Toxicology Exam 1

Front 1

what is the difference between a toxicant and a toxin?

Back 1

A toxicant can be any substance a toxin is only a natural substance

Front 2

All toxins are toxicants but not all toxicants are toxins (T/F)

Back 2

True
toxins are biological toxicants

Front 3

What is the difference between acute, subacute, subcronic and chronic toxicity?

Back 3

acute toxicity- the effect of a single dose or multiple doses over 24 hours

Subacute= the effect produced by daily expures from 1 to 30 days

Subchronic = the effect produced from daily exposure from 30 to 90 days

chronic = the effect produced by daily exposures from 3 months or more

Front 4

what is the chronicity factor?

Back 4

chronicity factor is the ratio of acute LD50 to chronic LD50. A low chronicity factor means that chronic toxicity is unlikley. A low chronicity factor is generally due to rapid metabolism

Front 5

What does a low chronicity factor indicate?

Back 5

A low chronicity factor indicates that chronic toxicity is unlikely most likely due to rapid metabolism

Front 6

What would the dose of a toxin that is extremely toxic be?

Back 6

extremely toxic = 1mg/kg or less

Front 7

What would the dose of a toxin that is highly toxic be?

Back 7

> 1-50 mg/kg

Front 8

What would the dose of a toxin that is moderately toxic be?

Back 8

>50-500mg/kg

Front 9

What would the dose of a toxin that is slightly toxic be?

Back 9

>,5 -5 g/kg

Front 10

What would the dose of a toxin that is pratcially non toxic be?

Back 10

>5-15 g/kg

Front 11

What is LD 0

Back 11

highest dose that does not cause any death

Front 12

What is LD 50

Back 12

dose that kills 50% of animals in a group

Front 13

What is LD 100

Back 13

lowest dose that kills all the animals in a group

Front 14

What is the risk factor?

Back 14

the risk factor can be calculated as the ratio between toxicity and risk use level (dose used in therapy)
The closer the toxic dose to the use dose the greater the risk (or lower your factor)

Front 15

What does a low risk factor indicate?

Back 15

The lower the factor the higher the risk

Front 16

Weak acids are more ionized in what pH

Back 16

basic

Front 17

What are the route of toxin exposure and what is the most common?

Back 17

The most common route of exposure is ORAL. However dermal route (insecticides) and inhalation (insecticides and toxic gases) are also seen.

Front 18

What effect will enzyme inhibitors and enzyme inducers have on toxins?

Back 18

enzyme inhibitors can decrease lethal synthesis
Enzyme inducers can increase lethal synethesis

Front 19

how does volume of distribution relate to drug diposition?

Back 19

the larger the volume of distribution the morel ikely the drug is to leave the extracellular space and enter the intracellular space or concentrate in tissues. Drugs with a Vd <1 have limited distribution, Vd>1 have a wide distribution

Front 20

What are common metabolism reactions in the liver? Which reactiosn are cats deficient in? Which reactions are cattle best at? What reactions are birds poor at ?

Back 20

The liver is primary site of biotransformation. Reactions in the liver are generally divided into phase I and phase II.
Phase I includes oxidation, reduction and hydrolysis
Phase II includes conjugation
Cats are deficient in conjugation due to a deficiency in glucuronly transferase
Ruminants and horses have higher levels of oxidative enzymes.
birds lack oxidative enzymes

Front 21

What is the importance of enterohepatic recirculation in toxicology?

Back 21

important to note in toxins because it determines how we use absorbents like activated charcoal. Drugs with enterohepatic recirculaion need repeated doses of activated charcoal

Front 22

What is first order kinetics

Back 22

most drugs follow first order kinetics meaning that the rate of remvoal of the durg from the plasma is proportional to the concentration persent at the given time. Constant half life

Front 23

What is zero order kinetics?

Back 23

zero order kinetics means that the rate of elimination of the drug remains constant no matter the amount. Process is saturable. These drugs have a half life that changes based on concentration

Front 24

If the 1/2 life of a drug that follows first order kinetics is 2 hours, how long will it take for the drug to reach 25% of its iniital blood level

Back 24

4 hours

Front 25

What is the strongest evidence of toxin diagnosis?

Back 25

confirmed diagnoeses- reached by using all criteria of diagnosis. these include: history, clinical findings, identification of source and lab work. The diagnosis is confirmed when these agree. Tetative diagnoses is the least evidence and presumptive diagnoses is the middle

Front 26

what are questions to ask to help determine if a toxicity has occured?

Back 26

suspected toxin type
does owner have container
was exposrue witnessed or evidence suggestive of ingestion
maximum amount
route of exposure
when did exposure occur
for farm animals, pertinent questions would also include: number of affected, number dead, type of management

Front 27

Do most toxins have a pathognomonic lesion, clinical signs or lab work?

Back 27

no
often lesions are similar to other disease processes and toxins.

Front 28

why might a postive chemical analysis not confirm toxicity or a negative chemical analysis not rule out a toxicity and why is chemical analysis often not useful in treatment?

Back 28

positive results may not indicate toxicity only exposure.

Front 29

What are general principles of sample submission?

Back 29

speciments should be submitted with a complete signalment, weight, history, PE, lab work
source should be on label
containers should be labeled with waterproof ink

Front 30

IMEF

Back 30

Southern California & Arizona

Front 31

what is the procedure for collecting and shipping blood and serum samples?

Back 31

collect the appropriate quantity of sample
serum should be frozen
blood should be refrigerated
(freezing causing hemolysis)
separate serum from blood follow appropriate procedures
appropriate tubes should be used

Front 32

What is the procedure for collecting and shipping forages and feed?

Back 32

collect sample
do not wash
green and silages should be frozen

Front 33

what factors should be addressed first in toxicologic emergencies?

Back 33

life threatening problems first: seizures, respiratory distress, shock

Front 34

what are things owners can do at home for toxicological emergencies?

Back 34

minimize stress at facility until docotr arrives in LA
transport to hospital with minmal stress (SA)
decontaminate with bath, emetic, wash eye, etc

Front 35

how do toxicological emergencies differ from other emergencies?

Back 35

even stable patients need immediate tx with toxins that cause acute toxicity

Front 36

methods of decontamination include??

Back 36

removal of the suspected source of toxicity
removal of the posion from site of absorption
decrease the rate of absorption
enhance elimination of the poison

Front 37

methods of removal of poison from the site of absorption include?

Back 37

emetics
gastric lavage and enterogastric lavage
rumentomy/gastrostomy/endoscopy
purgatives
skin and eye decontamination

Front 38

general rules of emesis ar>

Back 38

emetics are helpful if used within 1 to 2 hours of ingestion of toxin
emetics may not completely empty stomach contents but the eariler the better

Front 39

what are some contraindications of emetics

Back 39

unconsciousness due to rik of aspiration, corrosive toxins may cause further injury to esophagus, species that can't vomit

Front 40

what are some examples of at-home emetics?

Back 40

3% hydrogen peroxide, syrup of ipecac, NaCl solution, fresh ground mustard

Front 41

What are emetics used in the hospital?

Back 41

apomorphine and xylazine

Front 42

how does hydrogen peroxide work?

Back 42

causes vomiting via irritation of GI system

Front 43

in what species is hydrogen peroxide used?

Back 43

dogs, can be used in cats but not offten

Front 44

what are some adverse effects of hydrogen peroxide

Back 44

potential gastric ulceration/perforation in particular if GIT is severely compromised by toxin.
air embolism
gastric irritation

Front 45

how do at home emetics work (besides H2O2)

Back 45

acts as direct irritant

Front 46

why are some at home emetics not used?

Back 46

some feel these cause excessive irritation

Front 47

how does apomorphine work as an emetic?

Back 47

opioid agonist acts directly on crtz to induce vomiting

Front 48

in what species is apomorphine primarily used?

Back 48

dogs

Front 49

why is apomorphine not recommended in cats?

Back 49

more likely to cause excitement, CNS and respiratory depression, and excessive vomiting

Front 50

how is apomorphine administered

Back 50

Subconjunctival sac, IV or IM

Front 51

What are contraindications and side effects of apomorphine?

Back 51

not recommended in animals that are depressed
may cause excitement and respiratory depression i ncats

Front 52

how are side effects of apomorphine controlled

Back 52

side effects can be reversed with naloxone except for vomiting

Front 53

whaqt are some dopamine agonsits that can be used to reverse vomitting caused by apomorphine

Back 53

metoclopramide-
chloropromazine

Front 54

why are repeated doses of apomorphine not likly to be helpful if vomiting is not seen after first

Back 54

additional doses may inhibit vomiting or cause side effects

Front 55

how does xylazine cause vomiting

Back 55

alpha 2 agonist that induced vomiting by stimulation crtz

Front 56

in what species do we use xylazine for emesis

Back 56

cats

Front 57

how is xylazine administered for emesis

Back 57

iv, im, sc

Front 58

side effects for xylazine

Back 58

may cause cns and respiratory depression for several hours

Front 59

how can xylazine be revesred

Back 59

yohimbine

Front 60

how effective are purgatives in decreasing absorption?

Back 60

not effective but may be good when combined with activated charcoal

Front 61

side effects and contraindidcations of purgatives

Back 61

purgatives may increase vomiting
hypovolemia, dehydration, intestinal obstruction and corrosive toxins are contraindicated
magnesium sulfate may increase mganesium levels

Front 62

how does precipitation decrease absorption and what are some examples?

Back 62

the use of chemicals that precipitate the toxicant thereby decreaseing absorption (make less soluble)

Front 63

what is adsorption?

Back 63

physical binding of toxicant in the GIT to an unabsorable carrier to that it cannot be absorbed and is eliminted in the feces.

Front 64

what is an example of an absorbent?

Back 64

activated charcoal

Front 65

what substances are NOT bound by activated charcoal

Back 65

ethanol, methanol, heavy metal salts, fluoride and nitrate and nitrite, NaCl, chlorate, bleach, fertilizer, ammonia and cyanide

Front 66

What type of molecules does activated charcoal work best on

Back 66

large non-polar molecules.

Front 67

contrainidcations and side effects of activated charcoal

Back 67

comatose patients
induces vomiting

Front 68

how does ion trapping decrease intestinal absorption?

Back 68

involves ionizing toxins to they are less likely to be absorbed
weak bases are ionized with strong acids

Front 69

how effective is ion trapping

Back 69

not effective

Front 70

methods of enhancing the elimination of toxins/

Back 70

fluids
urine pH modifers
peritoneal dialysis

Front 71

when are fluids helpful in enhancing elimination?

Back 71

fluids will help renal elimination of renal excreted toxins in particular if a patient is dehydrated

Front 72

In what patients must fluids be used with caution?

Back 72

use caution in patients with renal and heart toxicity or previous illness (may cause fluid overload)

Front 73

what drugs are sometimes combined with fluid therapy to enhance elimination and what must be accomplished prior to giving these drugs?

Back 73

sometimes patients are fluid loaded and then diuretics are used to increase urine output (mannitol and lasix).
- volume must be restored before giving diuretics. If not GFR and toxin clearence may actually decrease due to hypovolemia
- it is debatable as to if diuretics will actually help clear toxins/ GFR vs. just eliminate water

Front 74

How do urin pH modifiers worK?

Back 74

by ionizing the molecule in the renal tubules it becomes trapped and is excreted. It is trapped by ionizing because ionized molecules cannot easily cross lipid membranes

Front 75

when does ionization work best, and when is it less effective?

Back 75

- ionization works best for weak acids and weak bases
- ionization can be performed when the counpound is not highly lipid bound, suitable pKa and is primarily distributed to the extracelllular space
-countraindcated in drugs with large volume of distribution , protein bound, lipid soluble or drugs metabolized in the liver or other tissues.

Front 76

what drugs can be used for acidification, when is it contraindicated and what are some examples?

Back 76

Ammonium chloride or methionine is used to acidify and ionize weak bases such as alkaloids or amphetamines. Acididication therapy is contraiindicated in patients with metabolic acidosis.

Front 77

What drugs can be used for alkalinziation, what are some potential adverse effects and what are some examples?

Back 77

soidum bicarbonate
ionizes weak acids such as NSAIDS or phenobarbital
may cause hypokalemia, hypernatremia, decreased ionized calcium and paradoxical CNS/intracelullar acidosis, secreased O2 delivery to tissues and volume overlaod

Front 78

when should hemodialysis or peritoneal dialysis be considered to eliminate toxins?

Back 78

hemodialysis and peritoneal dialysis can be performed when renal function is poor or to increase toxin elimination

Front 79

Methods of toxin dilution include

Back 79

milk and water

Front 80

when is toxin dilution recommended?

Back 80

when a corrosive toxicant has been ingested

Front 81

With what toxicants might lipid administration be beneficial and who would it help?

Back 81

-Helpful with lipid soluble toxicants like ivermectin
- lipids may help bind the lipid soluble toxin in the blood and thereby prevent the toxin from getting to the site of action

Front 82

If an animal presented to your hospital after being exposed to a toxicant which decontamination procedures would most likely be performed?

Back 82

1. contact poison control
2. activatted charcoal if vomiting is not contraindicated.

Front 83

why are organophosphates considered more dangerous than other insecticides?

Back 83

most organophosphates are highly toxic range. Sensitivity depends on species and type. BIRDS and FISH
More dangerous due to a close treatment and toxic range. They are not as selective for insects. They have a lower risk ratio

Front 84

What is the onset of clinical signs of organophosphates?

Back 84

mostly acute (often minutes when ingested).

Front 85

How does environment, quality of product, storage, vehicles, and age effect toxicity of organophosphates?

Back 85

toxicity decreased by degradation of the compound in the environment
- technical grades are more toxic than pure
organic solvents increase toxicity
drugs that require activation are less toxic to young animals due to decreased biotransformation.

Front 86

what sre some drug interactions with organophosphates?

Back 86

-malathion and coumaphos are synergistic
muscle relaxants and neuromuscular blockers increase toxicty
Enzyme inducers such as phenobarbital and chlorinated hydrocarbon insecticides may decrease or increase toxicity.
Enzyme inducers increase toxicity in cases of lethal synthesis such as malathion and parathion

Front 87

What is the difference between systemic or non-systemic organophosphatese and what are some examples?

Back 87

non-systemic = malathion and parathion
systemic = coumaphos and dichlorvos
systemic forms have a longer recovery and may have a longer time until onset of action. Clinical signs of systemic are more simular to organochlorines at certain stages of toxicty. Systmeic have a molecular structure that is more similar to organochlorines.

Front 88

What are some toxicokinetic concerns with organophosphates?

Back 88

most need enzymatic activation by the liver (parathion, malathion)
- tolerance may develop with continued exposure due to enzyme induction
- protein binding, enzyme induction and adaptation/alteration of cholinergic receptors when exposed to chornic excessive amount of Ach (decreasd/down regulation of Ach receptors) may lead to tolerance

Front 89

What is the mechanism of action of organophosphate in acute toxicosis?

Back 89

IRREVERSIBLE inhibition of acetylcholineterase causes neurologic stimulation

See muscarinic signs before nicotinic signs and neuromuscular stimulation

Excessive depolarization eventually results in ganglionic and neuromuscular blockade --> neuromuscular depression

Front 90

what is aging and why is it important in regards to organophosphates

Back 90

when organophosphates are changed chemicallly by organophosphates so that they are permanently dysfunctional
important because once aged ACHase cannot be reactivated by 2 PAM.

Front 91

what are the clinical signs of acute organophosphate toxicosis?

Back 91

- PNS/muscarinic stimulation. PSN signs are typically seen first and predominant in most tissues. (DUMBLES, bronchoconstriction)
-later ganglionic nicotinic stimulation causes vasoconstriction due to predomination of sympathetic in blood vessels. may see other sympathetic signs in other organs but typically PSN predominates
- Neuromuscular nicotinic stimulation causes neurlogic stimulation signs (remor, muscle fasciculation, etc)
- Nicotinic blackade causes neurlogic depression and can cause respiratory paralysis resulting in death
-signs of cns stimulation causes neurlogic excitement (seizures)
- signs of CNS depression may also be seen in particular after prolonged CNS stimulation resutling in coma, depression, etc

Front 92

what species are not reported to have seizures with organophosphates?

Back 92

ruminants

Front 93

can organophosphates be chemically tested for? If so is there a specimen of choice?

Back 93

can test for OP in rumen stomach contents, hair, and skin
-can also test actylcholinesterase activity

Front 94

Do oganophosphates have any specific antidote and what is the main type of supportive care require?

Back 94

atropine (partial antidote) and 2 PAM (full antidote) are antidotes

2 PAM can reactivate ACHase if it is not aged

supportive care involves tx of seizures and respiratory support

always treat life threatehing conditions first

Front 95

why is atropine only a partial antidote and is 2 PAM a full antidote?

Back 95

-atropine only blocks muscarinic effects
-2 PAM can decrease muscarinic (decrease parasympathetic activity) and nicotinic activty (decrease sympathetic, parasympathetic and NMJ activation

Front 96

Is 2 PAM or atropine needed in intermediate syndrome?

Back 96

typically these patients do not have muscarinic signs (due to muscarinic receptor down-regulation) therefore atropine is not generally recommended.

Front 97

how can atropine be used to confirm organophosphate toxicosis?

Back 97

give smaller dose of atropine similar to that used in anesthesia. IF the animal responds to the atropine it is likely not organophosphate toxicosis.

Front 98

what is the prognosis/recovery period for organophophates?

Back 98

best if treated early but recovery period can be long in some cases. high doese = rapid death

Front 99

Why are carbamates less toxic than organophosphates?

Back 99

-similar relative toxicity to organophophates but relative toxicity depends on species ad type.

- however less toxic than OP due to reversible inhibition and rapid metabolism

- somewhat more used then organophosphates d/t decreased toxicity

Front 100

what are some toxicokinetic concerns with carbamates?

Back 100

do not require liver activation and rapidly metabolized

Front 101

what is the mechanism of action of carbamates?

Back 101

similar to organophosphates but inhibition of acetylcholinesterase is reversible

Front 102

what are the clinical signs of carbamates?

Back 102

similar to acute toxicity with organophosphates.

Front 103

can carbamates be chemically tested for? If so, is there a specimen of choice and waht is the problem with acetylcholinesterase testing?

Back 103

-chemical testing is possible but toxicant id quickly degraded once absorbed so testing tissues is not very useful. Stomach contents therefore may be better
-Acetylcholinestrase activity can be checked but due to reversbile inhibition they maay also be less useful
-In other words by the time the sample reaches the lab the ACHase may no longer be inhibited because inhibition is reversible.
-Response to treatment may also help confirm diagnosis

Front 104

Do carbamates have any specific antidote and what is the main type of supportive care required?

Back 104

-Atropine is partial antidote
-2PAM is not used- may be more harmful

Front 105

What is prognosis/recovery period of carbamates

Back 105

recovery and prognoses are better than organophosphates, but large amounts can result in a poor prognosis.

Front 106

organochlorines toxicants include?
`

Back 106

diphenyl aliphatics (DDT, methoxychlor)
aryl hydrocarbons (lindane)
cyclodienes (Aldrin, toxaphene)

Front 107

what are some environmental concerns with organochlorines?

Back 107

very persistent in enviornment because they resist chemical or microbial decomposition (there are exceptions espceially if they are protected by a layer of soil)
-residues may appear naturally in animal tisssues due to environment contamination
-environmental residues may cause BIOACCUMULATION

Front 108

why is organochlorine toxicity less common currently?

Back 108

used in 1950s and early 1970s as insecticide and ectoparasiticide.

Front 109

what is the species sensitivity and susceptibility of organochlorines?

Back 109

all animals are susceptible but CATS are most sensitive

Front 110

what is the onset of clinical signs of organochlorines?

Back 110

typically acute toxicity (few minutes to 1 to 2 days) but dose dependent and with sublethal doses toxicity may be subactue (over several days)

Front 111

what are some toxicokinetic concerns with organochlorines?

Back 111

mainly distributed to fat then brain
-rapidly taken up and sotred in fat (fat acts like a sink) and is slowly released
-distribution to fat to some degree protects brain. However with large doses enough can accumulate in the brain to cause toxicity. slow release from fat casuses long half life and can prolong toxicity
-initial distirubtion to fat causes quick decrease in blood levels but slow release from the fat resutls in a long half life (may be weeks to months)
-also distributes to fetus
-metabolized by liver
-enzyme inducer
- can increase the toxicity of organophosphates with lethal synthesis (malathion, parathion) and decrease the toxicity of organophosphates without lethal synthesis
- metabolites of diphenyl aliphatics and cyclodienes are more toxic (lethal synthesis)
- excreted in bile (undergoes enterohepatic rercycling), feces, urine and milk

Front 112

what is the mechanism of action of organochlorines?

Back 112

-diphenyl aliphatics interfere with mechanism where soidum influx is stopped and potassium efflux is started during the action ptoential, this results in repetitive nerve discharges
-lindane may inhibit GABA binding
-Cyclodienese stimulate the CNS by an unknown mechanism

Front 113

what are the clinical signs of organochlorines?

Back 113

-mainly see CNS excitement
-often see seizures (may see CNS depression between seizures)
- may be explosive or slowly progressive
- abnormal posture and walking backward is seen in cattle
- birds show depression abnormal postures apparent blindness and death
-early gastrointestinal signs may also be seen

Front 114

Can organochlorines be chemically tested for?

Back 114

chemical analysis confrims acute toxicosis if the insecticide is in the blood, liver or brain, but levels do not correlate with severity of clinical signs
- brain concentrations are better correlated with toxicosis than fat. Remeber the fat takes up toxin thereby decreasing level in the brain and blood. After uptake by the fat the toxin is released back into the blood but it is a slow release. So fat levels may be greater than the blood or brain levels. This leads to a situation of where no toxicity occurs depsite high levels in th fat. However, if high levels are found in the brain then the clinical signs are likely related to the toxin

Front 115

do organochlorines have any specific antidote and what is the main type of supportive care required?

Back 115

no specific antidote, need to control seizues

Front 116

what is the prognosis/recovery period of organochlorines?

Back 116

-poor if comatose otherwise guarded to good
-recovery time is moderate
-signs such as seizures may last 48 to 72 hours but residues can persist for months to years.

Front 117

what is the definition of pyrethrins, pyrethroids, and pyrethrum?

Back 117

- pyrethrins are from pyrethrum flowers (chrysanthemum) they are natural
- pyrethroids are synthetic and divided into type 1 and type 2
-pyrethrum includes natural and sythetic forms

Front 118

what are some important differences between pyrethrins and pyrethroids?

Back 118

unstable in light and air so environmental toxicity limited by pyrethroids are more stable

Front 119

what is an important source of pyrethrins and pyrethroids?

Back 119

flea product and tick control in dogs and cats

Front 120

why are pyrethrums a relatively safe insecticides?

Back 120

highly toxic but considered to have low toxicity to animals. Dose used to kill insects is much lower than toic dose in aniamls

Front 121

what is species sensitivity and susceptibility of pyrethrins and pyrethroids?

Back 121

-dogs, cats, and large animals are susceptible
-cats may be more sensitive and some individuals seem to be more sensitive
-very toxic to fish and some birds

Front 122

how can the toxicity from pyrethrin and pyrethroids be increased? Which is more potent, pyrethrins or pyrethroids, and what type of pyrethroid is most toxic?

Back 122

-piperonyl butoxide is added to inhibit enzymes that inactivate pyrethrins. This will increase toxciity and is used commercially as pyrethrin synergist
-pyrethroids are more potent than pyrethrins
-type 2 are generally more toxic than type 1

Front 123

what are some toxicokinetics concerns with pyrethrins and pyrethroids?

Back 123

-very rapidly inactivated by plasma esterases and by liver enzymes
-rapid metabolism will decrease toxicity
-also metabolized in GIT

Front 124

what is the mechanism of action of pyrethrins and pyrethroids?

Back 124

-prolonged opening of soidum channels--> impulse conduction

Front 125

what are the clinical signs of pyrethrins and pyrethroids?

Back 125

-pyrethrins and pyrethroids primarily cause CNS excitement
-tremors are more common than seizures
-weakness may be seen with Tpye 2
=Gastrointestinal signs may also be seen
-Dermal exposure may cause allergic skin reaction
-Systemic anaphylactic reactions are rare.

Front 126

what are the clinical signs of pyrethrins and pyrethroids?

Back 126

CNS excitement
tremors, seizures
weakness
GIT signs
dermal exposure- allergic skin reactions
systemic anaphylactic rxn =rare

Front 127

can pyrethrins and pyrethroids be chemically tested for? If so, is there a specimen of choice?

Back 127

can be tested for but often low tissue levels (due to rapid metabolism) and difficult to detect, in addition tissue levels are not well correlated with clincial signs

Front 128

Do pyrethrins and pyrethroids have any specific antidote and what is the main type of supportive care required?

Back 128

-no antidote
- need to control tremors
-may need to treat skin reactions with anti-inflammatories, rarely treatemnt for anaphylaxis is needed

Front 129

what drug is considered more effective than valium in controlling pyrethrin induced tremors?

Back 129

-methocarbamol (mainly for tremor and maybe seizure)
- for full on seizures (not tremor), diazepam or other anticonvulsant may be superior to methocarbamol but not all sources agree

Front 130

what is the prognosis/recovery period of pyrethrins and pyrethroids?

Back 130

-excellent in most cases unless signs are advanced
- moderate recovery time
- animals that recover generally take 24-48 hours

Front 131

What are sources of rotenone?

Back 131

-historically used to be placed on arrowheads to kill fish
-used as a pesticide in water to kill fish
-used for garden pest control
-used for ear mites in dogs, cats, and rabbits

Front 132

what is the species sensitivity and susceptibility of rotenone toxicosis?

Back 132

low toxicity to mammals
chickens are resistent

Front 133

what is the onset of clinical signs of rotenone toxicosis?

Back 133

acute most common

Front 134

what factors can increase rotenoone toxicity?

Back 134

formulation (emulsion is more toxic)
sometimes combined with pyrethrins
route more toxic by ingestion and inhalation

Front 135

what is the mechanims of action of rotenone toxicosis?

Back 135

-irritant to contact surfaces
-inhibits energy metabolism
- inhibition of NADH prevents formation of substances such as glutamate and pyruvate that need to oxidize by NAD to be fomred
-Rotenone also inhibits electron transport

Front 136

What are the clinical sings of rotenone toxicosis?

Back 136

in acute toxicosis inhibition of energy production results in gastrointestinal abnormalities and possibly neuroligc abnormalities (depression and excitment are seen)
-neurologic disease may lead to respiratory deprssion and death. Dyspnea may be seen prior to respiratory depression.
-local irritation to contact tissues such as the skin and eye may cause conjunctivitis, congestion and dermatitis
-chronic signs cause liver and kidney damage

Front 137

does rotenone have any specific lesions or bloodwork findings?

Back 137

-no specific findings
-not specific but may see hypoglycemia on bloodwork

Front 138

does rotenone have any specific antidote and what is the main type of supportive car required?

Back 138

no specific antitode
need to suppor GIT and treat seizures or respiratory depression.

Front 139

what is the prognosis of rotenone?

Back 139

excellent in most cases

Front 140

what food is D limonene found in?

Back 140

citrus peels

Front 141

What are sources of D limonene?

Back 141

control of lice, fleas, ticks
desiccant that destroyes insect cuticle
food additive and fragrance.

Front 142

what is the relative toxicity od D limonene?

Back 142

toxicity in cats occurs at 5x recmmoneded dose for dogs

Front 143

what is the species sensitivity nd susceptibility of D limonene

Back 143

dogs and cats are susceptible
cats are more sensitive than dogs

Front 144

what is the onset of clinical signs of D limonene?

Back 144

mostly acute for neurologic and cardiovascular abnormalities (minutes to hours)

Front 145

how can D limonene toxicity be ptoentitated?

Back 145

toxicity potentiated by piperonyl butoxise and other enzyme inhibitors

Front 146

what is the mechanism of action of D limonene?

Back 146

mechanism of neurologic and cardiovascular dysfunction is unknown
vasodilation caused by the toxin in central and peripheral vessels may be due to a neuronal mechanism.
idosyncratic skin leasions

Front 147

what are the clinical sings of D limonine

Back 147

nervous system dysfunction
cns dperession
may see neurlogic excietment
cardiovascular dysfunction
causes hypotension via vasodilation
hypotherma
acute necrotizing dermatitis

Front 148

does D limonene have any specific lesions or bloodwork findins?

Back 148

no

Front 149

does D limonene have any specific antidtoe, and what is the main type of supportive care required?

Back 149

no specific antidote
-cases with large skin lesions may need tx of vasodilation (fluids/vasopressors)

Front 150

what is the prognosis for D limonene toxicosis

Back 150

in animals with no skin lesions short recovery - 24 hours
skin lesions are longer recovery with poorer prognosis

Front 151

what are ths oruces/uses fo napthalene?

Back 151

found in mothballs, urinal disks and toilet bowel/diaper pan deoodarant blocks

Front 152

what is the species senstivity ans suceptibility of naphthalene?

Back 152

cats and dogs are suceptible
cats are more sensitive

Front 153

onset of cllinical signs of napthalene?

Back 153

acute but may be over several days
time may vary due to reate of absorption which is dependent on form. for exmaple whole moth balls take a dew days to be absorbed

Front 154

what are some toxicokinetic concerns with naphthalene?

Back 154

whole mothball in the GIT may take several days to be absorbed

Front 155

what is the mechanism of action of naphthalene?

Back 155

irritant to contact tissues like the GIT
metabolie causes oxidative injury to RC making them fragile resulting in hemolytic anemia (Heinz body)
oxidative injury - likely to cause liver and GIT issues
hemoglobinuria from red cell lysis can lead to secondary injury to kidneys

Front 156

what are the clinical signs of naphthalene?

Back 156

-primarily causes GI signs and evidence of hemolytic anemia (pale, yellow gums, tachycardia), but may also see liver damage and secondary renal injury
-seizures and cataracts (in neonates)
breath odor

Front 157

what are specific bloodwork findings associated with naphthalene toxicosis

Back 157

hemolytic anemia and heinz bodies. methemoglobin (brown blood)

Front 158

what is the prognosis of napthelene toxicosis

Back 158

depends on complications. can be poor if compilcations like liver and renal disease develop and prolonged recovery if severe hemolytic anemia

Front 159

what are the sources of nicotine?

Back 159

contaminated feed with nicotine sulfate as plant insecticide
wild tobacoo may be source in farm animals
sources of exposure in small animals include chewing tobacoo, nicotine patches, nicotine gum, cigarettes or cigars

Front 160

onset of clinical signs of nicotine?

Back 160

acute toxicity (course of signs rapid, within a few minutes to an horu)

Front 161

what are some toxicokinetic concerns with nicotine?

Back 161

urinary excretion decreased when urine is alkaline

Front 162

what is the mechanism of action of nicotine?

Back 162

GI irritation may be partly due to caustic effect
neurologic signs are due to nicotinic agonism
nicotinic agonism causes ganglionic and neuromuscular stimulation at small doses and intially at high doses.
Later nicotinic receptor agonism causes ganglionic and neuromuscular blockade because the persistentn depolarization leads to inability of the cell to repolarize

Front 163

what are autonomic signs associated with nicotine

Back 163

neurologic
-autonomic signs- neurologic stimulation. Parasympathetic signs tend to predominate in most tissues except blood vessels.
para= diarrhea, urination, miosis, bradycardia, emesis, lacrimation, salivation (DUMBLES).
Sympathetic = vasoconstriciton
later blockage of nicotine receptors occurs due to persistent situmation resulting in normal heart rate and vasodilation.

Front 164

What are some neuromuscular signs of nicotine?

Back 164

initially see stimulation- tremors, etc
followed by paralysis

Front 165

central effects of nicotine include?

Back 165

CNS stimulation results in excitement, seizure and tremor followed by depression.
CNS and nueromuscular depression- repsiratory paralysis- death
vomiting

Front 166

Does nicotine have any specific antidote and what is the main type of supportive care required?

Back 166

Decontamination- gastric lavage with diluted soluntion of potassium permangante, tannic acid or tincutre of iodine
acidification of urine may help excretion
mecamylamine as a ganglionic blocker only can have some benefit early in case
atropine therapy for PS effects
control neurlogical excitement

Front 167

What is the prognosis of nicotine?

Back 167

poor in large doses but typically in small doses recovery is generally short (<24 hours)

Front 168

What are sources of DEET?

Back 168

insect repellent
combined with fenvalerate as a repellant and insecticide for dogs/cats

Front 169

what is the relative toxicity of DEET

Back 169

acute toxicity
slightly toxic

Front 170

what is the species sensitivity and susceptibility of DEET?

Back 170

dogs and cats are susceptible but cats are more senstive
neonates are more sensitive

Front 171

onset of clinical signs of DEET toxicity?

Back 171

acute or subactue

Front 172

what are some toxicokinetic concerns with DEET

Back 172

neurotoxicity mechanism is unknown
may cause irritation of the skin and mucous membranes

Front 173

what are the clinical signs of DEET toxicity?

Back 173

primarily neurologic excitement
gatrointestinal signs
skin irritation

Front 174

Does DEET toxicity have any specific antidote and what is the main type of supporitve care required?

Back 174

no specific antidote
the main thing is to control CNS excitement

Front 175

What is the prognosis for DEET toxicosis

Back 175

toxicity is RARE

Front 176

Amitraz sources and uses include?

Back 176

flea and tick collars
sources include: ingestion of the dip or accidental ingestion of the collar and dermal absorption following dermal exposure

Front 177

What is the species sensitivity and susceptibility of amitraz?

Back 177

never used in horses due to induction of intestinal stasis
cats are also more sensitive

Front 178

onset of clinical signs of amitraz?

Back 178

acute to subacute

Front 179

Amitraz is a good insect repellent in horses (T/F)

Back 179

false, amitraz causes intestinal stasis

Front 180

Onset of clinical signs of amitraz

Back 180

acute to subacute

Front 181

drugs and other factors tha can increase the toxicity of amitraz?

Back 181

meperidine or sympathomimetic amines increase toxicity
stress increases toxicity

Front 182

what is the mechanism of action of amitraz?

Back 182

alpha 2 adrenergic agonist in the CNS is believed to result in sedation and cardiovascular instability
alpha 2 adrenergic agonist in the PNS is believeed to result in cardiovascular instability
weak MAO inhibition may also contribute to neurlogic toxicty
Mild irritant to the GIT and skin

Front 183

what are the clinical signs of amitraz?

Back 183

primarily CNS depression but may also see ataxia, possibly seizures and vocalization

cardiovascular instability can cause hypotension and is due to bradycardia and vasodilation
hypothermia
mydriasis
gastrointestinal abnormalities such as intestinal motility
urination/PU
death often due to CNS depression resulting in respiratory depression or colic in horses

Front 184

does amitraz have any specific lesions or bloodwork findings?

Back 184

HYPERGLYCEMIA (due to alpha 2 receptor activation) may be clue but is not specific
chemical analysis is possible

Front 185

Does amitraz have any specific antidote and what is the main type of supportive care required?

Back 185

- Alpha 2 adrenergic antagonists (yohimbine or atipamezole) are an antidote

- main supportive care is to monitor for respiratory depression and decontamination

Front 186

What is the prognosis of amitraz?

Back 186

good in most cases
moderate recovery period (24 to 72 hours)

Front 187

What are some common macrocyclic lactone brand names?

Back 187

includes drugs such as ivermectin (heart gaurd, Ivomec), moxidectin, selamectin, milbemycin, doramectin, eprinomectin, abamectin

Front 188

what are uses/sources of macrocyclic lacones?

Back 188

-endectocide from cattle, swine, sheep and horses
- prevention of heart worm disease in dogs and cats
-also used for treatment of various external and internal parasites, in dogs, cats, rabbits and other species
-abamectin
-sources include overdose and use of large dose of products formulated for large animals in dogs. Ingestion of ant traps by dogs will rarely causes toxicity, but can cause obstruction

Front 189

what is the species sensitivity and susceptibility of macrocyclic lactones? why are some speciese more sensitives

Back 189

many species are susceptible
certain dog breeds- collies and herding breeds

Front 190

onset of clinical signs of macrocyclic lactones?

Back 190

acute

Front 191

what are some toxicokinetic concerns with macrocyclic lactones

Back 191

ivermectin most known
long half life after skin administration

Front 192

what is the mechanim of action of macrocyclic lactones?

Back 192

GABA agonist- neuronal inhibiton

Front 193

what are the clinical signs of macrocyclic lactone

Back 193

mainly CNS depression seen, may also see stupor, coma, mydriasis, neurologic blindness, ataxia, tremor. Seizures can alos be seen.
-other signs may include GI signs, bradycardia and sinus arrhythmias
-may progress to respiratory/cardiac depression resulting in death

Front 194

Do macrocyclic lactones have any specific antidote? What supportive care is required?

Back 194

decontamination may need multiple doeses of activate charcoal
physostigmine IV
picrotoxin is specific antidote- but has narrow safety margin

Front 195

What is the prognosis of macrocyclic lactones?

Back 195

depends on dose, but may need long term care
can be very long (>1 week) due to long half life

Front 196

what insecticides are long lived in the environment or have environmental concerns?

Back 196

organochlorines- BIOACCUMULATION

Front 197

what insecticides have an acute toxicity?

Back 197

all of the them are primarily acute but some can also be subacute and chronic

Front 198

what insecticides have a well recognized subacute to chronic toxicity?

Back 198

organophosphates- delayed/intermediate syndrome
-organochlorines- chronic with low doses
-napthalene- whole moth balls slow absorption in GIT

Front 199

what insecticides are highly to moderately toxic?

Back 199

all of them except DEET and D Limonene

Front 200

what insecticides are unsafe due to similar therapeutic and toxic doses?

Back 200

organophosphates

Front 201

to what insecticides are fish and/or reptiles and/or birds most sensitive?

Back 201

pyrethrins very toxic to fish and birds
rotenone very toxic to fish and cold blooded animals
with organophosphates and carbamates some sources report birds and fish are more sensitive

Front 202

to what insecticides are dogs or cats most sensitive?

Back 202

cats= organocholrines, D limonene, napthalene

dogs= macrocyclic lactones in some K9

Front 203

what insecticides are not used in horses, and generally not in cats?

Back 203

horses- amitraz due to intestinal stasis
cats are also sensitive to amitraz and are more sensitive than dogs

Front 204

to what insecticides are avians sensitive or resistant?

Back 204

chickens are resistant to rotenone
some birds are sensitive to pyrethrins and organophosphates/carbamates

Front 205

what insecticides are neonates more sensitive too?

Back 205

- OP without lethal synthesis
-Carbamates
-DEET

Front 206

are any insecticides not well absorbed or poorly distributed?

Back 206

-all are well distributed
-absorption varies but most can be absorbed to some degree by all routes

Front 207

where are most insecticides metabolized and excreted?

Back 207

most are metabolized in the liver and excreted in urine and bile
OC have significant bile exretion
Rotenone is mainly excreted in feces
Macrocyclic lactones are excreted mainly unchanged in the feces (these also have long half life and long recoery time due to the long half life)

Front 208

what insecticides have lethal synthesis

Back 208

Organophosphates
Organochlorines
rotenone forms toxic metabolites in some liver reaction

Front 209

why is bile or feces excretion important

Back 209

important because excretion in bile or feces means repeated closes of activated charcoal should be given

Front 210

what insecticides cause mainly CNS excitement

Back 210

organophosphates, carbamates, organochlorines, pyrethrins (mainly tremors), nicotine, DEET
-sometimes depression can also be seen with some of these

Front 211

what insecticides cause mainly CNS depression?

Back 211

Ivermectin, amitraz, rotenone and D limonene= mainly CNS depression but may also see excitment

Front 212

Which insecticides cause significant direct cardiovascular dysfunction?

Back 212

amitraz (similar to xylazine)
D limonene (vasodilation)

Front 213

what insecticides cause skin lesion?

Back 213

D limonene (TEM or EM like)
Pyrethrins (type 1 hypersensitivity)

Front 214

what insecticides and other toxins cause hemolytic anemia

Back 214

napthalene

Front 215

what insecticides and toxins cause hypoglycemia

Back 215

rotenone

Front 216

what insecticides cause mainly CNS depression?

Back 216

Ivermectin, amitraz, rotenone and D limonene= mainly CNS depression but may also see excitment

Front 217

Which insecticides cause significant direct cardiovascular dysfunction?

Back 217

amitraz (similar to xylazine)
D limonene (vasodilation)

Front 218

what insecticides cause skin lesion?

Back 218

D limonene (TEM or EM like)
Pyrethrins (type 1 hypersensitivity)

Front 219

what insecticides and other toxins cause hemolytic anemia

Back 219

napthalene

Front 220

what insecticides and toxins cause hypoglycemia

Back 220

rotenone

Front 221

What insecticides and toxins causing hyperglycemia?

Back 221

amitraz

Front 222

which insecticides have a specific lesion on necropsy or physical examination

Back 222

none

Front 223

what insecticides are associated with a poor prognosis?

Back 223

most only have a poor prognosis in large doses but insecticides with higher relative toxicity, lethal synthesis or decreased metabolism tend to have a worse prognosis
prognosis is always poor once multiple organ failure develops. Insecticides that lead to CNS excitement such as organophosphates and organochlorines seem to quickly lead to this sequela in particular with large doses and delayed supportive care

Front 224

what insecticides are associated with a good prognosis?

Back 224

cabamates, pyrethrins, DEET, D limonene, Rotenone all tend to have a good prognosis in cases of limited exposure

Front 225

For what insecticdes is chemical analysis possible? Do any have a specimen of choice?

Back 225

only citrus oil has no test for chemical analysis
organophosphates- acetylcholinesterase activity and chemical analysis
-carbamates acetylcholinesterase activity, chemical analysis of stomach contents best due to rapid metabolism but can also test tissues
-organochlorine - brain
-pyrethrins- worry about rapid metabolism

Front 226

which insecticides that are commonly used in veterinary products have limited toxicity?

Back 226

fipronil- Frontline-GABA agonist
imidacloprid (advantage)
methoprene (Frontline plus)
nitenpyram (Capstar

Front 227

how are anticoagulants classified?

Back 227

First Generation: Warfarin, pindone, chlorophacinone

Second Generation: Brodifacoum, bromodiolone, diphenadione

Front 228

what are sources/used of anticoagulants?

Back 228

used to kill rodents as prepared baits or powders for mixing with bait material, some are used medically as anticoagulants, ingestion of baits or eating contaminated foods, swine, dogs, and cats can be poisoned by eating rats or mice killed by these, malicious

Front 229

what is the species sensitivity ans suceptibility of anticoagulants?

Back 229

dogs are most suceptible
order or sensitivity is pigs>dogs>cats>ruminants>horses>chickens

Front 230

what is the onset of clinical signs of anticoagulants?

Back 230

toxicity is subacute. It takes 3 to 5 days to see clinical signs. It is more acute with second generation, but it still generally takes a few days after ingestion to see clinical signs

Front 231

what factors increase toxicity with anitcoagulants

Back 231

factors that enhance bleeding
vitamin K deficiency, oral antibiotics/sufonamide therapy or high dietary fat, enzyme inhibitors, presence of other drug or diseases that causes hemorrhage, liver disease, presence of drugs that displace the anticoagulant from albumin

Front 232

what factors decrease toxicity?

Back 232

pregnancy or lactation, enzyme inducers

Front 233

what are the clinical signs of anticoagulant toxicosis?

Back 233

it depends on the site of bleeding
respiratory distress, neurologic, cardiovascular deterioration if severe blood losses

Front 234

do anticoagulants have any specific lesions or bloodwork findings?

Back 234

no specific lesions. Lesions will depend on the site of bleeding
blood work not specific but will often be consistent with blood loss
activated coagulation time (ACT)
PT/PTT
PIVKA

Front 235

what will be elevated first with anticoagulant toxicosis PT/PTT and why?

Back 235

PT b/c it tests the extrinsic pathway which involves factor VII. Therefore it is prolonged first because Factor VII has the shortest 1/2 life

Front 236

which clotting test is least sensitive and which is most sensitive?

Back 236

ACT is the least sensitive
PIVKA is said to be the most sensitive and specific. Other disease will increase the PIVKA test and some feel the PT is just as good for early detectioin

Front 237

Can anticoagulants be chemically tested for if so is there a specimen of choice?

Back 237

best for definitive diagnosis
detection in blood (preferred in live animal) serum, or plasma in a live animal
other smaples that may be submitted include liver (preferred in dead animals) GI contents, vomitus and baits

Front 238

Do anticoagulants have any specific antidote? What is the main type of treatment for anticoagulant rodenticides?

Back 238

stable patient
detoxification
antidote is vitamin K1. Vitamin K1 will not stop active bleeding
coagulation parameters should be checked a few days after cessation of therapy
unstable patient
decontamination is not helpful since posion is alreaady absorbed
antidote is fresh frozen plasma for aniaml with coagulopathy and minimal blood loss or while blood for animals in need of clotting factors and red blood cell. FFP will give immediate clotting factor. Vitamine K1 is alos given as in stable patient to help liver activate factors
-supportive care/monitoring, fluid therapy oxygen therapy, minimize restraint and handling, thoracocentesis/pericardiocentesis/abdomiocentresis should be avoided unless respiratory/cardiac distress from hemorrhage is life threatening
-coagulation monitoring as in stable patient

Front 239

how long is vitamin K given and how long before the liver starts making new factors after giving vitamin K1?

Back 239

-coagulation parameters are significantly shortened within 24 to 48 hours of vitamine K1 therapy
-Generally takes 12 to 48 hours for clotting factors to normalize depending only severity of toxicity.

Front 240

why is vitamin K3 not used in treatment?

Back 240

vitamin K3 (menadione) is not effective
vitamin K3 can cause heinz body anemia and is nephrotoxic. It is also poorly stored and requires metabolism for activity so its onset of action is slow and requires a larger amount

Front 241

what is the prognosis and recovery period of anticoagulants?

Back 241

generally a few days but it depends on the amount and location of bleeding.
Treatment is long for second generation 3 to 4 weeks and shorter for first generation 1 to 2 weeks. if unknown type should treat for long period

Front 242

What is the other name of vitamine D3 what are vitamin D analoges?

Back 242

Vitamin D3 is chloecalciferol
calcipotrol, calcipotriene are vitamine D analoges

Front 243

what are sources/uses of vitamin D toxicosis? What is the most common source? What source rarely causes toxicity?

Back 243

ingestion of cholecalciferol rate poisons
feeding on poisoned rodents
consumptiono f large doses of vitamin D
ingestion of psoriasis medications with vitamin d3 analogs creams
ingestion of poisonous plants containing vitamin D analogs

Front 244

what is the sepcies sensitivity ans suceptibility of cholecalciferol

Back 244

all animals are susceptible
dogs and cats are most frequently poisoned
cats are more sensitive than dogs
young animals are more sensitive than adults

Front 245

what factors increase toxicity with cholecalciferol

Back 245

predisposing factor include renal disease, hyperparathyroidism, ingestion of high calcium and phosphorus in diet

Front 246

what are some toxicokinetic concerns with cholecalciferol?

Back 246

absorbed from the GIT
binds to serum vitamin D binding protein and transported to the liver
cholecalciferol is metabolized in the liver by hydroxylation via 25 hydroxylase to 25 hydroxychloecalciferol
calcefidiol is converted to 1,25 dihydroxycholecalciferol by 1-alpha-hydroxylase in the kidney
-metabolites are very lipid soluble so they are slowly eliminated
-metabolism is dependent on form
-metabolites mainly excreted in the bile then in feces
-vitamin D can be excreted in milk at toxic level

Front 247

what is the species sensitivity and susceptibility of cholecalciferol?

Back 247

all animals are susceptible
-dogs and cats are most frequently poisoned
-cats are more sensitive than dogs
- young animals are more sensitive than adults

Front 248

what factors increase toxicity with cholecalciferol?

Back 248

predisposing factor include renal disease, hyperparathyroidism, ingestion of high calcium and phosphorus in diet

Front 249

what are some toxocokinetic concerns with cholecalciferol?

Back 249

absorbed from the GIT
binds to serum vitamin D binding protein and transported to the liver
cholecalciferol is metabolized in the liver by hydroxylation via 25 hydroxylase to 15

Front 250

what form of the vitamin D3 metabolites is most active and which form predominated?

Back 250

calcefidiol is the main vitamin D form in circulation becaues of inhibition of 1 alpha hydroxylase by calcitriol
calcitriol is the 500 times greater vitamin D receptor binding than calcifediol and 1000 times greater binding than cholecalciferol

Front 251

what is the mechanism of action of cholecalciferol toxicosis?

Back 251

toxicity is mainly the result of hypercalcemia and hyperphosphatemia

early mechanisms of action hypercalcemia of hypercalcemia are receptor and intracellular mediated events and are mainly seen in the gastrointestinal tract, kidenys, heart and nervous system

- later in toxicity increased calcium and phosphorus results in soft tissue mineralization in areas such as kidneys, cardiac and lung tissues, vascular walls and stomach

Front 252

what are the clinical signs of cholecalciferol toxicosis?

Back 252

generally appear within 24 to 36 hours. Main organs afffected include the gastrointestinal system, cardiovascular system, nervous system and kidneys
Gastrointestinal: GI injury is severe, anorexia, vomiting (bloody), abdominal pain, constipation, or bloody diarrhea
Renal: initially PU and PD, later in toxicity anuria can be seen with acute renal failure, weakness, renal disease can also worsen GI injury via uremia
Cardiovasuclar- cardiac arrhythmias (often causes bradycardia) and hypertension
CNS- mainly CNS depression: weakness, lethargy, depression, coma
other CNS signs may include twitching and seizure

Front 253

What blood work abnormalities (CBC, chemistry, urinalysis) would be seen in cholecalciferol toxicosis?

Back 253

CBC, chemistry and urinalysis
- hyercalcemia (>11 mg/dl in dogs and 12 to 18 mg/ dl in cats)
- hyperphosphatemia
- hypnatremia and hypokalemia

Front 254

what lesions are seen in cholecalciferol toxicosis?

Back 254

calcification of the kidneys, blood vessels, stomach and other tissues is the most specific lesion

Front 255

what are differentials for cholecalciferol toxicosis?

Back 255

differentials for hypervitiminosis D and hypercalcemia will be most useful
other differential list may also be helpful but they are most helpful when you see them with hypercalcemia
Differentials for hypervitaminosis D

Front 256

why can it be difficult to make a diagnosis when you have hypercalcemia and renal failure?

Back 256

hypercalcemia is a cause of renal failure and renal failure can cause hypercalcemia

Front 257

why can it be difficult to make a diagnosis when you have hypercalcemia and renal failure?

Back 257

hypercalcemia is a cause of renal failure and renal failure can cause hypercalcemia

Front 258

what radiograph finding may be seen with vitamin d toxicosis?

Back 258

calcification of tissue of radiograph

Front 259

can cholecalciferol be chemically tested for if so is there a specimen of choice?

Back 259

you can test serum serum levels of 25 hydroxycholecalciferol

Front 260

how would PTH, PTHrp and phos levels possibly differ in renal disease, neoplasia, primary hyperparathyroidism and vitamin D toxicosis?

Back 260

renal disease= high PTH, low PTHrP and high phos
vitamin D toxicosis= low PTH, low PTHrP and high phos
neoplasia = low PTH, high PTHrP and low phos
Primary hyperparathyroidism- high PTH, low PTHrP and low phos

Front 261

Does cholecalciferol have any specific antidote and what is the main type of supportive care required?

Back 261

no specific antidote but several drugs amy help to lower calcium levels such as
- normal saline IV
-furosemide
- glucocorticoids such as prednisone or prednisolone
-calcitonin
-sodium bicarbonate
-pamidronate disodium
-also consider low calcium diet

Front 262

what should be done prior to lasix/furosemide administration and holwng is therapy givien

Back 262

restore volume prior to lasix to protect kidney
therapy should continue until serum CA is normal

Front 263

what is the prognosis/recovery period of cholecalciferol

Back 263

good if treated early
guarded to poor in severe hypercalcemia
grave in animals with hematemesis
toxicity is short to long depending on degree of injury cause by toxin
treatment may be long due to slow elimination

Front 264

does bromethalin look different from other rodenticides?

Back 264

no it is often similar color /texture

Front 265

what are sources/used of bromethalin

Back 265

general use pesticide
ingestion of rat poison
secondary poisoning of non target animals (possible in cats)

Front 266

what is the relative toxicity of bromethalin

Back 266

highly toxic in dogs and cats

Front 267

what is the species sensitivity and susceptibility of bromethaline

Back 267

dogs and cats are susceptible
cats more senstive
guinea pigs are resistant

Front 268

onset of clinical sings of bromethalin?

Back 268

acute seen with dosees greater then the LD50
lower doses can cause slower onset
cats tend to have a more subacute toxicity

Front 269

what are some toxicokinetic concerns with bromethalin?

Back 269

highly lipophilic- rapidly absorbed
wide distribution with the highest concentrations in fat and brain
metabolized by N demthylation in the liver to the metabolite which is more toxic

Front 270

what is the mechanism of action of bromethalin toxicosis

Back 270

neurlogic abnormalities noted are thought to be due to uncoupling of oxidative phosphorylation resutling in lack of atp
insufficient energery fo atp depdent Na and K ion channel pumps results in cerebral edema due to accumulati onf Na in th cells, may also cause lipid perodidation resulting in brain injury

Front 271

what are the clinical signs of bromethalin toxicosis?

Back 271

clinical signs are varied and dose dependent cats tend to have a slower onset and lower doses cause a slower onset.
in acute toxicosis (w/in 24 hrs) CNS stimulation is most prominent. In some subacute cases in particular the cat the signs may be consistent with a spinal lesion.
Acute CNS signs are generally CNS excitement. Generalized seizures may be precipitated by light or noise.
Animals may also show CNS depression

Front 272

does bromethalin have any specific lesions or bloodwork findings?

Back 272

no but may see cerebral edema, myelin edema, myelin splitting, axonal swelling confined genally to CNS

Front 273

can bromethalin be chemically tested for i?

Back 273

chemical analysis is not routinely available can use several specimens including vomitus and bait

Front 274

does bromethalin have any specific antidote and what is the main type of supportive care required?

Back 274

no specific antidote
dexamthosone may be helpful
mannitol for cerebral edema
antioxidants for oxidative injury

Front 275

what is the prognosis/recovery period of bromethalin

Back 275

if exposure is not severe animals may recover but sever exposure is fatal

Front 276

what are the sources/uses of strychnine?

Back 276

restricited use pesticide
currently used to control gophers and squirrels
ingestion of bait intended for other animals
dogs and cats and wild birds eating poisoned rodents
malicious poisoining

Front 277

what is the relative toxicity of stychine?

Back 277

extremely toxic in horses, cattle, pigd, gods and highly toxic in cats.

Front 278

what is the species sensitivity and suceptbility of strychnine?

Back 278

all animals = susceptible
dogs- most frequently poisoned more sensitive than cats
horses, cattle, pigs are very sensitive
poultry are resistant

Front 279

onset of clinical signs of strychnine

Back 279

acute, signs seen to 10 to 120 minutes

Front 280

what other factors alter strychnine toxicity?

Back 280

vomiting decreases toxicity
presence of food in stomach may prevent emesis and enhance toxicity or may decrease toxicity by decreasing absorption
small amoutns ingested over time may not cause poisoning because of rapid elimination

Front 281

what are some toxocokinetic concenrs with strychnine

Back 281

rapidly abosrbed
does not accumulate
cross BBB
metabolized in liver
excreted in urine as unchanged and metabolites
most lethal dose eliminated in 24 hours

Front 282

what is the mechanism of action of strychnine toxicosis?

Back 282

blocks the postsynaptic effect of glycine in the spinal cord
tonic seizures

Front 283

what are the clinical signs of strychnine toxicosis?

Back 283

rapid onset and rapid death
neurologic system- excitement
seizures
respiratory failure

Front 284

does strychnine have any specific lesions or bloodwork findings

Back 284

none, may note rapid rigor mortis

Front 285

can strychnine be chemically tested for if so is there a specimen of choice

Back 285

urine in a live animal and stomach contents in a dead animal or specimens of choice. usually can be detected in the liver

Front 286

does strychnine have any specific antidote and whats the main type of supportive care required?

Back 286

no specific antidote
control seizures

Front 287

useful anitconvulsants in strychnine poisoning?

Back 287

pentobarbital to effect
thibarbiturates in cats
methocarbamol, guaifensin, xylazine
diazepam

Front 288

what are some specific considerations in strychnine decontamination

Back 288

specific considerations for decontamination
sodium bicarbonate is contraindicated in lavage, precipitation of alkaloid by diluted solution of tannic acid or potassium peermaganate
enhancing renal excretion with fluid therapy or ammonium chloride or methionine to acidfy urine

Front 289

what is the prognoses/recovery period for strychnine?

Back 289

good if treated early

Front 290

does zinc phosphide persist in the environment?

Back 290

stable when dry but decomposes in air or bait within 2 weeks

Front 291

what are sources/uses of zinc phosphide

Back 291

most products are restricted use pesticides
available as grain, bait, or tracking powder
sources include: accidental ingestion, caged birds exposed by ingesting food contaminated for killing mice

Front 292

what is the relative toxicity of zinc phosphide?

Back 292

highly toxic

Front 293

what is the species sensitivity and suceptibility of zinc phosphide

Back 293

birds are most sensitive

Front 294

onset of clinical signs of zinc phosphide

Back 294

tpyically acute within 15 minutess
sometimes delayed

Front 295

what factors alter toxicity of zinc phosphide?

Back 295

gastric acid enhances toxicity
an empty stomach may decrease toxicity due to decreased acidity
=dogs may survive after eating on an empty stomach
vomiting decreases toxicityq

Front 296

what is the recovery period of zinc phosphide?

Back 296

in hospital genrally 48-72 hours

Front 297

what is the species sensitivity and susceptibility of bromethaline

Back 297

dogs and cats are susceptible
cats more senstive
guinea pigs are resistant

Front 298

onset of clinical sings of bromethalin?

Back 298

acute seen with dosees greater then the LD50
lower doses can cause slower onset
cats tend to have a more subacute toxicity

Front 299

what are some toxicokinetic concerns with bromethalin?

Back 299

highly lipophilic- rapidly absorbed
wide distribution with the highest concentrations in fat and brain
metabolized by N demthylation in the liver to the metabolite which is more toxic

Front 300

what is the mechanism of action of bromethalin toxicosis

Back 300

neurlogic abnormalities noted are thought to be due to uncoupling of oxidative phosphorylation resutling in lack of atp
insufficient energery fo atp depdent Na and K ion channel pumps results in cerebral edema due to accumulati onf Na in th cells, may also cause lipid perodidation resulting in brain injury

Front 301

what are the clinical signs of bromethalin toxicosis?

Back 301

clinical signs are varied and dose dependent cats tend to have a slower onset and lower doses cause a slower onset.
in acute toxicosis (w/in 24 hrs) CNS stimulation is most prominent. In some subacute cases in particular the cat the signs may be consistent with a spinal lesion.
Acute CNS signs are generally CNS excitement. Generalized seizures may be precipitated by light or noise.
Animals may also show CNS depression

Front 302

does bromethalin have any specific lesions or bloodwork findings?

Back 302

no but may see cerebral edema, myelin edema, myelin splitting, axonal swelling confined genally to CNS

Front 303

can bromethalin be chemically tested for i?

Back 303

chemical analysis is not routinely available can use several specimens including vomitus and bait

Front 304

does bromethalin have any specific antidote and what is the main type of supportive care required?

Back 304

no specific antidote
dexamthosone may be helpful
mannitol for cerebral edema
antioxidants for oxidative injury

Front 305

what is the prognosis/recovery period of bromethalin

Back 305

if exposure is not severe animals may recover but sever exposure is fatal

Front 306

what are the sources/uses of strychnine?

Back 306

restricited use pesticide
currently used to control gophers and squirrels
ingestion of bait intended for other animals
dogs and cats and wild birds eating poisoned rodents
malicious poisoining

Front 307

what are some toxocokinetic concerns with zinc phosphide?

Back 307

gastric acid causes hydrolysis
gas in lungs may cause toxicity to persons txing animal

Front 308

what is the mechanism of action of zinc phosphide toxicosis?

Back 308

exact mechanism is unknown- irritation of the GIT due to corrosive effects resutls in vomiting blood early in intoxication
reducing compound- phosphine is reducing compound which can complex to metals such as copper, iron and other metals
enzyme dysfunciton also reuslts in inhibiton of oxidative phosphorylation and therefore decreased energy production
phosphine gas can increase damaging reacitve oxygen species formed by the reuction of oxygen
tissues affected are mainly the brain, heart, liver, kidney, and lungs
damage of the blood vessels and erythrocyte membranes and respiratory mucosa is also noted
acute toxicosis is due to absorbed phosphine gas and intact zinc phosphide may cause liver or kidney damage later

Front 309

what are the clinical signs of zinc phosphide toxicosis

Back 309

onset is rapid
mainly see GIT, resp, cardiovascular and neurologic signs but many organs can be affected
-neurologic signs are mainly CNS excitement, dogs may show CNS stimulation, signs such as "mad dog running", yelping and convulsions, gastroenteritis may be hemorrhagic
death is usually due to tissue anoxia and may be seen within 3 to 48 hours
in animals that recover may see delayed hepatic and renal injury with associated clinical signs

Front 310

does zinc phosphide be chemically tested for if so if there is speciment of choice

Back 310

zinc phosphide can be tested for in various issues
specimens should be rapidly frozen

Front 311

does zinc phosphide have any specific antidote, decontamination procedures or supportive care

Back 311

gastic lavage
alkalinzaiton of stomach
oral antacids

Front 312

what is the progonsis/recovery time of zinc phopshide

Back 312

animals that vomit may recover
animals with severe signs of tissue damage have a guarded to poor

Front 313

what are sources/uses of fluoracetate?

Back 313

currently it is only used in the US as a livestock protection collar (LPC) for controlling coyotes preying on sheep and goats
Sources- eat poisoned animals

Front 314

what is the relative toxicity of flluoroacetate?

Back 314

extremely to highly toxic

Front 315

what is the species sensitivity and susceptibility of fluoroacetate

Back 315

dogs are very sensitive
birds are most resistant

Front 316

onset of clinical signs of fluoroacetate

Back 316

acute

Front 317

what is the recovery period of fluoroacetate

Back 317

depends on degree of injury and death is common in animals that show clinical signs
death can occur in 3 to 5 hours with lethal doses rare to live more than 48 hours

Front 318

what are some toxokinetic concerns with fluoracetate

Back 318

readily absorbed from the GIT lung or open wounds but no intact skin
distributed throughout the body without accumulation in a particular tissue
fluroacetate is metabolized to monofluroacetic acid by hydrolysis.
-Fluoroacetate and its metabolites are eliminated in the urine within a few days

Front 319

what is the mechanism of action of fluoroacetate toxicosis

Back 319

GI signs partly due to direct GI irritant
Cardiac and neurologic signs are due to inhibition of energy production
-combines with acetyl coenzyme A to form fluroacetyl CoA which combines with oxaloacetate to form flurocitrate
-flurocitrate competes with citrate for the active site of the citric acid cycle enzyme

Front 320

what are the clinical signs of fluoracetate toxicosis

Back 320

rapid onset of clinical signs and signs are dependent on species
In dogs mainly see signs of CNS stimulation and GI irritation
other signs include hyperthermia due to seizures, and death within 2 to 12 hours
in horses, cattle, sheep, goats see signs of heart failure

in cats and pigs signs are a combination of cns and cardiac signs

Front 321

does fluoroacetate have any specific lesions or bloodwork findings

Back 321

non-specific
lesions typically due to CNS excitement and cardiac failure
may see rapid rigor mortis
blood chemistry may show hypocalcemia and other findings associated with shock and convulsions

Front 322

can fluoroacetate be chemically tested for if so is there a specimen of choice

Back 322

-chemical analysis for floroactetate is difficult
-specimens are gastric contents and vomitus
-can test for elevated citrate in the kidney tissue or blood but it is not diagnosic/specific for fluroacetate

Front 323

Does fluoroacetate have any specific antidote and was is the main type of supportive care required

Back 323

limewater precipitates fluoracetate and therefore may be helpful in decontamination
-acetate donors which compete with the poison at vital biochemical steps to reduce conversion to fluroacetate may be helpful these inlcude Glycerol monoacetate, ethanol 50% and acetic acid 5% soln is an alternative but is less effective, acetamide soln.
-Sodium bicarbonate may reduce toxicity
-other supportive care of seizures and shock

Front 324

what rodenticides generally have an acute toxicity?

Back 324

vitamin D, bromethalin, strychnine, zinc phosphide, fluroacetate

Front 325

what rodenticides have a well recognized subacute to chronic toxicity

Back 325

anticoagulant rodenticides are always subacute to chronic

bromethaline
zinc phosphide is often acute but can sometimes have delayed hepatic and renal injury

Front 326

what rodenticides are highly to moderately toxic

Back 326

all highly to moderate
choliceferol and strychnine is extremely toxic in some species

Front 327

to what rodenticides are birds most sensitive

Back 327

zinc phosphide

Front 328

to what rodenticides are dogs or cats most sensitive

Back 328

cats- vitamin D, bromethalin, fluoroacetate
dogs- anticoagulant (dogs more than cats but pigs are most sensitive) strychnine (dogs more than cats but large animals are more sensitive

Front 329

to what rodenticides are large animals more sensitive

Back 329

strychnine
pigs very sensitive to anticoagulants

Front 330

what rodenticides are neonates more sensitive too

Back 330

vitamin D

Front 331

to what rodenticide are guinea pigs resistant

Back 331

bromethalin

Front 332

what rodenticides have lethal synthesis

Back 332

vitamin D, bromethalin

Front 333

what rodenticides cause mainly CNS excitement

Back 333

zinc phosphide, fluoroacetate, bromethalin, strychnine

Front 334

what rodenticides cause hypercalcemia

Back 334

vitamin D toxicosis

Front 335

which rodenticides cause bleeding

Back 335

anticoagulant rodenticides

Front 336

what rodenticides and other toxins have elicitable seizures

Back 336

rodenticides - bromethalin, strychnine, zinc phosphide
other toxins = metaldehyde

Front 337

what are the sources/uses of metaldehyde?

Back 337

restricted use pesticide
used alone or in combination with other compounds- as a molluscicide
solid fuel in certain camp stove

Front 338

what is the relative toxicity of metaldehyde

Back 338

moderately toxic

Front 339

what is the species sensitivity and susceptibility of metaldehyde

Back 339

acute toxicty
usually seen within 1 to 3 hours of ingestion

Front 340

what is the recovery period of metaldehyde

Back 340

can last up to 5 days but generally only last about 12 to 72 hours

Front 341

what factors increase toxicity with metaldehyde

Back 341

more toxic by inhalation

Front 342

what factors decrease toxicity of metaldehyde?

Back 342

enzyme inducers such as phenobarbital may decrease toxicity

Front 343

what are some toxocokinetic concerns with metaldehyde

Back 343

metaldehyde is readily absorbed from the GIT
acetaldehyde is formed in the stomach when gastric acid hydrolyzes metaldehyde to acetaldehyde and therefore some acetaldehyde is also absorbed
-acetaldehyde is also formed via by metabolism of metaldehyde by liver microenzymes
-acetaldehyde is metabolized by hepatic aldehyde dehydrogenase to acetic acid which can enter the TCA cycle and be broken down to water and CO2
-both metaldehyde and acetaldehyde cross the blood brain barrier

Front 344

what is the mechanism of action of metaldehyde in acute toxicosis?

Back 344

causes direct GI irritation
neurotoxicity may be due to acetaldehyde or metaldehyde
decreased norepineprhine and serotonin appears to be due to increases MAO leading to break down of norepinephrine and serotonin. Decreased levels can lead to seizures
-decreased GABA levels may cause convulsive seizures
-Dogs that survive the acute phase may develop liver failure
l

Front 345

what are the clinical signs of metaldehyde toxicosis?

Back 345

-primarily neurologic excitement
-convulsions are usually stimulated by external stimuli in cats and sometimes elicitable in dogs
-hyperthermia is likely due to muscle tremors and can be severe
-convulsions may lead to hyperthermia and CNS depression and death by respiratory failure
- other signs may inlcude GI and cardiovascular signs
- dogs that survive the acute phase may develop live failure within 2 to 3 days

Front 346

Does metaldehyde have any specific lesions or bloodwork findings?

Back 346

-no specific lesions or bloodwork
-formedaldehyde or acetaldehyde odor in the stomach contents

Front 347

can metaldehyde be chemically tested for if so is there a specimen of choice

Back 347

analysis of stomach contents for metaldehyde or acetaldehyde

Front 348

what is the main treatment of metaldehyde and are their any specific antidotes

Back 348

-Decontamination is standard and Milk or sidum bicarbonate to decrease absorption
-control seizures
-diazepam, pentobarbital (enzyme inducer), propofol
-Muscle relaxants such as methocarbamol and guiafensen
-xylazine and acepromazine in horses
-other supportive care control hyperthermia, fluid therapy for acidosis, diuresis and maintenance requirement

Front 349

What are sources/uses of PCP

Back 349

-only used by certified applicators as a wood preservative to protect lumbar from fungal rot and wood-boring insects

-Sources: licking wood treated with pentachlorophenol, inhalation of toxic amounts from treated walls in sheds and barns
-toxicity usually associated with fumes in crowded barns but is rare due to decreased use

Front 350

what is the relative toxicity of PCP

Back 350

high to moderately toxic

Front 351

onset of clinical signs of PCP

Back 351

acute or chronic

Front 352

what factors increase toxicity with PCP

Back 352

high ambient temperatures, oily or organic solvent

Front 353

what factors decrease toxicity of PCP

Back 353

cold temperatures, antithyroid drugs and presence of body fat

Front 354

what are some toxocokinetic concerns with PCP?

Back 354

-readily absorbed from the GIT by inhalation and from intact skin
-distributed throughout the body with some accumulation in body fat
-metabolized by conjugation to glucuronic acid
-excreted in urine
-residues in tissues and fat are depleted from teh body within 1 week of exposure

Front 355

what is the mechanism of action of PCP in acute toxicosis?

Back 355

-irritation of the respiratory tract mucousa and skin
-uncouples oxidative phosphorlyation and blocks or decrease ATP
-Uncoupling increases oxygen demand in an effort to produce ATP
-end result in neurotoxicity, hyperthermia and metabolic acidosis

Front 356

What are the clinical signs of PCP toxicosis?

Back 356

acute toxicosis, onset and duration may be so fast that no signs are seen.
acute- diffuse organ involvement- neurologic excitement (seizures) and hyperthermia

Front 357

Does PCP have any specific lesions or bloodwork findings

Back 357

acute and chronic toxicity findings are non specific
may see changes due to shock and seizures with acute. The blood may be very dark. Rapid rigor mortis
-with chronic toxicity hyperkeratosis of the skin and villous like hyperplasia of urinary bladder in chronic cases

Front 358

Can PCP be chemically tested for if so there is a specimen of choice.

Back 358

chemical analysis in blood and urine in live animals and kidneys and skin in dead animals

Front 359

what is the main treatment of PCP and are their any specific antidotes

Back 359

standard decontamination
supportive care for seizures and hyperthermia

Front 360

what is the prognosis with PCP

Back 360

if animal survives 24 hours, chances for complete recovery are fair

Front 361

what are sources/uses of 2,4-D

Back 361

generally sprayed forages
sources: include accidental ingestion of concentrations or sprays (cattle), grazing freshly sprayed pastures (Cattle), access to freshly sprayed lawns (pets)

Front 362

what is the relative toxicity of 2,4-D

Back 362

moderately toxic

Front 363

onset of clinical signs of 2,4-D

Back 363

acute

Front 364

what species is most sensitive to 2,4-D and what species are susceptible

Back 364

cattle and dogs are the most susceptible
dogs are more sensitive than othrspecies

Front 365

what factors increase toxicity with 2,4-D

Back 365

alter the metabolism of plants resulting in toxicity by increasing accumulation of nitrate and cyanide
improve palability of some poisonous plants thereby increasing toxicity to animals

Front 366

what are some toxocokinetic concerns with PCP?

Back 366

readily absorbed from the GIT
poorly absorbed from the skin
well distributed
metabolized in liver
excreted mainly unchanged in the urine y tubular secretion
meat residues in cattle and sheep are unlikely unless exposed to very high concentrations

Front 367

what is the mechanism of action of 2,4-D acute toxicosis

Back 367

=Gastrointestinal and neurologic signs
= irritation of the GI mucosa
= uncouple oxidative phosphorlation and depress ribonuclease synthesis
= in dogs may directly affect skeletal muscle membranes

Front 368

what are the clinical signs of 2,4-D toxicosis?

Back 368

-Ruminants: gastrointestinal signs, depression, muscle weakness, and emaciation with no convulsion

Dogs: gastrointestinal signs, neurolgic signs

Front 369

does 2,4-D have any specific lesions or bloodwork findings

Back 369

no specific findings
rumen stasis with ingested food is a characteristic finding

Front 370

Does 2,4D have any specific lesions or bloodwork findings

Back 370

no specific findings
rumen stasis with ingested food is a characterstic finding

Front 371

Can 2,4-D be chemically tested for if so is there a specimen of choice

Back 371

chemically analysis by analytical methods are expensive and time ocnsuming

Front 372

what is the main treatment of 2,4-D and are their any specific antidotes

Back 372

no specific antidote
need supportive care and during decontamination alkaline diuresis can be considered

Front 373

what is the prognoses for 2,4D

Back 373

good if exposure is moderate

Front 374

what are the sources/uses of ipyridyl hericides

Back 374

paraquat is RUP and diquat is GUP. It is a broad spectrum desiccant contact herbicide
concentrated forms for agriculture use and dilute forms for lawn and garden

Front 375

what is the relative toxicity of dipyridyl herbicides

Back 375

moderately to highly toxic

Front 376

what species is most sensitive to dipyridyl herbicides and what species are susceptible

Back 376

all animals are suceptible especially dogs

Front 377

what is the onset of clinical signs with dipyridyl herbicides

Back 377

acute GI but pulmonary toxicity delayed with paraquat
-chronic toxicity also described with smaller doses

Front 378

what factors increase toxicity with dipyridyl herbicides

Back 378

toxicity is enhanced by a selenium or vitamin E deficiency, depletion of tissue glutathione and oxygen therapy

Front 379

what are some toxocokinetic concerns with dipyridyl herbicides

Back 379

diquat is poorly absorbed from the GIT
paraquat is absorbed from the GIT and also from the skin
paraquat is distributed all over the body and achieves high concentrations in the lungs
energy dependent uptake of paraquat by the lungs occurs at a critical level and is time dependent
diquat is not taken up by the lungs like paraquat
minimal metabolism
paraquat is excreted within 24 hours mainly unchanged in the urine
small amounts can be detected in urine for up to 21 days

Front 380

what is the mechanism of action of dipyridyl herbicides in acute toxicosis

Back 380

caustic to mucous membranes resulting in severe GI ulceration
other organ injury is mainly respiratory with paraquat and gastrointestinal diquat due to reactive oxygen species formation
-production of free radicals results in membrane damage, damage to DNA and damage to cell enzymes ultimately resulting in cell death
-With paraquat the lung is particularly susceptible due to accumulation in lung tissue and the kidneys due to excretion
-in chronic cases there may be less all at once massive damage to the lungs but rather slow damage and healing with scar tissue

Front 381

what are the clinical signs of dipyridyl herbicides toxicosis (paraquat)

Back 381

Paraquat:
- acute toxicosis: early signs are mainly GI abnormalities (caustic so may see vomiting anorexia) but may also see neurologic abnormalities (seizures,depression, and ataxia) at high doses may cause dypsnea
-delayed: primarily due to respiratory dysfunction. Respiratory signs include tachypnea, dyspnea, harsh respiratory sounds and cyanosis
-liver and renal failure may be seen after 2 to 3 days

Subacute or chronic toxicosis: respiratory signs due to progressive pulmonary fibrosis

Front 382

what are the clinical signs of diquat?

Back 382

minimal pulmonary signs
mainly see GI, liver, renal, and neurologic signs

Front 383

do dipyridyl herbicides have any specific lesions or blood work findings

Back 383

nonspecific
pulmonary lesions with paraquat instertial pneumonia
GI, liver, renal

Front 384

can dipyridyl heribcides be chemically tested for if so is there a specimen of choice

Back 384

speciments are suspected plants, stomach, contents and urine in acute cases or lung in chronic
urine samples may be negative after 48 hours

Front 385

what is the prognosis with dipyridyl herbicides

Back 385

poor for paraquat