vitamin-k-semiquinone-radical and Cat-Diseases

This article focuses on the 3 most commonly used rodenticide types: anticoagulants, bromethalin, and cholecalciferol. It is important to verify the active ingredient in any rodenticide exposure. Many owners use the term D-con to refer to any rodenticide regardless of the brand or type of rodenticide. The Environmental Protection Agency released their final ruling on rodenticide risk mitigation measures in 2008 and all products sold had to be compliant by June 2011, changing to consumer products containing either first-generation anticoagulants or nonanticoagulants, including bromethalin and cholecalciferol. These regulations have caused an increase in the number of bromethalin and cholecalciferol cases.

Topics: Aniline Compounds; Animals; Anticoagulants; Antidotes; Cat Diseases; Cats; Cholecalciferol; Dog Diseases; Dogs; Rodenticides; Vitamin K

Acute liver injury and acute liver failure are syndromes characterized by a rapid loss of functional hepatocytes in a patient with no evidence of pre-existing liver disease. A variety of inciting causes have been identified, including toxic, infectious, neoplastic, and drug-induced causes. This article reviews the pathophysiology and clinical approach to the acute liver injury/acute liver failure patient, with a particular emphasis on the diagnostic evaluation and care in the acute setting.

Topics: Animals; Cat Diseases; Cats; Chemical and Drug Induced Liver Injury; Diet Therapy; Dog Diseases; Dogs; Liver Failure, Acute; Prognosis; Vitamin K

The mechanism of toxicity and agents of anticoagulant rodenticides are discussed. The diagnosis of anticoagulant poisoning is outlined and discussed by applying clinical, laboratory, and therapeutic response measures as a means to confirm poisoning. Additional therapeutic concerns and newly developed diagnostic tests are discussed. Application of the therapeutic and diagnostic measures provides a successful plan to manage anticoagulant poisonings.

Topics: Animals; Anticoagulants; Cat Diseases; Cats; Dog Diseases; Dogs; Rodenticides; Vitamin K

A Somali cat was presented with recurrent anorexia, lethargy, vomiting and icterus. A macrocytic-hypochromic, regenerative haemolytic anaemia was identified and hereditary pyruvate kinase deficiency was confirmed by means of breed-specific DNA mutation analysis. The case was complicated by the presence of markedly elevated serum liver enzyme activities, hyperbilirubinaemia, coagulopathy and ultrasonographic evidence of gall bladder choleliths and extrahepatic bile duct obstruction. The choleliths consisted of 100 per cent bilirubin, likely because of chronic haemolysis and haeme degradation. In conclusion, haemosiderosis and bilirubin cholelithiasis can be a consequence of chronic haemolysis in pyruvate kinase-deficient cats, as seen in human beings with a variety of chronic haemolytic disorders.

Topics: Anemia, Hemolytic; Animals; Belgium; Bilirubin; Cat Diseases; Cats; Cholelithiasis; Euthanasia, Animal; Female; Hemosiderosis; Pyruvate Kinase; Radiography; Splenomegaly; Vitamin K

Clinical features were evaluated in seven adult cats (six males, one female) with haemorrhage and presumptive anticoagulant rodenticide intoxication. Haemorrhage appeared as thoracic haemorrhage, otic bleeding, haematoma, melena, haematochezia, and petechiation. The most common other presenting signs were lethargy, anorexia, and tachypnoea or dyspnoea. Six cats were anaemic, four cats were mildly thrombocytopenic (58000-161000/ microL), and three had slightly decreased plasma protein or albumin values. The prothrombin time (30.3->100 s, reference range: 16.5-27.5 s) and activated partial thromboplastin time values (32.6->100 s; reference range: 14-25 s) were markedly prolonged in all cats. All cats received vitamin K(1)subcutaneously or orally (3.7-5 mg/kg body weight initially) and depending on severity of signs five cats were transfused with fresh whole blood. Plasma coagulation times improved in all cats and returned to normal in 1-5 days. Rodenticide poisons represent an important but relatively rare cause of haemorrhage in cats and can be effectively treated.

Topics: Administration, Oral; Animals; Anticoagulants; Cat Diseases; Cats; Female; Germany; Hemorrhage; Injections, Subcutaneous; Male; Partial Thromboplastin Time; Poisoning; Prothrombin Time; Radiography; Records; Retrospective Studies; Rodentia; Rodenticides; Vitamin K

Severe congenital deficiency of factor X was diagnosed in a 3-year-old castrated male domestic shorthair cat with clinical signs of generalized seizures and prolonged bleeding after venipuncture. Heritability of factor X deficiency was suspected because of a prolonged Russell's viper venom time in the dam and reductions in factor X activity in the dam and 1 sibling. To our knowledge, factor X deficiency in cats has not been reported previously. Definitive diagnosis for animals with clinical signs of coagulopathy may require repetition of coagulation screening tests using different assay methods or specific coagulation factor analyses.

Topics: Animals; Blood Coagulation; Cat Diseases; Cats; Factor X; Factor X Deficiency; Male; Partial Thromboplastin Time; Prothrombin Time; Vitamin K

Deficiencies of the vitamin K-dependent coagulation factors were identified in a Devon rex cat which had bled after castration. Haemorrhage was controlled by plasma transfusion. Clotting times were normalised by oral administration of vitamin K. This report confirms the existence of this bleeding disorder in a Devon rex cat in the United Kingdom.

Topics: Administration, Oral; Animals; Blood Coagulation; Blood Coagulation Disorders; Blood Coagulation Factors; Castration; Cat Diseases; Cats; Hemorrhage; Male; Partial Thromboplastin Time; Postoperative Complications; Prothrombin Time; Vitamin K; Vitamin K Deficiency

Two Devon Rex cats from the same litter, which had no evidence of liver disease, malabsorption of vitamin K or chronic ingestion of coumarin derivatives, were found to have plasma deficiencies of factors II, VII, IX and X. Oral treatment with vitamin K1 resulted in the normalization of these coagulation factors. After taking liver biopsies it was demonstrated that the coagulation abnormality was accompanied by a defective gamma-glutamyl-carboxylase, which had a decreased affinity for both vitamin K hydroquinone and propeptide. This observation prompted us to study in a well-defined in vitro system the possible allosteric interaction between the propeptide binding site and the vitamin K hydroquinone binding site on carboxylase. It was shown that by the binding of a propeptide-containing substrate to gamma-glutamylcarboxylase the apparent KM for vitamin K hydroquinone is decreased about 20-fold. On the basis of these in vitro data the observed defect in the Devon Rex cats can be fully explained.

Topics: Amino Acid Sequence; Animals; Blood Coagulation Disorders; Carbon-Carbon Ligases; Cat Diseases; Cats; Factor X; Kinetics; Ligases; Liver; Molecular Sequence Data; Peptides; Prothrombin; Substrate Specificity; Vitamin K

A coagulopathy attributable to a deficiency of vitamin K-dependent clotting factors (II, VII, IX, and X) was diagnosed in 3 Devon Rex cats. There was no evidence for exposure to vitamin-antagonist-related rodenticides. The cats did not have evidence of hepatic disease, gastrointestinal disease, or fat malassimilation. Oral treatment with vitamin K1 resulted in normalization of clotting factor concentrations. However, when treatment was discontinued in 2 cats, prothrombin and activated partial thromboplastin values became prolonged again, although the cats did not have clinical signs of a bleeding disorder.

Topics: Animals; Blood Coagulation Disorders; Breeding; Cat Diseases; Cats; Factor VII Deficiency; Factor X Deficiency; Female; Hemophilia B; Hypoprothrombinemias; Male; Partial Thromboplastin Time; Pedigree; Prothrombin; Prothrombin Time; Vitamin K; Vitamin K Deficiency