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Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

PCP is used for what?

A

Wood preservative

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2
Q

What ways can you get exposed to PCP?

A

dermal, inhalation, GIT

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3
Q

MOA PCP

A

uncouples oxidative phosphorylation to decrease ATP

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4
Q

Major CS of PCP

A

metabolic acidosis, hyperthermia, weight loss, CNS seizures and hyperkeratosis

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5
Q

Dx for PCP

A

rapid rigor mortis, test kidney in dead, urine and blood in live- metabolic acidosis

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6
Q

What is 2,4-D

A

phenoxy derivatives of fatty acids- amides and benzoicacids- herbicides

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7
Q

How to get toxicosis from 2,4-D

A

from freshly sprayed lawns or pastures- canines and bovines

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8
Q

Who has a shorter half life of 2,4-D in? Canine or bovine

A

Canine

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9
Q

Increasing pH of urine enhances excretion of 2,4-D, T or F?

A

true

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10
Q

MOA 2,4-D

A

uncouples oxidative phosphorylation to decrease ATP

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11
Q

CS ruminants and canines fr 2,4-D

A

ruminants- GIT

canines- GIT and neuro

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12
Q

Toxicity of paraquat/diquat

A

mod-high toxicity

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13
Q

What enhances toxicity of paraquat/diquat?

A

Vit E def, depletion of tissue glutathione and O2 therapy

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14
Q

Which is absorbed through GIT? Paraquat or diquat?

A

Paraquat- GIT, skin

Diquat- poorly through GIT

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15
Q

paraquat/diquat MOA

A

reduced by NADPH to produce single O causing free radicals and membrane damage

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16
Q

paraquat/diquat can have acute, delayed or chronic reactions, T/F?

A

true- acute GI signs
delayed are pulmonary signs
chronic pulmonary fibrosis

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17
Q

After 48 hrs post exposure what may be negative to test for paraquat/diquat?

A

Urine

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18
Q

What can you NOT give with paraquat/diquat toxicosis?

A

OXYGEN, give antioxidants!

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19
Q

T/F alkaline pH (especially in rumen) enhances hydrolysis of urea by urease to ammonia?

A

TRUE

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20
Q

What age is the MOST tolerant of NPN?

A

3-6 weeks old

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21
Q

MOA NPN

A

NH3 inhibits citric acid cycle -> lack of energy and decrease cellular respiration and tissue damage

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22
Q

NPN has a rapid onset of action? T/F

A

true

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23
Q

Clinical signs NPN

A

bloat, alkaline rumen, stasis, anorexia, teeth grinding, colic

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24
Q

What samples do you use to NPN?

A

feed, and NH3 in blood, freeze specimens immediately except blood

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25
Q

Tx of NPN tox?

A

acetic acid/vinegar with large volume of cold water and NaHCO3 for acidosis

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26
Q

Ionophores are used for?

A

anti-coccidials

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27
Q

what species is most sensitive/susceptible to monensin?

A

equine (and turkeys)

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28
Q

Which drugs increase tox of ionophores?

A

tiamulin, glycosides, fluoroquinolones, chloramphenical, erythromycin and sulfonamindes- inhibit microsomal enzymes

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29
Q

MOA ionophores

A

disrupt transmembrane electrochemical gradients- mitochondria main target. Sequester Ca and decrease ATP and energy made by mito

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30
Q

CS for animals with ionophore tox?

A

eq- heart and some skeletal muscle
bv and av-skm and heart
k9, ov, pc- skm

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31
Q

Na enters the brain passively and is actively removed, T/F?

A

true

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32
Q

MOA water deprivation

A

Na in brain inhibits anaerobic glycolysis -> decrease energy, causes water to come into brain- edema

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33
Q

CS water deprivation

A

circling, pivoting, head-pressing, blindness, inability to drink/eat
Av- depression, ascites, collapse

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34
Q

Lesions water deprivation

A

pinpoint ulcers, GI congestion, edema, eosin meningoencephalitis in porcine

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35
Q

Tx water deprivation

A

small amounts of water GRADUALLY over 2-3 d, antiseizure meds

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36
Q

What is included in ethylene glycol that can increase P?

A

Rust remover

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37
Q

Ethylene glycol does NOT go through lethal synthesis? T/F

A

false it does

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38
Q

Which part metabolite causes the most problems?

A

oxalic acid

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39
Q

MOA ethylene glycol

A

direct GI irritation and CNS depression, metabolites cause metabolic acidosis and ARF

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40
Q

There are acute or delayed signs from ethylene glycol, T/F?

A

true
acute- met acid, PU, GI signs, CNS depression, ataxia
delayed- (24-72 hrs) oliguric RF, seizure, coma, anuria, renal pain

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41
Q

Ethylene glycol lesions

A

hem gastroenteritis, pulm edema, tubular necrosis of kidneys, Ca oxalate crystals

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42
Q

Lab dx ethylene glycol

A

increased serum osm and anion gap, low USG, hypocalcemia, hyperglycemia, azotemia, hyperphos, hyperkalemia, increased PCV/TP, CaO crystals

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43
Q

Tx of ethylene glycol

A

1) fomepizole, 2)ethanol

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44
Q

Propylene glycol is pleasantly flavored, T/F?

A

false- it is unpleasant

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45
Q

High concentrations of what causes lactic acidosis with propylene glycol?

A

D-lactic acid

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46
Q

T/F propylene glycol is metabolized to toxic metabolites

A

false

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47
Q

what CS does propylene glycol cause?

A

Heinz body anemia

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48
Q

CS of alcohol tox

A

cns depression, vomiting, metabolic acidosis, irritate MM

Chronic- L/K damage

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49
Q

Tx for methanol tox

A

ethanol or fomepizole- competitive inhibitors of alcohol dehydrogenase

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50
Q

MOA for bleach

A

with acid, release of chlorine/chloramine gas and hypochlorous acid

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51
Q

tx for bleach tox

A

milk and water

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52
Q

three types of detergents (least to most toxic)

A

non-ionic

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53
Q

T/F cationic detergent is contraindicated to use emesis/gastric lavage for tx

A

true it is contraindicated

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54
Q

An animal that smells like lemon/citrus can have a tox of what?

A

D-limonene

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55
Q

D-limonene is used for what?

A

Topical for fleas/ticks shampoo

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56
Q

CS for D-limonene

A

necrotizing dermatitis, CNS depression

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57
Q

Tx for D-limonene

A

shampoo/mild dish soap to wash off

58
Q

xylitol MOA

A

insulin release -> hypoglycemia and hypokalemia -> L failure, GI hemorrhage, DIC

59
Q

Tx xylitol

A

Dex inj and then CRI, oral feeding sugar, antiemetic, fluid therapy, antacids/GI protectants

60
Q

Dermal exposure to phenolic compounds causes what?

A

coag necrosis, ulcers, white plaques, and later eschar formation

61
Q

Oral exposure to phenolic compounds causes what?

A

ulceration and necrosis of GIT

62
Q

Which chemical causes green or black urine?

A

phenolic compounds

63
Q

T/F emetics/gastric lavage contraindicated with phenol compound toxicosis

A

true

64
Q

methylxanthines are made of what three things?

A

caffeine, theophylline, and theobromine

65
Q

MOA methylxanthines

A

inhibit phosphodiesterase and antagonize adenosine receptors

66
Q

CS methylxanthines

A

theoph: GI

Caf/theo: clonic convulsions, arrhthymias, seizures, coma, VPCs

67
Q

Tx methyxanthines

A

AC, fluids, methocarbamol, diaz, B blockers, lidocaine

68
Q

T/F organic Fe> irritant and astringent than inorganic Fe

A

false, inorganic>organic

69
Q

T/F divalent is less irritating/astringent than trivalent

A

true

70
Q

T/F iron is absorbed in the SI via an electron dependent carrier

A

true

71
Q

What is irons electron carrier called?

A

transferrin extracellular (ferritin intracellular)

72
Q

What is overdose due to, iron is natural in the body right?

A

When the free iron concentration saturates transferrin causing there to be free Fe circulating

73
Q

MOA Fe

A

circulating free Fe causes free radical lipid peroxidation and damage to membranes- vasculitis

74
Q

CS Fe parenteral and orl prep

A

parenteral- anaphylactoid rxn, shock, death
oral- stage 1: nausea, vom, diarrhea
Stage 2: “apparent” recovery
Stage 3: most serious (12-96 hrs) severe metabolic effects- V, D, hemorrhage, CV collapse
Stage 4: GI obstruction

75
Q

Tx Fe tox

A

w/in 4 hrs emetics/gastric lavage (not AC), milk of magnesia, sucralfate, chelation therapy- deferoxamine**

76
Q

Toxicity of inorganic arsenic

A

Tri > pent > organic

77
Q

How toxic is inorganic arsenic?

A

highly toxic

78
Q

Which species is most susceptible to inorganic arsenic

A

herbivores

79
Q

MOA inorganic arsenic

A

inhibition of lipoic acid inhibits or slows glycolysis and citric acid cycle -> inhibits oxidative enzymes and inactivates glutathione, capillary endo cells are most sensitive

80
Q

CS inorganic arsenic

A

GI and cardio collapse, colic**

81
Q

Tx inorganic arsenic

A

chelation- Dimercaprol (BAL) or demercaptosuccinic acid (Succimer)- safer but less effective than BAL

82
Q

Name the two names for organic acid and species they go with

A

porcine-arsanilic acid

poultry- roxarsone

83
Q

CS arsanilic acid

A

porcine- incoord, ataxia, partial paralysis, peripheral neurologic but GOOD APPETITE, possible blindness
poultry-CNS depression, ANOREXIA, coma and death (no peripheral neurotox)

84
Q

CS roxarsone

A

porcine- hyperexcitability, tremors, collapse, NO blindness

poultry- incoord and ataxia, PERIPHERAL neurotox

85
Q

T/F puppies are most susceptible to lead tox because they eat everything and have increased absorption

A

true

86
Q

T/F lead is easily degraded in environment

A

false it is not

87
Q

T/F acid environmenet decreases absorption of lead

A

false, it increases it

88
Q

MOA lead

A

dysfunction of enzyme receptors and structural proteins, disurpt heme synthesis causing premature release of nRBCs

89
Q

CS lead

A

GIT (SA), CNS (LA)- roaring, megaesophagus, anemia; hematopoietic

90
Q

Lesions for lead

A

cerebral cortical necrosis and poliomalacia in bovine, inclusion bodies, BASOPHILIC STIPPLING

91
Q

T/F 99% of lead is attached to RBCs

A

true

92
Q

T/F serum is the best sample to test for lead

A

FALSE whole blood**

93
Q

Tx for lead toxicosis

A

Ca EDTA for chelation
can also use succimer, DMSA or BAL
fluids, mannitol, propofol/phenobarb, cathartic
ALSO SURGERY IF FOREIGN BODY

94
Q

Which crosses the BBB?
Ca EDTA
Succimer
BAL

A

BAL crosses the BBB, use when CNS signs

95
Q

Which is more hydrophilic, succimer or BAL?

A

succimer

96
Q

Uses of zinc

A

part of many enzymes and proteins, for growth, cell proliferation, collagen formation, skin etc

97
Q

T/F acid environment increases Zn release and absorption

A

true

98
Q

What does zinc bind to?

A

2/3 to albumin and 1/3 to B-macroglobulin

99
Q

MOA zinc

A

unknown but excess zinc interferes with absorption and utilization of copper and iron -> hemolytic anemia

100
Q

hematologic lesions of zinc

A

regenerative HA, icterus, hemoglobinuria
also prerenal azotemia
can cause PANCREATITIS

101
Q

what type of tube do you use to sample blood for zinc?

A

dark/navy blue tube for trace elements (no Zn stearate)

102
Q

Tx for zinc toxicosis

A

first try to decontaminate then try surgery, make sure to stabilize patient
can chelate with Ca EDTA

103
Q

T/F increased [Cu] in liver is due to imbalances between Cu, molybdenum and sulfate

A

true

increased sulfate decreases Cu absorption

104
Q

Which species are resistant to Cu tox?

A

swine and poultry

105
Q

MOA/CS copper

A

accum in liver > necrosis, RBCs get metHb and can’t carry O2 -> liver, kidney, organ damage

106
Q

Which form of Cu tox is more common, chronic or acute?

A

chronic!! acute NOT common

107
Q

Lesions with copper tox

A

icterus, hemolysis, methemoglobinuria, liver is enlarged/yellow/friable, “gunmetal” kidney, “black berry jam” spleen with “portwine” urine

108
Q

Dx copper tox

A

see increased liver enzymes 3-6 weeks before hemolytic crisis (when liver fails), also hemoglobinuria and HA

109
Q

how to PREVENT cu tox

A

easier to prevent than treat, add Mo to sheep feed make sure enough sulfur
to treat can use a chelator- D-penicillimine to increase Mo

110
Q

T/F decreased Mo causes a Cu deficieny

A

false- INCREASED Mo causes a Cu deficieny

111
Q

Which states have Mo rich soil?

A

Fl, Ca, Or, Nv

112
Q

Which species are resistant to Mo tox?

A

equine and porcine (bovine MOST susceptible)

113
Q

CS Mo tox?

A

green diarrhea after 8-10 days, rough hair coat and depigmentation (ESPECIALLY around eyes), anemia, osteoporosis and exostosis, lameness

114
Q

Tx for Mo tox?

A

Cu glycinate subQ or Cu sulfate in diet

115
Q

Se def diseases are?

A

white muscle/nutritional muscle dystrophy (lambs/calves/foals)
hepatosis dietetica in pigs
exudative diathesis in chicks
nutritional pancreatic atrophy in chickens
porcine stress syndrome in pigs

116
Q

3 types of accumulators (plants) in Se tox

A

obligate, faculatative, passive

117
Q

Name the 9 Se rich states

A

N and S Dakota, Wy, Montana, Ne, Ks, Ut, Co, NM

118
Q

T/F selenium toxicity most to least

Organic Se > selanate = selenite > selenide > synthetic Se compounds

A

true

119
Q

What type of environment increases formation of selanate?

A

arid alkaline

120
Q

Is elemental Se absorbed easily in water?

A

No it is INSOLUBLE- not absorbed

121
Q

Where does Se accumulate?

A

hair and hoof (chronic exposures)

122
Q

MOA Se

A

Se replaces S in AA, cause malformed proteins- decrease tissue glutathione

123
Q

Acute, subacute and chronic Se tox CS

A

Acute- GI, resp (edema) when PO; neuro signs when parenteral
Subacute- “blind staggers”
1- aimless walking, circling, normal resp/temp
2-incoordination, walking on knees, anorexia
3-colic, hypothermia, emaciation, blindness, paresis, coma
In pigs “porcine focal symmetrical poliomyelomalacia”
Chronic- “alkali disease”, rough hair coat, loss of hair, hoof deformities, stiff joints, partial blindness

124
Q

Se prevention

A

Easier- take animals away from high Se rich soil, add Cu to diet, high protein diet, increase sulfur containing compounds

125
Q

T/F only crude oils are highly irritant to MM and skin, not refined petroleum products

A

False- BOTH are

126
Q

Are more or less volatile compounds more toxic because of increased absorption?

A

More volatile (low BP), MORE pneumotoxic potential

127
Q

T/F sweet crude more toxic than sour crude

A

true

128
Q

Aromatic hydrocarbons cause what?

A

bone marrow suppression

129
Q

Can the oily substance aspirated into the lungs of petroleum products be eliminated by cough or ciliary activity?

A

no

130
Q

MOA petroleum products

A

aspiration pneumonia or chemical pneumonitis -> inhalation, swelling, inflammation, edema, bronchoconstriction and necrosis -> hypoxia and bacterial pneumonia

131
Q

CS petroleum products

A

aspiration pneumonia, bovine hyperkeratosis, smell like oil/kerosene, CNS signs (hydrocarbons), ulceration of trachea

132
Q

Lab dx petroleum products

A

panleukopenia, x ray asp pneumonia

133
Q

T/F emetic/gastric lavage and steroids contraindicated in petroleum product toxicosis?

A

true

134
Q

Fluoride has a high affinity for what elements?

A

Ca, Al, and Fe

135
Q

Whats more common, acute or chronic toxicity with Fl?

A

chronic

136
Q

Which species is most susceptible to Fl tox?

A

dairy cattle

137
Q

T/F CaF2 > tox than NaF

A

FALSE- NaF. CaF2

138
Q

Where is Fl stored?

A

teeth (especially in young)

139
Q

MoA chronic Fl tox?

A

brown/black tooth discoloration, altered and decaying bone/teeth

140
Q

CS chronic Fl tox?

A

lame, painful gait, bony extoses, fractures, brown teeth, emaciation, lesions on mandible, metacarpals, ribs, spine and joints

141
Q

Specimen for Fl tox?

A

BONE

142
Q

Tx Fl tox

A

Al salts, Cacarbonate, defluorinated phosphate PO to form insoluble compounds

Toxicology (3 decks)

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