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Toxicology 5172 (Fall 2014) > L4: CV and Hematopoietic Toxicity (Martyniuk) > Flashcards

L4: CV and Hematopoietic Toxicity (Martyniuk) Flashcards

1
Q

1st generation anticoagulant

A
  • warfarin
  • short half-life (15hr)
  • low potency, requires multiple feedings
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2
Q

2nf generation anticoagulant

A
  • brodifacoum
  • long half-life (20d)
  • high potency, kills in single feeding
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3
Q

anticoagulant MOA

A

inhibits vitamin K epoxide reductase and prevents formation of Vit. K dependent clotting factors
-results in excess inactive vitamin K and inability to clot

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4
Q

CS of anticoagulant

A

(delayed onset as active vitamin K is used up)

-depression, anorexia, anemia initially –> dyspnea, hemorrhage, hematoma, prolonged bleeding

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5
Q

3 most common methods of dx of anticoagulant

A
  • Hx of exposure
  • evidence of coagulopathy
  • response to vitamin K therapy
  • Tests: increased PT or PTT time
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6
Q

Tx of anticoagulant

A

-Recent: emesis, adsorbent, cathartic therapy
-Vit. K administration
+/-transfusion if severe
-2nd generation requires longer tx than 1st generation

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7
Q

nitrate toxicosis source and MOA

A

fertilizers and plants (Johnson grass, lambsquarters, Black nightshade, pigweed)
-converted to nitrite, which causes vasodilation and formation of MetHb

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8
Q

nitrate toxicosis species susceptibility

A

pigs>cattle>sheep>horses

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9
Q

CS of nitrate toxicosis

A

Based on lvl of MetHb:

70% - death

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10
Q

Dx of nitrate toxicosis

A
  • nitrate lvls in feed/water
  • plasma, serum lvls
  • eye post-mortem
  • body cavity smells like ammonia
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11
Q

Tx of nitrate toxicosis

A
  • IV methylene blue for ruminants

- ascorbic acid in cats/horses

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12
Q

cardiac glycosides source

A

avocados
lily of the valley
oleander
foxglove

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13
Q

cardiac glycoside MOA

A

inhibits Na-K ATPase pump through competition w/ K for binding sites –> hyperkalemia, inc. intracellular Na

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14
Q

CS of cardiac glycoside toxicity

A

trembling, staggering, dyspnea

racing heart rate and rhythm/arrythmia, weak pulse

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15
Q

Dx of cardiac glycoside toxicity

A

based on Hx, access, symptoms, analysis of vomit

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16
Q

Tx of cardiac glycoside toxicity

A

GI decon if recent
propranolol to tx arrythmias**
tx hyperkalemia with sodium bicarb, calcium glucamate
Digibind if propanolol ineffective (binds glycosides)

17
Q

cantharidin source

A

blister beetles found in alfalfa
Spanish fly
-usually affects horses

18
Q

cantharidin MOA

A
  • inhibits protein phosphatases

- mucosal irritant

19
Q

CS of cantharidin toxicity

A
  • colic, frequent urination, D contraction with heart beat, shock
  • severe irritation and ulceration of oral, GI, and bladder
  • cardiac toxicity
20
Q

Dx of cantharidin toxicity

A 
alfalfa hay consumption
beetles in hay or stomach
hypocalcemia, inc. BUN
ulceration of mm
cardiac necrosis
21
Q

Tx of cantharidin toxicity

A

GI decon and protection (sucralfate), abx

22
Q

cyanide sources

A 
wild cherry
white clover
fresh Sorghum spp.
fertilizers/pesticides/rodenticides
fumigants
combustion
23
Q

cyanide MOA

A

inhibition of cytochrome oxidase, which prevents cellular aerobic respiration

24
Q

CS of cyanide

A

-sudden death, dyspnea, weakness, tremors

25
Q

Dx of cyanide

A
  • classic: cherry red blood that is slow to clot
  • stomach contents smell like almonds
  • Hx of ingestion
26
Q

Tx of cyanide toxicity

A

-INDUCE MetHb formation with sodium nitrite to bind cyanide
-sodium thiosulfate to inc. form. of thiocyanate, which binds cyanide
+/- tx MetHb with methylene blue

27
Q

methylxanthine source

A

(caffeine, theobromine, theophylline)

chocolate, coffee, meds

28
Q

methylxanthine MOA

A
  • 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.
29
Q

CS of methylxanthine toxicity

A
  • v/d, diuresis
  • hyperactivity
  • panting
  • tachycardia
  • ataxia
  • tremors, seizures
  • coma
  • death from arrythmia/resp. failure
30
Q

Dx of methylxanthine toxicity

A
  • Chem. analysis of stomach contents, plasma, serum, urine or liver
  • theobromine in serum
31
Q

Tx of methylxanthine toxicity

A
  • GI decon (emesis, act. charc.)
  • monitor EKG
  • tx seizures with diazepam or barbiturates
  • maintain resp.
  • fluid diuresis
32
Q

gossypol source

A

pigment glands of cottonseed

  • an oily substance
  • usually requires chronic exposure to cause toxicity
  • non-ruminants more sensitive
33
Q

gossypol MOA

A
  • chelates iron and causes anemia
  • reduces protein availability
  • inhibits dehydrogenases leading to dec. energy and protein production; may also cause oxidative stress
34
Q

CS of gossypol toxicity

A
  • weight loss, weakness, dyspnea
  • edema 2ary to heart failure
  • myocardial necrosis
35
Q

Dx of gossypol toxicity

A
  • Hx of cottonseed ingestion
  • cardiac necrosis, edema, vacuoloization
  • chem. analysis
36
Q

Tx of gossypol toxicity

A

remove source
high protein diet
Vit. A, iron, lysine
tx symptoms

Toxicology 5172 (Fall 2014) (8 decks)

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