Lymphoreticular system Flashcards

Question

Coagulation cascade | Common pathway

Answer 1

Starts with activation of Factor X Activated FX binds activated Factor V and calcium on the platelet surface This complex converts prothrombin (FII) to thrombin (FIIa) Thrombin converts fibrinogen (FI) to fibrin (FIa) Fibrin crosslinked by activated FXIII

Answer 2

Anti-thrombin III - inhibits thrombin and activated FX Activity of ATIII increased by heparin from the endothelium Protein C - inactivates Factors V and VIII Fibrinolysis (enzymatic breakdown of fibrin by plasmin)

Answer 3

Most common cause of thrombocytopaenia Platelet numbers extremely low (often s syndome - concurrent immune mediated thrombocytopaenia and anaemia Primary - antibodies produced against platelets antigens Secondary - many causes (other immune diseases (SLE), drugs or vaccine, neoplasia, infectious) Diagnosis of exclusion/response to treatment

Answer 4

Glanzmann's thrombasthenia - defect in GPIIbIIIa - Ottermans and Great Pyrenees, Quarter horse - Defective platelet aggregation and abnormal clot retraction Canine thrombopathia - abnormal GPIIbIIIa exposure and impaired degranulation - Basset hounds Bovine thrombopathia - defect not know (Simmentals), mild to severe bleeding

Answer 5

Physiological - transient - epinephrine induced splenic contraction Reactive (secondary) - Increased thrombopoietin and possibly IL6 - Inflammation, haemorrhage, iron deficiency Essential thrombocytemia - Myeloproliferative disorder - Marked peristent incerase in platelets - Bone marrow megakaryocytes increased and may have abnormal morphology - Function variable - may see petechiae and ecchymoses or thrombosis

Answer 6

Clinical signs: mucosal bleeding (GI, epistaxis, haematuria etc.) Bleeding may be absent No petechiae - use to differentiate from other platelet disorders See prolonged buccal mucosal bleeding time without thrombocytopaenia Clotting time usually normal but PTT msy be prolonged due to decrease in factor VIII] Common in dogs (rare in cats and horses)

Answer 7

All multimers are present but as decreased concentrations Variable severity of bleeding but not until concentration of vWF are <20% Most common - 90% cases Dobermans Autosomal inheritance so males and females equally affected

Answer 8

Qualitative abnormalities in vWF structure and function Often disproportionate decrease in large multimers Severe and uncommon Seen in German short haired and wire haired pointers Autosomal recessive

Answer 9

Absence of all vWF multimers (<0.1%) Seen in Scottish Terriers, Chesapeake Bay Retrievers, Shetland Sheepdogs and Dutch Kooiker Autosomal recessive

Answer 10

Measure levels of vWF:Ag - Collect blood into EDTA or citrate - If using citrate as anticoagulation - dilute blood:citrate at ratio of 1:9 - vWF levels will be decreased by clots in the sample and by haemolysis but are inaffected by lipaemia - Separate plasma immmediately, freeze and ship overnight ELISA: quantative measurement of vWF using specific antibodies -<50% considered decreased Immunoelectrophoresis: used to separate relative amounts of different multimers - required for diagnosis of type II Genetic test to detect carriers

Answer 11

Transfusion to supply vWF Cryoprecipitate best - concentration of vWF 5-10x greater than in plasma - give at dose of 1 unit/10kg Plasma can be given at 6-12 ml/kg if cryoprecipitate nto available Whole blood if animal is anaemic Desmopressin (DDAVP)as a pre-op prophylaxis for dogs with type I vWD Causes release of vWF from endothelium Give dose of 1 nanog/kg SQ 30 min prior to surgery Intranasal preparation

Answer 12

Factors II, VII, IX and X are produced in the liver Are activated by a vitamin K dependent carboxylase - this step requires reduced vitamin K Production of reduced vitamin K requires the action of vitamin K reductase Vitamin K reductase is inhibited by coumarin - type redenticides This leads to a lack of active factors II, VII, IX and X and a coagulopathy Extrinsic, intrinsic and common pathways affected Factor VII has the shortest half life so will decrease 1st PT is often prolonged 1st in early vitamin K deficency Main clinical sign: haemorrhage Test results: elevation in PT and PTT, platelet numbers and buccal mucosal bleeding time should be normal but mild thrombocytopaenia is possible - due to consumption associated with haemorrhage, FDP's may also be elevated

Answer 13

Emetics, cathartics, activated charcoal if ingestion of rodenticide is recent Transfusions of whole fresh blood or fresh frozen plasma to replace coagulation factors May also need packed red cells if severe anaemia is present Vitamin K therapy: - Can be given orally or parenterlly (SQ) - Loading dose of SQ and then lower dose 8h later - Same dose can be given orally with a fatty meal

Answer 14

Transfusions of whole blood or plasma to replace factor deficiency and red cells Use of fresh or frozen plasma will give a small amount of factor Administration of cryoprecipitate - 10x more factor VIII vs plasma

Answer 15

Mixed haemostatic defect Results when excessive coagulation leads to widespread thrombosis Haemorrhage eventually results as all coagulation factors are consumed Not a primary event but secondary to other underlying disease (neoplasia, liver disease, immune mediated diseases, infectious diseases) May be chronic or acute Haemostatic abnormalities: thrombocytopaenia, prolonged PT and PTT, elevated FDP's, decrease fibrinogen, decreased antithrombin III

Answer 16

``` Stop the coagulation process Heparin (different regimes) Transfusion of whole blood, plasma or cryoprecipitate as source of antithrombin III Aspirin to stop platelet activation Correct other underlying abnormalities Prognosis - poor ```

Answer 17

Family Retroviridae, subfamily Oncovirinae, genus Gammaretrovirus Replicates in many tissues, non-cytopathic Prevalence of 1-2% in 'healthy' cats in UK, 20% in symptomatic cats Transmission: shed in saliva, nasal secretions, faeces, urine, milk, short survival outside of body - Intimate prolonged contact - Neonates (in utero, nursing) - Blood transfusions Persistent viraemia, transient viraemia, latent infection, localised infection

Answer 18

``` Inappetence Weight loss, wasting Poor coat condition Lymphadenopathy Persistent fever Pale mm Ocular disease Gingivitis Stomatitis Infections of skin, urinary bladder, upper resp tract Persistent diarrhoea Seizures, behavioural changes and other neuro disorders Queen's - abortions ```

Answer 19

Immunosuppression - most common manifestation of FeLV Depletion of interference with function of lymphocytes +/- neutrophils Susceptible to co-infection - common for FeLV+ cats to have concurrent infection (opportunistic pathogens)

Answer 20

Bone marrow suppression: viral infection of haemopoietic stem cells and stromal cells - Anaemia: non-regenerative, aplastic anaemia, regenerative (10%) - Thrombocytopaenia - Granulocytopaenia Myelodysplasia -> myelodysplastic syndrome Leukaemia (all cell lines susceptible)

Answer 21

FeLV+ cats, >60x increased risk of lymphoma Expect to develop in 25% of FeLV+ cats within two years of diagnosis Most often mediastinal (thymic) and multicentric Some cats with lymphoma test FeLV- but have virus in tumours

Answer 22

Immunoassay - screening (ELISA) Immunofluorescent antibody test (IFA) - confirms Polymerase chain reaction (PCR) - confirms Viral culture - gold standard confirms Antibody tests - not for diagnosis

Answer 23

Systemically well: - General preventative helath care - Neuter and confine indoors Sick: - Supportive care - Treat secondary illness - Confine indoors

Answer 24

Family Retroviridae, genus Lentivirus, RNA virus, five subtypes - similar to HIV, not zoonotic Clinical findings: stomatitis, neoplasia, ocular inflammation (uveitis, chorioretinitis), anaemia and leucopaenia, opportunistic infections, renal insufficiency

Answer 25

``` CBC: neutropaenia, anaemia common, thrombocytopaenia, co-infection with Mycoplasma haemofelis - haemolytic anaemia Serum biochemical profile: no particular abnorm, +/- polyclonal gammapathy Tests: - Antibody test - develop with 60d - IFA - detects antibodies - Western blot - confirms - PCR - Viral isolation ```

Answer 26

``` Supportive therapy: - antibiotics (aerobes) - cautious use of glucocorticoids in combo with antibiotics (gingivitis, stomatitis) - lactoferrin - possibly in stomatitis Antiviral therapy: - Zidovudine - Reduce plasma load - Generally well tolerated but check for Heinz body haemolytic anaemia and non-regenerative anaemia ```

Answer 27

``` Prevent exposure to virus Virus readily killed but disinfectants, dies within a few hours in environment Low risk transmission by social contact Do not breed fro FIV+ queens If FIV+ queen, hand rear kittens ```

Answer 28

Subgroup A: - present in almost all FeLV-infected cats - transmitted cat-cat - basis from production of other subgroup - least pathogenic Subgroup B: - recombination of subgroup A with endogenous FeLV proviral sequences - oncogenic Subgroup C: - arises from mutation of subgroup A - non-regenerative anaemia

Answer 29

Fatal disease, domestic and non-domestic cats Causative agent: feline coronavirus, enveloped, ssRNA virus Replicates in cytoplasm FIP in 5-10% of FCoV infections Vasculitis, complement activation, excessive cytokine formation Clinical signs: consequences of vasculitis and secondary organ damage Incubation period: weeks - months Onset: sudden or insidious

Answer 30

Present in large portion of healthy cat population Oronasal transmission Virus replicates in enterocytes Clinical signs mild/inapparent - V and D, upper resp signs

Answer 31

FCoV may undergo mutations to FIPV Infects macrophages -> systemic infection FIP = clinical disease syndome result from ineffective immune reponse

Answer 32

Early: - Pyrexia - Inappetence/anorexia, weight loss - Diarrhoea - Listlessness, dehydration - Jaundice (icterus) Effusive vs non-effusive form (sometimes mixed) - Effusive: abdominal, pleural, pericardial effusions - Non-effusive: dry or granulomatous form, predisposition to eye, brain and CNS, kidney, liver, localised regions of intestine

Answer 33

Often difficult AM (esp dry form) CBC: Lymphopaenia, neutrophilia with mild left shift, mild non-regenerative anaemia, may also be normal Serum biochem: Hyperglbulinaemia (polyclonal increase in gamma globulins, albumin:globukin ratio <0.5) hyperbilirubinaemia, usually not azotaemic, may also be normal Fluid analysis: clear, straw - yellow colour, high protein content, viscous, cellularity variable

Answer 34

Grave prognosis - no cure usually, palliative treatment Options: - Suppotive/palliative care - Abx, SQ fluids, nutrition, rest, thoracocentesis - Immune modulators - Glucocorticoids +/- chlorambucil - Aspirin? - Oral polyprenyl immunostimulant

Answer 35

Haematropic mycoplasmas: - Mycoplasma haemofelis: anaemia, pleiomorphic (rods, rings or spherical), gram negative, young entire males - Candidatus Mycoplasma haemominutum: - Candidatus Mycoplasms turicensis Pathogenesis: - Mycoplasmas attach to RBC -> immune-mediated destruction - Concurrent diseases, immunosuppression -> enhanced disease - If recover from infection -> chronic infection fro variable time

Answer 36

Fleas Blood transfusion Female cats to neonates - in utero, nursing Fighting? Oral? Experimentally: IP, IV and PO infected blood, urine and saliva not thought to be infective

Answer 37

Acute: lethargy, inappetence/anorexia, fever (39-41), anaemia, splenomegaly, icterus Chronic: normal to subnormal temperature, weakness, depression, weight loss/emaciation, icterus and splenomegaly less likely

Answer 38

Regenerative anaemia: varies in severity (PCV 15-18%), reticulocytosis, regenerative morphology, if acute onset may be pre-regenerative Erythrophagocytosis and autoagglutination may be present Leucocyte count variable: - Leucocytosis with monocytosis in acute forms - Normal counts in chronic forms - Leucopaenia in moribund cases

Answer 39

Doxycycline: 5-10mg/kg orally bid for 14-21d Potentially adverse effects: GIT effects, abdominal discomfort, vomiting, inappetence/anorexia, oesophagitis, oesopharyngeal stricture formation Flea control Supportive care: blood transfusion, immunosuppresive therapy (pred)

Answer 40

No treatment - 1/3 with uncomplicated acute disease die | Regeneration - destruction + immune response to organism -> recovery

Answer 41

``` Pallor Lack of exercise intolerance Weakness Haemic murmur Red urine Jaundice Dependent oedema Black faeces Swollen udder ```

Answer 42

``` Caudal vena caval syndrome Enzootic haematuria Ruptured uterine artery Ruptured aorta Haemonchosis Fasciolosis Lice, mites and ticks Pyelonephritis Abomasal ulcer Intraluminal intestinal haemorrhage Gastric ulceration in pigs Proliferative haemorrhagic enteropathy in pigs (PIA) ```

Answer 43

``` Leptospirosis Postparturient haemoglobinuria Bacillary haemoglobinuria Protozoa (Babesia, Eperythrozoon) Chronic copper poisoning Cold water ingestion Brassica spp poisoning (rape, kale, cabbages) Drug induced Blood transfusion Autoimmune haemolytic anaemia ```

Answer 44

``` Deficiency of cobalt or copper Iron deficiency Acute bracken poisoning (enzootic haematuria) Faciolosis Lymphosarcoma Chronic renal disease (amyloidosis, pyelonephritis) Anaemia of inflammatory disease Radiation damage ```

Answer 45

Clinical signs: - Haematuria with blood clots - Freq urination - Thickened bladder may or may not be palpable per rectum - Other signs of chronic progressive anaemia - Internal bleedings Diagnosis: - Most common cause of haematuria in cattle - Pyelonephritis also causes haematuria but not necessarily anaemia

Answer 46

``` Sand, DA, 'stress' Diagnosis: - Occult blood in faeces/black stinking dung - Free air in the abdomen - Abdominal pain ```

Answer 47

Species and breed variation in susceptibility Copper is stored and accumulated in the liver Some centrilobular necrosis occurs as liver copper concentrations rise Sudden release of copper from the liver - acute fatal syndrome develops

Answer 48

Clinical signs: jaundice, pallor, haemoglobinuria, depression, death (24-48h) Clinical path: Blood copper elevated, liver copper elevated, increased plasma AST Necopsy: swollen yellow liver, swollen gunmetal kidneys, jaundice everywhere

Answer 49

Treatment: - Ammonium tetrathiomolybdate (ATM) 2.7 mg/kg IV 2-3d intervals 3-6 treatments - Ammonium molybdate 100mg + sodium aulphate 1g oral daily - Sodium calcium edetate 70mg/kg IV 2d - Somnulose 10ml IV

Answer 50

Dietary copper < 10 ppm Cu absorption inhibitors (Mo, Zn, Fe and soil) Avoid prolonged feeding of concentrates

Answer 51

Starting 4-6 weeks before calving there is transfer of immunoglobulins (Ig) into the udder IgG1 is actively transferred into colostrum Following ingestion of colostrum by the calf, Ig is absorbed by the epithelial cells of the SI and passes via the lymphatic system to the peripheral blood circulation Systemic production in the calf by IgG and IgM Local protection of intestine by: 1. re-secretion of IgG into the gut lumen 2. passage of IgA in colostrum (and milk) through the gut lumen

Answer 52

Primary - uncommon Secondary - antibodies attach to RBC membranes: - Alterations in RBC membrane produced by primary infectious, neoplastic or other immune-mediated disease process - Antigen-antibody complex deposition on RBC surface - Drugs that cause immunoproteins to react indirectly with RBCs

Answer 53

Heinz bodies are precipitations of oxidatively denatured haemoglobin on RBC membrane Can be caused by rarely used drugs (methylen blue, phenothiazine) or plants (onions, Brassica spp: rape, kale) Exception: red maple leaf toxicity

Answer 54

Exotic, Equine infectious anaemia virus (lentivirus) | Persistent infection: no treatment, lifelong carriers

Answer 55

``` Most common cause Mild-moderatre regenerative anaemia Pathogenesis: - Iron sequestration - anti-bacterial mechanism - Defective erythropoietin - Decreased RBC lifespan ```

Answer 56

Lack of colostrum/poor quality Failure to nurse Failure of absorption Measure IgG conc - <12-18h oral colostrum unless foal has system disease process - or IV plasma - 1l = 2g in blood (2l usually required) - Repeat measuring/transfusions as necessary

Answer 57

Destruction of foal's RBC by antibodies present in colostrums directed against foal's RBC antigens Blood group incompatibility between mare and foal Clinical signs: - First 4d of life - Weakness, lethargy, increased hr and rr, icterus, pale mm Diagnosis on clinical signs and haemolytic cross match Treatment: - 24-48 hours - prevent further colostrum intake - Over that, supportive care - Blood transfusion: mare's washed red cells (not plasma) or typed donor

Answer 58

Arab foals - autosomal recessive inheritance Lack of functional T and B lymphocytes Fatal by several months of age Can test for SCID gene