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23 spring: pharm > Test 4: 62: plants > Flashcards

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
Q

how to treat cardiac glycosides

A

GI decontamination: gastric lavage or vomiting, activated charcoal

treat arrhythmias

check potassium levels

digoxin

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26
Q
A

asclepias speciosa
milkweed

cardiac glycoside

milkweed:; asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex

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27
Q

what does asclepias look like

A

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

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28
Q

asclepias cause —

A

cardiac glycoside → arrythmia and death

cardenolides

can also effect respiratory, GI, CNS → dyspnea, colic, diarrhea, muscle tremors, seizures, and head pressing

milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex

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29
Q

monarch butterflies retain — from — plants

A

cardenolides: cardiac glycoside

Birds that eat them experience intense emetic effects and avoid eating monarchs in the future

asclepias (milkweed)

milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex

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30
Q

clinical signs of asclepias

A

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

milkweed: asclepias
thin or thick leaves
umbels of white or red flowers
seed pod has silky hairs
some have milky sap or latex

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31
Q
A

convallaria
lily of the valley

seeds have high concentrations of cardenolide cardiac glycosides
skin of fruit and flowers- abdominal pain and diarrhea

not requires

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32
Q
A

digitalis
floxglove

cardiac glycosides are digoxin, digitoxin, and digitonin, found
in all parts of the plant

NOT REQUIRED

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33
Q
A

nerium oleander
evergreen
white, pink or red flowers with 5 or more petals
cardiac glycoside

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34
Q

what does nerium oleander look like

A

nerium oleander
evergreen
white, pink or red flowers with 5 or more petals
25 ft tall
cardiac glycoside

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35
Q
A

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

not required

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36
Q
A

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

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37
Q

Taxus toxicity

A

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

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

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38
Q

clinical signs of taxus ingestion

A

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

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

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39
Q
A

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
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40
Q

senecio toxicity

A

pyrrolizidine alkaloid
liver disease → secondary photosensitization

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41
Q
A

senecio longilobus
scaggily

pyrrolizidine alkaloid
liver disease → secondary photosensitization

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42
Q

pyrrolizidine alkaloids are found in — will build up in the blood and when exposed to UV light will cause

A

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
Q

how does pyrrolizidine alkaloids work

A

PAs are converted to toxic pyrroles

affect the endoplasmic reticulum of liver cells, inhibiting mitosis and the
replication of hepatocytes

senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization

44
Q

clinical signs of pyrrolizidine alkaloids

A

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
Q

pathologic changes of pyrrolizidine alkaloids

A

◦ Megalocytosis
◦ Bile duct hyperplasia
◦ Fibrosis

senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization

46
Q

path with Megalocytosis, Bile duct hyperplasia and Fibrosis is suggestive of

A

pyrrolizidine alkaloids

senecio longilobus
pyrrolizidine alkaloids →pyrroles →liver disease →photosensitization

47
Q
A

astragalus and oxytropis spp
locoweed

neurotoxic

48
Q

astragalus and oxytropis toxicity

A

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
Q

clinical signs of astragalus and ocytropis exposure

A

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
Q

how to diagnose atragalus and oxytropis

A

locoweed- neuro toxic
swainsonine → oligosacchardie accumulation

cytoplasmic vacuolation
swainsonine in serum
↓ serum α-mannosidase activity

51
Q

how to prevent atragalus and oxytropis ingestion in cattle

A

food aversion

feed locoweed then dose with lithium chloride

52
Q
A

eupatorium rugosum
white snakeroot

53
Q

toxin in eupatorium rugosum

A

neurotoxin
tremetone- requires microsomal activation to become toxic
causes skeletal and mycocardial degeneration
secreted in milk- milk sickness, trembles
pasteurization does NOT detoxify

white snakeroot
eupatorium

54
Q

clinical signs of eupatorium rugosum ingestion

A

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
Q

treatment for eupatorium rugosum

A

no specific antidote
supportive care
horses have difficulty swallow- fed by NG tube
discard milk

56
Q
A

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

NOT required

57
Q
A

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

NOT required

58
Q
A

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

NOT required

59
Q
A

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

NOT REQUIRED

60
Q
A

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
Q

diagnostics of acer ingestion

A

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
Q

treatment for acer rubrum

A

red maple → hemolytic anemia in horses

guarded prognosis

Blood transfusions may be needed to address intravascular hemolysis and coagulopathies
IV fluids
methylene blue?

63
Q

allium

A

wild onions, garlic, leeks and chives

bulbs, hollow narrow basal leaves, 6 part flower

attack blood and bone marrow

64
Q

allium toxicity

A

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

wild onions, garlic, leeks and chives

65
Q

clinical signs of allium ingestion

A
  • 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

wild onions, garlic, leeks, and chives → anemia and heinz bodies

66
Q
A

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

not required

67
Q
A

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

Calcium oxalate: philodendron and dieffenbachia

68
Q

dieffenbachia bowmannii toxicity

A

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
Q
A

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

rhododendron, kalmia, pieris all grayanotoxins

70
Q
A

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

rhododendron, kalmia, pieris all grayanotoxins

71
Q
A

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

rhododendron (azalea), kalmia, pieris all grayanotoxins

72
Q
A

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

rhododendron (azalea), kalmia, pieris all grayanotoxins

73
Q

clinical signs of grayanotoxin exposure

A

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

rhododendron (azalea), kalmia, pieris all grayanotoxins

74
Q

how to treat grayanotoxin exposure

A

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

rhododendron (azalea), kalmia, pieris all grayanotoxins

75
Q
A

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

Calcium oxalate crystals: dieffenbachia bowmannii (dumbcane) and philodendron

arisema- jack in the pulpiy
spathephyllum- peace lily
zantedeshia aethiopica- calla lily

76
Q

which plants produce calcium oxalate crystals when damaged

A

Calcium oxalate crystals: dieffenbachia bowmannii (dumbcane) and philodendron

arisema- jack in the pulpiy
spathephyllum- peace lily
zantedeshia aethiopica- calla lily

77
Q
A

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

potato is a type of nightshade!

78
Q
A

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
Q
A

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
Q

solanum toxicity

A

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
Q
A

podophyllum peltatum
mayapple

not required

82
Q
A

phytolacca americana
pokeweed

oral irritation, hypersalivation, vomiting, colic, bloody diarrhea, depression, prostration, and death (rare)

not required

83
Q
A

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
Q

juglans nigra toxicity

A

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
Q
A

beteroa incana
hoary alyssum

muscle toxic
horse- laminitis and limb edema
abortion

not required

86
Q
A

hypericum perforatum
st johns wort

skin and integument toxic

not required

87
Q
A

vicia villosa
hairy vetch

skin and integument toxic

not required

88
Q

— plant makes oxalate poisoning that attacks UT

A

amaranthus
red rooted pigweed

89
Q

amaranthus toxicity

A

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
Q

Perirenal edema is a characteristic lesion in pigs and cattle consuming —

A

Amaranthus

oxalate poisoning →urinary system

binds to calcium and magnesium → impairs cell membrane function and cellular metabolism → kidney failure from oxalate nephrosis and death

91
Q

oxalate poisoning treatment

A

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
Q
A

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
Q
A

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

not required

94
Q

symptoms of quercus ingestion

A

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
Q

treatment for quercus ingestion

A

oak

attack renal system

fresh food and water
Oral calcium hydroxide can help neutralize residual tannic acid in the rumen
IV fluids

96
Q
A

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
Q

lupinus toxicity

A

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
Q
A

pinus ponderosa

repro toxic

Isocupressic acid causes premature parturition or abortion in cattle

99
Q

toxicity of pinus ponderosa

A

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
Q
A

veratrum californicum
western false hellebore
moutain meadows > 8500 ft

repro toxic

101
Q

clinical signs of veratrum californicum ingestion

A

western false hellebore
repro toxic

cyclopia
shortened legs and tracheal agenesis

moutain meadows

102
Q

robinia toxicity

A

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
103
Q

clinical signs of robinia ingestion

A

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

23 spring: pharm (46 decks)

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