L4: CV and Hematopoietic Toxicity (Martyniuk) Flashcards
1st generation anticoagulant
- warfarin
- short half-life (15hr)
- low potency, requires multiple feedings
2nf generation anticoagulant
- brodifacoum
- long half-life (20d)
- high potency, kills in single feeding
anticoagulant MOA
inhibits vitamin K epoxide reductase and prevents formation of Vit. K dependent clotting factors
-results in excess inactive vitamin K and inability to clot
CS of anticoagulant
(delayed onset as active vitamin K is used up)
-depression, anorexia, anemia initially –> dyspnea, hemorrhage, hematoma, prolonged bleeding
3 most common methods of dx of anticoagulant
- Hx of exposure
- evidence of coagulopathy
- response to vitamin K therapy
- Tests: increased PT or PTT time
Tx of anticoagulant
-Recent: emesis, adsorbent, cathartic therapy
-Vit. K administration
+/-transfusion if severe
-2nd generation requires longer tx than 1st generation
nitrate toxicosis source and MOA
fertilizers and plants (Johnson grass, lambsquarters, Black nightshade, pigweed)
-converted to nitrite, which causes vasodilation and formation of MetHb
nitrate toxicosis species susceptibility
pigs>cattle>sheep>horses
CS of nitrate toxicosis
Based on lvl of MetHb:
70% - death
Dx of nitrate toxicosis
- nitrate lvls in feed/water
- plasma, serum lvls
- eye post-mortem
- body cavity smells like ammonia
Tx of nitrate toxicosis
- IV methylene blue for ruminants
- ascorbic acid in cats/horses
cardiac glycosides source
avocados
lily of the valley
oleander
foxglove
cardiac glycoside MOA
inhibits Na-K ATPase pump through competition w/ K for binding sites –> hyperkalemia, inc. intracellular Na
CS of cardiac glycoside toxicity
trembling, staggering, dyspnea
racing heart rate and rhythm/arrythmia, weak pulse
Dx of cardiac glycoside toxicity
based on Hx, access, symptoms, analysis of vomit
Tx of cardiac glycoside toxicity
GI decon if recent
propranolol to tx arrythmias**
tx hyperkalemia with sodium bicarb, calcium glucamate
Digibind if propanolol ineffective (binds glycosides)
cantharidin source
blister beetles found in alfalfa
Spanish fly
-usually affects horses
cantharidin MOA
- inhibits protein phosphatases
- mucosal irritant
CS of cantharidin toxicity
- colic, frequent urination, D contraction with heart beat, shock
- severe irritation and ulceration of oral, GI, and bladder
- cardiac toxicity
Dx of cantharidin toxicity
alfalfa hay consumption beetles in hay or stomach hypocalcemia, inc. BUN ulceration of mm cardiac necrosis
Tx of cantharidin toxicity
GI decon and protection (sucralfate), abx
cyanide sources
wild cherry white clover fresh Sorghum spp. fertilizers/pesticides/rodenticides fumigants combustion
cyanide MOA
inhibition of cytochrome oxidase, which prevents cellular aerobic respiration
CS of cyanide
-sudden death, dyspnea, weakness, tremors
Dx of cyanide
- classic: cherry red blood that is slow to clot
- stomach contents smell like almonds
- Hx of ingestion
Tx of cyanide toxicity
-INDUCE MetHb formation with sodium nitrite to bind cyanide
-sodium thiosulfate to inc. form. of thiocyanate, which binds cyanide
+/- tx MetHb with methylene blue
methylxanthine source
(caffeine, theobromine, theophylline)
chocolate, coffee, meds
methylxanthine MOA
- competitive antagonist of adenosine receptors, which mitigate inhibitory effects –> CNS stimulation, vasodilation, tachycardia
- prevents Ca reuptake –> m. contractility
- inhibits phosphodiesterase, inc. cAMP and GMP conc.
CS of methylxanthine toxicity
- v/d, diuresis
- hyperactivity
- panting
- tachycardia
- ataxia
- tremors, seizures
- coma
- death from arrythmia/resp. failure
Dx of methylxanthine toxicity
- Chem. analysis of stomach contents, plasma, serum, urine or liver
- theobromine in serum
Tx of methylxanthine toxicity
- GI decon (emesis, act. charc.)
- monitor EKG
- tx seizures with diazepam or barbiturates
- maintain resp.
- fluid diuresis
gossypol source
pigment glands of cottonseed
- an oily substance
- usually requires chronic exposure to cause toxicity
- non-ruminants more sensitive
gossypol MOA
- chelates iron and causes anemia
- reduces protein availability
- inhibits dehydrogenases leading to dec. energy and protein production; may also cause oxidative stress
CS of gossypol toxicity
- weight loss, weakness, dyspnea
- edema 2ary to heart failure
- myocardial necrosis
Dx of gossypol toxicity
- Hx of cottonseed ingestion
- cardiac necrosis, edema, vacuoloization
- chem. analysis
Tx of gossypol toxicity
remove source
high protein diet
Vit. A, iron, lysine
tx symptoms
