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CSB336 > Toxinology > Flashcards

Toxinology Flashcards

1
Q

What is anaphylaxis?

A

A severe life-threatening systemic hypersensitivity reaction *Note: ‘systemic’ can also called ‘generalised’*

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2
Q

By what mechanism does anaphylaxis cause death?

A

Upper airway obstruction, severe bronchospasm, or by profound anaphylactic shock

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3
Q

What are the two main types of anaphylaxis?

A

IgE dependent and IgE independent (also called non-allergic anaphylaxis and anaphylactoid reaction)

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4
Q

What is the key trigger for the majority of antigen-induced immune-mediated anaphylaxis?

A

IgE dependent activation of mast cells and basophils

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5
Q

True or false: rapid systemic development of anaphylaxis does not occur in persons who have previously been sensitised to the antigen

A

False - it occurs in those who have.

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6
Q

Describe IgE independent anaphylaxis

A
  • A clinical syndrome with identical symptoms to anaphylaxis and with release of the same inflammatory mediators, but follows non-immunological mechanisms
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7
Q

True or false: IgE independent anaphylaxis may occur on first exposure to an agent and doesn’t require a sensitisation period

A
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8
Q

List some things that can trigger IgE independent anaphylaxis

A
  • Radiography contrast media
  • Opioids
  • Muscle relaxants
  • Physical factors/exercise/temperature
  • IV immunoglobulin
  • Transfusion reaction to cellular elements (IgG, IgM)
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9
Q

Anaphylaxis results from the sudden release of mast cell and basophil derived mediators into circulation; name three of these.

A
  • Histamine
  • Cytokines
  • Chemokines
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10
Q

Synthesis of new mediators results from immunological reaction stimulation or any agent capable of producting a sudden ssytemic regranulation of mast cells or basophils; name three of these mediators.

A
  • Leukotrienes
  • Tumour necrosis factor
  • Prostaglandin
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11
Q

What is the pathophysiology of IgE dependent anaphylaxis?

A
  • Allergen-specific IgE molecules bind to mast cells and basophils via specialised receptors where they stay ready for a subsequent exposure
  • When challenged there is a specific allergen release of mediators and cytokines, causing symptoms of anaphylaxis
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12
Q

What is the pathophysiology of IgE independent anaphylaxis?

A

Certain allergens/substances can trigger the mast cell cascade directly without involving IgE as the initial mediator; reactions are dose-dependent

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13
Q

What is the effect of mast cell activation and granule release on the GIT, airways, and blood vessels?

A
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14
Q

Describe the clinical presentation of anaphylaxis

A
  • Rhinitis
  • Conjunctival erythema, tearing
  • Flushing
  • Itching
  • Urticaria
  • Angioedema
  • Dysphagia
  • Stridor
  • Throat and/or chest tightness
  • Dyspnoea/bronchospasm
  • Cough
  • Wheeze
  • Cyanosis
  • Palpitations
  • Tachy or bradycardia
  • ECG changes (T and ST changes)
  • Hypotension
  • CA
  • Vascular headache (typically ‘throbbing’)
  • Dizziness/syncope
  • Confusion
  • N+V+D
  • Abdo/pelvic pain
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15
Q

Describe the grading system for systemic hypersensitivity reactions and corresponding symptoms for each one

A
  • Mild - skin and subcutaneous tissues only
    • Generalised erythema, urticaria, periorbital oedema, angioedema
  • Moderate - features suggesting respiratory/cardiovascular/GIT involvement
    • Dyspnoea, stridor, wheeze, N+V, diaphoresis, throat/chest tightness, abdo pain
  • Severe - hypoxia, hypotension, neurological compromise
    • Cyanosis, SpO2 <92%, hypotension, confusion, syncope, LOC, incontinence
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16
Q

What two conditions can mimick upper airway oedema?

A
  • Dystonic reactions mimicking a swollen tongue
  • Acute oesophageal reflux (sudden onset of painful throat that feels like swelling; *acid reflux*)
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17
Q

Describe anaphylaxis mx

A
  • Remove causal agent
  • High flow O2 or IPPV
  • Adrenaline and salbutamol if indicated
  • Consider PIT if result of bite/sting
  • IV access, fluid therapy if indicated
  • ECG monitoring
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18
Q

Describe adrenaline and its use in rx of anaphylaxis

A
  • Alpha recepter agonist - reverses peripheral vasodilation, reduces angioedema and urticaria
  • Beta1 adrenergic stimulation - has positive inotropic and chronotropic effects on cardiac muscle
  • Beta2 adrenergic stimulation - leads to bronchodilation and stabilises mast cells by inhibiting histamine activation
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19
Q

True or false: Australian venomous snakes mainly cause systemic toxicity rather than local effects.

A

True

20
Q

Discuss pathophysiology of coagulopathy with regard to snake bites

A
  • Many snake venoms contain procoagulant toxins that activate the coagulation cascade
  • These cause venom-induced consumptive coagulopathy (VICC)
  • Brown snakes, tiger snakes, and taipans can cause significant coagulopathy
21
Q

Discuss the pathophysiology of neurotoxicity with regard to snake bites

A
  • Paralysis is a classic effect
  • Neurotoxicity is due to presynaptic neurotoxins which disrupt neurotransmitter release fom the terminal axon and are associated with cellular damage
  • This does not respond to antivenom
  • Manifests as progressive descending flaccid paralysis
  • First sign is ptosis, following by respiratory muscle paralysis peripheral weakness
22
Q

Discuss the pathophysiology of myotoxicity with regard to snake bites

A
  • Myotoxins damage skeletal muscles
  • Local or generalised muscle pain, tenderness, weakness
  • Muscle tissue breakdown causes release of myoglobin into the blood
  • Myoglobin can damage the kidneys (rhabdomyolysis); it is associated with myoglobinuria and rapidly increasing creatine kinase
23
Q

Describe presentation less than one hour following snake bite (varies depending on snake and pt)

A
  • Headache
  • N+V
  • Abdo pain
  • Transient hypotension associated with confusion or loss of consciousness
  • Coagulopathy
  • Regional lymphadenitis
  • Oedema
24
Q

Describe presentation one to three hours following snake bite

A
  • Paresis/paralysis of cranial nerves e.g. ptosis, double vision
  • Ophthalmoplegia, dysphonia, dysphagia, myopathic facies
  • Haemorrhage from mucosal surfaces, needle punctures
  • Tachycardia, hypotension
  • Tachypnoea, shallow tidal volume
25
Q

Discuss presentation more than three hours following snake bite

A
  • Paresis/paralysis of truncal and limb muscles
  • Paresis/paralysis of respiratory muscles (respiratory failure)
  • Peripheral circulatory failure (shock), hypoxaemia, cyanosis
  • Rhabdomyolysis
  • Dark urine (due to myoglobinuria or haemolysis)
26
Q

Describe the examination of a pt with a snake bite

A
  • Examine patient on exposed areas for bite marks or scratches
  • Look for local and regional tender lymphadenopathy
  • Perform a neurological assessment looking specifically for ptosis or diplopia or other evidence of muscle weakness
  • Examine muscles for tenderness and swelling
  • Check for myolysis; dark or red urine indicative of myoglobinuria (positive for “blood” and so may be mistaken for haematuria)
27
Q

Why is the onset of envenomation syndrome likely to be more rapid in children?

A

Higher ratio of venom to body mass

28
Q

Justify the PIT

A

The PIT impedes lymphatic flow, which is how many venoms gain circulatory access

29
Q

For what does the ARC recommend the use of PIT?

A
  • All Australian venomous snakes including sea snakes
  • Funnel web spider
  • Blue-ringed octopus
  • Cone shell snail
  • Bee, wasp, and ant stings in allergic pts
30
Q

What does the ARC not recommend the PIT for?

A
  • Other spider bites (PIT funnel web only)
  • Jellyfish stings
  • Fish stings (stonefish etc)
  • Bites or stings from scorpions, centipedes, beetles
31
Q

Describe phase one of funnel web spider toxicity

A
  • Occurs within minutes of the bite
  • Symptoms include:
    • Pain at the bite site
    • Perioral tingling
    • Piloerection (goosebumps)
    • Fasciculations (most prominent in the face, tongue and intercostals)
    • Fasciculations (may progress to more overt muscle spasm: masseter and laryngeal involvement may constitute a threat to the airway)
    • Tachycardia
    • Hypertension
    • Cardiac arrhythmias
    • N+V
    • Abdominal pain
    • Gastric dilatation
    • Diaphoresis
    • Pupillary asymmetry
    • Lacrimation
    • Salivation
    • Frank pulmonary oedema
    • Altered level of consciousness
32
Q

Describe phase two of funnel web spider toxicity

A

Resolution of the overt cholinergic and adrenergic crisis. Untreated pts may have gradual onset of refractory hypotension, apnoea, and CA

33
Q

What is the key toxin in redback spider bites and its chemical effect?

A

Alpha-latrotoxin - it acts as a presynaptic neurotoxin that stimulates the release of catecholamines from sympathetic nerves and acetylcholine from motor nerve endings in a syndrome known as latrodectism

34
Q

What clinical presentation is consistent with redback spider bites?

A

Local and/or spreading pain which can be generalised or regional, often severe

Increased and/or local sweating

Hypertension

Nausea

malaise

Insominia

Tender and swollen regional lymph nodes

Local piloerection

35
Q

Which direction should bee stings be scraped off?

A

Sideways

36
Q

How does the toxin carried by paralysis ticks induce its effect?

A

Causes progressive paralysis by interfering with presynaptic transmission in motor nerves; it can also cause a relapsing fever and other reactions

37
Q

Should you remove a paralysis tick from a pt?

A
38
Q

Describe the presentation of a box jellyfish sting

A
  • Severe localized pain
  • Wide (0.5 -1cm) erythematous lines (Whip weal with frosted ladder pattern)
  • Confusion, agitation
  • Pulmonary oedema
  • Unconsciousness
  • Collapse with respiratory failure and/or cardiac arrest
39
Q

Describe the typical presentation of Irukandji syndrome

A
  • Severe lower back pain
  • Muscle cramps
  • Nausea and vomiting
  • Restlessness
  • Anxiety and “sense of Impending doom”
  • Pulmonary oedema
  • Hypertension
  • Onset usually 5 -120 minutes post envenomation (average 30 minutes)
40
Q

True or false: vinegar or salt water are to be used for nematocyst (jellyfish sting) removal, not fresh water as it activates them

A

True

41
Q

What is the presentation of and indications for box jellyfish antivenom?

A
  • Cardiac arrest
  • Decreased LOC
  • Cardiac and/or respiratory distress or collapse
  • Total surface area affected > than half the surface area of one limb
  • Intractable pain unrelieved by pain relief management
  • Presentation: ampoules with 20,000 units of antivenom
42
Q

Describe box jellyfish antivenom administration

A
  • Adult/Child (Non-cardiac Arrest)
    • IVI 20,000 units
      • Preferred route
      • Administered over 10 minutes
    • IMI 60,000 units
      • May need multiple injection sites
  • Adult/Child (Cardiac Arrest)
    • IVI 20,000 units
      • Administered over 2 – 5 minutes
      • May be repeated up to 60,000 units
    • In this setting ensure that basic cares and standard cardiac arrest management have been instigated first
  • Be aware of potential for anaphylaxis
43
Q

Describe bluebottle jellyfish sting mx

A
  • Pick off any adherent tentacles with fingers
  • Rinse stung area well with seawater to remove invisible stinging cells - vinegar is not recommended
  • Place the victim’s stung area in hot water (no hotter than the rescuer can comfortably tolerate)
  • If local pain is unrelieved by heat, or if hot water is not available the application of cold packs or wrapped ice may be effective
44
Q

What is the pathophysiology of blue-ringed octopus contact?

A

Sting contains tetrodotoxin, which causes motor paralysis due to neuronal sodium channel blockade

45
Q

What is the presentation of cone shell snail or blue ringed octopus envenomation?

A
  • Painless bite
  • Numbness of lips and tongues
  • Respiratory difficulty leading to paralysis of respiratory muscles (death can occur within 30 minutes of bite)
46
Q

What are the divisions of clinical syndromes due to plant toxins?

A

*Note: dangerous ones are bracketed*

  • Gastrointestinal irritants (toxalbumins)
  • Cardiac toxins (cardiac glycosodes e.g. frangipani, oleander, and is also carried by some cane toads)
  • Proconvulsant plants
  • Hallucinogenic plants
  • Anticholinergic plants
  • Other hallucinogenic plants
  • “Stinging” plants
47
Q

List the types of seafood poisoning

A
  • Tetrodoxtoxin poisoning (sodium channel blocking neurotoxin - pufferfish)
  • Paralytic shellfish poisoning (mussels, oysters, clams, pipis, scallops, abalone, rock lobster, crab contaminated by eating dinoflagellate algae**)
  • Neurotoxic shellfish (NSP) poisoning (mollusks contaminated with brevetoxins)
  • Diarrhetic shellfish poisoning (bivalves)
  • Encephalopathic (amnesic) shellfish poisoning (domoic acid)
  • Ciguatera toxin poisoning (warm water finfish carrying ciguatera toxin)
  • Scombroid poisoning (ingestion of spoiled fish with high histamine levels; also called histamine fish poisoning)

CSB336 (14 decks)

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