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From Flashcardlet > Toxins and Venom > Flashcards

Toxins and Venom Flashcards

0
Q

What are the clinical sighs of aldicarb toxicity?

A

Muscarinic overstimulation

SLUDGE

Salivation, lacrimation, urination/urinary incontinence, defecation/diarrhea, gastric cramping, and emesis

Additional symptoms of the cholinergic toxidrome include miosis, bronchorrhea, bradycardia, and lethargy

Niconitic overstimulation: tachycardia, hypertension, muscle fasciculations, tremors, respiratory depression, respiratory failure

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1
Q

What is the MOA of aldicarb?

A

Carbamate

Inhibits acetylcholinesterase leading to hyper excitability of cholinergic receptors

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2
Q

Minimum lethal dosage of EG in dogs vs cats?

A

4.4-6.6 ml/kg dogs, 1.5 ml/kg cats

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3
Q

List the pathway for ethylene glycol.

A

EG, glycoaldehyde, glycolate, glyoxylate, oxalate
(al-co-oxy-oxa)

ADH converts EG to glycoaldehyde AND glycoaldehyde to glycolate

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4
Q

What is the rate limiting step in EG pathway?

A

glycolate to glyoxylate

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5
Q

What are the most toxic metabolites of EG on a per weight basis?

A

glyoxylate and glycoaldehyde; HOWEVER, b/c of its longer half life and greater systemic accumulation, GLYCOLATE is thought to be the major mediator IN VIVOR

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6
Q

The CNS effects that occur during the first 12 hours of exposure to EG thought to be due to…

A
  1. aldehyde metabolites
  2. hyperosmolality
  3. metabolic acidosis
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7
Q

Clinical signs during 30 min to 12 h exposure to EG?

A

Depression, incoordination, ataxia, seizures, paresis, vomiting, coma, PU/PD, proprioception deficits, LMN signs, muscle fasciculations, hypothermia

Like me when drunk:)

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8
Q

Clinical signs from 12 h to 24 h exposure to EG?

A

Sometimes resolution CNS signs (cats sometimes remain severely depressed), tachycardia, tachypnea, hypothermia, muscle fasciculations

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9
Q

Clinical signs 24-72h post exposure to EG?

A

Severe GI signs, oliguria/anuria, seizures, death, anorexia, oral ulcerations, ptyalism

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10
Q

Rise in osmolal gap ocurs as early as __ hr in cats and dogs and typically peaks by ___ hrs dogs.

A

1 hr, 6 hrs

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11
Q

How long does the osmolal gap remain elevated after EG ingestion?

A

up to 18 h

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12
Q

What is the normal osmolal gap?

A

10 mOsm/kg

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13
Q

What method is best to determine the osmolal gap?

A

freezing point depression

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14
Q

What normally develops in 3 hr of ingestion of EG?

A

high anion gap normochloremic metabolic acidosis

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15
Q

Why does EG cause hypocalcemia?

A

chelation of calcium with oxalic acid to form calcium oxalate crystals

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16
Q

Hyperglycemia is seen in over 70% of patients with EG toxicity. Proposed mechanims?

A
  1. aldehyde induced inhibition of glucose metabolism
  2. increased epinephrine
  3. increased endogenous cortisol
  4. uremia
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17
Q

When are calcium oxalate crystals seen?

A

w/i 3 hr in cats, 4-6 hr dogs

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18
Q

What can be done to the urine to help determine if EG toxicity?

A

Wood’s lamp the urine - will fluoresce up to 6 h after ingestion of toxin

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19
Q

What can cause a false positive EG test?

A
  1. propylene glycol
  2. glycerol
  3. lactate dehydrogenas
  4. lactic acid
  5. less than 50 mg/dl EG
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20
Q

What causes acidosis with EG toxicity?

A
  1. Metabolic products of EG (glycolic acid aka glycolate)

2. Increased lactic acid production caused by NAD depletion during EG metabolism

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21
Q

Disadvantages to using ethanol to tx EG tox?

A
  1. exacerbates hyperosmolality
  2. exacerbates osmotic diuresis
  3. worsens metabolic acidosis by enhancing formation of lactate from pyruvate
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22
Q

How does ethanol cause hypoglycemia?

A

Metabolized to acetaldehyde which impairs gluconeogenesis

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23
Q

Advantages of 4MP?

A
  1. Greater affinity for ADH than ethanol

2. Not associated with CNS depression, hyperosmolality, or osmotic diuresis

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24
Q

What’s different b/t cats and dogs regarding use of 4MP?

A

Cats require much higher doses, up to 6 times higher

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25
Q

What therapies are used to prevent metabolism of glycoxylic acid (glyoxalate) to toxic end products?

A

Thiamine (converts it to alpha hydroxy and beta ketoadipate) and pyridoxine (converts it to glycine then hippurate, needs benzoate)

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26
Q

Signs of muscarinic overstimulation?

A

PNS: vomiting, diarrhea ptyalism, urination, bradycardia, miosis, bronchorrhea, tenesmus

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27
Q

Signs of nictotinic overstimulation?

A

SNS: tachycardia, hypertension, mydriasis

CNS: agitation, coma, respiratory depression/failure

NM jxn: muscle fasciculation, weakness, paralysis

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28
Q

Anastasio, JVECC, 2011. What were the most common clinical signs of acute aldicarb toxicity?

A

vomiting (M 93%), ptyalism (M 86%), diarrhea (M 80%), tremors (N 73%)

others: dull mentation, bradycardia (M), increased resp effort, miosis (M), ataxia (N), hyperthermia, tachycardia (N), mydriasis (N), tenesmus (M), resp failure (N)

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29
Q

DDx for acute aldicarb toxicity?

A
  1. intoxication (other carbamate, OPs, nicotine, phenothiazines,
    mushrooms with muscarine)
  2. envenomation (spider, scorpion, neurotoxic snake)
  3. Infectious dz (botulism, lepto, encephalitis, meningitis)
  4. Neuro dz (epilepsy, cerebral vasculitis, subarachnoid or subdural hemorrhage or hematoma)
  5. metabolic dz (uremia, hypo or hyper glu, myxedema coma, thyrotoxicosis)
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30
Q

What is methiocarb?

A

molluscicide and insecticide, carbamate, less toxic than aldicarb

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31
Q

How do you make a definitive diagnosis of aldicarb toxicity?

A

gas chromatography or mass spectrometry on tissue, urine, vomit, stomach contents

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32
Q

How is measuring AChE activity helpful with aldicarb tox?

A

<25% diagnostic if C/S fit

Not reliable in cats b/c of presence of pseudocholinesterase in feline erythrocytes

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33
Q

What was most common lab abnormalities with aldicarb tox?

A
  1. lactic acidosis

2. hyperglycemia

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34
Q

How does atropine help with aldicarb tox?

A

parasympatholytic - helps with muscarinic sings (not nicotinic)

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35
Q

What are side effects of atropine?

A

GI stasis, constipation and prolonged retention of toxin, dry mouth, thirst, mydriasis, tachycardia, dysphagia, if severe then dyspnea, ataxia, muscle tremors, resp failure, death

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36
Q

How is aldicarb excreted?

A

kidneys

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37
Q

What about aldicarb causes respiratory failure?

A

peripheral - profound NM weakness d/t nictonic overstim

central - depression of medullary resp center

others: aspiration pneumonia, bronchorrhea, bronchoconstriction

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38
Q

How could diphenhydramine be helpful with aldicarb tox?

A

blocks nicotinic receptor overstimulation (only been shown effective due to OP tox, not carbamate tox)

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39
Q

How is 2-PAM helpful?

A

oximes decrease toxicity of cholinesterase inhibitors by reactivating cholinesterases (used for OP tox, not really needed for carbamate b/c spontaneous hydrolysis occurs that rapidly reactivates AChE); HOWEVER, may be synergistic with atropine with carbamate toxicity from human studies

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40
Q

What was survival in aldicarb tox paper?

A

91%

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41
Q

What 6 systems are evaluated on the SSS?

A 
pulmonary
cardiovascular
local wound
GI system
hematologic system
CNS
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42
Q

In humans, SSS > ___ is considered severe?

A

8

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43
Q

Immediate adverse effects of antivenom.

A

Bradycardia, 2nd degree AV block, agitation, injection of pinnae and sclera, vomiting, fever, nausea, tachycardia, trembling, anaphylaxis

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44
Q

OPCA is ___ times as otent as ACP

A

5.2

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45
Q

Size of ACP vs OPCA

A

150 kDa vs 50 kDa

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46
Q

Intralipid is from what fat?

A

soybeal oil based emulsion of long chain triglycerides

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47
Q

Fat overload syndrome can cause…

A

fat embolism, hyperlipidemia, hepatomegaly, icterus, splenomegaly, thrombocytopenia, increased clotting times, hemolysis

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48
Q

Adverse effects on pulmonary system from ILE.

A

increased PAP, increased venous admixture, decreased PaO2/FiO2, increased A-a, intrapulmonary shunting

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49
Q

ILE improvement theories

A
  1. Improved myocardial performance by providing energy substrate
  2. Drug sequestration or lipid sink theory
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50
Q

The higher the log P value, the more lipophilic a drug or chemical becomes. T/F

A

T

P>1

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51
Q

How does heparin treat complications of ILE?

A

Heparin causes the release of LPL and hepatic lipase from endothelium, an can potentially act as the rate limiting step in metabolism of triglycerides

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52
Q

Side effects of cholinesterse inhibitors.

A

Pharnygeal and bronchial secretions, increased pharyngeal and bronchial secretions, diarrhea and enhanced GI peristalsis, increased urination, resp depression, arrest if desensitization blockade (abundance Ach at synapse)

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53
Q

What is a cholinergic crisis?

A

result of cholinergic overload at NM jxn secondary to inhibition of cholinesterase

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54
Q

Atropine MOA in cholinergic crisis.

A

competes with acetylcholine for the postsynaptic muscarinic receptor (does nothing for nicotinic receptors but helps with bronchospasm and bronchorrhea)

55
Q

Neurotoxin from Clostridium tetani

A

tetanospasm - prevents release of inhibitory neurotransmitters and results in unopposed muscle excitation and dysautonomia

56
Q

Beneficial effects of Mg for tetanus?

A

Nonspecific calcium channel blocker (decreases calcium entry into presynaptic terminals and decreases release of ACh)

Decreases sensitivity of postsynaptic motor endplates to ACh - relaxation

57
Q

What is the earliest sign of Mg toxicity?

A

deep tendon hyporeflexia

58
Q

Effects of venom A?

A

Irreversible, pre-synaptic acting neurotoxin composed of acidic peptide and basic protein.

Acidic: noncompetitive CCB blocks ACh release

Basic: acts like PLA2 to hydrolyze acetyl bond on phospholipids

59
Q

Effects of venom B?

A

edema, tissue necrosis

proteolytic enzymes and cytotoxins

hyaluronidase and collagenase spread venom, protease cause coagulopathy

60
Q

Most common signs of cats vs dogs with essential oil products. Genovesse, JVECC, 2012

A

Cats - behavioral changes, seizures, tremors
Dogs - lethargy

92% clinical signs, 50% resolved with bath, 50% needed more care

61
Q

What are terpenes?

A

essential oils that are rapidly orally and dermally absorbed d/t lipophilic nature

62
Q

Salbutamol (albuterol) inhaler toxicity dogs…

A

tachycardia, hypokalemia, oral burns!! (pressurized hydrocarbons cause frostbite)

63
Q

Incidence of neurotoxicity from rattlesnake envenomation?Julius, JVECC, 2012

A

5.4%

64
Q

Findings from Julius, JVECC, 2012, Neurotoxicity in cats/dogs from rattlesnake envenomation.

A
  1. incidence 5.4%
  2. No diff b/t type of antivenom or #vials and neurotox, LOH, or survivial
  3. 11.8% PPV, half survived
  4. Overall mortality 18%
  5. Cats * longer LOH
  6. Cats overrepresented with neuro signs
  7. Diphenhydramine and colloids assc’d with survival
65
Q

Crotalidae polyvalent immune Fab (ovine) antivenom made from…

A

Eastern and Western diamondbacks, Mojave rattlesnake, cottonmouth

66
Q

ACP antivenom made from….

A

horses inoculated with Eastern and Western diamondback, Central and South American rattlesnakes, Fer-de-Lance

67
Q

What is myokymia?

A

muscle fasciculation associated with envenomation

MOA: interaction of venom components with calcium or calcium binding sites on the nerve membrane

68
Q

MOA of Mojave toxin?

A

inhibits ACh release at PRESYNAPTIC terminal of the NM jxn, causing inhibition of NM transmission and eventually complete NM blockade

69
Q

MOA for hypokalemia from snake envenomation?

A

release of endogenous epinephrine that stimulates beta receptors on the cell surface, thereby stimulating Na-K-ATPase pumps, leasing to intracellular shift of potassium

70
Q

Toxic dose 5FU

A

5 mg/kg, lethal at 40 mg/kg

71
Q

Signs os 5FU toxicity

A

CNS (seizures, depression, ataxia, tremors), respiratory (cyanosis, distress), GI (diarrhea, vomiting, salivation), cardiac arrhythmias, death, severe myelosuppression, ocular signs

72
Q

5-FU MOA

A

metabolism of 5FU into fluorouridine triphosphate that then interferes with RNA synthesis and fxn; inhibits thymidylate synthase via FdUMP which leads to depletion of thymidine 5’ monophopshate and thymidine 5’ triphosphate thus accumulating deoxyuridine mono- and tri- phosphate - goes into new DNA and doesn’t work well leading to cell death

73
Q

How do you treat seizures from 5-FU?

A

phenobarb, meperidine, anesthesia - diazepam not effective

74
Q

What is the neurotoxin MOA coral snakes?

A

postsynaptic alpha-neurotoxins; block the nicotinic acetylcholine receptors of NM jxns and cause a curare-like effect characterized by vasomotor instability, CNS depression, and muscle paralysis

75
Q

Coral snake venom inhibits….plt aggregation.

A

ADP

76
Q

What lab parameters were elevated in all coral snake dogs?

A

AST and CK

77
Q

T/F - Both dogs and cats show hemolysis after coral snake envenomation.

A

F - only dogs

78
Q

Clinical signs of marijuana toxicity

A

CNS depression, ataxia, mydriasis, increased sensitivity to motion or sound, hyperesthesia, ptyalism, tremors, acute onset urinary incontinence

79
Q

Toxic compound marijuanan.

A

delta-tetrahydrocannabinol (delta-THC)

80
Q

MOA permethrins

A

modulate sodium ion channels, causing them to say open for a longer period of time, resulting in repetitive discharging of excitable cells

81
Q

How do you know of a drug is lipid soluble?

A

partition coefficient, log P reported to indicate lipophilicity, higher values = greater lipophilicity

82
Q

MOA for lipids

A
  1. Lipid sink

2. Cardioprotective by provision of FAs which are major substrate of cardiac ATP production, + cardiac inotropic effects

83
Q

Potential adverse effects of lipids

A

acute allegic rxns, anaphylactoid reactions, fat overload syndrome (liver, fat embolism, thrombocytopenic, coagulopathy), sepsis, neuro signs, thrombophlebitis

84
Q

Osmolality of 20% lipids

A

350 mOsm/kg

85
Q

Lipid antidote

A

heparin

86
Q

Most common clinical sign from SSRI intoxication

A

CNS depression (JVECC, 2012)

neuro and GI most common overall signs

87
Q

How is serotonin made?

A

from tryptophan via enzymes tryptophan hydroxylase and tryptophan decarboxylase

88
Q

Where is serotonin made?

A

most in CNS and enterochromaffin cells, some platelets

95% stored in GI enterochromaffin cells and plts

89
Q

Where is serotonin stored in CNS?

A

presynaptic vesicles of serotonergic neurons, pineal gland, and catechoalminergic neurons

metabolized by monoamine oxidase (MAO)

90
Q

What SSRI was associated with dose effect on clinical signs?

A

fluoxetine (JVECC, 2012)

91
Q

What is the toxin in mountain laurel (rhododendron) and MOA.

A

grayanotoxins - bind to sodium channels in excitable cell membranes of nerve, heart, skeletal muscle which increases membrane permeability of sodium ions in the excitable membranes, thus maintaining the cells in the state of depolarization

92
Q

Salicylate toxicity MOA

A

uncouples oxidative phosphorylation and disturbs Krebs

93
Q

Antidote for salicylate toxicity

A

none

94
Q

Principle tx of salicylate toxicity

A
  1. urinary alkalinization to increase rate of excretion

2. hemodialysis effective

95
Q

Mechanism of GI signs in salicylate toxicity

A

Direct antagonism of prostaglandins which normally serve to increase epithelial cell turnover and mucus/bicarb secretion

96
Q

What acid base disturbance seen with severe salicylate toxicity?

A

respiratory alkalosis or mixed (metabolic acidosis with respiratory alkalosis)

Toxin directly stimulates respiratory center causing tachypnea and respiratory alkalosis –> kidneys get rid of bicarb which makes it worse for impending metabolic acidosis (lactate and ketoacids)

97
Q

What type of metabolic acidosis seen with salicylate tox?

A

increased AG metabolic acidosis (lactate and ketoacids accumulate d/t uncoupling of oxidative phosphorylation)

98
Q

What lung problem can occur with salicylate toxicity?

A

noncardiogenic pulmonary edema

99
Q

Goals of urinary alkalinization with salicylate toxicity?

A

NaHCO3 to keep urine pH 7.5-8 and blood pH 7.35-7.5

Increases renal excretion 10-20X

100
Q

Why is it important to prevent hypokalemia with salicylate toxicity?

A

Potassium reabsorption prevents excretion of an alkaline urine b/c of the exchange of potassium for hydrogen in the distal tubule (intercalated type A cell)

101
Q

What is the rational for empirically supplementing glucose with salicylate toxicity

A

neuroglycopenia can occur despite a normal blood glucose

102
Q

Amphetamine toxicity MOA

A

indirect-acting sympathomimetic amines and clinical signs d/t enhanced adrenergic stimulation and serotonin syndrome. Hyperdynamic sage can cause severe hyperthermia with rhabdomyoloysis, CNS signs, AKI, metabolic abnormalities

103
Q

Cocaine MOA

A

inhibits presynaptic neuronal uptake of dopamine, NE, and serotonin, and causes blockade of fast sodium channels = neuro and cardio signs

104
Q

Phencyclidine MOA

A

dissociative that antagonizes NMDA operated calcium channels; causes marked CNS depression or stimulation; increased ICP, also acts on delta-receptors causing dysphoria and hallucinations

105
Q

What 2 drugs may antagonize the effects of amphetamines and cocaine by antagonizing or blocking catecholamines

A

chlorpromazine, haloperidol

106
Q

Why do dogs become PU/PD after ingestion of cholecalciferol?

A

inhibition of ADH

107
Q

MOA of cardiac arrhythmias after cholecalciferol ingestion?

A
  1. mineralization of heart
  2. changes in ratio of IC to EX ion concentratione
  3. increase in depolarization threshold
108
Q

Tx cholecalciferol ingestion?

A

Tx hypercalcemia - saline diuresis to induce calciuresis, furosemide, glucocorticoids, salmon calcitonin (can cause anaphylaxis), pamidronate

calcitonin and pamidrongate inhibit osteoclastic activity

109
Q

LD50 bromethalin dogs vs cats

A

dogs 4.7 mg/kg, cats 1.8 mg/kg

110
Q

MOA bromethalin

A

uncouples oxidative phosphorylation, Na, K ATPase pumps fail, in goes water – cerebral edema and neuro predominate as clinical signs

Enterohepatic recirculation, lots of charcoal

111
Q

Histopathologic evidence of bromethalin toxicity?

A

diffuse white matter vacuolation (spongy degeneration) with microgliosis

112
Q

What enhances zinc phosphide toxicity?

A

food b/c gastric acid secretion; once ingested and in acidic environment zinc phosphide hydrolyzed to phosphine gas and free radicals

113
Q

Strychnine MOA

A

prevents uptake of glycine at inhibitory synapses of Renshaw cells in CNS; inhibition of an inhibitory pathway called disinhibition, results in net excitatory effect from excessive afferent input and efferent response

114
Q

Risks of gastric lavage

A

hypoxia, dysrhytmias, laryngospasm, perforation of GI tract or pharynx, fluid and electrolyte abnormalities, aspiration pneumonia, aspiration pneumonitis

115
Q

Contraindications to gastric lavage

A

loss of protective airway reflexes (unless patient indubated), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high risk of aspiration potential, risk of GI hemorrhage due to an underlying medical or surgical condition, hyponatremia if lavage with water

116
Q

If gastric lavage performed at 60 minutes post ingestion, mean recovery of markers?

A

8.6-13%

117
Q

Theories for ILE

A
  1. Lipid sink - sequestration of lipophilic compounds in the newly created lipid compartment
  2. Myocardial energy substrate improving cardiac performance
  3. Increasing cardiac calcium to restore myocardial fxn
  4. Increasing the overall fatty acid pool, which overcomes inhibition of mitochondrial fatty acid metabolism (eg, bupivicaine toxicity)
118
Q

List drugs/toxins that are not absorbed by activated charcoal.

A
  1. Hydrocarbons
  2. Lithium
  3. Ferrous sulfate (conflicting reports)
  4. Potassium
  5. Ethanol
119
Q

Urinary alkalinization is useful for what toxins?

A

SALICYLATES, PHENOBARBITAL, methotrexate, chlorpropamide, 2.4-dichlorophenoxyacetic acid, diflunasil

120
Q

Contraindications to urinary alkalinization?

A

Renal failure, heart failure (sodium load) - relative

121
Q

Complications of urinary alkalization?

A

Hypokalemia most common, hypocalcemia, coronary vasoconstriction (alkalemia shifts curve to left), cerebral vascoconstriction

122
Q

When should whole bowel irrigation be considered?

A

Sustained release or enteric coated drugs in patient presenting 2 hours after ingestion

123
Q

Contraindications for WBI?

A

bowel obstruction, perforation, ileus, recent surgery, hemodynamic instability, vomiting, GI hemorrhage

124
Q

How do you perform WBI?

A

Enteral administration (NG tube) of large amounts of polyethylene glycol electrolyte solution, osmotically active, liquid stool, no net absorption or secretion so no significant changes in water or electrolytes occur

125
Q

MOA zinc phospide rodenticides

A

After ingestion, phosphine gas produced by hydrolysis of zinc phospide in acidic moist stomach; phosphine gas rapidly absorbed across gastric mucosa then who knows…possible inhibition cytochrome C oxidase, inhibition serum acetyl cholinesterase activity, formation of reactive hydroxyl radicals, inhibition of catalase and peroxidase resulting in lipid peroxidation

Food increases absorption b/c dec gastric acidity

126
Q

Tx zinc phosphide tox?

A

increase stomach pH (aluminum hydroxide, calcium carbonate, magnesium) then make vomit or do gastric lavage, charcoal probably not helpful, but give anyway

127
Q

What kind of drug is PPA

A

sympathomimetic amine, acts as an alpha-adrenergic receptor agonist and indirectly through increased release of stored norepi by alpha- and beta-adrenergic receptors

128
Q

PPA toxicity (JAVMA, 2011, findings)

A

Dose dependent side effects, 61% dogs showed signs including agitation, vomiting, mydriasis, lethargy, tremor/twitching, panting, bradycardia, tachycardia, hypertension, erythema, one dog died that ate 145 mg/kg (therapeutic dose 1-1.5 mg/kg)

129
Q

What is the toxin in bath salts?

A

methylene-dioxypyrovalerone (MDPV) - inhibit NE and dopamine reuptake and act as central system stimulants, clinical signs extreme sympathetic stimulation

130
Q

What’s used in humans to treat frostbite?

A

aspirin and prostacyclin

131
Q

SSRI toxicosis cats, JVECC, 2013, findings.

A
  1. 24% clinical signs
  2. Sedation > GI > CNS stimulation = CV = hyperthermia
  3. No deaths
  4. venlafaxaine had most clinical signs
  5. No assc’n b/t dose ingested and clinical signs
132
Q

Where is serotonin made normally?

A

raphe nuclei

133
Q

Systemic effects of serotonin?

A

vasoconstriction, plt aggregation, intestinal peristalsis, bronchoconstriction

134
Q

SSRI MOA

A

block reuptake of serotonin in presynapse, increasing serotonin at synaptic cleft

From Flashcardlet (19 decks)

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