Haematology Flashcards
absolute decrease in platelet count
Absolute decrease in platelet count, it’s a clinical sign and NOT a diagnosis
predisposition of thrombocytopenia
cocker spaniels, poodles, greyhounds (physiologic decreased platelet number), CKC spaniels (hereditary macrothrombocytopaenia)
cause of thrombocytopenia
primary (idiopathic/IM), secondary (infectious, neoplasia, drugs)
- Increased platelet destruction: immune mediated thrombocytopenia, infection, drug induced, disseminated intravascular coagulation
- Decreased platelet production: drug-induced megakaryocytic hypoplasia, Myelophthisis
signs of thrombocytopenia
may be no clinical signs or signs of bleeding, haematuria, melena, petechial haemorrhages, epistaxis
diagnosis of thrombocytopenia
always do a blood smear
- clinical exam, lab diagnostics
- Haematocrit, platelets, total protein, urine colour
o low platelet count, normal coagulation panel, pancytopenia + megakaryocytic hypoplasia (bone marrow suppression), platelet bound antibody (IM)
- Differential WBC count, biochemistry profile, radiography, PT and aPTT
treatment of thrombocytopenia
depends on cause, cage rest, IM give prednisolone, doxycycline (E.canis + haemobarotonella), desmopressin and transfusion is not recommended
BMBT procedure
- Position the animal in lateral recumbency with manual restraint
- Place a 5-cm wide strip of gauze around the maxilla to fold up the upper lip, causing moderate engorgement of the mucosal surface
- Position the Sim plate against the upper lip mucosa and push the trigger
- Start a stopwatch when the incisions are made
- Blot the blood with a gauze or blotting paper placed 1-3mm ventral to the incision without dislodging the clot
- Stop the stopwatch when the incision ceases to bleed
- Normal times are 2-3 minutes
platelet dsyfunction
- Congenital: vWD
- Acquired: drugs (prostaglandin inhibitors, atb, vaccines), secondary to diseases (monoclonal gammopathies, ehrlichiosis, uraemia, retroviral infections, drug therapy, liver disease)
immune mediate thrombocytopenia predisposition
Most common acquired primary haemostatic defect in dogs
middle-aged female dogs, cocker spaniels, old English sheep-dog
cause of I.M thrombocytopenia
characterised by IM destruction of antibody coated platelets
signs of I.M thrombocytopenia
petechiae, epistaxis, haematemesis, melena, haemturia
diagnosis of I.M thrombocytopenia
made by excluding other diseases and initiating immunosuppressive drug therapy, exclude vector-borne diseases (ehrlichia, anaplasma, borrelia, leishmania, babesia, bartonella, drugs)
- haematology: thrombocytopenia with/without anaemia (degree of bleeding/presence of IHA)
- Bone marrow punction: megakaryocytic hyperplasia (occasionally: megakaryocytic hypoplasia with free megakaryocyte nuclei)
treatment of I.M thrombocytopenia
immunosuppressive drugs, glucocorticoids
prognosis of I.M thrombocytopenia
good, rarely fatal
predisposition of Von Willebrand
severe form may become obvious in neonate
- Type 1: Airedale, akita, dachshund, Doberman, golden, poodles, etc
- Type 2: German short/wirehaired pointed
- Type 3: Scottish terrier, Shetland sheepdog, cocker spaniel, labs, Maltese
cause of VW
typically an inherited disorder
Types of VW
Type 1:
- most common type, decreased concentration or activity of vWF
- partial lack of VWF
- typically mildest manifestation
- autosomal dominant inheritance with incomplete penetrance
Type 2:
- low to normal concentration of an abnormal vWF
- associated with a partial lack of VWF
- more severe clinical manifestation possible
- autosomal recessive inheritance
Type 3:
- absence of circulating vWF
- typically severe clinical manifestation
- autosomal recessive inheritance
signs ofVW
excessive bleeding during/after surgery, petechiae and ecchymoses, perinatal death, abortion, stillbirth, epistaxis, urinary tract haemorrhage, gastrointestinal haemorrhage
diagnosis of V.W
PFA-100 test (closure time) and BMBT is prolonged
- BMBT, activated clotting time, activated partial thromboplastin time (APTT), prothrombin time (PT)
treatment of VW
transfusion with plasma/fresh blood. Desmopressin (DDAVP) may have some beneficial effect
prognosis of VW
incurable, problems are usually mild and inconsequential, risk of life-threating haemorrhagic
differential of VW
haemophilia, anticoagulant rodenticide poisoning, thrombocytopenia, hereditary platelet defects, acquired platelet dysfunction
secondary haemostat defects predisposition
more common in dogs than cats
cause of 2nd hemeostatic defect
severe liver disease, rodenticide poisoning (vit K deficiency), congenital deficiency (haemophilia), systemic diseases (neoplasia, DIC, toxins, severe bleeding)
signs of 2nd hemeostatic defect
aematoma, intracavitary bleeding, delayed bleeding after venepuncture, haemorrhagic shock, exercise intolerance, collapse, lameness, masses
diagnosis of secondary hemeostatic defects
- clinical exam, lab diagnostics, haematocrit, platelets, total protein, urine colour, differential WBC, biochemistry, radiography, PT and aPTT
- measurement of coagulation time
- intrinsic and common pathway of blood coagulation: aPTT, ACT
- extrinsic and common pathway of blood coagulation: PT
- common pathway of blood coagulation: TT (thrombin time)
vitamin K def cause
ingestion of Vit K antagonist, malabsorption in dogs and cats (obstructive cholestasis, IBD, liver disease), Vit K dependent
sign of vitamin K deficient
excessive/prolonged bleeding, spontaneous haematomas, lethargy, weakness, pale/white gums, acute shock from blood loss
diagnosis of Vitamin K deficiency
- PT prolonged, aPPT prolonged
- FDP (fibrin degradation products) positive in more than half of affected dog
- mild thrombocytopenia, anaemia (regenerative), hypoproteinameia
treatment of vitamin K deficiency
peracute: induce vomiting, give activated charcoal
- transfusion
- Vit K: SC, IV (possible anaphylactic reaction), PO, rehydration
- after last dose repeat PT in 48h
DIC cause
variety of diseases, eg infections, neoplasia, immune-mediated haemolytic anaemia, pancreatitis, severe trauma
1st phase DIC
- inflammatory process is a major factor in patients who develop DIC
- haemostasis dysfunction and microvascular thrombosis ischemia and further endothelial injury
- hypercoagulability blood stasis endothelial damage
2nd phase DIC
- Massive consumption of coagulation factors and platelets leads to haemostasis disorders and subsequently to bleeding
- DIC is not a specific disorder but rather a common pathway in a variety of disorders
signs of DIC
bleeding, coagulopathy, hypovolemic shock
diagnosis of DIC
- Haematology: regenerative haemolytic anaemia, hemoglobinemia, schistocytes, thrombocytopenia, neutrophilia
- Biochem: hyperbilirubinemia, azotaemia, increased liver enzymes, panhypoproteinemia
- Haemostatic abnormalities: thrombocytopenia, prolonged aPTT, schiscoytosis, d-dimer test
treatment of DIC
heparin low dose SC, removal of underlying cause, fluid therapy, plasma blood products
prognosis of DIC
grave, mortality rate 54%, frequently fatal
differentials of DIC
immune mediated thrombocytopenia, inherited coagulation disorder, von Willebrand’s disease, anticoagulant rodenticide poisoning, acute liver disease
cause of thrombosis
blood stasis, decreased activity of natural anticoagulants, decreased fibrinolysis
what is thrombosis associated with
cardiomyopathy, hyperadrenocorticism, IMHA, protein-losing enteropathy/nephropathy
signs of thrombosis
melena, diarrhoea, vomiting, severe abdominal pain, seizure, tremors, anxiety
diagnosis of thrombosis
thromboelastrography haematosis analyser system (TEG) in large number of dogs with overt thrombosis TEG is normal
treatment of thrombosis
anticoagulants, pain management
hypoproteinemia
Can have only albumin decreased
- Hepatic production decreased
o Negative APP = inflammation/infection
o CBC, CRP and clinical ex
- Also glomerulopathy
o Urinarlysis UPCR
- Hepatic damage
o Microcytosis, creased U,chol, BG = imaging, bile test, biopsy
- Only decreased globulin
o Increased protein catabolism – cancer? Hyperthyroidism?
Further investigation: hormone testing, abdo US
- Rare immunodeficiency in young: Consider electrophoresis
Both decreased
- Haemorrhage
- 3 space loss? Vasculitis, pleuritis, peritonitis, PLD
- GI loss? PLE
If antigenic stimulation occurs, can result in normal/elevated globulin concentration
pahhyperproteinemia def
Presenting sign of lower than normal serum protein levels
pahhyperproteinemia predisposition
same as primary disease entities, basenji, yorkies
panhypoproteinemia cause
Cushing’s, liver neoplasms with excessive production, haemoconcentration/dehydration, protein-losing enteropathy
panhyperproteinemia signs
signs of primary disease process until chronic when generalised peripheral edema, pleural/abdominal effusion, weight loss
prognosis of panhyperproteinemia
depends on primary disease process, increasing serum albumin, resolution of edema, ascites
electrophoresis
- at pH 8.6 all serum proteins carry negative charge and migrate from cathode to anode
- proteins can be separated in an electric field on the basis of their molecular charge densities and weight
- normal reference values
o albumin, globulin - abnormal values
o polyclonal gammopathy, monoclonal gammopathy
hyperglycaemia
Cause: diabetes, pancreatic disease, hyperadrenocorticism and hyperthyroidism
Signs: -> PU -> PD -> dehydration
- stress -> increased RR + HR, increased BP, dilated pupils
Extra: differentiate stress from pathological HG = measure frucosamine
hypoglycaemia cause
error, toxicosis, drugs, PSS, hypoadrenocorticism, paraneoplastic syndrome, young, sepsis, insulinoma
lactate
- Increased lactate = marker for hypoperfusion, useful in critically ill patients
- Increased defensive mechanisms in hypoxic state enables energy production protects from acidosis
- Lactate concentration increases proportional to the severity of hypoperfusion and with severity of insult
- Unfavourable if there’s no returning to normal conc within 24-48hr
- Trend is superior to one measurement
predisposition of leukocyte disorder
- younger animals differ from adults = increased leukocytes
- sighthounds have lower count = decrease leukocytes
- decrease in total leukocyte count seen with aging (tervurens, lab and beagles)
- greyhounds have abnormal eosinophils (granules don’t stain)
- Birman cats show atypical neutrophil granulation
cause of leukocyte disorder
most common: inflam, stress + glucocorticoids, exercise + epinephrine
negative prognostic sign for leukocyte disorder
- degenerative L shift
- leukemoid reaction = extra neutrophils can’t solve problems
- toxic neutrophils
- severe/persistent lymphopenia
differential for leukocyte disorder
inflammation, stress and glucocorticoids, exercise and epinephrine
neutropenia predisposition
collies have 2 inherited forms of neutropenia (trapped neutrophil syndrome and canine cyclic hemopoiesis)
neutropenia cause
overwhelming demand and increased migration from circulation to tissues
decreased survival of cells
decreased or ineffective granulopoiesis
chemotherapy (azathioprine, cyclophosphamide
doxorubicin)
oestrogen-toxicity in dogs
chloramphenicol in cats
phenybutazone in dogs, cephalosporins
pathogenesis of neutropenia
Generally, a result of; (1) overwhelming demand and increased migration from circulation to tissues, (2) decreased survival of cells and (3) reduced or ineffective granulopoiesis
signs of neutropenia
frequent infections, unexplained fever, diarrhoea, joint pain
treatment of neutropenia
treatment is secondary infection, transfusion may also be necessary
prognosis of neutropneia
good
predisposition of neutrophil dysfunction
Irish setters and crosses, Weimaraners and dobermans
pathogenesis of neutrophil dysfunction
reduced neutrophil function due to decreased expression of adhesion molecules CD11 and CD18
types of neutrophil dysfunction
canine LAD – Irish setters
- inherited neutrophil dysfunction in Weimaraner Dobermans
- Chédiak – higashi syndrome
- pelger-huet anomaly – persistent L shift
pelger-huet anomaly predisposition
DSH cats, American +English foxhound, border collie, Boston terrier, cocker spaniel, GSD
cause of pelger-huet anomaly
genetic changes
pathogenesis of pelter Huet anomaly
RARE anomaly of granulocytes
signs of pelter-huet anomaly
incidental finding of apparent continual left shift despite animal appearing clinically normal, with normal white blood cell count
diagnosis, treatment and prognosis of pelter heat anomaly
D: haematology
T: none
P: excellent
differentials for pelter huet anomaly
shift to the left associated with active inflammatory response. Pseudo-pelger-Huet anomaly seen with inflammation, infection, neoplasia or drug therapy
cause of anaemia
haemorrhage (acute or chronic) or haemolysis
pathogenesis of anaemia
blood loss, increased erythrocyte destruction and decreased erythrocyte production
- Microcytic, normocytic, macrocytic (MVC, average size of RBC)
- hypochromic, normochromic (MCHC haemoglobin relative to volume of packed erythrocytes)
physiologic anaemia
splenic relaxation (anaesthetics, tranquilisers), young animals (under 4 months), haemodilution – not true anaemia
signs of anaemia
hypovolemic shock, pale MM, lethargy, tachypnoea, tachycardia, exercise intolerance
diagnosis of anaemia
physical examination, finding/history
History
* family history, exercise intolerance, pallor, localised/generalised bleeding, FeLV/FIV, malnutrition, chronic inflammation, travel history
Physical examination
* pallor, jaundice, lymphadenopathy, hepatomegaly, tachycardia, occult blood in stool, haematuria
CBC
* anaemia patients have a low packed cell volume (PCV), RBC count, and haemoglobin concentration
Reticulocyte count
* quantitative measurement of reticulocytes is most important lab test
Peripheral blood smear evaluation
* morphological changes of the RBCs can help to determine the underlying cause of anaemia
Biochemsitry:
Urinalysis
- haemoglobinuria and bilirubinaemia
Slide agglutination
treatment of anaemia
transfusion, identify and treat underlying cause, repeat CBC to monitor on response to therapy
regenerative anaemia def
Decreased circulating erythrocyte mass accompanied by an appropriate, compensatory increase in erythrocyte production and release of reticulocytes
cause of regenerative anaemia
blood loss, immune mediated disease, oxidant injury, RBC parasites, mechanical RBC fragmentation, inherited RBC abnormalities
signs of regenerative anaemia
presence of polychromatophils (Except equines) counting reticulocytes
non regenerative def
Decreased circulating erythrocyte mass in absence of an appropriate bone marrow response. Bone marrow doesn’t produce or release an adequate number of reticulocytes/erythrocytes
non-reg cause
inflammatory disease, chronic renal disease, chronic liver disease, neoplasia, endocrine disease, nutrition/mineral deficiencies, infectious agents, toxicities
non-reg signs
pale MM, tachypnoea, tachycardia, bounding pulse
diagnosis of non-reg
- haematology – anisocytosis, low reticulocytes
- biochemistry: total serum protein, erythropoietin
immune mediate haemolytic anaemia def
Disease in which body attacks its own RBC
IMHA predisposition
young to middle-aged adults, cocker spaniels, poodle, old English sheepdog, doberman
IMHA cause
infection, drugs, vaccination, neoplasia, toxins and other infections or inflammatory conditions
IMHA signs
lethargy, tachypnoea, tachycardia
diagnosis IMHA
routine testing, PCV, slide agglutination test, radiograph, abdominal ultrasound, infectious disease panel, coombs test
treatment IMHA
immunosuppressive drugs, treat underlying cause
prognosis IMHA
fair for chronic cases, 50% mortality for acute cases
def polycytemia
Abnormally increased RBC, haematocrit (PCV), and haemoglobin concentration due to relative, transient or absolute increase in number of circulating RBC
predisposition polycytemia
primary = 2-8 years
cause polycytemia
primary = unknown, secondary = pathological or physiological response
relative polycytemia
- Decrease in plasma volume produced an elevated PCV even though RBC mass is normal or decreased
- Erythropoiesis isn’t increased
- Plasma volume may be decreased from decreased fluid intake or rapid loss: marked dehydration from water deprivation, vomiting, diarrhoea, heat stroke, burns, hyperventilation, diuresis and with a shift of vascular fluid into the interstitial space
- Transient polycytemia can occur with splenic contraction
absolute polycytemia - primary
- Increase in RBC volume that isn’t related to EPO concentration
- Primary polycytemia is also referred to as polycytemia vera
- Polycytemia vera is a rare myeloproliferative disorder caused by clonal proliferation of erythroid precursors of bone marrow stem cells. Proliferation results in excessive production of mature RBCs independent of EPO
absolute polycyemia secondary
- Occurs with congenital or acquired disorders that cause increase production of EPO
- Considered appropriate in conditions associated with systemic hypoxia: congenital heart defects, chronic pulmonary disease, upper airway obstruction, brachycephalic syndrome, high altitude
- Inappropriate polycytemia occurs when EPO levels rise in absence of systemic hypoxia
- Local renal hypoxia or EPO-producing tumours can lead to secondary inappropriate polycytemia, renal tumours, hydronephrosis, hyperadrenocorticism, hyperthyroidism, etc.
polycytemia dangerous?
increases blood viscosity decreased capillary blood flow blood cell sludging tissue hypoxia thrombosis
signs of polycytemia
primary: brick red MM, hepatosplenomegaly + secondary: seizures, blindness, PUPD, bleeding
diagnosis of polycytemia
- Physical examination findings: clinical signs related to polycytemia occurs with PCVs > 60/70%
- Clinical signs of relative polycytemia are related to dehydration and can include prolonged CRT, decreased skin turgor, hypotension and tachycardia
- Signs; lethargy, anorexia, splenomegaly, MM brick red/hyperaemia/cyanotic, GI bleeding, epistaxis etc
- CBC, biochemical panel, pulse oximetry/blood gas, serum EPO concentration, bone marrow aspirate, radiography, echocardiography, abdo radiography and abdo ultrasound
treatment polycytemia
phlebotomy, simultaneous IV fluid therapy, myelosuppression (hydroxyurea)
Phlebotomy
- blood removed till clinical signs resolve or target haematocrit reached ,ml (removed) = kg x 0.09 x 1L/kg X (actual PCV- wanted PCV) divide actual PCV
prognosis polycytemia
reasonable with ongoing treatment, may survive for many years with regular phlebotomy or cytotoxic therapy
primary bone marrow def
- Disease or failure from any cause can lead to nonregenerative anaemia and pancytopenia with diffuse marrow involvement, granulocytes are affected first, followed by platelets and finally RBCs
primary bone marrow
Aplastic anaemia
* Reported in dogs, cats, ruminants, horses and pigs with pancytopenia and a hypoplastic marrow replaced by fat. Most cases are idiopathic/include infection, drug therapy, toxic ingestion
Pure red cell aplasia (PRCA)
* Only the erythroid line is affected, characterised by nonregenerative anaemia with severe depletion of red cell precursors in the bone marrow. It’s been reported in dogs, cats and may be primary or secondary … most commonly immune mediated
Primary leukaemia
* Uncommon to rare in domestic species has been reported in dogs, cats, cattle, goats, sheep, pigs and horses
* Retroviruses are cause in some cattle, cats, primates and chickens
* Leukaemia can develop in myeloid or lymphoid cell lines and are further classified as acute or chronic
transfusion - dogs excluded from donating blood if:
- previously transfused
- bite, abscess, pyoderma
- surgical implants
- vomiting or diarrhoea
- elevated body temp
when can blood products be better than whole blood?
- for specific therapy
- decreased risk of transfusion reactions
- smaller volume needed
- better utilisation of blood
when to give fresh whole blood?
- severe haemorrhages, DIC, coagulopathy, vWD, haemophilia A
what’s crossmatching?
- directly testing for the presence of antibodies against the antigens between donor and recipient
- obligatory in dogs that have already been transfused and in dogs with unknown history
Crossmatching protocol: if positive for agglutination = not a match
how much blood from 1 donor
- up to 20% of blood volume
- max vol = 16-18mL/kg during 2 years
should you heart blood bag?
no -growth of microorganisms
how do you know transfusion was successful?
PCV + TP before then 1,6 + 24 hr after
transfusion in cats
- resting always obligatory
- 3 blood groups + naturally occurring antibodies
how much blood does patient need
- V (ml) = kg x 85 x (goal PCV – real PCV) divide donors PCV
- usually around 10-22ml/kg
rate of transfusion
- 0.25ml/kg for 30 minutes, then 5-10ml/kg/h
- severe haemorrhage 22ml/kg/h
- cardio patients = 3-4ml/kg/h + diuretic therapy before
slide agglutination test
- used to differentiate true autoagglutination from rouleaux formation (nonimmune RBC adhesion)
- 1 drop of EDTA-anticoagulated blood is placed onto a microscope slide and mixed with saline (1-2 drops in dogs, 3-4drops in cats)
- Slide is rocked back and forth, then evaluated for the formation of microagglutination
- Coverslip: placed on mixture and slide evaluated under a microscope for microagglutination
- True agglutination appears as “clusters of grapes” while rouleaux appear as “stacks of coins”
Increase BUN
GI haemorrhage, raw meat diet
urea and creatinine
kidney
urea and creatinine, TP, ALB
dehydration
- Bilirubin, urea, creat, CRP
leptospirosis and babesiosis
- BUN, creat, decreased Na/K and decreased BG
= hypoadrenocorticism
Decreased BG + decreased BUN
= PSA (porto systemic asatomosis
low albumin
edema
high CRP
infection, neoplasia, trauma, CHF, pregnancy
A:G = albumin/globulin
- Normal, also when panhypo/hyperproteinemia
- Decreased = decreased albumin and/or increased globulin
- Increased = decreased globulin
- high potassium in cats often with urethral obstruction
