Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Toxicology > Quiz > Flashcards

Quiz Flashcards

1
Q

Why study toxicology?

A

Animal poison control center fields about 100,000 cases/year. Most cases do not result in serious toxicosis, you need to know when and how to treat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How often are poisonings malicious?

A

It is very rare! only 1-2% are malicious. Most involve pesticides, drugs like aspirin and caffeine, ethylene glycol and cyanide.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a toxin/toxicant?

A

A compound that causes toxicity . Can be a synthetic or natural compounds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Toxicology

A

The study of poisons. Is concerned with identification, treatment, and assessing risks of poisons. In a clinical, regulatory and environmental setting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Xenobiotic

A

foreign substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Antidote

A

Historically- remedy to counteract a poison. Current- any substance that prevents/relieves the effects of a toxicant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do some veterinarians call the universal antidote?

A

Activated charcoal.

But no antidote really works on all toxicants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Manmade chemicals

A

More than 50,000. Potential toxicants include pesticides, cleaning products, pharmaceuticals, industrial chemicals, etc,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Natural products

A

Toxic plants, at least 800 species with millions of compounds. Microbes, vitamins, and animal venoms. Don’t understand them all- like grapes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are natural or synthetic poisonings worse?

A

Just depends on the situation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Additive compounds

A

Two compounds when together both have their full effect (1+1=2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antagonistic compounds

A

When one compound prevents the full action of another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Synergistic compounds

A

Two compounds that when together magnify each others effects (1+1=5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What factors of toxicity are related to the chemical?

A

Chemical structure, affinity to molecules, the toxicants carrier.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What factors of toxicity are related to exposure?

A

Dose, route of entry, duration of exposure (acute, chronic, subacute)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What factors of toxicity are related to the subject?

A

species, age (young or old), health status, history (other medications they might be on), gender (might matter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does environment influence toxicosis?

A

Body temperature, outside temperature (where the microbes can survive), stomach pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Species differences

A

Differences in the capacity for biotransformation. Cats are deficient in glucuronidation. Dogs are deficient in acetylation. Pigs are deficient in sulfation. Pregnancy can also alter metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acute exposure

A

Single dose exposure or several doses within a 24 hour period. ex: snake venom, bottle of aspirin, rate poison

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sub-acute/subchronic exposure

A

Exposure over 7 to 90 days. ex: lawn pesticides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic exposure

A

Protracted exposure (6 months- lifetime). ex: lead paint, well water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Dose-response relationship

A

Central concept of toxicology; assumes a cause and effect relationship and that response is proportional to dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Toxicokinetics

A

Exposure and dose are NOT the same. Most important veterinary toxicants are absorbed by oral or dermal routes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ADME

A

Absorption, Distribution, Excretion and Metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does metabolism usually do?

A

It usually detoxifies a compound and increases its elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bioactivation

A

Occasionally metabolism will increase the toxicity of a compound. ex: benzoapyrene, aflatoxin, acetaminophen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mechanisms of toxicity

A

1) Delivery from site of exposure to target. 2) Reaction of the ultimate toxicant with the target molecule. 3) Cellular dysfunction and resultant toxicities. 4) Repair (apoptosis tissue regneration) or disrepair (tissue necrosis, fibrosis, cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Cellular damage caused by toxicity

A

Can result from free radical damage, inhibition of energy production, disruption of enzyme function. ex: arsenic, acetaminophen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Organ system dysfunction by toxicity

A

Not associated with specific cellular injury, but lethal to intact organism. ex: insecticides, rodenticides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Top ten toxic foods for dogs

A

Alcohol, avocados, chocolate, coffee and caffeine, fruits with pits/seeds, grapes and raisins, macadamia nuts, onions and garlic, xylitol, yeast dough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Top ten toxins for dogs and cats

A

Prescription drugs, insecticides, organophosphates, OTC drugs, house hold products, human foods, veterinary medications, rodenticides, plants, lawn products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How important is it to take a history?

A

Pretty much the most important thing ever!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Known exposure

A

Owner saw or highly suspects that animal ingested a particular compound. Initial contact if often by phone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Unknown exposure

A

Animal presents with symptoms but no known cause. Much more difficult to diagnose and treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what to evaluate for immediate life-threatening problems when toxic animals come in?

A

Cardiovascular function and output (HR), Respiratory (RR), Temperature, Having siezures (other CNS problems)? Hemorrhaging?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Who are candidates for intubation?

A

unconscious, paralyzed and severe respiratory distress patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Ventilation may be needed if there is….

A

Hypoventalation and hypercapnia (PCO2 > 45 mmHg). Metabolic acidosis (pH 7.35). Hypoxia (PaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do you prevent aspiration of vomitus?

A

Comes down to positioning. Head should be below the body. With large animals keep them on an incline with keeping head below the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do we control hyperactivity (seizures)?

A

Diazepam is the treatment of choice- repeat every 10 minutes for 2x the effect. Phenobarbital. Methocarbamol- skeletal muscle relaxation to control seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How do we treat depression?

A

Analeptics, Doxapram- increased respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How do we treat tachycardia and arrhythmias?

A

Need to correct acid-base, electrolyte or fluid disorders. Lidocane or propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do we treat hypertension?

A

Nitroprusside via constant IV infusion. Hydralazine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Fluid therapy to control cardiovascular function

A

Balanced electrolyte solution for shock and dehydration. Monitor urine output. Inotropic drugs like dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Stabilize the patient

A

Priority in animals that present with severe clinical signs. Potential diagnostic testing- EDTA tube, 2 serum tubes. Once patient is stable, perform a complete PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Obtain a complete history

A

Most important and most overlooked part of diagnosing toxicity. Once patient is stable, question owner to narrow down causes of toxicity. 4 major themes: health history, clinical signs, environment, diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

History: health history

A

Ask about Vx history, any medications and suppliments, genetic diseases, ect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

History: current clinical history

A

How long has the problem been present? When was the animal observed first sick? If animal was found dead- when were they last seen healthy? What is the size of the herd?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

History: clinical signs

A

Although you never want to diagnose based only on clinical signs because so many toxicities have the same signs. But it helps choose treatment because you know what organ system is effected. CNS, GI, Renal, Hepatic, Cardiac, Hematopoietic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

History: environment

A

Type of environment in which the animal lives will greatly determine next line of questions to ask: indoor only, indoor/outdoor, fenced yard vs roaming.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

History: diet

A

What are they eating? Method of feeding, moldy or spoiled food, drinking water source, water supply changes?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Formulate rule-out list

A

Popular list of differential diagnoses. Make sure not to have blinders on! Could be infection, metabolic, ect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Ancillary support

A

Ensure adequate urine output. Monitor respiratory, cardiac and neurological status. Manage clinical signs as they develop. Manage secondary hepatic or renal injury. Administer GI protectants and anti-emetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Symptomatic care

A

Maintain body temperature- avoid heat lamps. Alleviate pain. Prevent irritation of skin and membranes with demulcents, milk, sucralfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Decontamination measures

A

Only after animal has been fully stabilized. Two most common methods are emesis and activated charcoal, might consider cathartics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Emesis

A

Prevents toxicant absorption! Given if you suspect oral exposure, should be done within 60 minutes of ingestion. Don’t use for very basic or acidic compounds, chronic exposures and minor toxicities. Always save the vomitus for analysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Emesis rule of thumb

A

Induce emesis if a toxic dose of a substance was ingested, no vomiting has occurred yet, and activated charcoal is not an option. There is little evidence that shows emesis improves the outcome in poisoned animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Activated charcoal

A

Prevent toxicant absorption. The earlier you give the more effective it is. Give orally, can be mixed with baby food. Repeat dose every 5 hours. Don’t give to a sedated animal without airway protection- aspiration risk. Don’t give if toxican is a corrosive agent or non-polar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Charcoal rule of thumb

A

Give if substance is known/thought to be absorbed, ingestion was very recent, undergoes enterohepatic circulation, the animal can tolerate it, there is no immediate need to administer oral medication. Have to wait at least 2 hrs between giving charcoal and a oral medication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Cathartics

A

Facilitate toxicant removal. Decrease GI transit time, increase movement of toxins, or charcoal-toxin complex, and decrease possible adsorption of the toxin. Use as a adjunct to activated charcoal therapy to reduce transit time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Mineral Oil

A

Type of Cathartic. Do not use with activated charcoal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Saline Cathartic

A

MgSO4 or Na2SO4. Can add to charcoal or use later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Corrosives, strong acids or bases toxicants

A

To prevent absorption use dilution instead of emesis (Dilute with milk, water or eggs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Dermal Exposures

A

To prevent absorption bathe in liquid dish soup, rinse well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Lipid infusion

A

New treatment for preventing absorption. Off label use of intravenous lipids. Promising adjunct to conventional treatments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Do most toxic agents have a specific antidote?

A

No they do not. If there is one, use it, but mostly treatment is symptomatic and supportive

66
Q

Analytic testing

A

No one test will screen for all toxicants. Multiple tests to cover everything becomes costly. So have to narrow down to general type of agent involved.

67
Q

Common toxins associated with an increased anion gap

A

> 30 mEq/L: suggests metabolic acidosis. Ethylene glycol, Ethanol, Iron, Methanol, Salicylates (aspirin), Strychnine

68
Q

Common toxins associated with CNS depression

A

Ivermectin, cholinesterase inhibitors, organophosphate insecticides, carbamate insecticides, blue-green algae, slaframine, lead, locoweed, ethylene glycol

69
Q

Common toxins associated with seizures

A

Bromethalin, chocolate, lead, organochlorine insecticides, pyrethrins/pyrethroids, syrchnine, water deprivation/sodium ion toxicosis, water hemlock.

70
Q

4 parts to accurately diagnosing any toxicity

A

History, clinical signs, pathology/necropsy, chemical analysis

71
Q

How do you prevent further exposures?

A

Change pasture, feed, water, ect. Remove baits, old pesticides. Bathe or flush for cutaneous or ocular exposures. Educate your clients!!

72
Q

Chemicals that cause neurotoxicity

A

Both “all natural” and synthetic. Largest class of chemicals inducing toxicosis. Clinical signs can be grouped by peripheral vs. central and excitatory vs. depressive.

73
Q

Organophosphate pesticides

A

Agricultural and residential use had increased since OCPs (degrade faster, used in flea collars, bug baits). Parathion, malathion, and chlorpyrifos. High water solubility and acute toxicity.

74
Q

Prganophosphates mechanism of action

A

Irreversible inhibition of acetylcholine esterase activity. Cholinergic overstimulation within minutes to hours

75
Q

Clinical signs of anti-esterase toxicity

A

May last 1-5 days- include respiratory distress and collapse. Muscarinic- SLUDGE-M. Nicotinic- muscle fasciculations. CNS.

76
Q

Species specific clinical signs. Don’t forget- won’t always see textbook versions

A

Horses- colic and dehydration. Cattle- rumen stasis (no miosis). Cattle/sheep- severe depression. Dogs/cats- CNS stimulation-> convulsions. Cats- chlorpyrifos cause severe nicotinic signs

77
Q

Diagnosing anticholinesterase toxicity

A

Correct history and clinical signs. Atropine challenge- administer, if normal signs of atropine are observed in 15 mins toxicity is NOT due to cholinesterase inhibitor. Decreased RBC AChE. May see pulmonary edema and petechial hemorrhage in GI mucosa

78
Q

Treating anti-esterase toxicity

A

GI decontamination, bathing in exposure was dermal. Atropine sulfate for muscarinic signs (won’t stop nicotinic signs). Oximes can reactivate AChE. Diazepam or barbiturates for seizures. Time.

79
Q

Pathology in dog with OP toxicity

A

Will see vacuolization of the brain

80
Q

Organophosphate induced delayed neurotoxicity

A

OP compounds can produce significant inhibition of neuropathy target esterase can delay neuropathy. Characterized by axonal degeneration of long motor neurons. Hindlimb weakness and paralysis. No treatment

81
Q

Ivermectin

A

Produced by Steptomyces avermitilis. Worm medication in cats/dogs. Anthelminthic in livestock. OD can cause ataxia and disorientation in any breed. In collies, shepherds and shelties smaller amounts can cause toxicity because BBB does not block ivermectin

82
Q

Ivermectin mechanism of action

A

Increases GABA release, enhances GABA binding and is a direct GABA receptor agonist. Increased inhibitory input decreases ability to respond to other stimuli. Doses can cumulate

83
Q

Ivermectin clinical signs

A

Onset is hours to 1 day. Ataxia, lethargy, mydriasis, coma, blindness, ect. Collies- recumbency and seizures. Respiratory distress typically precedes death.

84
Q

Ivermectin diagnosis

A

History of administration, brain concentration > 100ppb, measure GI content, liver, fat, feces. No diagnostic bloodwork or lesions

85
Q

Ivermectin treatment

A

GI decontamination for recent exposures (charcoal- multiple times). Supportive care, barbiturate for convulsions. Prognosis depends of exposure dose, Should test dogs prior to administering them higher doses of ivermectin.

86
Q

Bromethalin

A

Single dose rodenticide. Kills in 3-5 days. Parents and metabolite uncouple oxidative phosphorylation in CNS

87
Q

Nicotine

A

Rodenticide. Usually stimulate then block nicotinic ACh receptor

88
Q

Metaldehyde

A

Rodenticide. Sources: fuel for small heaters and molluscicides. Metabolism to acetaldehyde = CNS excitation

89
Q

Mycotoxins

A

Fungal metabolites which cause pathological, physiological and/or biochemical alterations usually on several organ systems. Can affect all species.

90
Q

Slaframine

A

Produced by black patch fungus. Seen in center, south eastern and southwestern USA. Is a ACh mimic, primarily acts as a muscarinic cholinergic agonist, especially in exocrine glands. Most common in horses and cattle.

91
Q

Clinical signs of slaframine

A

Copious salivation is the primary sign, can be only sign. Bloat, diarrhea, frequent urination. May see feed refusal.

92
Q

Slaframine diagnosis

A

Diagnose by consumption of clover, identification of black patch in clover. Have to differentiate from OPs and Botulism

93
Q

Slaframine treatment

A

Remove source, maintain hydration and electrolytes. Can treat with atropine, rarely fatal- signs should cease within 48 hours.

94
Q

Fumonisin

A

Metabolite of Fusarium spp. Found mostly on corn. Occurs in years of drought followed by wet weather. Presence of Fusarium spp is not indicative of fumonisin.

95
Q

Fumonisin mechanism of action

A

Acts by inhibition of sphingosine-N-acetyltransferase causing increased levels of sphinganine (cytotoxic). Affects vascular endothelial cells-> stroke, hepatic injury, and pulmonary edema. Species susceptible- horses, swine, and rabbits.

96
Q

Two diseases fumonisin toxicity causes

A

Equine leucoencephalomalacia (ELEM) and porcine pulmonary edema (PPE)

97
Q

Porcine pulmonary edema

A

Clinical signs include inactivity, increased RR, and decreased HR. Develop lethal pulmonary edema within 4-7 days of consuming contaminated feed. Abdominal effort and open mouth breathing occurs within hours of death.

98
Q

Diagnosis of PPE

A

Analysis of feed for fumonisin with clinical signs. Increase in serum and tissue sphingoid base. Increased liver enzymes, total bilirubin, bile acids and cholesterol. Post-mortem pathology shows pulmonary edema, hepatic lesions and necrosis.

99
Q

Equine leukoencephalomalacia

A

Main target is brain and liver- acute onset of ataxia, drowsiness, hysteria that get progressively worse. Hepatoxicity- jaundice, encephalopathy, coma and convulsions are terminal. Near 100% mortality

100
Q

ELEM diagnosis

A

Analysis of feed and clinical signs. Severe liver injury and lesions- increased cholesterol and liver enzymes. Post-mortem CNS necrosis and liquefaction

101
Q

Treating fumonism toxicity

A

No treatment available. Isolate affected animals. Change feed. Pigs usually recover within 48 hrs.

102
Q

Tremorgenic mycotoxins

A

Elicit intermittent/sustained tremors in vertebrates. Sources- food, garbage, compost. Clinica signs- dimished activity and immobility-> hyperexcitability.

103
Q

Tremorgenic mycotoxins mechanism of action

A

Release of neurotransmitters from synaptosomes in the CNS

104
Q

Ammoniated feed toxicosis

A

Non-protein nitrogen sources are added to cattle feed. Found in high concentrations in some mineral licks. Species affected- bovine, caprine, ovine. Leads to excitability “bovine bonkers”

105
Q

Ammonia toxicity/imidazoles clinical signs

A

Hyperexcitaility- rapid blinking, trembling, rapid RR, SLUD, tonic convulsions. Animals alternate between hyperexcitability and normal. Onset rapid- 15 mins to several hrs. Death within 24 hrs

106
Q

Ammonia toxicosis diagnosis

A

History of exposure, clinical signs. Differentials- OP, cyanide, grain overload, meningitis. Analyse feed or blood/rumen for ammonia levels. Increased ammonia, glucose, BU, and decreased blood pH

107
Q

Ammonia toxicosis treatment

A

Imidazole- no treatment, just feed removal, might need sedation. NPN- no treatment, water and vinegar by stomach tube

108
Q

Strychnine

A

Seeds for Strychos-nux vomica. Often used as a malicious poison.

109
Q

Strychnine mechanism of action

A

Rapidly absorbed and distributed to blood, liver and kidney. Rapid elimination. Competitive antagonist at postsynaptic glycine receptors. Glycine is an inhibitory transmitter, so antagonism results in stimulation of all muscles

110
Q

Strychnine toxicity clinical signs

A

Rapid onset, begins with anxiety, restlessness, “grinning”, ears twitch. Proceeds to violent tetanic seizures. Sawhorse stance. Death from respiratory failure, exhaustion.

111
Q

Strychnine toxicity diagnosing

A

Clinical signs, hyperthermia in dogs. Chemical analysis of bait, stomach contents or liver. Elevated CPK and LDH. Lactic acidosis, hyperkalemia and leukocytosis. Rule out- OP, tetanus, metaldehyde, Pb

112
Q

Strychnine toxicity treatment

A

Need to control seizures and prevent asphyxiation. Given pentobarbital or methocarbamol. Gastric lavage, activated charcoal and forced diuresis. Ammonium chlorida to trap strychnine

113
Q

Salt toxicity

A

Water deprivation (most common) or eating large amounts of salt. Most common is pigs.

114
Q

Salt toxicity mechanism of action

A

Diffusion of sodium into CSF when plasma Na levels are high. When plasma Na level drop, sodium leaves CSF slowly, attracting water to maintain osmotic balance. Increases CSF volume and pressure.

115
Q

Clinical signs of salt toxicity

A

Primarily CNS and includes salivation, increased thirst, abdominal pain and diarrhea. Cattle may be belligerent and uncoordinated

116
Q

Diagnosis of salt toxicity

A

Na levels high especially in CSF. >2000ppm is diagnostic in swine and cattle. Differentiate from polio, lead, pesticides, encephalitis

117
Q

Treatment of salt toxicity

A

Slow rehydration (over days). Serum sodium levels should be lowered at a slow rate. IV hyperosmotic fluids low in NA, loop diuretics- to prevent pulmonary edema

118
Q

Pharmaceuticals

A

Neuroactive substances. Top- vicodin, synthyroid, zocor and lipitor, lisinopril. Clinical signs in animals can be similar to human toxicity

119
Q

Alprazolam (Xanax)

A

Benzodiazeprine. ASPCA receives many calls about this.

120
Q

Alprazolam mechanism of action and clinical signs

A

Acts on the CNS. Signs- ataxia, depression, vomiting, tremors, tachycardia, diarrhea, ptyalism, hypothermia. Appear with 30 minutes of ingestion, If there were especially high doses, may initially show CNS excitation

121
Q

Alprazolam diagnosis and treatment

A

Dx- based on suspect and clinical signs. Tx- standard decontamination procedures, can use antagonist flumazenil. Need close monitoring. Fluids and medications to support respiratory function.

122
Q

Zolpidem (Ambien) mechanism of action

A

Non-benzodiazepine hypnotic drug. Inhibits neuronal excitation by binding to the benzodiazepine omega-1 receptors

123
Q

Zolpidem clinical signs

A

Rapid absorption from GI tract. Ataxia, vomiting, lethargy, disorientation, hyper-salivation, hyperactivity, panting. Signs usually resolve by 12 hours

124
Q

Zolpidem diagnosis and treatment

A

Dx- suspect and clinical signs. Tx- supportive and symptomatic

125
Q

Phenoxyacetic acid herbicides

A

Scott’s weed and feed, Silvex. Low toxicity in most animals, dogs are very susceptible. Affected animals usually exposed to concentrate or predisposed through kidney damage or genetics. MOA unknown.

126
Q

Phenoxyacetic acid clinical signs

A

GI effects (sometimes only sign in dogs). Muscle affects- rigid muscles, ataxia, seizures, rumen atony, myotonia with serious toxicosis. Renal tubular degeneration, hepatic necrosis.

127
Q

Phenoxyacetic acid diagnosis

A

Oral and GI ulcers, enteritis, rumen stasis, congestion of kidney/liver, hyperemia of lymph nodes. Chemical analysis of serum, urine.

128
Q

Phenoxyacetic acid treatment

A

Emesis, lavage or bath decontamination. Activated charcoal/cathartic. Ion trapping to enhance excretion. Prognosis good for treated animals

129
Q

Ergot alkaloids

A

Produce in grains by Claviceps purpurea. Alkaloids are dopamine serotonin agonists which produce hallucinations. Lead to decreased prolactin secretion. Smooth muscle contractions- uterus and peripheral vasculature- causes abortion and ischemia

130
Q

Ergot clinical signs

A

Reduced feed intake and weight gain, heat intolerance and retain winter coat. Necrotizing ergotism- lameness, gangrene of extremities. Fat necrosis, poor reproductive performance

131
Q

Clinical signs of ergotism in horses and pigs

A

Horses- abortion, weak foals, prolonged gestation. Pigs- causes infertility and early parturition, decreased milk production.

132
Q

Ergotism diagnosis and treatment

A

Evidence of sclerotia in feed, fescue in forage. Treat by removing source, prevent secondary infections. Metoclopromide and domperidone increase prolactin secretion and normalize gestation in mares.

133
Q

Inophores

A

Compounds that form lipid soluble complexes with cations. Used as antibiotics. Used to improve milk production in dairy cattle

134
Q

Inophores mechanism of action

A

Act by increasing Na and Ca, leads to mitochondrial swelling and cell death, especially in muscle. Usually a feed-mixing error. Horses are most susceptible. Poultry are the least sensitive

135
Q

Inophores clinical signs

A

Occur 12-72 hrs after ingestion. Anorexia, colic, sweating, in-coordinated, and weak (horses). Unlikely but poultry- down with legs and wings out, dogs- posterior paresis, cats- polyneuropathy from salinomycin.

136
Q

Inophores diagnosis

A

Increased muscle enzymes and myoglobinuria. Elevated liver values. Decreased K and Ca (horses). Chemical analysis of feeds, liver (not blood). Differentiate from other colic, Vit E and Se deficiency, white snakeroot, botulism

137
Q

Inophores treatment

A

No specific treatment or antidote. Feed change must be made immediately until all diagnostic procedures are completed. Supportive therapy. Animals may die later due to exercise intolerance

138
Q

Tetanus (clostridium tetani)

A

Mostly affects cattle. Spores in a puncture wounds, can be ingested. Toxins acts by blocking release of GABA and glycine. Results in overstimulation of muscles leading to stiffness and tetany

139
Q

Tetanus clinical signs

A

Stiffness and reluctance to move, twitching and tremors, lockjaw, unsteady gait, stiff tail, bloat-> collapse, spasm, death

140
Q

Tetanus treatment

A

Antitoxin is available- only works very early on. Supportive therapy, prognosis is very poor.

141
Q

Common respiratory toxins: ventilatory muscle paralysis

A

Botulism, tetanus, snake venom, OP insecticides, strychnine

142
Q

Common respiratory toxins: respiratory center depression

A

Barbiturates, opiodes, ethylene glycol, hypnotics, sedatives, tricyclic antidepressants, crude oil

143
Q

Anticoagulant & anticoagulant rodenticides mechanisms of actions

A

Inhibits Vit K epoxide reductase. Prevents formation of Vit K dependent clotting factors (II, VII, IX, X)

144
Q

Anticoagulant & anticoagulant rodenticide toxicity clinical signs

A

Delayed onset of clinical signs (3-5 days) as clotting factors are consumed. Depression, anorexia, anemia, dyspnea, nosebleeds, bleeding gums, bloody feces. Hemorrhage into chest/abdomen and hematoma. Prolonged bleeding from injection sites noted

145
Q

Anticoagulant & anticoagulant rodenticide toxicity diagnosis

A

History of exposure, evidence of a coagulopathy and response to vitamin K therapy. Hematological tests: increased PT/PTT

146
Q

Anticoagulant & anticoagulant rodenticide toxicity treatment

A

If it has been within the last few hours- emetic, adsorbent, cathartic therapy. Vitamin K administration. Therapy for 10-14 days for warfarin, 30 days for second generation compounds. Severe cases may require a transfusion

147
Q

Nitrate toxicosis

A

Found in fertilizers, many plants, contamination of water. Converted to nitrite- nitrite anion causes vasodilation and oxidized ferrous iron in hemoglobin to the ferric state forming methemoglobin. Results in oxygen starvation of tissues

148
Q

Nitrate toxicosis clinical signs and diagnosis

A

Levels of metHb. Diagnosis by nitrate levels in feed or water. In suspected nitrate deaths save eye for analysis of nitrate.

149
Q

Nitrate toxicosis treatment

A

IV or aqueous solution of methylene blue- good for ruminants, urine becomes dark green. Use ascorbic acid in cats and horses. Educate farms about nitrate accumulation

150
Q

Cardiac glycosides

A

Contain glycosides- inhibit the sodium-potassium ATPase pump through competition with potassium for binding sites

151
Q

Cardiac glycoside toxicity clinical signs and diagnosis

A

Clinical signs can occur from 1 hr to weeks after ingestion, depending on plant species. Trembling, staggering and dyspnea. Increased Ca and Na. Racing HR, arrhythmia, weak pulse. Dx- based on history, suspect, clinical signs, and analysis of vomit

152
Q

Cardiac glycoside toxicity treatment

A

GI decontamination (if recently eaten), treat arrhythmia with propanolol, treat hyperkalemia if needed, use digoxin immune Fab fragments if propranolol ineffective.

153
Q

Cyanide toxicity

A

Usually a problem with consumption of wilted leaves and seeds of wild cherry, ect. Also found in fertilizers, pesticides/rodenticides, fumigants, combustion.

154
Q

Cyanide toxicity mechanism of action

A

Not toxic when dry, as hydrogen cyanide is volatile. Mechanism of toxicity is inhibition of cytochrome oxidase

155
Q

Cyanide toxicity clinical signs

A

Generally occur within 15 mins to a few hrs after consumption. Classic symptom is cherry red blood that is slow to clot. Stomach contents smell like almonds. Sudden death, dyspnea, weakness, tremors.

156
Q

Cyanide toxicity diagnosis

A

Made by history of ingestion and unclotted red blood. As well as analysis of frozen stomach contents

157
Q

Cyanide toxicity treatment

A

Two steps: 1) Induce methemoglobin formation with sodium nitrite to bind cyanide. 2) Give sodium thiosulfate to increase formation of thiocyanate by rhodanese. Thiocyanate in non-toxic and elminated. If necessary, treat metHb with methylene blue

158
Q

Methylxanthines

A

Caffeine, theobromine, theophylline, chocolate, medications. Most common around the holidays (chocolate). Unsweetened baking chocolate is especially toxic. Caffeine tablets and cocoa bean mulch are also a common problem in horses

159
Q

Methylxanthine mechanism of action

A

Competitive antagonist of adenosine receptors; causes CNS stimulation, vasoconstriction and tachycardia. Prevents Ca reuptake leading to increased skeletal and cardiac muscle contractility. Inhibits phosphodiesterase, increases cyclic AMP and GMP concentrations

160
Q

Methylxanthine toxicity clinical signs

A

Vomiting, diarrhea, diuresis, hyperactivity, “bounce”, panting, tachycardia, hypertension, ataxia, tremors, seizures, coma. Death is from arrhythmias or respiratory failure

161
Q

Methylxantine toxicity diagnosis

A

Chemical analysis of stomach contents, plasma, serum, urine or liver. Theobromine can be detected in serum for 3-4 days after ingestion (long half-life)

162
Q

Methylxantine toxicity treatment

A

GI decontamination (induction of emesis, repeated admin of charcoal). Monitor EKG (treat arrhythmias with lidocaine-not cats!). Treat seizures with diazepam or barbiturates, maintain respiration, fluid diuresis may increase excretion

Toxicology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions