Exam 2: Plants affecting the liver and integument Flashcards
Know the 3 major categories of photosensitization
Primary photosensitization: Photodynamic compound in plant absorbed during digestion or direct contact with skin
Secondary photosensitization: Diseased liver is unable to appropriately metabolize phylloerythrin (from chlorophyll) and it causes photosensitization
(Parenchymal liver disease, Biliary liver disease)
**Congenital defects in porphyrin metabolism
**
What are clinical signs of photosensitization?
Photophobia, Excessive Tearing. Swelling, redness, increase in sensitivity of non-pigmented skin, ooze serum Around lips, Eyes, Ears, Coronary band of hooves. Hair and skin slough leaving ulcerated areas.
How do primary photosensitizers cause these clinical signs?
Primary photosensitization develops when animals eat plants containing pigments (polyphenolic compounds) which are readily absorbed from the gastrointestinal tract and accumulate in the skin.
Familiarize yourself with images of the 5 primary photosensitizing plants in powerpoint.
st johns wart
buckwheat
bishops weed
spring parsley
cow parsnip
Define Hepatobiliary or secondary photosensitization.
Diseased liver is unable to appropriately metabolize phylloerythrin (from chlorophyll) and it causes photosensitization
(Parenchymal liver disease, Biliary liver disease)
What toxic alkaloid most commonly causes hepatotoxicity leading to secondary photosensitization?
Secondary or hepatogenous photosensitization in animals occurs more commonly than primary photosensitization. Liver disease, the underlying cause of secondary photosensitivity, results from ingestion of plants containing compounds toxic to the liver.
A variety of hepatotoxic compounds are found in plants, the most important of which are pyrrolizidine alkaloids (PA) These are found principally in the plant families Asteraceae, Boraginaceae, and Fabaceae.
What is the mechanism of action for this toxin (alsike clover, red clover) and why does this lead to photosensitizaton?
Biliary occlusion blocks the normal elimination route of phylloerythrin, a breakdown product of chlorophyll, through excretion in the bile. Phylloerythrin then accumulates in the blood where it circulates through the skin causing oxidative cellular damage when it is exposed to ultraviolet light. The resulting intense inflammatory response is most severe in the non-pigmented skin.
What are clinical/diagnostic signs for PA induced toxicity?
Symptoms of Liver Failure: Jaundice
Abdominal distension
Abnormal copper accumulation
Diarrhea, tenesmus, Rectal prolapse
Weight Loss
Abnormal Neurological signs of hepatic encephalopathy:
Yawning
Drowsiness
Aimless wandering
Head pressing
Dermatitis nonpigmented skin
Familiarize yourself with 5 PA containing plants in powerpoint.
Groundsel, tansy ragwort
Senecio species (Packera spp.), Asteraceae Family
Hounds tongue
Cynoglossum officinale
Heliotropium europaeum
Fiddle Neck Amsinckia spp. Boraginaceae
Crotolaria spp. Rattlepod
How do steroidal sapogenins contribute to secondary photosensitization?
Form crystalloid material blocking biliary system
Insoluble crystalloid substance in bile duct
What are 4 plants that produce steroidal sapogenins in powerpoint?
Agave lecheguilla
Bear grass
Nolina texana
Lantana
Lantana camara
puncture vine, goat’s head
What congenital conditions could be a differential diagnosis for primary and secondary photosensitization.
Congenital disease:
Aberrant Porphyrin Metabolism (Type II)
Congenital Porphyria
cattle, pigs, cats, and humans
Defective hemoglobin formation results in production of an excess of Type I porphyrins due to deficiency of Uroporphyrinogen III cosynthetase
Autosomal recessive
Protoporphyria
Clinical Signs
Excess of coproporphyrin I and uroporphyrin I colors urine amber or reddish brown.
Bones, urine, and teeth (especially the deciduous teeth) fluoresce pink when irradiated with near-ultraviolet light.
Prolonged exposure to sunlight causes photosensitization with hyperemia, vesicle formation, and superficial necrosis of unpigmented portions of the skin.
Name plant recently associated with acute hepatoxicity from contaminated hay
Carboxyatractyloside: cocklebur
