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103 Cards in this Set
- Front
- Back
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What are the 9 essential metals with potential for toxicity?
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Chromium, cobalt, copper, iron, magnesium, manganese, molybdenum, selenium, and zinc
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What are the 5 essential metals with important toxic implications in Vet Med?
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Copper, iron, molybdenum, selenium, and zinc
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What are "non-essential" metals?
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Metals that have no known biological function
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What are 6 important non-essential metals in vet med?
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Arsenic, beryllium, cadmium, lead, mercury, nickel
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What are the 3 most important non-essential metals in vet med?
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Arsenic, lead, and mercury
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What are metal-binding proteins called?
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Metallothioneins
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What are glycoproteins important for iron transport called?
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Transferrin
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What is the storage protein for iron?
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Ferritin
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What converts ferrous to ferric iron?
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Ceruloplasmin
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What is the essential trace nutrient that forms ternary complex with insulin receptors facilitating attachment of insulin?
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Chromium
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Supplementing cattle's diet with chromium when they are travel-stressed significantly decreases _________ and increases ____________
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Decreases serum cortison
Increases serum immunoglobulins |
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What is cobalamin (form of Cobalt) required for?
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It is an essential component of vitamin B12 required for the production of RBCs and prevention of pernicious anemia
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What is copper a/w with in all living cells?
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Oxidative processes
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What are 3 types of copper metalloenzymes?
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Type A oxidases, Type B monamine oxidases, and superoxide dismutase
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What is the role of Type A oxidases?
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i.e. Lysyl oxidase plays major role in elastin and collagen synthesis
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What is the role of Type B monamine oxidases?
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i.e. Cytochrome c-oxidase catalyzes a key reaction in energy metabolism
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What is the role of superoxide dismutase?
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Scavenges superoxide radicals reducing them to H2O2
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Most iron is bound to ________
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Hemoglobin
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What form of iron binds to molecular oxygen?
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Ferrous (Fe2+)
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What does iron deficiency cause?
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Anemia, impaired intellectual development, decreased resistance to infections, and possibly increased susceptibility to lead & cadmium toxicity
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Magnesium is a cofactor many enzymes, including key enzymes in the ________ cycle, converting ________ to __________
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Glycolytic cycle, converting glucose to pyruvate
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What does magnesium deficiency lead to?
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Neuromuscular irritability, tetany, and seizures
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Manganese is a cofactor for a number of enzymatic reactions, particularly those involved in which 3 things?
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Phosphorylation, cholesterol, and fatty acid synthesis
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What does manganese deficiency lead to?
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Impaired growth, skeletal abnormalities, and disturbed repro. function
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Molybdenum is a component of xanthine oxidase, which has a role in ________ metabolism
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Purine
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Molybdenum deficiency is synonymous with ___________ toxicity as these 2 metals have an inverse relationship
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Copper (Molyb. deficiency = copper toxicity & Molyb. toxicity = copper deficiency)
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What is selenium a/w in RBC's?
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Glutathione peroxidase and enzyme of the antioxidant defense system
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Selenium is also found in type 1 idothyronine deiodinase which catalyzes the conversion of ______ to ____
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T4 to T3
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What does selenium deficiency cause?
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Causes white muscle disease in lambds and calves, which is a form of nutritional muscular dystrophy
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Zinc is required as a cofactor for more than 200 ____________
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Metalloenzymes
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What are the 6 major categories of metalloenzymes that require zinc as a cofactor?
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Oxidoreductases, transferasres, hydrolases, lyases, isomerases, ligases
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What are some other roles of zinc?
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Essential for the development and normal function of the nervous system, has a role in immune function and cytokines, and also in membrane stabilization of proteins and lipids
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What does zinc deficiency cause?
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Impaired growth, delayed sexual maturation, increases susceptibility to infections, impaired healing, loss of hair, etc.
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What is the major storage organ for copper toxicity?
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Liver
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What happens once the liver reaches it's limit of copper? (in ruminants)
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Hepatic necrosis ensues and it releases copper into systemic circulation, where it has a strong oxidizing effect on RBCs and hemoglobin
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What is the difference b/w copper toxicity in ruminants vs. in dogs?
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Ruminants have a finite amount that causes toxicity. Oversupplementing causes acute toxicity.
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Where exactly does the copper accumulate?
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In the lysosomes in the hepatocytes in the liver.
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What is the CS seen once the copper enters the systemic circulation?
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Hemoglobinuria b/c RBC's and hemoglobin are being lysed
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What is the hallmark sign of copper toxicity? (at necropsy)
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Gun-metal blue kidneys
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Will goats most likely have chronic or acute copper tox.?
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Chronic
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How do dogs deal with copper toxicity? (what happens in their body?)
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They will stop absorbing the copper once the level is high and start excreting it. They can accumulate much more than ruminants.
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What will copper tox. cause in dogs?
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Slow insidious liver failure
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What does iron tox. initially cause? And what does it ultimately lead to?
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Initial necrosis of GI mucosa. Ultimately, multi-system organ failure and cardiovascular collapse.
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What does selenium toxicity cause (at the molecular level)?
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Acute poisoning may deplete intermediate substrates such as glutathione and S-adenosylmethionine, disrupting their enzyme activities. Production of free radicals. Replacement of Se in place of Sulfure in proteins disrupting normal fxn
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What are CS and lesions seen with selenium tox.?
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Petechial hemorrhages on myocardium, pulmonary edema, tetanic spasms, sudden death after acute toxic exposures
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What are the signs most commonly seen in dogs and pigs with zinc tox.?
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Severe intravascular hemolysis and gastroenteritis
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What is the possible zinc tox. mechanism?
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Mechanism not well understood. May be due to excess zinc interfering with copper and iron storage and utilization.
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What does arsenic tox. cause at a molecular level?
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Inhibit cellular respiration by binding to sulfhydryl compounds (tissue resp. enzyme)
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What are the signs seen with arsenic tox.?
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Severe gastroenteritis and neurological signs related to cellular energy depletion
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What are the mechanisms of lead tox.?
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Binds to cellular & enzymatic sulfhydryl groups, which results in inactivation of enzymes involved in heme synthesis. Also competes w/ca++ ions, which alters nerve & muscle transmission. Also inhibits membrane-associated enzymes & alters vit D metabolism.
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What are the signs of lead tox.?
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Depression, behavior changes, anemia, ataxia, tremors, seizures, sudden death
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What are the mechanisms of mercury tox.?
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Inorganic Hg causes direct tissue necrosis & renal tubular necrosis. Organic Hg interfere w/ metabolic activity & prevent synthesis of essential proteins, which leads to cellular degeneration & necrosis.
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Characteristics of clostridium?
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Gram-positive
Facultative anaerobe Rods Sporulating |
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Clostridium - exogenous or endogenous?
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Both (most commonly in soil when exogenous and often from intestinal tract when endogenous)
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What is a prophylactic measure to clostridial diseases?
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Vaccination with bacterin-toxoids or toxoids
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What are the 3 pathotypes of Clostridium?
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Neurotoxic, histotoxic, and enteric
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What pathotype is Clostridium perfingens?
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Enteric
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What are the 2 types of C. perfingens that affect goats?
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Type C & D
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Which type of C. perfingens are newborn animals most typically susceptible to?
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Type C
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What CS are seen with infection of neonatal calves, lambs, and goats with type C?
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Hemorrhagic necrotic enteritis, enterotoxemia, nervous signs, tetany, opisthtonos
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What can incite multiplication of type C in the abomasum and small intestine?
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Damage to GI mucosa, often by poor quality feed
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C. perfingens type D affects sheep of all ages except _________
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Neonates
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What does C. perfingens type D cause?
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Enterotoxemia, sudden death, overeating
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Rapid multiplication of type D and production of E-toxin are favored by excess dietary _______ in the small intestine
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Starch
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What are the effects of E-toxin on the CNS and other tissues?
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Sudden death, preceded in some cases by CS such as opisthotonos and convulsions, with agonal struggling
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What is a hallmark lesion of type D enterotoxemia?
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Pulpy kidney (but not usually in goats)
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What are some signs of enterotoxemia in sheep & goats?
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Off feed, lethargic, kicking @ belly, lying on side, panting, crying out, diarrhea, opisthotonos, death
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Tx. for enterotoxemia?
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Not successful in severe cases: IV fluids, antibiotic therapy, oxygen, analgesics
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Prevention of enterotoxemia?
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3-way vaccine of C. perfingens type C & D and C. tetani
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What causes chronic passive congestion?
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Systemic obstruction at vena cava in the diaphragm or mediastinum can affect hepatic outflow and systemic venous return. Right-sided heart failure elevated pressure w/in the caudal vena cava. Endocardiosis can also lead to it.
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How does chronic passive congestion affect the liver histologically?
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Will initially cause distention of central veins and centrilobular sinusoids. Persisten centrilobular hypoxia leads to atrophy of loss of hepatocytes and eventually centrilobular fibrosis.
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What would the liver look like with acute congestion?
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Slightly enlarged, blood flowing freely form any cut surface, intrinsic lobular pattern may be slightly more pronounced (mainly on cut surface) due to the centrilobular areas being congested
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What would the liver look like with chronic congestion?
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Diffusely enlarged, rounded edges, focal fibrous thickening of capsule, lobular pattern is enhanced, "nutmeg liver"
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What are some sources of copper toxicity?
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Lack of molybdenum in diet, excess copper in diet, fungicides can cause accumulation in soil, algaecides can cause accumulation in water
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How does copper get to the kidneys?
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Excess copper is absorbed by the kidney (primarily by liver, but then by kidney)
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What is the suggested copper:molybdenum ratio in ruminants' diet?
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6:1 to 10:1
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Which animals are most sensitive to copper?
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Sheep
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When are CS seen in sheep & ruminants with copper tox.?
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When animal becomes stressed
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What CS are seen in sheep and ruminants with copper tox.?
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Massive liver necrosis, intravascular hemolysis of RBC (hemoglobinuria, icterus), anorexia, death, elevated liver enzymes
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What lesions are seen in sheep with copper tox.?
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Hemoglobinuria, dark red to bluish-black kidneys, swollen friable liver
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How can copper toxicity be treated?
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Often unsuccessful --> aim to reduce liver copper levels. Use ammonium molybdate, sodium thiosulfate, &/or D-penicillamine.
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What's an autogenous vaccine?
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Vaccines made from bacteria isolated from a specific herd
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What is the largest gland in the body?
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Liver
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Where should a liver biopsy been done on a goat?
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On the right 9th intercostal space
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What is Ivermectin's MOA?
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Action on GABA &/or glutamate-gated chloride channels induces reduction of motor activity & paralysis
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What type of parasites will Ivermectin affect?
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Insects, ascarids, and nematodes
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How does Ivermectin kill parasites?
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Paralyzes pharyngeal pump and parasite dies due to lack of nutrients. It also reduces egg prod. by female
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What is thiamine hydrochloride?
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Pharmaceutical form of thiamine (vitamin B1)
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What would thiamine deficiency cause in goats?
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Polioencephalomalacia
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How do ruminants get thiamine?
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Microbes naturally produce it
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What is thiamine deficiency in ruminants called?
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Poliencephalomalacia (PEM)
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What animals are most affected by thiamine deficiency?
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Cattle, sheep, and less commonly, goats
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What are some indicators a/w PEM?
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Sudden changes in diet, feeds high in molasses, moldy hay, rumen acidosis, and dietary stress of weaning
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How does PEM (neuronal swelling occur)?
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Energy production in the neurons is impaired due to the pentose phosphate pathway being impeded. Cellular osmotic gradients cannot be maintained and neuronal swelling results in PEM.
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What are the gross lesions seen with PEM?
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Cerebral edema, brain herniation if severe, yellow discoloration of cerebrocortical gray matter, edematous separation and necrosis, atrophy of gyri
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What are CS of PEM?
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Depression, stupor, ataxia, head pressing, apparent cortical blindness, dorsomedial strabismus, opisthotonos, convulsions, and recumbency w/ paddling & death
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How is thiamine deficiency treated?
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Thiamine replacement at 10 mg/kg for 2 days. Cerebral edema can be reduced with furosamide, mannitol, or dexamethasone.
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What is penicillamine?
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A chelating agent (forms stable water-soluble complexes that are excreted by the kidneys)
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What is penicillamine used for?
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Copper-storage associated hepatopathies, lead & mercury toxicities
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Besides getting rid of metals, what else is penicillamine good for?
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It is anti-fibrotic & inhibits collagen cross-linking, promoting its degradation. It is also anti-rheumatic, which improves lymphocyte function. Also combines with cysteine to form complex that is readily excreted (to treat cystine urolithiasis).
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What is the withdrawal time for penicillamine?
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Milk - min. 3 days
Meat - 21 days |
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In what species is penicillamine used for cystine urolithiasis?
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Dogs
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In what species is penicillamine used only for lead poisoning?
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Birds and cats
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