Term
| Which of the following are clinical signs of grape poisoning in dogs? |
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Definition
a. increase in BUN, Creatinine and ALT
b. ataxia, weakness, vomiting and diarrhea
c. decreased urine output
d. increased urine output
e. a, b, d
f. a, b, c |
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Term
| What are the histologic findings in a dog with grape poisoning? |
|
Definition
a. Brownish-yellowing crystals in renal pelvis
b. acute tubular necrosis of the prox. convoluted tubules
c. acute tubular necrosis of the distal tubules
d. erythema of serosa and mucosa
e. multifocal small red intestinal foci
f. all except h
g. all except c
h. fibrinous thickening of the splenic capsule |
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Term
| What is the possible proposed mechanisms for grape poisoning in dogs? |
|
Definition
a. nephrotoxicity
b. tannins
c. pesticides
d. heavy metals
e. glucose overload
f. excesss vitamin D
g. hypovolemic shock
h. renal ischemia
i. all of the above |
|
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Term
| These plants have neurologic, cardiac and hematologic effect? |
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Definition
| Ericcaeae (heath/heather family), Solanaceae (Night-shade family), Proteaceae (macadamia nuts), Cardiac glycoside containing plants, Taxaceae (Yew family), Alliaceae (Allium spp.) |
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Term
| Members of the Ericaceae that produce the grayanotoxins: |
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Definition
| Ericaceae family: Kalmia (laurel, lambkill, calfkill) and Rhododentron |
|
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Term
| Range and Habitat of Ericaceae: |
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Definition
Natural: Woods/ mountains of SE Applachia to Mid-atlantic coast;
Cultivated: mild temperate climates esp. Rododendron and Azalea |
|
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Term
| What is the function of the Grayanotoxin? |
|
Definition
Affects calcium channels
Neurotoxin |
|
|
Term
| Rhododendron spp. toxic characteristics |
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Definition
| All parts of plant is toxic esp. the foliage. 2-3 leaves=SEVERE toxicosis |
|
|
Term
| What seasons are most common for rhododendron toxicosis? |
|
Definition
| Winter and early spring (no other forage available) |
|
|
Term
| What is another name for grayanotoxin produced by rhododendron and how does it work? |
|
Definition
| Andromedotoxin: affects Na channels--binds and blocks inactivation of Na channels leading to a prolonged depolarization and excitation |
|
|
Term
| What are the clinical signs of grayanotoxin? |
|
Definition
| Salivation, oral irritation, V/D, weakness, incoordination, paralysis, impaired vision, lack of PLR, bradycardia, hypotension (vasodilation), +/- heart block, dyspnea, Depressiong, Prostration |
|
|
Term
| What is the therapy for grayanotoxin ingestion? |
|
Definition
| Early: Emesis, AC lavage following by a cathartic, atropine, other supporting therapy |
|
|
Term
| Name cause of toxicosis that can be treated using atropine: |
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Definition
|
|
Term
Onset of death from grayanotoxin is:
a. 6-12 hours
b. 12-24
c. 18-36 |
|
Definition
|
|
Term
| Solanaceae (nightshade) Family |
|
Definition
Datura stramonium (Jimson weed)
Mandragora officinarum (Mandrake)
Atropa belladona (deadly nightshade)
Nicotiana (Tobaccco) |
|
|
Term
| What is the common name for Jimsom weed (Datura stramonium)? |
|
Definition
| Angel's Trumpet: 2-5 feet with irregular toothed leaves. Seeds are small, rough dark brown |
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|
Term
| What species are affected by datura stramonium? |
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Definition
| All with pigs and horses most severe |
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|
Term
| What is the toxic principle behind datura stramonium (angels trumpet)? |
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Definition
| Tropane alkaloid (anticholinergic effects at muscarinic receptor in CNS) |
|
|
Term
| Datura stramonium clinical signs are: |
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Definition
| Appears like an atropine overdose: mydriasis (dilated pupil), blindess, dry mouth, thirst, paralytic ileus, bloat/colic, urine retention |
|
|
Term
| Name 2 plants with similar affects of Datura stramonium: |
|
Definition
| Mandragora officinarum and atropa belladona: both inhibit AcH |
|
|
Term
| Name a plant with the opposite affect as Datura stramonium: |
|
Definition
|
|
Term
| What is the toxic range of macadamian nuts? |
|
Definition
| 2.5-20 g/kg. 10 fold difference of dose associated with toxicity |
|
|
Term
| What is the toxic principle of Macadamian nuts? |
|
Definition
| Unknown. Doesn't kill animals--- |
|
|
Term
| What are the clinical signs for macadamian nut toxicity? |
|
Definition
| Paralysis/paresis (reversible), tremors. Hindlimbs are more commonly affected |
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|
Term
Which of the following are clinical pathologies of macadamian nut toxicity?
a. increased triglycerides at 4-6 hours post ingestion
b. lipase peaks at 12 hours post exposure
c. lipase peaks 24 hours post exposure
d. Amylase increase
e. Increase in triglycerides 8-12 hours post ingestion. |
|
Definition
a. increased triglycerides at 4-6 hours post ingestion
c. lipase peaks 24 hours post exposure |
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|
Term
| Name the plant sources of cardiac glycoside poisoning? |
|
Definition
Nerium oleander (oleander)
digitalis purpurea (foxglove)
Convallaria majalis (lily of the valley) |
|
|
Term
| What is the common name for the taxus spp.? |
|
Definition
|
|
Term
|
Definition
North America
small, flat, ianceolate leaves and seed cones with a fleshy covering |
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|
Term
| True or false. Toxic alkaloids from the taxus spp. exist in all parts of the plant: bark, leaves, seeds and aril |
|
Definition
| False. The do not exist in the aril. |
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|
Term
| True or false> The Yew is a cardiac glycoside |
|
Definition
| False. It is a cardiotoxin but not a cardiac glycoside. |
|
|
Term
All of the following are clinical signs of taxus ingestion except:
Bradycardia
Dyspnea
Fatigue
Collapse
Coma
Diarrhea
Vomiting +/-
Acute Death
Coma lasting several days |
|
Definition
| All but the coma lasting several days. This is an acute situation. |
|
|
Term
| How do you diagnosis taxus poisoning? |
|
Definition
| Clinical signs and the leaves may be present in the GI tract at post mortem |
|
|
Term
| What is the treatment for taxus spp.? |
|
Definition
| No specific therapy: supportive |
|
|
Term
| Name the common species of allium |
|
Definition
Allium cepa (onion)
Allium sativum (garlic)
Allium porrum (leek)
Allium schoenoprasum (chive) |
|
|
Term
| T or F. Allium causes n-succinyl disulfide bonds. |
|
Definition
| False. Cuases n-propyl disulfide bonds in RBCs resulting in heinz bodies, eccentrocytes and acute hemolysis and eccentrocytes |
|
|
Term
| Clincical signs associated with allium: |
|
Definition
| Weakness, tachypnea, icterus, anemia, hemoglobinuria |
|
|
Term
| Liver enzyme depleted by allium toxicosis |
|
Definition
| Glutathionone reductase. Allium is an oxidant and this liver enzyme helps reduce the oxidants. |
|
|
Term
| Name the plants that have primarily GI effects |
|
Definition
| Araceae (insoluble oxalates), Euphorbiaceae (toxalbumins, viscaceae |
|
|
Term
| T or F. Araceae has pre-formed crystals and on contact with mucus membranes cause irritation: Primarily local effects |
|
Definition
|
|
Term
| T or F: Araceae can be lethal. |
|
Definition
|
|
Term
| Name the members of the Araceae family |
|
Definition
Dieffenbachia: Dubmcane
Philodendron: Philodendron
Monstera: Ceriman; split leaf philodenran
Alocasia antiquorum or Colocasia--Elephant's Ear
Zantedeschia aethiopica: Calla Lily, arum lily
Spathiphyllum: Peace Lilly
Cladium: Caladium (also called elephan'ts ear) |
|
|
Term
| T or F. Araceae spp. are in the lily family |
|
Definition
|
|
Term
| What parts of the Araceae are toxic? |
|
Definition
| All parts are poisonous but the leaves are less often |
|
|
Term
| What is the mechanism behind the Araceae toxicosis? |
|
Definition
| Calcium oxalate crystals (preformed) are main problem. Also trigger the release of kinins and histamines: mechanical damage to mouth/mm |
|
|
Term
| T or F: Dubmcane has contractile cells called idioblasts |
|
Definition
| True. AKA Dieffenbachia contain oxalate crystals (raphides) in a gel matrix and when broken they release oxalate crystals. Like needles piercing through the tissues |
|
|
Term
| Name the clinical signs of Araceae: |
|
Definition
| pain/iritation upon chewing, headshaking, intense salivation, swelling of mm, dyspnea, Nausea/Vomiting, Diarrhea, 2cd dehydration/electrolyte imbalance and shock |
|
|
Term
| T or F. Arrhythmia, mydriasis, coma and death are common outcomes from Araceae poisoning. |
|
Definition
|
|
Term
| What is the treatment for Araceae? |
|
Definition
Rinse mouth, AC, Oral Calcium (milk/yogurt: percipitate any soluble oxalates), Histamines, symptomatic/supportive care, If V/D: give IV fluids
Signs subside after 2-4 hours of treatment but may persist for several days. |
|
|
Term
| name the members of the Euphorbiaceae Family |
|
Definition
Spurge Family
Ricinus communis
Euphorbia pulcherrima |
|
|
Term
| Name the phytotoxins associated with Euphorbiaceae Family |
|
Definition
Diterpine esters
Alkaloids
Glycosides
Lectins |
|
|
Term
| What is the other name for the Castor bean? |
|
Definition
Ricinus (tick) communis
Habitat: semi-tropical |
|
|
Term
| T or F. One can swallow a castor seed and be fine. |
|
Definition
| T. The degree of crushing is important for the release of the toxalbumin/lectin toxin |
|
|
Term
| T or F. The castor bean is one of the most toxic compounds of plants origin. |
|
Definition
| True. beans at 0.2% BW may cause toxicosis |
|
|
Term
| T or F. Castor oil contains ricin |
|
Definition
|
|
Term
| Describe the mech. of action for ricinus communis |
|
Definition
Two glycoprotein chains (A and B)
B chain: binds to galactoside-containing proteins on cell surface facilitating internalization
A chain: enters the ER and depurinates the 28S rRNA (inhibits protein synthesis) |
|
|
Term
| T or F. Acute toxicosis occurs with Ricinus communis |
|
Definition
| False. Takes a few hours to days. Characteristic lag period (think protein synthesis) |
|
|
Term
| Clinical signs of Ricinus |
|
Definition
| Vomiting with blood and diarrhea (often blood with tenesmus and abd. pain). Lesions: catarrhal to hemorrhagic gastroenteritis; petechial hemrrhages on serosal surfaces, necrotizing enteritis, edematous mesenteric ln. |
|
|
Term
| How do you diagnosis ricinus communis? |
|
Definition
| Hx of exposure, leukocytosis, increase ALT, alkaloids (ricinine) in gastric contents via LC/MS |
|
|
Term
| What is the specific antidotes for ricinus? |
|
Definition
| None. Supportive care. poor prognosis if well masticated/large quant. consumed or small animal |
|
|
Term
| Name the species in the Spurges family |
|
Definition
Euphorbia
E. pulcherrima-Poinsettia
E. marginata-Snow on the mountain
E. nutans-Spotted spurge |
|
|
Term
| Plants causing physical damage |
|
Definition
Nettle (urica and Laportea)
Poaceae ( Grass family: setaria, hordeum, cenchrus)
Cactaceae |
|
|
Term
| Name the most common route of exposure in small animals of common household products |
|
Definition
oral (69%)
Combo of oral and dermal (21%) |
|
|
Term
| Most common toxicant in SA from ASPCA Poison Control Center in 2011 |
|
Definition
Human prescription drugs 21%
Human OTC 15%
Chocolate 14%
Household Productions 9% |
|
|
Term
| 2008 Most common Toxins in SA from ASPCA |
|
Definition
| Human Meds, Insecticide, Foods, Rodenticides, Vet Meds, then Plants |
|
|
Term
|
Definition
- Time since exposure:dictates decontam
- Deter,ome time to clinical signs onset (depends on toxicant, dose, species)--guides monitoring/obs. period
-Time since clinical signs |
|
|
Term
| What percentage of permanent Antifreeze is EG? |
|
Definition
| 95% however it is diluted with 50%$ water for use in engines |
|
|
Term
| What is the mortality rate of EG ingestion? |
|
Definition
75%
used as malicious poisoning |
|
|
Term
| Toxic doses for Cats and Dogs, Cattle |
|
Definition
Cats: 1.5 ml EG/kg
Dogs 4.6 mL EG/kg
Death in 12 hours from 9.5 mL/kg
Cattle: 6-10 ml/kg |
|
|
Term
| T or F. Reaches peak levels in blood 1-4hrs and causes mild CNS intoxication |
|
Definition
|
|
Term
| EG is rapidly metabolized by liver enzymes by: |
|
Definition
alcohol dehydrogenase to toxic organic acids----acidosis
Hypocalcemia
Ca Oxalate crystals in kidneys |
|
|
Term
| T or F: The half life of EG is approx. 3 hrs. |
|
Definition
|
|
Term
| Describe the stages of EG toxicity |
|
Definition
Acute: 30-12 hrs
Vomiting, ataxia, depression, PU/PD
Renal Stage (12-24-72 hrs)-cats on the earlier side dogs on the later side: vomiting, ataxia, depression, PU/PD |
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