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Toxicology > Other Toxins > Flashcards

Other Toxins Flashcards

1
Q

Possible complications of Rattlesnake envenomation

A

Thrombocytopenia
Prolongation of clotting times
Anemia (hemolysis +/- blood loss)
Myocardial damage

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2
Q

Cantharidin toxicosis pathogenesis

A

Causes irritation to the mucous membranes

Interferes with family of enzymes— phosphoprotein phosphatases

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3
Q

Horses with cantharidin toxicosis develop signs of:

A
  1. GI disease (colic, diarrhea)
  2. Urinary system disease (renal failures, cystitis)
  3. Cardiac disease (arrhythmias)
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4
Q

Which spp are most susceptible to copper toxicosis?

A

Sheep

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5
Q

Which dietary supplements reduce ruminant copper accumulation?

A

Dietary molybdenum, sulfur, zinc & iron

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6
Q

Sheep diet concentration greater than what ratio makes them susceptible to copper poisoning

A

Copper to molybdenum ratio: greater than 10:1

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7
Q

Pathogenesis of copper toxicosis

A

Absorption, binding to albumin & transcuprein proteins
—> transport to liver
—-binds to ceruloplasmin (hepatic metalloprotein)

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8
Q

Effects of copper tox on the liver

A

Necrosis of liver parenchymal cells
Swelling of kupffer cells
—> followed by sudden spontaneous or stress-related release of copper into bloodstream

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9
Q

Acute phase of copper toxicosis results in

A 
Reduce blood glutathione
Increase RBC fragility
Hemoglobin oxidation
Methemoglobin formation
—> resulting IV hemolysis leads to anemia, icterus & hemoglobinuric nephrosis
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10
Q

Gross lesions of Copper toxicosis

A

Liver: yellow & friable, larger/smaller than normal
Spleen: enlarged & congested
Kidney: hemoglobin casts in tubules cause kidneys to appear dk red or blue-black

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11
Q

Mercury causes 2 clinical syndromes (depending on its form)

A
  1. Acute poisoning from inorganic mercury salts

2. Chronic neurologic damage from organomercurials

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12
Q

Acute inorganic mercury toxicosis causes

A 
Ulceration of the mouth, esophagus & remainder of GI tract
— diarrhea/anorexia
Anorexia
Gastroenteritis
Wt loss 
Acute nephrosis/nephritis
Alopecia
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13
Q

Organic mercury fungicides & methyl mercurycauses

A

Brain damage
Blindness
Incoordination
Proprioceptive deficits

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14
Q

Intravenous doxycycline causes

A 
Supraventricular tachycardia
Systemic arterial hypertension
Discomfort
Collapse
Death
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15
Q

Most common adverse reactions of enrofloxacin in horses includes

A

Mild diarrhea
Neurologic signs
Orthopedic disorders in young animals

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16
Q

Beta adrenergic receptor agonists at high doses cause what clinical signs

A

Nervousness
Mild agitation
Sweating
Increased heart rate

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17
Q

Examples of blood doping agents

A

Erythropoietin & Darbepoetin

18
Q

Dimethyl sulfoxide (DMSO) at concentrations greater than 50% results in

A

Severe hemolysis

19
Q

Diocytl sodium succinate (or Docusate) negative side effects

A 
Agitation
Abdominal pain
Dehydration
Watery diarrhea
Intestinal mucosal damage
Collapse
Death
20
Q

Horses at higher risk for developing negative side effects of lidocaine

A

Geriatric
Neonatal horses
Horses with hypoproteinemia

21
Q

Clinical signs of menadione sodium bisulfide (vitamin K3) in horses

A 
Weakness
Stiffness
Colic
Laminitis
Depressed appetite

clinical signs occur in 4 to 48 hours

22
Q

Menadione sodium bisulfide (vitamin K3) can be a cause of

A

Acute tubular necrosis

—azotemia, proteinuria, hematuria, hyperkalemia, hypochloremia, hyponatremia

23
Q

Nonprotein nitrogen (NPN) is converted by ruminal bacteria to

A

Ammonia
— by enzyme urease
— used for bacteria protein synthesis — dep on available carbohydrate source

24
Q

What is the most commonly used form of NPN: nonprotein nitrogen

A

Urea

25
Q

NPN-induced ammonia toxicosis usually results from:

A
  1. Inadequate or improper feed mixing
  2. Error in calculating the amount for inclusion in feed
  3. Inadequate adaptation to NPN
  4. Inclusion in carbohydrate deficient rations
  5. Unrestricted consumption of palatable liquid NPN formulations
26
Q

Which body system is the primary target of NPN intoxication

A

CNS

27
Q

Ammonium ion pathogenesis within the CNS

A
  • amino acid disturbances
  • alterations in neurotransmission
  • cerebral energy deficits
  • alteration of nitric oxide syntehsis
  • brain edema
28
Q

Ammonium ion pathogenesis in brain edema

A

Increased astrocyte osmolality & cytotoxic oxidative & nitrosative damage

29
Q

Treatment of hyperammonemia in cattle

A

Administer 20-30 liters of water orally

2-6 liters of vinegar (reduce rumen pH)

30
Q

Ammoniation of feed can lead to

A

Hyper excitability syndrome called bovine bonkers

31
Q

Purpose of ionophores are commonly added to cattle & poultry feed for what purpose?

A

Growth promotant & anti-coccidial properties

32
Q

How do ionophores promote growth in cattle?

A

Result in more prioprionic acid production int eh rumen (which improved feed efficiency)

33
Q

Ionophores pathogenesis

A

Ionophores bind & transport ions across cell & organelle membranes
— direction of movement depends on concentration gradient of particular ion

— at cellular level ionophores affect mitochondrial function & result in loss of aerobic energy production

34
Q

Tetrachlorvinphos (TCVP) is what kind of toxin?

A

Organophosphorus insecticide

— fed to horses, cattle & swine as a pass-through larvicide

35
Q

Tetrachlorvinphos (TCVP) mechanism

A

Cholinesterase inhibitor

**intoxication associated with overstimulation of muscarinic and nicotinic cholinergic receptors

36
Q

Organophosphate & carbamate insecticides inhibit

A

Acetylcholinesterase (AChE) at cholinergic nerve synapses & at. Neuromuscular junctions—> causes acetylcholine to accumulate at nerve junctions & cause excessive synpatic action

37
Q

Acetylcholine is a neurotransmitter at which locations:

A

Postganglionic parasympathetic neurons in smooth mm, cardiac mm, or exocrine glands
Neuromuscular junctions of somatic nervous system
Postganglionic neurons of autonomic nervous system

38
Q

Muscarinic signs include

A

SLUD (salivation, lacrimation, urination & defecation)
—>ptylaism, excessive tracheobronchial secretions & sweating, bronchospasms & laryngospasms, lacrimations, nausea, darrhea, miosis & bradycardia

39
Q

Nicotinic clinical signs

A 
Muscle fasciculations
Tremors
Weakness
Ataxia
Flaccid paralysis
Vomiting
Paralysis of resp muscles
40
Q

Orgranophosphate tox clinical signs

A

Muscarinic signs first,
Then nicotinic signs
CNS effects (hyperactivity & seizures)

41
Q

Diagnosis of OP or carbamate toxicosis includes

A
  1. History & clinical signs consistent with the toxicosis
  2. Response of animals to treatment with atropine
  3. Determining cholinesterase inhibition (whole blood, retina, brain), corresponding with adverse clinical effects
  4. Detection of the insecticide in biological tissues (GI contents or tissues)

Toxicology (5 decks)

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