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315 Cards in this Set
- Front
- Back
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Name 4 sources of large animal nitrates
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1. fertilizers-eaten in clump like salt or taken up by crops
2. decaying organic matter (old hay in barns) 3. water contaminated with fertilizer/decaying matter(manure) runoff 4. plants under stress (drought) |
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Name the 2 most common weeds known to accumulate nitrate
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pigweed
johnson grass |
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name the 3 most common crop plants that accumulate nitrate
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corn
sorghum sudan grass *Sudex is a hybrid of sudan and sorghum* |
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What part of the plant contains the most nitrate?
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lower 1/3 of the plant
*corn, wheat, or oat seeds are not a problem, it is the stover/straw part |
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Which has a higher nitrate concentration?
silage or hay |
hay
hay doesnt lose its nitrate content silage loses 60% bc bacterial degradation/protein encorporation |
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What factors cause plants to accumulate excess nitrate?
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environmental stresses
esp. DROUGHT |
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T/F High silage and concentrate diets are a source of high nitrates for dairy cows.
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False
silage loses 60% of nitrates due to bacterial degradation seeds contain only 1% of the plants nitrates |
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Which form causes more systemic problems, nitrate or nitrite?
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Nitrite
nitrate must be reduced to nitrite to cause systemic problems |
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What level of nitrate in forage is toxic to ruminants?
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>1%
moderate morbidity and moderate to high mortality |
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What level of nitrate in water is toxic to ruminants?
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>500ppm
moderate morbidity and moderate to high mortality |
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Name 4 sources of large animal nitrates
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1. fertilizers-eaten in clump like salt or taken up by crops
2. decaying organic matter (old hay in barns) 3. water contaminated with fertilizer/decaying matter(manure) runoff 4. plants under stress (drought) |
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Name the 2 most common weeds known to accumulate nitrate
|
pigweed
johnson grass |
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name the 3 most common crop plants that accumulate nitrate
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corn
sorghum sudan grass *Sudex is a hybrid of sudan and sorghum* |
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What part of the plant contains the most nitrate?
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lower 1/3 of the plant
*corn, wheat, or oat seeds are not a problem, it is the stover/straw part |
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Which has a higher nitrate concentration?
silage or hay |
hay
hay doesnt lose its nitrate content silage loses 60% bc bacterial degradation/protein encorporation |
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List these animals in order of susceptibility to nitrates
sheep horse pig cow |
cow>sheep>horse>pig
*monogastric animals are fairly resistant to systemic nitrate problems (fertilizer in dogs causes GI problems) |
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What is the mechanism of action of nitrite in the body?
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converts regular hemoglobin to methemoglobin which is chocolate brown
*methemoglobin cant carry oxygen |
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What enzyme is responsible for getting rid of metHb formed in the body?
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Methemoglobin reductase (diaphorase)
*overwhelmed in nitrate toxicosis |
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What are clinical signs of acute nitrate toxicosis?
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METHOMOGLOBIN BLOOD (chocolate brown)
abortion 3-5 d after acute toxicosis depress/leth, weakness, dyspnea cyanosis weak, rapid pulse |
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Onset time and course of action of Nitrate toxicosis
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onset time: 1/2 hr to several days
course: minutes to 2 hours |
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What systems does nitrate toxicosis affect?
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respiratory
RBCs |
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What clinical signs are seen with chronic nitrite toxicosis?
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abortion
infertility decreased milk production goiter in newborn |
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What is the onset time of chronic Nitrate toxicosis?
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weeks
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What is chronic nitrate toxicosis most likely associated with?
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induced iodine or vitamin A deficiency
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Name 3 ways to diagnose nitrate toxicosis
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1. look for methemoglobin by putting blood on a piece of white paper (chocolate brown)
2. analyze nitrate content of feed or water 3. nitrate content of aqueous humor or serum >40ppm *false positives in aborted calves |
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What 2 toxic compounds are found in Sorghum?
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nitrates
cyanide-->volatizes with drying so hay is not a cyanide issue |
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How do you treat nitrate toxicosis?
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-reducing agent to reduce methemoglobin to hemoglobin
ascorbic acid (methylene blue is first choice if available) -activated charcoal and cold water may help |
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What are 3 ways to prevent nitrate toxicosis
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1. check nitrate levels in forage in drought years before feeding (esp. sorghum)
2. raise cutter bar, ensile forages, or wait at least 1 week after drought ending rain 3. increase carbs, vitamins and I in diet **can try Bova-Pro supplement |
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What is responsible for Fescue toxicity?
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endophyte fungus- Neotyphodium coenophialum
95% chance that fescue is infected |
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Can a previously uninfected Fescue plant become infected wtih Neotyphodium coenophialum?
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NO
*infected plants tend to crowd out the uninfected however and take over the pasture |
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What parts of a fescue plant are toxic?
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all parts
seed heads in mid-summer may be more toxic |
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Name 2 factors that can increase fescue's toxicity
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fertilization
drought |
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Name the mycotoxin responsible for fescue toxicity and how much is necessary to cause problems
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ergovaline
>200ppb |
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In what species are fescue toxicity signs most prevalent?
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cattle
mares during last 30d of gestation may also be seen in sheep |
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Name 3 physiologic affects of ergot alkaloids from fescue
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1. vasconstriction of smooth muscle-->esp distal arteries of back legs and switch of tail
2. hypothalamic thermoregulation disruption 3. prolactin inhibition because they are dopamine AGONISTS |
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Name 4 Fescue Syndromes that affect cattle
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Summer Slump
Fescue Foot Fat Necrosis Syndrome Reproductive dysfunction syndrome |
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What are the clinical signs of Summer Slump in cattle?
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generalized ADR , neuroendocrine
(increased body temp of 2-3 F, poor weight gain, failure to shed, decreased conception, heat intolerance, decreased immunity, diarrhea, salivation) *caused by ergot alkaloids from fescue |
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What are the lesions associated with Fescue Foot Syndrome in cattle and what time of year are they generally seen?
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gangrenous necrosis of feet/tail
*affects blood vessels late fall-winter |
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Name 4 effects of Reproductive dysfunction syndrome
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-prolongs gestation by 27 days
foal is dysmature/weak or stillborn with long and langy feathered hooves<BR>-thickened edematous placenta-may have red bag presentation<BR>agalactia-->no udder development<BR>-dystocia<BR>-retained placenta |
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What is the most common way to diagnose fescue toxicity in a mare
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history of exposure with compatible clinical signs
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How would you treat fescue toxicosis in a mare?
How would you prevent it? |
-domperidone (dopamine antagonist)
-take mare off fescue pasture/hay during last month of gestation or feed domperidone for the last 15 days |
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What 2 ergot peptide alkaloids are produced by Claviceps purpurea?
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ergotamine
ergosine |
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What fungus paratizes rye, wheat, barley and various other grasses?
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Claviceps purpurea
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What 2 tremorgenic mycotoxins are produced by Claviceps paspali?
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paspalanine
paspalitrems |
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On what plant can Claviceps paspali be found and where is it usually located?
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Dallis grass
southern states |
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Name 3 body systems that are associated with Claviceps purpura and name a syndrome associated with each.
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-CNS-acute nervous ergotism in cattle (horses)
-blood vessels-chronic gangrenous ergotism in cattle (horses, swine, sheep) -reproductive-ergotism in swine |
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What is the onset time and course of action of Acute Nervous Ergotism?
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onset: 1-5d
course:1-7d |
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What is the onset time of Chronic gangrenous ergotism and what time of year does it occur?
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onset: 1 week
winter (similar to fescue foot) |
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Name 1 similarity and 1 difference between reproductive ergot problems in horses and swine
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similarity:causes agalactia in both, both are related to prolactin
difference: mare gestation is lengthened 27 days while sow gestation is shortened 3-5 days |
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What syndrome is caused by ergots produced by Claviceps paspali and what body system does it affect?
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Dallis grass staggers
CNS |
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Name 3 differentials for Dallis Grass Staggers and how you would differentiate
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-acute nervous ergotism (Claviceps purpura-ergotamine, ergosine)
-Bermuda grass staggers -perennial ryegrass staggers *check forages |
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How would you treat ergot toxicosis?
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-symptomatic treatment
-clip seed heads off with mower -antibiotics for gangrenous ergotism |
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What is the common name for Taxus spp?
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Yew
Japanese and English are the most common |
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What are the toxins present in Yew and where are they found?
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taxine A & B-->present in all parts of the plant except the fruit of the berry
*mature leaves are more toxic than younger leaves |
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What species are most commonly affected by Yew poisoning?
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-cattle
-poisonings occur in most species including birds -deer are fairly resistant |
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How do Taxines in Yew plants cause toxicity?
i.e. mech of action |
-negative inotropic effect on the heart, Ca & Na channel antagonism
-leads to heart stoppage in DIASTOLE -heart will be enlarged *added bonus of unknown convulsions in dogs |
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What body systems are involved in Yew toxicity?
What are the clinical signs? |
Heart
CNS in dogs in addition usually sudden death, convulsions in dogs |
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How do you diagnose Yew toxicity?
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history of access and necropsy findings
-leaves in stomach -enlarged globular heart -lung edema and congestion with increased pericardial fluid |
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How would you treat Yew toxicity?
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-avoid excitement
-atropine for bradycardia -after HR increases, give activated charcoal + saline cathartic |
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What is the scientific name for Buckeye?
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Aesculus
(Yellow Buckeye, Ohio Buckeye, Horse Chestnut) |
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What are the toxic parts of Aesculus?
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all parts are toxic
-nuts, young growth, and sprouts are most toxic |
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What species are most commonly affected by Buckeye?
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cattle
can also be seen in horses |
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Compare low doses of buckeye toxins to high doses
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neurotoxic at low doses
hemolytic at high doses |
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What toxins in Aesculus cause toxicity?
What system does it affect? |
(buckeye)
likely a mixture of triterpenoids and saponins (Aesculin?) -CNS (small GI component from saponins) |
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What is the most common clinical sign associated with Buckeye?
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goose stepping!
(saw horse stance, incoordination, ataxia) |
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What is the onset time of Buckeye toxicosis?
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12-16 hours
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What 4 things would you use to treat Aesculus toxicosis?
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(buckeye)
-Gi detox-->lavage(difficult), activated charcoal and cathartic -ace to calm them (consider xylazine or methocarbamol) -steroids and B vitamins -fluids and electrolytes |
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What are the common names for the two species of Quercus discussed?
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White oak (1 yr for achorns)
Black oak (2 yrs for achorns) |
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Discuss which species are most susceptible to Quercus toxicity and which others are resistant
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most common in cattle/calves
-can occur in sheep/goats/horses -swine are resistant -deer-->proline in saliva is resistant -goats have inducible tannase to allow foraging |
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What is the most toxic part of an oak tree
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buds and achorns-especially the cap
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What is the morbidity and mortality associated wtih Quercus toxicity?
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low to moderate morbidity
moderate to high fatality |
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What is the toxic principle of Quercus
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tannin a gallotannin, is hydrolyzed to gallic acid and pyrogallol in the rumen
-gallic acid (polyhydroxyphenol) precipitates proteins |
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How do the tannins in oak cause toxicity
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tannins are hydrolyzxed to gallic acid which causes GI irritation by increasing absorption of phenolic compounds
-this causes precipitation of plasma proteins and damages endothelial cells and renal tubular epithelium-->interstitial edema of the kidney (this causes backpressure leading to perirenal edema) |
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What are the body systems involved in Oak toxicity?
What is the onset time and course of disease |
Renal
GI onset: 3-14 days course:7 days |
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Describe clinical signs related to Quercus toxicity
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initial
-anorexia/depress/weakness, atonic rumen (gravel), mucous nasal discharge -constipation, mucous covered feces later signs -black tarry diarrhea -elevated lumbar spine (gaunt) -VENTRAL EDEMA, pu/pd, dehydration, hyposthenuria, hematuria |
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How would you diagnose Quercus?
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History of ingestion, clinical signs, lesions (clin path associated wtih renal failure)
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How would you treat oak toxicity?
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-restore renal perfusion-fluids/electrolytes
-lavage-oils or activated charcoal (remember, not both!) -reestablish rumen motility-transfaunation (legume hay, vit B, propylene glycol) -prevention-10% Ca(OH)2 in grain to precipitate tannins |
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When would you see Quercus toxicity?
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In the fall when achorns are present in abundance
-In spring when there is little grass but buds are present on trees |
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What is the scientific name for Red Maple
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Acer rubrum
*all maples are in the genus Acer |
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What is the most toxic part of the Acer tree?
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leaves are toxic when wilted or dry (fresh is controversial)
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What is the toxic element of Maple leaves?
What other plant contains these same toxins? |
Gallic acid and pyrogallol
Quercus (oak) |
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How do gallic acid and pyrogallol cause Maple toxicity?
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oxidative reactions due to methemoglobin and heinz bodies, acute hemolysis
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What are the body systems involved in Acer rubrum toxicity
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(red maple)
RBCs hepatic renal |
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What are the clinical signs associated with Red maple toxicity?
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(acer rubrum)-->acute hemolytic disease
early-->weakness, depress/leth, anorexia, hemoglobinemia, hemoglobinuria later-->polypnea, tachycardia, cyanosis anemia, heinz bodies, methemoglobin and icterus |
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What is the onset time and course of action for Acer rubrum toxicosis?
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(red maple)
onset:1-3 days course: 3-5 days |
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How would you treat Acer rubrum toxicosis?
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-no specific antidote
-URGENT supportive care -if very early-activated charcoal -ascorbic acid -fluids/electrolytes-keep kidneys flushed -diuretics -whole blood transfusions -NO STRESS |
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What species is most likely to be affected by a Red Maple toxicosis?
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horse
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What is the common name for Juglans nigra
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Black walnut
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Toxic principle of Juglans nigra
What species is affected? |
unknown (Juglone?)
horse |
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How do black walnut shavings cause toxicity?
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-allergic reaction to shavings causes severe laminitis (alpha 1 receptors) and swelling of coronary band and legs
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In horses, what limbs would be most affected by Juglans nigra toxicity?
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(black walnut)
thoracic limbs |
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What body systems are affected by black walnut toxicity?
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Dermal (vascular, skeletal)
may see resp difficulties, horse is distressed(incr. HR, RR, temp), his belly will probably hurt |
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How would you treat Juglans nigra toxicity?
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remove bedding!
treat laminitis -pain-bute or banamine -prazocin (alpha blocker) -nifedipine (Ca blocker) -nitroglycerin on fetlocks-improve circulation -cold hose legs -deep soft bedding (sand) |
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Name the 5 cyanogenetic plants
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Prunus-wild/chokecherry
Sorghum-sudan or johnsongrass Linum-Flax Beta-sugar beets (tops) Triglochin-arrowgrass |
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What is the toxic principle of cyanogenetic plants?
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cyanide containing glycosides
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What is the mechanism of action for cyanogenetic plants?
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CN binds to cytochrome oxidase and shuts down cellular respiration
HISTOTOXIC ANOXIA |
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What 3 factors increase [CN]?
What decreases [CN]? |
1. frost
2. wilting 3. mechanical damage -drying out-free cyanide is fairly volatile and escapes |
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What body systems are involved in cyanogenetic plant toxicity?
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Respiratory
RBCs |
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What is the onset time of cyanogenic toxicity?
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RAPID 15-60min
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What species is most commonly affected by cyanogenetic plant toxicity?
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ruminants-they have the mechanism to encorporate CN
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A goat presents DOA
-there are scuff marks around the body -mucous membranes appear bright red, as do the lungs, but intestines appear normal -at necropsy leaves are found in the abomasum and there is a bleachy or bitter almont odor What is the most likely diagnosis? |
cyanogenetic plant
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What are the lesions associated with cyanogenetic plants?
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-bright red blood-lots of O2 (may not clot well)
-subendocardial and epicardial hemorrhages -odor on breath or stomach contents of bitter almonds/bleach/mousy |
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What level of CN in a forage sample is dangerous?
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>200ppm
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How would you treat choke cherry toxicity?
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must restore cell respiration!
-sodium nitrite and sodium thiosulfate-->give IV together -nitrite oxidizes Hb to MetHb which has a higher affinity for CN than cytochrome oxidase -this forms cyanomet HB then thiosulfate grabs the CN with rhadanese(liver enzyme) to form nontox thiocyanate which can be excreted |
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In what toxicity is it beneficial to create a controlled nitrite poisoning?
|
cyanogenetic plant toxicity
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Name the 4 primary plants involved in photosensitization
|
Hypericum perforatum-St. John’s Wort
Fagopyrum sagittatum-Buckwheat Medicago sativa-Alfalfa Trifolium spp-White Clover |
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Name the 3 secondary plants involved in photosensitization
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Lantana-Lantana, red sage
Tetradymia-Horsebrush Microcystis or Anabaena-blue green algae |
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What toxic principles are involved with primary plant photosensitization?
|
hypericin
fagopyrin |
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What toxic principles are involved in secondary plant photosensitization?
What do they do? |
lantadene A and Tetradymol
-injure liver and cause a buildup of phylloerythrin |
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What is the mechanism of action for plant toxins involved in photosensitization?
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-interact with UV light to form free radicals which damage DNA or RNA
-this changes the cell permeability in the dermis/epidermis -pyrogen and histamine are released in skin cells |
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What body system is involved in photosensitization?
What are the clinical signs? |
skin
-erythema of light colored skin, dermatitis, sloughing, fissures, fever, coronitis, photophobia *may see hepatic damage (esp secondary plants) |
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What is the onset time of photosensitization?
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1-5 days
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What species are most affected by by photosensitization plants?
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cattle
horses |
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What would you test to aid in diagnosis of a photosensitization plant toxicity in addition to a history of access to plants?
|
liver function
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How would you treat an animal who ingestedTrifolium?
|
trifolium=clover
topical skin treatment and avoid sunlight -antihistamines-prevent further histamine release -corticosteroids-prevent further formation of histamine -antibiotics, protective ointments-prevent secondary infections |
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Name the 3 resin containing plants
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-rhododendron maximum
-kalmia latifolia-mountain laural -azalea spp |
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What is the toxic dose of a resin containing plant?
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0.2% of body weight
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What is the toxic principle in resin containing plants?
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grayanotoxins (Andromedotoxins)
-complex alcohol (tetracyclic polyol) |
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Where is grayanotoxin found?
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in the leaves, nectar, and honey of resin containing plants
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What is the mechanism of action of grayanotoxin (in resin containing plants)?
|
binds Na channels and prolongs depolarization which allows Ca to enter the cell causing an inotropic effect leading to bradycardia, hypotension and AV block
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What body systems are involved in grayanotoxicity?
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Heart, CNS, GI
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What is the onset time for grayanotoxicity caused by consumption of mountain laural, rhododendron, or azaleas?
What is the course of disease? |
onset: 4-6 hours post ingestion
course: death within 1-2 days |
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What time of year would you expect to see a gryanotoxin toxicity (redundancy much?)
|
late winter or early spring when snow has covered all other vegetation and those leaves look TASTY!
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What species are most affected by consumption of rhododendron or azaleas and what is the main clinical sign associated with each?
|
cows-projectile vomit
sheep/goats-ooze ingesta from mouth horse-cant vomit so painful retching signs shared by all-CV EFFECTS, salivation/burning in mouth, diarrhea, muscle weakness, impaired vision |
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How would you treat a toxicity resulting from ingestion of resin containing plants
|
-oral detox-lavage and activated charcoal (may have to consider rumenotamy because it can be difficult to get plant material out)
-supportive care fluids, electrolytes, warmth atropine-bradycardia treat arrhythmias antiemetics |
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What is the scientific name for water hemlock?
|
cicuta maculata
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Where would cicuta maculata be found?
|
in wet areas, along streams, ditches
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What is the most toxic part of a water hemlock plant?
|
roots-tubers
1 tuber can kill and adult cow/horse |
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What is the toxic principle in cicuta maculata?
|
(water hemlock)
cicutoxin complex alcohol-resinoid found in lower stem and root |
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What is the mechanism of action of cicutoxin?
|
(water hemlock-resin containing plant)
powerful CNS convulsant |
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Cicutoxin from water hemlock affects the CNS in 2 ways.
list them: |
1. effects Na and K channels
2. acts as gaba antagonist |
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what is the onset time for water hemlock toxicity?
|
30-60 minutes
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What are the clinical signs associated with cicuta maculata?
|
(water hemlock)
-acute onset of violent TETANIC seizures -champing jaws, salivation -twitching, tremors, convulsions -resp distress, asphyxia from convulsions -dilated pupils, abdominal pain, increased temp -coma, death |
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How would you diagnose a water hemlock toxicity?
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History, signs, rumen contents
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How would you treat cicutoxin toxicity?
|
disease is often too rapid!
symptomatic -control convulsions-pentobarbital -resp support-intubate lavage-prompt and vigorous activated charcoal and repeat as necessary |
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What 2 things used as fertilizer can increase copper content in pasture?
|
poulty litter
swine manure |
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What 2 minerals interact with copper in dogs?
|
iron
zinc |
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What species is most susceptible to chronic copper toxicosis?
|
sheep
*cattle and goats are more likely to suffer a Cu deficiency |
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What is the ideal ratio of Cu:Mo in sheep diets?
When would you see problems? |
6:1
>10:1 |
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What 5 breeds of dogs have heritable copper problems?
What is the age group most likely affected? |
Bedlandington terrier
West Highland terrier White terrier Skye terrier Doberman 2-6yrs |
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What is the mechanism of action of a chronic copper toxicosis?
|
Cu builds up slowly in liver lysosomes (wks-months) then a significant stress causes Cu to be dumped into blood, this causes hemolysis and liver necrosis
|
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What are the body systems involved in a chronic copper toxicosis?
Clinical signs? |
Liver
RBCs Renal -vomiting(dogs), hemolytic anemia, hemoglobinuria, anorexia, weakness, icterus |
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What lesions are associated with chronic copper toxicosis?
|
icterus
gun-metal colored kidneys enlarged spleen |
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What preventative measure is often taken in dogs predisposed to copper toxicity?
|
liver biopsy around 1 yr of age
DNA microsatellite marker for gene in Bedlingtons |
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What other problem involving the liver is often associated wtih Cu accumulation
|
primary cholestasis
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How would you treat a sheep with chronic copper toxicosis?
What is the prognosis? |
ammonium tetrathiomolybdate
fluids for kidney hemoglobin problems steroids ascorbic acid (avoid acidosis) POOR prognosis |
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How would you prevent chronic Cu toxicity in a flock of sheep once 1 has succombed?
|
0.5 g/hd/d of Na molybdenate for 3 wks
correct Cu:Mo ratio in diet (be sure to keep M0<5ppm |
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How would you treat chronic copper toxicity in dogs?
|
fluids, steroids, ascorbic acid, Vt E
S-adenosylmethionine (glutathione precursor) to help decrease oxidative stress |
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Why might propholactic zinc decrease incidence of Cu toxicity in dogs?
|
induces metallothionein in intestinal cells to bind Cu and slough into the gut
-could also give penicillamine or Trientine |
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What are some sources of Zinc?
|
nuts and bolts
pennies after 1983 zinc oxide ointments (desitin) misfornulated diets galvanized containers, cages monopoly game pieces calamine lotion, dandruff shampoo |
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What are the two types of zinc toxicity and what species are most affected by each?
|
acute-->dogs (think pennies!)
may also see in zoo animals new wire disease in birds/ferrets chronic-->cattle (think diet) these species are indescriminant eaters! |
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How is zinc excreted?
|
in bile and pancreatic secretions
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What systems are involved with chronic zinc toxicity?
acute zinc toxicity? |
-GI, RBC, hepatic, renal, bone
-GI, RBC, hepatic, renal |
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Chronic consumption of zinc interes with uptake from the GI tract of what 2 minerals?
What role does this play in bone formation? |
Cu and Fe
Cu is involved in lysyl oxidase enzyme necessary for bone collagen formation |
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What are the clinical signs of acute zinc toxicosis?
|
vomiting and hemolytic anemia-very consistent
hemoglobinuria, icterus, DIC depress/leth, anorexia, diarrhea |
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How would you diagnose zinc toxicity?
|
elevated serum or liver Zn conc
radiograph for hardware clin path-anemia, elevated liver enzymes, hemoglobinuria, DIC, signs of kidney dysfunction |
|
|
How would you treat Zn toxicity?
|
symptomatic
-antiemetic (metaclopromide, low doze phenothiazine) -fluids to flush kidneys -transfusions -remove foreign body -cathartic-canned pumpkin! CaEDTA for high serum Zn levels |
|
|
Name the 4 most common liver toxicants
|
-acetaminophen
-Pine oil, phenol disinfectants -Minerals-Cu, Zn, Fe Endotoxins (garbage) others: halothane, penny royal oil, Xylitol, mycotoxins (aflatoxin, fumonisin), mushrooms (amanita phalloides), Rimadyl, some plants |
|
|
Name the 5 most common hemolytic toxicants
|
-acetaminophen
-Cu, Zn -Anionic surfactants -Onions (dogs, cats) others: snake bites, DMSA, propylene glycol, methylene blue (cats), phenol, Vit K3 parenterally -Red maple (horses) |
|
|
What are some sources of lead for small animals?
|
pre 1960 PAINT
lead weights (fishing) putty, solder roofing materials, linoleum board game tokens, stained glass framing |
|
|
Large animal sources of lead
|
paint
grease, motor oil, lubricants batteries caulking compounds putty lead shot (less common now) |
|
|
What 4 things can lead to increased Pb absorption
(normally 2-10% absorbed from GIT) |
age (young>old)
macro mineral deficiency binding of lead to Ca binding proteins acidic environment |
|
|
What is considered the sink for Pb?
How does it get there and how long does it take? |
bone
lead is deposited on RBCs then soft tissues (liver, kidney) then by 7-10 days has deposited in bone |
|
|
T/F lead can cross the BBB and placenta
|
True!
|
|
|
How is lead excreted?
|
feces
urinary route plays a role when lead is chelated milk-lactating animals excrete significant amounts |
|
|
What body systems does lead affect?
|
multi-systemic!
GIT, CNS (PNS), RBCs, renal |
|
|
What mineral does lead compete with and replace in enzymes?
|
Zinc
|
|
|
How does lead affect the hematopoeitic system?
|
inhibits heme synthesis enzymes (Alanine dehydratase and synthetase)
|
|
|
What part of the kidney is most affected by lead?
|
tubular epithelial cells
|
|
|
There are 2 lead toxicity syndromes. What are they and what are some key clinical signs?
|
GI syndrome-->acute toxicity
vomiting, anorexia, tender abdomen-dogs rumen stasis-cows constipation followed by diarrhea +/-blood CNS syndrome dogs-depression to hysteria, barking, muscle tremors, tonic clonic seizures **may be intermittent cattle-BLINDNESS, head pressing, bellowing, muscle tremors, rhythmic ear twitch, head bob/jaw champing ataxia, incoordination horses-roaring water fowl-weakness, diarrhea, lethargy, coma, death, droopy wings |
|
|
List 2 differentials for lead toxicity GI syndrome in dogs
list 4 differentials for CNS syndrome |
gastritis (garbage), arsenic
distemper, encephalitis, organochlorides, strychnine, metaldehydes, OPs and carbamates |
|
|
How would you treat lead poisining?
What must you be careful to prevent? |
chelation with EDTA (treat 2-5 days, rest for same, check levels, retreat if necessary)
-must use CaNa2EDTA to prevent hypocalcemia DMSA (dimercaptosuccinic acid)-removes lead from ST and bone BEST for birds, good for cats and dogs Penicillamine-better for copper but good in chronic lead cases Thiamin-CATTLE |
|
|
How does EDTA work to treat lead poisoning?
Are there side effects to EDTA? |
chelates extracellular Pb from bone but not soft tissue
lead will redistribute from soft tissue to bone once it is removed which reduces body burden EDTA can be nephrotoxic |
|
|
What can penicillamine be used to treat?
|
Cu, Pb, As, and Zn
|
|
|
What species are affected by Inorganic Arsenic? What are some sources for them?
|
cattle-old pesticides and salt treated lumber
cats and dogs-syrupy ant bait |
|
|
What is the mechanism of action for inorganic arsenic?
|
combines with SH groups of key metabolic enzymes (Lipoic acid) and shuts down cellular respiration
is also directly corrosive to capillaries and is a potent toxicant of vascular system |
|
|
What two toxicants shut down cellular respiration and how might you them apart?
|
cyanogenetic plants and inorganic arsenic
cyanogenetic plants will cause bright red blood and mucous membranes while inorganic arsenic will cause hyperemic GUTS |
|
|
What are the key clinical signs of acute inorganic arsenic toxicity
|
intense abdominal pain
severely hyperemic gut signs of shock |
|
|
How long can an animal live if subacutely poisoned with inorganic arsenic and what are the key clinical signs?
|
4-7 days
severely hyperemic gut, PU/PD progressing to anuria dehydration, acidosis cool extremities from poor circulation |
|
|
Name 3 histological signs of inorganic arsenic poisoning
|
-gi epithelial necrosis
-renal tubular necrosis -hepatic fatty degeneration |
|
|
What is contraindicated in treatment of inorganic arsenic?
|
cathartics
activated charcoal is indicated as is treatment of shock and dehydration and lavage if caught between 1-4 hours after ingestion |
|
|
What are some antidotal treatments for inorganic arsenic?
|
BAL given IM (painful)
DMSA Sodium thiosulfate bland diet |
|
|
What factors could lead to organic arsenical toxicity?
|
poorly balanced diet
lack of water, dehydration and renal disease |
|
|
What body systems are affected by organic arsenicals?
|
PNS-demyelination and axonal damage
|
|
|
Clinical signs of organic arsenicals?
|
blindness, weakness
remain bright and alert and will eat and drink but may not be able to walk erythema in light skinned animals |
|
|
What is the prognosis of organic arsenical toxicity?
|
they usually recover in 5-7 days if offending feed is removed and plenty of fresh water is provided
|
|
|
What are some common ionophores used and what are they used for?
|
monenson
lasolocid salinomycin used as coccidiostats and to increase feed efficiency (antibiotic potential?) -they are compounds from streptomyces fungi that facilitate transfer of ions across membranes |
|
|
List these animals in order of monensoin susceptibility
sheep, chickens, swine, cattle, horse |
horse>sheep>swine>cattle>c hicken
|
|
|
What potentiates monensin toxicity?
|
-concurrent exposure to macrolides
-some antibiotics that inhibit cytP450 |
|
|
What ionophore is most likely to cause problems in dogs?
|
lasalocid
|
|
|
What are the target organs of ionophore toxicity?
What happens? |
heart
skeletal muscle GI free radical formation leading to lipid peroxidation catecholamine release leads to intracellular Ca accumlation causing mitochondrial Ca accumulation-->swelling and opening of MPTP with decreased ATP formation and cell necrosis |
|
|
Discuss species differences in heart vs skeletal muscle prevalence of ionophore damage (horse, cattle, rabbits, sheep, cats, dogs, pigs)
|
horse and cat: heart>skeletal
cattle and rabbits: heart=skeletal sheep, pig, dog: skeletal>heart |
|
|
How would you diagnose ionophore toxicity?
|
anorexia, gi problems or death folloing use of a new concentrate or mineral should cause you to stop and wonder if you should get that mineral analyzed
Clin path: signs of muscle damage! (increased CK, AST< LDH) ECG abnormalities |
|
|
How would you treat ionophore toxicity?
|
activated charcoal-binds ionophores AND endotoxins!
fluids steroids-may decrease amount of CT formed Vit E/selenium for free radicals stall rest 6 wks |
|
|
What is in blister beetles that causes irritation?
What types of hay most commonly contain blister beetles? |
cantharidin
3rd cutting hay (July) alfafa (medicago!) from southwest US crimped hay *more likely on hay from periphery of pasture |
|
|
What species is most susceptible to Cantharidin toxicity?
How much would it take? |
horses
about 30 beetles |
|
|
What body systems are involved in blister beetle toxicity?
What are the most common clinical signs? |
GI, Renal, Cardiac
pollakiuria, synchronous diaphragmatic flutter (hiccups), fever can also cause salivation, shock and muscle tremors |
|
|
What is gossypol and where does it come from?
|
polyphenolic pigment in glands of cotton seeds
its a cumulative toxicant with a long 1/2 life in the body |
|
|
What is the mechanism of action of gossypol?
|
inhibits protein synthesis and a variety of enzymes (lactic dehydrogenase, GSH-transferase)
inhibits reproductive hormone balance and sperm motility/morph. |
|
|
What are the body systems involved in gossypol toxicity?
What is the main clinical sign? What are lesions associated wtih it? |
cardiac, hepatic, reproduction
thumps (tachypnea) -hydrothorax, hydropericardium, pulmonary edema, dilated/flabby heart with necrosis, icterus, ascites, anemia **sudden death syndrome in lambs |
|
|
List 6 cardiac toxicants
|
1. ionophores
2. endotoxins 3. selenium deficiency/toxicosis (LA) 4. Cantharidin (blister beetles!) 5. plants-yew, rhododendron, Mt. laural 6. gossypol-swine and young ruminants (rare) |
|
|
List 8 things that can cause rear leg paresis in dogs
|
1. bromethalin low dose (CNS)
2. 2, 4-D (myotonia w/ rigid muscles) 3. disk disease/trauma 4. botulism (flaccid muscles) 5. ionophores 6. tick paralysis 7. low dose tremorgin mycotoxin (roquefortine) 8. macadamia nuts |
|
|
What is the mechanism of action for sodium toxicosis?
|
passive movement of Na across BBB along with inhibition of enerfy production necessary to actively transport Na back out of CSF
Na loss from blood via the kidney or reintroduction of water creates an imbalance so water follows sodium into the CNS causing edema can also get intracellular fluid loss as water leaves brain cells to enter CSF which causes brain shrinkage and retraction from clavarium, also get meningeal vessel bleeding |
|
|
What body systems are involved in Na toxicosis in cattle and what is the main clinical sign?
|
CNS, GI
blindness |
|
|
What body systems are involved in Na toxicosis in swine and what are the main clinical signs?
|
CNS syndrome
star gazing, jaw champing, blind, eosinphil cuffing of brain |
|
|
What body systems are involved in poultry Na toxicosis and what are some clinical signs?
|
cardiovascular
hypertension, depress/leth, dyspnea, ascites and edema |
|
|
How would you treat Na toxicosis in a dog?
|
replace free water deficit SLOWLY (50% day one, 50% day 2)
once rehydrated use furosemide for Na exretion **carefully monitor Na every few hours and dont decrease too quickly! |
|
|
Molds are classified into field or storage fungi, where is most mycotoxin produced?
|
field
if grain is dried to <13.5% moisture there should be no additional mycotoxin production |
|
|
What fungus produces aflotoxins and what plant is it associated with?
|
Aspergillus flavus
corn (esp. in drought years or if there is insect damage) |
|
|
What is a quick way to screen corn for aflotoxins and what is it detecting?
|
black light
kojic acid, another metabolite of Aspergillus flavus (50% false pos but only 10% false neg) |
|
|
Name the 4 aflotoxins found in feed, which is most prevalent, and which is most toxic
|
B1, B2, G1, G2
B1 is most prevalent and most toxic |
|
|
What aflotoxin is measured in milk by the FDA and why?
|
Aflatoxin M1 which is a metabolite of B1
it is carcinogenic |
|
|
Which animals are the most susceptible to aflotoxins and which are most resistant?
|
poulty and young swine are the most likely to have toxicoses-poultry horses, dogs, young animals and breeding animals are susceptible
finishing animals-cattle, swine, and sheep are most resistant |
|
|
What are the three mechanisms of action of aflatoxins?
|
1. decrease RNA synthesis, primarily in liver
2. immunosuppressive (cell mediated) 3. decrease synth of clotting factors sum:hepatotoxic and carcinogenic |
|
|
What are the clinical signs of aflotoxins?
|
general ADR, hepatotoxic (icterus, bile duct hyperplasia, hemorrhages, ascites, hydrothorax)
|
|
|
How could you treat and prevent aflotoxin problems?
|
-anticaking clays-bind aflatoxin in intestine
-remove or blend contaminated feed -check corn in drought years before feeding, dry picked corn down |
|
|
Where does trichothecene come from?
What is the most common trichothecene? |
Fusarium molds
vomitoxin-produced in corn and small grains during WET seasons **pink or rose color** |
|
|
What species are most susceptible to vomitoxin?
|
swine and dairy cattle
dogs can also be affected poultry, sheep and beef are fairly resistant |
|
|
What are trichothecenes refered to as?
|
Feed refusal factor
|
|
|
What are the main clinical signs of T-2 and DAS (trichotecenes)
How about vomitoxin? |
dermal/oral necrosis
feed refusal, possible diarrhea, vomiting in some pigs and dogs *all inhibit protein synth and are immunosuppressive at high doses |
|
|
How would you treat trichothecene toxicoses?
|
dilution is the only solution to pollution
can try anti-caking clays but they wont work too well could also try MTB 100 (yeast) |
|
|
What are the 2 toxins produced by Fusarium molds?
|
zearalenone
vomitoxin |
|
|
Describe the perfect situation for growth of zearalenone
|
presence of fusarium mold on corn stored on the cob at >14% moisture in open air cribs at 8-15% C
varying temps is important bc the mold likes to grow at warmer temps but likes to produce zearalenone at lower temps |
|
|
What species is most likely to be affected by zearalenone
|
swine
|
|
|
What is the mechanism of action of zearalenone?
|
acts as an estrogen
zearalenone is metabolized to zearalenol which is in Ralgro an estrogenic implant |
|
|
What is the body system most affected by zearalenone?
|
reproductive
estrogenizes males, females have prolonged estrus and signs of heat |
|
|
What are the 2 toxins produced by Fusarium molds?
|
zearalenone
vomitoxin |
|
|
Describe the perfect situation for growth of zearalenone
|
presence of fusarium mold on corn stored on the cob at >14% moisture in open air cribs at 8-15% C
varying temps is important bc the mold likes to grow at warmer temps but likes to produce zearalenone at lower temps |
|
|
What species is most likely to be affected by zearalenone
|
swine
|
|
|
What is the mechanism of action of zearalenone?
|
acts as an estrogen
zearalenone is metabolized to zearalenol which is in Ralgro an estrogenic implant |
|
|
What is the body system most affected by zearalenone?
|
reproductive
estrogenizes males, females have prolonged estrus and signs of heat |
|
|
What is the primary hay mycotoxin and what is it produced by?
|
slaframine
Rhizoctonia leguminicola, usually on clover (alfalfa) |
|
|
What is slaframine often referred to as?
|
slobber factor
|
|
|
What species are affected by slaframine
|
HORSES
goats possible in sheep and cattle |
|
|
What is the mechanism of action of slaframine?
|
it is a parasympathomimetic alkaloid metabolized in liver to ketoimine (similar to ach) that works on cholinergic receptors associated wtih exocrine salivary gland
**cant cross BBB bc of charge |
|
|
What causes ELEM (equine leucoencephalomalacia)
|
Fumonisins B1 and B2 produced by Fusarium verticilloides growing on CORN
|
|
|
When would fumonisins be found on corn?
|
if there was a dry season followed by a wet harvest
*could be co-contaminated with aflatoxin OR vomitoxin (not usually both) |
|
|
What species are most affected by fumonisins?
|
all equidae (even mini donkeys)
swine are next most susceptible |
|
|
Contrast morbidity and mortality of fumonisin cases with other myocotoxins
|
fumonisins have a low morbidity and high case mortality whereas most other have the high morbidity but low mortality
|
|
|
What is the mechanism of action of fumonisins?
|
inhibit sphingolipid biosynthesis which is important for myelin formation and integrity in the brain (no big deal)
-also important in heart/endothelial cells-responsible for swine pulmonary edema problem |
|
|
There are two syndromes associated wtih fumonisin in horses. What are they and what are the main clinical signs of each?
Which is most common? |
CNS (MOST COMMON)-blindness and bizarre maniacal behavior
hepatic-YAWNING, head pressing, cyanosis, jaundice, petechial hemorrhages on mucosal membranes |
|
|
Liquifactive necrosis of the white matter in the brain of a horse indicates what?
|
fumonisin toxicity
|
|
|
a horse presents in February with bizarre behavior and appears to be blind. What are some differentials and how could you rule them out?
|
fumonisin-correct
EEE and West Nile would also appear this way-->they generally occur in summer when the bugs are out |
|
|
list some sources of tremorgens
|
-aspergillus
-penicillium-->Penitrem A and Roquefortine neotyphodium lolli endophyte in perennial ryegrass-lolitrems A and B -bermuda grass toxin -fumitremorgen from ergot sclerotia on grass heads |
|
|
Name and differentiate where you would find the two tremorgens produced by Penicillium molds
|
Penitrem A-moldy dairy products and walnut hulls
Roquefortine-decaying organic matter *often found together |
|
|
What mycotoxins are on the Blodges top 5 of canine toxicants but get no respect in the literature?
|
Penitrem A and roquefortine
|
|
|
What is the mech of action of Penitrem A?
|
facilitates transmission of impulses across motor end plates and inhibits inhibitory neurotransmitters (GABA and glycine)=increased excitatory stimulus!
|
|
|
What are 2 ruleouts for goosestepping in cattle?
|
buckeye and tremorgens
|
|
|
Name some clinical signs of tremorgens
|
muscle tremors, paralysis/prostration (often w/ low doses), nystagmus, salivation, clonic/tonic convulsions
ataxia/high stepping |
|
|
How would you treat tremorgen toxicities?
|
large animals recover from grass problems unaided
dogs-symptomatic methocarbamol or pentobarbital for muscle tremors/convulsions |
|
|
What is the scientific name of marijuana and list in order the toxic parts of the plant
|
Cannabis sativa
flowering tops>flowers>leaves>stems/seeds |
|
|
What is the main toxin in cannabis?
What is the body system it affects? |
tetrahydrocannabinol (THC)
CNS (depressant) |
|
|
What is the prognosis for marijuana overdose?
|
good to excellent but recovery may take 1-4 days
|
|
|
List 6 Calcium oxalate sources
Which one is the most toxic? |
dumbcane Diefenbachia **most toxic
philodendron jack in the pulpit ariseama caladium pothos skunk cabbage |
|
|
Which parts of calcium oxalate plants are the most toxic?
|
all parts are toxic
stalks more so than leaves |
|
|
What species are most susceptible to calcium oxalate toxicity?
|
dogs, cats, birds and lizards
|
|
|
What is the mechanism of action of calcium oxalate?
|
mechanical damage from Ca oxalate needles in IDIOBLAST cells
(these can be visualized on a slide for ID) |
|
|
What is the onset time and what are some clinical signs?
|
onset is immediate and lasts up to 14 days
affects GI TRACT head shaking, salivation , vomiting, diarrhea, dyspnea from laryngeal edema and loss of voice (dumb) |
|
|
How would you treat Calcium oxalate toxicity?
|
-rinse mouth with water (milk may precip soluble oxalates)
-demulcents -fluids metaclopramide to stop vomiting |
|
|
What lesions are associated wtih grape/rasin toxicity?
|
affects GI and RENAL systems
will see enlarged kidneys w/ proximal tubular nephrosis and hyaline casts |
|
|
What is the initial sign if too many grapes are ingested?
|
vomiting
|
|
|
How would you treat a dog with raisin toxicity?
|
-emetic followed by activated charcoal and a saline cathartic if caught within 3 hours
-must monitor BUN and creatinine for 3 days IV isotonic fluids for 2 days furosemide and dopamine |
|
|
What is the prognosis for a dog with raisin toxicity?
|
if there are renal signs the prognosis is guarded
|
|
|
Name 7 bulbs that you wouldnt want your dog to eat
|
tulip-tulippa
Iris Hyacinth-Hyacinthus Amaryllis-Hippeastrum Daffodil, jonquil-narcissus *Autumn crocus-Colchicum *Glory lily-Gloriosa |
|
|
What is the body system affected in consumption of bulbs and what are some clinical signs?
|
GI
vomiting, salivation, diarrhea may be some kidney problems from cholchicine |
|
|
What is the most likely way for an animal to get a toxicosis from a christmas tree?
|
drink the water
could get it from chewing on needles |
|
|
What species is most susceptible to Christmas tree toxicity?
Why? |
cats
they are deficient in glucuronyl transferase which is necessary to conjugate the monocyclic carbon alcohols (phenols, pine oil, pinene) for excretion |
|
|
What is the mechanism of action of Christmas tree toxicity?
|
phenol like compounds are protoplasmic poisons that denature and precipitate proteins
may be oxidizers and produce free radicals |
|
|
What are the body systems involved in Christmas tree toxicity?
|
hepatic, GI, renal
|
|
|
What are the common names of some of the Lilium genus?
|
easter lily
tiger lily asiatic lily |
|
|
What species is most susceptible to lilium toxicity?
|
cats-takes less than 1 leaf
|
|
|
What body systems are affected by lilium toxicity and what are some common clinical signs?
|
GI, renal
vomiting and polyuria early, progressing to anuria |
|
|
How would you treat a cat who had eaten a lily?
|
*early treatment is key (w/in 6h)
metaclopramide for persistent vomiting and IV isotonic saline fluid diuresis at 2x maint. for 3-4 days |
|
|
Name 9 renal toxicants
|
ethylene glycol, NSAIDS, cholecalciferol
phenols, pine oil, Christmas trees boric acid, herbicides (dipyridyl) aminoglycosides and sulfonamides cantharidin plants-Oaks and Red Maple in LA, lilies, grapes, raisins in SA |
|
|
What is the scientific name for tobacco?
|
Nicotiana tabacum
|
|
|
Name 2 toxic principles involved in tobacco
|
nicotine (pyridine alkaloid)
Anabasine (teratogen) |
|
|
What is the mechanism of action of nicotine?
|
mimic ACh at gangli, NMJs and some areas of CNS
-it is a depolarizing ganglionic blocker (first it depolarizes, then it blocks) |
|
|
What are the body systems affected and clinical signs associated with ingestion of tobacco?
|
CNS, Cardiovascular
excitation, hyperactivity, shake, shiver, twitch nausea, vomit, diarrhea, urinate, lacrimate decreased HR initially then increases with blockade, pulse will be weak and thready respiration will go from rapid and shallow to very slow to DEAD |
|
|
What are some differential diagnoses for Tobacco poisoning?
|
strychnine, roquefortine, OP's Carbamates
|
|
|
What is phoradendron flavescens and where is it found?
|
mistletoe
parasatizes oak and walnut trees |
|
|
What is the toxic principle of mistletoe?
|
-sympathomimetic amines like tyramine, choline, and B-phenylethylamine
-oxytocin-like substance (indian abortifactant) PHORATOXIN(toxalbumin)-GI irritant |
|
|
What body system is affected and what are some clinical signs?
|
GI
vomiting, diarrhea, colic, bradycardia |
|
|
How would you treat mistletoe toxicity?
|
fluids and electrolytes are the most important
can give atropine for bradycardie lavage and give activated charcoal |
|
|
What is the toxic principle of Poinsettas?
|
euphorbin-irritant in juice or sap that irritates GI tract and may irritate eyes
|
|
|
What is the scientific name for Holly?
|
Ilex opaca
|
|
|
What is the toxic principle of Ilex opaca and in what part of the plant is it found?
|
Glucosidic saponins in all parts of the plant
some caffeine and theobromine |
|
|
What body system is affected by Holly toxicity and what are some clinical signs?
|
GI
salivation, vomiting, diarrhea shake head and smack lip (it burns!) |
|
|
What is the scientific name for the destroying angel mushroom and what toxins does it contain?
|
Amanita phalloides
AMANITINS and Phalloidins(these are destroyed by stomach acid) |
|
|
What do Amanitins and Phalloidins do to the body?
|
alpha and beta amanitins are cyclic polypeptide alkaloids which are potent liver and kidney toxins
-inhibit nuclear RNA polymerase II-inhibits protein synth at ribosomes-cell dies |
|
|
What body systems are involved in cyclopeptide Amanita toxicity and what are clinical signs?
|
GI, liver, kidney
initial-violent vomiting, diarrhea (may be bloody), abdominal cramps, these signs improve in 60 hours 3-5 days after ingestion-signs of severe liver and kidney failure-animal dies from severe hypoglycemia |
|
|
Name the 4 groups of mushrooms involved in toxicities
|
1. cyclopeptides
2. muscarinic 3. isoxazoles 4. Psilocybin and Psilosin |
|
|
Name 4 differentials for Cyclopeptide mushroom toxicity
(ie: GI with liver) |
blue green algae
cycad palm aflotoxins acetaminophen |
|
|
How would you treat Amanitin toxicity?
|
emesis and lavage
multiple doses of activated charcoal (every 2-6 hours) fluids and electrolytes treat for liver insufficiency-plasma extenders, whole blood, dextrose, low protein diet Pen G may reduce uptake of amatoxins |
|
|
What are some examples of muscarinic mushrooms and what is their toxic principle?
|
Amanita muscaria (fly mushroom)
Inocybe and Clitocybe (more toxic) Muscarine-acts like acetylcholine but is uncontrolled since Acetylcholinesterase cannot break it down |
|
|
What body systems are affected and what are the clinical signs of muscarine?
|
GI and ANS
SLUD constricted pupils, bradycardia abdominal pain-intestinal spasms |
|
|
How would you treat a toxicosis caused by muscarinic mushrooms?
|
early oral decontamination
atropine-counteract secretions and bradycardia |
|
|
What 2 catagories of mushrooms does the fly mushroom fit into?
|
isoxazoles and muscarinic mushrooms
|
|
|
What 2 mushrooms fit into the isoxazole group?
|
amanita pantherina
amanita muscaria-fly mushroom |
|
|
What are the toxic principles in isoxazole mushrooms and what are their actions?
|
ibotenic acid-mimics glutamate(excitatory)
muscimol-GABA-A aganist-acts like a dose of Diazepam, decreases motor activity and causes ataxia |
|
|
What body systems are involved in isoxazole mushroom toxicity and what are some clinical signs?
|
CNS
chewing movements, miosis, opisthotonus, seizures, paddling, resp depression, coma |
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How would you treat an isoxazole mushroom toxicity?
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agressive oral decontamination and supportive care
-Diazepam or barbiturates for seizures, may need ventilatory support |
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What are the hallucinogenic or sacred mushrooms called?
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Psilocybe and Paneolus
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What is the toxic principle of Psilocybe and Paneolus?
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Psilocybin which is metabolized to Psilosin
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What is the mechanism of action of Psilosin and what are some clinical signs?
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psilosin acts like serotonin and stimulates 5-HT2 receptors
it is psychoactive (hallucinogenic) ataxia, vocalization, aggression, nystagmus increased HR, BP, and tem mydriasis, tremors or mild seizures but no coma |
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name the three cardiac glycosides
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foxglove-digitalis
lilies of the valley-convallaria oleander-nerium |
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What part of the cardiac glycoside plants are toxic?
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all parts are fairly potent
oleander is THE WORST |
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What is the mechanism of action of cardiac glycosides
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cause cardiac arrhythmias due to incomplete AV block (changes Na-K ATPase in cell membrane)
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What body systems are involved in cardiac glycoside toxicity?
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CV, GI
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What is the onset time and course of action of cardiac glycosides?
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fast!
onset 30 min-3hrs initially GI then CV |
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How would you treat a cardiac glycoside toxicity?
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GI detox-emesis, lavage, activated charcoal, saline cathartic
supportive care-mnitor serum K, ECG -lidocaine/phenytoin for arrhythmias f-fluids and electrolytes -digibind for severe cases-antibody prep |
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What is the difference between venom and poison?
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venom is injected while poison is from contact
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What are the three classes of constituents in venoms and poisons and give an example of each
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low molecular weight substances-prostaglandins and biogenic amines(histamine)-->mediators of allergy, inflammation and pain
peptides-neurotoxins, anticoagulants, antigens -enzymes-hyaluronidase, phospholipases, thrombin-like enzymes, collagenase, proteases |
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How would you treat a reaction brought on by a sting from a member of Hymenoptera?
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antihistamines-stop release of new histamine
glucocorticoids-open bronchiole tree sympathomimetics-epinephrine |
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What is transmitted through a ticks saliva to the host to cause tick paralysis
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holocyclotoxin (neurotoxin)
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What are some differential diagnoses for tick paralysis?
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botulism
OP induced delayed neuropathy |
