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Principles of Science > Toxicology > Flashcards

Toxicology Flashcards

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1
Q

How does paracetamol toxicity occur and to what species?

A

Highly toxic to cats! Occurs via saturation of metabolic pathways. Conjugated by glutathione- glutathione promptly depleted. Cellular death. Cats lack metabolic capacity to detoxify paracetamol

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2
Q

What are the clinical manifestations of paracetamol toxicity?

A

Early (<4hr)- progressive cyanosis, weakness and lethargy
4-24hr- facial and paw oedema, V+, depression, methaemoglobinaemia
Days- severe methaemoglobinaemia, hepatic necrosis

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3
Q

What is the treatment for paracetamol toxicity?

A

Doesn’t respond to O2 therapy.
Emesis (optimal w/in 2hrs)- apomorphine (Ds), xylazine (Cs)
Activated charcoal
Antidote- acetylcysteine (precursor of glutathione)
Additional- SAMe, ascorbic acid

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4
Q

What are the clinical manifestations of NSAID toxicity?

A

Early- GI erosion, ulceration and poss perforation, V+/D+, rarely CNS symptoms (ataxia, lethargy, drowsiness)
Late- RF, hepatic impairment
Largely due to COX-1 inhibition. Therapeutic action due to COX-2 (PG suppression)

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5
Q

What is the treatment for NSAID toxicity?

A

Decontamination: emesis (optimal w/in 3hrs)- dogs apomorphine; activated charcoal (repeat doses)
Prevention of gastric ulceration: H2-R antagonists (cimetidine, ranitidine, famotidine), proton pump inhibitors (omeprazole), ulcer healing/ coating agent (sucralfate)
PG supplementation- misoprostol
Maintenance of renal function- IVFT

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6
Q

What are the clinical effects of theobromine toxicity?

A

V+/ D+, PD, salivation- dehydration. CNS/ myocardial stimulation (tremor, convulsions, tachycardia, hypertension), RF. Fatal cases- severe convulsions/ circulatory failure

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7
Q

What is the treatment for theobromine toxicity?

A

Emesis- apomorphine
Repeat dose activated charcoal
Adequate rehydration
Monitor vital signs, ECG, benzodiazepines for CNS stim, tx of arrhythmia (lidocaine/ B blocker)

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8
Q

What are tremorgenic mycotocins?

A

Fungal metabolites produced by mould. Penitrem A may interfere w/ release of NTs (glutamate, aspartic acid and GABA). Onset of action usually w/in 3hrs- V+, ataxia, tremors, rigidity w/ hyperextension of extremities, hyperactivity, hyperaesthesia, tachycardia, panting, tachypnoea, nystagmus and blepharospasm. Svere- convulsions, coma w/ paddling, rhabdomyolysis

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9
Q

What is the treatment for tremorgenic mycotoxin toxicity?

A

Decontamination: emesis (apomorphine), gastric lavage, activated charcoal (recirculation)
Anticonvulsants- benzodiazepines, barbiturates, methocarbamol
Supportive care- rehydration, cooling, ventilation, antiemetics

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10
Q

What are the allium sp and what is their mechanism of toxicity?

A

Large group of plants incl leeks, onions, shallots, garlic
Contain organosulphoxides, trauma to plant converts to organic sulphur compounds. Within erythrocytes reduce the protective effect of the antioxidant, glutathione (remains in oxidative state). Mixed sulphide bond forms between Hb and glutathione–> heinz body formation. Damaged erythrocytes removed inducing anaemia.

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11
Q

What are the clinical effects of allium sp toxicity?

A 
Variable onset, signs of haemolysis can be delayed for 1-5d, heinz bodies w/in 24hr.
GI effects (V+, inappetance, onion smelling breath), heinz body anaemia (lethargy, pale MM, tachycardia, tachypnoea), haematurea and haemoglobinurea
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12
Q

What is the management for allium sp toxicity?

A

Emesis. Activated charcoal. Monitor haem parameters. IVFT. Anti-emetics if needed
Supportive- high protein diet may restore glutathione, supplemental O2 in severe cases, oxyglobin/ blood transfusion in crictal

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13
Q

What is the mechanism of toxicity of anticoagulant rodenticides?

A

Inhibit vit K reductase. Thus depletion of vit K and so reduction in factors II, VII, IX and X- essential for production of fibrin.

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14
Q

What are the clinical effects of anticoagulant rodenticide toxicity?

A

Clinical effects rare. Delay between exposure and effects due to 1/2 life. Onset 24-72hrs. Elevation of PT time. Main effect is haemorrhage. May present w/ dyspnoea, lethargy, weakness or anorexia. Bruising, bleeding from gums, GIT, nose, wounds.

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15
Q

What is the treatment for anticoagulant rodenticide toxicity?

A

Not always necc
If required- decontamination by emesis (apomorphine, xylazine) or activated charcoal. If elevation in PT/ symptomatic then Vit K therapy. In severe intoxication whole blood transfusions may be required.

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16
Q

What are the clinical signs of molluscicide (metaldehyde) toxicity?

A

Hypersalivation, V+, D+, ataxia, panting, tremors, convulsions, hyperthermia.
Resp and cardiac effects less common.
Fatalities usually due to resp failure.

17
Q

What is the management for molluscicide toxicity?

A

Most common fatality for VPS. Emetics? Gastric lavage? Activated charcoal.
Management of convulsions- benzoizepines, propofol+ midazolam. Consider referral?

18
Q

What is the presentation of Vipera berus toxicity?

A

European adder- only venomous snake in UK. Can cause significant morbidity but low mortality. Dry bites. Venom- proteases, peptide hydrolases, hyalyronidase and phospholipases.
Hypovolaemia and local oedema (incr vasc perm), cardiac effects, renal impairment may be due to hypovolaemic shock.

19
Q

What is the tx for vipera berus toxicity?

A

IVFT, antivenom. Monitor BO, pulse, resp, temp, ECG, BT (check for coagulopathy), renal and hepatic parameters
Analgesia- opiod (not NSAIDs due to renal risks), abx (rare), antihistamines

20
Q

What adverse reactions can occur to vipera berus antivenom?

A

Uncommon
Early (anaphylactic)- urticaria, V+, fever, tachycardia. In severe there can be hypotension, bronchospasm. Tx- adrenaline, steroids and antihistamines
Serum sickness- days after, fever, urticaria, joint pain, lymphadenopathy. Tx- steroids and antihistamines

21
Q

What is lipid rescue therapy?

A

Used to tx dogs poisoned w/ lipophilic drugs: moxidectin, avermectin, ivermectin. Thought that lipid component formed in blood acts as a sink for lipophilic substances making them unavailable to act on their target Rs.

22
Q

What is xylitol toxicity?

A

Found in chewing gum, naturally occurring in fruit and beg. Rapid stimulator of insulin release. Requires gastric decontamination and monitoring.
Hypoglycaemia tx- frequent small meals, glucose/ dextrose, ECG monitoring
Hepatotoxicity tx- consider immediate dextrose therapy, SAMe

23
Q

What is the effect of the MDR-1 gene mutation of collies, shepherd dogs?

A

MDR-1 codes for P-gp- a large transporter protein which acts as an efflux pump. Most commonly associated w/ toxicity from MLs (ivermectin, moxidectin, doramectin, milbemycin, selamectin), loperamide, vinca alkaloids (vincristine)

24
Q

What are endotoxins vs exotoxins?

A

Endotoxins- lipid A portion of LPS of G-ve OM.
Exotoxins- classically produce by G+ve, protein and heat labile e.g. collagenases, haemolysins, also produced by some G-ve e.g. cholera toxin, E Coli enterotoxins. Useful as basis for vaccine

25
Q

What is the pathophysiological effect of endotoxins?

A

Interaction w/ R on macrophage membrane, recognized by PRRs on host cells. Stimulates production of TNF and IL-1. Induces fever, leucopenia, hypotension, activation of C3, DIC, shock and death

26
Q

What are some examples of neurotoxins?

A

Botulinum toxin- blocks release of ACh at synapse and NMJ–> flaccid paralysis and death
Tetanus- blocks release of NTs at inhibitory synapses causing uncontrolled excitatory synapse activity- paralysis

27
Q

What are superantigens?

A

E.g. staphylococcus aureus TSST-1. Immunomodulators which induce massive T cell activation and cytokine release. Binds to invariable regions on MHCII on APC- process of T cell activation is short circuited.

28
Q

What physiological differences in neonates influence drug handling?

A

Decr GI motility, underdeveloped gut flora and immature mucosal enzymes all lead to decr absorption of some drugs
Incr total body water (polar drugs have a larger vol of distribution)
Immature liver metabolic capacity
Decr GFR and renal tubule function

29
Q

Describe monensin toxicity in horses?

A

From eating feed meant for sheep. CS related to neuronal, skeletal muscle and cardiac muscle effects of ionophores. Susceptibility due to low 1st pass metabolism in horses compared to ruminants making systemic bioavailability much higher than sheep.

30
Q

Why are pyrethroids toxic to cats?

A

Probably due to ineffective metabolism- lack of glucuronidyl transferase. Target is voltage dependent sodium channel- leads to repetitive firing of neurons

31
Q

What are the 5 primary agents of concern wrt food poisoning?

A 
Camplylobacter
Salmonella
Listeria
E Coli
Norovirus
Other: s.aureus, bacillus cereus, c.perfringens, c.botulinum, vibrio parahaemolyticus. TSE
32
Q

What is campylobacter?

A

Curved G-ve rod. C.jejuni (poultry), C.coli (pigs). Microaerophilic, thermophillic. Endemic in animals. Dx by culture of faeces (blood agar w/ abx selection, 48hrs). Zoonotic

33
Q

How does campylobacter cause dz?

A

Incubation 2-5d. Colonises the SI and causes enteritis. D+, V+, stomach pains, cramps, fever, unwell. Cooking always kills Campylobacter

34
Q

What is listeriosis?

A

Can grow at low temp. Transmitted in faeces- soil, vegetation, silage, udder. Ingestion can cause encephalitis and bacteraemia causing abortion. Grows and proliferates in epithelial cells, phagosomal escape, cytosolic replication, direct cell to cell spread. Normal adults rel resistant and cooking always kills.

35
Q

What is norovirus?

A

Winter vomiting bug (ssRNA). Person to person spread, food or food handles. Faeces. Calicivirus. Small infective dose. Resistant in environment. Cooking and disinfection always kill the virus.

36
Q

What is E coli O157?

A

Shiga toxin producing Coli= STEC. Toxin encoded by bacteriophage which infects the E COli. Toxins- ST 1 and ST 2. Some D+ and haemorrhagic colitis in calves but generally just carry. Adheres to villus surface and injects toxin into cells, causing vascular damage, oedema, thrombi. Cooking destroys pathogen. Detection by culture and latex agglutination test
Carriage by calves–> beef. Can get onto cooked foods. Only need low dose–> haemorrhagic colitis and haemolytic uraemic syndrome–> RF

37
Q

What is Salmonella?

A

Many animals carry small no. Infectious dose quite high. Vaccination reduced carriage by FAs, broilers and layers. Control means incidence significantly decr. Cooking always kills. Dx by culture and serotyping.

38
Q

What are the other causes of food borne dz?

A

S.aureus- heat stable enterotoxins, must be incubated 6-12hrs for toxin to form
Bacillus cereus- rice, cooking activates spores, toxin produced during subsequent incubation
C.perfingens type A- 5% strains produce enterotoxin
C.botulinum- faeces and soil- botulinum toxin in heated, anaerobic foods (canned/ bottled)
Vibrio parahaemolyticus- shellfish

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