POS- Week 1 Flashcards
Toxicity associated with HRT/Oral contraceptives
Low toxicity along with powder flower food, silica gel, zinc oxide cremes
Why is Paracetamol toxic?
Toxicity occurs via saturation of metabolic pathways. Toxic metabolite conjugated by gluthione but this is promptly depleted. Leads to OXIDATION and the formation of NAPQI
CCWhy does NAPQI lead to cellular death
NAPQI is the result of oxidation of paracetamol and binds to essential amino acids and results in cellular death
Clinical manifestation of paracetamol toxicity a) <24 hrs c) days after
a) <4 hrs: Progressive cyanosis, brown/blue MM, weakness and lethargy
b) Facial/Paw Oedema, vomiting, depression, methhaemaglobin
c) Severe methaemaglobinaema, hepatic necrosis
Cyanosis DOES NOT RESPOND TO OXYGEN THERAPY
What colour is Methaemaglobin? Significance in toxicity
Methaemaglobin is brown (apparent from 4-24 hrs) and days ahead post paracetamol toxicity.
Toxic metabolite NAPQI
At what dose should ingestion of paracetamol be treated?
Cat: 20mg/kg (i.e. any ingestion)
DogL 150mg/kg
Treatment for Paracetamol toxicity
Emesis (within 2 hrs) Apomorphin or Xylazine
Antidote: Acetylcystiene (precursor of glutathione)
Also SAMe
Ascorbic acid
Antidote for Paracetamol; how does it work?
Acetylcystiene which is a precursor of gluthione (try to prevent pathway being saturated so oxidation pathway doesn’t happen = NAPQI)
Continue treatment until clinically well
How to induce emesis in a) cat b) dog
a) Cat: Xyazine
b) Dog: Apomorphine
NSAID’s toxicity is largely due to ___ inhibition
NSAIDs toxicity is largely due to COX-1 inhibition
Carprofen and meloxicam are examples of
COX-2 inhibitors. (Flunixn and Phenylbutazone are non-selective)
Early and Late clinical manifestations of NSAIDs toxicity
Early: Gastrointestinal erosion, ulceration and potentially perforation. Vomiting/Diarrhoea (bloody), rarely CNS signs
Late: Renal/ Hepatic failure
NSAIDs treatment
No specific Antidote.
Emesis (optimal within 3 hrs, apomorphine/xyalizine)
Activated charcoal
Prevention of gastric ulceration: H2 receptor antagonists, proton pump inhibitors. ulcer healing
Supplement prostaglandin, maintenance of renal function (fluid therapy)
Examples of a) H2 receptor antagonist b) proton pump inhibitor
a) h2 receptor antagonist: Cimetidine, Ranitidine
b) proton pump inhibitor: Omeprazole
Approx toxic dose of a) white chocolate b) milk chocolate
Theobromine is toxic component of chocolate
a) white chocolate: 2200g/kg!!!!!!
b) milk chocolate: 9g/kg
c) dark choc: 1.25 g/ kg
Clinical effects of Theobromine toxicity
Vomiting/Diarrhoea/ Polydipsea/ Salivation/ Dehydration
CNS / Myocardial stimulation - tremor convulsion/ tachycardia
Renal failure
Severe cases- severe convulsions/ circulatory failure
Management of Theobromine toxicity
Emesis- apomorphine/ activated charcoal/ adequate rehydration
ECG/ Benzodiazapine for CNS stim.
Treatment of arrthymia (lidocaine/ beta blocker)
Tremorgenic Mycotoxins
Mycotoxins are fungal metabolites produced by mould. Normally mouldy food waste. Penitrem A/ Roquefortine.
How does toxicity come about from Penitrem A
Penitrem A is a Tremorgenic Mycotoxin (mould).
Interfers with release of neutrotransmitters (glytamate, aspartic acid/ GABA)
- Within 3 hrs whole body muscle tremors, tachycardia, nystagmus, bleparospasm
Onset of effects of Penitrem A
Usually within 3 hours; vomiting/ataxia whole body muscle tremors, rigidity with hyperextension of exrememeties, tachycardia, tachypnoea, nystagmus
Management of Tremorgenic Mycotoxins
from mould e.g. Penitrem A.
Decontaimination (emesis/ apomorphine./ activated charcoal)
Anticonvulsants (benzodiapine, barbiturate)
Allium species includes…
Which part is toxic
Large group of plants (>600), mostly pereenial bulbous herbs inc LEEKS, ONIONS, SHALLOTS, SPRING ONIONS, GARLIC/ CHIVE.
Contain organosulphoxides
Toxic dose of Allium species
e.g. onions/leeks/shallots.
>0.5% of body weight (therefore 5 g/kg)
Leads to Heinz body formation and anaemia
Clinical effects of Allium species
Due to organosulphoxides, forms mixed sulphide bond between haemaglobin and gluthione resulting in formation of Heniz bodies = damaged erythrocytes removed from circulation