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Flashcards in Cyanide (FINAL) Deck (60)
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1

Which species are most likely to get cyanide poisoning?

Large animals

2

What are possible sources of cyanide poisoning in large animals?

  • Ingestion of cyanogenic plants
    • Wild cherry (Prunus spp)
    • Sudan grass, Johnson grass, and sorghums

3

What does sudan grass, Johnson grass, and sorghum contain?

Cyanogenic glycosides that can liberate toxic amounts of HCN

4

What species is this?

Chokecherry (Prunus spp)

 

5

What is this?

Sorghums (Sorghum spp)

 

6

What can be a source of cyanide poisoning in small animals?

Hydrogen cyanide and cyanide salts have many uses that lead to poisoning in small animals

7

What is used as a fumigant rodenticide that can cause poisoning in small animals?

Hydrogen cyanide gas

8

What compound do some fertilizers contain that is toxic to small animals?

Cyanamide

9

T/F: Sodium nitroprusside is used as a hypotensive

TRUE

10

Combustion of what produces HCN gas that can poison small animals?

Many plastic compounds

11

What are some cyanogenic plants that cause toxicity in small animals?

  • Prunus spp
    • Cherries, apples, plums, apricots
  • Some species of lima bean and cassava roots (tapioca)

12

What is cyanide also known as?

Hydrogen cyanide (HCN), hydrocyanic acid, or prussic acid

13

Is HCN a volatile gas?

YES

14

T/F: HCN will disappear as the plant dries and also from the rumen contents

TRUE

15

What is HCN's characteristic odor?

Bitter almond or ammoniacal

16

Is HCN an irritant to mucous membranes

Of course it is

17

What does the CN- radical form?

Complexes with a number of chemicals, such as ferric ion, cupric, and molybdenum

18

Does cyanide have an antithyroid effect?

No--thiocyanate SCN has an antithyroid effect

19

What are the toxic levels of cyanide?

Greater than 200ppm in the plant is toxic

20

What is the acute oral MLD of HCN?

2-2.3 mg/kg in all species

21

Which species are more/less susceptible to cyanide toxicosis?

  • Ruminants are more susceptible than horses and swine
  • Sheep are less susceptible than cattle

22

Why are ruminants more susceptible to HCN poisoning?

Hydrolysis by the rumen microflora causes release of cyanide from cyanogenic plants

23

What happens to cyanogenic plants when damaged?

  • Plant damage (stunting, wilting, trampling, frost, drought, or treatment w/ 2,4-D herbicides)
    • Causes release of beta-glucosidase that causes hydrolysis of cyanogenic glycosides and release of cyanide (HCN)

24

What is the order of cyanogenic glycoside concentrate in plant parts?

Seeds > leaves > bark > stems > fruit

25

Which plant stage contains more glycoside?

Young/growing

26

What soil condition might increase cyanide poisoning?

High N or low P--may increase glycoside

27

T/F: Plants can contain large amounts of free HCN and cyanogenic glycoside

TRUE

28

T/F: Rapid ingestion and ingestion of large portions of a cyanogenic plant can cause toxicosis

TRUE

29

Where is HCN absorbed from?

HCN is rapidly absorbed from the GI tract, by inhalation, and from intact skin

30

Where is HCN distributed?

Throughout the whole body

31

Where is CN- metabolized?

In the presence of thiosulfate, CN- is metabolized by serum and liver sulfurtransferase (rhodanese) to thiocyanate (SCN-) which is relatively less toxic and is excreted in the urine

32

Excretion of HCN?

Small amounts are excreted in the urine or expired air

33

What happens to excess CN- in tissues/blood?

It binds with ferric iron and cupric copper of the mitochondrial cytochrome oxidase

--> this blocks electron transport and inhibits the cells from utilizing available oxygen --> histotoxic anoxia particularly in the brain

34

Does CN- toxicosis respond to oxygen therapy

NO--cells can't utilize the available oxygen

35

T/F: Anaerobic glycolysis leads to metabolic acidosis in HCN toxicosis

TRUE

36

What might cyanide inhibit following toxicosis?

May inhibit enzymes of glycolysis and citric acid cycle and decrease cellular energy

37

What effect does cyanide have?

A prominent vasoconstrictor effect

38

Does HCN toxicosis cause neuronal damage?

Yes, due to histotoxic anoxia

39

What occurs following chronic HCN toxicity?

  • Neuronal degeneration and demyelination of the spinal cord and brain
  • Low levels of cyanide are goitrogenic due to thiocyanate

40

T/F: Both peracute and acute poisoning can have an extremely rapid onset

TRUE

41

T/F: Animals may die from poisoning without manifesting clinical signs

TRUE

42

What are the clinical signs of acute poisoning?

  • Signs occur in rapid succession and include tachypnea, apparent anxiety, severe panting, gasping, and behavioral alarm
  • Other signs may be muscle tremors, salivation, lacrimation, urination, defecation, severe colic, vomiting, prostration, bright red mucous membranes (from hyperoxygenation of the blood), clonic convulsions, and rapid death

43

T/F: Signs of acute HCN poisoning will vary among species

FALSE--signs are similar in all species

44

How long does it take for animals to die from acute poisoning?

About 4-5min from onset of clinical signs

45

What are the clinical signs of chronic poisoning?

  • Posterior paralysis, urinary incontinence and cystitis, which may result in infection
  • Constipation due to lower spinal cord degeneration
  • May have goitrogenic effect

46

Which sample is positive for cyanide poisoning?

Far left

47

What are the lesions associated with cyanide toxicosis?

  • Bright red mm, cherry-red blood that may not clot or will slowly clot
  • GI tract and lungs show congestion and petechial hemorrhages
  • Plants may be seen in rumen contents
  • May be smell of cyanide, although it leaves the rumen contents rapidly

48

What specimens are used for chemical analysis?

What should be done to the specimens?

  • Forage (200ppm considered toxic), blood (stays longer than in tissues), rumen contents, liver, muscle, brain, and heart (if taken w/in 4hrs of death)
  • Brain and heart are good specimens
  • All specimens (except blood) should be frozen immediately and kept frozen until analysis

49

What can be used as a preservative for plant specimens?

Adding 1-3% solution of mercuric chloride--prevents hydrolysis

50

Is chemical analysis useful for emergency situations?

No--results take days

51

What is elevated on the lab diagnosis?

  • Elevated thiocyanate levels in urine
  • Lactic acidosis and increased anion gap
    • Good indicators for presence and severity of cyanide poisoning

52

What is the sodium picrate paper test?

  • Commercial kit test to detect toxic levels of cyanide in the rumen contents or plant
  • Yellow color changes to brick red in a few minutes (in airtight glass jar)

53

Diagnosis?

  • History of consuming cyanogenic plants, bright red mm, and odor of cyanide are indicative of cyanide toxicosis
  • Chemical analysis confirms diagnosis

54

DDx?

  • Carbon monoxide (causes bright red blood)
  • Hydrogen sulfide
  • Nitrate
  • Urea

55

How can you differentiate between cyanide toxicosis and hydrogen sulfide poisoning?

H2S causes rapid death by inhibition of cytochrome oxidase, but blood and tissues will be dark

56

How can you differentiate between nitrate and cyanide toxicity?

Nitrate can cause rapid death (with little exposure), but the blood is chocolate brown colored

57

How is urea poisoning similar/different from cyanide poisoning?

Urea may cause rapid death with few lesions, but causes severe colic, nervous and behavioral effects, and the odor of ammonia in the rumen

58

Treatments?

  • Sodium nitrite 20% IV at 10-20mg/kg
  • Sodium thiosulfate orally
  • Oxygen therapy is beneficial in addition to nitrite-thiosulfate
  • Vinegar (4L) in 12-20 L cold water orally to slow microbial hydrolysis
  • Mineral oil as a laxative

59

How does sodium nitrite work as a treatment?

  • 20% IV at 10-20mg/kg
  • Immediately improves perfusion by causing vasodilation
  • Causes methemoglobin which can bind the CN- and reactivate cytochrome oxidase (too slow to account for the rapid improvement)

60

How does sodium thiosulfate work as treatment?

  • 20% IV at 600mg/kg (?)
  • Converts CN- to thiocyanate (SCN) which is less toxic and is excreted in urine