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Haematology Flashcards

1
Q

absolute decrease in platelet count

A

Absolute decrease in platelet count, it’s a clinical sign and NOT a diagnosis

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2
Q

predisposition of thrombocytopenia

A

cocker spaniels, poodles, greyhounds (physiologic decreased platelet number), CKC spaniels (hereditary macrothrombocytopaenia)

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3
Q

cause of thrombocytopenia

A

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

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4
Q

signs of thrombocytopenia

A

may be no clinical signs or signs of bleeding, haematuria, melena, petechial haemorrhages, epistaxis

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5
Q

diagnosis of thrombocytopenia

A

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

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6
Q

treatment of thrombocytopenia

A

depends on cause, cage rest, IM give prednisolone, doxycycline (E.canis + haemobarotonella), desmopressin and transfusion is not recommended

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7
Q

BMBT procedure

A
  • 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
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8
Q

platelet dsyfunction

A
  • Congenital: vWD
  • Acquired: drugs (prostaglandin inhibitors, atb, vaccines), secondary to diseases (monoclonal gammopathies, ehrlichiosis, uraemia, retroviral infections, drug therapy, liver disease)
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9
Q

immune mediate thrombocytopenia predisposition

A

Most common acquired primary haemostatic defect in dogs

middle-aged female dogs, cocker spaniels, old English sheep-dog

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10
Q

cause of I.M thrombocytopenia

A

characterised by IM destruction of antibody coated platelets

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11
Q

signs of I.M thrombocytopenia

A

petechiae, epistaxis, haematemesis, melena, haemturia

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12
Q

diagnosis of I.M thrombocytopenia

A

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)

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13
Q

treatment of I.M thrombocytopenia

A

immunosuppressive drugs, glucocorticoids

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14
Q

prognosis of I.M thrombocytopenia

A

good, rarely fatal

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15
Q

predisposition of Von Willebrand

A

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

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16
Q

cause of VW

A

typically an inherited disorder

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17
Q

Types of VW

A

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

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18
Q

signs ofVW

A

excessive bleeding during/after surgery, petechiae and ecchymoses, perinatal death, abortion, stillbirth, epistaxis, urinary tract haemorrhage, gastrointestinal haemorrhage

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19
Q

diagnosis of V.W

A

PFA-100 test (closure time) and BMBT is prolonged
- BMBT, activated clotting time, activated partial thromboplastin time (APTT), prothrombin time (PT)

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20
Q

treatment of VW

A

transfusion with plasma/fresh blood. Desmopressin (DDAVP) may have some beneficial effect

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21
Q

prognosis of VW

A

incurable, problems are usually mild and inconsequential, risk of life-threating haemorrhagic

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22
Q

differential of VW

A

haemophilia, anticoagulant rodenticide poisoning, thrombocytopenia, hereditary platelet defects, acquired platelet dysfunction

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23
Q

secondary haemostat defects predisposition

A

more common in dogs than cats

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24
Q

cause of 2nd hemeostatic defect

A

severe liver disease, rodenticide poisoning (vit K deficiency), congenital deficiency (haemophilia), systemic diseases (neoplasia, DIC, toxins, severe bleeding)

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25
Q

signs of 2nd hemeostatic defect

A

aematoma, intracavitary bleeding, delayed bleeding after venepuncture, haemorrhagic shock, exercise intolerance, collapse, lameness, masses

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26
Q

diagnosis of secondary hemeostatic defects

A
  • 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)
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27
Q

vitamin K def cause

A

ingestion of Vit K antagonist, malabsorption in dogs and cats (obstructive cholestasis, IBD, liver disease), Vit K dependent

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28
Q

sign of vitamin K deficient

A

excessive/prolonged bleeding, spontaneous haematomas, lethargy, weakness, pale/white gums, acute shock from blood loss

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29
Q

diagnosis of Vitamin K deficiency

A
  • PT prolonged, aPPT prolonged
  • FDP (fibrin degradation products) positive in more than half of affected dog
  • mild thrombocytopenia, anaemia (regenerative), hypoproteinameia
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30
Q

treatment of vitamin K deficiency

A

peracute: induce vomiting, give activated charcoal
- transfusion
- Vit K: SC, IV (possible anaphylactic reaction), PO, rehydration
- after last dose repeat PT in 48h

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31
Q

DIC cause

A

variety of diseases, eg infections, neoplasia, immune-mediated haemolytic anaemia, pancreatitis, severe trauma

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32
Q

1st phase DIC

A
  • 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
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33
Q

2nd phase DIC

A
  • 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
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34
Q

signs of DIC

A

bleeding, coagulopathy, hypovolemic shock

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35
Q

diagnosis of DIC

A
  • Haematology: regenerative haemolytic anaemia, hemoglobinemia, schistocytes, thrombocytopenia, neutrophilia
  • Biochem: hyperbilirubinemia, azotaemia, increased liver enzymes, panhypoproteinemia
  • Haemostatic abnormalities: thrombocytopenia, prolonged aPTT, schiscoytosis, d-dimer test
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36
Q

treatment of DIC

A

heparin low dose SC, removal of underlying cause, fluid therapy, plasma blood products

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37
Q

prognosis of DIC

A

grave, mortality rate 54%, frequently fatal

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38
Q

differentials of DIC

A

immune mediated thrombocytopenia, inherited coagulation disorder, von Willebrand’s disease, anticoagulant rodenticide poisoning, acute liver disease

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39
Q

cause of thrombosis

A

blood stasis, decreased activity of natural anticoagulants, decreased fibrinolysis

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40
Q

what is thrombosis associated with

A

cardiomyopathy, hyperadrenocorticism, IMHA, protein-losing enteropathy/nephropathy

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41
Q

signs of thrombosis

A

melena, diarrhoea, vomiting, severe abdominal pain, seizure, tremors, anxiety

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42
Q

diagnosis of thrombosis

A

thromboelastrography haematosis analyser system (TEG) in large number of dogs with overt thrombosis TEG is normal

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43
Q

treatment of thrombosis

A

anticoagulants, pain management

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44
Q

hypoproteinemia

A

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

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45
Q

pahhyperproteinemia def

A

Presenting sign of lower than normal serum protein levels

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46
Q

pahhyperproteinemia predisposition

A

same as primary disease entities, basenji, yorkies

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47
Q

panhypoproteinemia cause

A

Cushing’s, liver neoplasms with excessive production, haemoconcentration/dehydration, protein-losing enteropathy

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48
Q

panhyperproteinemia signs

A

signs of primary disease process until chronic when generalised peripheral edema, pleural/abdominal effusion, weight loss

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49
Q

prognosis of panhyperproteinemia

A

depends on primary disease process, increasing serum albumin, resolution of edema, ascites

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50
Q

electrophoresis

A
  • 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
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51
Q

hyperglycaemia

A

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

52
Q

hypoglycaemia cause

A

error, toxicosis, drugs, PSS, hypoadrenocorticism, paraneoplastic syndrome, young, sepsis, insulinoma

53
Q

lactate

A
  • 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
54
Q

predisposition of leukocyte disorder

A
  • 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
55
Q

cause of leukocyte disorder

A

most common: inflam, stress + glucocorticoids, exercise + epinephrine

56
Q

negative prognostic sign for leukocyte disorder

A
  • degenerative L shift
  • leukemoid reaction = extra neutrophils can’t solve problems
  • toxic neutrophils
  • severe/persistent lymphopenia
57
Q

differential for leukocyte disorder

A

inflammation, stress and glucocorticoids, exercise and epinephrine

58
Q

neutropenia predisposition

A

collies have 2 inherited forms of neutropenia (trapped neutrophil syndrome and canine cyclic hemopoiesis)

59
Q

neutropenia cause

A

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

60
Q

pathogenesis of neutropenia

A

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

61
Q

signs of neutropenia

A

frequent infections, unexplained fever, diarrhoea, joint pain

62
Q

treatment of neutropenia

A

treatment is secondary infection, transfusion may also be necessary

63
Q

prognosis of neutropneia

A

good

64
Q

predisposition of neutrophil dysfunction

A

Irish setters and crosses, Weimaraners and dobermans

65
Q

pathogenesis of neutrophil dysfunction

A

reduced neutrophil function due to decreased expression of adhesion molecules CD11 and CD18

66
Q

types of neutrophil dysfunction

A

canine LAD – Irish setters
- inherited neutrophil dysfunction in Weimaraner Dobermans
- Chédiak – higashi syndrome
- pelger-huet anomaly – persistent L shift

67
Q

pelger-huet anomaly predisposition

A

DSH cats, American +English foxhound, border collie, Boston terrier, cocker spaniel, GSD

68
Q

cause of pelger-huet anomaly

A

genetic changes

69
Q

pathogenesis of pelter Huet anomaly

A

RARE anomaly of granulocytes

70
Q

signs of pelter-huet anomaly

A

incidental finding of apparent continual left shift despite animal appearing clinically normal, with normal white blood cell count

71
Q

diagnosis, treatment and prognosis of pelter heat anomaly

A

D: haematology
T: none
P: excellent

72
Q

differentials for pelter huet anomaly

A

shift to the left associated with active inflammatory response. Pseudo-pelger-Huet anomaly seen with inflammation, infection, neoplasia or drug therapy

73
Q

cause of anaemia

A

haemorrhage (acute or chronic) or haemolysis

74
Q

pathogenesis of anaemia

A

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)

75
Q

physiologic anaemia

A

splenic relaxation (anaesthetics, tranquilisers), young animals (under 4 months), haemodilution – not true anaemia

76
Q

signs of anaemia

A

hypovolemic shock, pale MM, lethargy, tachypnoea, tachycardia, exercise intolerance

77
Q

diagnosis of anaemia

A

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

78
Q

treatment of anaemia

A

transfusion, identify and treat underlying cause, repeat CBC to monitor on response to therapy

79
Q

regenerative anaemia def

A

Decreased circulating erythrocyte mass accompanied by an appropriate, compensatory increase in erythrocyte production and release of reticulocytes

80
Q

cause of regenerative anaemia

A

blood loss, immune mediated disease, oxidant injury, RBC parasites, mechanical RBC fragmentation, inherited RBC abnormalities

81
Q

signs of regenerative anaemia

A

presence of polychromatophils (Except equines) counting reticulocytes

82
Q

non regenerative def

A

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

83
Q

non-reg cause

A

inflammatory disease, chronic renal disease, chronic liver disease, neoplasia, endocrine disease, nutrition/mineral deficiencies, infectious agents, toxicities

84
Q

non-reg signs

A

pale MM, tachypnoea, tachycardia, bounding pulse

85
Q

diagnosis of non-reg

A
  • haematology – anisocytosis, low reticulocytes
  • biochemistry: total serum protein, erythropoietin
86
Q

immune mediate haemolytic anaemia def

A

Disease in which body attacks its own RBC

87
Q

IMHA predisposition

A

young to middle-aged adults, cocker spaniels, poodle, old English sheepdog, doberman

88
Q

IMHA cause

A

infection, drugs, vaccination, neoplasia, toxins and other infections or inflammatory conditions

89
Q

IMHA signs

A

lethargy, tachypnoea, tachycardia

90
Q

diagnosis IMHA

A

routine testing, PCV, slide agglutination test, radiograph, abdominal ultrasound, infectious disease panel, coombs test

91
Q

treatment IMHA

A

immunosuppressive drugs, treat underlying cause

92
Q

prognosis IMHA

A

fair for chronic cases, 50% mortality for acute cases

93
Q

def polycytemia

A

Abnormally increased RBC, haematocrit (PCV), and haemoglobin concentration due to relative, transient or absolute increase in number of circulating RBC

94
Q

predisposition polycytemia

A

primary = 2-8 years

95
Q

cause polycytemia

A

primary = unknown, secondary = pathological or physiological response

96
Q

relative polycytemia

A
  • 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
97
Q

absolute polycytemia - primary

A
  • 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
98
Q

absolute polycyemia secondary

A
  • 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.
99
Q

polycytemia dangerous?

A

increases blood viscosity  decreased capillary blood flow  blood cell sludging  tissue hypoxia  thrombosis

100
Q

signs of polycytemia

A

primary: brick red MM, hepatosplenomegaly + secondary: seizures, blindness, PUPD, bleeding

101
Q

diagnosis of polycytemia

A
  • 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
102
Q

treatment polycytemia

A

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

103
Q

prognosis polycytemia

A

reasonable with ongoing treatment, may survive for many years with regular phlebotomy or cytotoxic therapy

104
Q

primary bone marrow def

A
  • 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
105
Q

primary bone marrow

A

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

106
Q

transfusion - dogs excluded from donating blood if:

A
  • previously transfused
  • bite, abscess, pyoderma
  • surgical implants
  • vomiting or diarrhoea
  • elevated body temp
107
Q

when can blood products be better than whole blood?

A
  • for specific therapy
  • decreased risk of transfusion reactions
  • smaller volume needed
  • better utilisation of blood
108
Q

when to give fresh whole blood?

A
  • severe haemorrhages, DIC, coagulopathy, vWD, haemophilia A
109
Q

what’s crossmatching?

A
  • 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
110
Q

how much blood from 1 donor

A
  • up to 20% of blood volume
  • max vol = 16-18mL/kg during 2 years
111
Q

should you heart blood bag?

A

no -growth of microorganisms

112
Q

how do you know transfusion was successful?

A

PCV + TP before then 1,6 + 24 hr after

113
Q

transfusion in cats

A
  • resting always obligatory
  • 3 blood groups + naturally occurring antibodies
114
Q

how much blood does patient need

A
  • V (ml) = kg x 85 x (goal PCV – real PCV) divide donors PCV
  • usually around 10-22ml/kg
115
Q

rate of transfusion

A
  • 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
116
Q

slide agglutination test

A
  • 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”
117
Q

Increase BUN

A

GI haemorrhage, raw meat diet

118
Q

urea and creatinine

A

kidney

119
Q

urea and creatinine, TP, ALB

A

dehydration

120
Q
  • Bilirubin, urea, creat, CRP
A

leptospirosis and babesiosis

121
Q
  • BUN, creat, decreased Na/K and decreased BG
A

= hypoadrenocorticism

122
Q

Decreased BG + decreased BUN

A

= PSA (porto systemic asatomosis

123
Q

low albumin

A

edema

124
Q

high CRP

A

infection, neoplasia, trauma, CHF, pregnancy

125
Q

A:G = albumin/globulin

A
  • Normal, also when panhypo/hyperproteinemia
  • Decreased = decreased albumin and/or increased globulin
  • Increased = decreased globulin
  • high potassium in cats often with urethral obstruction

Internal (12 decks)

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