Other Toxins Flashcards
Possible complications of Rattlesnake envenomation
Thrombocytopenia
Prolongation of clotting times
Anemia (hemolysis +/- blood loss)
Myocardial damage
Cantharidin toxicosis pathogenesis
Causes irritation to the mucous membranes
Interferes with family of enzymes— phosphoprotein phosphatases
Horses with cantharidin toxicosis develop signs of:
- GI disease (colic, diarrhea)
- Urinary system disease (renal failures, cystitis)
- Cardiac disease (arrhythmias)
Which spp are most susceptible to copper toxicosis?
Sheep
Which dietary supplements reduce ruminant copper accumulation?
Dietary molybdenum, sulfur, zinc & iron
Sheep diet concentration greater than what ratio makes them susceptible to copper poisoning
Copper to molybdenum ratio: greater than 10:1
Pathogenesis of copper toxicosis
Absorption, binding to albumin & transcuprein proteins
—> transport to liver
—-binds to ceruloplasmin (hepatic metalloprotein)
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
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
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
Mercury causes 2 clinical syndromes (depending on its form)
- Acute poisoning from inorganic mercury salts
2. Chronic neurologic damage from organomercurials
Acute inorganic mercury toxicosis causes
Ulceration of the mouth, esophagus & remainder of GI tract — diarrhea/anorexia Anorexia Gastroenteritis Wt loss Acute nephrosis/nephritis Alopecia
Organic mercury fungicides & methyl mercurycauses
Brain damage
Blindness
Incoordination
Proprioceptive deficits
Intravenous doxycycline causes
Supraventricular tachycardia Systemic arterial hypertension Discomfort Collapse Death
Most common adverse reactions of enrofloxacin in horses includes
Mild diarrhea
Neurologic signs
Orthopedic disorders in young animals
Beta adrenergic receptor agonists at high doses cause what clinical signs
Nervousness
Mild agitation
Sweating
Increased heart rate
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:
- Inadequate or improper feed mixing
- Error in calculating the amount for inclusion in feed
- Inadequate adaptation to NPN
- Inclusion in carbohydrate deficient rations
- 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
- History & clinical signs consistent with the toxicosis
- Response of animals to treatment with atropine
- Determining cholinesterase inhibition (whole blood, retina, brain), corresponding with adverse clinical effects
- Detection of the insecticide in biological tissues (GI contents or tissues)
