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Critical Care > Environmental emergencies > Flashcards

Environmental emergencies Flashcards

1
Q

What are the three protective mechanisms of the body against heat stroke?

A

Thermoregulation, acute-phase response, increased expression of intracellular heat shock proteins

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2
Q

How does the carboxyhaemoglobin affect the oxygenhaemoglobin curve?

A

An increase Carboxyhaemoglobin will shift the oxygenhaemoglobin curve left and lower than normal

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3
Q

When does carbon monoxide cause overt signs? and neurological dysfunction? and loss of conciousness?

A

> 15% and >30% and >50%

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4
Q

When are the delayed neurological sequelae of carbon monoxide toxicity?

A

between 3-240 days post-intoxication

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5
Q

What is the main treatment for carboxyhaemaglobin?

A

Oxygen therapy, FiO2 100% = 40-80min half life of CO

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6
Q

What is methaemaglobin?

A

Inactive form of haemaglobin when the iron molecule is oxidised to the ferric (Fe3+) state

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7
Q

Which way does the cruve shift with methaemaglobinaemia?

A

LEFT

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8
Q

Why are feline haemaglobins more susceptible to oxidative damage?

A

Feline haemaglobin has 8 sulfhydryl groups and canine has 4 sulfhydryl groups. The feline spleen is less effective at filtering out oxidative damage??

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9
Q

What are the antioxidant defences in the erythrocyte?

A

Glutathionine, XX, XX

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10
Q

What are Heinz bodies?

A

Aggregates of denatured haemaglobin within erythrocytes that form as oxidated-haemaglobin is metabolised. Ghost cells

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11
Q

What causes methaemaglobinaemia?

A

Paracetamol, laryngeal sprays, nitrates, nitrites (nitroglycerin/nitroprusside), congenital (methaemoglobin reductase deficiency), allium plants, zinc, methylene blue, mothballs, repeated propofol in cats, copper

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12
Q

Diagnosis of methaemaglobin?

A

20% on co-oximetry

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13
Q

Treatment of methaemaglobin?

A

Remove source, oxygen, N-acetylcystine

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14
Q

What is the MOA of N-acetylcystine?

A

Interacts with NAPQI

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15
Q
A
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15
Q

What are the risks of methylene blue?

A

Can cause oxidative damage itself, in cats more so, and can potentiate haemolytic anaemia.

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15
Q

What is the MOA of methylene blue?

A

Increases rate of reduction of metHb through increasing NADPH dehydrogenase.

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16
Q

What are the 5 causes of hypoxia?

A

Hypoventilation, Low FiO2, Ventilation-perfusion mismatch, Right to left shunting, Diffusion

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17
Q

What factors and proteins are affected by vit K?

A

2, 7, 9, 10, protein C and S

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18
Q

Which factor has the shortest half life? and how long

A

Factor 7 and 6.5hrs

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19
Q

Order of affected factors in VIt K deficiency?

A

Factor 7, PT, Factor 9, APTT

20
Q

What are the difference between FP and FFP?

A

Labile factors of 5 and 8 (decreased activity in FP)

21
Q

What is the pathophys of cholecalciferol rodenticide tox?

A

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.

22
Q

What is the MOA of frusemide in calciuresis?

A

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.

23
Q

What are treatments for hypercalcaemia?

A

IV fluids, emesis/decontamination, frusemide, steroids, biphosphanates, calcitonin

24
Q

What is the diagnostic criteria for anaphylaxis?

A

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

25
Q

What are the MOA of the 4 histamine receptors?

A
  • 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
26
Q

What are the mediators released from mast cells?

A

Histamine, typtase, heparin, cytokines, platelet activating factor

27
Q

What are biochem findings for grape/raisin ingestion

A

Hyperphos, hyperCa, increased renal value

28
Q

What is MOA of TCAs?

A

Inhibition of pre synaptic amine pumps responsible for reuptake of norepinephrine and serotonin

29
Q

What is atropine MOA?

A

Muscarinic acetylcholine inhibitor, vagolytic as competes with binding sites of acetylcholine at SA and AV nodes

30
Q

Cyanobacteria can produce major toxins…?

A

Microcystins, anatoxins

31
Q
A
32
Q

What is the MOA of microcystins from cyanobacteria?

A

Enters hepatocytes. Induces free radical formation and mitochondrial alterations.

33
Q

What are the clinical signs of microcystin toxicity?

A

V/D, hyperK, hypoGlu, seizures, nephrotixicity, hepatic failure, death

34
Q

What are treatments for microcytin ingestion?

A

Rifampin (competes for uptake), prophylactic treatment including glutathione, silymarin, cyclosproine A, antixoxidants (vit E, selenium)

35
Q

What are the three types of anatoxin

A

Anatoxin-a, homoanatoxin-a, anatoxin-a(s)

36
Q

What are the MOA of anatoxins?

A

Anatoxin-a, homoanatoxin-a are Cholinergic agonists.
Anatoxin-a(s) is an acetylcholinesterase inhibitor.

37
Q

What is the active ingredient and effect of onion and garlic intoxication?

A

Organosulfoxides. Oxidative damage to the RBC -> heinz body formation, methaemaglobin formation leading to haemolysis, haemaglobinuria and secondary nephrosis

38
Q

What are clinical signs of onion and garlic toxicity?

A

GI signs, impaired oxygen transportation (resp signs), haemolysis, antithrombotic effect

39
Q

What are the treatments for onion and garlic toxicity?

A

Emesis, activated charcoal, IVFT, blood transfusion for anaemia, oxygen therapy, antioxidants (vit E, NAC, vit C)

40
Q

What is the MOA of mycotoxins?

A

Metabolites produced by fungi that cause neurotoxicosis. Primarily penitrem A (Penicillum species) and also roqueforine C.

41
Q

What are clinical signs of myoctoxin ingeston?

A

Muscle tremors, ataxia, seizures, vomiting, diarrhoea, hyperaesthesia, nystagmus, hyperthermia

42
Q

What diagnostics for mycotoxin ingestion?

A

Elevation in liver enzymes, azotaemia, CK increase, dehydration. Could test suspected foodstuffs, stomach ingesta or vomitus for presence of penitrem A or roqueforine C.

43
Q

What are treatments for mycotoxin ingestion?

A

Decontamination, benzodiazepines, methocarbamol, IVFT, antiemetics, intra-lipid.

44
Q

What are the MOA of intralipid?

A

Lipid sink (sequesters lipophilic compounds), improved myocardial performance (there are specifics to this which are not included), provides kcal

45
Q

What are the side effects of intralipid?

A

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

46
Q

What are the properties of venom?

A

Phospholipase A2 (inflammatory), Thromboxane A2 (platelet aggregation), Proteases (platelet dysfunction), Hyaluronidase and collagenases (allow venom dissemination)

47
Q

What is the mechanism of phospholipase A2?

A

Anticoagulation via anti-Xa activity

48
Q
A

Critical Care (8 decks)

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