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Year 3 MOD > Clinical Pathology- Haematology: Anaemia > Flashcards

Clinical Pathology- Haematology: Anaemia Flashcards

1
Q

What is the definition of anaemia?

A

Reduction in RBC mass
Value below reference interval for any of: PCT/Hct, RBC, total Hb

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2
Q

What causes anaemia?

A

Inadequate production by the bone marrow
Increased destruction
Loss (haemorrhage)

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3
Q

Typically which causes of anaemia are regenerative and non-regenerative?

A

Inadequte production from bone marrow- non-regenerative

Increased destruction- usually regenerative

Loss (haemorrhage)- regenerative but not enough,

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4
Q

What are the responses to anaemia?

A

2-3 diphosphoglycerate (2,3-DPG) increases in erythrocytes which lowers oxygen-Hb affinity causing better O2 delivery to peripheral tissues

Alterations in tissue perfusion- increased EPO, stimulates bone marrow to increase eryhtropoiesis

Alterations in behavious to reduce oxygen requirment

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5
Q

Why can cats respond to anaemia better?

A

Cats have different oxygen affinity haemoglobins- changing levels of these gives them a mix of Hbs able to response over a range of oxygenation conditions

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6
Q

What are the clinical signs of anaemia?

A

Pallor
Weakness
Excercise intollerance
Tachycardia
Tachypnoea
‘Haemic’ murmur- more viscous blood creating more sound

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7
Q

What history should be collected from an anaemic animal?

A

Signalment
Acute or chronic onset of signs
Weakness, lethargy, excercise intolerance
Evidence of external blood loss
Access to toxins, recent drug therapy
Urine normal?
Abroad?

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8
Q

What should be checked in a physical examination when anaemia is suspected?

A

Pallor, weakness
Tachycardia, bounding or hyperkinetic pulse
Tachypnoea, dyspnoea
Haemic murmur
Icterus
Petechiation
Evidence of bleeding
Pyrexia
Lymphadenopathy
Abdominal pain/mass
Splenomegaly

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9
Q

What tests can be done on a potentially anaemic animal?

A

Full haemoatology- reticulocyt count required

TP, alb, glob

Coag screen/bleeding times

Saline agglutination/Coombs test

Biochem

Urinalysis

Diagnostic imaging

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10
Q

What degrees of severity are there for anameia based on PCT/Hct?

A

Mild- 30-60% in dogs, 20-24% in cats

Moderate- 18-28% in dogs, 15-19% in cats

Severe- <18% in dogs, <15% in cats

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11
Q

What erythrocyte indexed and regenerative response can be used for classification of anaemia?

A

Erythrocyte indexes- MCV, MCHC (mean corpiscular volume, mean haem concentration):
Microcytic/normocytic/macrocytic/hypochromic/normochromic

Regenerative responses- regenerative vs non-regen

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12
Q

What are hallmarks of regenerative anaemia?

A

Reticulocytosis and polychromasia

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13
Q

How can polycromatophils and reticulocytes be seen?

Identify the polychromatophils and reticulocytes in the images?

A

Poly chromatophils seen with routine romanowsky stains

Reticulocytes are seen with ‘special stains’- new methylene blue

Large red are polychromatophils
RBCs with blue are reticulocytes- shows ribosomes

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14
Q

All flowers are roses but not all roses are flowers

Sub in polychromatophils and reticulocytes

A

All polychromatophils are reticulocytes but not all reticulocytes are polychromatophilic

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15
Q

How long does it take for reticulocytes to increase after anaemia?

A

Initially anaemia will appear non-regenerative

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16
Q

What are the main causes of regenerative anaemias?

A

Haemorrhage

Haemolysis

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17
Q

What types of reticulocytes do feline have?

A

Aggregate and punctate (less stained) which last up to 10 days before reaching mature RBC

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18
Q

How can an acute haemorrhage be identified?

A

Results in hypovolaemic shock
Proportional loss of all blood components

Presents as- pallor, tachycardia, weak peripheral pulses, poor peripheral perfusion, cold extremities

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19
Q

How much blood loss can often lead to fatality?

A

>30%

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20
Q

How does PCV and TP vary with acute haemorrhage?

A

Immediatley PCV is 45% lost in proportion

24 hours later PCV drops to 30% adn TP drops as interstitial fluid moves into circulation

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21
Q

What is required for chronic blood loss?

A

Bleeding for >2 weeks

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22
Q

What can chronic blood loss lead to?

A

Iron deficiency anaemia- IDA after consumption of iron stores

Iron stores are abundant in adults so it takes > 1 month

Initially regenerative

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23
Q

What does IDA cause to happen to RBCs?

A

The extra division of the precursor in attempt to reach the optimal cytoplasmic haemoglobin concentration as not enough can be produced leadining to microcytic hypochromic RBC being produced

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24
Q

1) What usually causes IDA?
2) What else can cause IDA?
3) How can it be diagnosed?

A

1) Most common cause is chronic bleeding- NSAIDs, steroids, neoplasia, Ulcers, CRF, parasitic infections
2) Dietary deficiency- rare (puppies, kittens slow to tansfer to solid food, vegan diet)
3) Microcytic and hypochromic anaemia

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25
Q

What are the different arrows pointing to in this image?

What kind of anaemia is this?

A

Iron deficiency anaemia

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26
Q

What is the name for increased destruction of RBCs, what are the two types?

A

Haemolysis

Immune mediates

Non-immune mediated

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27
Q

What can cause immune-mediated and non-immune mediated haemolysis?

A

Immune mediated:
immune-mediated- primary or secondary to infecion/neoplasia

Non-immune mediated:
Oxidative damage- onions, paracetamol in cats, zinc
Intra-erythrocytic parasites
Mechanical damage- angiopathic anaemia

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28
Q

What is the most common cause of haemolysis and why does it happen?

A

Immune mediated haemolytic anaemia

Production of antibodies against patiensts red blood cells by macrophages or complement system involvment

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29
Q

Describe the process of extravascular haemolysis

A

Antibody binds to RBC and macrophage binds and phagocytosis of RBC
Spherocytes arise from partial phagocytosis

Haem converted to unconjugated bilirubin

Unconjugated bilirubin conjugated by liver and excreted with bile

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30
Q

Why can extravascular haemolysis result in jaundice?

A

If liver capacity is over whelmed from conjugated bilirubin it can lead to hyperbilirubinaemia as well as bilirubinuria and jaundice

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31
Q

What are the clinical signs of extravascular haemolysis?

A

Variable onset and severity of signs
Pallor
Lehtargy
Tachycardia, tachypnoea
Splenomegaly
Mild lymphadenopathy

+/- jaundice

32
Q

How does intravascular haemolysis occur and what does it lead to?

A

Intravascular cell lysis
Extensive complement activation

Leads to:

Haemoglobinaemia
Haemoglobinuria

Renal compromise- tubular epithelial damage- free haemoglobin
Jaundice

33
Q

What are the clinical signs of intravascular haemolysis?

A

Sudden onset- severe illness

Pallor

Collapse

Jaundice

Tachycardia/tachypnoea

Splenomegaly

Haemoglobinuria

34
Q

How is IMHA diagnosed?

A

Clinical signs

Haematology-
typically regenerative
autoagglutination
sphertocytes- especially if many
Leukocytosis with left shift

Direct antiglobulin test (coomb’s test)
Demonstration of anti-RBC antibodies

35
Q

What exceptions are there of regeneerative IMHA?

A

1/3 of patients present with poorly regenerative anaemia which could be from:

Acute onset (<3-5 days) so pre-regenerative

Immune-targeting of RBC precursors in the bone marrow

36
Q

What are intravascular hosts a sign of?

A

Intravascular lysis

37
Q

What causes autoagglutination and how does it present?

A

Antierythrocyte IgM

or

Very high antierythrocyte IgG

Appears as red cells cluster as grapes

38
Q

What is the difference between agglutination of RBC vs Rouleaux formation?

A

Agglutination- antibody mediated clumping- may be temp dependent, strongly supportive IMHA

Rouleaux formation- stacking of RBCs due to increased plasma proteins coating RBCs- caused bny inflammation, cancer, normal in horse and cats

39
Q

What is the purpose of the saline agglutination and how is it done?

A

Rouleaux disappear and agglutinates stay therefore allowing distinguishing

1 drop of anti coagulated +4 or more drops of saline

40
Q

What is the purpose of the coomb’s test and when can it not be done?

A

Used to detect presence of antiRBC antiboides and complement RBCs using rabbit antisera

Cannot be done if agglutionation is already evident

41
Q

How does the alvedia antiglobulin test work and what does it test for?

A

Immuno-chromatographic technology

Detects for presence of immunoglobulin and/or C3 components binding to RBC surface with a colour change

42
Q

What are the possible triggers for secondary IMHA?

A

Drugs

Vaccines

Neoplasia

Inflammatory diseases

Infectious diseases

43
Q

What tests are for IMHA and what further tests can be done?

A

Smear checking for autoagglutination
Saline agglutination test

Coomb’s test

Antiglobulin test

Further tests- Biochemistry/urinalysis, Imaging, PCR, PT/aPTT

44
Q

Describe the biochemistry and urinalysis of IMHA?

A

Biochem:

Elevated ALT and AP
Hyperbilibrubinaemia
Possible azotaemia

Urinalysis:

Haemoblinuria
Billirubinuria
Proteinuria

45
Q

What is non-regeneerative anaemia and what are its causes?

A

Absence of reticulocytes- make sure its not pre-regen

Causes- primary marrow disease, other diseases affecting marrow function, lack of erythropoietin

46
Q

What can cause intramarrow disease for non-regeneratvie anaemia?

A

Idiosyncratic drug reactions

Oestrogen toxicity

Pure red cell aplasia

Aplastic pancytopenia

Myelofibrosis/myelosclerosis

Myelodysplastic syndromes

Bone marrow sample required for confirmation

47
Q

What drugs can give idiosyncratic drug reactions?

A

Unpredictable individual adverse reactions

Implicated:
Oestrogen
Antibiotics
NSAIDs
Anticonvulsants
Antivirals
antifungals
methimazole

48
Q

What does oestrogen toxicity cause and how can it be caused?

A

Causes pancytopenia- thrombocytopenia, neutropenia, anemia

Causesd from exogenous oestrogen or endogenous- sertoli cell tumours

49
Q

How is oestrogen toxicity treated?

A

Bactericial antibiotics

Blood/platelet rich transfusions

Removal of offending neoplasm

Prognosis very poor

50
Q

What is red cell aplasia?

What are its causes and treatment?

A

Only when red cell line is affected

No erythroid precursors in the BM

Myriad of causes- most likely immune

Treatment- remove any suspected initiating cause, cross matched transfusions, immunosuppressive therapy

51
Q

What is aplastic anaemia and how is it treated?

A

Pancytopenia

Treatment- supportive, as in oestrogen toxicity, immunosupression

52
Q

What is myelofibrosis?

What is it secondary too?

How is it treated?

A

Proliferation of collagen and reticulin fibres in bone marrow

Secondary to- chronic damage to marrow stroma, retroviral infection, idiopathic

Treatment- crossmatched transfusions, immunosupression, anabolic steroids?

53
Q

What is anaemia of chronic disease?

A

Very common

Normocytic, normochromic non-regenerative anaemia

Mild to rarely moderate

Doesn’t require specific therapy- should resolve after chronic disease cured

54
Q

What is anaemic of chronic kindey disease?

A

Normocytic, normochromic, non regenerative anaemia

Reduced erythropoietin production

Reduced red cell survival

Reduced erythropoiesis

Haemorrhage- thrombocytopathies, GI ulceration

55
Q

How can anaemia of chronic kidney disease be treated?

A

Increase EPO concentrations

Minimide blood loss- gut protectants, H2 blockers

56
Q

What feline retroviruses can cause non-regenerative anaemia?

A

FIV- erythroid dysplasia, maturation arrest

FeLV- usually non-regen, occasionally macrocytic- multiple mechanisms (red cell aplasia, aplastic anaemia, anaemia of chronic disease)

57
Q

How is IDA treated?

A

Determine and treat underlying cause

Iron supplementation

Bloof packed red cell transfusion

58
Q

How can IMHA be treated?

A

Complete all tests before starting therapy- immunosuppresant may mask disease

Treat underlying disease if secondary

Combination of immunesuppressive therapy, antithrombotic therapy and supportive therapy

59
Q

What can be used for the immunosuppressive therapy?

A

Predisone- first line but side effects

Dextamethasone- may be used if oral not tolerated

Azathioprine- delayed onset 2-3weeks, can cause hepatotoxicity and myelosupression, toxic in cats

Ciclosporin- not myelosuppressive

Mycofenolate mofetil- low toxicity but expensive, GI side effects and monitoring

Leflunomide- monitoring haematology and liver tests

60
Q

What are the corticosteroid side effects?

A

Polyuria/polydipsia/polyphagia

Muscle wastage and poor excercise tolerance

GI signs- gastritis, ulceration, pancreatitis

Long term use detrimental to many organ systems

Rationale for use of 2nd immunosupressant

61
Q

When is a second immunosupressant needed for treatment of IMHA?

A

Clinical features of severe/life threatening disease

No response to corticosteroids over first 7d

Patient with or at risl of severe corticosteroid side effects

62
Q

How can immunoglobulins be used to treat IMHA?

A

Human IVIG

Block fc receptors in macrophages and bind/block circulating antibodies

Salvage therapy if not responding to 2 immunosupressants

63
Q

How much treatmenr should be used for IMHA and how long for?

A

Start high and gradually reduce doses if anaemia under control

Minimum 2-3 weeks between dose reductions

Typically for 4-8 months

Some may come off after period of months and relapse some for life

64
Q

Why is antithrombotic therapyused for treatment of IMHA?

A

High risk of thromboembolic disease in IMHA-
severe intravascular haemolytics most at risk, anticoagulant/antiplatlet drug

65
Q

What specific drugs are used for antiplatelets and anticoagulants?

A

Antiplatelets- clopidogrel, asprin

Anticoagulants- unfractionate heparin, dalteparine

66
Q

What other supportive therapy can be used for IMHA?

A

Blood transfusion- base on clinical situation of patient

Gastroprotectants- omeprazole

67
Q

What is neontatal isoeryhthrolysis?

A

Dogs:
Rare in puppies
Destruction of neonates RBCs by maternal antibody
Sensitised DEA1.1 negative bitch- positive puppies affected

Cats:
rare
Type A or AB born to type B queen
British short hair

68
Q
A
69
Q

What is microangiopathic haemolytic anaemia?

How is it caused?

A

RBCs are mechanically damaged or fragmented as they pass through fibrin meshworks in microvasculature

Damaged cells rapidly removed

Caused by mechanical damage:
Altered vasculature
Fibrin nets
Glomerulonephritis
Vascular anomalies/congential defects

70
Q

What are schistocytes and what can cause them?

A

Fragmented RBCs

Caused by:
DIC
Glomerulonephritis
Neoplasia esp endothelial tumours
Vascular anomalies

71
Q

What are acanthocytes and what can cause their formation?

A

Multiple rounded projections of variable length- unevenly spaced- on RBCs

Liver disease
Splenic HSA
Lymphoma
Glomerulonephritis

72
Q

What can cause oxidative injury in dogs and cats and what does it result in?

A

Onions and zinc in dogs
Paracetamol in cats

Results in:

Methaemoglobinaemia
Heinz body formation
RBC membrane oxiation

RBC destroyed- tend to lyse and phagocytosed

73
Q

What are heinz bodies?

What causes them?

What stain highlights them?

A

Round pale inclusions on inner surface of RBC membrane

Aggregated of denatured haemoglobin

New methyl blue stain highlights them

74
Q

What is the treatment for oxidative damage?

A

Immediate withdrawl of offending cause

Supportive care

N-acetyl cysteine for paracetamol poisoining

75
Q

What is intrinsic haemolytic anaemia?

A

Rare inherited metabolic defects

Pyruvate kinase deficiency

Phosphofructokinase deficency

Osmotic fragility

76
Q

What blood parasites are their?

A

Babesia canis

Babesia gonis

Ehrlichia

Anaplasma

Mycoplasma haemofelis

77
Q

What is mycoplasmosis?

How is it diagnosed and treated?

A

Mycoplasma haemofelis

Regenerative haemolysis- due to immune mediated haemolysis

May not be the primary cause of anaemia

PCR recomended- smear is hard

Doxycycline- for 21 days, cats remain carriers, flush meds
Prednisolone- ifimmune mediated component

Year 3 MOD (42 decks)

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