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Toxicology Exam 2 > Tox Exam 2 Feed & Water Related Toxicants > Flashcards

Tox Exam 2 Feed & Water Related Toxicants Flashcards

1
Q

What is the most commonly used non-protein nitrogen (NPN)?

A

urea

it is also the most toxic one

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2
Q

Explain MOA of urease.

A

urease breaks down urea into ammonia (NH3) and CO2

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3
Q

Urease is found in ______.

A

rumen microflora

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4
Q

What species are susceptible to NPN toxicity.

A

cattle and horses

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5
Q

Optimal temp and pH for urease activity?

A

temp optimum=49* C
pH optimum=7.7-8.0
peak ammonia levels are 1/2-2 hrs post ingestion

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6
Q

T/F Alkaline pH enhances hydrolysis of urea by urease.

A

TRUE–this is bc urea is a weak base

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7
Q

T/F Animals less than 1 yr are more sensitive.

A

TRUE–but very young animals–3-6 wks are tolerant

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8
Q

T/F Animals who are routinely exposed to NPN have a lower toxic dose.

A

FALSE–animals who are preconditioned to NPN are more tolerant

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9
Q

What factors increase NPN toxicity?

A

fasting, dehydration or low water intake, hepatic insufficiency, diet low in carb (E) and protein but high in fiber, feeds rich in urease (soybeans), stress, increased rumen temp and pH

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10
Q

ADME of NPN?

A

A=non-ionized ammonia is absorbed–ionized ammonia is NOT absorbed
D=non-ionized ammonia crosses the cell membranes, BBB and placenta
M=non-ionized ammonia converted by liver to urea; too much ammonia (> liver capacity)–>hyperammonemia
E=urea excreted in urine–or recycled in saliva of ruminants

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11
Q

pH around 5-6.5 ammonia will be in ______ form?

A

ionized

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12
Q

pH around 8-9 ammonia will be in _______ form?

A

non-ionized

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13
Q

Is it preferred for ammonia to be in non-ionized or ionized form in the rumen?

A

ionized! want it to stay in the rumen to allow microbes to convert it to protein–do not want it absorbed systemically–which leads to increased blood ammonia levels and toxicity

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14
Q

Describe how microbes in the rumen utilize urea.

A

Use urease to convert urea into ammonia. Ammonia aminates ketoacids (from soluble carbs) to amino acids. These amino acids form bacterial protein. Bacterial protein can then be converted into animal protein.

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15
Q

MOA of ammonia?

A

Inhibits citric acid cycle–lack of energy, decreased cellular respiration, tissue damage.

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16
Q

T/F Toxicity of urea is actually due to ammonia; urea is harmless.

A

TRUE!

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17
Q

What is the cause of death d/t urea poisoning?

A

respiratory or cardiac failure

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18
Q

Onset of clinical signs d/t urea poisoning?

A

rapid onset–30 mins to 3 hrs

convulsions and death w/in 1-2 hrs

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19
Q

Clinical signs of urea poisoning?

A

restlessness, aggression, muscle tremors, salivation, teeth grinding, colic, sternal recumbency while standing on hind limbs, bloat, rumen stasis, usually NO D+, saw horse stance, excitable, hallucinations

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20
Q

Changes seen in blood due to urea poisoning?

A

increased blood ammonia, anaerobic glycolysis, blood lactate, metabolic acidosis, blood glucose, BUN, serum K & P, transaminases, PCV

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21
Q

Pathology of urea poisoning?

A

no characteristic lesions
congestion and degeneration of liver/kidneys
dead animals extremely bloated
ammonia odor and rumen alkalotic

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22
Q

T/F Postmortem exam very helpful in diagnosing urea poisoning.

A

FALSE–not helpful–only see bloat and that rumen alkalotic (greater than 7.5 pH)

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23
Q

Specimens used for the diagnosis of urea poisoning?

A

feed for urea and blood, rumen fluid, vitreous for ammonia

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24
Q

Differential diagnosis for urea poisoning?

A

Agents which cause colic–> caustics, inorganic arsenic–generally cause D+ (often bloody) & no CNS signs
Lead, metaldehyde, CH pesticides–no abnormal posture, jumping, maniacal behavior in urea as in CH px
Organophosphates–cause parasympathomimetic signs & respond to atropine therapy
Grain engorgement, nitrate px, enterotoxemia, cyanide px–differentiate by necropsy & lab tests

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25
Q

Prognosis for urea poisoning?

A

Much better if animal is urinating, if animal ceases to urinate then bad prognosis bc unable to excrete urea.

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26
Q

Treatment of urea poisoning?

A

Relieve bloat first. Acetic acid 5% or vinegar to cattle, sheep, goats followed by large amounts of cold water.
Symptomatic–>normal saline for dehydration, Na bicarb IV for acidosis, rumenotomy

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27
Q

Reasoning behind using vinegar & cold water to treat urea poisoning?

A

vinegar helps to acidify the rumen & cold water helps to lower rumen temperature–high temp & alkalotic environment in rumen favor urease activity

28
Q

FYI: extra information from video regarding different rumen pHs

A

urea tox=8-9.2 high grain diet=5.5-6.2
protein overload=7.5-8.5 mild grain indig=4.5-5.5
fasting=6.3-7.5 actue grain overload=3.4-4.5

29
Q

Names of some ionophores?

A

monensin, lasalocid, salinomycin, narasin, semduramicin sodium, laidlomycin propionate K

30
Q

Use of ionophores?

A

anticoccidial/coccidiostat prevention in cattle, poultry, goats.
reduce bloat, reduce rumen acidosis & growth promoter in cattle. monensin approved to improve milk efficiency in dairy cattle. prevention of tryptophan-induced atypical bovine pulmonary emphysema.

31
Q

Sources of ionophore poisoning?

A

chickens, cattle, swine–>eating feeds containing more than recommended levels
horses, sheep, dogs–>eating feeds w/ added ionophores (accidental or intentional)
horses–>malicious poisoning

32
Q

What animals are susceptible to ionophore poisoning?

A

ALL!

33
Q

What animal is most sensitive to ionophore poisoning? Second most sensitive?

A

horses most sensitive–followed by adult turkeys

34
Q

Chemical properties of ionophores?

A

slightly soluble in water, soluble in organic solvents & oils, form lipid soluble complexes w/ polar cations (Na,K,Ca,Mg) that are transported across cell membranes

35
Q

T/F Horses that ingest the recommended levels of ionophores for cattle are poisoned.

A

FALSE–NOT poisoned

36
Q

Concurrent administration of these drugs increases toxicity of ionophores?

A

cardiac glycosides, tiamulin, chloramphenicol, erythromycin, sulfonamides

37
Q

ADME of ionophores?

A

A=about 50% ruminants, most of it in monogastrics
D=throughout body, blood/tissue levels relatively small–does not accumulate
M=rapidly by p450 oxidative demethylation enzymes in liver
E=mainly in bile

38
Q

Why is metabolism of ionophores in horses slower than in other species?

A

horses have less oxidative demethylases

39
Q

Clinical signs for ionophore poisoning?

A

ACUTE in onset, ACUTE in death—like heart attack in humans
horses–>rapid onset–anorexia, profuse sweat, colic, depression, incoordination, hypervent, tachycardia, arrhythmia, prostration, die
cattle–>anorexia, D+, depression, labored breathing, ataxia, prostration, death
poultry–>anorexia, D+, ataxia, resting on knees w/ wings–legs directed outward, decreased egg production
dogs–> ataxia, muscle weakness of hind limbs, resp paralysis, dysuria, constipation, depression

40
Q

Pathology of ionophore poisoning?

A

horses–>cardiac muscle lesions–pale w/ white steaks of necrosis in myocardium
note: if horses survive may not reach previous performance due to cardiac lesions
sheep/swine/dogs–>skeletal muscle lesions–pale
cattle/poultry–>BOTH skeletal and cardiac muscle lesions

41
Q

Lab diagnosis of ionophore poisoning?

A

increased enzymes of muscle origin (CPK, ASK), increased LDH and ALP enzymes, decreased serum Ca and K, no change in Na, increased PCV

42
Q

Differential diagnosis of ionophore poisoning for horses?

A

colic, blister beetles (cantharidin toxicosis), azoturia

43
Q

Differential diagnosis of ionophore poisoning for cattle?

A

vit E/selenium deficiency, poisonous plants–>
skeletal muscle: coffee senna, coyotillo, white snakeroot
cardiotoxic: taxus, vetch, oleander, milkweed

44
Q

Differential diagnosis of ionophore poisoning for poultry?

A

nutrition myopathy, coffee senna, botulism, Na/water deprived, mycotoxicosis, round heart dz, downer syndrome

45
Q

Specimens for diagnosis of ionophore poisoning?

A

best sample is feed, GI contents, liver, feces

46
Q

Treatment for ionophore poisoning?

A

no specific antidote.
decreased absorption–>charcoal, mineral oil, saline cathartics
symptomatic–>IV fluids/electrolytes, K for hypoK

47
Q

T/F Vit E & selenium may decrease muscle damage from ionophore poisoning esp in cattle and swine.

A

TRUE

48
Q

T/F If a horse survives ionophore poisoning they are safe to ride again.

A

FALSE–do not ride for months! monitor cardiac function for months after

49
Q

Sources of water deprivation/sodium salt toxicosis?

A

feeding brine, whey, garbage.
ingestion of salt licks or ice-melts.
drinking water containing salt.

50
Q

Factors that cause excess Na/H20 deprivation?

A

overcrowding, frozen H2O, unpalatable (medicated) H2O, lack of H2O

51
Q

What species are most susceptible to water deprivation?

A

pigs, cattle, poultry

52
Q

What species are least susceptible to water deprivation?

A

dogs

53
Q

ADME for sodium?

A

A=rapidly through GIT
D=all over body, enters brain passively, removed actively
E=excess absorbed rapidly excreted in urine as long as there is enough water present

54
Q

Normal Na levels in plasma and normal Na levels in CSF?

A

plasma=135-145 mEq/L

CSF=130-140 mEq/L

55
Q

Restricted water intake and dehydration can increase Na plasma and CSF levels to?

A

plasma= 150-190 mEq/L

CSF=145-185 mEq/L

56
Q

Animals can tolerate more than ___% salt in feed if they have free access to water.

A

10%

57
Q

Sodium chloride is normally present at about ____% in feed.

A

0.5-1%

58
Q

MOA of Na in the brain?

A

high Na in the brain inhibits anaerobic glycolysis–>lack of energy necessary for active transport
Na trapped in brain attracts water bc of osmotic gradient, results in cerebral edema!

59
Q

T/F There are acute, subchronic and chronic forms of water deprivation/Na salt toxicosis.

A

FALSE–only acute form

60
Q

Clinical signs of water deprivation/Na toxicosis?

A

early constipation, thirst, V+, polyuria, metabolic acidosis, intermittent convulsive seizures–last from 30 sec to 2-3 mins interrupted by other signs, circling, pivoting, head-pressing, blindness, deafness, lateral recumbency, inability to eat or drink, coma, death
poultry–only show depression, ascites, collapse

61
Q

Pathology of water deprivation/Na toxicosis?

A

gastric congestion or inflammation w/ pinpoint ulcer filled w/ clotted blood. fluid in body cavities or organ edema, prominent cerebral edema.

62
Q

What is pathognomonic in pigs for water deprivation/Na toxicosis?

A

eosinophilic meningoencephalitis–>filling of cerebral and meningeal perivascular spaces w/ eosinophils
but only seen if animal dies early

63
Q

T/F Convulsive seizures caused by water deprivation/Na toxicosis are elicited by stimuli.

A

FALSE. are NOT elicited by stimuli

64
Q

Differential diagnosis of water deprivation/Na toxicosis?

A

encephalitic dz–trauma, tumor, heat stroke, viral encephalomyelitis
CH insecticide, roxarsone, pseudorabies in pigs

65
Q

Treatment for water deprivation/Na toxicosis?

A

give small amounts of fresh water (.5% of BW) gradually over 2-3 days–if animal can drink (recovery is 50%).
IV fluids (5% dextrose) & furosemide in small animals
anticonvulsants in small animals

66
Q

Prognosis for water deprivation/Na toxicosis?

A

once start showing signs of CNS damage–poor

mortality is about 50%

67
Q

What can occur if give too much water too rapidly to an animal suffering from water deprivation/Na toxicosis?

A

aggravate cerebral edema–lead to death

Toxicology Exam 2 (8 decks)

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