q

What metabolic disturbance do adults presenting with salicylate poisoning predominates?

A

Reps alkalosis > metabolic acidoses

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3
Q

What metabolic disturbance do children presenting with salicylate poisoning predominates?

A

Metabolic acidosis > resp alkalosis

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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
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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
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6
Q

What is severe salicylate poisoning?

A

1, CNS features, acidosis or > 700mg/L
2. Consider HD and I+V

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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.

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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
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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

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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
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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
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12
Q

What is the antidote to benzo OD?

A

Flumazenil

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13
Q

How long does flumezanil last?

A

1 hour

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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

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15
Q

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

A

Oculogyric crisis
Muscle spasms - torticollis/opisthonus

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16
Q

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

A
  1. Increased QRS
  2. Arrhythmias
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17
Q

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

A
  1. Proycylidine
  2. Diazepam
  3. Bicarbonate if QRS >120ms
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18
Q

What are the features of lithium toxicity? (6)

A
  1. n/v
  2. diarrhoea
  3. ataxia
  4. confusion
  5. increased tone
  6. clonus
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19
Q

What is the treatment for lithium toxicity?

A

Supportive
Dialysis

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20
Q

What are the effects of sulfanylurea overdose?

A
  1. Low glucose
  2. Low potassium
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21
Q

What is the treatment for sulfanylurea overdose?

A

Octreotide

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22
Q

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

A
  1. Bronchospasm in asthmatics
  2. Hypoglycaemia in children
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23
Q

What does sotalol OD cause in particular?

A

Torsades des pointes

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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)
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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
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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
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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
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28
Q

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

A
  1. Glucagon
  2. Intralipid
  3. HIET
  4. Vasopressors/ionotropes
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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
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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
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31
Q

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

A
  1. Acidosis
  2. Hypergylcaemia
  3. Raised amylase
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32
Q

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

A
  1. Blindness
  2. Parkinsonian features
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33
Q

What is the treatment for methanol poisoning? (4)

A

Ethanol
Fomepizole
Folinic acid
Bicarbonate if acidotic

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34
Q

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

A

Appear drunk, no smell alcohol

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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`
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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
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37
Q

What can occur in petrol ingestion?

A

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

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38
Q

What is the pathophysiology of organophosphate poisoning?

A

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

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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

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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

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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

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42
Q

What is the mechanism of pralidoxime?

A

Reactivate acetylcholinesterase inhibited by organophosphates allowing metabolisation of acetylcholine.

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43
Q

What can lead to cyanide poisoning? (3)

A
  1. Polyurethane burning
  2. Fruit kernels
  3. Finger polish remover
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44
Q

What are the features of cyanide poisoning? (4)

A
  1. Metabolic acidosis
  2. Seizures
  3. Pulmonary oedema
  4. Arrhythmias
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45
Q

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

A
  1. Remove clothes
  2. Wash exposed skinW
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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
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47
Q

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

A
  1. Sodium thiosulphate
  2. Sodium nitrate
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48
Q

What is the best treatment for inhaled cyanide poisoning?

A

5g hyroxycobalamin IV (Cyanokit)

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49
Q

What is the max dose of lidocaine?

A

3mg/kg
max 200mg

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50
Q

What is the maximum dose of lidocaine with adrenaline?

A

7mg/kg
max 500mg

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51
Q

What is the maximum dose of bupivicaine?

A

2mg/kg
150mg

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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

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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
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54
Q

What drugs can cause methaemoglobinaemia?(7)

A

benzene derivatives
chloroquine
dapsone
prilocaine
metoclopramide
nitrites (nitroglycerin, NO, sodium nitroprusside)
sulphonamides

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

56
Q

What is the treatment for methaemoglobinaemia?

A

Methylene blue

57
Q

What is the triad of symptoms in serotonin syndrome?

A
  1. Change in mental staus
  2. Autonomic hyperactivity
  3. Neuromuscular manifestations
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

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

60
Q

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

A

Cryoheptadine

61
Q

What are the tx options for NMS? (2)

A
  1. Bromocriptine (first line)
  2. Dantrolene
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
63
Q

What level of methaemagobinaemia should be treated? (2)

A
  1. > 30% methaemaglobin
  2. Any evidence of tissue hypoxia
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?

65
Q

How is the toxicity of something calculated?

A

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

66
Q

How do cholinergic drugs act?

A

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

67
Q

Name anticholingergic medication? (7)

A
  1. Tricyclic antidepressants (amitryptyline)
  2. oxybutynin
  3. olanzepine
  4. quetiapine
  5. clozapine
  6. chlorpromazine
  7. prochlorperazine
68
Q

What type of toxidrome does Sarin gas cause?

A

Cholinergic

69
Q

Over what level does acute radiation syndrome?

A

> 0.5 Sv (Sievert)

70
Q

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

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Opiates
  4. Amphetamines
  5. Theophylline
  6. Sulfonyureas
  7. TCAs
  8. Chloroquines
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

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

73
Q

When should PEP be considered? (2)

A

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

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 malignancy 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

100
Q

How is arsenic poisoning managed?

A

Chelation with succimer or dimercaprol

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 >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 of VHF?

109
Q

What are some of the more common notifiable diseases?

A
  1. Meningitis/encephalitis
  2. Botulism
  3. Cholera
  4. Covid
  5. Invasive group A step
  6. MMR
  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.
120
Q

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

A
  1. Remove from source
  2. High flow 02
121
Q

What are the effects of hydrogen sulphide poisoning at 1.low and 2. high concentrations?

A

1.Bronchospasm, Methaemoglobinaemia, respiratory paralysis, cyanosis, convulsions, coma, cardiac arrhythmias, and death within minutes.

  1. irritate the eyes and respiratory tract, resulting in sore throat, cough, and dyspnoea.
122
Q

What is the appearance and odour of chlorine gas?

A

Green/yellow appearance

Bleach like odour

123
Q

Where will chlorine gas accumulate when mixed with air?

A

Low areas as it is heavier than air

124
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)
125
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
126
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
127
Q

What chemical causes burns in button batteries?

A

Sodium hydroxide (Strong alkali)

128
Q

What time frame can button batteries cause symptoms?

A

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

129
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
130
Q

What is the initial investigation of choice for button battery ingestion

A

AP + lateral neck/chest/abdo XR

131
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 1 gram sucralfate oral suspension every 10 mins
    (max 3 doses)
132
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