Final Quizes and Exams Flashcards

1
Q

What is a “Standard Operating Procedure” and why are SOPs used so often in large operations or organizations?

A

Step by step instructions for carrying out complex (usually) routine operations

  1. Increase efficiency
  2. Quality Output
  3. Uniformity of performance
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2
Q

What organisms drive the evolution of chemical defenses (toxins) and of physical defenses in plants?

A

Chemical defenses: herbivory by insects and microbes

Physical defenses: herbivory by large herbivores (mammals, etc.)

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3
Q

How do the internal environments of simple stomachs differ from rumens?

A

Simple stomach: no microbes, lower water content, very low pH of 2

Rumen: many microbes, high water content, neutral to slightly acidic pH (6-7)

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4
Q

What are three factors that affect severity of poisonings in animals?

A

Ruminant vs. monogastric

Animal condition (sick, pregnant, lactating, etc.)

Rumen microbes/sudden diet change

And more…

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5
Q

List the direct and indirect agricultural impacts of toxicants. Clearly indicate which are direct and which are indirect.

A

Direct: death, abortion

Indirect: low weight animals, increased purchase of herbicide, loss of forage in invaded fields

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6
Q

In general, what is a “natural toxicant”?

A

Chemical produced by a living organism that can cause physical harm to another living organism

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7
Q

Define LD50. What does it stand for, what does it mean, and why is it important?

A

Lethal dose – 50; the dosage at which 50% of test subjects die; this is the level that can cause acute toxicity, below this dosage it is sublethal or chronic

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8
Q

What are the major components of a glycoside and which part groups toxins into classes?

A

Glycone (sugar), aglycone (non-sugar or steroidal part, R which usually classifies the molecule into a toxin group

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9
Q

What are the two ways can you tell Larkspur and Monkshood apart in the field? Be specific.

A

Larkspur have hollow stems which monkshood do not

Larkspur have a spur off the back of the flower, while monkshood flowers are hood-shaped

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10
Q

What are the two types of alkaloids present in larkspur? Which of the two is most toxic? Of greatest concern?

A

MDL is of more concern because they are present in higher concentrations, but MSAL alkaloids are inherently more toxic

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11
Q

Pacific (or Western) yew contains the chemical precursors to what life-saving drug and for what purpose is that drug used?

A

Taxol which is used to treat breast cancer

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12
Q

What are four native or crop species that accumulate nitrate?

A

Common sunflower, ragweed, sudan grass, alfalfa, sweet clovers

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13
Q

What is the difference between hemoglobin and methemoglobin?

A

Hemoglobin has Fe 2+; methemoglobin is oxidized and has Fe 3+

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14
Q

Label the nitrogen cycle by writing in the correct answer with the corresponding letter under the image.

A
  1. Nitrogen-fixing bacteria in root nodules of legumes
  2. Nitrogen-fixing bacteria in soil
  3. Nitrification (or nitrifying bacteria)
  4. Nitrifying bacteria
  5. Assimilation
  6. Ammonification
  7. Denitrification (or denitrifying bacteria)
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15
Q

What are the clinical signs of cardiac glycoside poisoning seen with GI tract, heart, and during postmortem exam?

A

GI Tract = hemorrhagic enteritis, abdominal pain/diarrhea

Heart = heart block, arrythmias, hypotension, hyperkalemia

Postmortem = myocarditis, cardiac lesions, cardiac glycosides detected in serum, urine, tissues, stomach contents

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16
Q

How does the ingestion of plant tissues containing high levels of non-toxic cyanogenic glycosides ultimately lead to sudden death by cyanide poisoning in ruminants? Feel free to use bullet points and/or drawings to explain the full mechanism

A
  1. Ingest forage with high levels of cyanogenic glycosides
  2. C.G.s stored in cell vacuoles are released when fresh leaves are chewed, torn, or experiencing frost/drought
  3. C.G.s undergo enzymatic hydrolysis after being exposed to plant/microbial enzyme B-glucosidase. The sugar is cleaved from the molecule resulting in a cyanohydrin
  4. Cyanohydrin spontaneously breaks down into a ketone/aldehyde and HCN
  5. Excess HCN is absorbed into the blood and binds with hemoglobin
  6. Hemoglobin then delivers the cyanide to the tissues
  7. CN binds non-competitively to cytochrome oxidase in the ETC
  8. ETC shuts down and cells become starved for oxygen and energy, eventually resulting in death
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17
Q

You have a hay crop that was heavily fertilized with nitrogen at the beginning of the season, but drought hit soon after. You suspect high nitrate concentration in the plants. What can you do to keep from poisoning your animals? Give at least three options.

A
  1. Get plant material and water tested
  2. Chop for silage
  3. Raise cutter bar 6 inches
  4. Acclimate animals to high-nitrate feed slowly
  5. Keep animals away from fertilizers
  6. Control weeds
  7. Feed to low risk animals
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18
Q

In general, what is a main treatment(s) for each of the following types of poisoning? (Specifics on dosing not necessary – note: “resting” is not considered a main treatment)

Oleander

Cyanide

Larkspur

Nitrate

Cicutoxin (water hemlock)

A
  1. Oleander: Atropine sulfate, gastric lavage, activated charcoal, rumenotomy
  2. Cyanide: sodium thiosulfate, sodium nitrite
  3. Larkspur: neostigmine
  4. Nitrate: IV methylene blue
  5. Cicutoxin (water hemlock): no antidote, sodium pentobarbital
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19
Q

Examine the graph below and answer the following questions:

  1. This graph describes seasonal changes in what species or group of species?
  2. Correctly label the axes** and **briefly explain what this graph means.
  3. Based on this graph, when is it considered “safe” to graze areas with this plant?
A
  • Tall Larkspur
  • At the beginning of the season, palatability is low, and toxicity is extremely high.As the plant grows, toxicity declines with just a slight increase at seed set.On the other hand, palatability increases.The most dangerous time to graze animals is the “toxic window”.At this stage, toxicity is still relatively high, and the plant is palatable enough for animals to want to eat it.This is the window when animal poisoning is most likely.
  • Sheep can graze before the toxic window. Cattle can as well if there is enough other forage available. All animals can safely graze after the toxic window though nutritional quality of the plants has decreased by then.
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20
Q

What plant was responsible for killing two priests at a dinner party in Dingwall, Scotland in 1856?

A

Aconite (Monkshood)

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21
Q

Curare produces the toxin known as d-tubocurarine, a powerful muscle relaxant. What did indigenous tribes in South America use this plant extract as?

A

Arrow Poison

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22
Q

Members of the Lewis and Clark Expedition may have been accidentally poisoned by eating the roots of which plant?

A

Death camas

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23
Q

According to the video on “undetectable poisons”, which poison used to be commonly used to commit murder? It was even a preferred method of H. H. Holmes, America’s first serial killer.

A

Arsenic

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24
Q

The ingestion of which plant shows up in the medical literature as a method of suicide, particularly among nursing-home patients?

A

Arsenic

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25
Q

Socrates famously committed suicide by consuming a drink made from what plant?

A

Poison Hemlock

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26
Q

What is a “Standard Operating Procedure” and why are SOPs used so often in large operations or organizations.

A

Step by step instructions for carrying out complex (usually) routine operations

  1. Increase efficiency
  2. Quality Output
  3. Uniformity of performance
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27
Q

Name two physical and two biological factors that can affect plant growth in general.

A

Physical: soil (pH, moisture, aeration, humus), or climate (light, wind, frost)

Biological: competition (inter- and intraspecific), management (fire, biological control,

grazing), disease

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28
Q

What drives the evolution of chemical defenses (toxins) and physical defenses in plants?

A

Chemical defenses: herbivory by insects and microbes

Physical defenses: herbivory by large herbivores (mammals, etc.)

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29
Q

Briefly discuss how metabolic processes are similar between plants and animals as well as how they differ? Why are these differences important?

A

Similarities: complex biochemical pathways, waste production, similar base needs (nutrients, water, temp., shelter

Difference: animals remove wastes through excretion while plants accumulate wastes in vacuoles

Importance: leads to the formation of secondary plant chemicals (metabolites)

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30
Q

What are the four coping methods that wildlife might employ to deal with “injurious” plants? Very briefly explain each

A
  1. Avoidance – animals avoid plants higher in toxins, taste and then avoid, fear of trying new things
  2. Dilution – combine with large amounts of other species that are not toxic to dilute the effect
  3. Degradation – chemicals are broken down within the GI tract by acidity or microorganisms
  4. Detoxification – occurs in the liver after toxins have been absorbed into the blood stream
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31
Q

How does the ingestion of plant tissues containing high levels of non-toxic cyanogenic glycosides ultimately lead to sudden death by cyanide poisoning in ruminants? Feel free to use bullet points and/or drawings to explain the full mechanism.

A
  1. Ingest forage with high levels of cyanogenic glycosides
  2. C.G.s stored in cell vacuoles are released when fresh leaves are chewed, torn, or experiencing frost/drought
  3. C.G.s undergo enzymatic hydrolysis after being exposed to plant/microbial enzyme B-glucosidase. The sugar is cleaved from the molecule resulting in a cyanohydrin
  4. Cyanohydrin spontaneously breaks down into a ketone/aldehyde and HCN
  5. Excess HCN is absorbed into the blood and binds with hemoglobin
  6. Hemoglobin then delivers the cyanide to the tissues
  7. CN binds non-competitively to cytochrome oxidase in the ETC
  8. ETC shuts down and cells become starved for oxygen and energy, eventually resulting in death
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32
Q

Matching: Please match the following toxins with the correct associated plant/genera. Put the correct letter in the space provided next to each toxin.

  • __ Cyclopamine A. Spring parsley
  • __ Anagyrine B. Penicillium
  • ___ Furanocoumarins C. Fiddleneck
  • ___ Coniine D. Western false hellebore
  • ___ Protoanemonins E. Ponderosa pine
  • ___ Swainsonine F. Black henbane
  • ___ Pyrrolizidine alkaloids G. Locoweed spp.
  • ___ Isocupressic acid H. Lupine spp.
  • ____ Aflatoxin I. Poison hemlock
  • ___ Scopolamine J. Baneberry
A
  1. __D__ Cyclopamine A. Spring parsley
  2. _H__ Anagyrine B. Penicillium
  3. __A__ Furanocoumarins C. Fiddleneck
  4. __I__ Coniine D. Western false hellebore
  5. __J__ Protoanemonins E. Ponderosa pine
  6. __G__ Swainsonine F. Black henbane
  7. __C__ Pyrrolizidine alkaloids G. Locoweed spp.
  8. __E__ Isocupressic acid H. Lupine spp.
  9. __B__ Aflatoxin I. Poison hemlock
  10. __F__ Scopolamine J. Baneberry
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33
Q

Why do some animal and plant species become problematic when introduced to new locations/continents?

A

They are freed from their natural predators and diseases, are better at utilizing resources, reproduce more quickly, etc.These qualities allow newly introduced species to outcompete native plants, establish populations, and spread quickly.

34
Q

Briefly describe what Jonathan Foley considers to be the other inconvenient truth.

A

The inconvenient truth is that we have to feed nearly 10 billion people by 2050 but need to dramatically reduce our environmental impacts.

35
Q

According to Marla Spivak, bees dying reflects what two issues?

A

Flowerless landscape

Dysfunctional food system

36
Q

What is a weed? Why do we care about weeds? What are the downsides to controlling for weeds?

A

Any plant that we deem valueless. We care because these plants impair food production, aren’t horticulturally important, cause damage to natural systems, etc. Controlling for weeds can kill non-target, native plants, affect insect populations and then everything that depends on those insects, etc.

37
Q

Puncture vine contains saponins, the ingestion of which can cause what liver disorder?

A

Biliary occlusive photosensitization

38
Q

How are protoanemonins created following the ingestion of certain plants in the Ranunculaceae family?

A

Ranunculin is exposed to plant enzymes during ingestion and converted to protoanemonins

39
Q

Diarrhea results from excessive consumption of which two plants?

A

Leafy spurge and Western yarrow

40
Q

Which species is least affected by pyrrolizidine alkaloids in Senecio spp. and how much more of these plants can this species tolerate?

A

Sheep – can consume 20x more

41
Q

Define biocontrol

A

The use of insects, microbes, and pathogens specific to a weed species to control and eventually eliminate invasive populations of that weed

42
Q

Why should a cow that has aborted her calf be watched closely? What could happen if you don’t?

A

The cow could have retained part or all the placenta which can lead to a secondary bacterial infection.If left untreated, the infection could cause a permanent loss of fertility

43
Q

What conditions favor blue green algal blooms in stock ponds? Define any technical terms.

A

Eutrophication – excessive loading of nitrogen and phosphorus in aquatic systems through agricultural run off

High temps

Stagnant water

44
Q

What three syndromes are associated with Lupine toxicosis?

A

Crooked calf disease

Acute fatal neurological disease in sheep

Lupinosis

45
Q

Generally, what is a teratogen?

A

Any substance (chemical, radiation, plant toxin, etc.) that can cause birth defects

46
Q

What conditions must be met for a plant compound to actually be teratogenic?

A

Right species

Right gestational period

High enough dose/concentration

Cross placenta easily

47
Q

How is cyclopia caused in sheep fetuses? Be a detailed as possible.

A

Ingestion of Western false hellebore with high concentrations of cyclopamine on the 14th day of gestation

48
Q

Which species cause(s) crooked calf disease? What are the symptoms?

A

Lupine and Poison hemlock

Symptoms: limb deformity, vertebral column malformation, cleft palate

49
Q

In animals with severe liver damage, why does the ingestion of chlorophyll lead to photosensitization of non-pigment skin?

A

Chlorophyll gets broken down into phylloerythrin which can’t be filtered out by the damaged liver. So, it builds up in the blood, reacts with UV light when it reaches the skin, and those reaction products then cause cellular damage.

50
Q

What are three ways for determining if your animal is suffering from primary or secondary photosensitization?

A

Remove from sun and food source

  • If recover happens, it is primary photosensitization
  • If no recover, biopsy liver

Look for signs of liver damage such as jaundice

Determine the plant species ingested

51
Q

Explain the mechanism of action of pyrrolizidine alkaloids and state what type of liver damage is seen at low doses and high doses.

A
  • PAs ingested
  • Liver bioactivates PAs in pyrroles
  • Pyrroles inhibits mitosis and replication of hepatocytes
  • Causes death of hepatocyte

High doses: hepatocellular necrosis

Low doses: less severe necrosis, characteristic pathological changes of fibrosis develop, similar changes in kidneys, pulmonary hypertension, and right heart failure

52
Q

Explain the mechanism of action for lectin (ex. Ricin) poisoning.

A
  • Binds to receptor sites on cell membrane leading to endocytosis of lectin
  • Passes through chain of organelles to reach the endoplasmic reticulum
  • Depurinates ribosomes (inactivation): 1 molecule can do this at a rate of 1500 ribosomes per minute
  • Cell death
53
Q

Explain the mechanism of action for poisoning by plants in the Nightshade family.

A
  • Blocks the action of cholinesterase
  • Accumulation of acetylcholine in synaptic cleft
  • Inhibits parasympathetic nervous system
54
Q

TOXIN

PLANT NAME

  1. Solanine
  2. Protoanemonins
  3. Ricin
  4. Hypericin
  5. Pyrrolizidine alkaloids
  6. Saponins
A

TOXIN

PLANT NAME

  1. Solanine

Bitter nightshade (Solanum dulcamara)

  1. Protoanemonins

Blister/bur buttercup; baneberry

  1. Ricin

Castor bean (Ricinus communis)

  1. Hypericin

St. John’s wort (Hypericum perforatum)

  1. Pyrrolizidine alkaloids

Fiddleneck/Groundsel/Hound’s tongue

  1. Saponins

Puncture vine or Lantana

55
Q

What type/group of toxin is a lectin? Where are lectins most concentrated in the plant?

A

Glycoprotein; concentrated in seeds

56
Q

How are protoanemonins created following the ingestion of certain plants in the Ranunculaceae family?

A

plant

Ranunculin ————> protoanemonins

enzymes

57
Q

Which treatment is most commonly prescribed for livestock GI tract issues resulting from plant ingestion? (Hint: You should probably have this on hand at all times)?

A

Activated charcoal

58
Q

What is the difference between primary and secondary photosensitization

A

Primary photosensitization – reversible because just a severe dermatitis caused by the interaction of plant pigments in the blood and UV light

Secondary photosensitization – while identical in mechanism, this version is actually a symptom of liver damage (~80%) and more common

59
Q

What is phylloerythrin?

A

Metabolic by-product of the breakdown of chlorophyll

60
Q

Pyrrolizidine alkaloids are not toxic initially. What happens in the animal to make them toxic? Be sure to name the toxic compound.

A

PAs are bioactivated by the liver into toxic pyrroles

61
Q

Explain the mechanism of action in lectin poisoning.

A
  1. Binds to receptor sites and triggers endocytosis
  2. Passes through chain of organelles to endoplasmic reticulum
  3. Depurinates ribosomes – 1 molecule can do this to 1500 ribosomes per minute
  4. Cell death
62
Q
  1. Explain the mechanism of action in nightshade poisoning.
A
  1. Blocks the action of cholinesterase
  2. Accumulation of acetylcholine
  3. Inhibits parasympathetic nervous system
63
Q

Due to the suggestible state induced in a user, “street-grade” scopolamine has earned what nickname?

A

Zombie drug

64
Q

In Victorian England, what did women use extract of Belladonna (derived from Deadly nightshade) for, believing it increased their attractiveness?

A

Dilate pupils

65
Q

What was important about the case study discussed in class? How did this case change veterinary diagnostics in Europe?

A
  • First locoism case in Europe
  • Now screen for this especially when ataxia and hypermetria, etc. are present
66
Q

The 20-year-old male horse initially presented with what two symptoms?

A

Hypermetria

Trembling & fright reactions

67
Q

Once admitted to the vet clinic, how was the horse medically treated? Be specific

A

Diazepam to calm

Dopamine to increase kidney function and urine output

Isotonic fluids with potassium

68
Q

Ultimately, what was determined to be the source of the swainsonine that poisoned the horse?

A

Unknown

Presence of Astragalus/Oxytropis not confirmed in feed

Unable to do mycological exam on hay

69
Q

According to your research, what is estimated economic impact each year due to loss of livestock from locoism?

A

$300 million per year

70
Q

What are two ways of preventing ingestion of locoweed by livestock?

A
  • Keep animals away from plants when they are most toxic & palatable
  • Conditioned avoidance using lithium bolus to make animal sick when exposed to plant
  • Supplement protein to prevent ingestion of locoweed
71
Q

Which plant genera are associated with locoism in North America?

A

Astragalus & Oxytropis

72
Q

Historically, which two disorders are associated with selenium toxicity? Which one is no longer associated with selenium toxicity and why?

A

Alkali Disease

Blind staggers – no long; actually caused by sulfate toxicity

73
Q

What conditions can affect selenium uptake by plants?

A

Chemical form, soil pH, temperature, moisture, species & stage of growth

74
Q

What is meant by “obligate” selenium accumulator vs. “secondary” selenium accumulator? Give an example of each.

A
  • Obligate = Se required for growth & can accumulate Se in tissues up to 10x as much as what is present in soil (as high as 10,000 ppm)
    • Examples: Prince’s plume, two-grooved milkvetch, woody aster, rayless goldenweed
  • Secondary = Se not required for growth but can still accumulate Se in plant tissues
    • Examples: white prairie aster, broom snakeweed, gumweed, saltbush, indian paintbrush, beardtongue
75
Q

If you have a horse that you suspect has locoweed poisoning, why is it also important to consider sagebrush poisoning? How can you tell the difference?

A

Sagebrush poisoning symptoms are nearly identical & usually only occur in horses

With sagebrush, will recover in 1-2 months once ingestion is stopped & animal is provided with good food sources

76
Q

How do symptoms of chronic selenium poisoning differ among horses, cattle, and sheep? In general, what are the major symptoms for acute poisoning?

A

Chronic Poisoning? -

  • Horses: abnormal hoof wall growth w/ uneven growth, circular ridges, and cracking
  • Cattle: defective growth but don’t lose hoof wall
  • Sheep: marked reduction in fertility but no keratin-related lesions

Acute poisoning?

  • Sudden death from cardiac insufficiency and pulmonary edema
77
Q

Step by step, how does swainsonine cause locoism?

A
  1. Inhibits cellular enzymes
  2. Intracellular waste products build up in lysosomes
  3. Increased # and size of lysosomes
  4. Decreased internal space and disruption of cellular function
78
Q

How do toxic levels of selenium affect keratinocytes? Why does excess selenium cause hair to break (classical symptom)?

A
  • complex effects on cellular function that alter cell division and growth, specifically causing degeneration and necrosis of cells that produce keratin
  • Selenium replaces sulfur in the structure of keratin, creating a weaker molecule
79
Q

How and why do sloths risk their lives once a month?

A

They descend from the forest canopy to the forest floor to defecate

80
Q

In the plant episode of The Life of Mammals, grooves found in a cave wall in east Africa were originally attributed to ancient Egyptians mining for gold and precious stones. But, elephants actually created the marks in the cave wall. Why did the elephants do this?

A

To supplement their diets with the salt crusted onto the cave walls