https://en.wikivet.net/api.php?action=feedcontributions&user=JamesSwann&feedformat=atomWikiVet English - User contributions [en]2024-03-29T12:23:13ZUser contributionsMediaWiki 1.35.0https://en.wikivet.net/index.php?title=Platelet_Abnormalities&diff=90299Platelet Abnormalities2010-09-05T20:42:11Z<p>JamesSwann: /* Clinical Significance */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
[[Platelet|Platelets]] (or thrombocytes) are responsible for primary haemostasis, the formation of a temporary platelet plug that initially seals any breach to a blood vessel wall. These breaches are then sealed more completely by the formation of a fibrin clot mediated by the coagulation factor cascade. <br />
<br />
Bleeding disorders may occur if platelets are deficient ('''thrombocytopaenia''') or if the platelets are unable to function adequately ('''thrombocytopathia'''). [[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]] (ITP) is one common cause of thrombocytopaenia and this may be a primary or secondary disease. '''Thrombocytosis''' refers to an increase in the blood platelet concentration above the normal level.<br />
<br />
Thrombocytopaenia and thrombocytopathia lead to disorders of primary haemostasis but, in general, this is less serious than the disorders of secondary haemostasis caused by deficiencies in the [[Coagulation Factor Deficiency|coagulation factors]]. <br />
<br />
==Thrombocytopaenia==<br />
Thrombocytopaenia is the most common haematological abnormality as platelet numbers are subject to fluctuation in a large number of different diseases. Care should be taken however to ensure that this finding is not caused by an artefact of sampling that leads to the formation of platelet clumps. The normal blood platelet concentration of the dog is 175-500x10^9 but clinical disease is not usually observed until this level falls below 50x10^9 and spontaneous haemorrhage is observed only when the level falls below 20x10^9. Reductions in the number of platelets may be caused by a failure to produce adequate numbers in the bone marrow in the process of megakaryopoiesis, increased destruction of existing platelets or sequestration of platelets outside of the circulation. <br />
*Diseases that cause '''[[Bone Marrow - Anatomy & Physiology|bone marrow]] suppression'''<br />
**'''Aplastic anaemia''' caused by ingestion of bracken or administration of oestrogens, [[Chloramphenicol|chloramphenicol]] or [[Sulphonamides|sulphonamide]] antibiotics. Prolonged use of phenylbutazone or salicylate may cause the same disease.<br />
**'''Infectious diseases''' that reduce stem cell function, including [[Distemper|canine distemper]], [[Canine Parvovirus|canine parvovirus]] and [[Feline Panleucopaenia|feline panleucopaenia virus]].<br />
**'''Myelophthisis''', the displacement of the normal cell lines of the bone marrow by another cell or tissue type may also reduce the function of the megakaryocytes. Possible diseases in this category include '''myelofibrosis''' and '''immunoproliferative''' or '''myeloproliferative''' neoplastic disease.<br />
**'''Radiotherapy''' or myelosuppressive '''chemotherapy''' may cause reversible bone marrow suppression.<br />
*Diseases that cause '''increased destruction of platelets'''<br />
**'''[[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]]''' is a common autoimmune disease that leads to the production of antibodies against platelets and their subsequent destruction by cells of the monocyte phagocyte system (MPS).<br />
**'''Infectious diseases''' that cause destruction of platelets include [[Bovine Viral Diarrhoea Virus|bovine viral diarrhoea]] (BVD), [[Classical Swine Fever|classical swine fever]] and [[Infectious Canine Hepatitis|infectious canine hepatitis]]. The parasites ''[[Ehrlichia platys|Anaplasma platys]]'', ''[[Ehrlichia phagocytophila|Anaplasma phagocytophilum]]'' and ''[[Ehrlichia canis]]'' may also cause infectious thrombocytopaenia. Any severe bacterial infection, including those caused by [[:Category:Staphylococcus species|''Staphylococci'']] and the Gram negative bacteria that produce endotoxin (e.g. [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas spp.'']] or [[Salmonella|''Salmonella spp.'']]) may also result in the destruction of platelets.<br />
*Diseases that cause '''sequestration of platelets''' usually involve some enlargement of the spleen, as this is the major organ where platelets are stored outside of the circulation. Examples include:<br />
**[[Haemangiosarcoma]] of the spleen and liver<br />
**Splenic enlargement under general anaesthesia maintained with agents such as [[Barbiturates|barbiturates]] and [[Phenothiazines|phenothiazines]]<br />
*'''Artefactual''' or spurious thrombocytopaenia<br />
**'''Cavalier King Charles spaniels''' have a relatively small number of giant platelets (macrothrombocytes) but they do not suffer from bleeding disorders as they maintain a similar total platelet mass as do dogs of other breeds.<br />
**If venepuncture is traumatic, '''platelet clumps''' may form and these will not be counted by automated machines. The presence of clumps can be investigated by making a blood smear and examining the feathered edge for large agglomerations of platelets.<br />
<br />
==Thrombocytopathia==<br />
Defects in platelet function may be congenital defects or they may be acquired with a number of diseases. Congenital thrombocytopathias are rare inherited diseases which are characterised by defects in platelet adhesiveness, aggregation or factor release. The defects are usually associated with particular breeds, such as '''Chediak-Higashi syndrome''' in blue smoke Persian cats.<br />
<br />
Causes of acquired thrombocytopathia include:<br />
*Infection with ''[[Angiostrongylus vasorum]]'', the canine lungworm, which also causes a consumptive coagulopathy.<br />
*'''Hypergammaglobulinaemia''' as occurs with multiple myeloma and some forms of (B-cell) lymphoma may affect platelet function.<br />
*Administration of large volumes of some '''[[Colloids|colloid solutions]]'''.<br />
*Administration of certain '''pharmaceutical products''', including [[NSAIDs|non-steroidal anti-inflammatory drugs]] and [[Cephalosporins|cephalosporins]].<br />
<br />
==Thrombocytosis==<br />
Increases in platelets above the normal level may occur due to '''physiological''' or '''pathological''' processes. <br />
*Physiological<br />
**'''Splenic contraction''' pushes sequestered platelets into the circulation. This phenomenon is especially marked in horses which have a muscular splenic capsule. <br />
**'''Splenectomy''' prevents the sequestration of platelets in the spleen, resulting in constantly increased levels of platelets.<br />
**As part of a response to '''[[Anaemia - Introduction|anaemia]]''', a '''reactive thrombocytosis''' is often documented and this may precede signs of regeneration.<br />
*Pathological<br />
**'''Essential thrombocythaemia''' is a rare myeloproliferative disease that results in the excessive production of platelets which function abnormally. Affected animals suffer from bouts of spontaneous haemorrhage.<br />
<br />
==Clinical Significance==<br />
Other than essential thrombocythaemia, thrombocytosis has no clinical importance except as an indicator of another disease process. Thrombocytopaenia and thrombocytopathia both result in reductions in the effectiveness of primary haemostasis, producing bleeding disorders. Since bleeding points are usually sealed by a fibrin clot, disorders of primary haemostasis tend to be less severe than those caused by deficiencies of the coagulation factors. Common signs of a disorder of primary haemostasis include:<br />
*'''Petechial''' or '''ecchymotic''' haemorrhages on the skin or mucous membranes.<br />
*'''Haemorrhages from the mucous membranes''', producing haematuria, haematochezia, haematemesis, haemoptysis and melaena.<br />
*'''[[Anaemia - Introduction|Anaemia]]''' with reactive [[Neutrophilia|neutrophilia]] and [[Monocytosis|monocytosis]] if the haemorrhage is severe.<br />
<br />
Severe platelet deficiencies may be managed with transfusions of whole blood or, in the USA, with transfusions of platelet cryoprecipitate. With both techniques however, it is likely that the transfused platelets have only a short half life in the recipient. <br />
<br />
The use of '''vincristine''' (a drug also used in chemotherapy for neoplasia) has been advocated in cases of thrombocytopaenia as it causes the release of immature platelets from the bone marrow.<br />
<br />
[[Category:Haemorrhagic Diseases]]<br />
[[Category:To Do - James]][[Category:Haematology Changes]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Platelet_Abnormalities&diff=90298Platelet Abnormalities2010-09-05T20:41:47Z<p>JamesSwann: /* Thrombocytosis */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
[[Platelet|Platelets]] (or thrombocytes) are responsible for primary haemostasis, the formation of a temporary platelet plug that initially seals any breach to a blood vessel wall. These breaches are then sealed more completely by the formation of a fibrin clot mediated by the coagulation factor cascade. <br />
<br />
Bleeding disorders may occur if platelets are deficient ('''thrombocytopaenia''') or if the platelets are unable to function adequately ('''thrombocytopathia'''). [[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]] (ITP) is one common cause of thrombocytopaenia and this may be a primary or secondary disease. '''Thrombocytosis''' refers to an increase in the blood platelet concentration above the normal level.<br />
<br />
Thrombocytopaenia and thrombocytopathia lead to disorders of primary haemostasis but, in general, this is less serious than the disorders of secondary haemostasis caused by deficiencies in the [[Coagulation Factor Deficiency|coagulation factors]]. <br />
<br />
==Thrombocytopaenia==<br />
Thrombocytopaenia is the most common haematological abnormality as platelet numbers are subject to fluctuation in a large number of different diseases. Care should be taken however to ensure that this finding is not caused by an artefact of sampling that leads to the formation of platelet clumps. The normal blood platelet concentration of the dog is 175-500x10^9 but clinical disease is not usually observed until this level falls below 50x10^9 and spontaneous haemorrhage is observed only when the level falls below 20x10^9. Reductions in the number of platelets may be caused by a failure to produce adequate numbers in the bone marrow in the process of megakaryopoiesis, increased destruction of existing platelets or sequestration of platelets outside of the circulation. <br />
*Diseases that cause '''[[Bone Marrow - Anatomy & Physiology|bone marrow]] suppression'''<br />
**'''Aplastic anaemia''' caused by ingestion of bracken or administration of oestrogens, [[Chloramphenicol|chloramphenicol]] or [[Sulphonamides|sulphonamide]] antibiotics. Prolonged use of phenylbutazone or salicylate may cause the same disease.<br />
**'''Infectious diseases''' that reduce stem cell function, including [[Distemper|canine distemper]], [[Canine Parvovirus|canine parvovirus]] and [[Feline Panleucopaenia|feline panleucopaenia virus]].<br />
**'''Myelophthisis''', the displacement of the normal cell lines of the bone marrow by another cell or tissue type may also reduce the function of the megakaryocytes. Possible diseases in this category include '''myelofibrosis''' and '''immunoproliferative''' or '''myeloproliferative''' neoplastic disease.<br />
**'''Radiotherapy''' or myelosuppressive '''chemotherapy''' may cause reversible bone marrow suppression.<br />
*Diseases that cause '''increased destruction of platelets'''<br />
**'''[[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]]''' is a common autoimmune disease that leads to the production of antibodies against platelets and their subsequent destruction by cells of the monocyte phagocyte system (MPS).<br />
**'''Infectious diseases''' that cause destruction of platelets include [[Bovine Viral Diarrhoea Virus|bovine viral diarrhoea]] (BVD), [[Classical Swine Fever|classical swine fever]] and [[Infectious Canine Hepatitis|infectious canine hepatitis]]. The parasites ''[[Ehrlichia platys|Anaplasma platys]]'', ''[[Ehrlichia phagocytophila|Anaplasma phagocytophilum]]'' and ''[[Ehrlichia canis]]'' may also cause infectious thrombocytopaenia. Any severe bacterial infection, including those caused by [[:Category:Staphylococcus species|''Staphylococci'']] and the Gram negative bacteria that produce endotoxin (e.g. [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas spp.'']] or [[Salmonella|''Salmonella spp.'']]) may also result in the destruction of platelets.<br />
*Diseases that cause '''sequestration of platelets''' usually involve some enlargement of the spleen, as this is the major organ where platelets are stored outside of the circulation. Examples include:<br />
**[[Haemangiosarcoma]] of the spleen and liver<br />
**Splenic enlargement under general anaesthesia maintained with agents such as [[Barbiturates|barbiturates]] and [[Phenothiazines|phenothiazines]]<br />
*'''Artefactual''' or spurious thrombocytopaenia<br />
**'''Cavalier King Charles spaniels''' have a relatively small number of giant platelets (macrothrombocytes) but they do not suffer from bleeding disorders as they maintain a similar total platelet mass as do dogs of other breeds.<br />
**If venepuncture is traumatic, '''platelet clumps''' may form and these will not be counted by automated machines. The presence of clumps can be investigated by making a blood smear and examining the feathered edge for large agglomerations of platelets.<br />
<br />
==Thrombocytopathia==<br />
Defects in platelet function may be congenital defects or they may be acquired with a number of diseases. Congenital thrombocytopathias are rare inherited diseases which are characterised by defects in platelet adhesiveness, aggregation or factor release. The defects are usually associated with particular breeds, such as '''Chediak-Higashi syndrome''' in blue smoke Persian cats.<br />
<br />
Causes of acquired thrombocytopathia include:<br />
*Infection with ''[[Angiostrongylus vasorum]]'', the canine lungworm, which also causes a consumptive coagulopathy.<br />
*'''Hypergammaglobulinaemia''' as occurs with multiple myeloma and some forms of (B-cell) lymphoma may affect platelet function.<br />
*Administration of large volumes of some '''[[Colloids|colloid solutions]]'''.<br />
*Administration of certain '''pharmaceutical products''', including [[NSAIDs|non-steroidal anti-inflammatory drugs]] and [[Cephalosporins|cephalosporins]].<br />
<br />
==Thrombocytosis==<br />
Increases in platelets above the normal level may occur due to '''physiological''' or '''pathological''' processes. <br />
*Physiological<br />
**'''Splenic contraction''' pushes sequestered platelets into the circulation. This phenomenon is especially marked in horses which have a muscular splenic capsule. <br />
**'''Splenectomy''' prevents the sequestration of platelets in the spleen, resulting in constantly increased levels of platelets.<br />
**As part of a response to '''[[Anaemia - Introduction|anaemia]]''', a '''reactive thrombocytosis''' is often documented and this may precede signs of regeneration.<br />
*Pathological<br />
**'''Essential thrombocythaemia''' is a rare myeloproliferative disease that results in the excessive production of platelets which function abnormally. Affected animals suffer from bouts of spontaneous haemorrhage.<br />
<br />
==Clinical Significance==<br />
Other than essential thrombocythaemia, thrombocytosis has no clinical importance except as an indicator of another disease process. Thrombocytopaenia and thrombocytopathia both result in reductions in the effectiveness of primary haemostasis, producing bleeding disorders. Since bleeding points are usually sealed by a fibrin clot, disorders of primary haemostasis tend to be less severe than those caused by deficiencies of the coagulation factors. Common signs of a disorder of primary haemostasis include:<br />
*'''Petechial''' or '''ecchymotic''' haemorrhages on the skin or mucous membranes.<br />
*'''Haemorrhages from the mucous membranes''', producing haematuria, haematochezia, haematemesis, haemoptysis and melaena.<br />
*'''[[Anaemia – Introduction|Anaemia]]''' with reactive [[Neutrophilia|neutrophilia]] and [[Monocytosis|monocytosis]] if the haemorrhage is severe.<br />
<br />
Severe platelet deficiencies may be managed with transfusions of whole blood or, in the USA, with transfusions of platelet cryoprecipitate. With both techniques however, it is likely that the transfused platelets have only a short half life in the recipient. <br />
<br />
The use of '''vincristine''' (a drug also used in chemotherapy for neoplasia) has been advocated in cases of thrombocytopaenia as it causes the release of immature platelets from the bone marrow.<br />
<br />
[[Category:Haemorrhagic Diseases]]<br />
[[Category:To Do - James]][[Category:Haematology Changes]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_Mediated_Haemolytic_Anaemia&diff=90297Immune Mediated Haemolytic Anaemia2010-09-05T20:39:22Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''IMHA'''<br><br />
'''Autoimmune haemolytic anaemia (AIHA)'''<br><br />
'''Pure red cell aplasia (PRCA)'''<br />
|}<br />
<br />
==Description==<br />
Immune-mediated haemolytic anaemia (IMHA) is the result of a [[Type II Hypersensitivity|type II antibody-mediated immune response]] directed against molecules expressed on the surface of erythrocytes. The clinical presentation of the disease depends on the isotype of antibody produced and the severity of the anaemia.<br />
<br />
[[IgM]] antibodies are capable of fixing complement on the surface of red blood cells leading to the assembly of a membrane attack complex. This complex causes the direct lysis of erythrocytes and '''intravascular haemolysis'''. Since IgM antibodies have a high avidity, they are also able to co-ordinate the formation of large numbers of red blood cells into aggregates, a phenomenon known as '''auto-agglutination'''.<br />
<br />
Some types of [[IgG]] antibody are able to directly activate the complement cascade but, in most cases, these antibodies are not able to cause intravascular haemolysis of agglutination and they are therefore described as '''incomplete''' antibodies. These antibodies act as opsonins and, through their interaction with Fc receptors expressed by cells of the hepatosplenic monocyte-phagocyte system (MPS), they promote the uptake and destruction of the red blood cells to which they are bound. These types of antibody therefore cause '''extravascular haemolysis'''.<br />
<br />
IMHA may occur as a '''primary''' disease with no apparent cause or it may be '''secondary''' to another systemic insult. Possible secondary causes of IMHA include bacterial and parasite infections (including ''[[Babesia canis]]'' in dogs and ''[[Mycoplasma haemofelis]]'' in cats), adverse drug reactions, neoplasia (especially myeloproliferative and lymphoproliferative disease) and live vaccines, although the association between vaccination and immune-mediated disease remains controversial. <br />
<br />
The majority of cases of IMHA affect only the circulating red blood cells resulting in a strongly regenerative anaemia as the bone marrow stem cells respond to the disease. In a small number of cases, antibodies are produced that affect the stem cells of the erythroid lineage in the bone marrow, resulting in a non-regenerative anaemia that still bears many of the same clinical features as IMHA. Although the two diseases have been considered separately in the past, they really represent two ends of a spectrum of immune-mediated disease directed at cells of the erythroid line. <br />
<br />
The widespread lysis of red blood cells causes disease in the following ways:<br />
*Blood '''oxygen carrying capacity''' is greatly reduced causing exercise intolerance, collapse and tissue hypoxia.<br />
*The release of '''endogenous procoagulant''' molecules from lysed cells increases the risk of thromboembolism in various tissues, particularly the lungs, spleen and liver.<br />
<br />
==Signalment==<br />
Primary IMHA occurs with greater frequency in Cocker spaniels<ref>Weinkle TK, Center SA, Randolph JF, Warner KL, Barr SC, Erb HN. '''Evaluation of prognostic factors, survival rates, and treatment protocols for immune-mediated hemolytic anemia in dogs: 151 cases (1993-2002).''' ''J Am Vet Med Assoc. 2005 Jun 1;226(11):1869-80.''</ref><ref>McAlees TJ. '''Immune-mediated haemolytic anaemia in 110 dogs in Victoria, Australia.''' ''Aust Vet J. 2010 Jan;88(1-2):25-8.''</ref>, Old English sheepdogs and standard Poodles but any breed of dog may be affected. Middle-aged, entire female animals have been shown to be at increased risk of developing the disease in some studies.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Affected animals often present acutely with sudden-onset collapse or severe exercise intolerance. On exmaination, the following signs may become evident:<br />
*'''Pallor''' and/or '''[[Icterus|icterus]]''' of the mucous membranes as the release of bilirubin from lysed red blood cells may result in pre-hepatic jaundice in severely affected animals.<br />
*A '''haemic heart murmur''' and a '''hyperdynamic peripheral pulse''' due to the reduction in viscosity of the blood.<br />
*'''Hepatosplenomegaly''' may be apparent in cases of extravascular haemolysis where the activity of the MPS is greatly increased.<br />
*'''Tachypnoea''' frequently occurs as animals attempt to compensate for reduced tissue oxygenation and blood oxygen carrying capacity.<br />
*'''Dyspnoea''' may occur in animals which develop pulmonary thromboemboli or disseminated intravascular coagulation.<br />
<br />
===Laboratory Tests===<br />
On presentation, full biochemical and haematological analysis of blood samples are indicated to confirm the diagnosis and to obtain a baseline measurement to assess the efficiacy of future treatment. Several tests are also available that have a higher specificity for the diagnosis of IMHA.<br />
====Haematology====<br />
Affected animals have a reduced [[Packed Cell Volume|packed cell volume]] (PCV) or haematocrit (HCT) and often a reduced haemoglobin concentration. IMHA causes a strongly [[Anaemia - Introduction|regenerative anaemia]] and evidence of macrocytosis (increased MCV) should be apparent after 48-72 hours in dogs. A blood smear is extremely useful in evaluating cases of IMHA as '''spherocytes''' are often visible. These small, dense red blood cells are formed due to partial phagocytosis of red blood cells by the MPS. Polychromasia should also be visible on a blood smear from an animal undergoing regeneration and reticulocytosis can be confirmed using a supravital stain such as new methylene blue.<br />
<br />
Reactive [[Platelet Abnormalities|thrombocytosis]] and leucocytosis may be present with any cause of anaemia.<br />
<br />
====Biochemistry====<br />
Serum bilirubin concentration will be elevated and this may be usfficiently severe to cause [[Icterus|icterus]]. The serum [[urea]] concentration may also be elevated as the kidneys receive less oxygen than normal causing a pre-renal azotaemia. A similar process of tissue hypoxia may also result in elevations in liver enzymes such as ALT and AST.<br />
<br />
====Other Tests====<br />
An '''in-saline agglutination''' test may be used to diagnose cases of IMHA that involve auto-agglutination. A drop of whole blood is mixed with a drop of plain saline on a glass slide and agitated for 30-60 seconds. A positive result is recorded if evident aggregates form but the slide should be evaluated under a microscope as rouleaux formation may result in a similar gross appearance. <br />
<br />
A '''Coomb's test''' can be used to diagnose cases of IMHA that are caused by incomplete antibodies. The red blood cells from a patient are mixed with Coomb's antiserum (IgG antiobies directed against IgG) and, in cases where the patient has IMHA with antibodies attached to the surface of the erythrocytes, the antiserum will result in the formation of aggregates of cells. The titre of the test should be evaluated as weakly positive results may occur with other diseases.<br />
<br />
In cases of pure red cell aplasia, a Coomb's test may still be positive but, experimentally, a definitive diagnosis can only be made by transfusing the serum of one animal to another and documenting the development of anaemia in the recipient.<br />
<br />
A diagnosis of PRCA is made more easily by examining '''bone marrow aspirates''' (or core biopsy) for evidence of erythroid hypoplasia and a reduction in the erythroid: myeloid ratio of the marrow stem cells.<br />
<br />
===Diagnostic Imaging===<br />
Imaging may be indicated to rule out other potential causes of the signs observed but it is not necessary to make a diagnosis of IMHA. Hepatosplenomegaly will be the major findings on both radiographs and ultrasound scans.<br />
<br />
==Treatment==<br />
Affected animals often present acutely and may require intensive care. The ultimate aim of long-term treatment for IMHA is to control the autoimmune response.<br />
<br />
===Stabilisation===<br />
In animals that have lost a large percentage of their [[Packed Cell Volume|PCV]] acutely, it is likely that a [[Blood Products|blood transfusion]] will be required. Since animals with IMHA are not usually hypovolaemic, packed red blood cells are often transfused to replace erythrocytes without significantly expanding the plasma volume. In emergency situations, whole blood or synthetic haemoglobin molcules (such as Oxyglobin [tm]) may be used to support the oxygen carrying capacity of the patient. Oxygen may be provided to tachypnoeic and dyspnoeic patients by facemask, nasal catheter or flow-by. <br />
<br />
===Immunosuppressive Therapy===<br />
Whatever supportive measures are taken, the autoimmune response must be controlled to prevent the continuing lysis of red blood cells. The following types of drug are typically used to achieve this goal:<br />
*'''Corticosteroids''' such as prednisolone and dexamethasone are used universally as a first-line treatment for IMHA as they are frequently effective, act rapidly and are available in a variety of preparations. Traditionally, very high doses of corticosteroids have been used to try to control the autoimmune response but dose rates beyond 2-3 mg/kg/day may be associated with significant adverse effects. More recently, there has been a move to add further immunosuppressive agents (see below) in a polypharmaceutical approach which allows the clinician to keep the corticosteroid dose rate at a reasonable level. Corticosteroids act to control both the cell- and antibody-mediated immune responses.<br />
*'''Azathioprine''' is frequently used in the management of IMHA and it has effects on both cell- and antibody-mediated immune responses. It may take 3-4 weeks of treatment before the patient experiences the maximal effects of the drug. Azathioprine is a cytotoxic drug and gloves should be worn to administer tablets. Owners or keepers should be made aware that the active drug or its metabolites may be present in the saliva and other secretions of animals receiving the drug.<br />
*'''Ciclosporin A''' is a fungal metabolite that inhibits a signaling molecule (ciclophilin) involved in T cell activation. Since B cells require T cell help to become activated, differentiate into plasma cells and produce antibodies, there is a rationale for the use of ciclosporin in cases of IMHA but there are currently no reports of its relative efficacy compared to the other immunosuppressive drugs. <br />
*Other less commonly-used drugs include danazol (a steroid related to testosterone), mycophenolate mofetil and cyclophosphamide. Cyclophosphamide was used widely in the management of IMHA but two separate studies have shown that its use is associated with higher rates of mortality<ref>Grundy SA, Barton C. '''Influence of drug treatment on survival of dogs with immune-mediated hemolytic anemia: 88 cases (1989-1999).''' ''J Am Vet Med Assoc. 2001 Feb 15;218(4):543-6.''</ref><ref>Burgess K, Moore A, Rand W, Cotter SM. '''Treatment of immune-mediated hemolytic anemia in dogs with cyclophosphamide.''' ''J Vet Intern Med. 2000 Jul-Aug;14(4):456-62.''</ref><ref>Mason N, Duval D, Shofer FS, Giger U. '''Cyclophosphamide exerts no beneficial effect over prednisone alone in the initial treatment of acute immune-mediated hemolytic anemia in dogs: a randomized controlled clinical trial.''' ''J Vet Intern Med. 2003 Mar-Apr;17(2):206-12.''</ref>.<br />
*'''Human gamma globulin''' is a variably popular product that is thought to act by occupying Fc receptors on cells of the MPS and therefore preventing phagocytosis of opsonised red blood cells. Studies investigating the effects of this drug have produced variable results, with some showing that it makes little difference to outcome<ref>Whelan MF, O'Toole TE, Chan DL, Rozanski EA, DeLaforcade AM, Crawford SL, Cotter SM. '''Use of human immunoglobulin in addition to glucocorticoids for the initial treatment of dogs with immune-mediated hemolytic anemia.''' ''J Vet Emerg Crit Care (San Antonio). 2009 Apr;19(2):158-64.''</ref> and others suggesting that it may be useful in the short-term control of cases that are refractory to other immunosuppressive regimes<ref>Kellerman DL, Bruyette DS. '''Intravenous human immunoglobulin for the treatment of immune-mediated hemolytic anemia in 13 dogs.''' ''J Vet Intern Med. 1997 Nov-Dec;11(6):327-32.''</ref>. Human gamma globulin is not widely available in veterinary practices and it is very expensive.<br />
*Due to the risk of thrombo-embolism caused by the release of endogenous procoagulant molecules, low doses of '''heparin''' or '''aspirin''' are often administered to dogs with IMHA to try to prevent the formation of thrombi in the lungs, liver or spleen. There is some evidence to suggest that, if a dose of heparin is used which is individualised for a particular patient, there may be beneficial effects on survival<ref>Helmond SE, Polzin DJ, Armstrong PJ, Finke M, Smith SA. '''Treatment of immune-mediated hemolytic anemia with individually adjusted heparin dosing in dogs.''' ''J Vet Intern Med. 2010 May-Jun;24(3):597-605. Epub 2010 Apr 6.''</ref>. This effect is not observed if a constant dose of heparin is used for all patients<ref>Weinkle TK, Center SA, Randolph JF, Warner KL, Barr SC, Erb HN. '''Evaluation of prognostic factors, survival rates, and treatment protocols for immune-mediated hemolytic anemia in dogs: 151 cases (1993-2002).''' ''J Am Vet Med Assoc. 2005 Jun 1;226(11):1869-80.''</ref>.<br />
<br />
===Adjunctive Therapy===<br />
Animals with IMHA frequently suffer from concurrent vomiting, regurgitation and diarrhoea while hospitalised. These conditions are frequently managed with [[Gastroprotective Drugs|gastro-protectant drugs]] such as sucralfate, ranitidine and omeprazole to prevent the development of gastro-duodenal ulceration and [[Oesophagitis|oesophagitis]].<br />
<br />
Antibiotics are frequently administered to animals which present with acute haemolytic crises but these should be used judiciously on a case-by-case basis. <br />
<br />
==Prognosis==<br />
Most mortality occurs in the first two weeks after presentation and, overall, 30-50% of animals would be expected to survive for at least one year after initial treatment for IMHA<ref>'''Idiopathic immune-mediated hemolytic anemia: treatment outcome and prognostic factors in 149 dogs.''' ''Piek CJ, Junius G, Dekker A, Schrauwen E, Slappendel RJ, Teske E.'' J Vet Intern Med. 2008 Mar-Apr;22(2):366-73. Epub 2008 Mar 10.</ref>. <br />
==References==<br />
<references/><br />
<br />
[[Category:Antibody Mediated Autoimmune Diseases]]<br />
[[Category:To Do - James]]<br />
[[Category:Dog]][[Category:Cat]]<br />
[[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Cat_asthma&diff=89737Cat asthma2010-09-01T20:53:10Z<p>JamesSwann: Redirected page to Feline Asthma Syndrome</p>
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<div>#REDIRECT [[Feline Asthma Syndrome]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Feline_asthma&diff=89736Feline asthma2010-09-01T20:52:42Z<p>JamesSwann: Redirected page to Feline Asthma Syndrome</p>
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<div>#REDIRECT [[Feline Asthma Syndrome]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Feline_allergic_bronchitis&diff=89735Feline allergic bronchitis2010-09-01T20:52:19Z<p>JamesSwann: Redirected page to Feline Asthma Syndrome</p>
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<div>#REDIRECT [[Feline Asthma Syndrome]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Feline_Asthma_Syndrome&diff=89734Feline Asthma Syndrome2010-09-01T20:51:42Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Feline Allergic Bronchitis'''<br />
|}<br />
<br />
==Description==<br />
Feline asthma is an allergic airway disease that bears many similarities with asthma in humans and with [[Recurrent Airway Obstruction|recurrent airway obstruction]] (RAO) in horses. Affected animals become allergic to allergens present in their immediate environment, including house dust mites and fungal spores and produce [[IgE]] antibodies against these molecules. When later exposed to the same allergens, asthmatic cats suffer a form of type I hypersensitivity response localised in the bronchi and bronchioles and resulting in constriction of the airways.<br />
<br />
Cases of feline asthma may be divided into '''intrinsic''' and '''extrinsic''' disease. <br />
<br />
**'''Extrinsic asthma'''<br />
***Type I hypersensitivity in response to allergen challenge - mediated by [[IgE]]<br />
***Pathological changes:<br />
****Exudate into airways - mucus/ cells<br />
****Thickened airway walls - oedema, glandular and smooth muscle hypertrophy, vascular congestion<br />
****Altered fluidity of mucus (associated with goblet cell hyperplasia) -> less effective mucociliary apparatus<br />
**'''Intrinsic asthma'''<br />
***A proportion of cats there is an increased propensity for the bronchial smooth muscle to contract (increased bronchial reactivity) -> airway constriction<br />
<br />
==Signalment==<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
===Laboratory Tests===<br />
===Diagnostic Imaging===<br />
<br />
==Treatment==<br />
==Prognosis==<br />
==References==<br />
<br />
[[Category:Allergic Respiratory Diseases]][[Category:Cat]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Rupture_of_the_Oesophagus&diff=89680Rupture of the Oesophagus2010-08-31T22:59:47Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
This term refers to the perforation of all layers of the oesophagus and the leakage of air and ingesta into the surrounding tissues. The contents of the oesophagus are not sterile and bacteria are seeded into surrounding tissues when the oesophagus is ruptured. For most of its length, the oesophagus runs through the thoracic cavity within the mediastinum, meaning that ruptures in this location cause septic '''mediastinitis''' and '''pneumomediastinum'''. The mediastinum is continuous with the fascial planes of the neck and the spread of air and bacteria into this region leads to '''subcutaneous emphysema''' and '''cellulitis'''. It has been suggested that the spread of infection along fascial planes may be assisted by the motion of peristalsis or of pulsation in the carotid arteries. If the parietal pleural membrane (which lines the mediastinum) is also ruptured, infection and air can enter the pleural space (between the parietal and visceral pleurae), causing '''pyothorax''' and '''pneumothorax'''. If more air is drawn into the mediastinum or pleural cavity through the rupture during each inspiratory phase but not expelled during exhalation, a '''tension pneumothorax''' may develop, in which the contents of the thorax are gradually compressed by the accumulation of air. If infectious agents spread into the blood, there is a risk of systemic sepsis. Finally, if the perforation is caused by a sharp object in the region of the heart base, the great vessels arising from the heart may be lacerated causing '''fatal internal haemorrhage'''.<br />
<br />
Perforation may occur when sharp [[Oesophageal Foreign Body|foreign bodies]] become lodged in the oesophagus or when attempts are made to remove these objects endoscopically or surgically. Ruptures may also occur when anastomotic sites dehisce after oesophagectomy (as performed for the treatment of [[Oesophageal Neoplasia|oesophageal neoplasia]].)<br />
<br />
==Diagnosis==<br />
For a more complete description of oesophageal foreign bodies and their sequelae, see [[Oesophageal Foreign Body|here]]. The following sections refer specifically to the diagnosis and treatment of oesophageal ruptures.<br />
<br />
===Clinical Signs===<br />
These may include:<br />
*'''Dyspnoea''' due to pleural effusion (with pyothorax), pneumothorax or tension pneumothorax. <br />
*'''Subcutaneous emphysema''' over the neck and pectoral region.<br />
*'''Pyrexia''', depression, inappetence and lethargy due to infection and the acute phase response to inflammation.<br />
*'''Collapse''' when stressed due to the absence of any respiratory reserve function, due to internal haemorrhage or to septic shock.<br />
<br />
===Diagnostic Tests===<br />
A blood haematological profile may indicate signs of severe acute inflammation, including '''neutrophilic leucocytosis''' with a right or left shift. In severe cases, a leukaemoid response (with exuberant mobilisation of neutrophils from the bone marrow storage pool) may be observed. Markers of acute inflammation (such as '''fibrinogen''') will also be elevated.<br />
<br />
===Diagnostic Imaging===<br />
'''Plain radiographs''' of the chest may show:<br />
*'''Pleural effusion''' with contracture of the lung lobes and presence of radiodense material around and between lobes.<br />
*'''Pneumothorax''' or '''tension pneumothorax'''. If the latter condition is unilateral, a dorso-ventral radiograph will show that the contents of the mediastinum are pushed to one side by the expansion of the lung field on the affected side.<br />
*'''Expansion of the mediastinum''', best assessed on a dorso-ventral radiograph where the mediastinum will appear to be significantly wider than the vertebral column.<br />
*'''Emphysema''' in the fascial planes of the neck.<br />
<br />
'''Ultrasonography''' can be used to better assess the contents of the mediastinum and pleural space and to guide fine needle aspiration if samples are required.<br />
<br />
==Treatment==<br />
Animals that have developed a ruptured oesophagus have an extremely poor prognosis for survival and strong consideration should be given to euthanasia if the condition is diagnosed. If the condition is to be treated, referral to a specialist centre would be highly advisable. A possible treatment regime would include the following elements:<br />
*Provision of '''oxygen''' by intra-nasal catheter, flow-by or mask.<br />
*'''Broad spectrum intra-venous antibiosis''' using bactericidal drugs. Samples should be obtained from the thorax for bacterial culture and sensitivity (including anaerobic culture) and a drug that treats anaerobic bacteria should probably be used from the outset.<br />
*'''Drainage of pleural effusion''' by thoracocentesis or, preferably, implantation of a thoracostomy tube since repeated drainage is likely to be required. <br />
*Administration of '''intra-venous fluid therapy''' since the animal is likely to be inappetant and is likely to lose copious amounts of fluid into the exudates forming in the chest.<br />
*'''Surgical repair of the rupture''' with repeated '''lavage of the pleural cavity and mediastinum''' when the animal is sufficiently stable.<br />
*Provision of '''analgesia''' and intensive care monitoring in the post-operative period. If thoracostomy tubes are implanted, these can be used to lavage the pleural space with sterile saline at regular intervals.<br />
<br />
==Prognosis==<br />
Oesophageal rupture and its sequelae will be fatal in the majority of patients. <br />
<br />
[[Category:Oesophagus_-_Pathology]]<br />
[[Category:To_Do_-_James]]<br />
[[Category:Cat]][[Category:Dog]]<br />
[[Category:To Do - Review]]<br />
[[Category:Oesophageal_Disorders_-_Horse]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Platelet_Abnormalities&diff=89679Platelet Abnormalities2010-08-31T22:58:21Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
[[Platelet|Platelets]] (or thrombocytes) are responsible for primary haemostasis, the formation of a temporary platelet plug that initially seals any breach to a blood vessel wall. These breaches are then sealed more completely by the formation of a fibrin clot mediated by the coagulation factor cascade. <br />
<br />
Bleeding disorders may occur if platelets are deficient ('''thrombocytopaenia''') or if the platelets are unable to function adequately ('''thrombocytopathia'''). [[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]] (ITP) is one common cause of thrombocytopaenia and this may be a primary or secondary disease. '''Thrombocytosis''' refers to an increase in the blood platelet concentration above the normal level.<br />
<br />
Thrombocytopaenia and thrombocytopathia lead to disorders of primary haemostasis but, in general, this is less serious than the disorders of secondary haemostasis caused by deficiencies in the [[Coagulation Factor Deficiency|coagulation factors]]. <br />
<br />
==Thrombocytopaenia==<br />
Thrombocytopaenia is the most common haematological abnormality as platelet numbers are subject to fluctuation in a large number of different diseases. Care should be taken however to ensure that this finding is not caused by an artefact of sampling that leads to the formation of platelet clumps. The normal blood platelet concentration of the dog is 175-500x10^9 but clinical disease is not usually observed until this level falls below 50x10^9 and spontaneous haemorrhage is observed only when the level falls below 20x10^9. Reductions in the number of platelets may be caused by a failure to produce adequate numbers in the bone marrow in the process of megakaryopoiesis, increased destruction of existing platelets or sequestration of platelets outside of the circulation. <br />
*Diseases that cause '''[[Bone Marrow - Anatomy & Physiology|bone marrow]] suppression'''<br />
**'''Aplastic anaemia''' caused by ingestion of bracken or administration of oestrogens, [[Chloramphenicol|chloramphenicol]] or [[Sulphonamides|sulphonamide]] antibiotics. Prolonged use of phenylbutazone or salicylate may cause the same disease.<br />
**'''Infectious diseases''' that reduce stem cell function, including [[Distemper|canine distemper]], [[Canine Parvovirus|canine parvovirus]] and [[Feline Panleucopaenia|feline panleucopaenia virus]].<br />
**'''Myelophthisis''', the displacement of the normal cell lines of the bone marrow by another cell or tissue type may also reduce the function of the megakaryocytes. Possible diseases in this category include '''myelofibrosis''' and '''immunoproliferative''' or '''myeloproliferative''' neoplastic disease.<br />
**'''Radiotherapy''' or myelosuppressive '''chemotherapy''' may cause reversible bone marrow suppression.<br />
*Diseases that cause '''increased destruction of platelets'''<br />
**'''[[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]]''' is a common autoimmune disease that leads to the production of antibodies against platelets and their subsequent destruction by cells of the monocyte phagocyte system (MPS).<br />
**'''Infectious diseases''' that cause destruction of platelets include [[Bovine Viral Diarrhoea Virus|bovine viral diarrhoea]] (BVD), [[Classical Swine Fever|classical swine fever]] and [[Infectious Canine Hepatitis|infectious canine hepatitis]]. The parasites ''[[Ehrlichia platys|Anaplasma platys]]'', ''[[Ehrlichia phagocytophila|Anaplasma phagocytophilum]]'' and ''[[Ehrlichia canis]]'' may also cause infectious thrombocytopaenia. Any severe bacterial infection, including those caused by [[:Category:Staphylococcus species|''Staphylococci'']] and the Gram negative bacteria that produce endotoxin (e.g. [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas spp.'']] or [[Salmonella|''Salmonella spp.'']]) may also result in the destruction of platelets.<br />
*Diseases that cause '''sequestration of platelets''' usually involve some enlargement of the spleen, as this is the major organ where platelets are stored outside of the circulation. Examples include:<br />
**[[Haemangiosarcoma]] of the spleen and liver<br />
**Splenic enlargement under general anaesthesia maintained with agents such as [[Barbiturates|barbiturates]] and [[Phenothiazines|phenothiazines]]<br />
*'''Artefactual''' or spurious thrombocytopaenia<br />
**'''Cavalier King Charles spaniels''' have a relatively small number of giant platelets (macrothrombocytes) but they do not suffer from bleeding disorders as they maintain a similar total platelet mass as do dogs of other breeds.<br />
**If venepuncture is traumatic, '''platelet clumps''' may form and these will not be counted by automated machines. The presence of clumps can be investigated by making a blood smear and examining the feathered edge for large agglomerations of platelets.<br />
<br />
==Thrombocytopathia==<br />
Defects in platelet function may be congenital defects or they may be acquired with a number of diseases. Congenital thrombocytopathias are rare inherited diseases which are characterised by defects in platelet adhesiveness, aggregation or factor release. The defects are usually associated with particular breeds, such as '''Chediak-Higashi syndrome''' in blue smoke Persian cats.<br />
<br />
Causes of acquired thrombocytopathia include:<br />
*Infection with ''[[Angiostrongylus vasorum]]'', the canine lungworm, which also causes a consumptive coagulopathy.<br />
*'''Hypergammaglobulinaemia''' as occurs with multiple myeloma and some forms of (B-cell) lymphoma may affect platelet function.<br />
*Administration of large volumes of some '''[[Colloids|colloid solutions]]'''.<br />
*Administration of certain '''pharmaceutical products''', including [[NSAIDs|non-steroidal anti-inflammatory drugs]] and [[Cephalosporins|cephalosporins]].<br />
<br />
==Thrombocytosis==<br />
Increases in platelets above the normal level may occur due to '''physiological''' or '''pathological''' processes. <br />
*Physiological<br />
**'''Splenic contraction''' pushes sequestered platelets into the circulation. This phenomenon is especially marked in horses which have a muscular splenic capsule. <br />
**'''Splenectomy''' prevents the sequestration of platelets in the spleen, resulting in constantly increased levels of platelets.<br />
**As part of a response to '''[[Anaemia – Introduction|anaemia]]''', a '''reactive thrombocytosis''' is often documented and this may precede signs of regeneration.<br />
*Pathological<br />
**'''Essential thrombocythaemia''' is a rare myeloproliferative disease that results in the excessive production of platelets which function abnormally. Affected animals suffer from bouts of spontaneous haemorrhage.<br />
<br />
==Clinical Significance==<br />
Other than essential thrombocythaemia, thrombocytosis has no clinical importance except as an indicator of another disease process. Thrombocytopaenia and thrombocytopathia both result in reductions in the effectiveness of primary haemostasis, producing bleeding disorders. Since bleeding points are usually sealed by a fibrin clot, disorders of primary haemostasis tend to be less severe than those caused by deficiencies of the coagulation factors. Common signs of a disorder of primary haemostasis include:<br />
*'''Petechial''' or '''ecchymotic''' haemorrhages on the skin or mucous membranes.<br />
*'''Haemorrhages from the mucous membranes''', producing haematuria, haematochezia, haematemesis, haemoptysis and melaena.<br />
*'''[[Anaemia – Introduction|Anaemia]]''' with reactive [[Neutrophilia|neutrophilia]] and [[Monocytosis|monocytosis]] if the haemorrhage is severe.<br />
<br />
Severe platelet deficiencies may be managed with transfusions of whole blood or, in the USA, with transfusions of platelet cryoprecipitate. With both techniques however, it is likely that the transfused platelets have only a short half life in the recipient. <br />
<br />
The use of '''vincristine''' (a drug also used in chemotherapy for neoplasia) has been advocated in cases of thrombocytopaenia as it causes the release of immature platelets from the bone marrow.<br />
<br />
[[Category:Haemorrhagic Diseases]]<br />
[[Category:To Do - James]][[Category:Haematology Changes]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Peritonitis_-_Cats_and_Dogs&diff=89678Peritonitis - Cats and Dogs2010-08-31T22:56:32Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
'''Peritonitis''' is defined as [[Inflammation - Pathology|inflammation]] of the [[Peritoneal cavity - Anatomy & Physiology|peritoneum]]. The inflammatory response involves vasodilation, [[Exudate|exudation]] of protein-rich fluid, cellular infiltration, pain and, chronically, formation of fibrous adhesion. The disease can be classified into primary and secondary cases.<br />
<br />
'''Primary peritonitis''' occurs spontaneously without any pre-existing pathological process in the abdomen. In cats, [[Feline Infections Peritonitis (FIP)|feline infectious peritonitis]] is the most common cause of primary peritonitis.<br />
<br />
'''Secondary peritonitis''' occurs as the result of a pre-existing pathological process within the abdomen. It can be further classified into '''septic''' or '''non-septic''' peritonitis, where septic peritonitis results from direct bacterial infection of the peritoneal cavity. Septic peritonitis is the most common form in the dog and its causes include:<br />
*'''Perforation of the gastro-intestinal tract''' due to foreign bodies, [[Intussusception|intussuscepta]], invasive [[Neoplasia - Pathology|neoplasia]], deep ulceration or dehiscence of surgical wounds or biopsy sites. Peritonitis as a result of wound dehiscence is most likely to occur 3-5 days post-operatively. <br />
*'''Penetration of the abdomen''' by a stick, gunshot or other foreign body.<br />
*Rupture of an infected uterus ('''pyometra'''), biliary tract or urinary tract.<br />
The bacteria causing septic peritonitis or their products may spread systemically causing sepsis or endotoxaemia.<br />
<br />
'''Non-septic''' peritonitis may occur due to the leakage of bile, urine or pancreatic enzymes ('''chemical peritonitis''') or due to the presence of foreign substances such as barium or glove powder ('''physical peritonitis'''). In some cases of urinary tract or biliary tract rupture however, septic peritonitis may occur if the tracts were previously infected.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
The clinical signs are related to the presence of severe inflammation within the body cavity, with or without systemic infection.<br />
*'''Abdominal pain''', manifesting as a reluctance to move due to inflammation of the parietal peritoneum.<br />
*'''Depression''', anorexia and lethargy and non-specific signs of infection or systemic disease.<br />
*[[Vomiting|'''Vomiting''']] and [[Diarrhoea|'''diarrhoea''']] may occur due to alterations in intestinal motility and functional ileus.<br />
*'''Hypotension''' and (septic) [[Shock|'''shock''']] due to effusion of fluid into the peritoneum and systemic vasodilation.<br />
*'''Hypothermia''' or '''hyperthermia'''.<br />
<br />
===Laboratory Tests===<br />
====Haematology====<br />
As with any severe inflammatory process, '''leucocytosis''' will occur. Initially, this is caused by '''neutrophilia''' which may have a left shift or, if very severe, a degenerative right shift. Severe localised inflammation may stimulate a '''leukaemoid response''' with massive mobilisation of neutrophils from the bone marrow pools.<br />
<br />
'''Haemoconcentration''' (causing a raised packed cell volume (PCV) and total protein concentration) may occur due to loss of extracellular fluid.<br />
<br />
====Biochemistry====<br />
'''Hypoproteinaemia''' may occur due to loss of plasma proteins into the inflammatory [[Exudate|exudate]].<br />
<br />
'''Hypoglycaemia''' may occur in cases of septic peritonitis.<br />
<br />
Dehydration (which is also responsible for the haemococentration) may also result in pre-renal [[Azotaemia|azotaemia]], increased tissue '''lactate''' production and '''metabolic acidosis'''.<br />
<br />
'''Hypokalaemia''' may occur as a result of chronic vomiting and it may contribute to the intestinal ileus which often develops in cases of peritonitis.<br />
<br />
===Diagnostic Imaging===<br />
====Radiography====<br />
'''Plain radiographs of the abdomen''' may reveal the presence of free gas in the abdomen ('''pneumoperitoneum''') due to intestinal perforation or bacterial production. The normal serosal detail may be effaced due to the presence of an abdominal effusion and, if a horizontal beam decubitus radiograph is made, a '''fluid line''' may be apparent.<br />
<br />
In cases where neoplasia is thought to be the cause of the inflammatory process, thoracic radiograph should be assessed for signs of metastatic disease.<br />
<br />
====Ultrasonography====<br />
This modality has a high sensitivity for the detection of free fluid in the abdomen and it may be used to identify some specific causes of peritonitis, including abscesses of organs or rupture of the [[Biliary Tract - Rupture|biliary tract]].<br />
<br />
Ultrasound scans can also be used to guide '''abdominocentesis'''.<br />
<br />
===Other Tests===<br />
Free abdominal fluid can be collected under ultrasound guidance and submitted for cytological analysis. If fluid cannot be obtained on aspiration, '''diagnostic peritoneal lavage''' can be performed by istilling a small volume (~20 ml/kg) of warmed isotonic crystalloid into the abdomen, agitating the abdomen and then re-aspirating this fluid. Grossly, the fluid may contain vegetable fibres if the gastro-intestinal tract has ruptured or it may be evidently green (indicating the presence of bile) or haemorrhagic. On cytological examaintion, the sample should be assessed for the presence of neutrophils (and other leucocytes) with intracellular bacteria.<br />
<br />
Further possible tests include:<br />
*Measurement of '''amylase''' and '''lipase''' where the cause is suspected to be [[Pancreatitis - Dog and Cat|pancreatitis]]<br />
*'''Bile''' where [[Biliary Tract - Rupture|biliary tract rupture]] is suspected.<br />
*'''Creatinine''' and '''potassium''' if the effusion is thought to be a uroabdomen.<br />
*'''Glucose''' (<2.8 mmol/l) and '''lactate''' (>5.5 mmol/l) should be measured and, where their values are below those shown, the inflammation is likely to be septic.<br />
<br />
In cats with [[Feline Infectious Peritonitis]], the effusion usually has a high protein content (>35g/l) with a high globulin: albumin ratio. There is a variably high cellularity mainly composed of lymphocytes.<br />
<br />
==Treatment==<br />
It is vital to identify severe cases promptly as these will require emergency surgical intervention. Any of the following criteria is a major indication for surgery:<br />
*Presence of intracellular bacteria in leucocytes in the abdominal exudate<br />
*Pneumoperitoneum<br />
*Presence of penetrating injuries to the abdomen.<br />
<br />
===Medical Management===<br />
====Fluid Therapy====<br />
Aggressive fluid therapy with [[Crystalloids|crystalloid]] and [[Colloids|colloid]] should be given on initial presentation to improve haemodynamic parameters and this should be mainatined into the peri- and post-operative periods where appropriate and until the patient is normotensive. If the patient remaines hypotensive, the use of a vasopressor such as [[Dobutamine|dobutamine]], [[Dopamine|dopamine]] or even [[Vasopressin|vasopressin]] should be considered as animals in septic shock are likely to have systemic peripheral vasodilation.<br />
<br />
Glucose and potassium should be supplemented where these parameters are found to be abnormal and, in cases of severe metabolic acidosis, the use of sodium bicarbonate may be considered. This product should be used with care as overdoses may result in overshoot metabolic alkalosis, tissue anoxia due to a left-shift of the haemoglobin-oxygen dissociation curve and paradoxical cerebral acidosis as carbon dioxide (not bicarbonate) crosses the blood brain barrier.<br />
<br />
Septic peritonitis can cause [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation (DIC)]] which represents a very large therapeutic challenge. Plasma my be administered to replace used clotting factors and some authors advocate the use of low doses of heparin to prevent further coagulation.<br />
<br />
====Antimicrobial Drugs====<br />
Broad spectrum bactericidal antibiotics should be administered and, where possible, the choice of product should then be guided by culture and sensitivity of samples of peritoneal fluid. [[Escherichia coli|''Escherichia coli'']], [[:Category:Clostridium species|''Clostridium spp.'']] and ''[[Enterococcus faecalis]]'' are the species most commonly isolated in cases of septic peritonitis.<br />
<br />
===Surgical Management===<br />
Surgical intervention is indicated if the cause of peritonitis is undetermined or if it has been caused by intestinal rupture, intestinal obstruction or mesenteric avulsion. Abdominal lavage is a controversial procedure as it carries a risk of disseminating infection throughout the body and it is therefore indicated in cases of generalised peritonitis but should be used with care in cases of localised peritonitis. A volume of around 200 ml/k fluid should be used to lavage the abdomen and as much of this fluid as possible should be re-aspirated as its continued presence will hinder the immune system by diluting bactericidal factor and preventing leucocyte migration.<br />
<br />
It is beneficial to maintain peritoneal drainage after lavage by either '''open''' or '''closed''' drainage. Open drainage involves leaving part of the abdominal wall loosely sutured so that peritoneal fluid can leak out under gravity. The wound must be dressed under sterile conditions and there is a high risk of ascending infection and of continued protein loss with this technique.<br />
<br />
Closed drainage involves implanting a drain into the abdomen (often a '''Jackson Pratt drain''') to which suction can be applied to aspirate fluid from the peritoneal cavity. The drain usually has multiple fenestrations along its length so that it does not become blocked by omentum or fat. <br />
<br />
==Prognosis==<br />
Guarded. Peritonitis is a multifactorial disease and the consequence is fatal in most cases. A rapid diagnosis and treatment may improve the prognosis but it is generally poor in cases of septic peritonitis.<br />
<br />
==References==<br />
*Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company<br />
*Fossum, T. W. et. al. (2007) '''Small Animal Surgery (Third Edition)''' ''Mosby Elsevier''<br />
*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.<br />
*Tilley, L. P. & Smith, F. W. K. (2007) '''Blackwell's Five-minute Veterinary Consult: Canine & Feline (Fourth Edition)''' ''Blackwell Publishing''<br />
<br />
For further information on peritonitis see: [http://inpractice.bvapublications.com/cgi/reprint/26/7/358 maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=haemoabdomen&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT] In Practice article<br />
[[Category:Peritoneal_Cavity_-_Inflammatory_Pathology]]<br />
<br />
[[Category:To Do - Review]]<br />
[[Category:To_Do_-_James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Packed_Cell_Volume&diff=89677Packed Cell Volume2010-08-31T22:54:43Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''PCV'''<br />
|}<br />
<br />
==Description==<br />
The packed cell volume (PCV) is the percentage of the blood volume which is occupied by [[Erythrocyte|red blood cells]]. The PCV is usually estimated by subjecting a small blood sample to centrifugation to compress the blood cells into a minimal volume before the PCV is measured against a standard scale. <br />
<br />
==Clinical Significance==<br />
'''Reductions''' in PCV are synonymous with [[Anaemia - Introduction|anaemia]] and they occur most commonly with haemorrhage, haemolysis or failures in the erythroid lineage. In cases of acute haemorrhage, the PCV will not fall immediately because blood cells are lost in the same proportion as the aqueous solvent. The osmotic movement of fluid from the interstitial space results in haemodilution and subsequent reduction of the PCV.<br />
<br />
'''Increases''' in PCV usually occur in dehydrated animals in which the blood cells come to occupy a greater proportion of the blood volume, a process called '''haemoconcentration''' or '''relative polycythaemia'''. Other reasons for increases in PCV include:<br />
*'''Primary absolute polycythaemia''', a form of myeloproliferative disease that results in the increased production of red blood cells. <br />
*'''Secondary absolute polycythaemia''' which may be caused by the paraneoplastic production of erythropoietin (EPO) from renal tumours or it may occur as a response to the hypoxygenation of blood in animals with reverse-shunting [[PDA|patent ductus arteriosus]] (PDA) or [[Tetralogy of Fallot]]. <br />
<br />
Since PCV is not a measure of the actual number of red blood cells, anaemic animals may appear to have a normal or even increased PCV if they also become dehydrated. An example of this phenomenon occurs with [[Hypoadrenocorticism|Addison's disease]], where animals frequently have a non-regenerative anaemia which is masked by dehydration in an Addisonian crisis. <br />
<br />
[[Category:To Do - James]][[Category:Haematology Changes]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Monocytosis&diff=89676Monocytosis2010-08-31T22:53:59Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
Monocytosis refers to an increase in the number of [[Monocytes|monocytes]] (haematogenous macrophages) in the blood. It may be found in conjunction with other changes inidicative of a stress leucogram or it may occur independently of other changes to the haematological profile. The blood monocytes themselves represent a brief transitional stage as they quickly move into tissues and differentiate further to tissue macrophages. As such, monocytes rarely perform any notable functions but they been found to phagocytose red blood cells in cases of [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]. The major causes of monocytosis are:<br />
<br />
*'''Stress leucogram''' mediated by the production or administration of glucocorticoids. This phenomenon is also characterised by [[Neutrophilia|neutrophilia]], [[Eosinopenia|eosinopenia]] and [[Lymphopenia|lymphopenia]].<br />
*'''Chronic inflammatory processes''', including chronic bacterial infections and chronic inflammatory diseases of the liver ([[Chronic Hepatitis|chronic hepatitis]] and [[Cholangitis|cholangitis]]) and pancreas ([[Pancreatitis - Dog and Cat|chronic pancreatitis]]). Serum fibrinogen may also be elevated in such chronic processes and there may be a variable neutrophilia depending on the level of active inflammation.<br />
*'''Granulomatous disease''' results in monocytosis as monocytes are recruited to contain certain types of bacteria (namely ''[[Mycobacteria spp.]]'', ''[[Nocardia|Nocardia spp.]]'', ''[[Actinomyces species - Overview|Actinomyces]]'' and ''[[Rhodococcus equi]]'') or foreign objects. Severe granulomatous disease may also result in hypercalaemia as differentiated macrophages acquire the ability to produce activated vitamin D metabolites.<br />
*Certain types of monocytic or myelomonocytic '''chronic myeloid leukaemia''' may result in the presence of large numbers of monocytes in the blood.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphopenia&diff=89675Lymphopenia2010-08-31T22:52:37Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphopenia is a reduction in the numbers of lymphocytes in the blood. This phenomenon is most commonly associated with stress (as part of the '''stress leucogram''') or with viral infection. Its causes therefore include:<br />
*Viral infection with [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Infectious canine hepatitis]], [[Feline infectious enteritis|feline infectious enteritis]] or [[Bovine Viral Diarrhoea|bovine viral diarrhoea]] (BVD)<br />
*Bone marrow suppression caused by '''chemotherapy''' or '''radiotherapy'''. Since neutrophils have a much shorter circulating half life, they are the first cell line to fall with any insult to the bone marrow but lymphopenia may occur as part of a more severe pancytopenia.<br />
*Inherited or acquired immunodeficiency syndromes, including '''[[Equine Severe Combined Immune Deficiency|SCID]]''' (Severe Combined Immunodeficiency Syndrome) in Arab foals and [[Feline Immunodeficiency Virus|'''feline immunodeficiency virus''']] infection.<br />
*Stress leucogram, characterised by '''[[Neutrophilia|neutrophilia]]''', '''[[Monocytosis|monocytosis]]''', '''[[Eosinopenia|eosinopenia]]''' and '''[[Lymphopenia|lymphopenia]]'''. A similar pattern may occur with [[Canine Hyperadrenocorticism - Cushing's Disease|hyperadrenocorticism]] (Cushing’s disease) or exogenous corticosteroid therapy as these hormones selectively suppress lymphocytic activity and the inflammatory response in general. <br />
*Leakage of lymphatic fluid may result in loss of lymphocytes, as occurs with '''[[Lymphangiectasia|lymphangiectasia]]''' or '''[[Chylous Effusion|chylothorax]]'''.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphocytosis&diff=89674Lymphocytosis2010-08-31T22:51:55Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphocytosis refers to an increase in the number of circulating lymphocytes in the blood. The major causes of lymphocytosis are:<br />
*Several types of '''neoplasia''' may result in increases in the number of blood lymphocytes, including:<br />
**Stage V (leukaemic) [[Lymphoma|lymphoma]]<br />
**Acute lymphoblastic and chronic lymphocytic leukaemia<br />
**Bovine Leukosis caused by bovine leukaemia virus (BoLV)<br />
*'''Stress''' may result in the release of lymphocytes into the circulation, especially in young horses and cats. This response is mediated by the release of adrenaline from the adrenal medulla and it should not be confused with the stress leucogram produced by the release of the glucocorticoid hormones cortisol from the adrenal cortex. <br />
*Some cases of '''chronic infection''' may be associated with lymphocytosis but reactive hyperplasia in associated lymph nodes may not correlate with the numbers of circulating lymphocytes.<br />
*'''Physiological''' lymphocytosis is common in young animals of many species. In growing pigs, this may be associated with [[Mycoplasmas species - Overview|''Mycoplasma'']] infection.<br />
*In '''premature''' or '''dysmature equine neonates''', the normal neutrophil: lymphocyte ratio of approximately 2: 1 may be reversed to produce an apparent lymphocytosis. Such animals will also have an increased mean corpuscular volume (MCV) of their red blood cells.<br />
*'''Hypoadrenocorticism''' may result in lymphocytosis and/or [[Eosinophilia|eosinophilia]].<br />
<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Key-Gaskell_Syndrome&diff=89673Key-Gaskell Syndrome2010-08-31T22:51:00Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Autonomic Polyganglioneuropathy'''<br><br />
'''Feline Dysautonomia'''<br />
|}<br />
<br />
==Description==<br />
Key-Gaskell Syndrome refers to the clinical signs observed in cats with abnormal function of the sympathetic and parasympathetic nervous systems. It is similar to [[Grass Sickness|grass sickness]] in horses and, like this disease, it is often fatal.<br />
<br />
The syndrome has occurred as outbreaks<ref>Cave TA, Knottenbelt C, Mellor DJ, Nunn F, Nart P, Reid SW '''Outbreak of dysautonomia (Key-Gaskell syndrome) in a closed colony of pet cats.''' ''Vet Rec. 2003 Sep 27;153(13):387-92.''</ref> in the past in the UK, continental Europe and occasionally in the USA. It was first described by Key and Gaskell as a 'puzzling syndrome' causing pupillary dilatation in cats at the start of a major outbreak in the UK in 1982<ref>Key TJ, Gaskell CJ. '''Puzzling syndrome in cats associated with pupillary dilatation.''' ''Vet Rec. 1982 Feb 13;110(7):160.''</ref>. It is currently described only sporadically but recent reports suggest that the incidence of the disease may be increasing again.<br />
<br />
The cause of the dysautonomia is not known but numerous factors have been implicated and it is generally thought to occur after exposure to a toxin, possibly in dry food or vaccines. As with grass sickness, it has also been suggested that toxins produced by ''[[Clostridium botulinum]]'' may be involved in the pathogenesis of the disease and a recent study showed that cats with the disease developed significantly higher titres of IgA antibody to botulinum toxins C and D than healthy controls<ref>Nunn F, Cave TA, Knottenbelt C, Poxton IR. '''Association between Key-Gaskell syndrome and infection by Clostridium botulinum type C/D.''' ''Vet Rec. 2004 Jul 24;155(4):111-5.''</ref>. Whatever the cause, degenerative lesions develop in the autonomic ganglia, intermedio-lateral columns of spinal grey matter and in the axons of the sympathetic neurones.<br />
<br />
==Signalment==<br />
Historically, Key-Gaskell syndrome was reported most frequently in cats but the disease has now been shown to occur in dogs<ref>Schulze C, Schanen H, Pohlenz J. '''Canine dysautonomia resembling the Key-Gaskell syndrome in Germany.''' ''Vet Rec. 1997 Nov 8;141(19):496-7''</ref><ref>Wise LA, Lappin MR. '''A syndrome resembling feline dysautonomia (Key-Gaskell syndrome) in a dog.''' ''J Am Vet Med Assoc. 1991 Jun 15;198(12):2103-6.''</ref><ref>Rochlitz I, Bennett AM. '''Key-Gaskell syndrome in a bitch.''' ''Vet Rec. 1983 Jun 25;112(26):614-5. ''</ref>, particularly younger animals. There is no apparent sex predisposition but the Labrador Retriever breed may be predisposed to the development of dysautonomia.<br />
<br />
In a recent study of 65 dogs confirmed as having dysautonomia, those raised and housed in rural environments appeared to be at greater risk (56/65 dogs) for dysautonomia than dogs from urban environments<ref>Harkin KR, Andrews GA, Nietfeld JC. '''Dysautonomia in dogs: 65 cases (1993-2000).''' ''J Am Vet Med Assoc. 2002 Mar 1;220(5):633-9.''</ref>.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
The sympathetic and parasympathetic nervous systems are involved in the regulation of multiple organ systems, particularly the gastro-intestinal tract and the secretory glands. Common clinical signs therefore include:<br />
*'''Anorexia''' and '''constipation''' due to intestinal ileus.<br />
*'''Abdominal distension''' may occur as a result of generalised paralytic ileus.<br />
*'''[[Megaoesophagus]]''' due to failure of oesophageal motility. This may cause regurgitation and secondary aspiration pneumonia.<br />
*'''Depression'''<br />
*'''Bradycardia'''<br />
*Decreased '''lacrimation''' and '''salivation''' due to reduced tone in the parasympathetic nerves that stimulate secretion. The xerotsomia caused by reduced production of saliva may be apparent as dry mucous membranes on clinical examination.<br />
*'''Pupillary dilatation''' due to reduced tone of the constrictor muscle of the iris, usually controlled by the parasympathetic fibres of the short ciliary nerves.<br />
<br />
The most frequent clinical signs associated with the syndrome are depression, anorexia, constipation and regurgitation or vomiting. Incontinence (faecal and urinary) has been observed less frequently.<br />
<br />
===Diagnostic Imaging===<br />
[[Megaoesophagus|Oesophageal dilatation]] may be observed on '''plain radiographs of the chest'''. A 'trachea stripe sign' may also be visible due to the compression of the tissue between the oesophagus and trachea. <br />
<br />
Oesophageal hypomotility may be evident with barium contrast study or using fluoroscopy to observe the dynamic passage of food boluses into the stomach.<br />
<br />
===Pharmalogical Tests===<br />
Various provocative tests can be used to assess the autonomic nerbous systems of animals with suspected Key-Gaskell syndrome:<br />
*Topical ocular administration of dilute pilocarpine should result in miosis, which implies a postive result. However, not all animals respond and the response is dependent on the degree of damage to the postganglionic parasympathetic neuron causing (denervation) supersensitivity of the iris muscle.<br />
*Intra-venous or subcutaneous administration of atropine (a parasympatholytic) should result in an increase in the heart rate. A failure to respond implies a positive result.<br />
*Intra-dermal administration of histamine should result in a classical wheal and flare response but this may be dampened in those animals with dysautonomia. An absence of the wheal and flare response is therefore a positive result.<br />
<br />
=====Pathology=====<br />
[[Image:Ba 250 07.jpg|thumb|Histological section of a degenerate neuron from a cat with Key-Gaskell Syndrome<br><small>Copyright Susan Rhind 2007 RVC]]</small> <br />
*Histologically there is marked reduction in the number of neurones in all autonomic ganglia in the ventral horn of all levels of spinal cord accompanied by proliferation of non-neuronal cells. Similar changes are found in the brainstem nuclei of the cranial nerves and features of chromatolytic degeneration may be apparent in the ganglia, spinal cord and sympathetic axons.<br />
<br />
==Differential Diagnosis==<br />
There are few differential diagnoses for this clinical presentation but, early in the course of disease, other causes of [[Megaoesophagus|megaoesophagus]] should be considered.<br />
<br />
==Treatment==<br />
Treatment may be attempted with parasympathomimteic drugs but is largely supportive.<br />
===Supportive===<br />
Food should be provided from an elevated bowl or via a gastrostomy tube which can be left in place for several weeks if necessary. Total parenteral nutrition may be considered but this cannot be used as a long term option for nutrition and it is associated with many adverse effects.<br />
<br />
===Parasympathomimetic Drugs===<br />
Some dogs may show minor improvement on initiation of therapy with '''bethanechol''' or '''metoclopramide'''.<br />
<br />
==Prognosis==<br />
The prognosis is guarded or poor. Recovery rates in the cat are reported as 20-40% but it may take 2-12 months for the patient to recover fully. In the dog, recovery rates are lower. Even after making an apparent recovery, many animals are left with residual neurological deficits including intermittent regurgitation.<br />
<br />
==References==<br />
<references/><br />
* Hall J.H, Wimpson J. W. and Williams D.A, (2005), Disorders of the Pharynx and Oesophagus, in BSAVA Manual of Canine and Feline Gastroenterology, 2nd Edition, British Small Animal Association, Gloucester, pp 142-143<br />
* Harkin K.R, Andrews G.A, Nietfeld J.C, (2002), Dysautonomia in dogs: 65 cases (1993–2000) J Am Vet Med Assoc, Mar 1, 220(5): pp. 633-9<br />
<br />
<br />
<br />
[[Category:Oesophagus_-_Pathology]]<br />
[[Category:To_Do_-_James]]<br />
[[Category:Cat]]<br />
[[Category:Intestine_-_Functional_Obstruction]]<br />
[[Category:To_Do_-_James]]<br />
[[Category:Dog]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Imtp&diff=89672Imtp2010-08-31T22:49:44Z<p>JamesSwann: Redirected page to Immune Mediated Thrombocytopaenia</p>
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<div>#REDIRECT [[Immune Mediated Thrombocytopaenia]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_Mediated_Thrombocytopaenia&diff=89671Immune Mediated Thrombocytopaenia2010-08-31T22:49:17Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
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{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Idiopathic Thrombocytopaenic Purpura'''<br><br />
'''Evan’s Syndrome'''<br />
|}<br />
<br />
==Description==<br />
Immune-mediated thrombocytopaenia (ITP) occurs due to an autoimmune response directed against circulating platelets or megakaryocytes in the bone marrow. The destruction of cells is mediated by antibodies, making ITP a form of '''[[Type II Hypersensitivity|type II hypersensitivity]]'''. The antibodies bind to cells and act as a foundation for the assembly of serum complement components or as opsonins, promoting the uptake and destruction of platelets by cells of the monocyte-phagocyte system (MPS). The destruction of platelets usually results in severe [[Platelet Abnormalities|thrombocytopaenia]] and, if the blood level of platelets fall below approximately 50x10^9/l, the affected animal is at risk of mucosal haemorrhages. <br />
<br />
ITP may be '''primary''' (with no apparent underlying cause) or '''secondary''' to another disease process, to an infection or as a reaction to some drugs. ITP that occurs concurrently with [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA) is known as '''Evan’s syndrome'''.<br />
<br />
==Signalment==<br />
Primary ITP has been reported in cats but it is much more common in dogs. Breeds of dog at particular risk of ITP are similar to those that also suffer from IMHA, namely old English sheepdogs, cocker spaniels and poodles.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Most affected animals will present with some form of bleeding disorder and it is important to differentiate disorders of primary haemostasis (such as ITP and thrombocytopathia) from those of secondary haemostasis (such as Haemophilia A and B). Disorders of primary haemostasis are usually less severe than those of secondary haemostasis as, if the platelets are absent or non-functional, bleeding is often still prevented by the formation of a stable fibrin clot. Common features of a disease of primary haemostasis include:<br />
*'''Petechial haemorrhages''' of the mucous membranes and skin<br />
*Bleeding from mucous membranes, producing '''melaena''', '''haematochezia''', '''haematuria''', '''haemoptysis''' and '''haematemesis'''.<br />
*Haemorrhage into the retina or brain may produce '''blindness''' or '''neurological signs''', respectively.<br />
Affected animals may also show other, less specific signs:<br />
*'''Lethargy''', '''anorexia''' and weakness.<br />
*'''Pyrexia'''<br />
*'''Lymphadenopathy'''<br />
*'''Hepatosplenomegaly''' due to the fact that most destruction of platelets occurs in the MPS of the liver and spleen.<br />
<br />
===Laboratory Tests===<br />
Haematological analysis of a blood sample will show '''thrombocytopaenia''', often with extremely low platelet counts (e.g. 1-5x10^9/l). There may be a reactive [[Neutrophilia|neutrophilia]] and other features of a stress leucogram. Examination of a blood smear may show evidence of '''microthrombocytes''' (small platelets that have been partially phagocytosed by cells of the MPS, similar to spherocytes in IMHA) or immature '''macrothrombocytes''' (a sign of bone marrow platelet regeneration). The patient may be anaemic in cases of Evan’s syndrome or if significant haemorrhage has occurred.<br />
<br />
===Other Tests===<br />
Definitive diagnosis relies on the detection of serum anti-platelet antibodies but this test is not widely available.<br />
<br />
Other tests may also be used to exclude potential infectious causes of thrombocytopaenia such as ''[[Ehrlichia platys]]'' and ''[[Tick-borne Fever|Anaplasma phagocytophilum]]''. <br />
<br />
Faecal occult blood tests represent an unreliable way of detecting gastro-intestinal haemorrhage in cases of mild melaena. The animal must be deprived of meat, bismuth subsalicylate and ferrous sulphate for 3 days before the faecal samples are taken for analysis.<br />
<br />
===Diagnostic Imaging===<br />
Imaging is not required to make a diagnosis of ITP but it may be used to rule out underlying causes of the disease. The major features of abdominal ultrasonography and radiography in affected animals will be '''hepatosplenomegaly'''.<br />
<br />
==Treatment==<br />
===Stabilisation===<br />
Severely thrombocytopaenic animals or those suffering from neurological signs may require transfusions with whole blood. The platelets transferred in this process have only a very short half-life in the recipient and this technique is therefore of little use in the majority of patients where the immune response is not controlled.<br />
<br />
===Immunosuppressive Therapy===<br />
The ultimate goal of the therapeutic regime is to control the autoimmune response to prevent further destruction of platelets. The bone marrow stem cells will then be able to replace the platelets that have been lost in the disease. A variety of drugs have been used in the treatment of ITP but those in widespread use include:<br />
*'''Corticosteroids''' including prednisolone and dexamethasone act to suppress cell- and antibody-mediated responses. These drugs act quickly, are frequently effective and are widely available, making them the most commonly used drugs in the management of ITP.<br />
*Adjunctive immunosuppressive therapy may be provided with '''ciclosporin''', '''azathioprine''' or '''cyclophosphamide'''.<br />
*A recent prospective study indicated that '''human immunoglobulin''' may produce a significantly better outcome in cases of ITP. This product is thought to act by occupying sites (Fc receptors) on cells of the MPS that are usually used to recognise opsonised platelets and mediate phagocytosis. Although it seems to be highly effective, this product is extremely expensive.<br />
*'''Vincristine''' is occasionally used in cases of severe thrombocytopaenia as it is thought to cause the release of platelets from the bone marrow. The immature platelets released however are not completely functional. It also reduces macrophage function by inhibiting the assembly of microtubules necessary for phagocytosis.<br />
*'''Splenectomy''' may be performed in cases refractory to medical management to remove the cells responsible for the phagocytosis of platelets.<br />
<br />
==Prognosis==<br />
Similarly to IMHA, mortality is most likely in the initial stages of the disease and the mortality rate is approximately 30% in this period. Beyond this, the majority of animals recover well although they may require immunosuppressive treatment for several months to completely control the disease. <br />
<br />
==References==<br />
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company<br />
<br />
[[Category:Antibody Mediated Autoimmune Diseases]]<br />
[[Category:To Do - James]][[Category:Dog]][[Category:Cat]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Hypothyroid&diff=89670Hypothyroid2010-08-31T22:48:31Z<p>JamesSwann: Redirected page to Hypothyroidism</p>
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<div>#REDIRECT [[Hypothyroidism]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Cretinism&diff=89669Cretinism2010-08-31T22:48:13Z<p>JamesSwann: Redirected page to Hypothyroidism</p>
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<div>#REDIRECT [[Hypothyroidism]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphocytic_thyroiditis&diff=89668Lymphocytic thyroiditis2010-08-31T22:47:57Z<p>JamesSwann: Redirected page to Hypothyroidism</p>
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<div>#REDIRECT [[Hypothyroidism]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Hypoadrenocorticism&diff=89666Hypoadrenocorticism2010-08-31T22:45:43Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
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{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Addison's disease'''<br />
|}<br />
<br />
==Description==<br />
Addison's disease occurs due to a failure to produce adequate amounts of glucocorticoid and mineralocorticoid hormones from the adrenal cortex. The majority of cases are '''primary''' and occur due to an autoimmune response directed at the endocrine cells of the adrenal glands, resulting in adrenocortical atrophy. This is an example of a [[Type IV Hypersensitivity|type IV (delayed type) hypersensitivity response]]. Smaller numbers of primary cases are caused by haemorrhage, necrosis or neoplasia within the adrenal glands. '''Secondary''' hypoadrenocorticism occurs due to a reduction in the secretion of ACTH from the anterior pituitary gland. <br />
<br />
===Primary Hypoadrenocorticism===<br />
[[Image:Adrenal atrophy.jpg|thumb|125px|Image of an adrenal gland undergoing atrophy.<br><small>Copyright A. Jefferies 2008</small>]]<br />
<br />
There are several possible causes of primary hypoadrenocorticism, including: <br />
*'''Adrenal atrophy''' is thought to be an autoimmune disease caused by a type IV immune response. Affected animals have an increased risk of developing other immune-mediated diseases, including [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]. Grossly, the adrenal glands are small, difficult to locate and they are dark brown on cut sections. Histological analysis reveals the presence of an infiltrate of lymphocytes, plasma cells and macrophages. <br />
<br />
[[Image:Adrenal necrosis.jpg|thumb|125px|Histological section of an adrenal gland undergoing necrosis<br><small>Copyright A. Jefferies 2008</small>]]<br />
[[Image:Adrenal necrosis2.jpg|thumb|125px|Image of an adrenal gland undergoing necrosis. Note the areas of haemorrhage within the cortex of the gland.<br><small>Copyright A. Jefferies 2008</small>]]<br />
<br />
*'''Adrenal necrosis''' may be caused by certain infections or it may be a sequel to other metabolic diseases. In horses, [[Salmonella|'''salmonellosis''']] may cause adrenal necrosis in horses but, in small animals, necrosis is more likely to occur due to myoarteritis in uraemic animals resulting in ischaemia of the adrenal gland. Idiopathic necrosis may occur with no apparent cause. Grossly, the glands contain areas of red haemorrhage with yellow necrotic foci. <br />
<br />
*'''Bilateral adrenalectomy''' or '''mitotane therapy''' may cause iatrogenic hypoadrenocorticism. Mitotane, which is used in the treatment of hyperadrenocorticism (Cushing's disease) selectively destroys the zona fasciculata and reticularis while sparing the essential zona glomerulosa. Iatrogenic Addison's disease is a common sequel of its use.<br />
<br />
===Secondary Hypoadrenocortisism===<br />
Deficient pituitary secretion of ACTH. Often '''iatrogenic''' due to withdrawal of glucocorticoid treatment. Prolonged high dose treatment induce adrenal atrophy due to the effect of negative feedback on the pituitary. The withdrawal of drug must be gradual to allow to adrenal gland to return to function over a period of time. <br />
Usually little effect on mineralocorticoids as ACTH has little trophic effect on their production.<br />
<br />
===Pathophysiology===<br />
The glucococorticoid hormone '''cortisol''' enables animals to cope with stress while the minerlaocorticoid '''aldosterone''' plays a critical role in the regulation of sodium and potassium concentrations and of extracellular fluid volume. Aldosterone normally acts to increase sodium reabsorption and potassium excretion in the kidney so deficient aldosterone secretion will result in '''hyponatraemia''', '''hypochloraemia''' and '''hyperkalaemia'''. Since they are unable to regulate their body sodium concentration, Addisonian animals become severely dehydrated and hypovolaemic, reducing the perfusion of peripheral tissues. During an Addisonian crisis, this can result in gastro-intestinal haemorrhage and allow translocation of bacteria across the gut barrier.<br />
<br />
Deficiency of cortisol results in '''hypoglycaemia''' (as cortisol usually antagonises the action of insulin), increased circulating levels of [[Lymphocytosis|lymphocytes]] and [[Eosinophilia|eosinophils]] and increased skin pigmentation. This latter syndrome occurs as low levels of glucocorticoids allow increased ACTH production as negative feedback on the pituitary is removed or decreased. As ACTH is released, so is MSH (Melanocyte Stimulating Hormone), increasing the pigmentation of the skin in chronic cases of hypoadrenocorticism.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Addison's disease may present acutely as an '''Addisonian crisis''' or it may cause chronic disease over several months before it is diagnosed. Acutely, affected animals present in '''hypovolaemic [[Shock|shock''']] with severe '''dehydration''' and '''bradycardia''' (caused by hyperkalaemia). This feature of the crisis is extremely suggestive of Addison's disease as hypovolaemic animals would usually be expected to be tachycardic. As with any cause of hypovolaemia, the peripheral pulse is often weak, the capillary refill time is prolonged and the heart sounds may not be clearly audible on auscultation.<br />
<br />
Addisonian animals may suffer [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|'''vomiting''']] as part of an acute crisis or as a chronic intermittent syndrome. In the chronic form of the disease, animals are frequently '''anorexic''' and '''weak'''.<br />
<br />
===Laboratory Tests===<br />
Complete analysis of blood samples is indicated for animals presenting acutely and for those that have a history of chronic intermittent vomiting and anorexia. The following changes may be documented:<br />
*'''Haemoconcentration''' in an acute crisis due to rapid dehydration.<br />
*'''Non-regenerative anaemia''' in chronic form as glucocorticoid deficiency decreases erythropoeisis. Since it is possible for animals to undergo an acute crisis after suffering from hypoadrenocorticism for several weeks, any anaemia may be masked by the haemoconcentration that occurs due to hypovolaemia.<br />
*'''Electrolyte imbalances''' occur in 90% of patients, typically '''hyperkalaemia''', '''hyponatraemia''' and '''hypochloraemia'''. The sodium: potassium ratio of a normal animal is >27: 1 but this falls to <25: 1 in Addisonian animals.<br />
*'''Pre-renal [[Azotaemia|azotaemia]]''' is common as hypovolaemic animals are unable to maintain adequate renal perfusion. <br />
*'''Hypoglycaemia''' is a common finding in animals presenting in Addisonian crisis.<br />
*'''[[Eosinophilia]]''' and '''[[Lymphocytosis|lymphocytosis]]''' occur due to the deficiency in glucocorticoids. In such a severely ill animal, a stress leucogram would usually be expected so this pattern is highly suggestive of hypoadrenocorticism. An elevated blood [[Urea|urea]] concentration may also occur due to gastro-intestinal haemorrhage which is a common finding in animals with Addison's disease.<br />
<br />
===Other Tests===<br />
Additional tests are available to confirm the diagnosis and assess the need for further supportive treatment. An '''ACTH stimulation test''' should be performed as soon as possible in animals presenting acutely. The pre-stimulation sample can be taken immediately, the ACTH (tetracosactin) is administered and the post- sample is collected after 1.5-2 hours. Although the results of the test may not be available for 24-48 hours, it is very useful to confirm the diagnosis when acute renal failure is considered to be a major differential diagnosis. A positive result is recorded if the level of cortisol is initially low and if this fails to respond to the injection of ACTH.<br />
<br />
Since hyperkalaemia has significant effects on the membrane potential of excitable tissues, it is useful to perform an electrocardiogram ('''ECG''') to assess the function of the heart. Findings consistent with hyperkalaemia include small or absent P waves (indicating sino-atrial standstill), wide and small QRS complexes, short Q-T intervals, peaked T waves and long P-R intervals.<br />
<br />
===Diagnostic Imaging===<br />
'''Plain radiographs''' of the chest and abdomen may show signs of hypovolaemia, including '''microcardia''', '''pulmonary underperfusion''' and '''microhepatica'''. Animals with Addison's disease may also develop [[Megaoesophagus|megaoesophagus]] due to muscle weakness. Ultrasound scans of the adrenal glands may be indicated to detect any evident pathological process that may account for the hypoadrenocorticism.<br />
<br />
==Treatment==<br />
===Stabilisation===<br />
Since collpased, bradycardic animals are unlikely to survive for long, urgent intervention is required to stabilise these patients. '''Intra-venous 0.9% sodium chloride (saline) solution''' should be provided at shock rates to restore normovolaemia and begin to correct the electrolyte imbalances. Additional '''glucose''' can be added to fluids in hypoglycaemic animals but blood glucose levels should be monitored closely if this is undertaken. <br />
<br />
When the diagnosis has been made with some certainty, '''intra-venous glucocorticoid replacement therapy''' can be initiated together with a '''mineralocorticoid'''. Dexamethasone is the corticosteroid of choice as it has greater mineralocorticoid activity than other products. Although there is an intra-muscular injectable mineralocorticoid (desoxycorticosterone acetate) available in the USA, this is not usually required for stabilisation.<br />
<br />
[[Gastroprotective Drugs|'''Gastro-protectant drugs''']] (such as sucralfate, ranitidine or omeprazole) may be administered to vomiting animals and '''antibiotics''' should be provided to any animals that develop pyrexia.<br />
<br />
===Management===<br />
In the long term, animals with Addison's disease require only a mineralocorticoid on a daily basis with intermittent courses of glucocorticoids during times of stress. The mineralocorticoid '''fludrocortisone acetate''' is available in an oral preparation and this is used most commonly for management.<br />
<br />
During times of '''stress''', courses of corticosteroids (e.g. prednisolone) should be provided and '''table salt''' should be added to the diet. Water should be avaiable at all time and blood electrolyte levels should be monitored at regular intervals to ensure that the correct dose of fludrocortisone is used.<br />
<br />
==Prognosis==<br />
The prognosis for long term survival is excellent for animals with hypoadrenocorticism provided that any crisis is controlled. <br />
<br />
==References==<br />
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company<br />
<br />
[[Category:Cell Mediated Autoimmune Diseases]][[Category:To Do - James]][[Category:Dog]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Hernia,_Pleuroperitoneal_Diaphragmatic&diff=89665Hernia, Pleuroperitoneal Diaphragmatic2010-08-31T22:43:14Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
This is a very rare form of hernia which is caused by a defect in the [[Muscles Developmental - Pathology#Congenital diaphragmatic defects|skeletal muscle]] of the diaphragm. The defect prevents the animal from generating the negative intrathoracic pressure required for inspiration and small animals therefore usually die at or shortly after birth. Large animals may survive for considerable periods of time with no clinical signs or they may show signs of respiratory difficulty or abdominal pain (if abdominal organs are incarcerated in the defect).<br />
<br />
[[Category:Peritoneal_Cavity_-_Developmental_Pathology]]<br />
[[Category:To Do - Review]]<br />
[[Category:To_Do_-_James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Gastrinoma&diff=89664Gastrinoma2010-08-31T22:42:00Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{|cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Zollinger-Ellison Syndrome'''<br />
|}<br />
<br />
==Description==<br />
A gastrinoma is a neoplasm of pancreatic islet cells that secretes the hormone gastrin, an example of an ectopic paraneoplastic disease. The disease was first described by Zollinger and Ellison in humans in 1955 and it has since been recognised occasionally in dogs and cats. Gastrinomas are the least common of the islet cell neoplasia, the other types being [[Glucagonoma|glucagonomas]] and [[Insulinoma|insulinomas]]. <br />
<br />
The excessive secretion of gastrin leads to hyperplasia of the crypt cells of the antral gastric mucosa and hyperstimulation of gastric acid production from the [[Stomach and Abomasum - Anatomy & Physiology|parietal cells]] of the stomach. Antral hyperplasia may result in '''gastric outflow obstruction'''. The excessive secretion of gastric acid leads to [[Gastric Ulceration - Dog|'''gastro-duodenal ulceration''']] and [[Oesophagitis|'''oesophagitis''']] due to gastro-oesophageal reflux. In severe cases of the disease, deep gastric ulcers may erode blood vessels causing '''haemorrhage''' or perforate, causing septic [[Peritonitis - Cats and Dogs|'''peritonitis''']]. Gastrinomas have often metastasised to local lymph nodes or to the liver at the time of diagnosis. <br />
<br />
==Signalment==<br />
Gastrinomas have only ever been reported in a very few dogs and cats and the disease is extremely rare.<br />
<br />
==Diagnosis==<br />
===Clinical signs===<br />
Affected animals may show few clinical signs as the condition first develops but, in more advanced cases, the following signs may be documented:<br />
*'''Anorexia''' and severe '''weight loss'''<br />
*[[Vomiting|'''Vomiting''']] which may contain blood if blood vessels are eroded ('''haematemesis'''). Vomiting occurs due to gastric irritation and possible gastric outflow obstruction. <br />
*'''[[Diarrhoea]]''' which may show evidence of haemorrhage in the upper gastro-intestinal tract ('''melaena'''). Diarrhoea occurs due to the production of excessive volumes of gastric secretions and because gastrin reduces the ability of the intestine to absorb fluid and electrolytes. Malabsorption may occur due to small intestinal villous atrophy.<br />
*'''Collapse''' and '''shock''' if an ulcer perforates to cause peritonitis.<br />
*Severe haemorrhage may result in '''pallor''', '''tachycardia''', a '''haemic murmur''' and '''collapse'''<br />
Affected animals may also show signs of [[Oesophagitis|'''oesophagitis''']], including regurgitation and hypersalivation.<br />
<br />
===Laboratory Tests===<br />
====Haematology====<br />
If haemorrhage is occurring, the '''packed cell volume''' (PCV) and blood '''haemoglobin''' concentration may be abnormally low and there may be signs of regeneration after 48-72 hours. In cases of chronic haemorrhage, the blood [[Urea|urea]] concentration may be raised and, as '''iron''' reserves are expended, a microcytic hypochromic anaemia may develop.<br />
<br />
Areas of gastro-duodenal ulceration will be inflamed, producing a '''leucoytosis'''. This may be neutrophilic, monocytic or both depending on the stage of disease.<br />
<br />
====Biochemistry====<br />
Blood '''[[Urea|urea]]''' concentration may be elevated in cases of gastro-intestinal haemorrhage. Haemorrhage will lead to the loss of plasma proteins, producing a [[Hypoalbuminaemia|'''hypoalbuminaemia''']]. <br />
<br />
Repeated bouts of gastric vomiting may lead to the loss of gastric acid and intestinal fluid, producing '''hyponatraemia''', '''hypokalaemia''', '''hypochloraemia''' and '''metabolic alkalosis'''.<br />
<br />
===Diagnostic Imaging===<br />
'''Ultrasonography''' is most useful for detection of gastro-duodenal ulceration and of metastases in the liver, peritoneal cavity and local lymph nodes<ref>Robben JH, Pollak YW, Kirpensteijn J, Boroffka SA, van den Ingh TS, Teske E, Voorhout G. '''Comparison of ultrasonography, computed tomography, and single-photon emission computed tomography for the detection and localization of canine insulinoma.''' ''J Vet Intern Med. 2005 Jan-Feb;19(1):15-22.''</ref>.<br />
<br />
Ulceration and antral hyperplasia may also be visualised by '''endoscopy'''.<br />
<br />
===Other Tests===<br />
It is possible to measure the '''gastric pH''' using a pH meter placed into the stomach. The pH in affected animals will be persistently lower than that of normal animals.<br />
<br />
In humans, Zollinger-Ellison syndrome is diagnosed by directly measuring serum gastrin concentration before or after injecting secretin or calcium, which both stimulate secretion. These tests have all been performed in animals but, given the very low prevalence of the disease, they are not widely available. Serum gastrin concentration may be elevated in many other disease conditions and a single basal measurement is not sufficiently specific to make a diagnosis of gastrinoma in dogs<ref>Gabbert NH, Nachreiner RF, Holmes-Wood P, Kivela JH. '''Serum immunoreactive gastrin concentrations in the dog: basal and postprandial values measured by radioimmunoassay''' ''Am J Vet Res. 1984 Nov;45(11):2351-3.''</ref><ref>Happé RP, van der Gaag I, Lamers CB, van Toorenburg J, Rehfeld JF, Larsson LI. '''Zollinger-Ellison syndrome in three dogs.''' ''Vet Pathol. 1980 Mar;17(2):177-86.''</ref>.<br />
<br />
===Pathology===<br />
Post mortem examination of the pancreas of affected animals may reveal multiple variably sized neoplasms that feel firm because they have a large connective tissue mass. The tumours may be partially encapsulated and locally invasive. Metastases are commonly detected in the [[Liver - Anatomy & Physiology|liver]] or local lymph nodes.<br />
<br />
==Treatment==<br />
Ideally, the tumour should be excised surgically by performing a '''partial pancreatectomy'''. Intra-operative ultrasound scans can be performed if the mass is not evident within the pancreatic parenchyma. Any evident metastatic masses can also be biopsied or resected during the procedure. Gastric hyperacidity usually recurs soon after resection, probably due to the presence of extra-pancreatic metastases.<br />
<br />
The somatostatin analogue '''octreotide''' has been used pre- and post-opratively in the management of gastrinomas <ref>Altschul M, Simpson KW, Dykes NL, Mauldin EA, Reubi JC, Cummings JF. '''Evaluation of somatostatin analogues for the detection and treatment of gastrinoma in a dog.''' ''J Small Anim Pract. 1997 Jul;38(7):286-91.''</ref>but so few cases have been described that it is not clear if this therapy is beneficial. Adjunctive therapy with [[Gastroprotective Drugs|'''gastro-protectants''']] such as sucralfate and with '''inhibitors of gastric acid secretion''' (such as omeprazole, ranitidine or cimetidine) is also indicated to reduce the severity of gastro-duodenal ulceration and the signs it causes.<br />
<br />
==Prognosis==<br />
In approximately 85% of cases, gastrinomas have metastasised at the time of diagnosis and the tumour is likely to recur after surgical resection.<br />
<br />
==References==<br />
<references/><br />
[http://w3.vet.cornell.edu/nst/nst.asp?Fun=Image&imgID=7762 Image of pancreatic garstrinoma in a dog from Cornell Veterinary Medicine]<br />
<br />
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2)<br />
<br />
[[Category:Pancreas_-_Hyperplastic_and_Neoplastic_Pathology]][[Category:Endocrine_System_-_Pathology]][[Category:Dog]][[Category:Cat]]<br />
[[Category:Neoplasia]]<br />
[[Category:To_Do_-_James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Evan%27s_syndrome&diff=89663Evan's syndrome2010-08-31T22:41:24Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
==Description==<br />
Evan's syndrome refers to the concurrent presence of '''[[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]''' (IMHA) and '''[[Immune Mediated Thrombocytopaenia|immune-mediated thrombocytopaenia]]''' (ITP) in the same patient. Animals suffering from this disease have a poorer prognosis than those with either disease alone.<br />
<br />
[[Category:Dog]][[Category:Cat]][[Category:Antibody Mediated Autoimmune Diseases]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Erythropoietic_Porphyria&diff=89662Erythropoietic Porphyria2010-08-31T22:40:46Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Congenital Pink Tooth'''<br><br />
'''Porphyria'''<br />
|}<br />
<br />
==Description==<br />
Congenital erythropoietic porphyria is a rare disease that affects cattle, cats and occasionally pigs. It occurs due to a defect in the metabolism of the haem group of haemoglobin leading to the deposition of pigment molecules in the skin and teeth. <br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
The deposition of haem degradation products in the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]] results in red/pink discolouration, hence the name '''pink tooth'''.<br />
<br />
The pigment products which are deposited in the skin cause secondary [[Photosensitisation|'''photosensitisation''']]. This manifests as a crusting dermatitis in non-pigmented areas of the skin which are exposed to sunlight. Cattle are often affected over their face, around their eyes and over any white patches of the body.<br />
<br />
Some types of porphyria may cause '''anaemia''' in Siamese cats.<br />
<br />
===Differential Diagnoses===<br />
Discolouration of single teeth is more likely to be caused by '''pathological processes in the oral cavity''', including tooth root abscesses and pulpitis. '''Fluorosis''' may cause chalky mottling (odontodystrophy) and yellow/brown discolouration of teeth in cattle that are exposed to cement works effluent.<br />
<br />
===Pathology===<br />
At post-mortem examination, the bones are found to have the same pink/brown discolouration as the teeth.<br />
<br />
==Treatment==<br />
There is no specific treatment for porphyria. Affected animals should be kept out of sunlight.<br />
<br />
==Prognosis==<br />
Affected animals may suffer from severe burns if they exposed to sunlight but they may otherwise live normally.<br />
<br />
==References==<br />
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company<br />
<br />
[[Category:Teeth - Developmental Pathology]][[Category:Cattle]][[Category:Cat]][[Category:Pig]]<br />
[[Category:To_Do_-_James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Eosinophilia&diff=89661Eosinophilia2010-08-31T22:38:39Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Eosinophilia refers to an increase in the number of [[Eosinophil|eosinophils]] present in the blood or tissues. This form of leucocytosis is most commonly associated with parasitism or hypersensitivity reactions, including the following diseases:<br />
*Hypersensitivity Reactions<br />
**'''Flea bite hypersensivity''' is the most common cause of eosinophilia in cats and it may occur in animals with signs of [[Miliary Dermatitis|miliary dermatitis]]. Food hypersensitivity reactions and [[Atopic Dermatitis|atopic dermatitis]] may also be variably associated with eosinophilia.<br />
**'''[[Feline Eosinophilic Granuloma|Feline eosinophilic granuloma complex]]''' may be associated with blood or tissue eosinophilia. The eosinophilic ulcer form is rarely associated with systemic changes whereas eosinophilia is a near constant feature of the eosinophilic plaque. The linear granuloma is variably associated with blood eosinophilia.<br />
**'''Feline hypereosinophilic syndrome''' is a rare cause of eosinophilia that is associated with infiltration of various organs, particularly the liver and spleen, by eosinophils.<br />
**'''[[Enteritis, Eosinophilic|Eosinophilic enteritis]]''' is a form of infiltrative enteritis which may be focal or diffuse. The latter form of disease is especially common in German shepherd dogs as an idiopathic complex that may be accompanied by blood eosinophilia. The focal form may be associated with intestinal parasite infection. '''Multisystemic Eosinophilic Enteritis and Dermatitis (MEED)''', a rare form of equine [[Inflammatory Bowel Disease|inflammatory bowel disease]] may also be associated with blood eosinophilia.<br />
**'''[[Feline Asthma Syndrome|Feline asthma syndrome]]''', canine '''[[Pulmonary Infiltration with Eosinophilia|pulmonary infiltration with eosinophils (PIE)]]''' and equine '''eosinophilic pulmonary granulomas''' may all be associated with blood eosinophilia.<br />
*Parasite Infection - Both endo- and ecto-parasite infections may result in blood eosinophilia, in particular:<br />
**''[[Aelurostrongylus abstrusus]]'', the feline lungworm.<br />
**''[[Dirofilaria immitis]]'' which causes [[Heartworm]].<br />
**Gastro-intestinal parasites including ''[[Toxocara canis]]'' and the other toxascarids of dogs and cats.<br />
*Miscellaneous<br />
**The rare form of eosinophilic '''chronic myeloid leukaemia''' may result in the abnormally high production of eosinophils.<br />
**'''[[Hypoadrenocorticism]]''' or Addison's disease may be associated with eosinophilia, a feature that may help to differentiate it from other diseases as such severely ill animals would usually be expected to have a stress leucogram.<br />
**Eosinophilia may occur in '''pregnant small animals'''.<br />
**'''German shepherd dogs''' are particularly prone to the development of eosinophilia and this may or may not be related to the presence of concurrent enteritis.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Eosinopenia&diff=89660Eosinopenia2010-08-31T22:36:51Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Eosinopaenia refers to a reduction in the normal number of circulating blood [[Eosinophil|eosinophils]]. It ocurs most commonly as part of a stress leucocgram and in other situations that result in an increase in the circulating concentration of glucocorticoids:<br />
<br />
*'''Stress leucogram''', with which [[Neutrophilia|neutrophilia]], [[Monocytosis|monocytosis]] and [[Lymphopenia|lymphopaenia]] would also be expected. <br />
*'''Hyperadrenocorticism''' (Cushing's disease) results in a similar pattern due to an increase in endogenous glucocorticoids.<br />
*'''Iatrogenic hyperadrenocorticism''' caused by the administration of corticosteroids, even with the use of topical otic or ophthalmic preparations.<br />
<br />
<br />
Corticosteroids are thought to exert a depressive effect on lymphocytes which usually stimulate eosinophil production.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Canine_Leukocyte_Adhesion_Deficiency&diff=89659Canine Leukocyte Adhesion Deficiency2010-08-31T22:35:28Z<p>JamesSwann: </p>
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<div>{{unfinished}}<br />
<br />
{|cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
|'''CLAD'''<br><br />
'''Canine Granulocytopathy Syndrome'''<br />
|}<br />
<br />
==Description==<br />
Leucocyte adhesion deficiency (LAD) is caused by a defect in a surface molecule expressed by neutrophils which usually allows this type of cell to attach to vessel walls and move into tissues. The disease was first reported in a dog in 1987<ref>Giger U, Boxer LA, Simpson PJ, Lucchesi BR, Todd RF 3rd. '''Deficiency of leukocyte surface glycoproteins Mo1, LFA-1, and Leu M5 in a dog with recurrent bacterial infections: an animal model.''' ''Blood. 1987 Jun;69(6):1622-30.''</ref> and it bears similarities to leucocyte adhesion deficiencies in mice and humans. The surface molecule, the integrin subunit CD18, is affected by a mis-sense mutation of Cys-38-Ser and this results in a failure to express multiple integrin molecules as CD18 is a common subunit in several heterodimeric complexes. The disease is inherited in an autosomal recessive manner, with heterozygous carriers showing no signs of disease.<br />
<br />
Since stimulatory cytokines are still released from inflamed tissues, neutrophils are produced in greater numbers from the bone marrow and released into the circulation. As these cells are unable to enter tissues, affected animals develop a persistent [[Neutrophilia|neutrophilia]]. Neutrophils from affected animals also show defects in chemotaxis and phagocytosis.<br />
<br />
==Signalment==<br />
The genetic defect described above has only been described in dogs of the Irish setter breed and in a very small number of Irish setter crosses<ref>Debenham SL, Millington A, Kijast J, Andersson L, Binns M. '''Canine leucocyte adhesion deficiency in Irish red and white setters.''' ''J Small Anim Pract. 2002 Feb;43(2):74-5.''</ref>.<br />
<br />
==Diagnosis==<br />
LAD is a very rare disease and should only be seriously considered in Irish setters with relevant genetic history.<br />
===Clinical Signs===<br />
Affected animals show signs of recurrent infections without neutrophilic exudates. Signs which have been described include<ref>Trowald-Wigh G, Ekman S, Hansson K, Hedhammar A, Hård af Segerstad C. '''Clinical, radiological and pathological features of 12 Irish setters with canine leucocyte adhesion deficiency.''' ''J Small Anim Pract. 2000 May;41(5):211-7.''</ref>:<br />
*'''Pyrexia'''<br />
*'''Skin lesions''' including pyoderma, furunculosis and ulceration<br />
*'''Anorexia''' and failure to gain weight<br />
*'''Bone disorders''' including metaphyseal osteopathy, craniomandibular osteopathy and [[Osteomyelitis|osteomyelitis]]<br />
*Generalised '''lymphadenopathy'''<br />
<br />
===Laboratory Tests===<br />
Haematological analysis of blood samples will reveal a persistent neutrophilia.<br />
<br />
===Other Tests===<br />
Genetic tests are now available to screen for the mutation in the CD18 gene in Irish setters<ref>Verfaillie T, Verdonck F, Cox E. '''Simple PCR-based test for the detection of canine leucocyte adhesion deficiency.''' ''Vet Rec. 2004 Jun 26;154(26):821-3.''</ref>. Carrier animals can then be prevented from breeding in future. A study of Irish setters in Germany revealed a carriage rate of 11%<ref>Pfeiffer I, Brenig B. '''Frequency of the canine leucocyte adhesion deficiency (CLAD) mutation among Irish red setters in Germany.''' ''J Anim Breed Genet. 2005 Apr;122(2):140-2.''</ref>.<br />
<br />
==Treatment==<br />
Supportive therapy may be attempted with antibiotics for specific infections but this is associated with a poor success rate.<br />
<br />
More recently, various forms of stem cell therapy have been attempted to introduce cells capable of expressing CD18. Typically, CD34 positive (pluripotential) stem cells are transformed with a viral vector expressing CD18 before being transfused into puppies suffering from CLAD. The technique has achieved success when foamy virus or gamma retroviral vectors were used to transfect the stem cells<ref>Hai M, Adler RL, Bauer TR Jr, Tuschong LM, Gu YC, Wu X, Hickstein DD. '''Potential genotoxicity from integration sites in CLAD dogs treated successfully with gammaretroviral vector-mediated gene therapy.''' ''Gene Ther. 2008 Jul;15(14):1067-71. Epub 2008 Mar 27.''</ref><ref>Bauer TR Jr, Allen JM, Hai M, Tuschong LM, Khan IF, Olson EM, Adler RL, Burkholder TH, Gu YC, Russell DW, Hickstein DD. '''Successful treatment of canine leukocyte adhesion deficiency by foamy virus vectors.''' ''Nat Med. 2008 Jan;14(1):93-7. Epub 2007 Dec 23.''</ref>.<br />
<br />
==Prognosis==<br />
Affected animals are unlikely to survive beyond six months of age as they are unable to control widespread bacterial infections.<br />
<br />
==References==<br />
<references/><br />
<br />
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine (6th edition, volume 2)''' ''Saunders Elsevier''<br />
<br />
[[Category:Primary Innate Immunity Deficiencies]]<br />
[[Category:To Do - James]][[Category:Dog]][[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Cyclic_neutropenia&diff=89658Cyclic neutropenia2010-08-31T22:33:21Z<p>JamesSwann: Redirected page to Canine Cyclic Haematopoiesis</p>
<hr />
<div>#REDIRECT [[Canine Cyclic Haematopoiesis]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Cyclic_neutropaenia&diff=89657Cyclic neutropaenia2010-08-31T22:32:52Z<p>JamesSwann: Redirected page to Canine Cyclic Haematopoiesis</p>
<hr />
<div>#REDIRECT [[Canine Cyclic Haematopoiesis]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Gray_collie_syndrome&diff=89656Gray collie syndrome2010-08-31T22:32:18Z<p>JamesSwann: Redirected page to Canine Cyclic Haematopoiesis</p>
<hr />
<div>#REDIRECT [[Canine Cyclic Haematopoiesis]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Canine_Cyclic_Haematopoiesis&diff=89655Canine Cyclic Haematopoiesis2010-08-31T22:31:44Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Grey Collie Syndrome'''<br><br />
'''Cyclic Neutropaenia'''<br />
|}<br />
<br />
==Description==<br />
Cyclic haematopoiesis is a disease inherited in an autosomal recessive manner. It is associated with an insertion mutation in the gene AP3B1 and it results in defective production of blood cells by bone marrow stem cells. The disease has only been described in grey collies which are homozygous for the genetic mutation; heterozygous animals do not show clinical signs. <br />
<br />
From around 7 weeks of age, affected animals begin to show cyclic waves of [[Neutropenia|neutropenia]] and of other cell type reductions. The reductions in other cell types (including platelets, eosinophils and red blood cells) do not occur in synchrony with each other or the neutropenia and bouts of reduction are interspersed with periods of marked blood cell overproduction. The periods of neutropenia last for approximately 2-4 days and are associated with severe systemic infections, including pneumonia, oronasal infection, bacterial enteritis, septic arthritis and sepsis.<br />
<br />
During the periods when cell numbers are increased, it is thought that cytokines drive the production and deposition of amyloid proteins in various tissues, including the kidney, liver, spleen and pancreas. Almost all affected animals develop this further disease and it ultimately results in organ failure.<br />
<br />
Affected animals rarely survive to sexual maturity and the disease is transmitted by heterozygous carriers.<br />
<br />
==Signalment==<br />
The disease has only been described in grey collies which are homozygous for the genetic mutation.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
[[Image:Grey Collie Syndrome.jpg|thumb|Appearance of a puppy with Grey Collie syndrome<br><small>Copyright Michelle Tennis & Peggy Melton]]</small><br />
Affected animals have a '''diluted grey coat colour''' and are often '''smaller than their littermates'''. The majority of other clinical signs relate to the reductions in various types of cell, including:<br />
*'''Pyrexia''', '''lethargy''' and '''depression''' due to infection which develops rapidly in neutropenic animals.<br />
*Signs of specific infections, including dyspnoea, diarrhoea, oral, nasal and ocular discharge, joint pain and generalised lymph node enlargement.<br />
Most affected animals die within a few weeks of birth and rarely survive to 2-3 years.<br />
<br />
===Laboratory Tests===<br />
Alterations in cell numbers can be documented by serial blood samples and subsequent haematological analysis. <br />
<br />
===Other Tests===<br />
'''Bone marrow aspirates''' can be used to demonstrate alterations in the erythroid: myeloid ratio, changes that generally precede the fluctuations in blood cell levels. <br />
<br />
'''Genetic tests''' are available to detect the mutation. These tests can be used to detect heterozygous carriers and to prevent them from breeding.<br />
<br />
==Treatment==<br />
Supportive therapy is indicated to treat infectious disease, anaemia or bleeding disorders caused by reductions in blood cell numbers. For long term management of the condition, injections of recombinant G-CSF (Granulocyte-Colony Stimulating Factor) or SCF (Stem Cell Factor) may be used to stimulate the production of leucocytes from bone marrow stem cells. These products are expensive and not widely available but they may result in prolonged survival without significant adverse effects.<br />
<br />
==Prognosis==<br />
Unless treatment with recombinant cytokines can be initiated, affected animals have an extremely poor prognosis and are unlikely to survive beyond 2 years of age.<br />
<br />
[[Category:Primary Innate Immunity Deficiencies]]<br />
[[Category:Dog]]<br />
[[Category:To Do - James]]<br />
[[Category:To Do - Review]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Canine_Cyclic_Haematopoiesis&diff=89654Canine Cyclic Haematopoiesis2010-08-31T22:30:52Z<p>JamesSwann: /* Diagnosis */</p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Grey Collie Syndrome'''<br><br />
'''Cyclic Neutropaenia'''<br />
|}<br />
<br />
==Description==<br />
Cyclic haematopoiesis is a disease inherited in an autosomal recessive manner. It is associated with an insertion mutation in the gene AP3B1 and it results in defective production of blood cells by bone marrow stem cells. The disease has only been described in grey collies which are homozygous for the genetic mutation; heterozygous animals do not show clinical signs. <br />
<br />
From around 7 weeks of age, affected animals begin to show cyclic waves of [[Neutropenia|neutropenia]] and of other cell type reductions. The reductions in other cell types (including platelets, eosinophils and red blood cells) do not occur in synchrony with each other or the neutropenia and bouts of reduction are interspersed with periods of marked blood cell overproduction. The periods of neutropenia last for approximately 2-4 days and are associated with severe systemic infections, including pneumonia, oronasal infection, bacterial enteritis, septic arthritis and sepsis.<br />
<br />
During the periods when cell numbers are increased, it is thought that cytokines drive the production and deposition of amyloid proteins in various tissues, including the kidney, liver, spleen and pancreas. Almost all affected animals develop this further disease and it ultimately results in organ failure.<br />
<br />
Affected animals rarely survive to sexual maturity and the disease is transmitted by heterozygous carriers.<br />
<br />
==Signalment==<br />
The disease has only been described in grey collies which are homozygous for the genetic mutation.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
[[Image:Grey Collie Syndrome.jpg|thumb|Appearance of a puppy with Grey Collie syndrome<br><small>Copyright Michelle Tennis & Peggy Melton]]</small><br />
Affected animals have a '''diluted grey coat colour''' and are often '''smaller than their littermates'''. The majority of other clinical signs relate to the reductions in various types of cell, including:<br />
*'''Pyrexia''', '''lethargy''' and '''depression''' due to infection which develops rapidly in neutropenic animals.<br />
*Signs of specific infections, including dyspnoea, diarrhoea, oral, nasal and ocular discharge, joint pain and generalised lymph node enlargement.<br />
Most affected animals die within a few weeks of birth and rarely survive to 2-3 years.<br />
<br />
===Laboratory Tests===<br />
Alterations in cell numbers can be documented by serial blood samples and subsequent haematological analysis. <br />
<br />
===Other Tests===<br />
'''Bone marrow aspirates''' can be used to demonstrate alterations in the erythroid: myeloid ratio, changes that generally precede the fluctuations in blood cell levels. <br />
<br />
'''Genetic tests''' are available to detect the mutation. These tests can be used to detect heterozygous carriers and to prevent them from breeding.<br />
<br />
==Treatment==<br />
Supportive therapy is indicated to treat infectious disease, anaemia or bleeding disorders caused by reductions in blood cell numbers. For long term management of the condition, injections of recombinant G-CSF (Granulocyte-Colony Stimulating Factor) or SCF (Stem Cell Factor) may be used to stimulate the production of leucocytes from bone marrow stem cells. These products are expensive and not widely available but they may result in prolonged survival without significant adverse effects.<br />
<br />
==Prognosis==<br />
Unless treatment with recombinant cytokines can be initiated, affected animals have an extremely poor prognosis and are unlikely to survive beyond 2 years of age.<br />
<br />
[[Category:Primary Innate Immunity Deficiencies]]<br />
[[Category:Dog]]<br />
[[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Neutrophilia&diff=89653Neutrophilia2010-08-31T22:27:44Z<p>JamesSwann: /* Description */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Neutrophilia refers to an increase in the number of [[Neutrophil|neutrophils]] in the blood. In many cases, neutrophilia is accompanied by the release of substantial numbers of immature neutrophils into the blood stream from the bone marrow. The nuclei of these '''Band cells''' are not segmented and they appear to be elongated bent tubes in the cytoplasm. The presence of band cells in the blood indicates that there is an intense need for neutrophils to maintain normal blood levels as they are lost in a purulent process somewhere in the body. When the percentage of the total neutrophil population that is contributed by these immature forms is high, the neutrophilia is described as having a '''regenerative left shift'''.<br />
<br />
Very severe diseases that deplete the neutrophils may also exhaust the reserve supply of these cells in the bone marrow. In such situations, there is a neutropenia without band cells in the circulation, a phenomenon called a '''degenerative right shift'''. Some severe localised infections (including pyometras) may cause a neutrophilia of much greater magnitude than is usually observed. This so-called '''leukaemoid response''' may precede a right shift.<br />
<br />
There are numerous causes of neutrophilia and it is the most common and least specific abnormal finding when blood samples undergo haematological analysis. Common causes include:<br />
<br />
*'''Purulent Foci''' and '''abscesses''' in the body produce substantial neutrophilia. Examples include pyometra, severe pyoderma and empyema (purulent inflammation of a body cavity). In severe cases of purulent inflammation, neutrophils may appear '''toxic''' when observed on cytological slides. These toxic cells have evident, blue-staining cytoplasmic granules and some cytoplasmic vacuolation. These cells have decreased bactericidal capability and do not respond as quickly to chemotactic stimuli.<br />
<br />
*'''Bacterial infection''' may result in neutrophilia as neutrophils are the major type of leucocyte that act to control this type of pathogen. Some bacteria, particularly Gram positive species, are particularly pyogenic due to their ability to resist intracellular killing by neutrophils.<br />
<br />
*'''Necrosis''' of any tissue will result in neutrophilia. Common causes of tissue necrosis include burns, malignancies and infections.<br />
<br />
*'''Fungal infection''' with, for example ''[[Aspergillus spp.]]''.<br />
<br />
*'''Viral infection''' may cause a neutrophilia but neutrophils are often not the major type of inflammatory cell responding to the infection. Examples include [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Herpesviridae|equine rhinotracheitis virus]] (EHV-1) and [[Herpesviridae#Bovine herpesvirus -1|infectious bovine rhinotracheitis]] (IBR or BHV-1).<br />
<br />
*'''Parasitic infection''' may cause a neutrophilia but neutrophils are often not the major type of inflammatory cell responding to the infection and [[Eosinophilia|eosinophilia]] is more likely. Examples include [[Fasciolosis|fasciolosis]] and [[Toxoplasmosis|toxoplasmosis]].<br />
<br />
*'''Immune-mediated disease''' frequently causes a neutrophilia, often with a concurrent [[Monocytosis|monocytosis]]. Examples include [[Rheumatoid Arthritis|rheumatoid arthritis]], [[Systemic Lupus Erythematosus|systemic lupus erythematosus]] and [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA).<br />
<br />
*'''Miscellaneous factors''' that can cause neutrophilia include:<br />
**Excitement, fear and strenuous exercise in young animals.<br />
**Corticosteroids as part of a stress leucogram with concurrent [[Monocytosis|monocytosis]], [[Eosinopenia|eosinopenia]] and [[Lymphopenia|lymphopenia]]. The corticosteroids may be endogenous (with pain, stress or [[Canine Hyperadrenocorticism - Cushing's Disease|hyperadrenocorticism]]) or exogenous with medical therapy for a variety of other diseases.<br />
**As a response to any cause of [[Anaemia - Introduction|anaemia]].<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Neutrophilia&diff=89652Neutrophilia2010-08-31T22:26:43Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Neutrophilia refers to an increase in the number of [[Neutrophil|neutrophils]] in the blood. In many cases, neutrophilia is accompanied by the release of substantial numbers of immature neutrophils into the blood stream from the bone marrow. The nuclei of these '''Band cells''' are not segmented and they appear to be elongated bent tubes in the cytoplasm. The presence of band cells in the blood indicates that there is an intense need for neutrophils to maintain normal blood levels as they are lost in a purulent process somewhere in the body. When the percentage of the total neutrophil population that is contributed by these immature forms is high, the neutrophilia is described as having a '"regenerative left shift'".<br />
<br />
Very severe diseases that deplete the neutrophils may also exhaust the reserve supply of these cells in the bone marrow. In such situations, there is a neutropenia without band cells in the circulation, a phenomenon called a '''degenerative right shift'''. Some severe localised infections (including pyometras) may cause a neutrophilia of much greater magnitude than is usually observed. This so-called '''leukaemoid response''' may precede a right shift.<br />
<br />
There are numerous causes of neutrophilia and it is the most common and least specific abnormal finding when blood samples undergo haematological analysis. Common causes include:<br />
<br />
*'''Purulent Foci''' and '''abscesses''' in the body produce substantial neutrophilia. Examples include pyometra, severe pyoderma and empyema (purulent inflammation of a body cavity). In severe cases of purulent inflammation, neutrophils may appear '''toxic''' when observed on cytological slides. These toxic cells have evident, blue-staining cytoplasmic granules and some cytoplasmic vacuolation. These cells have decreased bactericidal capability and do not respond as quickly to chemotactic stimuli.<br />
<br />
*'''Bacterial infection''' may result in neutrophilia as neutrophils are the major type of leucocyte that act to control this type of pathogen. Some bacteria, particularly Gram positive species, are particularly pyogenic due to their ability to resist intracellular killing by neutrophils.<br />
<br />
*'''Necrosis''' of any tissue will result in neutrophilia. Common causes of tissue necrosis include burns, malignancies and infections.<br />
<br />
*'''Fungal infection''' with, for example ''[[Aspergillus spp.]]''.<br />
<br />
*'''Viral infection''' may cause a neutrophilia but neutrophils are often not the major type of inflammatory cell responding to the infection. Examples include [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Herpesviridae|equine rhinotracheitis virus]] (EHV-1) and [[Herpesviridae#Bovine herpesvirus -1|infectious bovine rhinotracheitis]] (IBR or BHV-1).<br />
<br />
*'''Parasitic infection''' may cause a neutrophilia but neutrophils are often not the major type of inflammatory cell responding to the infection and [[Eosinophilia|eosinophilia]] is more likely. Examples include [[Fasciolosis|fasciolosis]] and [[Toxoplasmosis|toxoplasmosis]].<br />
<br />
*'''Immune-mediated disease''' frequently causes a neutrophilia, often with a concurrent [[Monocytosis|monocytosis]]. Examples include [[Rheumatoid Arthritis|rheumatoid arthritis]], [[Systemic Lupus Erythematosus|systemic lupus erythematosus]] and [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA).<br />
<br />
*'''Miscellaneous factors''' that can cause neutrophilia include:<br />
**Excitement, fear and strenuous exercise in young animals.<br />
**Corticosteroids as part of a stress leucogram with concurrent [[Monocytosis|monocytosis]], [[Eosinopenia|eosinopenia]] and [[Lymphopenia|lymphopenia]]. The corticosteroids may be endogenous (with pain, stress or [[Canine Hyperadrenocorticism - Cushing's disease|hyperadrenocorticism]]) or exogenous with medical therapy for a variety of other diseases.<br />
**As a response to any cause of [[Anaemia - Introduction|anaemia]].<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphopenia&diff=89649Lymphopenia2010-08-31T22:03:03Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphopenia is a reduction in the numbers of lymphocytes in the blood. This phenomenon is most commonly associated with stress (as part of the '''stress leucogram''') or with viral infection. Its causes therefore include:<br />
*Viral infection with [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Infectious canine hepatitis]], [[Feline infectious enteritis|feline infectious enteritis]] or [[Bovine Viral Diarrhoea|bovine viral diarrhoea]] (BVD)<br />
*Bone marrow suppression caused by '''chemotherapy''' or '''radiotherapy'''. Since neutrophils have a much shorter circulating half life, they are the first cell line to fall with any insult to the bone marrow but lymphopenia may occur as part of a more severe pancytopenia.<br />
*Inherited or acquired immunodeficiency syndromes, including '''[[Equine Severe Combined Immune Deficiency|SCID]]''' (Severe Combined Immunodeficiency Syndrome) in Arab foals and [[Feline Immunodeficiency Virus|'''feline immunodeficiency virus''']] infection.<br />
*Stress leucogram, characterised by '''[[Neutrophilia|neutrophilia]]''', '''[[Monocytosis|monocytosis]]''', '''[[Eosinopenia|eosinopenia]]''' and '''[[Lymphopenia|lymphopenia]]'''. A similar pattern may occur with [[Canine Hyperadrenocorticism - Cushing's Disease|hyperadrenocorticism]] (Cushing’s disease) or exogenous corticosteroid therapy as these hormones selectively suppress lymphocytic activity and the inflammatory response in general. <br />
*Leakage of lymphatic fluid may result in loss of lymphocytes, as occurs with '''[[Lymphangiectasia|lymphangiectasia]]''' or '''[[Chylous Effusion|chylothorax]]'''.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Neutropenia&diff=89648Neutropenia2010-08-31T21:58:01Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Neutropenia refers to a reduction in number of [[Neutrophils|neutrophils]] circulating in the blood. As with deficiencies in other types of blood cell, neutropenia may occur due to failure to produce sufficient cells or due to excessive loss of cells as part of a pathological process. The major causes of neutropenia are:<br />
*Infections caused by '''Gram negative bacteria''' which are able to produce endotoxin.<br />
*Diseases that result in reduced production of cell in the [[Bone Marrow - Anatomy & Physiology|bone marrow]]. In these diseases, neutropenia may be accompanied by other '-penias' and this may result in deficiencies of all of the blood cell lines: '''pancytopenia'''. Examples of this type of disease include:<br />
**Radiotherapy and cytotoxic chemotherapy<br />
**Toxins including bracken, chloramphenicol, trimethoprim-potentiated [[Sulphonamides|sulphonamides]] in Dobermann dogs and oestrogens.<br />
**Infection with viruses that have a tropism for rapidly dividing cells, including [[Canine Parvovirus|canine parvovirus]], [[Canine Distemper|canine distemper]] and [[Infectious Canine Hepatitis|infectious canine hepatitis]]. [[Feline Panleucopaenia|Feline panleucopaenia]] may result in multiple '-cytopenias'. <br />
**Myelophthisis that may be due to myelofibrosis or to the growth of tumours that replace or displace normal [[Bone Marrow - Anatomy & Physiology|bone marrow]]. The most common type of tumour that cause myelophthisis are myeloproliferative or lymphoproliferative diseases.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_Mediated_Thrombocytopaenia&diff=89647Immune Mediated Thrombocytopaenia2010-08-31T21:48:34Z<p>JamesSwann: /* Immunosuppressive Therapy */</p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Idiopathic Thrombocytopaenic Purpura'''<br><br />
'''Evan’s Syndrome'''<br />
|}<br />
<br />
==Description==<br />
Immune-mediated thrombocytopaenia (ITP) occurs due to an autoimmune response directed against circulating platelets or megakaryocytes in the bone marrow. The destruction of cells is mediated by antibodies, making ITP a form of '''[[Type II Hypersensitivity|type II hypersensitivity]]'''. The antibodies bind to cells and act as a foundation for the assembly of serum complement components or as opsonins, promoting the uptake and destruction of platelets by cells of the monocyte-phagocyte system (MPS). The destruction of platelets usually results in severe [[Platelet Abnormalities|thrombocytopaenia]] and, if the blood level of platelets fall below approximately 50x10^9/l, the affected animal is at risk of mucosal haemorrhages. <br />
<br />
ITP may be '''primary''' (with no apparent underlying cause) or '''secondary''' to another disease process, to an infection or as a reaction to some drugs. ITP that occurs concurrently with [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA) is known as '''Evan’s syndrome'''.<br />
<br />
==Signalment==<br />
Primary ITP has been reported in cats but it is much more common in dogs. Breeds of dog at particular risk of ITP are similar to those that also suffer from IMHA, namely old English sheepdogs, cocker spaniels and poodles.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Most affected animals will present with some form of bleeding disorder and it is important to differentiate disorders of primary haemostasis (such as ITP and thrombocytopathia) from those of secondary haemostasis (such as Haemophilia A and B). Disorders of primary haemostasis are usually less severe than those of secondary haemostasis as, if the platelets are absent or non-functional, bleeding is often still prevented by the formation of a stable fibrin clot. Common features of a disease of primary haemostasis include:<br />
*'''Petechial haemorrhages''' of the mucous membranes and skin<br />
*Bleeding from mucous membranes, producing '''melaena''', '''haematochezia''', '''haematuria''', '''haemoptysis''' and '''haematemesis'''.<br />
*Haemorrhage into the retina or brain may produce '''blindness''' or '''neurological signs''', respectively.<br />
Affected animals may also show other, less specific signs:<br />
*'''Lethargy''', '''anorexia''' and weakness.<br />
*'''Pyrexia'''<br />
*'''Lymphadenopathy'''<br />
*'''Hepatosplenomegaly''' due to the fact that most destruction of platelets occurs in the MPS of the liver and spleen.<br />
<br />
===Laboratory Tests===<br />
Haematological analysis of a blood sample will show '''thrombocytopaenia''', often with extremely low platelet counts (e.g. 1-5x10^9/l). There may be a reactive [[Neutrophilia|neutrophilia]] and other features of a stress leucogram. Examination of a blood smear may show evidence of '''microthrombocytes''' (small platelets that have been partially phagocytosed by cells of the MPS, similar to spherocytes in IMHA) or immature '''macrothrombocytes''' (a sign of bone marrow platelet regeneration). The patient may be anaemic in cases of Evan’s syndrome or if significant haemorrhage has occurred.<br />
<br />
===Other Tests===<br />
Definitive diagnosis relies on the detection of serum anti-platelet antibodies but this test is not widely available.<br />
<br />
Other tests may also be used to exclude potential infectious causes of thrombocytopaenia such as ''[[Ehrlichia platys]]'' and ''[[Tick-borne Fever|Anaplasma phagocytophilum]]''. <br />
<br />
Faecal occult blood tests represent an unreliable way of detecting gastro-intestinal haemorrhage in cases of mild melaena. The animal must be deprived of meat, bismuth subsalicylate and ferrous sulphate for 3 days before the faecal samples are taken for analysis.<br />
<br />
===Diagnostic Imaging===<br />
Imaging is not required to make a diagnosis of ITP but it may be used to rule out underlying causes of the disease. The major features of abdominal ultrasonography and radiography in affected animals will be '''hepatosplenomegaly'''.<br />
<br />
==Treatment==<br />
===Stabilisation===<br />
Severely thrombocytopaenic animals or those suffering from neurological signs may require transfusions with whole blood. The platelets transferred in this process have only a very short half-life in the recipient and this technique is therefore of little use in the majority of patients where the immune response is not controlled.<br />
<br />
===Immunosuppressive Therapy===<br />
The ultimate goal of the therapeutic regime is to control the autoimmune response to prevent further destruction of platelets. The bone marrow stem cells will then be able to replace the platelets that have been lost in the disease. A variety of drugs have been used in the treatment of ITP but those in widespread use include:<br />
*'''Corticosteroids''' including prednisolone and dexamethasone act to suppress cell- and antibody-mediated responses. These drugs act quickly, are frequently effective and are widely available, making them the most commonly used drugs in the management of ITP.<br />
*Adjunctive immunosuppressive therapy may be provided with '''ciclosporin''', '''azathioprine''' or '''cyclophosphamide'''.<br />
*A recent prospective study indicated that '''human immunoglobulin''' may produce a significantly better outcome in cases of ITP. This product is thought to act by occupying sites (Fc receptors) on cells of the MPS that are usually used to recognise opsonised platelets and mediate phagocytosis. Although it seems to be highly effective, this product is extremely expensive.<br />
*'''Vincristine''' is occasionally used in cases of severe thrombocytopaenia as it is thought to cause the release of platelets from the bone marrow. The immature platelets released however are not completely functional. It also reduces macrophage function by inhibiting the assembly of microtubules necessary for phagocytosis.<br />
*'''Splenectomy''' may be performed in cases refractory to medical management to remove the cells responsible for the phagocytosis of platelets.<br />
<br />
==Prognosis==<br />
Similarly to IMHA, mortality is most likely in the initial stages of the disease and the mortality rate is approximately 30% in this period. Beyond this, the majority of animals recover well although they may require immunosuppressive treatment for several months to completely control the disease. <br />
<br />
==References==<br />
<br />
[[Category:Antibody Mediated Autoimmune Diseases]]<br />
[[Category:To Do - James]][[Category:Dog]][[Category:Cat]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphopenia&diff=89171Lymphopenia2010-08-30T20:24:40Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphopenia is a reduction in the numbers of lymphocytes in the blood. This phenomenon is most commonly associated with stress (as part of the '''stress leucogram''') or with viral infection. Its causes therefore include:<br />
*Viral infection with [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Infectious canine hepatitis]], [[Feline infectious enteritis]] or [[Bovine Viral Diarrhoea]] (BVD)<br />
*Bone marrow suppression caused by '''chemotherapy''' or '''radiotherapy'''. Since neutrophils have a much shorter circulating half life, they are the first cell line to fall with any insult to the bone marrow but lymphopenia may occur as part of a more severe pancytopenia.<br />
*Inherited or acquired immunodeficiency syndromes, including '''SCID''' (Severe Combined Immunodeficiency Syndrome) in Arab foals and [[Feline Immunodeficiency Virus|'''FIV''']] infection.<br />
*Stress leucogram, characterised by '''neutrophilia''', '''monocytosis''', '''eosinopenia''' and '''lymphopenia'''. A similar pattern may occur with hyperadrenocorticism (Cushing’s disease) or exogenous corticosteroid therapy as these hormones selectively suppress lymphocytic activity and the inflammatory response in general. Young horses may develop lymphopenia when exposed to even mild stress, such as handling.<br />
*Leakage of lymphatic fluid may result in loss of lymphocytes, as with '''[[Lymphangiectasia|lymphangiectasia]]''' or '''[[Chylous Effusion|chylothorax]]'''.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphopenia&diff=89170Lymphopenia2010-08-30T20:24:28Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphopenia is a reduction in the numbers of lymphocytes in the blood. This phenomenon is most commonly associated with stress (as part of the '''stress leucogram''') or with viral infection. Its causes therefore include:<br />
*Viral infection with [[Paramyxoviridae#Canine Distemper Virus (CDV)|canine distemper]], [[Infectious canine hepatitis]], [[Feline infectious enteritis]] or [[Bovine Viral Diarrhoea]] (BVD)<br />
*Bone marrow suppression caused by '''chemotherapy''' or '''radiotherapy'''. Since neutrophils have a much shorter circulating half life, they are the first cell line to fall with any insult to the bone marrow but lymphopenia may occur as part of a more severe pancytopenia.<br />
*Inherited or acquired immunodeficiency syndromes, including '''SCID''' (Severe Combined Immunodeficiency Syndrome) in Arab foals and [[Feline Immunodeficiency Virus|'''FIV''']] infection.<br />
*Stress leucogram, characterised by '''neutrophilia''', '''monocytosis''', '''eosinopenia''' and '''lymphopenia'''. A similar pattern may occur with hyperadrenocorticism (Cushing’s disease) or exogenous corticosteroid therapy as these hormones selectively suppress lymphocytic activity and the inflammatory response in general. Young horses may develop lymphopenia when exposed to even mild stress, such as handling.<br />
*Leakage of lymphatic fluid may result in loss of lymphocytes, as with '''[[Lymphangiectasia|lymphangiectasia]]''' or '''[[Chylous Effusions|chylothorax]]'''.<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Lymphocytosis&diff=89169Lymphocytosis2010-08-30T20:22:00Z<p>JamesSwann: /* Description */</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Lymphocytosis refers to an increase in the number of circulating lymphocytes in the blood. The major causes of lymphocytosis are:<br />
*Several types of '''neoplasia''' may result in increases in the number of blood lymphocytes, including:<br />
**Stage V (leukaemic) [[Lymphoma|lymphoma]]<br />
**Acute lymphoblastic and chronic lymphocytic leukaemia<br />
**Bovine Leukosis caused by bovine leukaemia virus (BoLV)<br />
*'''Stress''' may result in the release of lymphocytes into the circulation, especially in young horses and cats. This response is mediated by the release of adrenaline from the adrenal medulla and it should not be confused with the stress leucogram produced by the release of the glucocorticoid hormones cortisol from the adrenal cortex. <br />
*Some cases of '''chronic infection''' may be associated with lymphocytosis but reactive hyperplasia in associated lymph nodes may not correlate with the numbers of circulating lymphocytes.<br />
*'''Physiological''' lymphocytosis is common in young animals of many species. In growing pigs, this may be associated with [[Mycoplasmas Species - Overview|''Mycoplasma'']] infection.<br />
*In '''premature''' or '''dysmature equine neonates''', the normal neutrophil: lymphocyte ratio of approximately 2: 1 may be reversed to produce an apparent lymphocytosis. Such animals will also have an increased mean corpuscular volume (MCV) of their red blood cells.<br />
*'''Hypoadrenocorticism''' may result in lymphocytosis and/or [[Eosinophilia|eosinophilia]].<br />
<br />
<br />
[[Category:Haematology Changes]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Platelet_Abnormalities&diff=89168Platelet Abnormalities2010-08-30T19:58:52Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
[[Platelet|Platelets]] (or thrombocytes) are responsible for primary haemostasis, the formation of a temporary platelet plug that initially seals any breach to a blood vessel wall. These breaches are then sealed more completely by the formation of a fibrin clot mediated by the coagulation factor cascade. <br />
<br />
Bleeding disorders may occur if platelets are deficient ('''thrombocytopaenia''') or if the platelets are unable to function adequately ('''thrombocytopathia'''). [[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]] (ITP) is one common cause of thrombocytopaenia and this may be a primary or secondary disease. '''Thrombocytosis''' refers to an increase in the blood platelet concentration above the normal level.<br />
<br />
Thrombocytopaenia and thrombocytopathia lead to disorders of primary haemostasis but, in general, this is less serious than the disorders of secondary haemostasis caused by deficiencies in the [[Coagulation Factor Deficiency|coagulation factors]]. <br />
<br />
==Thrombocytopaenia==<br />
Thrombocytopaenia is the most common haematological abnormality as platelet numbers are subject to fluctuation in a large number of different diseases. Care should be taken however to ensure that this finding is not caused by an artefact of sampling that leads to the formation of platelet clumps. The normal blood platelet concentration of the dog is 175-500x10^9 but clinical disease is not usually observed until this level falls below 50x10^9 and spontaneous haemorrhage is observed only when the level falls below 20x10^9. Reductions in the number of platelets may be caused by a failure to produce adequate numbers in the bone marrow in the process of megakaryopoiesis, increased destruction of existing platelets or sequestration of platelets outside of the circulation. <br />
*Diseases that cause '''[[Bone Marrow - Anatomy & Physiology|bone marrow]] suppression'''<br />
**'''Aplastic anaemia''' caused by ingestion of bracken or administration of oestrogens, [[Chloramphenicol|chloramphenicol]] or [[Sulphonamides|sulphonamide]] antibiotics. Prolonged use of phenylbutazone or salicylate may cause the same disease.<br />
**'''Infectious diseases''' that reduce stem cell function, including [[Distemper|canine distemper]], [[Canine Parvovirus|canine parvovirus]] and [[Feline Panleucopaenia|feline panleucopaenia virus]].<br />
**'''Myelophthisis''', the displacement of the normal cell lines of the bone marrow by another cell or tissue type may also reduce the function of the megakaryocytes. Possible diseases in this category include '''myelofibrosis''' and '''immunoproliferative''' or '''myeloproliferative''' neoplastic disease.<br />
**'''Radiotherapy''' or myelosuppressive '''chemotherapy''' may cause reversible bone marrow suppression.<br />
*Diseases that cause '''increased destruction of platelets'''<br />
**'''[[Immune Mediated Thrombocytopaenia|Immune-mediated thrombocytopaenia]]''' is a common autoimmune disease that leads to the production of antibodies against platelets and their subsequent destruction by cells of the monocyte phagocyte system (MPS).<br />
**'''Infectious diseases''' that cause destruction of platelets include [[Bovine Viral Diarrhoea Virus|bovine viral diarrhoea]] (BVD), [[Classical Swine Fever|classical swine fever]] and [[Infectious Canine Hepatitis|infectious canine hepatitis]]. The parasites ''[[Ehrlichia platys|Anaplasma platys]]'', ''[[Ehrlichia phagocytophila|Anaplasma phagocytophilum]]'' and ''[[Ehrlichia canis]]'' may also cause infectious thrombocytopaenia. Any severe bacterial infection, including those caused by [[:Category:Staphylococcus species|''Staphylococci'']] and the Gram negative bacteria that produce endotoxin (e.g. [[:Category:Pseudomonas and Burkholderia species|''Pseudomonas spp.'']] or [[Salmonella|''Salmonella spp.'']]) may also result in the destruction of platelets.<br />
*Diseases that cause '''sequestration of platelets''' usually involve some enlargement of the spleen, as this is the major organ where platelets are stored outside of the circulation. Examples include:<br />
**[[Haemangiosarcoma]] of the spleen and liver<br />
**Splenic enlargement under general anaesthesia maintained with agents such as [[Barbiturates|barbiturates]] and [[Phenothiazines|phenothiazines]]<br />
*'''Artefactual''' or spurious thrombocytopaenia<br />
**'''Cavalier King Charles spaniels''' have a relatively small number of giant platelets (macrothrombocytes) but they do not suffer from bleeding disorders as they maintain a similar total platelet mass as do dogs of other breeds.<br />
**If venepuncture is traumatic, '''platelet clumps''' may form and these will not be counted by automated machines. The presence of clumps can be investigated by making a blood smear and examining the feathered edge for large agglomerations of platelets.<br />
<br />
==Thrombocytopathia==<br />
Defects in platelet function may be congenital defects or they may be acquired with a number of diseases. Congenital thrombocytopathias are rare inherited diseases which are characterised by defects in platelet adhesiveness, aggregation or factor release. The defects are usually associated with particular breeds, such as '''Chediak-Higashi syndrome''' in blue smoke Persian cats.<br />
<br />
Causes of acquired thrombocytopathia include:<br />
*Infection with ''[[Angiostrongylus vasorum]]'', the canine lungworm, which also causes a consumptive coagulopathy.<br />
*'''Hypergammaglobulinaemia''' as occurs with multiple myeloma and some forms of (B-cell) lymphoma may affect platelet function.<br />
*Administration of large volumes of some '''[[Colloids|colloid solutions]]'''.<br />
*Administration of certain '''pharmaceutical products''', including [[NSAIDs|non-steroidal anti-inflammatory drugs]] and [[Cephalosporins|cephalosporins]].<br />
<br />
==Thrombocytosis==<br />
Increases in platelets above the normal level may occur due to '''physiological''' or '''pathological''' processes. <br />
*Physiological<br />
**'''Splenic contraction''' pushes sequestered platelets into the circulation. This phenomenon is especially marked in horses which have a muscular splenic capsule. <br />
**'''Splenectomy''' prevents the sequestration of platelets in the spleen, resulting in constantly increased levels of platelets.<br />
**As part of a response to '''[[Anaemia – Introduction|anaemia]]''', a '''reactive thrombocytosis''' is often documented and this may precede signs of regeneration.<br />
*Pathological<br />
**'''Essential thrombocythaemia''' is a rare myeloproliferative disease that results in the excessive production of platelets which function abnormally. Affected animals suffer from bouts of spontaneous haemorrhage.<br />
<br />
==Clinical Significance==<br />
Other than essential thrombocythaemia, thrombocytosis has no clinical importance except as an indicator of another disease process. Thrombocytopaenia and thrombocytopathia both result in reductions in the effectiveness of primary haemostasis, producing bleeding disorders. Since bleeding points are usually sealed by a fibrin clot, disorders of primary haemostasis tend to be less severe than those caused by deficiencies of the coagulation factors. Common signs of a disorder of primary haemostasis include:<br />
*'''Petechial''' or '''ecchymotic''' haemorrhages on the skin or mucous membranes.<br />
*'''Haemorrhages from the mucous membranes''', producing haematuria, haematochezia, haematemesis, haemoptysis and melaena.<br />
*'''[[Anaemia – Introduction|Anaemia]]''' with reactive [[Neutrophilia|neutrophilia]] and [[Monocytosis|monocytosis]] if the haemorrhage is severe.<br />
<br />
Severe platelet deficiencies may be managed with transfusions of whole blood or, in the USA, with transfusions of platelet cryoprecipitate. With both techniques however, it is likely that the transfused platelets have only a short half life in the recipient. <br />
<br />
The use of '''vincristine''' (a drug also used in chemotherapy for neoplasia) has been advocated in cases of thrombocytopaenia as it causes the release of immature platelets from the bone marrow.<br />
<br />
[[Category:Haemorrhagic Diseases]]<br />
[[Category:To Do - James]][[Category:Haematology Changes]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_Mediated_Thrombocytopaenia&diff=89167Immune Mediated Thrombocytopaenia2010-08-30T19:58:00Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding="10" cellspacing="0" border="1"<br />
| Also known as:<br />
| '''Idiopathic Thrombocytopaenic Purpura'''<br><br />
'''Evan’s Syndrome'''<br />
|}<br />
<br />
==Description==<br />
Immune-mediated thrombocytopaenia (ITP) occurs due to an autoimmune response directed against circulating platelets or megakaryocytes in the bone marrow. The destruction of cells is mediated by antibodies, making ITP a form of '''[[Type II Hypersensitivity|type II hypersensitivity]]'''. The antibodies bind to cells and act as a foundation for the assembly of serum complement components or as opsonins, promoting the uptake and destruction of platelets by cells of the monocyte-phagocyte system (MPS). The destruction of platelets usually results in severe [[Platelet Abnormalities|thrombocytopaenia]] and, if the blood level of platelets fall below approximately 50x10^9/l, the affected animal is at risk of mucosal haemorrhages. <br />
<br />
ITP may be '''primary''' (with no apparent underlying cause) or '''secondary''' to another disease process, to an infection or as a reaction to some drugs. ITP that occurs concurrently with [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA) is known as '''Evan’s syndrome'''.<br />
<br />
==Signalment==<br />
Primary ITP has been reported in cats but it is much more common in dogs. Breeds of dog at particular risk of ITP are similar to those that also suffer from IMHA, namely old English sheepdogs, cocker spaniels and poodles.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Most affected animals will present with some form of bleeding disorder and it is important to differentiate disorders of primary haemostasis (such as ITP and thrombocytopathia) from those of secondary haemostasis (such as Haemophilia A and B). Disorders of primary haemostasis are usually less severe than those of secondary haemostasis as, if the platelets are absent or non-functional, bleeding is often still prevented by the formation of a stable fibrin clot. Common features of a disease of primary haemostasis include:<br />
*'''Petechial haemorrhages''' of the mucous membranes and skin<br />
*Bleeding from mucous membranes, producing '''melaena''', '''haematochezia''', '''haematuria''', '''haemoptysis''' and '''haematemesis'''.<br />
*Haemorrhage into the retina or brain may produce '''blindness''' or '''neurological signs''', respectively.<br />
Affected animals may also show other, less specific signs:<br />
*'''Lethargy''', '''anorexia''' and weakness.<br />
*'''Pyrexia'''<br />
*'''Lymphadenopathy'''<br />
*'''Hepatosplenomegaly''' due to the fact that most destruction of platelets occurs in the MPS of the liver and spleen.<br />
<br />
===Laboratory Tests===<br />
Haematological analysis of a blood sample will show '''thrombocytopaenia''', often with extremely low platelet counts (e.g. 1-5x10^9/l). There may be a reactive [[Neutrophilia|neutrophilia]] and other features of a stress leucogram. Examination of a blood smear may show evidence of '''microthrombocytes''' (small platelets that have been partially phagocytosed by cells of the MPS, similar to spherocytes in IMHA) or immature '''macrothrombocytes''' (a sign of bone marrow platelet regeneration). The patient may be anaemic in cases of Evan’s syndrome or if significant haemorrhage has occurred.<br />
<br />
===Other Tests===<br />
Definitive diagnosis relies on the detection of serum anti-platelet antibodies but this test is not widely available.<br />
<br />
Other tests may also be used to exclude potential infectious causes of thrombocytopaenia such as ''[[Ehrlichia platys]]'' and ''[[Tick-borne Fever|Anaplasma phagocytophilum]]''. <br />
<br />
Faecal occult blood tests represent an unreliable way of detecting gastro-intestinal haemorrhage in cases of mild melaena. The animal must be deprived of meat, bismuth subsalicylate and ferrous sulphate for 3 days before the faecal samples are taken for analysis.<br />
<br />
===Diagnostic Imaging===<br />
Imaging is not required to make a diagnosis of ITP but it may be used to rule out underlying causes of the disease. The major features of abdominal ultrasonography and radiography in affected animals will be '''hepatosplenomegaly'''.<br />
<br />
==Treatment==<br />
===Stabilisation===<br />
Severely thrombocytopaenic animals or those suffering from neurological signs may require transfusions with whole blood. The platelets transferred in this process have only a very short half-life in the recipient and this technique is therefore of little use in the majority of patients where the immune response is not controlled.<br />
<br />
===Immunosuppressive Therapy===<br />
The ultimate goal of the therapeutic regime is to control the autoimmune response to prevent further destruction of platelets. The bone marrow stem cells will then be able to replace the platelets that have been lost in the disease. A variety of drugs have been used in the treatment of ITP but those in widespread use include:<br />
*'''Corticosteroids''' including prednisolone and dexamethasone act to suppress cell- and antibody-mediated responses. These drugs act quickly, are frequently effective and are widely available, making them the most commonly used drugs in the management of ITP.<br />
*Adjunctive immunosuppressive therapy may be provided with '''ciclosporin''', '''azathioprine''' or '''cyclophosphamide'''.<br />
*A recent prospective study indicated that human immunoglobulin may produce a significantly better outcome in cases of ITP. This product is thought to act by occupying sites (Fc receptors) on cells of the MPS that are usually used to recognise opsonised platelets and mediate phagocytosis. Although it seems to be highly effective, this product is extremely expensive.<br />
*'''Vincristine''' is occasionally used in cases of severe thrombocytopaenia as it is thought to cause the release of platelets from the bone marrow. The immature platelets released however are not completely functional. It also reduces macrophage function by inhibiting the assembly of microtubules necessary for phagocytosis.<br />
*'''Splenectomy''' may be performed in cases refractory to medical management to remove the cells responsible for the phagocytosis of platelets.<br />
<br />
==Prognosis==<br />
Similarly to IMHA, mortality is most likely in the initial stages of the disease and the mortality rate is approximately 30% in this period. Beyond this, the majority of animals recover well although they may require immunosuppressive treatment for several months to completely control the disease. <br />
<br />
==References==<br />
<br />
[[Category:Antibody Mediated Autoimmune Diseases]]<br />
[[Category:To Do - James]][[Category:Dog]][[Category:Cat]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_Mediated_Thrombocytopaenia&diff=89166Immune Mediated Thrombocytopaenia2010-08-30T19:55:57Z<p>JamesSwann: </p>
<hr />
<div>{{unfinished}}<br />
<br />
{| cellpadding=”10” cellspacing=”0” border=”1”<br />
| Also known as:<br />
| '''Idiopathic Thrombocytopaenic Purpura'''<br><br />
'''Evan’s Syndrome'''<br />
|}<br />
<br />
==Description==<br />
Immune-mediated thrombocytopaenia (ITP) occurs due to an autoimmune response directed against circulating platelets or megakaryocytes in the bone marrow. The destruction of cells is mediated by antibodies, making ITP a form of '''[[Type II Hypersensitivity|type II hypersensitivity]]'''. The antibodies bind to cells and act as a foundation for the assembly of serum complement components or as opsonins, promoting the uptake and destruction of platelets by cells of the monocyte-phagocyte system (MPS). The destruction of platelets usually results in severe [[Platelet Abnormalities|thrombocytopaenia]] and, if the blood level of platelets fall below approximately 50x10^9/l, the affected animal is at risk of mucosal haemorrhages. <br />
<br />
ITP may be '''primary''' (with no apparent underlying cause) or '''secondary''' to another disease process, to an infection or as a reaction to some drugs. ITP that occurs concurrently with [[Immune Mediated Haemoytic Anaemia|immune-mediated haemolytic anaemia]] (IMHA) is known as '''Evan’s syndrome'''.<br />
<br />
==Signalment==<br />
Primary ITP has been reported in cats but it is much more common in dogs. Breeds of dog at particular risk of ITP are similar to those that also suffer from IMHA, namely old English sheepdogs, cocker spaniels and poodles.<br />
<br />
==Diagnosis==<br />
===Clinical Signs===<br />
Most affected animals will present with some form of bleeding disorder and it is important to differentiate disorders of primary haemostasis (such as ITP and thrombocytopathia) from those of secondary haemostasis (such as Haemophilia A and B). Disorders of primary haemostasis are usually less severe than those of secondary haemostasis as, if the platelets are absent or non-functional, bleeding is often still prevented by the formation of a stable fibrin clot. Common features of a disease of primary haemostasis include:<br />
*'''Petechial haemorrhages''' of the mucous membranes and skin<br />
*Bleeding from mucous membranes, producing '''melaena''', '''haematochezia''', '''haematuria''', '''haemoptysis''' and '''haematemesis'''.<br />
*Haemorrhage into the retina or brain may produce '''blindness''' or '''neurological signs''', respectively.<br />
Affected animals may also show other, less specific signs:<br />
*'''Lethargy''', '''anorexia''' and weakness.<br />
*'''Pyrexia'''<br />
*'''Lymphadenopathy'''<br />
*'''Hepatosplenomegaly''' due to the fact that most destruction of platelets occurs in the MPS of the liver and spleen.<br />
<br />
===Laboratory Tests===<br />
Haematological analysis of a blood sample will show '''thrombocytopaenia''', often with extremely low platelet counts (e.g. 1-5x10^9/l). There may be a reactive [[Neutrophilia|neutrophilia]] and other features of a stress leucogram. Examination of a blood smear may show evidence of '''microthrombocytes''' (small platelets that have been partially phagocytosed by cells of the MPS, similar to spherocytes in IMHA) or immature '''macrothrombocytes''' (a sign of bone marrow platelet regeneration). The patient may be anaemic in cases of Evan’s syndrome or if significant haemorrhage has occurred.<br />
<br />
===Other Tests===<br />
Definitive diagnosis relies on the detection of serum anti-platelet antibodies but this test is not widely available.<br />
<br />
Other tests may also be used to exclude potential infectious causes of thrombocytopaenia such as ‘’[[Ehrlichia platys]]’’ and ‘’[[Anaplasma phagocytophilum]]’’. <br />
<br />
Faecal occult blood tests represent an unreliable way of detecting gastro-intestinal haemorrhage in cases of mild melaena. The animal must be deprived of meat, bismuth subsalicylate and ferrous sulphate for 3 days before the faecal samples are taken for analysis.<br />
<br />
===Diagnostic Imaging===<br />
Imaging is not required to make a diagnosis of ITP but it may be used to rule out underlying causes of the disease. The major features of abdominal ultrasonography and radiography in affected animals will be '''hepatosplenomegaly'''.<br />
<br />
==Treatment==<br />
===Stabilisation===<br />
Severely thrombocytopaenic animals or those suffering from neurological signs may require transfusions with whole blood. The platelets transferred in this process have only a very short half-life in the recipient and this technique is therefore of little use in the majority of patients where the immune response is not controlled.<br />
<br />
===Immunosuppressive Therapy===<br />
The ultimate goal of the therapeutic regime is to control the autoimmune response to prevent further destruction of platelets. The bone marrow stem cells will then be able to replace the platelets that have been lost in the disease. A variety of drugs have been used in the treatment of ITP but those in widespread use include:<br />
*'''Corticosteroids''' including prednisolone and dexamethasone act to suppress cell- and antibody-mediated responses. These drugs act quickly, are frequently effective and are widely available, making them the most commonly used drugs in the management of ITP.<br />
*Adjunctive immunosuppressive therapy may be provided with '''ciclosporin''', '''azathioprine''' or '''cyclophosphamide'''.<br />
*A recent prospective study indicated that human immunoglobulin may produce a significantly better outcome in cases of ITP. This product is thought to act by occupying sites (Fc receptors) on cells of the MPS that are usually used to recognise opsonised platelets and mediate phagocytosis. Although it seems to be highly effective, this product is extremely expensive.<br />
*'''Vincristine''' is occasionally used in cases of severe thrombocytopaenia as it is thought to cause the release of platelets from the bone marrow. The immature platelets released however are not completely functional. It also reduces macrophage function by inhibiting the assembly of microtubules necessary for phagocytosis.<br />
*'''Splenectomy''' may be performed in cases refractory to medical management to remove the cells responsible for the phagocytosis of platelets.<br />
<br />
==Prognosis==<br />
Similarly to IMHA, mortality is most likely in the initial stages of the disease and the mortality rate is approximately 30% in this period. Beyond this, the majority of animals recover well although they may require immunosuppressive treatment for several months to completely control the disease. <br />
<br />
==References==<br />
<br />
[[Category:Antibody Mediated Autoimmune Diseases]]<br />
[[Category:To Do - James]][[Category:Dog]][[Category:Cat]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Evans_syndrome&diff=89165Evans syndrome2010-08-30T19:55:20Z<p>JamesSwann: Redirected page to Evan's syndrome</p>
<hr />
<div>#REDIRECT [[Evan's syndrome]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Evans_syndrome&diff=89164Evans syndrome2010-08-30T19:54:41Z<p>JamesSwann: Redirected page to Evan's Syndrome</p>
<hr />
<div>#REDIRECT [[Evan's Syndrome]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Evan%27s_syndrome&diff=89163Evan's syndrome2010-08-30T19:54:16Z<p>JamesSwann: Created page with "{{unfinished}} ==Description== Evan's syndrome refers to the concurrent presence of '''immune-mediated haemolytic anaemia''' (IMHA) and ''..."</p>
<hr />
<div>{{unfinished}}<br />
<br />
==Description==<br />
Evan's syndrome refers to the concurrent presence of '''[[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]''' (IMHA) and '''[[Immune Mediated Thrombocytopaenia|immune-mediated thrombocytopaenia]]''' (ITP) in the same patient. Animals suffering from this disease have a poorer prognosis than those with either disease alone.<br />
<br />
[[Category:Dog]][[Category:Cat]][[Category:Antibody Mediated Autoimmune Diseases]][[Category:To Do - James]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Idiopathic_thrombocytopenic_purpura&diff=89162Idiopathic thrombocytopenic purpura2010-08-30T19:51:13Z<p>JamesSwann: Redirected page to Immune Mediated Thrombocytopaenia</p>
<hr />
<div>#REDIRECT [[Immune Mediated Thrombocytopaenia]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune_mediated_thrombocytopenia&diff=89161Immune mediated thrombocytopenia2010-08-30T19:50:37Z<p>JamesSwann: Redirected page to Immune Mediated Thrombocytopaenia</p>
<hr />
<div>#REDIRECT [[Immune Mediated Thrombocytopaenia]]</div>JamesSwannhttps://en.wikivet.net/index.php?title=Immune-mediated_thrombocytopenia&diff=89160Immune-mediated thrombocytopenia2010-08-30T19:50:06Z<p>JamesSwann: Redirected page to Immune Mediated Thrombocytopaenia</p>
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<div>#REDIRECT [[Immune Mediated Thrombocytopaenia]]</div>JamesSwann