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2023 ECC Board Exam > Environmental/Toxicology > Flashcards

Environmental/Toxicology Flashcards

1
Q

What is the toxic dose for xylitol?

A

100mg/kg → hypoglycemia secondary to insulin stimulation (within 30-60 min)

500mg/kg → hepatotoxicity, acute hepatic necrosis (6-72 hours)

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2
Q

What is the MOA of anticoagulant rodenticide?

A

Inhibit Vitamin K epoxide reductase

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3
Q

What is the difference in terms of the treatment duration for 1st and 2nd generation anticoagulant rodenticide toxicity?

A

1st generation: 2 weeks
2nd generation: 4 weeks

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4
Q

For anticoagulant rodenticide intoxication, why do we measure PT instead of PTT?

A

PT is used to assess extrinsic pathway, and factor VII has the shortest half-life (6.2hr) → being able to detect the abnormalities earlier

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5
Q

For anticoagulant rodenticide intoxication, when should you check PT if vitamin K is not administered?

A

48 hours after exposure (this is when factor VII are all used up)

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6
Q

What is the onset of the clinical signs of cholecalciferol rodenticide toxicity?

A

4-36 hours

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7
Q

What is the lethal dose for cholecalciferol in dogs?

A

1.5 - 8 mg/kg

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8
Q

What is the MOA of bromethalin?

A

Uncoupling of oxidative phosphorylation → decrease ATP production → Na/K-ATPase not working → organ dysfunction (muscle tremor, seizure, hyperthermia, extreme hyperexcitability, cerebral edema)

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9
Q

What is the lethal dose of bromethalin for dogs and cats?

A

Dog: 4.7 mg/kg
Cat: 1.8 mg/kg

ER textbook: LD50 dog 2.4 mg/kg; cat 0.3 mg/kg

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10
Q

Does Strychnine cause a net inhibitory or excitatory effect of the CNS?

A

Net excitatory effect (because it inhibits the inhibitory pathway)

It blocks post-synaptic glycine receptor -> block the inhibitory effect of glycine on the spinal cord motor neuron -> exaggerated excitatory effect

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11
Q

What is the MOA of organophosphate toxicity?

A

Irreversibly binds to AChE → prevent breakdown of ACh → overstimulation of both the muscarinic and nicotinic receptors

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12
Q

True or False: Polyradiculoneuritis usually doesn’t cause autonomic dysfunction.

A

True

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13
Q

What is the MOA of metaldehyde toxicity?

A

In the stomach, metaldehyde undergoes partial hydrolysis in the stomach to produce acetaldehyde.
Metaldehyde decreases the concentration of GABA, serotonin and norepinephrine in the CNS → decrease the threshold for seizures.
Monoamine oxidase activity is increased following metaldehyde exposure.
Muscle tremors and the production of acidic metaldehyde metabolites cause severe electrolyte disturbances and metabolic acidosis.

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14
Q

What is the clinical triad for serotonin syndrome?

A

Altered mentation
Autonomic instability
Neuromuscular abnormalities

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15
Q

Where are most of the serotonin stored at?

A

Enterochromaffin cells and the myenteric plexus in the GI tract

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16
Q

List 5 effects of serotonin in peripheral nervous system.

A

Vasoconstriction
Bronchoconstriction
Urinary retention
Increased GI peristalsis
Platelet aggregration

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17
Q

Which amino acid is essential for serotonin formation?

A

Tryptophan

  • Serotonin is formed in the body by hydroxylation and decarboxylation of the essential amino acid tryptophan by tryptophan hydroxylase
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18
Q

Can serotonin cross the BBB?

A

No

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19
Q

What are the two receptors mainly responsible for serotonin syndrome?

A

5-HT1
5-HT2A

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20
Q

What are the 5 mechanisms of serotonin toxicity?

A

1) Increased L-tryptophan → increased serotonin level in the neuron
2) Amphataminase → increased release of serotonin
3) MAO inhibitors → decreased serotonin metabolism → increased pre-synaptic level
4) Selective serotonin reuptake inhibitors (SSRI) → increased serotonin level at the synapse
5) Serotonin agonist → increased serotonin receptor activation

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21
Q

What type of drug is cyproheptadine?

A

Non-specific 5-HT1A and 5-HT2 receptor antagonist

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22
Q

What type of drug is chlorpromazine?

A

5-HT2 receptor antagonist; dopamine D2 receptor antagonist; phenothiazine derivative
* Side effect: hypotension

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23
Q

Does xylitol bind to activated charcoal? What about ethylene glycol?

A

Both toxins do not bind to activated charcoal

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24
Q

For NSAID intoxication, normally how long should the treatment be?

A

At least 3 half-lives

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25
Q

What are the 5 indications for extracorporeal therapies in AKI patients?

A
  • Azotemia refractory to conventional medical management
  • Anuria or severe oliguria
  • Severe uremic signs
  • Severe electrolyte or acid-base disturbances
  • Life-threatening volume overload
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26
Q

What is the lethal dose of ethylene glycol in dogs and cats?

A

Dogs: 6.6 ml/kg
Cats: 1.5 ml/kg

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27
Q

What are the toxic metabolites of ethylene glycol?

A

Glycolic acid
Oxalic acid

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28
Q

In a retrospective study published in 2020 by Groover and colleague looking at extracorporeal blood purification in acutely intoxicated veterinary patients, what are the 4 most common complications? What is the survival rate and average time of hospitalization?

A

Complications (18.3%)
- Mild hypotension
- Thrombocytopenia
- Clotting of the extracorporeal circuit
- Hemorrhage

Survival rate: 83.3%
Average time of hospitalization: 49.2 ± 37.7 h

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29
Q

What is half-life of phenobarbital in dogs?

A

48 hours

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30
Q

What are half-life of diazepam and midazolam in dogs?

A

Diazepam: 2.5 hr
Midazolam: 1.9 hr

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31
Q

What is the dose of flumazenil for diazepam toxicity?

A

0.05 mg/kg IV

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32
Q

What is the MOA of Baclofen?

A

GABA agonist

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33
Q

Why opioid can cause miosis in dogs?

A

Opioid stimulates the visceral nuclei of the oculomotor nuclear complex and the parasympathetic nerve that innervates the pupil.

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34
Q

True or False: Naloxone is a synthetic derivative of oxymorphone.

A

True

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35
Q

What is the dose of naloxone and what is the onset and duration?

A

Dose: 0.01-0.04 mg/kg
Onset: 1-2 minutes
Duration: 45-90 minutes

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36
Q

Why in 𝜷-blocker overdose/toxicity, mild hyperkalemia may be seen (2 reasons)

A

1) decreased cellular uptake of K+
2) lower aldosterone levels (β-blocker can suppress the catecholamine-induced renin release)

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37
Q

In a study published in 2004 by Vnuk and colleagues about high-rise syndrome in cats, falling from which floor or about which floor is associated with thoracic trauma?

A

7th floor or above

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38
Q

There are four degrees of burn wounds, what is their depth?

A

First-degree: only epidermis affected
Second-degree:
- Epidermis + superficial part of dermis - Painful to touch, hair follicles preserved
- Epidermis + deep part of the dermis - hair follicle destroyed, decreased pain sensation
- Healing by contraction and epithelialization (may need surgery)
Third-degree: Epidermis + full thickness of dermis
- Insensitive to touch
Fourth-degree: full thickness burn with extension to muscles, bone and tendon

  • In the JVECC review paper in 2012, they use superficial, superficial & partial thickness, deep partial thickeness, full thickness
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39
Q

In burn injury, how many percentage of the body surface area being involved can have severe metabolic derangement?

A

> 20%

  • It is also classified as severe burn injury
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40
Q

In a study published in 2021 by Henriksson and colleagues about body surface area in dogs, what are the BSA of the follow body parts?
Head
Thorax
Abdomen
Thoracic limbs
Pelvic limbs

A

Head 14%
Thorax 18%
Abdomen 14%
Thoracic limbs 9%
Pelvic limbs 11%

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41
Q

In a study published in 2021 by Henriksson and colleagues about body surface area in cats, what are the BSA of the follow body parts?
Head
Thorax
Abdomen
Thoracic limbs
Pelvic limbs

A

Head 13%
Thorax 20%
Abdomen 15%
Thoracic limbs 7%
Pelvic limbs 12%

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42
Q

After severe burn injury, patients usually will experience two phases with very different hemodynamic status. What are these two phases and what are the timing?

A

1) Resuscitation phase (hypodynamic or ebb phase)
- immediately after injury till 24-72 hours later
- Hypovolemic, decreased cardiac output, increased vascular permeability, vasoconstriction, decreased peripheral blood flow
2) Hyperdynamic hypermetabolic phase (flow phase)
- 3-5 days after injury
- decreased vascular permeability, increased heart rate, and decreased peripheral vascular resistance resulting in an increase in CO
- Release of counter-regulatory hormones, cortisol, glucagon, and catecholamines are the drive

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43
Q

When do the exfoliation of tracheal epithelial lining of the trachea and main-stem bronchi occur after smoke inhalation?

A

3-5 days later

  • High risk of bronchial obstruction
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44
Q

What is the definition of primary and secondary hypothermia?

A

Hypothermia: core body temperature < 37 C (98.6 F)
Primary: caused by excessive exposure to low environmental temperatures.
Secondary: a result of disease, trauma, surgery, or drug-induced alteration in heat production and thermoregulation

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45
Q

Where is the thermoregulatory center in the body?

A

Hypothalamus

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46
Q

What are the 4 primary mechanisms of heat loss?

A

Convection - body surface to air
Conduction -body surface to object
Radiation
Evaporation

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47
Q

Why hypotension develops in hypothermic patients?

A

Vascular responsiveness to norepinephrine at the α1-receptor decreases

48
Q

Does hypothermia-induced bradycardia atropine responsive?

A

No

49
Q

Why during severe hypothermia patient’s respiratory rate and tidal volume usually reduce?

A

Decrease CO2 production from the tissue → decreased respiratory drive

50
Q

What is the most commonly seen acid-base imbalance during marked hypothermia?

A

Respiratory acidosis & metabolic acidosis

  • Metabolic acidosis - decreased blood buffering capacity, decreased hepatic metabolism, decreased acid excretion from the urine, increased lactate due to shivering and decreased tissue perfusion
51
Q

List 3 coagulation changes during hypothermia.

A

1) Thrombocytopenia (sequestration by the liver and spleen)
2) Decreased platelet aggregation (secondary to decreased production of thromboxane B2, decreased platelet granule secretion, attenuation of P selectin expression, and diminished expression of the von Willebrand factor receptor )
3) Prolonged aPTT/PT

52
Q

For every 1C decrease in the temperature, how will the HCT change?

A

Increase by 2%

53
Q

Explain the pathophysiology of cold diuresis.

A

Vasoconstriction (before core temperature drops) → relatively increased blood volume → diuresis

Core temperature drops → decreased response to vasopressin → unable to reabsorb water at collecting tubule

In moderate hypothermia, GFR decreases due to decreased cardiac output and renal blood flow

54
Q

Explain the cause of hyperglycemia during moderate hypothermia.

A

1) Decreased cardiac output and renal blood flow → reduced renal clearance of glucose
2) Decreased insulin sensitivity
3) Decreased insulin secretion from the pancreas

55
Q

What is the pathophysiology of rewarming shock?

A

Active external rewarming can cause peripheral vasodilation → relative hypovolemia and hypotension

56
Q

What is core temperature afterdrop during the rewarming process?

A
  • Usually happens at the beginning of the rewarming
  • The cold peripheral blood returns to the core → decrease core body temperature even more
  • These complications are most likely to occur when the extremities are warmed before the core; therefore application of external heat should be focused on the truncal regions of the body, not the extrem- ities.
57
Q

What is the pathophysiology of rewarming acidosis.

A

The return of the peripheral blood is colder and has higher level of lactate → causes acidosis

  • These complications are most likely to occur when the extremities are warmed before the core; therefore application of external heat should be focused on the truncal regions of the body, not the extrem- ities.
58
Q

What is the recommended rewarming rate?

A

0.5 - 2 C/hr

59
Q

When the environmental temperature increases, which two of the heat dissipation mechanisms are responsible for 70% of the thermoregulation?

A

Convection
Radiation

60
Q

What are the three protective mechanisms of the body during increased heat?

A

1) thermoregulation
2) acute-phase response
- leukocytosis
- synthesis of acute-phase proteins ↑
- stimulate the hypothalamic-pituitary-adrenal axis, - activate endothelial cells and WBCs
3) intracellular heat shock proteins
- protect against denaturation of intracellular proteins - help to regulate the baroreceptor response during heat stress → preventing hypotension

61
Q

Describe the pathophysiology of heat stroke

A

Release of IL-1 & IL-6 from the muscles + endotoxin from GI tract → WBCs & endothelium activation → proinflammatory and antiinflammatory cytokines + activation of coagulation cascade → microthrombosis & tissue injury → MODS

62
Q

What number of NRBC is highly associated with death?

A

18 NRBC/100 leukocytes

63
Q

When should the active cooling be discontinued in heat stroke to prevent rebound hypothermia?

A

103F

64
Q

List 8 poor prognosis indicators in heat stroke.

A

Hypoglycemia
DIC
MODS
> 18 NRBC/100 leukocyte
Hypocholesterolemia
Hyperbilirubinemia
Hypoalbuminemia
Elevated creatinine
Ventricular arrhythmias
Obesity
Seizure
Prolonged aPTT/PT

65
Q

At the same amperage, which will cause more severe injury, alternating current or direct current?

A

Alternating current

66
Q

What type of arrhythmias does low-voltage current more likely to cause? What about high-voltage current?

A

Low-voltage current: V-fib
High-voltage current: asystole

67
Q

Describe 4 types of hypersensitivity reactions and what immunoglobulins or cells are involved.

A
68
Q

List 5 anaphylaxis mediators in the classic pathway.

A

Histamine
Tryptophan
Heparin
Kallikreins
Proteases
Proteoglycans
Eosinophilic chemotactic factor of anaphylaxis
Neutrophil chemotactic factor of anaphylaxis

69
Q

What are the two mechanisms of anaphylaxis?

A

1) Classic pathway
Body is sensitized → IgE is produced and bind to mast cells or basophils (through FcεRI) → repeated exposure of the antigen → cross-link of bound IgE → cell degranulation (histamine, tryptophan, heparin, kallikreins, proteases, proteoglycans)
2) Alternative pathway
IgG-FcγRIII-macrophage pathway
The only difference is PAF is the main anaphylaxis activator

70
Q

Which anaphylaxis pathways cause more severe clinical signs?

A

Classic pathway (IgE)

71
Q

There are three types of histamine receptors. What are their functions?

A

H1: mediate coronary artery vasoconstriction & cardiac depression; bronchoconstriction, peripheral vasodilation
H2: mediate gastric acid production; when stimulated, produce coronary and systemic vasodilation & increases in HR and ventricular contractility
H3: presynaptic autoreceptor, inhibit histamine release and activation of sympathetic nerve system

72
Q

What is the epinephrine dose for anaphylaxis?

A

0.05 mcg/kg/min IV via CRI
2.5-5.0 mcg/kg IV

73
Q

If patient is on 𝜷-blocker and has anaphylaxis, what drug should you reach for?

A

IM or IV administration of glucagon

74
Q

What is the rationale of glucocorticoid in anaphylaxis?

A

Suppress the arachidonic acid cascade → reduce the severity of the late-phase inflammatory reaction (4-6 hours)

75
Q

Which type of hypersensitivity does serum sickness belong to?

A

Type III

76
Q

True or False: A while IgG can activate complement but F(ab’)2 cannot.

A

True

Fc is the part that binds to complement (C1q)

77
Q

What is the MOA of apomorphine?

A

Dopamine agonist (induce vomiting via D2 receptor)

78
Q

What is the dose for gastric lavage in dogs?

A

60 - 90 ml/kg for 5-10 times

79
Q

True or False: Intralipid 20% is hypertonic.

A

False

Isotonic (so can be given at peripheral vein)

80
Q

What is the antidote for ethylene glycol? What is the MOA?

A

Fomepizole (4-MP)

Fomepizole is a competitive inhibitor of alcohol dehydrogenase

81
Q

What are the two antidote for organophosphate?

A

Atropine
Pralidoxime chloride (2-PAM): competes for OP on acetylcholinesterase and prevents retention of OP on the receptor

82
Q

How is intralipid metabolized?

A

cleared up by skeletal muscles, splanchnic viscera, myocardial cells, and subcutaneous tissues
→ broken down into glycerol, free fatty acids, and choline

83
Q

Does activated charcoal work for bromethalin intoxication?

A

Yes

And it does undergo enterohepatic recirculation

84
Q

Does activated charcoal work for cholecalciferol intoxication?

A

Yes

it also does undergo enterohepatic recirculation

85
Q

List 4 treatments for cholecalciferol.

A

1) IV fluid therapy
2) Furosemide
3) Steroid administration (2–3 mg/kg/day prednisone or 0.1 mg/kg/day dexamethasone SP)
4) Bisphosphonates (pamidronate 1.05–2 mg/kg IV diluted in saline and given over 2 hours)

86
Q

Write down the metabolism of ethylene glycol and the enzymes involved.

A
87
Q

What clinical signs can glycoaldehyde cause?

A

CNS signs

  • Ethylene glycol itself is also CNS depressant and can cause GI irritation
88
Q

What metabolites from ethylene glycol contribute to AKI?

A

Glycolic acid → direct renal tubular epithelium injury
Oxalic acid → form calcium oxalate crystal and deposit in the tubular lumen

89
Q

In ethylene glycol intoxication, when does the second phase kicks in? What about 3rd phase? What are the clinical findings in each phase?

A

Second phase: 12-24 hours after ingestion
- Metabolic acidosis, hypocalcemia, tachyarrhythmias
Third phase: 24-72 hours in dogs and 12-24 hours in cats after ingestion
- AKI, oliguria

90
Q

In ethylene glycol intoxication, what is the earliest blood work change? What is normal osmolal gap?

A

Increased osmolal gap
Normal: < 10 mOsm/L

91
Q

Why hyperglycemia may be seen in ethylene glycol intoxication?

A

Aldehyde metabolites can inhibit glucose metabolism

92
Q

When does calcium oxalate monohydrate present in the urine?

A

3-6 hours after ingestion

93
Q

What is the time frame for Kacey test?

A

1-6 hr to 48-72 hr

94
Q

What is the MOA of fomepizole (4-MP) and ethanol?

A

inhibiting the function of alcohol dehydrogenase (ADH) so EG can be peed out

95
Q

What is the dose for 4-MP?

A

20mg/ kg 5% IV initially, followed by 15mg/kg IV at 12 and 24 hours and 5mg/kg IV at 36 hours

In cats, a higher dose is required at 125 mg/kg IV initially, then 31.25 mg/kg IV at 12, 24, and 36 hours

96
Q

True or False: Both COX-1 and COX-2 play a role in prostaglandin synthesis and maintenance of gastric mucosal integrity.

A

True

97
Q

Does aspirin under enterohepatic recirculation?

A

No

98
Q

What is the toxic dose for Naproxen and the organs involved?

A

> 5 mg/kg: GI signs
10–25 mg/kg: renal damage
50 mg/kg: CNS signs

99
Q

List 3 electrolyte abnormalities in dogs with grapes/raisins toxicity.

A

Hypercalemia
Hyperphosphatemia
Hypokalemia/Hyperkalemia

100
Q

What is the pathophysiology of cocaine toxicity? How is it metabolized?

A

Sympathomimetic effects from reuptake inhibition of NE, serotonin, and dopamine

Metabolized via hydrolysis by plasma and hepatic esterase and 10-20% is excreted unchanged in urine

  • Cocaine produces anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. This is achieved by reversibly binding to and inactivating sodium channels.
101
Q

What is the pathophysiology of Methamphetamine toxicity?

A

Sympathomimetic effects from inhibition of monoamine oxidase (MAO), increased catecholamine release, and direct dopamine and serotonin receptor agonism.

102
Q

What is the toxic dose for xylitol to cause hepatic necrosis and hypoglycemia?

A

Hypoglycemia: > 0.1 g/kg
Hepatic necrosis: > 0.5 g/kg

103
Q

What are the three main components in chocolate that contributes to its toxicity?

A

Caffeine
Methylxanthines
Theobromine

CNS stimulant

104
Q

True or False: In human studies of burn injury, inhalation injury is an independent predictor of death.

A

True

Particularly in patients with cutaneous burns ≥ 20% BSA

105
Q

According to 2016 NEJM Fire-Related Inhalation Injury, what is the recommended mechanical ventilation mode for smoke inhalation injury?

A

Pressure control, lung-protective ventilation

106
Q

In patient with burn injury, what lab abnormalities raises concerns for cyanide toxicity?

A

persistent metabolic acidosis despite hemodynamic normalization

107
Q

What is hunting reaction/response?

A

When the extremities/skin is exposed to cold temperature, there may be alternating vasoconstriction and vasodilation

108
Q

Name 4 substances in the crotalinae snake venom and the clinical signs caused by each substance.

A

Hyaluronidase - break-down of connective tissue
Phospholipase A2 - cytotoxicity, echinocytes, anti-Xa activity
Thromboxane - thrombocytopenia
snake venom metalloproteinases (SVMPs) - platelet dysfunction

Neurotoxin
Myotoxin

109
Q

True or False: The antivenom with F(ab’)2 has larger volume of distribution, less antigenic and shorter half-life compared to complete immunoglobins

A

True

110
Q

What are the toxins for Coral snakes?

A

Neurotoxin
Hemolysin

111
Q

How do elapid snake neurotoxin work?

A

Pre-synaptic: phospholipase A2 group of toxins → prevent release of acetylcholine

Post-synaptic: antagonist at acetylcholine receptors

112
Q

What is the Consensus formula (Parkland formula) for burn injury fluid therapy?

A

Administer isotonic crystalloid at 4ml/kg per percentage of TBSA in the first 24 hours, with half of this amount administered at the first 8 hours, and the remainder over the rest of 16 hours.

  • For cats: reduce the amount by 25-50%
113
Q

True or False: According to the ABA guidelines, preload-driven strategies for burn resuscitation are strongly recommended to prevent fluid overload.

A

False

Preload-driven strategies for burn resuscitation are not advisable because neither preload or cardiac output restoration is achievable within the first 24 hours.

114
Q

What is the recommended target urine output in patient with severe burn injury?

A

0.5-1 ml/kg/hr

  • Human:
    Adult 0.4 ml/kg/hr
    Pediatric 1 ml/kg/hr
115
Q

Mafenide acetate can be used in burn wound. What is the MOA?

A

Potent carbonic anhydrase inhibitor

116
Q

True or False: According to the ABA guidelines, vitamin C is recommended for severe burn injury.

A

True

117
Q

True or False: In severe burn injury, early and more aggressive surgical debridement attenuates hypermetabolic response and decreases infection rate.

A

True

2023 ECC Board Exam (24 decks)

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