Term
| Poultry litter and Swine manure are common sources of what potential toxin? |
|
Definition
Copper
also present in soil/plants, and as a feed additive |
|
|
Term
| Excessive dietary intake of which trace metals can induce secondary copper deficiency states? |
|
Definition
|
|
Term
| What organ acts as a reservoir for the body's copper? |
|
Definition
|
|
Term
| How is copper excreted from the body? |
|
Definition
|
|
Term
| Copper overload in the liver overwhelms what type of enzymes? |
|
Definition
| anti-oxidation enzymes ---> oxidative stress --> hepatocellular necrosis |
|
|
Term
| Lysyl oxidase, diamine oxidase, cytochrome oxidase, superoxide dismutase are all enzymes that depend upon which metal for normal function? |
|
Definition
|
|
Term
| What species is most highly susceptible to copper toxicity? |
|
Definition
|
|
Term
| T/F: non-ruminants can tolerate higher levels of copper than ruminants |
|
Definition
| True (esp. pigs and chickens) |
|
|
Term
| How does sulfur interact with molybdenum and copper? |
|
Definition
| Sulfur binds molybdenum resulting in overall higher levels of free copper |
|
|
Term
| How do phytates (fiber and lignin), calcium and casein, affect zinc bioavailability? |
|
Definition
| reduce zinc bioavailability |
|
|
Term
| How much of ingested zinc is actually absorbed? |
|
Definition
|
|
Term
| what dogs breeds have a reduced capacity to absorb zinc? |
|
Definition
| northern breeds i.e. Siberian Huskies and Alaskan Malamutes |
|
|
Term
| How does inflammatory bowel disease influence zinc absorption? |
|
Definition
| decreased absorption --> zinc deficiency |
|
|
Term
| NADH dehydrogenase, RNA/DNA polymerase, DNA transcription factors, alkaline phosphatase, superoxide dismutase, carbonic anhydrase all require which metal? |
|
Definition
|
|
Term
| What are zinc finger domains? |
|
Definition
| transcription factors, often involved in expression of genes that regulate growth and maintain genomic integrity |
|
|
Term
| How does zinc deficiency affect cellular membranes? |
|
Definition
| increases susceptibility to oxidative damagae |
|
|
Term
| Clinical signs associated with zinc deficiency |
|
Definition
| dermatologic problems/alopecia, poor wound healing/immune responses, impaired taste, fatigue |
|
|
Term
| Why are grazing animals especially susceptible to selenium toxicity? |
|
Definition
| plants tend to accumulate inorganic selenium from the soil (also may be contaminated by selenomethionine (yeast)) |
|
|
Term
| T/F: inorganic forms of selenium are more bioavialable than organic forms |
|
Definition
|
|
Term
| Why do cattle have a high selenium requirement? |
|
Definition
| 60% of ingested selenium is incorporated into bacterial proteins in the rumen |
|
|
Term
| How do free radicals destabilize cellular membranes? |
|
Definition
| free radicals extract electrons from membrane lipid component |
|
|
Term
| What important selenoprotein neutralizes free radicals? |
|
Definition
|
|
Term
| What is secondary ingestion of rat poison? |
|
Definition
| Pet consumes intoxicated rodents |
|
|
Term
| How does dicoumarol(moldy sweet clover) compare with warfarin? |
|
Definition
| Warfarin is a dicoumarol derivative, it is longer acting and more potent |
|
|
Term
| What are three non-anticoagulant rodenticides? |
|
Definition
| cholecalciferol, bromethalin, zinc phosphide |
|
|
Term
| T/F: first generation warfarin rodenticides are lethal following a single exposure |
|
Definition
| FALSE, continuous bait exposure is required |
|
|
Term
| What two enzymes are deactivated by anticoagulant rodenticides? |
|
Definition
| Cytosolic vitamin K reductase, Vitamin K epoxide reductase |
|
|
Term
| Hydroxycoumarins, indanediones, benzothiopyranones are examples of what class of rodenticides? |
|
Definition
| second generation (long-acting) anticoagulants |
|
|
Term
| What species is much less susceptible to toxicity from second generation (long-acting) anticoagulant rodenticides? |
|
Definition
|
|
Term
| T/F- you can identify the type of rodenticide bait based on appearance alone |
|
Definition
FALSE
Second generation long-acting anticoagulants, cholecalciferol and bromethalin can all appear as blue/green pellets |
|
|
Term
| Why are long acting second generation anticoagulant rodenticides more toxic than warfarin? |
|
Definition
| greater affinity for vitamin K epoxide reductase, additional affinity for cytosolic vitamin K reductase (aka. DT-diaphorase), accumulation in the liver, longer half life (enterohepatic recycling and greater lipid solubility (ie. larger volume of distribution)) |
|
|
Term
| What coagulation factor has the shortest half life and acts as a biomarker for antigoaculant toxicity? |
|
Definition
|
|
Term
| What coagulation factors are vitamin K dependent? |
|
Definition
|
|
Term
| Coagulation factors must undergo what reaction in order to participate in hemostasis |
|
Definition
|
|
Term
| What coagulation test will be abnormal in animals with anticoagulant rodenticide toxicity? |
|
Definition
| PT (prothromin time) - measures the extrinsic pathway which relies upon factor 7 (factor seven in the vitamin K dependent coagulation factor with the shortest half life, and therefore the first depleted, in cases of anticoagulant rodenticide toxicity. |
|
|
Term
| How soon post ingestion of anti-coagulant rodenticide will PT be elevated? |
|
Definition
|
|
Term
| T/F: 24 hours after ingestion of anti-coagulant rodenticides clinical signs indicative of coagulopathy are appreciable |
|
Definition
FALSE,
the half lives of the plasma clotting factors (factor 7 = 6 hours) result in a latency period between ingestion and overt clinical signs of 3-5 days |
|
|
Term
| What are some clinical signs indicative of anti-coagulant rodenticide toxicity? |
|
Definition
Factor deficiencies --> cavital bleeding
Pesudothrombocytopenia (platelet clumping) --> mucosal and subdermal bleeding |
|
|
Term
| T/F: long acting anticoagulant rodenticides can cross the placenta |
|
Definition
True
large enough dose may cause spontaneous abortions, tx mom early and aggressively |
|
|
Term
| T/F: long acting anticoagulant rodenticides cannot be transmitted into breast milk |
|
Definition
FALSE
if mom ingests a toxic dose treat and/or wean the babies |
|
|
Term
| What formulation of vitamin K (phytonadione) is preferred for the treatment of anticoagulant rodenticide toxicity? |
|
Definition
| oral formulation, injectable may be coagulopathic and may precipitate an anaphylactic reaction |
|
|
Term
| T/F: you should recheck PT 2-3 day after last vitamin K (phytonadione- oral) dose |
|
Definition
TRUE
if still prolonged continue vitamin K and additional 3 wks |
|
|
Term
| cholecalciferol toxicity can arise from ingestion of what four sources? |
|
Definition
| rodenticide, feed additives, calcinogenic plants (solanum sp), calcipotriene cream (human Rx) |
|
|
Term
| What is the bioactive form of Vitamin D3(cholecalciferol)? |
|
Definition
calcitriol <-- more lipophilic than cholecalciferol, greater penetrance of cell membranes and greater volume of distribution
--> calcitriol binds to membrane receptors and opens calcium channels resulting in high intracellular calcium concentration
---> calcitriol binds to cytosolic receptros and affects gene transcription |
|
|
Term
| What two biomechanical processes are responsible for the activation of cholecalciferol into calcitriol? In what organs do these reactions take place? |
|
Definition
Hydroxylation in the liver
CPY 450 in the kidney |
|
|
Term
| What is the pathophysiology of cholecalciferol toxicity? |
|
Definition
| bioactivation of cholecalficerol to calcitriol in the liver and kidney --> increased absorption of calcium from the gut, increased reabsorption of calcium in the kidneys, increased mobilization of calcium and phosphorous from body stores (i.e. bone) --> hypercalcemia results in vascular, renal, and cardiac mineralization |
|
|
Term
| T/F: Cats are less sensitive to cholecalciferol toxicity than dogs |
|
Definition
FALSE
the only rodenticide that cats are less sensitive to than dogs are the anticoagulants |
|
|
Term
| What are the three most common laboratory and clinical abnormalities seen in patients with cholecalciferol toxicosis |
|
Definition
1st: Pu/Pd (ADH inhibition)
then: hyperphosphatemia (>8 mg/dl)
finally: hypercalcemia (>12.5 mg/dl)
if untreated (2-4 days post ingestion): acute renal failure +/- hypertension, cardiac arrhythmias, seizures --> DEATH |
|
|
Term
| Why are bisphosphonates and salmon calcitonin considered for the treatment of cholecalciferol toxicity? |
|
Definition
| they both decrease mobilization of calcium from the bones helping to normalize serum calcium levels |
|
|
Term
| What are the big three treatments for cholecalciferol toxicity to maintain kidney function and enhance renal calcium excretion? |
|
Definition
SALINE DIURESIS and FUROSEMIDE enhance calcium excretion in the urine
PREDNISONE is a competative antagonist of calcitriol |
|
|
Term
| What is the toxic component often found in worm/grub shaped mole baits? |
|
Definition
bromethalin
but also tan, green/blue pellets and blocks (ie. CANT distinguish rodenticides based on appearance!!!)Wha |
|
|
Term
| What species can tolerate relatively high doses of bromethalin due to poor demethylation capability? |
|
Definition
guinea pigs
LD50 = >1000mg/kg |
|
|
Term
| What is the more toxic metabolite of bromethalin and what biochemical process results in its synthesis? |
|
Definition
| Bromethalin is demethylated in the liver to form DES-methylbromethalin (2-3X more toxic than bromethalin) |
|
|
Term
| How is bromethalin excreted from the body? |
|
Definition
| in the bile, enterohepatic recycline results in a long half life (6 days) |
|
|
Term
| What is the pathophysiology of bromethalin toxicity? |
|
Definition
| uncouple mitochondrial oxidative phosphorylation --> less ATP is produced and cells cannot maintain ion/fluid balance |
|
|
Term
| What tissue is especially sensitive to bromethalin, what histopathologic and clinical abnormalities result from toxicosis? |
|
Definition
CNS --> edema results in increased intracranial pressure which can lead to paralysis (k9, toxic dose < LD50, cats any dose) or convulsions (k9, toxic dose > LD50) and death
histopath: diffuse spongiosis in cerebral cortex and spinal cord |
|
|
Term
| T/F: Cats are more sensitive to bromethalin than dogs |
|
Definition
TRUE (slower onset of action and longer duration in cats)
Cats are more sensitive than dogs to all rodenticides EXCEPT anticoagulants |
|
|
Term
| T/F: the convulsant syndrome associated with bromethalin toxicosis is slowly progressive |
|
Definition
FALSE
convulsant syndrome (k9, dose > LD50) is rapidly progressive , focal to generalized motor seizures can be induced by light and sound |
|
|
Term
| T/F: the paralytic syndrome associated with bromethalin toxicosis can result in death due to respiratory failure |
|
Definition
TRUE,
paralytic syndrome (k9, dose |
|
|
Term
| What is the only definitive diagnosis for bromethalin toxicity? |
|
Definition
Post mortem via gas chromatography (brain, kidney, gastric contents)
and histopath of CNS white matter (spongiform degeneration) |
|
|
Term
| T/F: there is NO antidote for bromethalin toxicity |
|
Definition
| TRUE, treatment involves decontamination (repeated doses of charcoal due to enterohepatic recycling) and trying to reduce cerebral edema (mannitol) |
|
|
Term
| T/F: the main mechanism of toxicity follow ingestion of zinc phosphide rodenticide is heavy metal toxicity |
|
Definition
FALSE, doesn't contain enough zinc for toxic effects
Phosphide is converted to toxic phosphine gas by gastic acid, so fasted animals are less susceptible to toxicity because eating increases gastric acid secretion and facilitates the reaction |
|
|
Term
| How does phosphine gas interact with the body? |
|
Definition
| phosphine gas produces facilitates free radical formation --> cell damage is manifested as multi-organ failure |
|
|
Term
| When advising owners to decontaminate following ingestion of zinc phosphine why is it important to make sure the area is well ventilated? |
|
Definition
| Phosphine gas causes severe respiratory irritation! also peripheral vascular collapse, renal damage, pulmonary edema, and cardiac arrest |
|
|
Term
| What is the most common sign associated with zinc phosphide toxicosis? |
|
Definition
vomiting (rapid onset, w/in 15 min of ingestion) Try to make sure area is WELL VENTILATED as phosphine gas is a hazard to pets and people
rarely tremors and seizures |
|
|
Term
| T/F: There are no helpful laboratory tests and no antidote to treat zinc phosphide toxicity |
|
Definition
TRUE
Dx by odor of phosphine gas (rotten fish)
Tx: focus on decontamination (gastric lavage with oral maalox liquid or 5% NaHCO3 to neutralize gastric acid and slow chemical reaction)
and supportive care |
|
|
Term
| What is a common complication associated with zinc phosphide toxicity |
|
Definition
|
|
Term
| What is the toxic manifestation and treatment associated with ingestion of metaldehyde slug baits? |
|
Definition
acute CNS toxicity (convulsions, secondary acidosis)
tx: decontaminate, anti-convulsants, maintain ventilation and acid-base balance |
|
|
Term
| What is the toxic manifestation and treatment associated with ingestion of strychnine rodent baits? |
|
Definition
convulsions and respiratory arrest
tx: decontamination, anti-convulsants, maintain in QUIET ENVIRONMENT, maintain ventilation |
|
|
Term
| Toxicosis following ingestion of human Rx antidepressants, anxiolytics, and antipsychotic drugs is associated with disruption of what essential physiologic function? |
|
Definition
|
|
Term
| Monoamine antidepressant drugs function by increasing synaptic concentrations of serotonin (5-HT) and or catecholamines (norepi and dopamine) through what two mechanisms of action? |
|
Definition
1. inhibiting reuptake (SSRI, SSNRI, TCA)
2. inhibiting degredation by monamine oxidase (MAO) |
|
|
Term
| What two classes of antidepressant drugs cause the most severe toxicosis in companion animals? |
|
Definition
TCA (ex. clomicalm, elavil)
and MAO inhibitors (amitraz (aka mitaban)) |
|
|
Term
| If given chronically SSRIs (prozac, zoloft, paxil) can cause drug interactions through what mechanism? |
|
Definition
| impairment of CYP 450 oxidation of other drugs |
|
|
Term
| T/F: antidepressants are well absorbed PO and are eliminated from the body very slowly |
|
Definition
TRUE
they are very lipid soluble --> large volume of distribution |
|
|
Term
| Clinical signs associated with small overdoses of TCAs |
|
Definition
increased availability and persistance of norepinephrine results in anticholinergic effects:
mydriasis (dilated), decreased secretions, tachycardia
+ mild sedation and transient anorexia |
|
|
Term
| Clinical signs associated with large overdoses of TCAs |
|
Definition
increased availability and persistence of norepinephrine results in profound sedation/coma, seizure, cardiac arrhythmias
Cardiovascular collapse is the main cause of death in companion animal overdoses |
|
|
Term
| T/F: emesis is the best method of decontamination in cases of TCA overdose |
|
Definition
FALSE
TCAs lower the seizure threshold, only induce emesis within minutes of ingestion, otherwise use gastric lavage and activated charcoal with a cathartic
*same is true for amphetamine toxicosis |
|
|
Term
| T/F: Cholinesterase inhibitors are the most effective method of managing the toxic effects associated with TCA overdose in pets |
|
Definition
FALSE
cholinesterase inhibitors are clinically ineffective and cause unnecessary complications instead
monitor arrhythmias with EKG, and control seizures with anti-convulsants |
|
|
Term
| What are the three primary features associated with serotonin snydrome (ingestion of SSRI + MAO) |
|
Definition
Autonomic instability (esp. MAO)
neuromuscular hyperactivity
agitation
all of these signs result from increased CNS and peripheral serotonin (5-HT) availability |
|
|
Term
| What clinical signs are associated with SSRI toxicosis? |
|
Definition
| agitation, vocalization, muscle tremors, vomiting, tachycardia, hyperthermia, transient blindness |
|
|
Term
| What supportive treatment is indicated in cases of SSRI toxicity? |
|
Definition
-Cyprohepatidine (IV/rectal): general serotonin antagonist
-Beta 1 AR-antagonist: treat tachycardia and hypertension
-Methocarbmaol: control muscle tremors
cool with fluids to address hyperthermia, anti-convulsants if seizuring, antiemetics if persistant vomiting |
|
|
Term
| Amphetamines are ______ drugs |
|
Definition
| sympathomimetic, increase availability of dopamine and norepinephrine |
|
|
Term
| How can you enhance excretion of ADD/ADHD drugs (adderall, ritalin, desoxyn, vyvase)? |
|
Definition
|
|
Term
| What are clinical signs associated with amphetamine toxicosis? |
|
Definition
-agitation, hyperactivity
-autonomic signs (tachycardia, hypertension)
-tremors, seizures, hyperthermia, coma |
|
|
Term
| T/F: diazepam is the anticonvulsant drug of choice to treat amphetamin toxicosis |
|
Definition
FALSE
benzodiazepines may increase sympathomimetic-induced aggitation) control seizures with CHLORPROMAZINE (major tranquilizer)
other tx includes 1.5-2X maintenance IV fluid therapy to maintain renal function and enhance excretion, methocarbamol to control muscle tremors, beta blockers to control tachycardia and hypertension |
|
|
Term
| Why are ephedrine and pseudoephedrine more toxic than phenylephrine? |
|
Definition
phenylephrine is more specific in its action:
ephedrine and pseudoephedrine act as agonists at alpha and beta adernergic receptors and evoke the release of norepi from sympathetic nerves
phenylephrine only acts alpha1 adernergic agonist (+alpha 2 at high doses) |
|
|
Term
| Ephedrine, pseudoephedrine and phenylephrine are most common in what over the counter human drugs? |
|
Definition
| nasal decongestants, vasoconstrictive eye drops |
|
|
Term
| What is the mechanism of action of ant-asthma human Rx (albuterol, salmeterol)? |
|
Definition
|
|
Term
| T/F: Anti-Asthma beta 2 agonists are selective to the beta 2 receptor at all doses |
|
Definition
FALSE,
in overdose situations these drugs activate all Beta AR receptor subclasses (beta 1 and beta 2) -->increased CAMP --> bronchodilation, vasodilation, shift of plasma potassium and phosphorus into intracellular space (this results in ventricular arrhythmias) |
|
|
Term
| What drugs can be used to treat adrenergic bronchodilator (i.e. asthma drug) toxicity induced tachycardia and ventricular arrhythmia? |
|
Definition
Beta- AR antagonist (propranolol)
Lidocaine |
|
|
Term
| What two things should you monitor in patients with adrenergic bronchodilator (asthma Rx) toxicity? |
|
Definition
Monitor for arrythmias with ECG
Monitor plasma potassium levels and supplement if needed |
|
|
Term
| How are adrenergic bronchodilators excreted from the body? |
|
Definition
|
|
Term
| Amlodipine, diltiazem, verapamil are human anti-hypertension drugs that act by blocking calcium channels. What clinical signs are associated with companion animal toxicosis? |
|
Definition
| hypotension with reflex tachycardia and AV block arrhythmias |
|
|
Term
| What is the mechanism of action of benzodiazepine-based anxiolytics (xanax, valium, klonopin), and non-benzodiazepine hypnotics? |
|
Definition
| These two classes of drugs bind to closely located allosteric sites on inotropic (associated with increased conductance through Cl channels, results in neuroinhibition) |
|
|
Term
| T/F: Human anxiolytic (benzodiasepines) and hypnotic drugs have a wide margin of safety in companion animals |
|
Definition
|
|
Term
| What are clinical signs present with acute toxicity following ingestion of anxiolytic/hypnotic Rx? |
|
Definition
50% present with CNS depression (ataxia, paresis, dull mentation)
50% present with CNS stimulation (can inhibit neurotransmission of inhibitory neurons, i.e. disinhibition) |
|
|
Term
| What is the antidote for anxiolytic/hypnotic toxicosis? |
|
Definition
Flumazenil (use with care, can lower seizure threshold, short half life --> must readminister frequently)
also get baseline renal/hepatic chemistry in animals with pre-existing disease to monitor excretory capacity of these organs (may need to treat more aggressively) |
|
|
Term
| What is the mechanism of action of Baclofen (muscle relaxant)? |
|
Definition
| GABA b receptor agonist (G-protein associated) --> neuroinhibition in spinal motor neurons |
|
|
Term
| T/F: Baclofen toxicosis is of longer duration |
|
Definition
TRUE
-Overdose results in saturation of elimination mechanisms
-large volume of distribution
-slow clearance from CNS tissues |
|
|
Term
| What clinical signs are associated with Baclofen toxicosis? |
|
Definition
| Vomiting, araxia, dyspnea, respiratory paralysis, seizures |
|
|
Term
| How is baclofen excreted from the body? |
|
Definition
In the urine
in cases of overdose fluid diuresis helps promote excretion |
|
|
Term
| T/F: You should NOT treat seizures associated with baclofen toxicosis with diazepam? |
|
Definition
FALSE
Diazepam interacts with the GABA-a receptor, while baclofen binds to the GABA-b receptor
*do not treat seizures or CNS excitation related to pseudoephedrine or anxiolytic/hypnotic(i.e. benzodiazepine and related compounds) toxicosis with benzodiazepines |
|
|
Term
| Acetaminophen toxicosis in cats is associated with what dose, and what clinical abnormality? |
|
Definition
low doses of acetaminophen (10-100mg/kg) in cats results in methemoglobinemia due to limited phase 2 acetylation
clinical signs: chocolate colored blood and mucus membranes, tachypnea, tachycardia, >35% MetHb = dyspnea |
|
|
Term
| Acetaminophen toxicosis in dogs is associated with what dose, and what clinical abnormality? |
|
Definition
| high doses of acetaminophen (100-600 mg/kg) overwhelm phase 2 acetylation resulting in CYP 450 oxidation of acetaminophen --> formation of NAPQI --> oxidative injury to hepatocytes |
|
|
Term
| What clinical signs are associated with acetaminophen toxicosis in dogs and cats? |
|
Definition
| tachypnea, facial and/or paw edema, cyanotic to muddy colored mucus membranes |
|
|
Term
| What molecule can bind to NAPQI and prevent oxidative damage? |
|
Definition
Glutathione,
normally only 4% of acetaminophen is CYP 450 oxidized to NAPQI so small concentrations of glutathione are adequate to neutralize any that forms. In overdose situations sulfation and glucuronidation pathways for acetaminophen biotransformation are overwhelmed so much more NAPQI is formed. When gluathione concentration is depleted by >30, NAPQI accumulates and perpetuates oxidative damage to cells |
|
|
Term
| Where in the hepatic acinus is oncotic necrosis due to excess formation of NAPQI the most extensive? |
|
Definition
Zone 3/centrilobular
(ie. the middle of the acinus) because this coincides with the greatest concentration of CYP 450 tissue expression coupled to the lowest partial oxygen pressure (i.e. furthest away from the hepatic artery) |
|
|
Term
| What is the antidote for acetaminophen intoxication? |
|
Definition
N-acetylcysteine
an orally bioavailable form of cysteine, which is the rate limiting factor in glutathione synthesis. |
|
|
Term
| T/F: You should give multiple doses of activated charcoal with a cathartic every third dose in cases of acetaminophen toxicity |
|
Definition
TRUE
enterohepatic recycling results in very slow excretion of acetaminophen |
|
|
Term
| What is the treatment of choice for methemoglobinemia? |
|
Definition
Iron reducing agents: vitamin C, methylene blue
oxygen therapy if dyspnic |
|
|
Term
| Aside from N-acetylcysteine what other treatments are beneficial in protecting the liver from oncotic centrilobular necrosis following ingestion of a toxic dose of acetaminophen? |
|
Definition
Cimetidine: decreases CYP 450 activity, thereby reduces formation of NAPQI
SAM/Marin are antioxidants that are hepatoprotective (must me given long term (1-3 months)) |
|
|
Term
| What are common sources of slicylates other than asprin tablets? |
|
Definition
Acne creams and washes
Bengay/oil of wintergreen (VERY high concentrations in this product) |
|
|
Term
| What will increase the elimination of salicylates from the body?A |
|
Definition
| alkalinize the urine (eliminated in the kidney via filtration AND tubular secretion |
|
|
Term
| Why are cats more susceptible for salicylate toxicity than dogs? |
|
Definition
| poor glucuronidation capabilities |
|
|
Term
| Low dose toxicity associated with salicylates is characterized by what clinical signs? |
|
Definition
| thrombopathy (in the form of abnormal platelet aggregation) with signs of primary hemostatic disorder, esp. gastritis with focal hemorrhage |
|
|
Term
| High dose salycilate toxicity is characterized by what three clinical manifestations? |
|
Definition
Acidosis (respiratory and metabolic)
Dehydration and Hyperthermia (uncoupling of oxidative phosphorylation --> ATP energy is converted into heat) |
|
|
Term
| How do NSAIDS like ibuprofin (advil/motrin) and naproxen (aleve) induce gastropathy? |
|
Definition
| inhibition of mucosal cytoprotective prostanoids + direct chemical irritant effects on upper GI tract + prolonged clotting times ----> ulceration and bleeding |
|
|
Term
| How do NSAIDS like ibuprofin (advil/motrin) and naproxen (aleve) induce nephropathy? |
|
Definition
| in very young or very old patients, low volume circulatory states, +/- impaired liver function --> loss of mucosal cytoprotection in poorly perfused kidneys --> ARF and necrosis of the renal papillae w/ retention of sodium, potassium, and water |
|
|
Term
| Which is more toxic to dogs, ibuprofen or naproxen? |
|
Definition
| Naproxen (>5mg/kg is a toxic dose, half life is 72 hrs!) |
|
|
Term
| What treatment can be used to accelerate NSAID excretion? |
|
Definition
fluid diuresis with LRS
+/- furosemide (loop diuretic --> increase urine output), and dopamine (renal vasodilation -- monitor CV function***) |
|
|
Term
| What is the mechanism of toxicosis following ingestion of 5-flurouracil (human dermatalogical neoplasia Rx cream)? |
|
Definition
| Two active metabolites are incorporated into RNA and DNA and stop chain growth, these effects are greatest in rapidly dividing cells (ie. GI epithelium and bone marrow) |
|
|
Term
| T/F: ingestion of 5-Flurouracil is very treatable and most patients recover |
|
Definition
FALSE
prognosis is grave, especially in cats |
|
|
Term
| What are the three most common clinical signs associated with 5-Fluorouracil toxicosis? |
|
Definition
-Persistent vomiting
-Seizures, non-responsive to diazepam
(remember*** don't treat pseudoephedrine or anxiolytic/hypnotic overdoses with benzodiazepines either**)
-dose dependent myelosuppression (delayed effect) |
|
|
Term
| When monitoring cell counts in patients recovering from 5-Fluourouracil toxicosis when should you start expecting normal numbers of RBC/WBC/platelets? |
|
Definition
25 days post ingestion
*monitor CBC every 3-4 days |
|
|
Term
| What is an early indicator of toxicity following ingestion of calcipotriene (human psoriasis Rx)? |
|
Definition
serum phosphorous is elevated before hypercalcemia can be appreciated
prognosis is good if tx is initiated before appreciable hypercalcemia |
|
|
Term
| Fentanyl is active at what receptor type and class? |
|
Definition
| selective mu-opioid agonist |
|
|
Term
| T/F: Clinical signs associated with fentanyl toxicosis in dogs and cats include CNS stimulation and mydriasis (dilation) |
|
Definition
FALSE
CNS stimulation and mydriasis in CATS
CNS depression, respiratory depression, hypothermia and miosis (constriction) in DOGS |
|
|
Term
| What is the antidote for Fentanyl toxicosis? |
|
Definition
Nalaxone (short half life in dogs may necessitate repeated dosings)
additional tx:
thermal support and ventilation
diazepam for seizures (CATS) |
|
|
Term
| T/F: ingestion of OTC steroid/antibiotic creams result in mild GI signs that are generally self limiting |
|
Definition
|
|
Term
| What clinical signs is most common following ingestion of Zinc Oxide (diaper rash creams)? |
|
Definition
spontaneous vomiting (ZnO is a gastric irritant and was previously used as an emetic agent)
*heavy metal toxicity is not anticipated except in cases of HUGE overdoses |
|
|
Term
| What is the active toxicant present in Tea Tree Oil? How are these toxins most commonly absorbed and excreted? |
|
Definition
Terpenoids (ex. terpinen-4-ol, eucalyptol)
Dermal absorption is most common, but also readily absorbed via GI mucosa.
eliminated in the urine |
|
|
Term
| Nicotine can be rapidly and completely absorbed through what three routes? |
|
Definition
| intestinal, airway, and dermal |
|
|
Term
| What clinical signs are associated with low doses, or early stage of high doses of nicotine? |
|
Definition
hypertension and tachycardia (sympathetic stimulation, more common in CATS)
SLUD and bradycardia (parasympathetic stimulation, more common in DOGS)
general CNS stimulation |
|
|
Term
| If nicotine stimulates nicotinic cholinergic receptors why is the late stage of high dose toxicity characterized by CNS depression and cardiorespiratory failure? |
|
Definition
| overstimulation results in desensitization and eventual blockade (ie. NO neurotransmission) at peripheral and central nACH-R |
|
|
Term
| Ingestion of Zinc oxide, steroid, and/or antibiotic ointments cause what degree of toxicosis? |
|
Definition
Mild toxicosis
clinical signs are usually mild and self-limiting, little to no treatment is required |
|
|
Term
| Ingestion of Tea Trea Oil and Nicotine patches/cigarettes cause what degree of toxicosis? |
|
Definition
Moderate toxicosis
systemic clinical signs that require medical treatment but not expected to be life threatening with appropriate care |
|
|
Term
| Ingestion of 5-Fluorouracil, salicylates, fentanyl, and calcipotriene among others cause what degree of toxicosis? |
|
Definition
Severe toxicosis
if untreated permanent organ damage and death would result, prognosis is variable |
|
|
Term
| Via which route are cattle most commonly exposed to pesticides? |
|
Definition
|
|
Term
| What is the golden rule of toxicology? |
|
Definition
| it is the DOSE that makes a poison POISONOUS |
|
|
Term
| What is the mechanism of action of stage 1 toxicity due to organophosphates and carbamates? |
|
Definition
| Acetylcholinesterase inhibition --> accumulation of acetylcholine at muscarinic and nicotinic Ach-R --> SLUDGE/bradycardia and muscle tremors/ seizures/paralysis of muscles of respiration (most common cause of death) |
|
|
Term
| T/F: Carbamates are more rapidly metabolized than organophosphates resulting in shorter duration of toxicity and more mild clinical signs |
|
Definition
TRUE
Seizures and bradycardia are less common in cases of carbamate toxicity |
|
|
Term
| Animals have three types of cholinesterases, where are they located? |
|
Definition
|
|
Term
| Why might blood acetylcholinesterase activity be only mildly inhibited even if the patient is experiencing signs associated with significant organophosphate toxicity (ex. seizures, dyspnea)? |
|
Definition
-acetylcholinesterase may reactivate prior to analysis of the blood sample
-in vivo snythesis of RBC could result in increased levels of active RBC associated acetylcholinesterase
-unrelated drug/chemical interactions |
|
|
Term
| T/F: oximes can reactived achetylcholinesterase that has been phosphorylated by organophosphates |
|
Definition
TRUE
*Carbamated acetylcholinesterase cannot be reactivated by oximes |
|
|
Term
| T/F: Pyrethroids are synthetic |
|
Definition
TRUE
Pyrethrins are natural |
|
|
Term
| Pyrethrins and pyrethroids are safe and effective insecticides common in topical products for companion animals, what negative side effect is associated with these products? |
|
Definition
Paresthesia --> excoriations and ulcers
esp. at doses >40% |
|
|
Term
| What species should never be exposed to pyrethrins? |
|
Definition
CATS
*use etofenprox (pseudo-pyrethroid) |
|
|
Term
| How are pyrethrins excreted from the body? |
|
Definition
|
|
Term
| Why do clinical signs associated with type II pyrethrum toxicosis in rumants resemble cyanide toxicosis? |
|
Definition
| Rumen bacteria release free cyanide groups from type II pyrethrum |
|
|
Term
| T/F: pyrethrum can increase estrogenic activity |
|
Definition
TRUE
can have a negative impact on male fertility |
|
|
Term
| What are the three most important treatments for animals exhibiting signs of toxicity following topically applied pyrethrins? |
|
Definition
bathe in degreasing shampoo and apply vitamin E oil to treat paresthesia
treat ataxia and muscle tremors with IV methocarbamol
IV fluid therapy for dehydration |
|
|
Term
| Why are some dog breeds (collies, aussies) especially sensitive to the toxic effects of ivermectin? |
|
Definition
| high incidence of mutations within the MDRI gene resulting in drug accumulation within the brain |
|
|
Term
| What three clinical signs are most commonly present in dogs with ivermectin toxicosis? How does toxicity manifest differently in cats? |
|
Definition
ataxia, seizures, hyperthermia
in cats --> HYPOTHERMIA |
|
|
Term
| What antidote/specific treatment can be used in cases of severe or non-responsive ivermectin toxicity? |
|
Definition
| Intralipid (20% IV fat emulsion) |
|
|
Term
| What is the mechanism of acute signs associated with iron toxicosis? |
|
Definition
| direct corrosive effect on GI mucosa --> vomiting and diarrhea +/- blood |
|
|
Term
| What is the mechanism of the later signs associated with iron toxicosis? |
|
Definition
| mitochondrial dysfunction, interference with cellular respiration, free radical formation --> metabolic acidosis, hepatic necrosis, tachycardia, hypotension and continued GI abnormalities |
|
|
Term
| What time frame is best to measure serum iron levels in cases of suspected iron toxicosis? |
|
Definition
4-6 hours after exposure
also look for radiopaque material on abdominal rads |
|
|
Term
| T/F: The best way to decontaminate a patient with suspected iron toxicosis is with activate charcoal |
|
Definition
FALSE
activated charcoal doesn't bind iron (or lead, or zinc), instead use aluminum hydroxide or milk of magnesia --> insoluble iron hydroxide |
|
|
Term
| What is the chelating agent of choice for the treatment of iron toxicity? |
|
Definition
Deferoxamine
**DO NOT USE LONGER THAN 24 HRS --> pulmonary hypertension |
|
|
Term
| Clinical signs associated with lead toxicity in small animals |
|
Definition
| CNS depression or agitation, seizures (k9), blindness, ataxia, mild anemia, vomiting, abdominal pain, diarrhea or constipation |
|
|
Term
| Clinical signs associated with lead toxicity in large animals |
|
Definition
| blindness, head pressing, ataxia, circling, anorexia, rumen stasis/colic |
|
|
Term
| What is the chelating agent of choice in cases of lead toxicosis? |
|
Definition
Succimer
* monitor renal function, especially in cats |
|
|
Term
| Clinical signs associated with Zinc toxicosis in dogs? |
|
Definition
| Mild to moderate GI signs followed by intravascular hemolysis, elevated liver enzymes, icterus, and compromised renal function |
|
|
Term
| What is a common manifestation of chronic zinc toxicosis in horses? |
|
Definition
| non-specific degenerative arthritis |
|
|
Term
| T/F: the most effective treatment in cases of zinc toxicosis is surgical removal or gastric lavage (if small and accessible) |
|
Definition
TRUE, physical removal is MUCH better than chelation
*can try using calcium disodium EDTA to chelate |
|
|
Term
| What clinical signs are seen following exposure (usually k9) to bufo toad toxin? |
|
Definition
| hypersalivation, red MM, hyperthermia, dyspnea, non-specific CNS stimulation, over time cardiac arrhythmias (brady or tachy) |
|
|
Term
| What is the decontamination method of choice in cases of bufo toad toxicosis? |
|
Definition
flush mouth with water for 10-15 minutes
*emesis is not recommended due to rapid onset of CNS abnormalities |
|
|
Term
| What clinical signs are associated with blister beetle toxicosis? |
|
Definition
| Direct irritant effect on skin and GI muscous membranes --> colic, ulcers, muscle tremors, hyperthermia, shock |
|
|
Term
| What mortality rate is associated with blister beetle toxicosis in horses? |
|
Definition
|
|
Term
|
Definition
dermal toxin --> bulls eye lesion with black scab (eschar) --> large slowly healing ulcer
if large dose systemic coagulopathies are possible |
|
|
Term
| T/F: sphingomyelinase D is the most important component of brown recluse spider venom |
|
Definition
TRUE
Sphingomyelinase D causes neutrophil migration, platelet aggregation, intravascular coagulation, and dermonecrosis |
|
|
Term
| What is the treatment of choice for lesions associated with brown recluse spider bites? |
|
Definition
lavage, debride, bandage ulcer
Dapsone, inhibits neutrophil function and may limit severity of the lesion |
|
|
Term
| What species is most affected by scorpion venom? |
|
Definition
Dogs
*doesn't seem to have much effect on cats |
|
|
Term
| Scorpion venom is primarily what kind of toxin? |
|
Definition
Neuro toxin
delays opening of sodium channels --> inhibition of neuromuscular transmision |
|
|
Term
| T/F: scorpion sting requires aggressive treatment |
|
Definition
| FALSE usually self limiting (pain, puruitis, +/- tremors, ataxia) within 24 hrs supportive care is sufficient |
|
|
Term
| What is the mechanism of toxicity due to bee/wasp sting |
|
Definition
| histamine release and influx of basophils w/ degranulation --> pain, vasodilation, hypotension |
|
|
Term
| What are the four potential physiologic responses to bee/wasp sting? |
|
Definition
1. local edema/pain/erythema (sec to min)
2. regional " "
3. anaphylaxis (min)
4. delayed type hypersensitivity (DIC, vasculitis, arthritis) (3-14 days) |
|
|
Term
| T/F: total number of bee/wasp stings is more important than species implicated |
|
Definition
|
|
Term
| T/F: Gila monster (heloderma sp.) venom is primarily a DERMAL toxin |
|
Definition
TRUE
*no neurotoxins and no coagulopathies |
|
|
Term
| What clinical signs are associated with gila monster bites? |
|
Definition
| most damage due to force of bite --> localized edema, hemmorhage, echymoses, lymphangitis and pain +/- rare tissue necrosis |
|
|
Term
| T/F: most blue green algae is toxic |
|
Definition
|
|
Term
| Microcystins are ______ produced by Microcystis, Anabaena, Planktothrix, other genera |
|
Definition
| hepatotoxins <-- free radical formation and disruption of mitochondrial oxidative phosphorylation results in centrilobular necrosis |
|
|
Term
| Anatoxins are ______ produced by Anabaena, Planktothrix, Oscillatoria, Microcystis, other genera |
|
Definition
neurotoxins <-- irreversible anticholinesterase inhibitor results in peripheral cholinergic neurotransmision at the neuromuscular junction
*like OP toxicity, but cannot cross blood brain barrier |
|
|
Term
| Clinical signs associated with blue green algae toxicosis? |
|
Definition
microcystin --> diarrhea, icterus, shock
anatoxin a --> muscle tremors and paralysis
anatoxin as --> SLUDGE |
|
|
Term
| T/F: prognosis for animals affected by blue green algae toxicosis is extremely poor |
|
Definition
TRUE
most are found dead, toxicity is so rapidly progressive that treatment is rarely effective |
|
|
Term
| What clostridium botulinum toxins are associated with disease in animals? |
|
Definition
|
|
Term
| What is the mechanism of action of c. botulinum toxicity? |
|
Definition
| potent NEURO toxin --> prevent release of acetylcholine at neuromuscular junction --> progressive flacid paralysis |
|
|
Term
| What are the three ways horses/cattle acquire botulism? |
|
Definition
1. preformed in feed (C1)
2. contamination of wounds (B)
3. colonization of GI tract (B/C1) <-- shaker foals with GI ulcers |
|
|
Term
| Why are cattle less susceptible to botulisum than horses? |
|
Definition
| ruminal microbes can degrade the toxin reducing systemic absorption |
|
|
Term
| How are dogs most commonly exposed to enterotoxins and what are two organisms that are commonly implicated? |
|
Definition
from ingesting toxins in contaminated food/garbage
commonly implicated organisms are Staph aureus, and Bacillus cereus |
|
|
Term
| T/F: dogs with Staph aureus enterotoxemia usually display both vomiting and diarrhea |
|
Definition
TRUE (vom 1st, then dia)
B. cereus is usually limited to either an emetic form, or a diarrheal form |
|
|
Term
| Coral snake venom is primarily a _____ toxin |
|
Definition
| NEURO toxin --> muscle paralysis and CNS depression |
|
|
Term
| T/F: coral snake antivenom can cause allergic reactions |
|
Definition
TRUE
*specific antivenom is not readily available, however pretty good crossreactivity with antivenom from other species |
|
|
Term
| Which species is most susceptible to black widow spider venom? |
|
Definition
|
|
Term
| Pit Viper venom is primarily a _____ toxin |
|
Definition
| HEMO toxin --> inhibition of clotting factors, dramatic drop in blood pressure |
|
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