Brainscape's Knowledge GenomeTM

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


See full index

Toxicology > Blakley > Flashcards

Blakley Flashcards

1
Q

How are organochlorines absorbed

A

Well absorbed through skin and MM

Poorly absorbed through lungs and GIT

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

Distribution of organochlorines

A

Accumulate in lipid tissues; Readily detectable in liver, kidney brain and fetus

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

metabolism of organochlorines

A

dechlorinated slowly in the liver; many metabolites are highly toxic

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

how are organochlorines excreted

A

through the bile; enterohepatic recycling occurs

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

what is organochlorines mechanism of action

A

K efflux is hindered and Na depolarization is prolonged –> decreasing transmembrane resting potential (decreased firing threshold)

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

other mechanisms of action for organochlorines

A

increased synaptic activity, increased neurotransmitter release from presynaptic terminals and inhibition of GABA

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

what is the susceptibility of cats to organochlorines

A

5 times more susceptible than most species

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

what are the clinical manifestations of organchlorines

A

behavioral abberations (anciety, apprehension, head between legs, licking excessively), nervous phenomena (hypersensitivity, muscle twitching, jaw clamping, clonic tonic convulsions, opisthotonus), autonomic manifestations (minimal but do occur – salivation, diarrhea, dyspnea), locomotor disturbance (stiff gait, ataxia, incoordination)

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

PM findings with organochlorines

A

non-specific; GIT (hemorrhage and congestion), mild fatty degeneration of liver and kidney, degenerative changes in thyroid, pancreas, testis and adrenal glands

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

Treatment of organochlorines

A

Wash off skin, gastric lavage, activated charcoal, mineral oil (to force through and bind), sedation, IV lipid emulsion

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

residue concerns of organochlorines

A

milk and meat residues are a major concern due to reproductive, carcinogenic and immunosuppresive effects

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

diagnosis of organochlorines

A

analyze fat, milk, liver, kidney and GI contents

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

3 major groups of anticholinesterase compounds

A

organophosphates insecticides, carbamate insecticides and nicotinoid insecticides

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

residue concerns with anticholinesterase compounds

A

not a concern because rapidly degraded with short half life

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

absorption of anticholinesterase compounds

A

well absorbed by all routes including dermal and respiratory

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

distribution of anticholinesterase compounds

A

rapidly to all tissues; no accumulation in fat

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

excretion of anticholinesterase compounds

A

excreted rapidly in a few days

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

mechanism of action of anticholinesterase compounds

A

inhibition of acetylcholinesterase prevents break down of acetylcholine

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

enzymes affected by anticholinesterase compounds

A

pseudo(plasma) cholinesterase (non-specific) and true (RBC) cholinesterase (80%)

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

specific mechanism of action of organophosphate

A

forms a stable enzyme-organophosphate complex that is practically irreversible

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

specific mechanism of action of carbamates

A

carbamate enzyme complex is not as stable so enzyme inhibition is reversible

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

nicitinoid compound mechanism of action

A

binds to nicotinic receptors therefore no inhibition of acetylcholinesterase BUT need extreme high doses to bind a sufficient number of receptors to cause signs

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

clinical manifestations of anticholinesterase compounds

A

excessive muscarinic and nicotinic stimulation starting 5 minutes to 1-2 hours after exposure; diarrhea, vomiting, salivation, dyspnea due to bronchoconstriction, decreased HR, pupil constriction

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

with what anticholinesterase compound does delayed neurotoxicity occur with

A

organophosphates

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

clinical signs of delayed neurotoxicity (organophosphates)

A

develops 10D to 3M after exposure; irreversible effects of muscle weakness especially in hind limbs, knuckling, ataxia (flaccid paralysis), cats unable to retract claws, normal acetylcholinesterase

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

PM findings of delayed neurotoxicity (organophosphates)

A

axonal degeneration, peripheral neuropathy, degeneration of myelin sheath

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

diagnosis of delayed neurotoxicity (organophosphates)

A

histo exam of spinal cord, chemical analysis of tissues and history of previous exposure

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

PM findings for anticholinesterase compounds

A

few lesions, petechial hemorrhage and congestion on viscera, slight pulmonary edema

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

Diagnosis of anticholinesterase compounds

A

history, cholinesterase activity in heparinized blood (measured by Michel’s change in pH for organophosphates only or titrimetric pH stat for carbamates/organophosphates

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

factors that influence the measurement of cholinesterase activity

A

aging, enzyme denaturation, spontaneous reaction (carbamate)

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

treatment of anticholinesterase toxicity

A

atropine (non-competitive antagonist that blocks muscarinic receptors), 2-PAM (for organophosphates only, contraindicated in carbamates), wash, activated charcoal, bicarb and fluids

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

mechanisms of action of lead

A

based on the affinity of lead for SH or imidazole groups; binds to various macromolecules to impair their function
(enzymes, decreases cellular respiration and ATP production due to effect on mitochondria, embryotoxic, teratogenic, immunosuppression)

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

absorption of lead

A

1-2% in adults, 30-40% in young

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

distribution of lead

A

cumulative toxin; distributes to liver and kidney within the day, chronic exposure displaces Ca in bone (does NOT go to brain)

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

excretion of lead

A

kidney and minor excretion in milk

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

effect of lead on the GIT

A

irritation and gastroenteritis

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

effect of lead on nervous system

A

encephalopathy – capillary damage causes hemorrhage and congestion in the brain followed by edema and malacia +/- blindness and peripheral nerve damage

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

effect of lead on hemopoetic system

A

anemia associated with decreased iron uptake, increased RBC fragility, and impaired heme synthesis; can see basophilic stippling

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

effect of lead on kidney

A

degenerative changes – tubular necrosis, nephritis, fibrosis and hyaline degeneration (acid fast inclusion bodies)

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

effect of lead on respiratory system

A

swallowing mechanisms can be impaired by neuro dysfunction leading to aspiration pneumonia

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

duration of acute lead poisoning

A

short; typically less than 24 hours

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

clinical manifestations of acute lead poisoning (cattle)

A

behavioral changes (mania, bellowing, head pressing), locomotor disturbances (staggering and muscle tremors), nervous phenomena (clamping jaws, blindness, hyperaesthesia, intermittent tonic-clonic convulsions, opisthotonus), GIT (rumen stasis, salivation, abdominal pain)

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

clinical manifestation of subacute lead poisoning (cattle)

A

dullness and head pressing, variable locomotor disturbances, blindness, depression, hyperaesthesia, NO CONVULSIONS, grinding teeth, anorexia

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

lead poisoning in sheep

A

usually subacute and may have osteoporosis

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

lead poisoning in horses

A

usually chronic – colic, diarrhea, pharyngeal paralysis, aspiration pneumonia, inspiratory dyspnea, roaring

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

lead poisoning in swine

A

primarily GI signs, vomiting, few CNS signs

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

lead poisoning in dogs

A

anorexia, vomiting, colic, hyperexcitability, convulsions, hysterical bark

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

diagnosis of lead poisoning

A

lead analysis of liver and kidney

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

antemortem diagnosis of lead poisoning

A

heparinized blood, rumen contents, fecal contents

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

clinical pathology of lead poisoning

A

anemia, basophilic stipling, increased ESR, hypochromia, leptocytes, proteinuria, glucosuria

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

treatment of lead poisoning

A

chelation therapy (penicillamine, BAL, Ca EDTA)

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

supportive care of lead poisoned animals

A

force feeding, oral fluids, mannitol

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

residue concerns of lead poisoning

A

treatment of food animals is not recommended due to meat and milk residues

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

lead half life

A

many months

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

3 forms of mercury

A

elemental metal mercury, inorganic mercury, organic mercury

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

absorption of metal mercury

A

well absorbed by inhalation

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

inorganic mercury absorption

A

poor; burns skin

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

absorption of inorganic mercury

A

well absorbed by skin and GIT (lipophilic)

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

metabolism of mercury

A

converted to inorganic forms but in environment be converted to organic mercury (methyl mercury)

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

distribution of mercury

A

liver and kidney accumulate high quantities; fetus acts as a sink and protects mother)

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

excretion of inorganic mercury

A

urinary

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

excretion of organic mercury

A

bile and feces; 70D half life

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

mechanism of action of inorganic mercury

A

causes corrosive damage and tissue necrosis (irritation); binds with sulfhydryl groups causing reduced metabolic activity and degenerative change)

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

mechanism of action of organic mercury

A

interferes with metabolic activity causing degenerative changes

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

clinical manifestation of inorganic mercury

A

GIT and neurological syndrome; anorexia, vomiting, salivation, diarrhea, stomatitis, ulcers, ataxia, tremors, terminal convulsions, depression, paresis, hematuria, proteinuria, uremia, epistaxis, dyspnea, (alopecia and keratinization occur with chronic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

clinical manifestations of organic mercury

A

ataxia, tremors, terminal convulsions, depression, paresis, hematuria, proteinuria, uremia, epistaxis, dyspnea, (alopecia and keratinization occur with chronic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

PM of inorganic mercury

A

gastroenteritis, stomatitis, mucosal hemorrhage and edema, ulcers, interstitial nephritis, tubular necrosis, edema, bronchitis, hydrothorax, mild liver necrosis, encephalomalacia, cerebellar atrophy of offspring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

PM of organic mercury

A

interstitial nephritis, tubular necrosis, edema, bronchitis, hydrothorax, mild liver necrosis, encephalomalacia, cerebellar atrophy of offspring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

diagnosis of mercury

A

clinical manifestations and pathology of CNS and GIT; analysis of blood, liver or kidney for mercury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

treatment of mercury

A

success is limited by long half life and degenerative organ change; sodium thiosulfate, egg whites, milk, astringents; chelators such as BAL are used to treat pets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

residue concerns of mercury

A

major concerns due to milk and meat residues being lengthy and highly teratogenic nature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

forms of arsenic

A

organic (less toxic, CNS) and inorganic (severe GI signs and CNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

arsenic absorption

A

readily absorbed through skin or GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

arsenic distribution

A

accumulates in energy rich tissues (liver, kidney, GI epithelium); with chronic exposure will be in hair and hoof as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

excretion of arsenic

A

bile or urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

arsenic mechanism of action

A

metabolic poison that impairs cellular respiration and uncouples oxidative phosphorylation (degenerative changes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

mechanism of action of inorganic arsenic

A

chemical irritation, tissue degeneration and metabolic poison

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

clinical manifestation of acute inorganic arsenic

A

high mortality, sudden onset, vomiting, abdominal pain, weakness, ataxia, recumbency, shock, diarrhea and death within 3-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

clinical manifestations of subacute inorganic arsenic

A

duration of 2-7 days with more neuro signs; colic, vomiting, diarrhea, salivation, grinding teeth, dehydration and shock, muscle tremors, incoordination, clonic convulsions, hind end paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

clinical manifestations of chronic inorganic arsenic

A

vague, unthrifty animals with poor growth, indigestion, reduced milk production, abortion and buccal cavity ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

diagnosis of inorganic arsenic

A

clinical signs, analysis of liver, kidney, hair, or food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

arsenic half life

A

only a few days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

treatment of inorganic arsenic poisoning

A

BAL is first choice because will pull out of brain; sodium thiosulfate (sulfur binds arsenic), fluid therapy is essential for shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

types of organic arsenic used as feed additives

A

arsanilic acid (least toxic), roxarsone, nitrophenylarsonic acid (5x more toxic than arsanilic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

elimination rate of organic arsenic

A

rapidly eliminated – short withdrawal times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

clinical manifestation of acute organic arsenic

A

symptoms in about 1 week, incoordination, ataxia, paralysis, blindness, not anorexia and no GI signs (CONSUME FOOD UNTIL LATE STAGES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

clinical manifestations of chronic organic arsenic

A

similar signs to acute but to a lesser extent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

diagnosis of acute arsenic poisoning

A

history, neuro signs, feed analysis is best

89
Q

what does glutathione peroxidase assess

A

selenium deficiency

90
Q

normal function of selenium

A

stabilize cell membrane

91
Q

plant sources of selenium

A

astragalus (locoweed)

92
Q

absorption of selenium

A

well absorbed

93
Q

distribution of selenium

A

found in all tissues; will be at highest levels in oxidative and energy rich tissues (liver and kidney), can displace sulfur in hair and hoof, accumulates in fetus

94
Q

excretion of selenium

A

urine mostly; bile, sweat, lungs, hair and hooves

95
Q

selenium toxicity mechanism of action

A

causes lipid peroxidation and membrane damage; high levels reduces ATP formation; irritating orally

96
Q

clinical manifestations of acute selenium poisoning

A

sudden onset in 1-2 days with quick death; anorexia, depression, dyspnea, cyanosis, colic and shock

97
Q

PM of acute selenium toxicity

A

congestion, hemorrhage, enteritis with oral exposure, degenerative changes to liver and kidney

98
Q

manifestation of subacute selenium toxicity (blind staggers)

A

often a plant source, onset is days to weeks; wander aimlessly, anorexia, blind, impaired swallowing, head pressing, emaciation, dyspnea, death

99
Q

PM of subacute selenium toxicity

A

pulmonary edema, hydrothorax, gastroenteritis, ulcers, rumen necrosis and hyperemia

100
Q

chronic selenium poisoning manifestations (alkali disease)

A

onset is months, dullness, rumen stasis, impaction, hoof deformities, hair loss

101
Q

PM of chronic selenium poisoning

A

mild gastroenteritis, atrophy and dilation of heart, other organs show degeneration

102
Q

PM of selenium poisoning in swine

A

symmetrical spinal poliomalacia, necrosis of grey horns of L6-L9 leading to paralysis, continue to eat and drink

103
Q

diagnosis of selenium toxicity

A

tissue and feed analysis

104
Q

treatment and prevention of selenium toxicity

A

fluids for shock therapy, acetylcysteine, dietary supplementation with copper, arsenic or sulfur containing AA may bind Se

105
Q

factors influencing iron toxicity

A

young animals, especially pigs, have no mechanism to excrete excess iron until 8D of age; animals born with high iron stores are more susceptible; animals born with low Vit E/Se status are more susceptible.

106
Q

mechanism of action of iron toxicity

A

not fully understood! CV collapse and death from shock; observe increased permeability leading to fluid loss and hepatic necrosis (leading to hemorrhage)

107
Q

clinical manifestations of peracute iron toxicosis

A

anaphylactoid like reaction then death from shock within minutes to 1-2 hours; (injectables)

108
Q

clinical manifestations of subacute/classical iron poisoning

A

drowsiness, depression, coma and death in 4-5 hours, vomiting, diarrhea, melena, necrosis, icterus, hemoglobinuria, pale skin, dyspnea, acidosis, hemorrhage

109
Q

presenting complaint for subacute/classical iron poisoning

A

liver damage

110
Q

clinical manifestations of chronic iron poisoning

A

rickets and poor growth due to iron binding P and altering bone growth

111
Q

PM of iron toxicity

A

subacute will show periportal necrosis and iron deposits in kupffer cells; icterus

112
Q

treatment of iron toxicity prior to GI signs

A

milk of magnesia can be used to form insoluble iron hydroxide salts

113
Q

treatment of iron toxicity after GI signs

A

fluids for shock and acidosis, chelators such as deferoxamine (Ca EDTA has low affinity), vitamin E

114
Q

most effective treatment of iron toxicity

A

vitamin E because antioxidant activity prevents further liver damage

115
Q

differences in species susceptibility regarding copper

A

ruminants more susceptible monogastrics; sheep more susceptible than catte; llamas comparable to sheep but without the hemolytic crisis; bedlington terriers are predisposed; pigs/horses metabolize copper differently so not affected

116
Q

absorption of copper

A

well absorbed

117
Q

distribution of copper

A

found extensively in plasma bound to albumin, ceruloplasmin, oxidase enzyme or metallothionein; liver is primary storage organ

118
Q

can blood be used to diagnose copper toxicity

A

No; ceruloplasmin will be low with copper deficiency but remains within normal reference in copper toxicity

119
Q

excretion of copper

A

primarily in the feces; biliary excretion, though limited, is critical for homeostasis (bedlington terriers don’t have this –> chronic copper poisoning)

120
Q

acute copper toxicity mechanism of action

A

protein coagulant at high levels leading to severe gastroenteritis

121
Q

chronic copper toxicity mechanism of action (primary)

A

Cu has oxidative properties that occur when liver exceeds storage – lipid peroxidation begins (glutathione is depleted causing Hg in RBC to be oxidized to methemoglobin, damaged erythrocytes undergo hemolysis)

122
Q

what color is the blood with copper poisoning

A

chocolate brown

123
Q

phytogenous chronic copper poisoning (secondary)

A

copper is normal but low molybdenum – increased Cu absorption and decreased excretion, no liver damage present

124
Q

hepatogenous chronic copper poisoning

A

related to ingestion of plants that cause liver damage (pyrrolizidine alkaloids impair bile excretion leading to chronic Cu poisoning) or chronic active hepatitis

125
Q

factors preceding Cu exceeding liver storage capacity

A

declining plane of nutrition, shipping, lactation, exercise, stress

126
Q

manifestations of acute copper poisoning

A

death within 24 hours; abdominal pain, nausea, vomiting, salivation, shock, feces (green color), mild jaundice, gastroenteritis primarily (erosion and ulceration), congestion of other organs, no methemoglobin

127
Q

manifestations of chronic copper poisoning

A

hemoglobinuria, hemoglobinemia, methemoglobinemia (portwine urine, red plasma, chocolate brown blood), jaundice and increased liver enzymes, trembling and weakness

128
Q

PM changes with chronic copper poisoning

A

liver will have generalized icterus, enlargement and friable; kidney – hemorrhage, friable, degeneration, tubular necrosis, gun metal color; spleen – enlarged, black currant jam appearance; methemoglobin causes brown discoloration of tissues

129
Q

diagnosis of acute copper poisoning

A

signs of sudden death and gastroenteritis, GI contents may be blue green color, normal tissue levels

130
Q

diagnosis of chronic copper poisoning

A

analysis of feed for copper molybdenum levels (normal is 6-10:1); elevated liver enzymes, methemoglobin and hemoglobinuria; 1 or 2 sick and the rest on the brink of disaster

131
Q

treatment of copper poisoning

A

unsuccessful once hemolytic crisis occurs; ammonium molybdate orally, sodium thiosulfate, thiomolybdate (ideal but not available commercially)m chelators, add Mo/Zn to diet

132
Q

what mineral does molybdenum toxicity manifest as a deficiency of

A

copper

133
Q

differences of susceptibility of molybdenum toxicity

A

cattle/ruminants are more susceptible; young are more susceptible; pigs can tolerate high levels

134
Q

mechanism of action of molybdenum toxicity

A

interferes with copper storage by reducing absorption and enhancing secretion (also competes with Cu for Cu dependent enzymes); interferes with P absorption and mineral metabolism in bones (faulty bone development); interferes with phospholipid synthesis causing reduced growth and maintenance of myeline

135
Q

clinical manifestations of molybdenum toxicity in sheep

A

swayback, incoordination, ataxia, occasionally blind, depigmented stringy wool, usually young, rapidly growing animals

136
Q

clinical manifestations of molybdenum toxicity in cattle

A

emaciation, diarrhea, anemia, achromotrichia, enlarged joints, osteoporosis, reduced fertility and reduced milk production

137
Q

diagnosis of molybdenum toxicity

A

forage levels of Cu/Mo (2/1), tissue levels of Cu and Mo, response to Cu therapy

138
Q

treatment of molybdenum toxicity

A

copper sulfate as a mineral mix; injectable copper; copper oxide needles; chelated mineral mix

139
Q

absorption of zinc

A

well absorbed

140
Q

distribution of zinc

A

found in most tissues

141
Q

excretion of zinc

A

excreted in urine and bile

142
Q

zinc half life

A

2-3 days; may be longer if there is kidney damage associated with Zn exposure

143
Q

mechanism of action of zinc toxicity

A

oxidative damage; hapten induced immune dysfunction and DIC can also occur

144
Q

clinical manifestations of Zn (dogs)

A

anorexia, salivation, vomiting, diarrhea, bleeding, jaundice, intravascular hemolysis, heinz bodies, leukocytosis with left shift, regenerative anemia, bilirubinemia, hemoglobinuria, tubular nephrosis

145
Q

diagnosis of zinc toxicity

A

elevated blood zinc levels (must use proper tube for diagnosis to be accurate), radiographs, clin path

146
Q

treatment of zinc toxicity

A

surgery, blood, transfusions, heparin or dicoumarol, cimetidine to reduce acid secretion and decrease dissolving Zn

147
Q

what is the most necessary treatment for zinc toxicity

A

heparin or dicoumarol to prevent DIC

148
Q

complication of zinc toxicity

A

pancreatitis and DIC

149
Q

what time of year is blue-green algae toxicity seen

A

hot summer months

150
Q

why do you need to collect a water sample ASAP with blue-green algae

A

toxin can disappear from water within 24 hours

151
Q

factors affecting blue-green algae toxicity

A

species of algae, bacterial presence in bloom (cl. botulinum), growth conditions, sunlight/temperature, acummulation, decompisition, LPS endotoxins, after rapid growth there may be rapid lysis with release of endotoxins

152
Q

what N/P ratio favors green algae

A

high N/P ratio

153
Q

what N/P ratio favors blue-green algae growth

A

low N/P ratio (high P favors)

154
Q

what are the 3 species of blue-green algae

A

microcystis, anabena, aphanizomenon (mike, annie and fannie)

155
Q

what toxin is present in anabena (blue-green)

A

anatoxin-a; alkaloid, very fast death factor, not stable

156
Q

what is the mechanism of action of anatoxin-a (anabena)

A

postsynaptic depolarizing neuromuscular block, nicotinic agonist, anticholinesterase activity

157
Q

clinical manifestations of anabena (blue-green)

A

paralysis, tremors, convulsions (3-5 minutes after drinking), salivation, vomiting, diarrhea, dyspnea, death within 4 minutes

158
Q

PM of anabena toxicity (blue-green)

A

few distinct changes; agonal hemorrhage and congestion

159
Q

diagnosis of anabena toxicity (blue-green)

A

mouse bioassay

160
Q

treatment of anabena toxicity (blue-green)

A

artificial respiration for at least 30 hours; (anatoxin irreversibly binds cholinesterase enzymes – animals usually found dead); atropine may offer relief

161
Q

components of microcystis toxin (blue-green)

A

hepatotoxic and post-synaptic neuromuscular block (two peptides) – fast death factor

162
Q

mechanism of action of microcystis (blue-green)

A

hyperphosphorylation of proteins and keratin, tumor promotor, hepatotoxin induces necrosis and apoptosis

163
Q

clinical manifestation of microcystis (blue-green)

A

death within one hour, vomiting, hemorrhagic diarrhea, icterus, photosensitzation in survivors, convulsions

164
Q

PM of microcystis (blue-green)

A

liver will be swollen, mottled, congested, hemorrhage, necrosis and apoptosis; tubular nephritis; pulmonary hemorrhage; cardiac degeneration

165
Q

diagnosis of microcystis

A

mouse bioassay with water sample; liver pathology; hepatic enzymes elevated within 45 minutes

166
Q

aphanizomenon toxins

A

saxitoxin (paralytic shell fish poison, Na channel blocker, inhibits axonal transmission of nerve impulses); neurotoxins (neuromuscular action and inhibition of nerve conduction)

167
Q

clinical manifestations of aphanizomenon toxicity (blue-green)

A

paralysis, death associated with respiratory depression/depression of respiratory center

168
Q

PM of aphanizomenon toxicity (blue-green)

A

no specific lesions

169
Q

treatment of aphanizomenon toxicity (blue-green)

A

symptomatic; activated charcoal

170
Q

prevention of blue-green algae toxicity

A

copper sulfate in water, diquat, shade, lime (standard treatment), duckweed, chlorine, increase N/P ratio

171
Q

what is the standard prevention of blue-green algae toxicity

A

lime: removes P and increase N/P ratio to favor green algae growth; changes pH and may make cattle not want to drink it

172
Q

thiram (fungicide)

A

relatively non-toxic; hepatotoxic and skin irritant; rotten egg smell from cows; zero residues

173
Q

chorophenols (fungicide) – trichlorophenol and pentachlorophenol

A

uncouples oxidative phosphorylation; temperature of animal sky rockets (need to cool down); irritant;

174
Q

pentachlorophenol mechanism of action (fungicide)

A

powerful uncoupler of oxidative phosphorylation, inactivates respiratory enzymes, direct irritant

175
Q

clinical manifestations of pentachlorophenol (fungicides)

A

muscle weakness, incoordination, anorexia, immense increase in BT, dyspnea, sweating, dehydration, irritation to skin/resp tract, cardiac malfunction, terminal convulsions

176
Q

absorption and excretion of pentachlorophenols (fungicides)

A

rapid absorption and excretion (glucoronidation) – cats can’t metabolize

177
Q

treatment of pentachlorophenols (fungicide)

A

cold water bath, wash, lavage

178
Q

pentachlorophenols are present in (fungicide)

A

wood preservative, molluscacide and rug shampoo

179
Q

Maneb (carbamate fungicide)

A

contains Mg; causes depressio, anorexia and diarrhea; PM shows liver and kidney degeneration, congestion of lungs, thyroid hyperplasia

180
Q

Captan (fungicide)

A

low toxicity; clinical signs are dyspnea, anorexia, depression; PM shows hydrothorax, ascites and gastroenteritis

181
Q

what is dinitroorthocresol

A

an insecticide, herbicide and wood preservative

182
Q

absorption of dinitroorthocresol

A

fat soluble; absorbed by vapors, oral or cutaneous exposure

183
Q

mechanism of action of dinitroorthocresol

A

uncouples oxidative phosphorylation so increases body temperature

184
Q

symptoms of dinitroorthocresol

A

fever, weakness, dyspnea, anorexia, acidosis, liver/kidney damage, possible abortion, stains organs yellow

185
Q

treatment of dinitroorthocresol

A

lavage, bicarb, activated charcoal, cathartic and ice pacls

186
Q

effect of sulfur toxicity (fungicide)

A

irritation causing superpurgation and diarrhea; erythema, colic, dullness, ataxia, gastroenteritis, ulcers, erosions, liver and kidney congestion

187
Q

thiabendazole (fungicide and anthelmintic)

A

depression, anorexia and GIT disturbance

188
Q

mechanism of action of chlorates (herbicides)

A

strong oxidizing agent; methemoglobin formation, RBC damage, irritation (rumen stasis)

189
Q

symptoms of chlorate toxicity

A

diarrhea, vomiting, colic, hematuria, dyspnea, cyanosis, tissues are chocolate brown (looks like chronic Cu but no liver damage)

190
Q

treatments of chlorate toxicity

A

lavage, demulcent, methylene blue (none very effective)

191
Q

what rule is paraquat (herbicide) considered the exception to

A

the rule that herbicides are not very toxic; paraquat is quite toxic but there are species differences

192
Q

manifestation of acute paraquat toxicity

A

excitation, incoordination, ataxia, diarrhea, dyspnea, death within 10 days

193
Q

manifestation of chronic paraquat toxicity (herbicide)

A

progressive fibrosing pneumonitis

194
Q

mechanism of action paraquat (herbicide)

A

reduction of oxygen to superoxide anion – free radical damage in lung, lipid peroxidation, cell damage and impaired cell function

195
Q

other organ affects of paraquat (herbicide)

A

edema and hyaline membrane formation in lung, GIT irritation and ulcer, kidney and liver degeneration, eye and skin irritant

196
Q

treatment of paraquat toxicity (herbicide)

A

soap wash, lavage, adsorbents

197
Q

what is TCDD

A

a phenoxyderivative herbicide

198
Q

TCDD skin lesions (highest toxicity of phenoxyderivative herbicides)

A

hepatotoxic, carcinogenic, teratogenic, immunosuppresion, chloroacne (skin), fat accumulation

199
Q

what are 2,4 D derivative

A

phenoxyderivative herbicides

200
Q

2,4 D absorption and half life

A

oral and dermal absorption; excreted unchanged in urine with 18 hour half life

201
Q

mechanism of action of 2,4 D (herbicide)

A

uncouples oxidative phosphorylation so increases BT, decreased ribonuclease synthesis and damages muscle membranes

202
Q

clinical signs of 2,4 D (herbicide)

A

anorexia, rumen stasis, hind limb paralysis

203
Q

PM of 2,4 D (herbicide)

A

congestion and degeneration of organs, some hemorrhage

204
Q

what species is most sensitive to 2,4 D toxicity (herbicide)

A

dogs – myotonia, vomiting, bloody diarrhea, posterior weakness

205
Q

treatment of 2,4 D (herbicide)

A

wash, activated charcoal and fluids

206
Q

food residue concern with 2,4 D (herbicide)

A

low

207
Q

rotenone absorption and metabolism (acaricide)

A

poor absorption and rapid metabolism

208
Q

rotenone symptoms (acaricide)

A

nausea, vomiting, salivation, dyspnea, tremors, incoordination, paralysis

209
Q

treatment of rotenone (acaricide)

A

sedation (atropine is ineffective), good prognosis, residues are not a concern

210
Q

pyrethrins/pyrethroids (acaricide) absorption

A

well absorbed by lungs, orally or dermally

211
Q

mechanism of action of pyrethrins (acaricide)

A

alters Na channels to decrease ion fluxes; binds GABA

212
Q

clinical signs of pyrethrin toxicity (acaricide)

A

muscle tremors, excitation, paralysis, salivation, vomiting, dyspnea

213
Q

treatment of pyrethrin toxicity (acaricide)

A

rapid recovery usually; wash, emetics, activated charcoal, sedation

214
Q

amitraz absorption, metabolism and excretion (acaricide)

A

well absorbed, metabolized by oxidation and excreted in urine (limited residue concern because rapid)

215
Q

mechanism of action of amitraz toxicity (acaricide)

A

alpha adrenergic agonist, monoamine oxidase inhibitor, CV collapse and respiratory depression

216
Q

clinical manifestations of amitraz toxicity (acaricide)

A

decreased HR, ataxia, depression, vomiting, diarrhea, seizures

217
Q

PM of amitraz (acaricide)

A

non-specific with enlarged liver

218
Q

treatment of amitraz

A

wash, emetic, activated charcoal

Toxicology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions