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Bachelor of Paramedic Science > PME3 > Flashcards

PME3 Flashcards

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1
Q

As mental status is usually normal in alcoholic ketoacidosis (AKA), what are 2 main causes that should be considered for the symptoms?

A

hypoglycaemia
acute ethanol intoxication

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2
Q

Can box jellyfish sting cause respiratory and cardiac arrest within minutes?

A

yes

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3
Q

Do Insulin & sulphonylureatoxicity patients require madatory transport to hospital?

A

yes

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4
Q

GCS Eyes Score: No Response

A

1

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5
Q

GCS Eyes Score: Pain

A

2

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6
Q

GCS Eyes Score: Verbal

A

3

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7
Q

GCS Motor Score: Extension

A

2

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8
Q

GCS Motor Score: Flexion

A

3

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9
Q

GCS Motor Score: Localises to Pain

A

5

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10
Q

GCS Motor Score: No Response

A

1

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11
Q

GCS Motor Score: Obeys

A

6

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12
Q

GCS Motor Score: Withdraws to Pains

A

4

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13
Q

GCS Verbal Score: Confused

A

4

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14
Q

GCS Verbal Score: Innapropriate

A

3

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15
Q

GCS Verbal Score: Moans and Groans

A

2

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16
Q

GCS Verbal Score: No Response

A

1

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17
Q

GCS Verbal Score: Orientated

A

5

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18
Q

GCS Eyes Score: Spontaneous

A

4

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19
Q

How long does it toake for the oxidation in paracetamol overdose to result in irreversible damage and hepatic dysfunction and death?

A

2-3 days

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20
Q

Hs & Ts

Reversible Causes

A
  • Hypoxia
  • Hypothermia / hyperthermia
  • Hypokalaemia / hyperkalaemia (or other electrolyte derangements)
  • H+ (acidosis)
  • Toxicity
  • Tension pneumothorax
  • Tamponade
  • Thrombus (coronary / pulmonary)
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21
Q

Is supportive care including ventilation usually sufficient in opioid overdoses?

A

yes

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22
Q

List the common Serotonin (5HT) reuptake inhibitors.

A

fluoxetine (prozac)
sertraline
citalopram

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23
Q

List the common Serotonin noradrenaline reuptake inhibitors (SNRIs)

A

venlafaxine (effexor)
desvenlafaxine
duloxetine

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24
Q

List the common Tricyclic antidepressants (TCAs)?

A

amitryptyline
imipramine (endep)
nortryptyline

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25
Q

Other than depression, what conditions are tricyclic antidepressants diagnosed for?

A

insomnia
nocturnal enuresis
neuralgia
migraines
OCD

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26
Q

QAS Procedure - Paramedic Unwitnessed Cardiac Arrest

A

Shockable rhythm?

  • commence CPR immediatey
  • Pads on ASAP (even as a single officer)
  • Deliver single shock (with relevant joule setting)
  • Continue CPR and reassess/readminister shock every 2 min if indicated (6 cycles of 30:2)
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27
Q

QAS Procedure - Paramedic Unwitnessed Cardiac Arrest Refractory VF/VT

A
  • DRC: Nil pulse, commence CPR
  • Expose chest & apply pads in correct positions
  • Analyse in AED mode: shockable rhythm
  • Safety checks in full for first shock
  • Shock (1)
  • Commence 2 mins CPR & give sitrep
  • A: If airway clear consider early insertion of i-Gel
  • B: Attach EtCO2 to BVM
  • No i-Gel: commence 30:2
  • i-Gel in situ: ventilate at rate of 10/min with continuous compressions
  • Attach Corepatch (if using Corpuls3)
  • Plan for timely defibrillation: Charge at 1:45
  • Shock (2)
  • Plan your positioning & rotation of CPR operators
  • Position shoulder-to-shoulder and swap without interruption
  • Are bystanders / QPS / QFRS available for CPR?
  • IV access
  • Plan for timely defibrillation: Charge at 1:45
  • Shock (3)
  • Amiodarone 300mg IV slow push
  • Two ampoules of 3mL each = 6mL in 10mL syringe
  • Flush with 10-20mLs saline (use a small bag)
  • Plan your positioning & execute rotation of CPR operators
  • Plan for timely defibrillation: Charge at 1:45
  • Shock (4)
  • Plan your positioning & rotation of CPR operators
  • Position shoulder-to-shoulder and swap without interruption
  • Are bystanders / QPS / QFRS available for CPR?
  • Plan for timely defibrillation: Charge at 1:45
  • Shock (5)
  • Amiodarone 150mg IV slow push (last dose of amiodarone)
  • One ampoule = 3mL
  • Flush with 10-20mLs saline (use a small bag)
  • Plan your positioning & execute rotation of CPR operators
  • Plan for timely defibrillation: Charge at 1:45
  • ** Shock (6)**
  • Start adrenaline: 1mg IV & 10-20mL flush (1)
  • Replace pads, applying new pads anterior-posterior
  • And so on…*
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28
Q

QAS Procedure - Paramedic Witnessed Cardiac Arrest

A
  • Deliver 3x stacked DCCS unless delay of 20s
  • If shocks are delayed by more than 20s, commence CPR and give a single shock as soon as possible
  • Quickly check rhythm before each shock
  • After three stacked shocks:
  • 2min CPR cycle
  • Single shocks thereafter
  • If still in a shockable rhythm, give amiodarone
  • If Pt has >2mins ROSC can give another set of three stacked shocks for return to shockable rhythm.
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29
Q

Signs and symptoms in mixed cholinergic toxidromes

A

Miosis (pinpoint pupils) or mydriasis (dilated pupils)
Lacrimation
Salivation
Increased bronchial secretions
Bronchospasm
Brady-or tachycardia
Hypo-or hypertension
Vomiting
Urinary incontinence
Diarrhoea
Muscle weakness/paralysis
Fasciculations (muscle twitching)
Sweating

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30
Q

Signs and symptoms in serotonin syndrome toxidromes

A

Altered mental state
Tachycardia
Hypertension
Hyperreflexia (over responsive reflexes)
Lower limb rigidity
Clonus (rhythmic muscle contractions)/myoclonus (sudden brief muscle contractions)
Hyperthermia
Sweating

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31
Q

Signs and symptoms in anticholinergic toxidromes

A

Agitated delirium
Dilated pupils
Blurred vision
Dry mouth
Ileus (intolerance of oral intake)
Tachycardia
Hyperthermia
Urinary retention
Dry flushed skin

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32
Q

Signs and symptoms in opiate toxidromes

A

Decreased conscious state
Miosis (pinpoint pupils)
Bradypnoea/apnoea
Ventilatory failure

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33
Q

What are the risk factors of taking digoxin?

A
  • Renal function decline:
    Decreased excretion results in increased bioavailability
  • Hypokalaemia:
    Low K+ increases toxicity as K+ competes with digoxin forbinding sites at Na-K pump
  • Hypercalcaemia:
    Risk of bradycardia, AV blocks, ventricular ectopy
  • Hypomagnesaemia:
    General increase in toxicity
  • Drug interactions:
    Digoxin has a wide range of drug interactions
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34
Q

What are 2 herbicides that cause poisoning in Australia?

A

paraquat
glyphosate

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35
Q

What are antipsychotics prescribed for?

A

schizophrenia and bipolar disorder

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36
Q

What are common causes of mixed cholinergic toxidromes?

A

Carbamates
Chemical warfare agents
Organophosphates

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37
Q

What are common causes of opiate toxidromes?

A

Heroin
Morphine (All opiates)

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38
Q

What are common causes of serotonin syndrome toxidromes?

A

Amphetamines
Fentanyl
Lithium
MAO inhibitors
SSRIs
SNRIs
St. John’s wort
Tramadol
Tricyclic antidepressants

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39
Q

What are common causes of Sympathomimetic (mixed α-and β-adrenergic) toxidromes?

A

Amphetamines
Cocaine

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40
Q

What are common causes of Sympathomimetic (β-adrenergic) toxidromes?

A

Caffeine
Salbutamol
Theophylline

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41
Q

What are common causes of anticholinergic toxidromes?

A

Antipsychotics
Antihistamines
Atropine
Benztropine
Carbamazepine
Plant poisonings
Tricyclic antidepressants

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42
Q

What are some of the challenges of cardiovascular toxidromes?

A
  • Pt may become toxic without overdosing
  • Non-compliant, agitated patient (regardless of intentional or not)
  • Complex, compound, and often bizarre dysrhythmias
    • Many toxidromes can produce multiple blocks
  • High likelihood of refractory presentations:
    • Pulseless VT or VF resistant to defibrillation
    • Bradycardia resistant to atropine
  • Electrolytic and metabolic disturbances
    • Hypo-or hyper-glycaemia
    • Hypo-or hyper-kalaemia, -calcaemia
    • Generalised weakness, including of respiratory muscles
    • Nausea and vomiting
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43
Q

What are some potential sources of cyanide exposure?

A

Insecticides
Photographic solutions
Metal polishing materials
Jewellery cleaners
Acetonitrile
Electroplating materials
Synthetic products such as rayon, nylon, polyurethane foam, insulation, and adhesive resins
Seeds and fruit pits of Prunus species (e.g. apple seeds and cherry and apricot pits)
Smoke inhalation in closed-space fires

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44
Q

What are the pharmacodynamics of digoxin?

A

Inhibits function of the Na/K pump to increase intracellular sodium & restrict calcium loss

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45
Q

What are teh two naturally occurring seafood toxins?

A
  • Ciguatera fish poisoning: occurs due to ingestion of fish carrying ciguatera toxin.
  • Pufferfish (tetrodotoxin): consumption of poisonous fish
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46
Q

What are the 3 main metabolic pathways within the liver?

A

Glucuronidation
Sulphonation
Oxidation

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47
Q

What are the 4 extrapyramidal syndromes in antipsychotic toxidromes?

A

acute dystonia
akasthesia
parkinsonism
tardive dyskinesia

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48
Q

What are the cardiovascular ECG manifestations in poisoning?

A
  • Bradycardia
  • Tachycardia
  • PVCs
  • QRS prolongation
  • QT prolongation
  • Ventricular tachycardia
  • Ventricular fibrillation
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49
Q

What are the cardiovascular signs and symptoms in snake envenomation?

A
  • Tachycardia
  • hypotension/hypertension
  • BP lability
  • haemodynamic instability
  • Watch for hyperkalaemia
  • cardiac arrest most likely with brown snake bites
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50
Q

What are the cardiovascular signs and symptoms of CO toxicity?

A

Tachycardia
hypotension
haemodynamic instability
Myocardial hypoxia
ischaemia
infarction
cardiac dysrhythmias

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51
Q

What are the cardiovascular signs and symptoms of inhaled hydrofluoric acid toxidrome?

A

QT prolongation
peaked T waves,
Look for hypocalcaemia & hyperkalaemia;
expect TdP, VT

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52
Q

What are the cardiovascular signs and symptoms of topical hydrofluoric acid toxidrome?

A

QT prolongation
peaked T waves,
Look for hypocalcaemia & hyperkalaemia;
expect TdP, VT

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53
Q

What are the classes of anticonvulsants?

A
  • Voltage-gated Na+ channel blockade (excitation ↓)
  • Enhance GABA inhibition (inhibition ↑)
  • Calcium channel blockade (excitation ↓)
  • Inhibiting glutamate release & NMDA interaction (excitation ↓)
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54
Q

What are the clinical features of an opioid toxidrome?

A

CNS depression
Miosis
loss of airway reflexes
Respiratory depression
apnoea
Bradycardia
tachycardia (response to hypoxia and hypercarbia)
Nausea/vomiting
Hypothermia
skin necrosis
compartment syndrome
rhabdomyolysis

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55
Q

What are the clinical features of anticholinesterase pesticides?

A

ALOC
seizures
miosis/mydriasis
lacrimation
salivation
bronchorrhoea
bronchoconstriction
respiratory failure
bradycardia/tachycardia
hypotension/hypertension
Cardiacarrhythmias
emesis
diarrhoea
urinary frequency
fasciculations and muscle weakness
possibly paralysis

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56
Q

What are the clinical features of energy drink overdose?

A

insomnia
agitation
palpitations
tremor

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57
Q

What are the clinical features of progressive cyanide toxicity?

A

coma
confusion
drowsiness
respiratory depression
hypotension
bradycardia
tetany

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58
Q

What are the clinical features of severe ethanol withdrawal?

A

insomnia
anxiety
tachycardia
hypertension
tremor
hyperreflexia
irritability
fever
seizures
visual hallucinations
delirium

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59
Q

What are the clues that increase the likelihood of ABD being from an organic aetiology?

A

over 40 yrs with first presentation of psychosis or altered mental state
disorientation/ALOC
altered vital signs
visual, tactile or olfactory hallucinations
sudden onset
fluctuating conscious state

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60
Q

What are the CO toxicodynamics?

A

Displacement of oxygen reduces oxygen-carrying capacity of blood, causing hypoxaemia & hypoxia
Binding to mitochondrial cytochrome oxidase enzymes restricts their function in aerobic metabolism
Hypoxia & metabolic changes causes release of toxic species, triggering inflammation cascade
Compound effects cellular & neuronal damage, myelin damage, & significant acidosis
Also causes reoxygenation injuries (incl. apoptosis)

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61
Q

What are the coagulopathy signs and symptoms in snake envenomation?

A

oozing from bite/IV sites/gums
haematemesis
haematuria
bruising
intravascular haemolysis
risk of intracranial haemorrhage

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62
Q

What are the differential diagnosis of acute ethanol intoxication?

A

Encephalopathy (Wernicke or Hepatic)
Head injury
Intracranial infarction or haemorrhage
Post-ictal state
Psychosis
Hypoxia
Hypocarbia (low levels CO2)
Hypo/hyperthermia
Hypoglycaemia
Hyponatraemia (low sodium in blood)
Overdose or other toxin
Sepsis

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63
Q

What are the clinical features of early cyanide toxicity?

A

loss of consciousness within seconds to minutes.
agitation
collapse
seizures
headache
dyspnoea
tachypnoea
hypertension
tachycardia
nausea/vomiting

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64
Q

What are the extreme presentations in Wernicke encephalopathy?

A

hyperthermia
hypertonia
spastic paresis
dyskinesias
coma

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65
Q

What are the features of a funnel-web spider bite?

A

bite is painful
fang marks usually obvious
spider may remain attached to Pt until shaken off or removed

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66
Q

What are the features of a redback spider bite site?

A

majority of Pts feel bite, but only as pinprick - some may not feel it
local sweating at the site
sometimes local erythema or blanching or piloerection

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67
Q

What are the four categories that acute behavioural disturbance (ABD) can be classified into?

A

psychiatric disorders
(schizophrenia, bipolar, PTSD, psychosis)

substance related
(psychostimulants, cocaine, ketamine, LSD, cannabis, alcohol)

organic disorders
(hypoglycaemia, sepsis, hyoxia, head injury, dementia)

situational
(grief, overwhelming stress)

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68
Q

What are the four types of snake venom actions?

A
  • Coagulopathic
  • Neurotoxic: paralysis
  • Nephrotoxic: acute kidney injury (AKI)
  • Myotoxic: rhabdomyolysis (will cause secondary AKI)
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69
Q

What are the less common presentations in Wernicke encephalopathy?

A

stupor
hypothermia
cardiovascular instability
seizures
visual disturbances
hallucinations
alterations in behaviour

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70
Q

What are the limitations for the prone position when restraining patients?

A

not in prone position for longer than 2 minutes as it may impede breathing and result in positional asphyxia

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71
Q

What are the metabolic manifestations in poisoning?

A

Hypo/Hyperthermia
Hypo/Hyperkalaemia
Hyponatraemia
Hypoglycaemia
H+ ion (acidosis)
Toxicity
Thrombus

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72
Q

What are the neurological signs and symptoms in snake envenomation?

A

Neurotoxic paralysis
headache
ptosis
double vision
fixed dilated pupils
drooling
slurring
respiratory paralysis
weakness
lost deep tendon & spinal reflexes

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73
Q

What are the neurological signs and symptoms of CO toxicity?

A

ALOC
seizures
coma
headache
dizziness
concentration difficulties
disorientation
cortical blindness
ataxia
weakness

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74
Q

What are the parameters for the immediate life threat risk category of poisoning?

A

↓ GCS
Airway loss
↓ Resp
Shock
vomiting
aspiration

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75
Q

What are the parameters for the low risk category of poisoning?

A

Dose does notmeet toxic threshold
Drug has low toxicity

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76
Q

What are the parameters for the potential complication risk category of poisoning?

A

Dysrhythmias
Seizures

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77
Q

What are the parameters for the potential organ damage risk category of poisoning?

A

kidneys
liver

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78
Q

What are the parameters for the uncertain risk category of poisoning?

A

Dose uncertain
Drug uncertain

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79
Q

What are the respiratory signs and symptoms of CO toxicity?

A

Dyspnoea
tachypnoea
pulmonary oedema
resp. depression (late)

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80
Q

What are the serotonin syndrome altered mental status symptoms?

A

coma
seizures (pre-terminal)
headache
anxiety
hallucinations
disorientation
excitation
agitation

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81
Q

What are the serotonin syndrome autonomic hyperactivity symptoms?

A

mydriasis
dry mucous membranes
tachypnoea
tachycardia
dysrhythmias
hypertension
hyperthermia
hot flushed skin
diaphoresis
vomiting
diarrhoea

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82
Q

What are the serotonin syndrome neuromuscular symptoms?

A

ocular clonus (ping pong gaze)
tremors
inducible clonus
spontaneous clonus
muscle rigidity (esp. lower limbs),
hyperreflexia
bilateral Babinski signs
akisthesia (inability to remain still)

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83
Q

What are the signs and symptoms of acute dystonia?

A

facial grimacing
involuntary upward eye movement
muscle spasms of tongue, face, neck and back
laryngeal spasms

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84
Q

What are the signs and symptoms of akathisia?

A

restless
trouble standing still
pacing
feet in constant motion rocking back and forth

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85
Q

What are the signs and symptoms of aloholic ketoacidosis (AKA)?

A

tachypnoea
tachycardia
hypotension
diffuse epigastric tenderness on palpation

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86
Q

What are the whole of body signs and symptoms of and NSAID toxidrome?

A

nausea/vomiting
abdominal pain
haematemesis
renal failure
haematuria
malaena

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87
Q

What are the cardiovascular signs and symptoms of and NSAID toxidrome?

A

coagulopathy
hypotension
Tachycardia
thrombocytopenic purpura (rare)

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88
Q

What are the neurological signs and symptoms of and NSAID toxidrome?

A

CNS depression
coma
risk of haemorrhagic stroke

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89
Q

What are the metabolic signs and symptoms of and NSAID toxidrome?

A

electrolytic derangements

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90
Q

What are the neurological signs and symptoms of and NSAID toxidrome?

A

CNS depression
coma
risk of haemorrhagic stroke

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91
Q

What are the cardiovascular signs and symptoms of and NSAID toxidrome?

A

coagulopathy
hypotension
Tachycardia
thrombocytopenic purpura (rare)

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92
Q

What are the metabolic signs and symptoms of and NSAID toxidrome?

A

electrolytic derangements

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93
Q

What are the whole of body signs and symptoms of and NSAID toxidrome?

A

nausea/vomiting
abdominal pain
haematemesis
renal failure
haematuria
malaena

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94
Q

What are the signs and symptoms of and NSAID toxidrome?

A

CNS depression
coma
Tachycardia
hypotension
coagulopathy
thrombocytopenic purpura (rare)
electrolytic derangements
Nausea, vomiting
abdominal pain
haematemesis
haematuria
malaena
Renal failure

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95
Q

What ECG changes does the K+ blockade of sotalolol cause?

A

prolongs QT, risking R-on-T & Torsades des Points

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96
Q

What ECG changes does the Na+ blockade of propranolol cause?

A

prolongs PR-interval & QRS duration

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97
Q

What ECG changes does the Na+ blockade of propranolol cause?

A

prolongs PR-interval & QRS duration

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98
Q

What ECG changes does the K+ blockade of sotalolol cause?

A

prolongs QT, risking R-on-T & Torsades des Points

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99
Q

What are the neurological signs and symptoms of digoxin toxicity?

A

agitation
ALOC
fatigue
headache (key early sign)
visual disturbances

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100
Q

What are the cardiovascular signs and symptoms of digoxin toxicity?

A

Variety of dysrhythmias & heart blocks
High risk of PVCs, VT, VF

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101
Q

What are the respiratory signs and symptoms of digoxin toxicity?

A

Largely dependent upon CNS status

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102
Q

What are the neurological signs and symptoms of digoxin toxicity?

A

agitation
ALOC
fatigue
headache (key early sign)
visual disturbances

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103
Q

What are the cardiovascular signs and symptoms of digoxin toxicity?

A

dysrhythmias
heart blocks
PVCs
VF
VT

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104
Q

What are the signs and symptoms of funnel-web spider bite?

A
  • Lacrimation
  • Paraesthesia in lips; may see fasciculations of tongue
  • Salivation
  • Pulmonary oedema
  • Cyanosis
  • Hypertension, +/- tachycardia,
  • Tachypnoea
  • Nausea/vomiting
  • Sweating
  • Malaise
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105
Q

What are the whole of body signs and symptoms of metformin toxidrome?

A

nausea, vomiting
abdominal pain
renal failure
decreased urine output
hypothermia

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106
Q

What are the cardiovascular signs and symptoms of metformin toxidrome?

A

↓ cardiac output
↓ vascular resistance
dysrhythmias
hypotension → shock & death
tachycardia

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107
Q

What are the respiratory signs and symptoms of metformin toxidrome?

A

dyspnoea
hyperpnoea
tachypnoea

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108
Q

What are the signs and symptoms of metformin toxidrome?

A

fatigue
irritability
ALOC
seizures
coma
dyspnoea
tachypnoea
hyperpnoea
↓ cardiac output
↓ vascular resistance
dysrhythmias
tachycardia
hypotension → shock & death
nausea, vomiting
abdominal pain
hypothermia
decreased urine output
renal failure

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109
Q

What are the neurological signs and symptoms of metformin toxidrome?

A

ALOC
coma
fatigue
irritability
seizures

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110
Q

What are the whole of body signs and symptoms of metformin toxidrome?

A

nausea, vomiting
abdominal pain
renal failure
decreased urine output
hypothermia

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111
Q

What are the signs and symptoms of methanol toxicity?

A

coma
seizures
tachypnoea
metabolic acidosis
progressive obtundation (lethargy)

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112
Q

What are the signs and symptoms of neuroleptic malignant syndrome?

A

agitation
mydriasis
labile blood pressure
tachycardia
increased bowel sounds +/- diarrhoea
clonus
tremor
hyperreflexia

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113
Q

What are the signs and symptoms of opioid toxicity?

A

miosis
airway obstruction and respiratory depression, especially in children

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114
Q

What are the signs and symptoms of pseudoparkinsonism?

A

stooped posture
shuffling gait
rigidity
bradykinesia
tremors
pill-rolling motion of hand

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115
Q

What are the signs and symptoms of redback spider bite?

A
  • Gradual onset of severe pain which transits proximally
  • Hypertension, +/- tachycardia, sweating, malaise
  • Severe abdominal and/or chest pain
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116
Q

What are the signs and symptoms of tardive dyskinesia?

A

protrusion and rolling of the tongue
sucking and smacking movements of the lips
chewing motion
facial dyskinesia
involuntary movements of the body and extremities

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117
Q

What are the signs and symptoms usually seen in the >3 hours after a snake bite?

A

Respiratory & limb weakness progressing to flaccid paralysis
Rhabdomyolysis & hyperkalaemia
myoglobinuria
AKI
Risk of catastrophic haemorrhage, circulatory failure & arrest

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118
Q

What are the signs and symptoms usually seen in the first 1-3 hours after a snake bite?

A

Cranial nerve paralysis of facial muscles & pupils
Coagulopathy
haemoglobinuria
muscle damage
limb weakness

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119
Q

What are the signs and symptoms usually seen in the firt 60 minutes after a snake bite?

A
  • Headache
  • irritability
  • confusion
  • photophobia
  • blurred vision
  • tachycardia
  • BP lability
  • Nausea/vomiting
  • diarrhoea
  • sweating, ,
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120
Q

What are the three hypoglycaemic agent?

A

insulin (eg novomix)
sulphonylureas (eg glibenclamide, gliclazide, glimepiride)
biguanides (eg metform, diabex, diaformin)

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121
Q

What are the top three drugs that cause death in overdose?

A

opioids
benzodiazepines
psychostimulants

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122
Q

What are the ventilation rates?

A

20 per minute = 1/3
18 per minute = 1/3
16 per minute = 1/4
14 per minute = 1/4
12 per minute = 1/5

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123
Q

What are the whole of body manifestations in poisoning?

A
  • Hypo/hypertension
  • Hypovolaemia
  • Shock
  • Chest pain (pshychostimulants)
  • Ischaemia
  • Infarction
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124
Q

What are the whole of body signs and symptoms of CO toxicity?

A

Lactic acidosis
rhabomyolysis
disseminated intravascular coagulation
Renal failure
coexistence of hypo-or hyper-glycaemia worsens prognosis

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125
Q

What are the whole of body signs and symptoms of digoxin toxicity?

A

Appetite loss & anorexia
nausea
vomiting

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126
Q

What body areas should be avoided when applying physical restraint?

A

face, neck and chest

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127
Q

What can supine positioning contribut to in restrained patients?

A

the risk of aspiration

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128
Q

What causes alcoholic ketoacidosis (AKA)?

A

starvation

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129
Q

What causes hyperkalaemia?

A
  • any toxidrome causing muscle damage from hyperthermia, hypertonicity or hypoxia
  • direct trauma
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130
Q

What channel does methadone inhibit?

A

some K channels

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131
Q

What commercial process uses cyanide?

A

metal extraction (especially gold) andrecovery, metal hardening and in the production of agricultural and horticultural pest control

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132
Q

What condition presents with overdose of insulin?

A

hypoglycaemia

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133
Q

What condition presents with overdose of slphonylureas?

A

hypoglycaemia

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134
Q

What conditions is theophylline and caffeine (under a variety of brand names) usually prescribed for?

A

COPD
asthma
similar conditions

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135
Q

What do antiarrhythmic drugs do?

A

restrict ionic movement into or out of heart cells modulating the action potential

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136
Q

What do Cardiac glycosides target?

A

heart failure

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137
Q

What do Class II and beta blockers target?

A

dysrhythmias
hypertension

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138
Q

What do Class III and K+ blockers target?

A

Dysrhythmias

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139
Q

What do Class IV and Ca++ blockers target?

A

Dysrhythmias
Hypertension

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140
Q

What do Dermatonecrotic toxins target?

A

Skin damage/necrosis from toxin, particularly box jelly fish

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141
Q

What do haemolytic toxins target?

A

Rupture of erythrocytes, haemaglobinis released into the blood stream

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142
Q

What do haemotoxins cause?

A

disseminated intravascular coagulation andother coagulopathies

143
Q

What do myotoxins cause?

A

muscle damage and rhabdomyolysis (withsecondary AKI)

144
Q

What do necrotoxins cause?

A

cutaneous damage; infections,inflammation, necrosis (more likely with arachnidism)

145
Q

What do neurotoxins target?

A

the neuromuscular junction, blocking the transmission of signals across the gap between the motor end plate and muscle

ACh, NA, & GABA most commonly affected

146
Q

What do prokinetics do?

A

Increase gastric motility (rate of excretion)

147
Q

What do Tetrodotoxins target?

A

the axon, inhibiting the chemical message reaching the motor end plate.

These toxins have rapid onset, may last for hours, however no actual damage to nerve

148
Q

What do the effects of antiarrhythmic drugs cause?

A
  • Reduce force of contraction
  • Reduce excitability and ectopic beats
  • Reduce ability to respond to reentrystimuli
  • Reduce cardiac workload and blood pressure
149
Q

What does a box jellyfish look like?

A

Transparent bell, 15+ tentacles extend up to 3m in length

150
Q

What does an antidote do?

A
  • Neutralise toxin by chemically alteration
  • Directly counter the toxic effect (e.g. n-acetylcysteine for paracetamol OD)
  • Competitively block the receptor to cease toxic effects (e.g. naloxone for opioid OD)
  • Alter the drug physically, such as absorption into charcoal to prevent absorption
151
Q

What does Biguanides do?

A

Inhibits gluconeogenesis
increases insulin sensitivity

152
Q

What does digoxin do?

A

improve the strength and efficiency of the heart or control the rate and rhythm of the heartbeat

153
Q

What does irukandji look like?

A

Small, Body only 1-3cm diameter, transparent, only few tentacles, nearly invisible

154
Q

What does Sulphonylureas do?

A

increases insulin release
decreases insulin clearance

155
Q

What does the nmemonic DUMBELS stand for?

A

Diarrhea
Urination (uncontrolled)
Miosis
Bronchorrhea/Bradycardia
Emesis
Lacrimation
Salivation/Sweating

156
Q

What does the Wernicke encephalopathy triad include?

A

*Oculomotor disturbance (usually nystagmus and ocular palsies)
*Abnormal mentation (usually confusion)
*Ataxia (difficulty speaking)

157
Q

What drug is used to reverse severe oioid toxicity?

A

Naloxone (narcan)

158
Q

What do Class Ia, Ib, Ic & Na+ blockers target?

A

dysrhythmias

159
Q

What effects does Gamma-hydroxybutyric acid (GHB) (‘grievous bodily harm’, ‘fantasy’, ‘scoop’, ‘liquid X’, ‘liquid E’) cause?

A

sedation and psychotropic effects

160
Q

What happens to metabolism and excretion in an overdose causing shock?

A

poor liver and kidney perfusion reduces metabolism and excretion

161
Q

What is ethylene glycol most commonly found in?

A

radiator antifreeze
coolant
hydraulic fluids
solvent preparations

162
Q

What is insulin and what does it do?

A

Endogenous hormone that facilitates glucose entry into cells

163
Q

What is lithium prescribed for?

A
  • Bipolar disorder to lessen manic episodes (often in conjunction with anti-psychotics)
  • Schizophrenic disorders unresponsive to antipsychotics
  • Major depression, typically as an adjunct
164
Q

What is the antidote for opiate toxidromes?

A

Naloxone

165
Q

What is the approach for antidepressent toxidromes?

A
  • Verbal de-escalation; sedation for ABD; QPS; physical restraint; early sitrep & backup
  • Airway loss likely if unresponsive; vomitus & secretions likely
    • Suctioning; consider early advanced airway management
  • May have increased muscle tone and rigidity causing respiratory failure
  • Expect dysrhythmias & blocks; cardiogenic shock; expect deterioration, pads on
    • Early 12-lead & serial print-outs; look for wave / segment widening; look for hyperkalaemia
  • Expect metabolic derangement! Early BSL & repeat with CVS obs
    • Maintain normothermia and aggressively cool the hyperthermic patient
  • Toxicological risk assessment & early hospital notification; consider bypass
  • Rapid transport for advanced cares (decontamination, antidote, elimination, etc.)
166
Q

What is the approach for metformin overdose patients?

A

Safety: Hypoglycaemics can be agitated & violent
Verbal de-escalation/QPS/physical restraint
early sitrep & backup
Airway - suctioning; consider early advanced airway management
Early 12-lead & serial print-outs; pads on
BSL every five minutes
keep warm
Toxicological risk assessment
early hospital notification; consider bypass
Rapid transport for advanced cares

167
Q

What is the appropriate positioning for pts who are physically restrained?

A

on their side with hands in front of their body

168
Q

What is the cardiac arrest treatment in hypothermic pts <30 degrees?

A

Rewarmed as rapidly as possible:–
* Drugs should be withheld until the temperature is >30C and then double the regular intervals until temperature is 35C
* Defibrillation at maximum joules
* If initially unsuccessful furthershocks should be withheld until temperature is >30C
* Prolonged resuscitation untid resuscitation and not discontinuesd until Pt is >35C

169
Q

What is the cardiac output formula?

A

CO= HR x SV

170
Q

What is the clinical presentation of blue ringed octopus envenomation?

A
  • Minor bite
  • Numbness of lips and tongue within minutes
  • Numbness, nausea, vomiting, chest tightness
  • Respiratory failure may occur within 30 minutes
171
Q

What is the clinical presentation of cone shell envenomation?

A
  • Pain followed by numbness and swelling
  • In severe cases numbness can spread over the limb, throat,lips, blurred vision, partial paralysis and respiratory paralysis can occur within 30 minutes.
172
Q

What is the clinical presentation of irukandji syndrome?

A
  • Anxiety and restlessness
  • Respiratory distress
  • Tachycardia
  • Hypertension
  • Back, chest and abdominal pain
  • Nausea and Vomiting
173
Q

What is the clinical presentation of seafood toxins?

A
  • dizziness
  • respiratory paralysis
  • nausea
  • vomiting
  • cramps
  • diarrhoea
  • weakness
  • tingling
  • numbness
174
Q

What is the clinical presentation of seafood toxins?

A
  • dizziness
  • respiratory paralysis
  • nausea
  • vomiting
  • cramps
  • diarrhoea
  • weakness
  • tingling
  • numbness
175
Q

What is the clinical presentation of stingray envenomation?

A
  • Injury usually occurs from standing on tail, deep and extensive lacerations.
  • Venom from barb can cause systemic symptoms
  • Mortality usually results from trauma or exsanguination, particularly to chest or abdomen.
176
Q

What is the clinical presentation of stone fish/bullrout envenomation?

A
  • spines imbedded in skin, causing immediate and extreme pain
  • headache
  • seizures
  • respiratory distress
  • hypertension
  • vomiting
  • abdo pain
  • paralysis
  • Symptoms peak 30-90minutes, dissipate 6-12hrs
177
Q

What is the funnel-web spider bite management?

A
  • NO wash; apply PIB
  • Opioids
  • IV access
  • Ondansetron
  • Expect pulmonary oedema & shock; consider IPPV, fluids
  • Early hospital pre-notification; transport to major facility
178
Q

What is the HPI for aloholic ketoacidosis (AKA)?

A

history of prolonged heavy alcohol misuse
bout of particularly excessive intake terminated several days earlier by nausea, severe vomiting and abdominal pain

179
Q

What is the hunter criteria?

A

a criteria used to identify serotonin syndrome using signs and symptoms

180
Q

What is the lethal oral dose for caffeine toxicity?

A

greater than 150 to 200 mg/kg

181
Q

What is the management for anticholinesterase pesticide poisoning?

A
  • Wear universal precautions - gloves, eyewear, gown
  • Place patient in an well ventilated area equipped for cardiorespiratory monitoring and resuscitation
  • Treat potential early life threats including:
    • Coma
    • Hypotension
    • Seizures
    • Respiratory failure
  • Simultaneous resuscitation and decontamination
182
Q

What is the management for CO toxidrome?

A

Scene safety
All basic and supportive cares
IV access early
100% oxygen delivery regardless of SpO2
12-lead ECG & expect ischaemia & dysrhythmias in severe cases
Treat symptomatically
Consider also cyanide toxicity

183
Q

What is the management for psychostimulants?

A

safety
standard cares
verbal de-escalation
APS assistance
physical restraint
EEA
Sedation ABD

184
Q

What is the management for suspected blue-ringed octopus envenomation?

A
  • pressure bandages and immobilisation
  • provide cardio-respiratory support
  • manage as per appropriate CPG for adult or paediatric resuscitation
185
Q

What is the management for suspected bluebottle or minor jellyfish envenomation?

A
  • wash site (sea water)
  • remove tentacles

Consider:
* analgesia
* hot water immersion

186
Q

What is the management for suspected box jellyfish envenomation?

A

If in shock or cardio-respiratory arrest - CPR

  • copious flushing with vinegar
  • remove tentacles

Consider:
* analgesia
* box jellyfish antivenom
* magnesium sulphate

187
Q

What is the management for suspected cone shell envenomation?

A
  • Pressure immobilisation bandage
  • Manage as per snake bite
  • Provide cardio-respiratory support
  • Ventilations must be continued, paralysis will eventually abate
188
Q

What is the management for suspected cone shell envenomation?

A
  • Pressure immobilisation bandage
  • Manage as per snake bite
  • Provide cardio-respiratory support
  • Ventilations must be continued, paralysis will eventually abate
189
Q

What is the management for suspected irukandji envenomation?

A
  • copious flushing with vinegar
  • remove tentacles

Consider:
* analgesia
* magnesium sulphate
* GTN (if SBP ≥ 160 mmHg)

190
Q

What is the management for suspected stingray envenomation?

A
  • Immerse limb in water as hot as the patient can tolerate (max 45deg) with outburning skin. Provides pain relief
  • Pain relief as appropriate
  • Haemorrhage control if required
  • Do not remove spines, stablise
  • Transport. Wound may require surgical clean, AB’s and tetanus prophylaxis.
191
Q

What is the management for suspected stone fish/bullrout envenomation?

A
  • Immerse limb in water as hot as the patient can tolerate (max 45deg) with outburning skin. Provides pain relief.
  • Pain relief as appropriate
  • Do not remove spines, stabilise.
  • Transport. Wound may require surgical clean, AB’s and tetanus prophylaxis.
192
Q

What is the management of paraquat intoxication?

A

early decontamination
airway management - Do not administer supplemental oxygen unless oxygen saturation <88% - titrate to 88%
early intubation or surgical airway if stridor, dysphagia and dysphonia present
treat symptomatically

193
Q

What is the management of paraquat intoxication?

A

early decontamination
airway management - Do not administer supplemental oxygen unless oxygen saturation <88% - titrate to 88%
early intubation or surgical airway if stridor, dysphagia and dysphonia present
treat symptomatically

194
Q

What is the management of paraquat intoxication?

A

early decontamination
airway management - Do not administer supplemental oxygen unless oxygen saturation <88% - titrate to 88%
early intubation or surgical airway if stridor, dysphagia and dysphonia present
treat symptomatically

195
Q

What is the management of paraquat intoxication?

A

early decontamination
airway management - Do not administer supplemental oxygen unless oxygen saturation <88% - titrate to 88%
early intubation or surgical airway if stridor, dysphagia and dysphonia present
treat symptomatically

196
Q

What is the methanol toxicity pathophysiology?

A

the formation of formic acid, which binds to cytochrome oxidase, resulting in impairment of cellular respiration

197
Q

What is the name of the criteria used to diagnosis serotonin syndrome?

A

Hunter Criteria

198
Q

What is the number 1 cause of death in poisonings?

A

respiratory failure

199
Q

What is the order of preference for restraint of a patient?

A

simple reassurance
verbal de-escalation
pharmacological
physical restraint

200
Q

What is the order of preference for restraint of a patient?

A

simple reassurance
verbal de-escalation
pharmacological
physical restraint

201
Q

What is the paracetamol toxicokinetics?

A

sulphuration pathway cannot keep up, increased proportion of paracetamol enters the toxic oxidation pathway
glutathione stores rapidly overwhelmed by increased amount of NAPQI produced
Build-up of NAPQI results in acute hepatocyte injury through oxidation

202
Q

What is the pathophsiology of benzodiazepines?

A

enhance the effect of the neurotransmitter GABA at the GABAA receptor, resulting in sedative, hypnotic, anxiolytic, anticonvulsant and muscle relaxant properties

203
Q

What is the pathophysiology of alcoholic ketoacidosis (AKA)?

A

increased gluconeogenesis from non-carbohydrate sources which then converts to lactate

(starvation from lack of glucose and body trying to use other sources of fuel causing ketoacidosis)

204
Q

What is the pathophysiology of metformin overdose?

A

Blocks oxidative phosphorylation during cellular respiration, leading to build-up of lactate and failure to recycle H+

205
Q

What is the pathophysiology of theophylline and caffeine?

A

inhibition of phosphodiesterase, elevated concentrations of intracellular cyclic adenosine monophosphate (cAMP), increasing catecholamine activity, competitive antagonism of adenosine and changes in intracellular calcium transport

206
Q

What are the cardiovascular clinical features of theophylline and caffeine toxicity?

A

refractory hypotension
tachycardia
SVT
AF
VT

207
Q

What are the neurological clinical features of theophylline and caffeine toxicity?

A

anxiety
insomnia
seizures (severe toxicity)

208
Q

What are the cardiovascular clinical features of theophylline and caffeine toxicity?

A

refractory hypotension
tachycardia
SVT
AF
VT

hypokalaemia
hypophosphataemia
hypomagnesaemia
hyperglycaemia
lactic acidosis

209
Q

What are the respiratory clinical features of theophylline and caffeine toxicity?

A

tachypnoea

210
Q

What are the cardiovascular clinical features of theophylline and caffeine toxicity?

A

refractory hypotension
tachycardia
SVT
AF
VT

211
Q

What are the neurological clinical features of theophylline and caffeine toxicity?

A

anxiety
insomnia
seizures (severe toxicity)

212
Q

What are the respiratory clinical features of theophylline and caffeine toxicity?

A

tachypnoea

213
Q

What is the pharmacology of amphetamines?

A

enhance the release of catecholamines, blocking their reuptake, increasing stimulation of central and peripheral adrenergic receptors leading to a sympathomimetic toxidrome and higher doses causing central serotonin release

negative feedback loop

214
Q

What is the pharmacology of antipsychotics?

A

dopamine receptor antagonism
(60% once effector)

215
Q

What is the pharmacology of cocaine?

A

inhibits the reuptake of adrenaline and noradrenaline and stimulates the presynaptic release of noradrenaline leading to a sympathomimetic response mediated through both α-and β-adrenoreceptors

216
Q

What is the toxicokinetics of cyanide toxicity?

A

It binds to the ferric ion (Fe3+) of cytochrome oxidase and inhibits oxidative metabolism, leading to lactic acidosis
It stimulates release of biogenic amines, resulting in pulmonary and coronary vasoconstriction.
In the CNS,cyanide triggers neurotransmitter release, particularly N-methyl-D-aspartate (NMDA), which leads to seizures

217
Q

What is the pharmacology of Gamma-hydroxybutyric acid (GHB) (‘grievous bodily harm’, ‘fantasy’, ‘scoop’, ‘liquid X’, ‘liquid E’)?

A

dopaminergic effects increasing acetylcholine and serotonin levels and may interact with endogenous opioids

218
Q

What is the pharmacology of MAOI- A enzymes?

A

inactivates monoamines including 5HT (serotonin), Catecholamines (adrenaline, noradrenaline, dopamine) and Tyramine

219
Q

What is the pharmacology of MAOI- B enzymes?

A

inactivates monoamines including Tyramine, dopamine, & phenylethylamine

220
Q

What is the pharmacology of opioids?

A

act on various types of opioid receptors in the central and peripheral nervous systems

221
Q

What is the toxicokinetics of paraquat toxicity?

A

readily absorbed, distributed to all tissues but concentrates on the lungs and kidneys owing to active uptake in type II pneumocytes and renal tubular cells.
Causes the production of free oxygen radicals, which cause oxidative stress leading to lipid peroxidation of cell membranes, mitochondrial toxicity and cellular death.

222
Q

What is the presentation of a box jellyfish sting?

A
  • Commonly to the lower body
  • Instant severe intractable burning pain
  • Red whip or welt initially. Manifest into a whitefrosted ladder pattern
223
Q

What is the presentation of a box jellyfish sting?

A
  • Commonly to the lower body
  • Instant severe intractable burning pain
  • Red whip or welt initially. Manifest into a whitefrosted ladder pattern
224
Q

What is the presentation of a box jellyfish sting?

A
  • Instant severe intractable burning pain
  • Red whip or welt progressing to a whitefrosted ladder pattern
225
Q

What is the presentation of a box jellyfish sting?

A
  • Commonly to the lower body
  • Instant severe intractable burning pain
  • Red whip or welt initially. Manifest into a whitefrosted ladder pattern
226
Q

What is the presentation of a box jellyfish sting?

A
  • Commonly to the lower body
  • Instant severe intractable burning pain
  • Red whip or welt initially. Manifest into a whitefrosted ladder pattern
227
Q

What is the presentation of an irukandji sting?

A
  • Localised sting often minor and unnoticed
  • Symptoms may be delayed 20 mintures
  • Small area of redness
228
Q

What is the presentation of an irukandji sting?

A
  • Small area of redness
  • Symptoms may be delayed 20 mintures
229
Q

What is the presentation of an irukandji sting?

A
  • Localised sting often minor and unnoticed
  • Symptoms may be delayed 20 mintures
  • Small area of redness
230
Q

What is the presentation of an irukandji sting?

A
  • Localised sting often minor and unnoticed
  • Symptoms may be delayed 20 mintures
  • Small area of redness
231
Q

What is the presentation of an irukandji sting?

A
  • Localised sting often minor and unnoticed
  • Symptoms may be delayed 20 mintures
  • Small area of redness
232
Q

What is the QRS width for arrhythmia risk in TCA OD?

A

> 160ms (0.16 sec/4 small squares)

233
Q

What is the QRS width for arrhythmia risk in TCA OD?

A

> 160ms (0.16 sec/4 small squares)

234
Q

What is the QRS width for arrhythmia risk in TCA OD?

A

> 160ms (0.16 sec/4 small squares)

235
Q

What is the QRS width for arrhythmia risk in TCA OD?

A

> 160ms (0.16 sec/4 small squares)

236
Q

What is the QRS width for seizure risk in TCA OD?

A

> 100ms (0.1sec/2.5 small squares)

237
Q

What is the QRS width for seizure risk in TCA OD?

A

> 100ms (0.1sec/2.5 small squares)

238
Q

What is the QRS width for seizure risk in TCA OD?

A

> 100ms (0.1sec/2.5 small squares)

239
Q

What is the QRS width for seizure risk in TCA OD?

A

> 100ms (0.1sec/2.5 small squares)

240
Q

What is the R wave height in aVR for seizure and arrhythmia risk in TCA OD?

A

> 3mm

241
Q

What is the R wave height in aVR for seizure and arrhythmia risk in TCA OD?

A

> 3mm

242
Q

What is the R wave height in aVR for seizure and arrhythmia risk in TCA OD?

A

> 3mm

243
Q

What is the R wave height in aVR for seizure and arrhythmia risk in TCA OD?

A

> 3mm

244
Q

What is the redback spider bite management?

A
  • NO PIB! Wash, ice pack
  • Opioids
  • IV access
  • Ondansetron
  • Treat symptomatically
245
Q

What is the redback spider bite management?

A
  • NO PIB! Wash, ice pack
  • Opioids
  • IV access
  • Ondansetron
  • Hypertension can be significant; posture to reduce BP
  • Monitor
  • Early hospital pre-notification; transport to major facility
246
Q

What is the redback spider bite management?

A
  • NO PIB! Wash, ice pack
  • Opioids
  • IV access
  • Ondansetron
  • Hypertension can be significant; posture to reduce BP
  • Monitor
  • Early hospital pre-notification; transport to major facility
247
Q

What is the redback spider bite management?

A
  • NO PIB! Wash, ice pack
  • Opioids
  • IV access
  • Ondansetron
  • Hypertension can be significant; posture to reduce BP
  • Monitor
  • Early hospital pre-notification; transport to major facility
248
Q

What is the redback spider bite management?

A
  • NO PIB! Wash, ice pack
  • Opioids
  • IV access
  • Ondansetron
  • Hypertension can be significant; posture to reduce BP
  • Monitor
  • Early hospital pre-notification; transport to major facility
249
Q

What is the redback spider toxicodyanmics?

A
  • α-Latrotoxin stimulates Ca++ ingress into presynaptic neurons, resulting in exocytosis of noradrenaline and acetylcholine
  • Latroinsectitoxinsalso contribute to S+S via unknown effects
  • Painful and distressing, but unlikely to cause death
250
Q

What is the Sedation Assessment Tool (SAT) score for combative, violent, out of control with continual loud outbursts?

A

+3

251
Q

What is the Sedation Assessment Tool (SAT) score for combative, violent, out of control with continual loud outbursts?

A

+3

252
Q

What is the Sedation Assessment Tool (SAT) score for no response to stimulation and nil?

A

-3

253
Q

What is the Sedation Assessment Tool (SAT) score for responds to physical stimulation and few recognisable words?

A

-2

254
Q

What is the Sedation Assessment Tool (SAT) score for very anxious/restless and normal/talkative?

A

+1

255
Q

What is the Sedation Assessment Tool (SAT) score for very anxious and agitated and loud outbursts?

A

+2

256
Q

What is the Sedation Assessment Tool (SAT) score for very awake and calm/cooperative and speaks normally?

A

0

257
Q

What is the Sedation Assessment Tool (SAT) score forasleep but rouses if name is called and slurring or prominent slowing?

A

-1

258
Q

What is the suffix on the common name form for class II cardiac drugs

A

-lol

atenolol, bisoprolol, carvedilol, sotalol, propranolol

259
Q

What is the suffix of non cardiac affecting Class IV variant drugs?

A

-dipine

260
Q

What is the sulphonylureas pathophysiology?

A

Increase insulin release by pancreatic ẞ-cells by blocking K+ channels and forcing depolarisation, increasing Ca++, causing actomyosin filaments contraction, releasing insulin

261
Q

What is the TCA toxicity level for adults and paeds?

A

Adults 10-20mg/kg
Paeds 5mg/kg

262
Q

What is the TCA toxicity level for adults and paeds?

A

Adults 10-20mg/kg
Paeds 5mg/kg

263
Q

What is the timeframe and effects of hydrofluoric acid topical exposure?

A

70% HF for 20secs causes:
Full dermal penetration in 5mins
Full-thickness necrosis in 1hr
Complete necrosis of dermis & underlying structures in 24hrs

264
Q

What is the timing of development and symptoms of a funnel-web spider bite?

A

may develop within 10-15 minutes,
usually within 4 hours

265
Q

What is the timing of development and symptoms of a funnel-web spider bite?

A

may develop within 10-15 minutes,
usually within 4 hours

266
Q

What is the timing of development and symptoms of a funnel-web spider bite?

A

may develop within 10-15 minutes,
usually within 4 hours

267
Q

What is the timing of development and symptoms of a funnel-web spider bite?

A

may develop within 10-15 minutes,
usually within 4 hours

268
Q

What is the timing of development and symptoms of a redbackspider bite?

A
  • within minutes to hour:
    • significant local pain around the bit are
    • increased sweating around bite area
  • over hours:
    • pain becomes more severe and spreads proximally
    • diaphoresis
    • nausea
    • hypertensive
    • general malaise
  • severe cases may mimic acute abdo or cardiac chest pain
269
Q

What is the timing of development and symptoms of a redback spider bite?

A
  • within minutes to hour:
    • significant local pain around the bit are
    • increased sweating around bite area
  • over hours:
    • pain becomes more severe and spreads proximally
    • diaphoresis
    • nausea
    • hypertensive
    • general malaise
  • severe cases may mimic acute abdo or cardiac chest pain
270
Q

What is the timing of development and symptoms of a redbackspider bite?

A
  • within minutes to hour:
    • significant local pain around the bit are
    • increased sweating around bite area
  • over hours:
    • pain becomes more severe and spreads proximally
    • diaphoresis
    • nausea
    • hypertensive
    • general malaise
  • severe cases may mimic acute abdo or cardiac chest pain
271
Q

What is the timing of development and symptoms of a redback spider bite?

A
  • within minutes to hour:
    • significant local pain around the bit are
    • increased sweating around bite area
  • over hours:
    • pain becomes more severe and spreads proximally
    • diaphoresis
    • nausea
    • hypertensive
    • general malaise
  • severe cases may mimic acute abdo or cardiac chest pain
272
Q

What is the toxic dose of Metformin?

A

10g

273
Q

What is the toxic dose of NSAIDS?

A

greater than 400mg/kg

274
Q

What is the toxic dose of paracetamol?

A

greater than 150mg/kg

275
Q

What is the toxic dose of Phenelzine?

A

> 2mg/kg

276
Q

What is the toxic dose of tranylcypromine?

A

> 1mg/kg

277
Q

What is the toxicokinetics of CO toxicity?

A

Inhaled during respiration and binds to haemoglobin with affinity 200-240x that of oxygen (even higher for the foetus, also binds to mitochondrial enzymes within cells and distributed toall perfused tissues

278
Q

What is the toxicology of box jellyfesh venom?

A

impacts calcium channels in cell membranes, also haemolytic and dermatonecrotic

279
Q

What is the treatment approach for snake bites?

A
  • Immediate PIB & splinting
  • early sitrep, request backup if ALOC
  • Suctioning, expect vomitus, implement early advanced airway management
  • You MUST be prepared to ventilate the ALOC patient
  • expect hyperkalaemia due to rhabdomyolysis
  • Provide antiemetics & analgesics. Watch carefully for signs of anaphylaxis
  • Toxicological risk assessment & early hospital notification; consider bypass
  • Rapid transport for advanced cares (monovalent or polyvalent antidote, ICU)
280
Q

What is the treatment approach for snake bites?

A
  • Immediate PIB & splinting
  • early sitrep, request backup if ALOC
  • Suctioning, expect vomitus, implement early advanced airway management
  • You MUST be prepared to ventilate the ALOC patient
  • expect hyperkalaemia due to rhabdomyolysis
  • Provide antiemetics & analgesics. Watch carefully for signs of anaphylaxis
  • Toxicological risk assessment & early hospital notification; consider bypass
  • Rapid transport for advanced cares (monovalent or polyvalent antidote, ICU)
281
Q

What is the treatment approach for snake bites?

A
  • Immediate PIB & splinting
  • early sitrep, request backup if ALOC
  • Suctioning, expect vomitus, implement early advanced airway management
  • You MUST be prepared to ventilate the ALOC patient
  • expect hyperkalaemia due to rhabdomyolysis
  • Provide antiemetics & analgesics. Watch carefully for signs of anaphylaxis
  • Toxicological risk assessment & early hospital notification; consider bypass
  • Rapid transport for advanced cares (monovalent or polyvalent antidote, ICU)
282
Q

What is the treatment approach for snake bites?

A
  • Immediate PIB & splinting
  • early sitrep, request backup if ALOC
  • great symptomatically
283
Q

What is the treatment approach for snake bites?

A
  • Immediate PIB & splinting
  • early sitrep, request backup if ALOC
  • Suctioning, expect vomitus, implement early advanced airway management
  • You MUST be prepared to ventilate the ALOC patient
  • expect hyperkalaemia due to rhabdomyolysis
  • Provide antiemetics & analgesics. Watch carefully for signs of anaphylaxis
  • Toxicological risk assessment & early hospital notification; consider bypass
  • Rapid transport for advanced cares (monovalent or polyvalent antidote, ICU)
284
Q

What is the treatment for decompression illness?

A

laying the patient supine
100% oxygen
IV access
IV fluids

285
Q

What is the treatment for decompression illness?

A

laying the patient supine
100% oxygen
IV access
IV fluids

286
Q

What is the treatment for ethanols toxicity?

A

Consider:
oxygen (if hypoxic)
IV Access (if intent on fluid/med admin)
Ondansetron

287
Q

What is the treatment for ethanols toxicity?

A

Consider:
oxygen (if hypoxic)
IV Access (if intent on fluid/med admin)
Ondansetron

288
Q

What is the treatment for ethanols toxicity?

A

Consider:
oxygen (if hypoxic)
IV Access (if intent on fluid/med admin)
Ondansetron

289
Q

What is the treatment for ethanols toxicity?

A

Consider:
oxygen (if hypoxic)
IV Access (if intent on fluid/med admin)
Ondansetron

290
Q

What is the treatment for freezing injuries in a cold emergency?

A

Do not attempt rewarming until guaranteed re-freezing won’t happen
Removal of constricting items such as watches,bracelets and rings

291
Q

What is the treatment for hyperthermia?

A
  • Evaporative cooling
  • misting tepid (around 15C) water onto the patient and blowing warm air (around 40C) over them
  • Ice packs can be packed into the axilla and groin for further
  • cooling
  • cease cooling when pts temp reaches 39C
  • IV access
  • IV fluids (10-20ml/kg) - be mindful of pulmonary oedema
292
Q

What is the treatment for hyperthermia?

A
  • Evaporative cooling
  • misting tepid (around 15C) water onto the patient and blowing warm air (around 40C) over them
  • Ice packs can be packed into the axilla and groin for further
  • cooling
  • cease cooling when pts temp reaches 39C
  • IV access
  • IV fluids (10-20ml/kg) - be mindful of pulmonary oedema
293
Q

What is the treatment for hypothermia 30-35 degrees?

A

removal from the cold, damp conditions and passive rewarming
remove constricting items in localised cold injury

294
Q

What is the treatment for hypothermia 30-35 degrees?

A

removal from the cold, damp conditions and passive rewarming
remove constricting items in localised cold injury

295
Q

What is the treatment for hypothermia <30 degrees?

A

active re-warming:
* applying external heat source
* warm IV fluids
* warm air

296
Q

What is the treatment for hypothermia <30 degrees?

A

active re-warming:
* applying external heat source
* warm IV fluids
* warm air

297
Q

What is the treatment for non-freezing injuries in a cold emergency?

A

removal from the cold, damp conditions and passive rewarming

298
Q

What is the treatment plan for Hymenoptera envenomings?

A
  • Remove a bee stinger by scraping sideways with a straight-edged object such as a knife or credit card
  • Wash sting site with soap and water and apply a cold pack
  • Simple analgesics & NSAIDs can help with pain & inflammation
  • Antihistamines
  • Watch for anaphylaxis; treat per that CPG.
299
Q

What is toxicokinetics?

A

How the body absorbs, distributes, alters, and excretes toxicsubstances

300
Q

What is Wernicke encephalopathy (WE)?

A

acute neuropsychiatric syndrome that develops in certain alcohol-dependent individuals as a result of thiamine (B1) deficiency

301
Q

What is Wernicke encephalopathy (WE)?

A

acute neuropsychiatric syndrome that develops in certain alcohol-dependent individuals as a result of thiamine (B1) deficiency

302
Q

What might snake bite sites look like?

A
  • Mayappear as deep punctures or fine scratches
  • May have bruising
  • Appearance does not reliably indicate ‘dry’ or ‘wet’ bites
303
Q

What might snake bite sites look like?

A
  • Mayappear as deep punctures or fine scratches
  • May have bruising
  • Appearance does not reliably indicate ‘dry’ or ‘wet’ bites
304
Q

What might snake bite sites look like?

A
  • Mayappear as deep punctures or fine scratches
  • May have bruising
  • Appearance does not reliably indicate ‘dry’ or ‘wet’ bites
305
Q

What might snake bite sites look like?

A
  • Mayappear as deep punctures or fine scratches
  • May have bruising
  • Appearance does not reliably indicate ‘dry’ or ‘wet’ bites
306
Q

What mode is the first rhythm analysis done in?

A

AED

307
Q

What morbidities is chronic alcohol abuse is associated with?

A
  • Exacerbation of mental health conditions and psychosis
  • Wernicke’s encephalopathy
  • Cardiovascular disease
  • Chronic Liver disease
  • Pancreatitis
  • Nutritional deficiencies
  • Alcoholic Ketoacidosis
308
Q

What neurotransmitter do Selective serotonin reuptake inhibitors (SSRIs) act on

A

Serotonin (5HT) reuptake inhibitors

309
Q

What neurotransmitter do Selective serotonin reuptake inhibitors (SSRIs) act on

A

Serotonin (5HT) reuptake inhibitors

310
Q

What neurotransmitters do Tricyclic antidepressants (TCAs) act on?

A

5HT
noradrenaline reuptake inhibitors
receptor blockers

311
Q

What neurotransmittres do Serotonin noradrenaline reuptake inhibitors (SNRIs) act on?

A

5HT
noradrenaline reuptake inhibitors

312
Q

What observations should be undertaken on the restrained patient?

A

continual visual for signs of distress/difficulty
vital signs every 5 minutes of:
GCS
RR
SPO2
HR
BP
Perfusion assessment distal to mechanical restraint
BGL - initially
Temp - intially and then every 15 minutes

313
Q

What should the MAOI risk assessment identify?

A

type of MAOI

314
Q

What should you consider with regards to breathing in poisoned pts?

A

Adequate? Check and recheck the effect on respiratory drive (#1 threat!)

315
Q

What should you consider with regards to breathing in poisoned pts?

A

Adequate? Check and recheck the effect on respiratory drive (#1 threat!)

316
Q

What is the B in the ABCDER mnemonic for the risk assessment based approach in the poisoned patient?

A

Breathing
Adequate? Check and recheck the effect on respiratory drive (#1 threat!)

317
Q

What is the C in the ABCDER mnemonic for the risk assessment based approach in the poisoned patient?

A

Circulation
* Adequate? Shock? Dysrhythmias?

318
Q

What should you consider with regards to disability in poisoned pts?

A

Hs & Ts

319
Q

What is the D in the ABCDER mnemonic for the risk assessment based approach in the poisoned patient?

A

Disability
* 4 Hs & 4 Ts

320
Q

What is the E in the ABCDER mnemonic for the risk assessment based approach in the poisoned patient?

A

Exposure
* Surface decontamination
* isolate emesis
* ID causative agent

321
Q

What is the A in the ABCDER mnemonic for the risk assessment based approach in the poisoned patient?

A

Airway
Anticipate and prepare for airway loss or obstruction (vomiting, aspiration)

322
Q

What should you expect in digibind (digoxin-specific FB anti’b’s) toxicity Pts?

A

high level blocks
refractory VT/VF

323
Q

What should you look for when checking the body for exposure to a poison?

A

look for rashes and stings
suspect chemical if unkown cause

324
Q

What should you look for when checking the body for exposure to a poison?

A

look for rashes and stings
suspect chemical if unkown cause

325
Q

What symptoms of a thrombus will you see in organophosphate poisoning?

A

big pupurate clots throughout body

326
Q

What symptoms of a thrombus will you see in organophosphate poisoning?

A

big pupurate clots throughout body

327
Q

What symptoms of a thrombus will you see in organophosphate poisoning?

A

big pupurate clots throughout body

328
Q

What treatments should you consider when evidence of serious anticholinesterase pesticide poisoning is present?

A

atropine
oxygen
IPPV
IV access
IV fluid

329
Q

What treatments should you consider when evidence of serious anticholinesterase pesticide poisoning is present?

A

atropine
oxygen
IPPV
IV access
IV fluid

330
Q

What treatments should you consider when evidence of serious anticholinesterase pesticide poisoning is present?

A

atropine
oxygen
IPPV
IV access
IV fluid

331
Q

What type of drugs will cause dysrhythmias and seizures in overdose?

A

TCAs
Beta Blockers
Calcium Channel Blockers

332
Q

What type of drugs will cause dysrhythmias and seizures in overdose?

A

TCAs
Beta Blockers
Calcium Channel Blockers

333
Q

What type of drugs will cause dysrhythmias and seizures in overdose?

A

TCAs
Beta Blockers
Calcium Channel Blockers

334
Q

What type of drugs will cause dysrhythmias and seizures in overdose?

A

TCAs
Beta Blockers
Calcium Channel Blockers

335
Q

What type of foods have tyramine?

A

cheese
wine
pickled foods

336
Q

What type of toxicity/toxidrome does anticholinesterase pesticides cause?

A

cholinergic

337
Q

When does ethanol withdrawal syndrom usually present?

A

within 6 to 24 hours of cessation or reduction in ethanol consumption in dependent individuals

338
Q

When should NAC be administered to result in complete recovery from paracetamol overdose?

A

within 1st 8 hours

339
Q

Where are nematocysts primaily located on jellyfish?

A

the tentacles

340
Q

Which 2 irreversible MAOIs pose a greater risk of toxicity?

A

Tranylcypromine (Nardil)
Phenelzine (Parnate)

341
Q

Which drug is the common starting point for treating dpressive disorders?

A

SSRIs
SNRIs

342
Q

Which opioid is associated with seizure activity in an overdose?

A

Tramadol

343
Q

Which opioid receptor has thegreatest clinical effect?

A

mu

344
Q

Which opioide can produce a prolonged QT syndrome and hypoglycemia in an overdose?

A

Methadone

345
Q

Which reuptake process does Tramadol inhibit?

A

serotonin nd noradrenaline

346
Q

Whit signs and symptoms are evidence of severe toxicity?

A

seizures
coma
bronchospsm
bradycardia
hypotension
paralysis

347
Q

Whit signs and symptoms are evidence of severe toxicity?

A

seizures
coma
bronchospsm
bradycardia
hypotension
paralysis

348
Q

Whit signs and symptoms are evidence of severe toxicity?

A

seizures
coma
bronchospsm
bradycardia
hypotension
paralysis

349
Q

Who has higher risk factors for aspiration in benzodiazepine overdoses?

A

older people
cardiorespiratory comorbidities

350
Q

Why are Class 1c overdoses associated with significant morbidity & mortality?

A

due to complete sodium blockade & long effect

351
Q

Why can cocaine cause hypotension?

A

blocks fast sodium channels causing a toxic effect on the myocardium

352
Q

Why do wide complex tachyarrhythmias occur in cocaine toxicity?

A

Sodium and potassium channel blockades in addition to sympathomimetic, ischaemic and cardiomyopathic effects

353
Q

Why is theophylline and caffeine prescribed for COPD, asthma and similar conditions?

A

its sympathomimetic properties act as a bronchodilator

Bachelor of Paramedic Science (19 decks)

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