Test 4: 62: plants Flashcards

1
Q

cicuta douglasii look like

A

white flowers in umbel
tuberous root
hollow stem

water hemlock- causes acut death

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2
Q

clinical signs of Cicuta douglasii or C maculata exposure

A

water hemlock

acute death
cicutoxin- all parts of plant- neurotoxin that causes muscle tremors and convulsions

  • Hypersalivation, vigorous chewing and teeth grinding, urination, defecation
  • Progressing to ataxia, incoordination, seizures, and lateral recumbency → respiratory paralysis and asphyxia in 2-3 hrs

white flowers, tuberous root, hollow stem

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3
Q

if animals do not die right away form Cicuta gouglasii or C. maculata they can develop

A

myocardial degeneration and skeletal muscle degneration

water hemlock- tuberous, hollow stem, white flowers

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4
Q

treatment of cicuta douglasii and C. maculata ingestion

A

no antidote

GI decontamination if early
emesis
rumenotomy
vinegar?
pentobarbital to ↓ seizures

water hemlock: white flowers, tuberous root, hollow stem

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5
Q
A

conium maculatum
posion hemlock

marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell

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6
Q

conium maculatum look like

A

conium maculatum
posion hemlock

marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell

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7
Q

what kind of toxin for conium maculatum

A

piperidine alkaloid: coniine and G-coniceine

block spinal cord reflexes: first nicotinic muscle activation then paralysis

acute death

conium maculatum
posion hemlock

marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell

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8
Q

clinical signs of conium maculatum ingestion

A

salivation, abdominal pain,
muscle tremors and incoordination Followed by dyspnea, dilated pupils, weak pulse, urination, and defecation

Temporary blindness from prolapsed nictitating membrane

muscle activation → paralysis and respiratory failure and coma: death in 2-3 hrs

small amounts can be teratogenic if cows eat day 40-70 of gestation

conium maculatum
posion hemlock

marshy, moist ground
carrot like root with purple spots
fernlike leaves
white flowers
mouse urine smell

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9
Q
A

aconitum (monkshood)

sudden death

Restlessness, hypersalivation, muscle weakness, hypotension, dyspnea, and collapse
◦ Ruminants may bloat after becoming laterally recumbent

not required plant

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10
Q
A

delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur

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11
Q

what does delphinium look like

A

delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur

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12
Q

toxin of delphinium

A

diterpenoid alkaloids
MLA

The alkaloids reversibly bind to and
competitively block nicotinic acetylcholine receptors at the neuromuscular junction → muscle weakness and paralysis

similar to nicotine and snake bungarotoxin

delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur

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13
Q

what is toxic window of delphinium

A

cows really like to eat plant when it is growing or after rainstorm when it is most toxic

try not to let cattle graze duing this time

delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur

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14
Q

clinical signs of delphinium

A

sudden death

Initial signs in cattle include increased excitability, muscle weakness with stiffness, staggering, and a base-wide stance

NM blockage prevents burbing → bloat → pneumonia

delphinium- larkspur
leaves at base
hollow stems
blue, purple, red flowers: 5 sepals and 4 petals
upper sepal are elongated and form spur

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15
Q

Hydrogen cyanide (HCN) rapidly inactivates — causing —

A

cellular respiration causing acute death

binds to cytochrome oxidase and inhibits enzymes needed for cellular respiration

cherry red venous blood

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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16
Q

what needs to happen to cyanogenic glycosides to become toxic

A

damage to plant cells caused by chewing, crushing, drought, wilting, or freezing

rymen microorganism will turn cyanogenic glycosides into HCN

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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17
Q

clinical signs of cyanogenic glycoside

A

Sudden death

Early signs include rapid labored breathing, frothing at the mouth, dilated pupils, ataxia, muscle tremors, convulsions, tachycardia +/- arrhythmias

Ruminants regurgitate rumen contents when they become recumbent and bloat

Mucous membranes: bright red to cyanotic in the terminal stages as tissues become oxygen depleted

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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18
Q

bitter almonds odor is

A

cyanogenic glycosides

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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19
Q

treatment for cyanogenic glycosides

A

sodium nitrite: converts some hemoglobin to methemoglobin: cyanide will bind to met
sodium thiosulfate: binds to cyanide and form nontoxic product

can give ruminants sodium thiosulfate and vinegar

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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20
Q

how to reduce cyanogenic glycoside ingestion

A

dont let animals graze after plants are growing, drought or frost
* test for cyanide
* curing will kill cyanide
* purchase low cyanide plants (some sorghum plants)

prunus- chockcherry, pin cherry
sorghum - johnson grass, indian grass

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21
Q

how do high dose cardiac glycosides work

A

Cardiac glycosides inhibit cellular membrane sodium-potassium pumps to deplete intracellular
potassium and increase serum potassium → decreased conductivity → arrhythmias and cardiac block, death

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22
Q

low dose cardiac glycosides

A

Low doses can have the therapeutic effect of increasing
contractility, decreasing heart rate, and increasing cardiac output

high dose: severe arrhythmias and conduction disturbances leading to death

CG inhibit Na/K pump → ↑ potassium = decreased electrical conductivity and arrythmias

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23
Q

clinical signs of cardiac glycosides

A

acute death from arrythmias

  • Early signs include tachypnea, cold extremities, and rapid weak irregular pulses
  • Symptoms rarely persist more than 24 hours before death occurs +/- terminal convulsions

Cattle receiving ionophores are more susceptible to cardiac glycosides

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24
Q

Cattle receiving — are more susceptible to cardiac glycosides

A

ionophores

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25
how to treat cardiac glycosides
GI decontamination: gastric lavage or vomiting, activated charcoal treat arrhythmias check potassium levels digoxin
26
asclepias speciosa milkweed cardiac glycoside ## Footnote milkweed:; asclepias thin or thick leaves umbels of white or red flowers seed pod has silky hairs some have milky sap or latex
27
what does asclepias look like
milkweed:; asclepias thin or thick leaves umbels of white or red flowers seed pod has silky hairs some have milky sap or latex cardiac glycoside
28
asclepias cause ---
**cardiac glycoside** → arrythmia and death cardenolides can also effect respiratory, GI, CNS → dyspnea, colic, diarrhea, muscle tremors, seizures, and head pressing ## Footnote milkweed: asclepias thin or thick leaves umbels of white or red flowers seed pod has silky hairs some have milky sap or latex
29
monarch butterflies retain --- from --- plants
cardenolides: cardiac glycoside Birds that eat them experience intense emetic effects and avoid eating monarchs in the future asclepias (milkweed) ## Footnote milkweed: asclepias thin or thick leaves umbels of white or red flowers seed pod has silky hairs some have milky sap or latex
30
clinical signs of asclepias
acute death **cardiac glycoside** → arrythmia and death cardenolides can also effect respiratory, GI, CNS → dyspnea, colic, diarrhea, muscle tremors, seizures, and head pressing, inability to stand, dilated pupils recumbent animals: tetany and chewing movements ## Footnote milkweed: asclepias thin or thick leaves umbels of white or red flowers seed pod has silky hairs some have milky sap or latex
31
convallaria lily of the valley seeds have high concentrations of cardenolide **cardiac glycosides** skin of fruit and flowers- abdominal pain and diarrhea ## Footnote not requires
32
digitalis floxglove cardiac glycosides are digoxin, digitoxin, and digitonin, found in all parts of the plant ## Footnote NOT REQUIRED
33
nerium oleander evergreen white, pink or red flowers with 5 or more petals cardiac glycoside
34
what does nerium oleander look like
nerium oleander evergreen white, pink or red flowers with 5 or more petals 25 ft tall cardiac glycoside
35
zigadenus death camas **cardiotoxic**- steroidal alkaloids with zygacine and zygadenine **↓BP by dilating arteriols and constricting veins and ↓HR** **sheep**- salivation, nausea, vomiting, muscular weakness, and staggering, convulsions, coma and death ## Footnote not required
36
taxus: Yew shrub red to yellow fruits with single seed (fruit not toxic) all other parts are toxic cardiotoxic: taxine→ arrhythmias milk and meat withhold times
37
Taxus toxicity
cardiogenic taxine: inhibits Na/Ca exhange in myocardiac cells →arrhythmias milk from poisoned animals should not be used for at least 48 hours and animals be withheld from slaughter for 35 days ## Footnote taxus: Yew shrub red to yellow fruits with single seed (fruit not toxic) all other parts are toxic cardiotoxic: taxine→ arrhythmias careful of milk and meat
38
clinical signs of taxus ingestion
cardiogenic → Na/Ca → arrhythmias sudden muscle tremors, incoordination, nervousness, dyspnea, bradycardia, vomiting, diarrhea, convulsions, and death Death may occur several days after ingestion, however **sudden death** may sometimes be the only observed sign ## Footnote taxus: Yew shrub red to yellow fruits with single seed (fruit not toxic) all other parts are toxic cardiotoxic: taxine→ arrhythmias milk and meat withhold times
39
persea- avocado cardiogenic- myocardium and tissue of lactating mammary gland * horses: edematous swelling of the lips, mouth, eyelids, head, and neck, leading to upper respiratory distress * Some horses colic * pulmonary edema due to cardiomyopathy and heart failure
40
senecio toxicity
pyrrolizidine alkaloid liver disease → secondary photosensitization
41
senecio longilobus scaggily pyrrolizidine alkaloid liver disease → secondary photosensitization
42
pyrrolizidine alkaloids are found in --- will build up in the blood and when exposed to UV light will cause
senecio longilobus liver damage →phylloerythrin accumulates → secondary photosensitization → Exposure to UV light causes the phylloerythrin to fluoresce and cause oxidative injury to blood vessels and surrounding skin tissues
43
how does pyrrolizidine alkaloids work
PAs are converted to toxic pyrroles affect the endoplasmic reticulum of liver cells, inhibiting mitosis and the replication of hepatocytes ## Footnote senecio longilobus pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization
44
clinical signs of pyrrolizidine alkaloids
senecio longilobus pyrrolizidine alkaloids →pyrroles →liver disease →**photosensitization** excessive tearing, and swelling, redness, and increased sensitivity of nonpigmented skin Affected skin rapidly becomes reddened, painful, and raised, with serum often oozing through to form crusts in the hair After 2-3 weeks **hair and skin slough** off leaving ulcerated areas prone to secondary bacterial infections Lameness may be seen in horses when the skin over joints and the coronet is affected **Signs of liver disease** include jaundice, ascites, diarrhea, tenesmus, and rectal prolapse **Hepatic encephalopathy** may result in abnormal behaviors such as yawning, aimless wandering, head pressing, and incessant licking **In severe cases**, acute liver failure and death may precede photosensitization
45
pathologic changes of pyrrolizidine alkaloids
◦ Megalocytosis ◦ Bile duct hyperplasia ◦ Fibrosis ## Footnote senecio longilobus pyrrolizidine alkaloids →pyrroles →liver disease →**photosensitization**
46
path with Megalocytosis, Bile duct hyperplasia and Fibrosis is suggestive of
pyrrolizidine alkaloids ## Footnote senecio longilobus pyrrolizidine alkaloids →pyrroles →liver disease →**photosensitization**
47
astragalus and oxytropis spp locoweed neurotoxic
48
astragalus and oxytropis toxicity
neurotoxic **Swainsonine** inhibits lysosomal enzymes that aid in saccharide metabolism α-mannosidase inhibition causes cells(brain and organs) to accumulate complex sugars or oligosaccharides **passed through milk** some animals (horses, cattle and sheep) really like the taste
49
clinical signs of astragalus and ocytropis exposure
locoweed- neuro toxic swainsonine → oligosacchardie accumulation can cause repro issues- abortions, testicular atrophy (rams) weight loss and ill thrift horses: * Depression, circling, incoordination, staggering gait, unpredictable behavior * Especially when animal is stressed or excited * Can suddenly rear and fall over backward, making them unsafe to ride Cattle: * aggressive and difficult to handle
50
how to diagnose atragalus and oxytropis
locoweed- neuro toxic swainsonine → oligosacchardie accumulation cytoplasmic vacuolation swainsonine in serum ↓ serum α-mannosidase activity
51
how to prevent atragalus and oxytropis ingestion in cattle
food aversion feed locoweed then dose with lithium chloride
52
eupatorium rugosum white snakeroot
53
toxin in eupatorium rugosum
neurotoxin tremetone- requires microsomal activation to become toxic causes skeletal and mycocardial degeneration secreted in milk- milk sickness, trembles pasteurization does NOT detoxify ## Footnote white snakeroot eupatorium
54
clinical signs of eupatorium rugosum ingestion
neurotoxin- tremetone Initial signs include listlessness, depression, lethargy, and reluctance to move * Cattle will develop muscle tremors, signs of **colic**, constipation, bloody feces, and an acetone odor to the breath * **Tremoring** animals show stiffness and eventually become recumbent * Horses may signs of choking due to paralysis of pharyngeal muscles * Nursing animals may have milk run out the nostrils * Dark urine may be observed due to **myoglobinuria**
55
treatment for eupatorium rugosum
no specific antidote supportive care horses have difficulty swallow- fed by NG tube discard milk
56
horse chestnut aesculus * neurotoxin- aesculin and fraxin → aglycones in rumen which produce neuro signs- twitching, weakness, **hopping gait** * monogastrics- vomit and gastroenteritis * dorsal- medial stabismus * severe toxicity- hyperglycemia, glucosuria, and proteinuria ## Footnote NOT required
57
nicotiana tabacum ANS- mimic AcH **Small dose**: excitement, tachycardia, salivation, vomiting, colic, and diarrhea. Ruminants may bloat **high dose**: neuromuscular blockade with weakness, staggering, collapse, and rapid, weak, irregular heart rates **Very large ingestions** rapidly cause respiratory paralysis, blindness, prostration, coma, and death ## Footnote **NOT required**
58
bleeding hearts Dicentra neuro toxin Isoquinoline alkaloids Cattle may exhibit muscle tremors, running back and forth, and incoordination as **“spring staggers”** * **Projectile vomiting**, convulsions, and lateral recumbency with the head extended back and legs in rigid extension may develop depending on the amount of plant consumed ## Footnote **NOT required**
59
yellow star thistle centaurea solstitialis neurotoxin- destroys the dopaminergic nigrostriatal pathway that controls prehension and chewing of food → ↑ risk of aspiration pneumonia Signs do not occur until large quantities have been eaten for 30-60 days wooden expression, can't hold food in mouth, frothy saliva and continual chewing bilateral liquefactive necrosis in the globus pallidus and substantia nigra no treatment- euthanize ## Footnote NOT REQUIRED
60
acer red maple affect blood and bone marrow **horses**: acute **hemolytic anemia-** weakness, tachypnea, tachycardia, cyanosis, icterus, and **red-brown urine**, methemoglobinemia, and liver lipidosis and necrosis
61
diagnostics of acer ingestion
red maple * markedly reduced hematocrit, methemoglobinemia, Heinz bodies, and depletion of erythrocyte glutathione * Serum AST, SDH, protein, and bilirubin are usually elevated **horses**: acute **hemolytic anemia-** weakness, tachypnea, tachycardia, cyanosis, icterus, and **red-brown urine**, methemoglobinemia, and liver lipidosis and necrosis
62
treatment for acer rubrum
red maple → hemolytic anemia in horses guarded prognosis **Blood transfusions** may be needed to address intravascular hemolysis and coagulopathies IV fluids methylene blue?
63
allium
wild onions, garlic, leeks and chives bulbs, hollow narrow basal leaves, 6 part flower attack blood and bone marrow
64
allium toxicity
blood and BM toxic * N-propyl disulfide affects glucose-6- phosphate dehydrogenase in RBCs, interfering with the hexose monophosphate pathway * Insufficient phosphate dehydrogenase or glutathione fails to protect the RBCs from oxidative injury * Oxidized hemoglobin precipitates to form **Heinz bodies** * Affected RBCs are removed from the circulation and **anemia** results ## Footnote wild onions, garlic, leeks and chives
65
clinical signs of allium ingestion
* **Dark red-brown urine** as hemoglobinuria is usually the first noticeable sign of poisoning * Affected animals have **pale mucous membranes** and fast weak pulses, and may be observed staggering and collapsing * Breath, feces, urine, and milk of affected animals may **smell like onions** * **Heinz bodies** may be observed in cattle even if the amount of onion consumed is not enough to induce **anemia and hemoglobinuria** ## Footnote wild onions, garlic, leeks, and chives → anemia and heinz bodies
66
pteridium aquilinum bracken fern blood and BM toxic Thiaminase splits thiamin (vitamin B1) into its two inactive components ↓ thiamin = white brain matter necrosis and CNS depression Ptaquiloside is carcinogenic and depresses bone marrow →severe blood loss, anemia, thrombocytopenia, and leukopenia death from anemai or local tumor invasion around the bladder horse: muscle tremors, uncoordinated gait and paralysis, anorexia → **treat by giving thiamin** ## Footnote **not required**
67
dieffenbachia bowmannii dumbcane toxic to GI tract **calcium oxalate crystals**- When plant cells are broken open or crushed, needlelike calcium oxalate raphides are released, penetrating surrounding soft tissues ## Footnote Calcium oxalate: philodendron and dieffenbachia
68
dieffenbachia bowmannii toxicity
dumbcane GI toxic **calcium oxalate crystals**- plant damaged and releases needlelike calcium oxalate raphides that penetrating surrounding soft tissues rapidly occurring **oral pain and swelling of the lips and tongue**
69
kalmia- laurel grayanotoxin- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract ## Footnote rhododendron, kalmia, pieris all grayanotoxins
70
pieris - mountain fetter bush **grayanotoxin**- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract ## Footnote rhododendron, kalmia, pieris all grayanotoxins
71
rhododendron **grayanotoxin**- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract ## Footnote rhododendron (azalea), kalmia, pieris all grayanotoxins
72
rhododendron - azalea **grayanotoxin**- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract ## Footnote rhododendron (azalea), kalmia, pieris all grayanotoxins
73
clinical signs of grayanotoxin exposure
**grayanotoxin**- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract * Initial GI signs include anorexia, hypersalivation, vomiting, colic, and frequent defecation * Regurgitated rumen contents may cause aspiration pneumonia * Severely affected animals develop muscle weakness, bradycardia, cardiac arrhythmias, paralysis, and coma before death ## Footnote rhododendron (azalea), kalmia, pieris all grayanotoxins
74
how to treat grayanotoxin exposure
**grayanotoxin**- * Water-soluble diterpenoids bind cell membranes, affecting sodium channels and **causing prolonged depolarization of cells** * Primary effects are on the heart, nervous system, and GI tract **atropine for ↓HR** **early decontamination** ## Footnote rhododendron (azalea), kalmia, pieris all grayanotoxins
75
Philodendron toxic to GI tract **calcium oxalate crystals**- When plant cells are broken open or crushed, needlelike calcium oxalate raphides are released, penetrating surrounding soft tissues ## Footnote Calcium oxalate crystals: dieffenbachia bowmannii (dumbcane) and philodendron arisema- jack in the pulpiy spathephyllum- peace lily zantedeshia aethiopica- calla lily
76
which plants produce calcium oxalate crystals when damaged
Calcium oxalate crystals: **dieffenbachia bowmannii** (dumbcane) and **philodendron** arisema- jack in the pulpiy spathephyllum- peace lily zantedeshia aethiopica- calla lily
77
solanum nigrum black nightshade **tropane alkaloids**- competitively inhibit acetylcholine at postganglionic parasympathetic neuroeffector sites This results in * Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea * Dilated pupils * Tachycardia ## Footnote potato is a type of nightshade!
78
solanum dulcamera bittersweet nightshade **tropane alkaloids**- competitively inhibit acetylcholine at postganglionic parasympathetic neuroeffector sites This results in * Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea * Dilated pupils * Tachycardia
79
solanum tuberosum potato **tropane alkaloids**- competitively inhibit acetylcholine at postganglionic parasympathetic neuroeffector sites This results in * Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea * Dilated pupils * Tachycardia
80
solanum toxicity
night shades- potatoes ?! **tropane alkaloids**- competitively inhibit acetylcholine at postganglionic parasympathetic neuroeffector sites This results in * Decreased salivation and intestinal motility → colic, constipation or hemorrhagic diarrhea * Dilated pupils * Tachycardia
81
podophyllum peltatum mayapple ## Footnote not required
82
phytolacca americana pokeweed oral irritation, hypersalivation, vomiting, colic, bloody diarrhea, depression, prostration, and death (rare) ## Footnote not required
83
juglans nigra black walnut toxic to muscles →vasoconstriction of blood vessels in the presence of catecholamines and corticosteroids laminitis in horses ◦ Depression, edema of the lower legs, lameness, colic, and respiratory distress walnuts can get moldy and get tremorgenic mycotoxin penitrem A
84
juglans nigra toxicity
black walnut → muscle toxic walnuts can get **moldy** → tremorgenic mycotoxin penitrem A Wood shavings used as bedding causes **laminitis in horses** ◦ Depression, edema of the lower legs, lameness, colic, and respiratory distress vasoconstriction of blood vessels in the presence of catecholamines and corticosteroids
85
beteroa incana hoary alyssum muscle toxic horse- laminitis and limb edema abortion ## Footnote **not required**
86
hypericum perforatum st johns wort skin and integument toxic ## Footnote not required
87
vicia villosa hairy vetch skin and integument toxic ## Footnote not required
88
--- plant makes oxalate poisoning that attacks UT
amaranthus red rooted pigweed
89
amaranthus toxicity
attack urinary tract oxalate poisoning oxalate crystals rapidly **combine with serum calcium** and magnesium * **Sudden hypocalcemia** in the acute phase of poisoning impairs normal cell membrane function * Animals develop **muscle tremors** and weakness, collapse, and eventually die * Oxalates also **interfere with cellular energy metabolism** * In chronic poisoning, **death results from kidney failure due to oxalate nephrosis**
90
Perirenal edema is a characteristic lesion in pigs and cattle consuming ---
Amaranthus ## Footnote oxalate poisoning →urinary system binds to calcium and magnesium → impairs cell membrane function and cellular metabolism → kidney failure from oxalate nephrosis and death
91
oxalate poisoning treatment
amaranthus binds to calcium giving calcium does not help oral limewater Ca(OH)2 can prevent further absorption high levels of dietary calcium in a salt mix or pelleted alfala bind oxalate in the rumen
92
lilium kidney toxic in cats- * Vomiting, anorexia, and depression can first develop within 2 hours of exposure * Anorexia and depression continue as BUN, creatinine, potassium, and phosphorus rise 24-72 hours after exposure * Creatinine is often disproportionately higher than BUN
93
quercus oak effect urinary system **Gallotannins** are hydrolyzed in the rumen to smaller compounds that react with cell proteins, denaturing them and causing **cell death** ## Footnote not required
94
symptoms of quercus ingestion
oak Animals stop eating, become depressed, and develop intestinal stasis * PU/PD * Hard dark feces may later turn into **black tarry diarrhea** * Teething grinding and hunched back may be an indication of **abdominal pain** * Mucoid **hemorrhagic gastroenteritis** * Hemorrhages on various organs * Fluid in peritoneal and pleural spaces * **Pale, swollen kidneys covered with small hemorrhages** * **Renal tubular necrosis and liver necrosis** are characteristic
95
treatment for quercus ingestion
oak attack renal system fresh food and water **Oral calcium hydroxide** can help neutralize residual tannic acid in the rumen IV fluids
96
lupinus repro toxic quinolizidine( **Anagyrine**) and piperidine alkaloids in all plant parts Lupinosis is a severe liver, kidney, and muscle disease associated with a phomopsin-producing fungus **crooked calf disease**
97
lupinus toxicity
repro toxic quinolizidine( **Anagyrine**) and piperidine alkaloids in all plant parts crooked calf disease- * front leg Limb deformities – arthrogryposis * Vertebral column malformation – scoliosis, kyphosis, torticollis * Cleft palate
98
pinus ponderosa repro toxic **Isocupressic acid** causes premature parturition or abortion in cattle
99
toxicity of pinus ponderosa
repro toxic **Isocupressic acid** causes premature parturition or abortion in cattle * Marked decrease in uterine blood flow due to vasoconstriction * Progesterone levels progressively decline due to necrosis of the corpus luteum * edematous swelling of the vulva and udder and a mucoid vaginal discharge before premature parturition or abortion → difficult delivery * cow produce little to no colostrum
100
veratrum californicum western false hellebore moutain meadows > 8500 ft repro toxic
101
clinical signs of veratrum californicum ingestion
western false hellebore repro toxic **cyclopia** shortened legs and tracheal agenesis ## Footnote moutain meadows
102
robinia toxicity
black locust lectins in beans **affect GI tract** inhibit cellular protein synthesis in ribosomes * Anorexia and severe hemorrhagic diarrhea develop within several days of consuming a toxic dose * Progresses to dehydration and hypovolemic shock * Horses may develop dilated pupils and cardiac arrhythmias * Serum chemistry results reflect fluid and electrolyte loss and organ dysfunction
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clinical signs of robinia ingestion
black locust lectins in beans **affect GI tract** inhibit cellular protein synthesis in ribosomes * Anorexia and severe hemorrhagic diarrhea develop within several days of consuming a toxic dose * Progresses to dehydration and hypovolemic shock * Horses may develop dilated pupils and cardiac arrhythmias * Serum chemistry results reflect fluid and electrolyte loss and organ dysfunction