Environmental emergencies Flashcards
What are the three protective mechanisms of the body against heat stroke?
Thermoregulation, acute-phase response, increased expression of intracellular heat shock proteins
How does the carboxyhaemoglobin affect the oxygenhaemoglobin curve?
An increase Carboxyhaemoglobin will shift the oxygenhaemoglobin curve left and lower than normal
When does carbon monoxide cause overt signs? and neurological dysfunction? and loss of conciousness?
> 15% and >30% and >50%
When are the delayed neurological sequelae of carbon monoxide toxicity?
between 3-240 days post-intoxication
What is the main treatment for carboxyhaemaglobin?
Oxygen therapy, FiO2 100% = 40-80min half life of CO
What is methaemaglobin?
Inactive form of haemaglobin when the iron molecule is oxidised to the ferric (Fe3+) state
Which way does the cruve shift with methaemaglobinaemia?
LEFT
Why are feline haemaglobins more susceptible to oxidative damage?
Feline haemaglobin has 8 sulfhydryl groups and canine has 4 sulfhydryl groups. The feline spleen is less effective at filtering out oxidative damage??
What are the antioxidant defences in the erythrocyte?
Glutathionine, XX, XX
What are Heinz bodies?
Aggregates of denatured haemaglobin within erythrocytes that form as oxidated-haemaglobin is metabolised. Ghost cells
What causes methaemaglobinaemia?
Paracetamol, laryngeal sprays, nitrates, nitrites (nitroglycerin/nitroprusside), congenital (methaemoglobin reductase deficiency), allium plants, zinc, methylene blue, mothballs, repeated propofol in cats, copper
Diagnosis of methaemaglobin?
20% on co-oximetry
Treatment of methaemaglobin?
Remove source, oxygen, N-acetylcystine
What is the MOA of N-acetylcystine?
Interacts with NAPQI
What are the risks of methylene blue?
Can cause oxidative damage itself, in cats more so, and can potentiate haemolytic anaemia.
What is the MOA of methylene blue?
Increases rate of reduction of metHb through increasing NADPH dehydrogenase.
What are the 5 causes of hypoxia?
Hypoventilation, Low FiO2, Ventilation-perfusion mismatch, Right to left shunting, Diffusion
What factors and proteins are affected by vit K?
2, 7, 9, 10, protein C and S
Which factor has the shortest half life? and how long
Factor 7 and 6.5hrs
Order of affected factors in VIt K deficiency?
Factor 7, PT, Factor 9, APTT
What are the difference between FP and FFP?
Labile factors of 5 and 8 (decreased activity in FP)
What is the pathophys of cholecalciferol rodenticide tox?
Metabolised to 25-hydroxycholecalciferol -> renal 1-alpha hydroxylase-> 1,25 dihydroxycholecalciferol which binds to vitamin D receptors. 25-hydroxy is more toxic, causing an increase in calcium release and absorption.
What is the MOA of frusemide in calciuresis?
Inhibits Na Cl K co-transporter, therefore stops excretion of positive ions out of the lumen and therefore stops absorption of Mg and Ca into the lumen.
What are treatments for hypercalcaemia?
IV fluids, emesis/decontamination, frusemide, steroids, biphosphanates, calcitonin
What is the diagnostic criteria for anaphylaxis?
Acute onset AND respiratory orhypotension/collapse.
OR
Exposure to likely allergen adn two or more of the following: cutaneous signs, respiratory compromise, hypotension/collapse, GIT signs.
OR
Hypotension after exposure to known allergen
What are the MOA of the 4 histamine receptors?
- H1 receptor: activates smooth muscle contraction and endothelial changes → vasodilation and increased vascular permeability.
- H2 receptor: best known for modulating gastric acid secretion and regulation of cardiac myocytes.
- H3: involved in PERIPHERAL neurotransmitter release respectively, as well as mediating immune response
- H4 receptors: involved in CENTRAL neurotransmitter release respectively, as well as mediating immune response
What are the mediators released from mast cells?
Histamine, typtase, heparin, cytokines, platelet activating factor
What are biochem findings for grape/raisin ingestion
Hyperphos, hyperCa, increased renal value
What is MOA of TCAs?
Inhibition of pre synaptic amine pumps responsible for reuptake of norepinephrine and serotonin
What is atropine MOA?
Muscarinic acetylcholine inhibitor, vagolytic as competes with binding sites of acetylcholine at SA and AV nodes
Cyanobacteria can produce major toxins…?
Microcystins, anatoxins
What is the MOA of microcystins from cyanobacteria?
Enters hepatocytes. Induces free radical formation and mitochondrial alterations.
What are the clinical signs of microcystin toxicity?
V/D, hyperK, hypoGlu, seizures, nephrotixicity, hepatic failure, death
What are treatments for microcytin ingestion?
Rifampin (competes for uptake), prophylactic treatment including glutathione, silymarin, cyclosproine A, antixoxidants (vit E, selenium)
What are the three types of anatoxin
Anatoxin-a, homoanatoxin-a, anatoxin-a(s)
What are the MOA of anatoxins?
Anatoxin-a, homoanatoxin-a are Cholinergic agonists.
Anatoxin-a(s) is an acetylcholinesterase inhibitor.
What is the active ingredient and effect of onion and garlic intoxication?
Organosulfoxides. Oxidative damage to the RBC -> heinz body formation, methaemaglobin formation leading to haemolysis, haemaglobinuria and secondary nephrosis
What are clinical signs of onion and garlic toxicity?
GI signs, impaired oxygen transportation (resp signs), haemolysis, antithrombotic effect
What are the treatments for onion and garlic toxicity?
Emesis, activated charcoal, IVFT, blood transfusion for anaemia, oxygen therapy, antioxidants (vit E, NAC, vit C)
What is the MOA of mycotoxins?
Metabolites produced by fungi that cause neurotoxicosis. Primarily penitrem A (Penicillum species) and also roqueforine C.
What are clinical signs of myoctoxin ingeston?
Muscle tremors, ataxia, seizures, vomiting, diarrhoea, hyperaesthesia, nystagmus, hyperthermia
What diagnostics for mycotoxin ingestion?
Elevation in liver enzymes, azotaemia, CK increase, dehydration. Could test suspected foodstuffs, stomach ingesta or vomitus for presence of penitrem A or roqueforine C.
What are treatments for mycotoxin ingestion?
Decontamination, benzodiazepines, methocarbamol, IVFT, antiemetics, intra-lipid.
What are the MOA of intralipid?
Lipid sink (sequesters lipophilic compounds), improved myocardial performance (there are specifics to this which are not included), provides kcal
What are the side effects of intralipid?
Fat embolism, phlebitis, fat overload syndrome, coagulopathy, pancreatitis, worsening ARDS, interaction with other drugs, acute adverse pyrogenic reaction, allergic reaction to egg phospholipid/soybean component
What are the properties of venom?
Phospholipase A2 (inflammatory), Thromboxane A2 (platelet aggregation), Proteases (platelet dysfunction), Hyaluronidase and collagenases (allow venom dissemination)
What is the mechanism of phospholipase A2?
Anticoagulation via anti-Xa activity
