Other Toxins Flashcards by Cassie Baumgarten

Possible complications of Rattlesnake envenomation

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

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Cantharidin toxicosis pathogenesis

Causes irritation to the mucous membranes

Interferes with family of enzymes— phosphoprotein phosphatases

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Horses with cantharidin toxicosis develop signs of:

GI disease (colic, diarrhea)
Urinary system disease (renal failures, cystitis)
Cardiac disease (arrhythmias)

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Which spp are most susceptible to copper toxicosis?

Sheep

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Which dietary supplements reduce ruminant copper accumulation?

Dietary molybdenum, sulfur, zinc & iron

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

Copper to molybdenum ratio: greater than 10:1

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Pathogenesis of copper toxicosis

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

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Effects of copper tox on the liver

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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Acute phase of copper toxicosis results in

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

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Gross lesions of Copper toxicosis

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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Mercury causes 2 clinical syndromes (depending on its form)

Acute poisoning from inorganic mercury salts

2. Chronic neurologic damage from organomercurials

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Acute inorganic mercury toxicosis causes

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

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Organic mercury fungicides & methyl mercurycauses

Brain damage
Blindness
Incoordination
Proprioceptive deficits

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Intravenous doxycycline causes

Supraventricular tachycardia
Systemic arterial hypertension
Discomfort
Collapse
Death

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Most common adverse reactions of enrofloxacin in horses includes

Mild diarrhea
Neurologic signs
Orthopedic disorders in young animals

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Beta adrenergic receptor agonists at high doses cause what clinical signs

Nervousness
Mild agitation
Sweating
Increased heart rate

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Examples of blood doping agents

Erythropoietin & Darbepoetin

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

Severe hemolysis

Diocytl sodium succinate (or Docusate) negative side effects

Agitation
Abdominal pain
Dehydration
Watery diarrhea
Intestinal mucosal damage
Collapse
Death

Horses at higher risk for developing negative side effects of lidocaine

Geriatric
Neonatal horses
Horses with hypoproteinemia

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

Weakness
Stiffness
Colic
Laminitis
Depressed appetite

clinical signs occur in 4 to 48 hours

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

Acute tubular necrosis

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

Nonprotein nitrogen (NPN) is converted by ruminal bacteria to

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

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

Urea

NPN-induced ammonia toxicosis usually results from:

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

Which body system is the primary target of NPN intoxication

CNS

Ammonium ion pathogenesis within the CNS

- amino acid disturbances - alterations in neurotransmission - cerebral energy deficits - alteration of nitric oxide syntehsis - brain edema

Ammonium ion pathogenesis in brain edema

Increased astrocyte osmolality & cytotoxic oxidative & nitrosative damage

Treatment of hyperammonemia in cattle

Administer 20-30 liters of water orally | 2-6 liters of vinegar (reduce rumen pH)

Ammoniation of feed can lead to

Hyper excitability syndrome called bovine bonkers

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

Growth promotant & anti-coccidial properties

How do ionophores promote growth in cattle?

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

Ionophores pathogenesis

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

Tetrachlorvinphos (TCVP) is what kind of toxin?

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

Tetrachlorvinphos (TCVP) mechanism

Cholinesterase inhibitor | **intoxication associated with overstimulation of muscarinic and nicotinic cholinergic receptors

Organophosphate & carbamate insecticides inhibit

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

Acetylcholine is a neurotransmitter at which locations:

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

Muscarinic signs include

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

Nicotinic clinical signs

``` Muscle fasciculations Tremors Weakness Ataxia Flaccid paralysis Vomiting Paralysis of resp muscles ```

Orgranophosphate tox clinical signs

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

Diagnosis of OP or carbamate toxicosis includes

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)