Toxiciology Flashcards
(199 cards)
1
Q
What are the features of salicylate poisoning? (6)
A
- Increased RR
- Tinnitus
- Deafness
- Sweating
- Vasodilation
- Acid base disturbance
2
Q
What metabolic disturbance do adults presenting with salicylate poisoning predominates?
A
Reps alkalosis > metabolic acidoses
3
Q
What metabolic disturbance do children presenting with salicylate poisoning predominates?
A
Metabolic acidosis > resp alkalosis
4
Q
What is mild salicylate poisoning and how should it be managed?
A
- < 300mg/L
- Asymp and normal VBG then home at 6 hours
5
Q
What is moderate salicylate poisoning and how should it be managed?
A
- 300-700mg/L
- Urinary alkalization - PH 7.5-8.5 using sodium bicarbonate
6
Q
What is severe salicylate poisoning?
A
- CNS features, acidosis or > 700mg/L
- Consider HD and I+V
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.
8
Q
What are the features of TCA OD in conscious patients? (7)
A
Anti-cholinergic toxidrome
- Tachycardia
- Dry skin
- Dry mouth
- Dilated pupils
- Urinary retention
- Ataxia
- Jerky limb movements
9
Q
What signs do unconscious patients developed following TCA OD? (7)
A
- Divergent squint
- Hypertonia
- Hyper-reflexia
- Myoclonus
- Upgoing plantars
If comatose - areflexia and muscle facciditiy
10
Q
What ECG changes will be seen in TCA OD and which is the most sensitive?
A
- Increased QRS (most sensitive)
- Increased PR
- Tachy
- P waves can be lost in T - looks like VT
11
Q
What is the tx for TCA overdose? (5)
A
- If under 1 hour activated charcoal
- 50-100ml 8.4% bicarbonate
- Aim PH 7.5-7.55 (excessive is fatal) and normal QRS
- Avoid routine use anti-arrhythmics
- Severe consider glucagon or intralipid
12
Q
What is the antidote to benzo OD?
A
Flumazenil
13
Q
How long does flumezanil last?
A
1 hour
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
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
16
Q
What ECG changes will you see in haloeridol/chlorpromazine/similar drugs in OD? (2)
A
- Increased QRS
- Arrhythmias
17
Q
What is the treatment for haloperiol/chlorpromazine OD? (3)
A
- Proycylidine
- Diazepam
- Bicarbonate if QRS >120ms
18
Q
What are the features of lithium toxicity? (6)
A
- n/v
- diarrhoea
- confusion
- ataxia
- increased tone
- clonus
19
Q
What is the treatment for lithium toxicity?
A
Supportive
Dialysis
20
Q
What are the effects of sulfanylurea overdose?
A
- Low glucose
- Low potassium
21
Q
What is the treatment for sulfanylurea overdose?
A
Octreotide
22
Q
What are the features of unique to propanolol OD? (2)
A
- Bronchospasm in asthmatics
- Hypoglycaemia in children
23
Q
What does sotalol OD cause in particular?
A
Torsades des pointes
24
Q
What are the treatments of beta blocker OD without severe hypotension?
A
- Consider activated charcoal
- Atropine may work (pacing probably not)
- Glucagon 5-10mg IV (anticipate vomiting)
25
In severe beta-blocker OD with low BP what are 3 treatment options?
1. High dose Insulin Euglycaemic Therapy (HIET)
2. Intralipid
3. Ionotropes/vasopressors
26
What are the features of CCB OD? (6)
1. Bradycardia
2. AV block
3. Profound vasolidation
4. Metabolic acidosis
5. Hyperkalaemia
6. Hyperglycaemia
27
What is the treatment for CCB OD? (3)
1. Consider activated charcoal
2. Atropine +/- pacing
3. Calcium chloride 10% over 10 mins and consider repeating up to x 4
28
What are the treatment options for severe CCB OD? (4)
1. Glucagon
2. Intralipid
3. HIET
4. Vasopressors/ionotropes
29
What are the features of digoxin toxicity? (4)
1. Xanthopisa- yellow flashes/discolouration
2. Hyperkalaemia
3. Brady, increased PR/QRS
4. Arrhythmias
30
What is the treatment for digoxin toxicity? (4)
1. Digiblind/Digifab
2. Insulin/dex for increased K+ (rapid decrease with Digibind)
3. Atropine/pacing
4. Magnesium IV considered
31
What are the biochemical changes in acute methanol poisoning? (3)
1. Acidosis
2. Hypergylcaemia
3. Raised amylase
32
What are survivors of methanol poisoning at risk of? (2)
1. Blindness
2. Parkinsonian features
33
What is the treatment for methanol poisoning? (4)
Ethanol
Fomepizole
Folinic acid
Bicarbonate if acidotic
34
What are the early (<12 hours) features of ethylene glycol poisoning?
Appear drunk, no smell alcohol
35
What are the late features of ethylene glycol poisoning? (6)
1. CCF
2. Acidosis
3. Tachy/arrhythmias
4. Hypocalcaemia (can be profound)
5. Acute tubular necrosis
6. CN palsies`
36
What are the treatment options for ethylene glycol poisoning? (5)
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
37
What can occur in petrol ingestion?
Can be fine but aspiration lead to severe pneumonitis requiring steroids + resp support
38
What is the pathophysiology of organophosphate poisoning?
Inhibit cholinesterases which leads to build up of acetylcholine at nerve endings (cholinergic affect)
39
What are the features of organophosphate poisoning (cholinergic toxidrome)? (8)
S- alivation
L - acrimation
U - rination
D - efecation
G - I upset
E - mesis
M - iosis
M - muscle twitching
Bradycardia, paralysis and resp failure
40
What is the treatment for organophosphate poisoning and what is its mechanism
Atropine - blocks affect of acetylcholine at muscarinic receptors
Eases smooth muscle constriction and dries up secretions
41
What is the atropine dose in organophosphate poisoning?
2mg IV adult
0.02mg/kg children
Every 5 mins double dose until atropinisation
42
What is the mechanism of pralidoxime?
Reactivate acetylcholinesterase inhibited by organophosphates allowing metabolisation of acetylcholine.
43
What can lead to cyanide poisoning? (3)
1. Polyurethane burning
2. Fruit kernels
3. Finger polish remover
44
What are the features of cyanide poisoning? (4)
1. Metabolic acidosis
2. Seizures
3. Pulmonary oedema
4. Arrhythmias
45
What is the initial management of cyanide poisoning? (2)
1. Remove clothes
2. Wash exposed skinW
46
What is the antidote for severe cyanide poisoning and what is the risk of giving it?
1. Dicobalt edetate - Kelocyanor
2. If no cyanide can be fatal
47
What are the treatments for mild cyanide poisoning? (2)
1. Sodium thiosulphate
2. Sodium nitrate
48
What is the best treatment for inhaled cyanide poisoning?
5g hyroxycobalamin IV (Cyanokit)
49
What is the max dose of lidocaine?
3mg/kg
max 200mg
50
What is the maximum dose of lidocaine with adrenaline?
7mg/kg
max 500mg
51
What is the maximum dose of bupivicaine?
2mg/kg
150mg
52
What is the management of LA toxicity including dose?
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
53
How are hydrofluric burns managed? (4)
1. Irrigate normal saline ++
2. Calcium gluconate gel
3. Tx low Ca2+
4. In arrest - 60ml x 10% calcium chloride
54
What drugs can cause methaemoglobinaemia?(7)
sulphonamides (abx, prefix sulf-)
chloroquine
dapsone
prilocaine
metoclopramide
nitrites (nitroglycerin, NO, sodium nitroprusside)
benzene derivatives
55
What are the features of methaemoglobinaemia?
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
What is the treatment for methaemoglobinaemia?
Methylene blue
57
What is the triad of symptoms in serotonin syndrome?
1. Change in mental staus
2. Autonomic hyperactivity
3. Neuromuscular manifestations
58
What are the 3 major and 5 minor symptoms suggestive of neuroleptic malignant syndrome?
Major
1. Fever
2. Rigidity
3. Elevated CK
Minor
1. Tachycardia
2. Abnormal arterial pressure
3. Altered consciousness
4. Diaphoresis
5. Leucocytosis
59
Describe an anticholinergic toxidrome (8)
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
In cases of serotonin syndrome where other management options have failed, what is the treatment?
Cryoheptadine
61
What are the tx options for NMS? (2)
1. Bromocriptine (first line)
2. Dantrolene
62
What are the commonly used drugs in ED that might cause methaemaglobinaemia? (4)
1. Metoclopramide
2. Nitrites (including 'poppers' and GTN)
3. Local anaesthetics
4. Abx including dapsone
63
What level of methaemagobinaemia should be treated? (2)
1. > 30% methaemaglobin
2. Any evidence of tissue hypoxia
64
If initial management of beta blocker OD with low BP doesn't success (i.e. glucagon) what does toxbase suggest as second line?
HIET
65
How is the toxicity of something calculated?
From the Lethal Dose 50 (LD50) = concentration required to kill 50% of exposed individuals
66
How do cholinergic drugs act?
Class of medication that increase/mimic activity of acetylcholine and lead to parasympathetic activity increase
67
Name anticholingergic medication? (7)
1. Tricyclic antidepressants (amitryptyline)
2. oxybutynin
3. olanzepine
4. quetiapine
5. clozapine
6. chlorpromazine
7. prochlorperazine
68
What type of toxidrome does Sarin gas cause?
Cholinergic
69
Over what level does acute radiation syndrome?
> 0.5 Sv (Sievert)
70
What are the paeds 'one pill killers?' (8)
1. Beta blockers
2. Calcium channel blockers
3. TCAs
4. Amphetamines
5. Opiates
6. Sulfonyureas
7. Theophylline
8. Chloroquines
71
When should we not offer PEP to a patient who has unprotected sex with a patient who is HIV positive?
If partner has been on ART > 6 months and has had an undetectable viral load in last 6 months
72
When should PEP be offered routinely (4)
If unknown or detectable vial load and:
1. Receptive anal sex
2. Receptive vaginal sex
3. Occupational exposure
4. Needle sharing
73
When should PEP be considered? (2)
Unknown or detectable viral and:
1. Insertive vaginal sex
2. Insertive anal sex
74
When is PEP not recommended? (2)
1. Sex/splash/injection in high risk group but not known HIV
2. Human bite in HIV positive
75
What PEP should be offered?
Tenovir + emtricitabne (Truvada) combination and raltegravir OD for 28 days
76
When should PEP be started?
ASAP (ideally <24hours)
77
After what period is PEP not effective?
>72 hours
78
What is a tetanus prone wound? (5)
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
What are high risk tetanus prone wounds? (3)
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
What is full tetanus immunisation? (3)
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
What is partial tetanus immunisation? (2)
1. Over 11 years, priming course but last dose >10 years
2. 5-11 years with priming course but no pre-school booster
82
If fully immunised against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound
Nothing
83
If partially immune against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound
1.Nil
2. Vaccine dose
3. Vaccine and TIG
84
If no immunisation against tetanus what do you require following a:
1. clean wound
2. tetanus prone wound
3. high risk tetanus prone wound
1. Vaccine
2. Vaccine and TIG
3. Vaccine and TIG
85
What dose of TIG should be given in tetanus? (4)
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
What is a clean wound re: tetanus risk?
< 6 hours
non-penetrating
87
What level of TCA overdose is considered life threatening?
> 10mg/kg
88
What causes the ECG changes associated with TCA overdose?
Sodium channel blockade
89
What ECG change in TCA OD is predictive of:
1. seizures
2. arrhythmia
1. QRS > 100ms
2. QRS >160ms
90
What should be used to target sodium bicarbonate treatment for TCA OD? (2)
1. Narrow QRS
2. PH 7.5-7.55
91
What is the mechanism behind malignant hyperpyrexia?
- genetic abnormality of the ryanodine receptor and excitation-contraction coupling in the skeletal muscle when exposed to certain triggers
92
What does malignant hyperpyrexia lead to?
- 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
How should malignant hyperpyrexia be treated? (4)
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
What is the toxic dose of paracetamol?
10g or >200mg/kg
95
What dose of paracetamol is considered safe?
75mg/kg (therapeutic excess)
96
What is the maximum weight to be used when calculating NAC dose?
110kg
97
How common are anaphylactoid reactions with NAC tx?
10-50%
98
What is intralipid made up of? (4)
1. Soya oil
2. Egg
3. Phospholipids
4. Glycerol
99
What can be used as an adjunct to managing digoxin toxicity?
Magnesium sulphate
Natural antagonist of digoxin. Low magnesium can lead to significant affects even with relatively small OD
100
How is arsenic poisoning managed?
Succimer or dimercaprol
Both metal chelating agents that treat mercury/lead/gold poisoning
101
How should life threatening acute hypercalcaemia be managed?
IV pamidronate
102
What is the mechanism of action of Paraquat poisoning?
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
How is Paraquat poisoning managed?
1. Mild hypoxia tolerated 85-88%
2. Anti-oxidants e.g NAC
3. Supportive care
104
What is the mechanism of action of cocaine?
Sodium channel blocker and inhibits noradrenaline and serotonin reuptake
105
What are the sympathominetic effects from the sodium channel blockade of cocaine?
1. Hyperthermia
2. Hypertension
3. Cardiac conduction abnormalities
4. Vasconstriction - IHD/SAH
106
What are the 4 families of viruses that cause VHF?
1. Arenavirus
2. Filovirus
3. Bunyavirus
4. Flavivirus
107
How are VHF transmitted?
Percutaneous/mucosal contact with bodily fluids
108
What is the incubation period of VHF?
21 days
109
What are some of the more common notifiable diseases? (9)
1. Meningitis/encephalitis
2. Covid
3. Invasive group A step
4. MMR
5. Botulism
6. Cholera
7. Rabies
8. SARS
9. VHF
110
How does cement cause injury? (5)
1. Insidious onset
2. Caustic injury and liquefactive necrosis
3. When it reacts with water cement powder produces highly alkali calcium hydroxide (PH >12)
4. Dry powder can still cause burn
5. Can lead to silicosis
111
Describe the local and systemic mechanism for hydrofluoric burns?
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
112
What are the dermal signs of HF burns?
Grey and sloughy
Patients can report deep pain but not have any dermal evidence
113
What can ingested HF lead to?
Cardiac arrest within 30 mins to 6 hours
114
Describe how phosphorous causes:
1. Local burns
2. Respiratory issues
3. Systemic toxicity
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
115
What is the treatment for phosphorous toxicity?
Supportive
116
What do phosphorous burns appear like?
Yellow appearance and smell of garlic
117
What is unique about the smell of hydrogen sulphide?
1. Smells rotten eggs
2. Proportion of population can't smell it
3. Smell diminishes at high concentrations.
118
What is the priority when managing hydrogen sulphide poisoning? (2)
1. Remove from source
2. High flow 02
119
What are the effects of hydrogen sulphide poisoning at:
1. low
2. high concentrations?
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.
120
What is the appearance and odour of chlorine gas?
Green/yellow appearance
Bleach like odour
121
Where will chlorine gas accumulate when mixed with air?
Low areas as it is heavier than air
122
What are the local and systemic affects of chlorine?
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)
123
What concentrations of chlorine are needed to cause:
1. acute symptoms
2. fatality
1. > 15 parts per million (ppm)
2. 430ppm for 30 mins
124
How do button batteries cause damage to patients?
- 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
125
What chemical causes burns in button batteries?
Sodium hydroxide (Strong alkali)
126
What time frame can button batteries cause symptoms?
From 2 hours after ingestion up to 28 days (Even after removed)
127
What are the risk factors for injury with regards to button batteries? (5)
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
128
What is the initial investigation of choice for button battery ingestion
AP + lateral neck/chest/abdo XR
129
Whilst waiting for surgical removal of battery what other intervention can be attempted if:
1. > 1year
2. Any age
If ingestion occurred LESS than 12 hours ago;
1. >1 year give 10 mls honey every 10 mins (max 6 doses)
OR
2. Any age give 1g sucralfate oral suspension every 10 mins
(max 3 doses)
130
What is the management for button batteries:
1. above clavicle
2. below diapragm
1. Time critical surgical emergency
2. D/w surgical team - likely follow up xr 24-48 hours
131
How do organophosphates act?
Inhibit acetycholinesterase which breaks down acetylcholine leading to increased parasympathetic activation/CNS affects and progressive paralysis
132
What is SLUDGEM used for and what does is mean?
Signs/symptoms of organophosphate poisoning/ cholinergic toxidrome
Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
Miosis
133
What other signs/symptoms will nerve agent poisoning cause aside from SLUDGEM? (6)
Bronchospasm
Bradycardia
Sweating
Progressive paralysis of res muscles
Coma
Death
134
What is the pathophysiology of organophosphate poisoning?
Inhibit cholinesterases which leads to build up of acetylcholine at nerve endings
135
What are the features of organophosphate poisoning? (8)
S- alivation
L - acrimation
U - rination
D - efecation
G - I upset
E - mesis
M - iosis
M - muscle twitching
Bradycardia, paralysis and resp failure
136
What is the treatment for organophosphate poisoning and what is its mechanism
Atropine - blocks affect of acetylcholine at muscarinic receptors
Eases smooth muscle constriction and dries up secretions
137
What is the atropine dose in organophosphate poisoning?
2mg- IV adult
0.02mg/kg (20mcg/kg) children
Every 5 mins double dose until atropinisation
138
What is the mechanism of pralidoxime?
Reactivate acetylcholinesterase inhibited by organophosphates allowing metabolisation of acetylcholine.
139
What can lead to cyanide poisoning? (3)
1. Polyurethane burning
2. Fruit kernels
3. Finger polish remover
140
What are the features of cyanide poisoning? (4)
1. Metabolic acidosis
2. Seizures
3. Pulmonary oedema
4. Arrhythmias
141
What is the antidote for severe cyanide poisoning and what is the risk of giving it?
1. Dicobalt edetate - Kelocyanor
2. If no cyanide can be fatal
142
What are the treatments for mild cyanide poisoning? (2)
1. Sodium thiosulphate
2. Sodium nitrate
143
What is the best treatment for inhaled cyanide poisoning?
5g hyroxycobalamin IV (Cyanokit)
144
How do vesicants (Mustard, Lewisite) cause injury?
Damage DNA leading to cell death in exposed tissue
145
How should vesicant (Mustard, Lewisite) poisonings be managed?
Decontamination
Supportive treatment
146
How do pulmonary agents (Chlorine/Phosgene) cause damage?
Damage cell membranes in respiratory tract + lungs leading to airway irritation + oedema.
Severe = death
147
Which substances does the BTS guidelines state specifically that oxygen may be harmful in?
Paraquat
Bleomycin
148
What are the target SATs in paraquat and bleomycin poisoning and why?
85-88%
Oxygen maybe harmful
149
How does methane exposure lead to hypoxia?
Simple asphyxiant
- only harmful in enclosed space with no ventilation
- Displaces oxygen and leads to oxygen poor enviroment
- can also causes pneumonititis (rare)
150
What is GHB?
Gamma-Hydroxybutyrate
Precursor metabolite of GABA
151
What is the relationship between alcohol and GHB?
GHB requires alcohol dehydrogenase to metabolise it. Therefore, if taken with alcohol can delay/inhibit onset
152
What is the classic presentation of GHB?
Fluctuating from GCS 3 to very agitated and difficult to manage. CNS and respiratory depression.
153
What is the pathophysiology of cyanide poisoning?
- 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.
154
What is the pathophysiology of Yew Tree poisoning?
- 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.
155
What are the effects of Yew Tree poisoning?
- QRS prolongation, decreased myocardial contractility and prolonged atrioventricular conduction time
- broad complex tachyarrhythmias difficult to shock
- bradycardia
156
What is the management of Yew Tree Poisoning?
No specific tx:
1. Activated charcoal
2. Management of arrhythmias
3. Pacing
157
What is the clinical course of iron poisoning? (7)
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
158
What is not indicated in Fe poisoining?
Activated charcoal
159
What investigations maybe useful in Fe poisoning?
1. XR as tablets radio-opaque
Can consider bowel irrigation
160
What is the treatment for iron poisoning?
Desferrioxamine
161
What can desferrioxamine cause?
Anapx
hypotension
ARDS
162
If giving desferrioxamine before Fe level back what confirms it was appropriate?
Iron-desferrioxamine complex causes orange/red urine
163
In paracetamol level what level is:
1. Safe
2. Needs bloods but not NAC empirically
3. Needs NAC
4. Likely to be toxic
1. <75mg/kg
2. <150mg/kg
3. >150mg/kg
4. >200mg/kg
164
What are 2 types of rat poison used?
1. Arsenic (historical)
2. Vit K antagonists
165
What is the treatment for 'super warfarin) rat poisons?
1. Activated charcoal
2. Vit K IV
166
What is considered highly toxic and relatively harmless in terms of LD50?
Extremely toxic = <5mg/kg
Relatively harmless = >15mg/kg
167
Describe the nicotinic/muscarinic affects NA poisoning?
Cholinergic toxidrome effects both nicotinic and muscarinic receptors. Atropine predominantly affects muscarinic.
Nicotonic receptors = HTN/tachycardia/mydriasis (dilation)
Muscarinic = brady/hypotension/meiosis (constriction)
168
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?
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
169
What are the two main blistering (vesicant) chemical warfare agents?
1. Mustards
2. Arsenic containing Lewisite
170
What is the antidote to Lewisite?
Dimercaprol 3mg/kg IM
171
Describe the characteristics of Sulphur mustard (HD) (5)
1. Reacts chemically with bleach
2. Combustible
3. Products of combustion toxic
4. Vaporises at room temperature, increases in moist environment
5. Lipophilic
172
How can sulphur mustard be removed from skin?
Warm detergent solution
173
If contaminated with liquid sulphur mustard, what should be ensured?
Remove within minutes and if some residual noted later also remove as it will off-gas vapour
174
What are the systemic complications of sulphur mustard poisoning?
Crude alkylating agent which can damage DNA and result in suppression of bone marrow, sepsis and death.
175
What is the smell of sulphur mustard (mustard gas) and why is this relevant clinically?
Garlic or mustard
Olfactory threshold below that which toxicity occurs and therefore is an early warning to exposure
176
Describe the characteristic of Chlorine gas (2)
1. 2.5 x heavier than air
2. Gas at room temperature
177
What are the clinical features of chlorine gas toxicity? (4)
1. Mild - mucous membrane irritation
2. Bronchospasm
3. Acute lung injury / ARDS
4. Skin/eye irritation in high concentration and burns in very high
178
How does chlorine gas cause damage?
Partially dissolves in water to form hydrochloric acid and hydrochlorous acid - deposits onto mucous membranes/skin/airways.
179
How should chlorine toxicity exposure be managed? (3)
1. Inhalational injury - oxygen, bronchodilators
2. Irrigate to skin
3. Ocular irrigation until normal PH
180
What are the 3 types of nerve agent?
1. G agents - invented in Germany 1930s. Sarin, soman and tabun
2. V agents (VX + VG)
3. Novichocks 'newcomer'
181
Once 'atropinisation' achieved, what rate should the infusion be set at?
20% of the total dose that achieved atropinisation /hr
182
How should Sarin/soman/tabun/VX and VG be managed?
As per organophosphates e.g. atropine/praloxidime/seizure control
183
When is HIV PEP most effective?
< 1 hour
184
What is the initial management of cement burns?
Remove affected clothing and irrigate thoroughly with water
185
What is the maximum weight for dose calculation of NAC?
110kg
186
When should intralipid be used and when should it be considered?
Give in arrest
Consider with CV instability
187
What is the maximum bolus dose of intralipid 20%?
12ml/kg
188
What additional treatment can be considered in digoxin toxicity?
Magnesium 2g IV
189
What does the AAGBI guideline for LA toxicity recommend for adrenaline dosing in arrest?
Use smaller amounts - 1mcg/kg
190
What is the treatment so severe hypercalcaemia (>3.5 or severe symptoms)
Pamidronate 30-90mg IV
191
What is the treatment of severe hypermagnesia? (4)
1.Calcium gluconate 10% 30mls
2. IVI
3. Furosemide
4. Consider HD
192
What is the dose of activated charcoal?
1g/kg
Max 50g
193
What is the dose of dantrolene?
2.5 mg/kg
194
What is the dose of naloxone in life threatening opiate OD:
1. Paeds
2. Adults
1. 100mcg/kg (max 2mg) - repeat a 1 mins intervals till max 2mg then review diagnosis
2. 400mcg - 800mcg - 800mcg - 2mg then review diagnosis (1 mins between each dose)
195
What is the immunisation schedule for tetanus in the UK? (3)
1. Primary Course:
8, 12, and 16 weeks
2. First Booster:
3 years (pre-school)
3. Second Booster:
14 years
196
What is 2-PAM?
Pralidoxime
197
What receptor does pralidoxime act on predominantly?
Nicotinic
198
What type of paralysis does botulism cause?
Descending
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