Brainscape's Knowledge GenomeTM

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


See full index

Toxicology Exam 2 > Tox Exam 2 Herbicides and Fungicides > Flashcards

Tox Exam 2 Herbicides and Fungicides Flashcards

1
Q

Source of phenoxy derivatives of fatty acids (2, 4-D) poisoning in cattle?

A

accidental ingestion of concentrates or sprays, grazing freshly sprayed pastures

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

Source of 2,4-D poisoning in pets?

A

freshly sprayed lawns

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

T/F 2,4-D sprayed forages at recommended concentrations can cause poisoning.

A

FALSE. do NOT cause poisoning

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

Which species are most susceptible to 2,4-D poisoning?

A

cattle & dogs

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

Which species are most sensitive to 2,4-D poisoning?

A

dogs

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

ADME of 2,4-D?

A

A=readily from GIT, poorly from skin
D=all over, liver, kidney, brain
M=1/2 life short (few hrs) but longer in dogs (up to 3-4 days)–mainly metabolized by hydrolysis
E=mainly unchanged in urine–tubular secretion

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

Is 2,4-D an acidic or basic toxin?

A

acidic

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

T/F Acidifying the urine will increase 2,4-D toxin excretion?

A

FALSE–alkalinization

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

T/F Meat residues in cattle/sheep are unlikely unless exposed to high concentrations of 2,4-D.

A

TRUE

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

Chemical properties of 2,4-D?

A

Alters metabolism of plants which increases toxicity by increasing accumulation of nitrate or cyanide. May increase palatability of plant.
Not stable in environment, not degraded by rumen microflora, do NOT alter rumen microflora.

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

MOA of 2,4-D?

A

irritation of GI mucosa, affects skeletal muscle in dogs, degeneration of liver/kidneys

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

Clinical signs of 2,4-D?

A

mainly GI & neuromuscular signs

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

Clinical signs of 2,4-D in ruminants?

A

anorexia, rumen atony, bloat, D+, ulcers in gastric mucosa

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

Clinical signs of 2,4-D in dogs?

A

anorexia, V+, bloody D+, muscle weakness (esp posterior muscles), ataxia, rigidity of skeletal muscles

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

Clinical signs of 2,4-D in swine?

A

V+, D+, muscle weakness, depression

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

T/F Rumen stasis with ingested food is a characteristic finding of 2,4-D poisoning.

A

TRUE

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

Specimens used in the diagnosis of 2,4-D poisoning?

A

forage, water, kidney, urine, liver, stomach contents, poo

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

Lab diagnosis of 2,4-D poisoning?

A

elevated ALP (alkaline phosphatase), LDH (lactate dehydrogenase), CPK (creatine phosphokinase)

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

Treatment of 2,4-D poisoning?

A

no specific antidote, detox by washing skin or activated charcoal, supportive/symptomatic–IV fluids, antidiarrheals, rumenatorics

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

Name the 2 dipyridyl herbicides that we discussed in lecture.

A

paraquat & diquat

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

Is paraquat (PQ) a RUP or a GUP?

A

RUP

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

Is diquat (DQ) a RUP or a GUP?

A

GUP

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

Are PQ & DQ stable in the environment?

A

NO! rapidly degraded by light and soil

PQ binds strongly to soil

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

Are PQ & DQ stable in neutral, acidic & alkali conditions?

A

stable in neutral and acidic–but destroyed in alkali

25
Q

T/F PQ/DQ are caustic to membranes & cause characteristic ulcers.

A

TRUE

26
Q

What species are susceptible to dipyridyl herbicidal toxicity?

A

ALL, esp dogs

27
Q

What factors increase PQ toxicity?

A

selenium-vit E deficiency, depletion of tisssue glutathione & oxygen therapy

28
Q

ADME of dipyridil herbicides?

A 
A= (DQ)--poorly absorbed from GIT, (PQ)--absorbed from GIT & skin
D= (PQ) all over body--high concentration in lung (10x other tissues)
M= (PQ) minimal metabolism
E= (PQ) w/in 24 hrs unchanged in urine
29
Q

MOA of dipyridil herbicide toxicity?

A

Reduced by NADPH to produce singlet oxygen which reacts with lipids in cell membranes to form hydroperoxidases. Production of free radicals, membrane damage, cellular degeneration & necrosis–esp lungs.

30
Q

Clinical signs of acute dipyridyl herbicide toxicity?

A

early–> V+, anorexia, depression, high doses may cause ataxia, dyspnea, seizures
delayed–> 2-7 days, resp signs–tachypnea, dyspnea, harsh sounds, cyanosis, decreased pulmonary compliance

31
Q

Clinical signs of subacute or chronic dipyridyl herbicide toxicity?

A

after 7 days up to 3 wks, resp signs d/t pulmonary fibrosis

32
Q

Pathology of dipyridyl herbicide toxicity?

A

pulmonary edema, congestion & enlargement of liver, kidneys and spleen, hemorrhage, fibrosis, failure of lung to collapse, lingual ulcers

33
Q

Specimens that are used to diagnose dipyridyl herbicide toxicity?

A

suspected plant, stomach contents, urine in acute cases, lung in chronic cases

34
Q

T/F Radiology can be used to detect mild changes in the lungs due to PQ/DQ toxicity.

A

TRUE

35
Q

Differential diagnosis for dipyridyl herbicide toxicity?

A

pneumonias, inhalant toxicants such as toxic gases/vapors/dusts, zinc phosphide also stimulates CNS/convulsions + resp signs

36
Q

Treatment for dipyridyl herbicide toxicity?

A 
no specific antidote
detox-->emetics, charcoal, bentonite/fuller's earth choice, saline cathartics after adsorbent
supportive-->fluids, hemo/peritoneal dialysis
biochemical antags (antioxidants)-->orgotein (superoxide dismutase), acetylcysteine, ascorbic acid, niacin, riboflavin
37
Q

T/F Giving O2 early in dipyridyl herbicide toxicity is crucial in preventing further lung damage.

A

FALSE–O2 contraindicated early bc may increase lung damage

38
Q

T/F Treatment for dipyridul herbicide toxicity must be started before 24 hrs post exposure for it to be helpful.

A

TRUE

39
Q

Prognosis for dipyridul herbicaide toxicity?

A

guarded or grave

40
Q

Is pentachlorophenol (PCP) a herbicide or a fungicide?

A

fungicide–prevents fungal infections in plants

41
Q

PCP is used as a _____ preservative.

A

wood–protects limber from fungal rot & wood boring insects

42
Q

Causes of pentachlorophenol toxicosis in livestock & pets?

A

licking wood treated w/ PCP, ingesting contaminated water or feeds, vapors can penetrate skin, inhalation of toxic amounts from treated walls in sheds & barns

43
Q

T/F An animal can still get pentachlorophenol toxicosis by inhaling treated walls in sheds and barns even months/years post application.

A

TRUE

44
Q

T/F PCP is still used in wood preserving solutions, insecticides & herbicides for home & garden use.

A

FALSE–no longer used for these purposes

45
Q

Factors increasing PCP toxicity?

A

high temp–can give off toxic vapors, oily/organic solvent vehicle, previous exposure, poor condition, newborn, hyperT

46
Q

Factors decreasing PCP toxicity?

A

cold temp, antithyroid drugs, presence of body fat

47
Q

ADME of PCP?

A

A=readily through GIT, inhalation, intact skin
D=throughout body–accumulation in fat
M=1/2 life 1.5-2 days
E=glucuronides excreted in urine; residue in tissues/fats depleted from body w/in 1 wk of exposure

48
Q

Chemical properties of PCP?

A

irritant to mucous membranes, resp tract, skin–older preparation contained dioxins which are carcinogenic/teratogenic

49
Q

T/F PCP persists in water, sewage & soil.

A

FALSE–bacterial decomposition prevents their persistence in the environment

50
Q

T/F There are 3 different types of PCP toxicosis–subacute, acute & chronic.

A

FALSE–just 2 types–acute & chronic

51
Q

Describe the clinical signs of acute PCP toxicity.

A

very fast onset–fever, tachycardia, dyspnea, cyanosis, seizure, collapse, death
newborn pigs–hyperthermia, skin irritation, rapid death

52
Q

Describe the clinical signs of chronic PCP toxicity.

A

anorexia, decreased milk production, anemia, fetal malformations, abortions–fever & resp distress may be absent

53
Q

MOA of PCP toxicity?

A

uncouples oxidative phosphorylation & blocks/decreases ATP–increased O2 demand to produce ATP–O2 demand > O2 supply

54
Q

Pathology of PCP toxicity?

A

rapid rigor mortis, local irritation of skin & MM, pulmonary congestion & edema, degenerative changes in liver/kidneys, dark blood due to hypoxia
chronic cases–hyperkeratosis of skin & villous like hyperplasia of urinary bladder mucosa

55
Q

Lab diagnosis of PCP toxicity?

A

antemortem–>chem analysis of blood/urine

postmortem–>skin & kidney

56
Q

Differential diagnosis of PCP toxicity?

A

heat stoke, toxicants causing resp insufficiency–nitrate (brown blood, no fever), CO (bright red blood, no fever), pesticides (marked neuromuscular signs, autonomic signs), parachute infectious dz

57
Q

Treatment of PCP toxicity?

A

no specific antidote
detox–>emetics, gastric lavage w/ 5% Na bicarb, activated charcoal or mineral oil, soap/water on skin
symptomatic–>O2 therapy, lower body temp (cold water/ethanol), IV fluids (NO glucose), electrolytes, prophylatic use of ABs & vitamins to prevent secondary bacT infections d/t liver/kidney/GI damage

58
Q

Prognosis of PCP toxicity?

A

survives past 24 hrs–chances of complete recovery are far

Toxicology Exam 2 (8 decks)

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