cardiotoxicity Flashcards

1
Q

Ld 50 of Caffeine, theophylline and
theobromine - methylxanthines in dogs

A

300mg/kg

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2
Q

LD50 due to Caffeine, theophylline and
theobromine - methylxanthines in cats

A

200mg/kg

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3
Q

cardiac dearangements due to macrolids

A
  • ECG changes (QT prolongation)
  • Myocardial damage
  • Generates oxidative stress
  • Also seen with fluoroquinolones and ketolides
  • Prolongation of cardiac repolarisation and sudden death syndrome
    • Ventricle fibrillation
    • Prevalence in animals (dogs) is not known
    • Cardiotoxicity of cytostatic agents
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4
Q

discuss pathogenesis of macrolids in cardiotoxicity

A
  • HERG block leading to
  • increased action potential duration, EADs and heterogenecity of repolirization
  • leading to qt prolongation
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5
Q

explain how monensim works in cows

A
  • it is a cocciciostants
  • Slow release devices (rumen bolus) or in feed medication
  • Carboxylic ionophores exert antimicrobial activity (grampositivebacteria) - microbiological NOEL
  • In the rumen:
    • Reduction of gram-positive bacteria and acetic acid
    • and butyric acid producing bacteria
    • Promotion of propionic acid producing gram negative bacteria
  • leading to Increased feed utility - treatment of rumen acidosis and ketosis
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6
Q

Carboxylic ionophores: causing cellular alkolosis

describe their mechanism ie movement of electolytes

A

monensin

NA into the cell

K and H out of cell

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7
Q

Carboxylic ionophores: causing cellular acidity

describe their mechanism ie movement of electolytes

A
  • Salimomycin
  • narasin
  • k out
  • h in
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8
Q

mechanism for inophores

A

increase influx of ca into the cell

leading to increased mm necrosis

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9
Q

cs of coccidostatics

A
  • In several animal species:
    • anorexia, diarrhoea, depression,
    • hypoactivity/reluctance to move,
    • dyspnea, leg weakness, ataxia
    • and recumbency
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10
Q

tx for coccidiostatics

A

Treatment:

  • no antidote
  • Feedchange,
  • adherence to species restrictions
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11
Q

histological lesion of monensin intoxication in horse

A
  • Infiltration of neutrophils and
  • lymphocytes in necrotic muscle fibers
  • Mitochondrial swelling/disrupted christae.
  • Myelin figures and lipid vesicles
  • Cellular (myocyte) necrosis. Ruptured fibres,
  • hypercontraction bundles
  • Inflammatory reaction: macrophage invasion
  • Tissue fibrosis - chronic heart failure
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12
Q

clinical signs of ionophore
intoxications

A
  • Anorexia
  • Diarrhea (monensin and
  • lasalocid)
  • Depression
  • Hypo-activity
  • Reduced feed conversion
  • Dyspnea
  • Leg weakness
  • Ataxia, recumbency
  • Growth depression
  • Drop in egg production
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13
Q

which lesions do u see in horses due to ionophore/coccidostats

A

cardiac lesions

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14
Q

which animal show the most muscle lesions due to ionophores

A

Muscle lesions: sheep > pigs > dogs > cattle > horses

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15
Q

cs of monensin in humans

A
  • they take them to increase mm mass
  • Sickness, nausea, abdominal pain,
    myoglobinuria, weakness, severe muscle pain,
    tachycardia
  • Death after 6 days: acute rhabdomyolysis & renal
    failure
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16
Q

lab findings for monensia

A
  • increased mm enzyms
  • CK 233.200 U/L (ref range < 80U/L)
  • LDH 13.100 U/L (ref range 240-480 U/L)
  • Creatinine 2,0 mg/dL (ref range 0,2-1,4 mg/dL)
17
Q

which drugs prevents monensin demythylation through drug to drug interaction

A

drugs that inhibit cyp3A

they will inhibit monensin as well

and the drug will

18
Q

which drugs reduce tolerance for monencin

A
  • tiamulin,
    macrolides
  • and fluoroquinolones
19
Q

this drug cause death in chicken when combined with monencin

A
  • tiamulin and monensin
20
Q

this drug cause death in pigs when combined with monencin

A

valnemulin and monensin