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Veterinary Toxicology > Integumentary System Toxicology > Flashcards

Integumentary System Toxicology Flashcards

1
Q

What are the 2 pathways of toxicant absorption through the skin?

A
  1. transappendageal - through hair follicles
  2. epidermal
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2
Q

What are the 4 oxidation states of selenium?

A
  1. -2 = selenides
  2. 0 = elemental
  3. +4 = selenites
  4. +6 = selenates
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3
Q

Why is selenium an essential nutrient? What roles does it play?

A

component of >30 selenoproteins

  • iodothyronine deiodinases: activates/deactivates thyroid hormones
  • glutathione peroxidase, thioredoxin reductase: oxidative stress defense

immune function, reproduction, biotransformation reactions, neurotransmitter turnover

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4
Q

What are the 3 major plant sources of selenium?

A
  1. obligate indicators - require high concentrations of Se to grow (woody aster, goldenweed, prince’s plume, locoweeds)
  2. facultative indicators - survive in high Se and accumulate high levels, but do not require high levels to grow (other asters, saltbush, ironweed, snakeweed)
  3. non-accumulators - other plants that grow on seleniferous soils
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5
Q

Why is Canadian maritime province soil deficient in selenium? Where are levels high?

A

acidic soil renders Se unavailable

western Canada, AZ, CO, SD, ND, ID, KS, NE, NV, NM, UT due to low rainfall and alkaline soils

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6
Q

What is a common cause of iatrogenic selenium toxicity? What are 2 other additional (rare) causes?

A

Se use for prevention of musculoskeletal disorders (white muscle disease)

  1. errors in food formulation
  2. mine wastes from cooper or silver mines
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7
Q

Where is selenium absorbed? How does absorption vary based on chemical form?

A

duodenum (some jejunum and ileum)

  • elemental Se = low absortion
  • selenomethionine, selenocysteine, selenite = high absorption
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8
Q

How are selenite, selenate, selenomethionine, and selenocysteine absorbed?

A

passive diffusion via brush-border membranes

sodium cotransport system

SM/SC = amino acid transport mechanisms

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9
Q

How is selenium mostly eliminated? What is indicative of this?

A

urine (+ feces, expired air)

garlic odor due to dimethylselenide

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10
Q

What are the 3 mechanisms of toxicity selenium? What cells are most susceptible? What does this lead to?

A
  1. reacts with thiols leading to generation of ROS, oxidative stress, and cellular damage (lipid peroxidation)
  2. depletes GSH and S-adenosylmethionine
  3. replaces sulfur in proteins, impairing enzyme activity and cellular function (decreases cell division and growth)

keratinocytes and sulfur-containing keratin —> weakening of hooves and hair

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11
Q

What mechanisms of toxicity of selenium were noted in birds and swine?

A

BIRDS = embryotoxicity due to DNA and RNA polymerase inhibition

SWINE = focal symmetrical poliomyelomalacia of ventral horns of the spinal cord

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12
Q

What species are most susceptible to selenium toxicity? What are some clinical signs of acute selenosis?

A

horses

  • depression, weakness, anorexia
  • dyspnea, cyanosis
  • garlicky odor (dimethylselenide) to breat
  • nasal discharge, salivation, teeth grinding
  • watery diarry
  • incoordination, sweating, tachycardia, tetanic spasms
  • dog-sitting (pigs)
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13
Q

In what species does subchronic selenosis occur? What are some clinical signs?

A

pigs —> symmetrical poliomyelomalacia

  • ataxia, posterior paralysis
  • quadriplegia, sternal recumbency
  • coronary band separation
  • alopecia
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14
Q

What species commonly develop chronic selenosis (alkali disease)? What are some clinical signs? What is not seen?

A

cattle, horses (also sheep, pigs, poultry)

  • lameness (animals graze on knees)
  • hair loss in tail and mane
  • horn and hoof deformities (horizontal rings and cracks)
  • vitality, anemia, joint stiffness

anorexia

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15
Q

How are waterfowl and poultry affected by selenium toxicity? What are 3 common manifestations?

A

teratogenesis

  1. underdeveloped feet
  2. underdeveloped or missing lower/upper beaks
  3. underdeveloped or missing eyes
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16
Q

How is acute selenium toxicosis treated?

A
  • terminate exposure
  • IV fluids, oxygen, ventilation
  • administer vitamin E or N-acetylcysteine
  • treat symptoms
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17
Q

How is chronic selenium toxicosis treated? How should the diet be altered?

A
  • ARSENIC SALT to accelerate biliary excretion in poultry, cattle, and pigs
  • selenium antagonists

provide Se-deficient rations with increased proteins to bind free Se

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18
Q

What are the 2 major functions of molybdenum?

A
  1. component of metalloenzymes responsible for purine metabolism, uric acid (antioxidant) production, sulfur-containing amino acids metabolism, and drug/toxicant metabolism —> xanthine oxidase/dehydrogenase, aldehyde oxidase, sulfide oxidase
  2. binds to alpha-macroglobulin on RBC membranes to enhance resistance to rupture
19
Q

What are 3 major sources of molybdenum? When does toxicosis occur?

A
  1. naturally found in copper, lead, and tungsten ores
  2. combustion of fossil fuels
  3. in high amounts in the soil and forage in FL, OR, NV, and CA, where Mo fertilizers are used to increase nitrogen fixation in legumes, and pastures near production plants

if copper deficiency is present

20
Q

What commonly competitively inhibits molybdenum uptake? In what 3 ways is it commonly excreted?

A

sulfate —> shares a common transport pathway in the intestine and kidney

  1. bile - cattle
  2. urine - lab animals
  3. milk - ruminants
21
Q

In what species is molybdenum toxicosis most common? What factor drives toxicosis?

A

ruminants, especially cattle (and younger animals)

dietary Cu:Mo ratio (4:1 or 10:1) —> high dietary sulfur levels exacerbate toxicity because it decreases Cu absorption

22
Q

What is the three-way interaction of Mo-Cu-S?

A
  1. dietary S is converted to sulfide in the rumen, which bind Cu, decreasing its absorption (increased Mo in diet increases conversion)
  2. Mo and S form thiomolybdates in the rumen that bind Cu, making it insoluble and decreases absorption
  3. when rumen Cu is low, thiomolybdates are absorbed and impair systemic Cu metabolism by increasing/urinary loss of Cu and depleting activities of Cu-dependent enzyes
23
Q

What Cu-dependent enzymes are typically affected by molybdenum toxicity? What are 2 results?

A
  • ceruloplasmin: Cu-transport and Fe metabolism
  • lysyl oxidase: collagen synthesis
  • tyrosinase: melanin synthesis
  • cytochrome C oxidase: mitochondrial electron transport (aerobic metabolism)
  • dopamine-beta-hydroxylase: catecholamine metabolism
  • superoxide dismutase: oxidant defense
  1. impairment of myeline maintenance and function = enzootic ataxia in lambs
  2. alteration of Zn metabolism
24
Q

In what species is acute molybdenum toxicosis most common? What are the main clinical signs? Lesions?

A

cattle and sheep

  • feed withdrawal, lethargy weakness
  • hind limb ataxia progresses to front, recumbency
  • profuse salivation, ocular discharge, mucoid feces

hydropic degeneration of hepatocytes and renal tubules

25
Q

What are the main 5 clinical signs of chronic molybdenum toxicosis?

A
  1. severe, persistent diarrhea (peat scours) - green, liquid feces containing gas bubbles
  2. achromotrichia and alopecia due to tyrosinase depletion that reduces melanin synthesis
  3. emaciation, decreased milk production, delayed puberty, bone fractures, lameness, limb deformities, muscular degeneration
  4. swayback/enzootic ataxia in lambs with stiff backs and legs making it difficult to rise
  5. microcytic hypochromic anemia
26
Q

What is important in the diagnosis of suspected molybdenum toxicosis? How is it diagnosed?

A

distinguishing between primary copper deficiency and secondary copper deficiency related to excessive molybdenum exposure

  • clinical signs in a herd and concentrations of Mo in blood, liver, and kidneys
  • levels of Cu and Mo in feeds/forages
  • levels of Cu and Mo in tissues (poor correlation between tissue levels of Cu and clinical disease)
27
Q

What are the 3 major differentials to rule out for molybdenum toxicosis?

A
  1. emaciation or unthriftiness - parasites, selenosis, fluorosis, ergotism
  2. diarrhea - metal poisonings, GI infections
  3. lameness or bone abnormalities - fluorosis, selenosis, ergotism, lead poisoning
28
Q

What are the 2 major treatments for molybdenum toxicosis?

A
  1. addition of Cu to diets to achiecve 4:1 to 10:1 Cu:Mo ratio (additional Cu necessary to counter S effects - S:Mo should be <100:1)
  2. administer Cu - injectable copper glycinate or copper edetate (Cu-EDTA)
29
Q

What is photosensitization? What are the 4 classifications?

A

abnormal sensitivity of the skin to UV light common in herbivores (NOT SUNBURN)

  • TYPE I = primary*
  • TYPE II = aberrant endogenous pigment synthesis (porphyria)
  • TYPE III = secondary/hepatogenous*
  • TYPE IV = idiopathic
30
Q

What is the pathogenesis of photosensitization?

A
  • photodynamic compounds in nonpigmented skin are activated by UV absorption, leading to higher energy states and reactions with biological substrates or molecular oxygen and production of ROS
  • ROS cause oxidative damage of macromolecules and organelles
  • damage results in increased permeability and release of lytic enzymes and cytoplasmic extrusion
  • edema, cell death, ulceration with superficial blood vessels and epidermis as the primary targets —> skin sloughs off
31
Q

What is primary photosensitization? How can it be chemically induced?

A

photodynamic compounds are ingested, injected, or absorbed through the skin and react with light in non-pigmented skin to cause severe dermatitis

  • phenothiazines in antipsychotics and antihistamines
  • polycyclic aromatic hydrocarbons
  • sulfonamides
  • tetracyclines
  • antifungals
  • NSAIDs
32
Q

What 3 plants cause primary photosensitization? What are the toxic principles?

A
  1. Fagopyrum esculentum (buckwheat) - fagopyrin
  2. Hypericum perforatum (St. John’s wort) - hypericin
  3. Ammi majus (bishop’s weed) - furnocoumarins (seeds are most phototoxic)
33
Q

What causes aberrant pigment metabolism? In what animals does this cause photosensitization?

A

porphyrin arises from inherited or acquired defective functions of enzymes involved in heme synthesis (TYPE II)

cattle and cats - congenital erythropoietic porphyria, bovine erythropoietic protoporphyria

34
Q

What causes secondary/hepatogenous photosensitization (III)? In what animals is this most common?

A

phylloerythrin, a microbial breakdown product of chlorophyll in the GIT —> hepatic disease/dysfunction or biliary occlusion prevents its excretion, causing concentrations in circulation to increase, reach the skin, and activate by light

livestock —> poor prognosis

35
Q

What 2 plants most commonly cause secondary/hepatogenous photosensitization? What species are most affected? What is the toxic principle?

A
  1. Panicum virgatum (switch/panic grass) - sheep, lithogenic saponin (diosgenin)
  2. Agave (lecheguilla) - goats and sheep, diosgenin
36
Q

What additional 2 plants also contain diosgenin?

A
  1. puncture vine (Tribulus terrestris)
  2. beargrass (Nolina texana)

(secondary/hepatogenous photosensitization - III)

37
Q

What skin areas are most commonly affected by photosensitization?

A

areas of little to no hair and light-colored skin

  • lips, nose, eyes, coronary bands
  • white skin on face, back, and legs
  • udders, teats, tongue
  • severe phylloerythrinemia and bright sunlight can induce lesions in black-coated animals
38
Q

What are the initial and later clinical signs of photosensitization? What is commonly seen in the hepatogenous form?

A
  • INITIAL: photophobia, excessive tearing, swelling, redness, increased sensitivity of nonpigmented skin
  • LATER: pruritis, blisters, ulceration, exudation, scabs, cutaneous edema, fissuring epithelium, sloughing of non-pigmented skin, secondary bacterial infection, licking behavior (cattle, sheep, deer) results in glossitis, corneal edema, and blindness

signs of liver disease - icterus

39
Q

Photosensitization:

A
40
Q

Photosensitization, sheep:

A

whole body can be affected if it has recently been sheared

41
Q

What causes facial eczema during photosensitization?

A

mycotoxin sporidesmin produces severe cholangitis and pericholangitis, which leads to biliary obstruction and restriction of phylloerythrin excretion

42
Q

How is photosensitization diagnosed? How can Type II and Type III be diagnosed?

A
  • history or evidence of exposure to photosensitizing agents or hepatotoxins
  • clinical signs/lesions restricted to lightly pigmented areas with sparse hair cover
  • liver serum enzymes

TYPE II = porphyria levels in blood, feces, and urine, signalment, clinical signs

TYPE III = liver serum enzymes and histologic signs of liver disease

43
Q

How is photosensitization treated?

A
  • provide ample shape/sheltering
  • grazing only allowed in darkness
  • parenteral corticosteroids
  • basic wound management: lavage, debridement, closure, and antibiotics to avoid secondary bacterial infections

Veterinary Toxicology (29 decks)

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