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

Clinical Pathology- Haematology: Anaemia Flashcards

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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
What are the different arrows pointing to in this image? What kind of anaemia is this?
Iron deficiency anaemia
26
What is the name for increased destruction of RBCs, what are the two types?
Haemolysis Immune mediates Non-immune mediated
27
What can cause immune-mediated and non-immune mediated haemolysis?
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
28
What is the most common cause of haemolysis and why does it happen?
Immune mediated haemolytic anaemia Production of antibodies against patiensts red blood cells by macrophages or complement system involvment
29
Describe the process of extravascular haemolysis
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
30
Why can extravascular haemolysis result in jaundice?
If liver capacity is over whelmed from conjugated bilirubin it can lead to hyperbilirubinaemia as well as bilirubinuria and jaundice
31
What are the clinical signs of extravascular haemolysis?
Variable onset and severity of signs Pallor Lehtargy Tachycardia, tachypnoea Splenomegaly Mild lymphadenopathy +/- jaundice
32
How does intravascular haemolysis occur and what does it lead to?
Intravascular cell lysis Extensive complement activation Leads to: Haemoglobinaemia Haemoglobinuria Renal compromise- tubular epithelial damage- free haemoglobin Jaundice
33
What are the clinical signs of intravascular haemolysis?
Sudden onset- severe illness Pallor Collapse Jaundice Tachycardia/tachypnoea Splenomegaly Haemoglobinuria
34
How is IMHA diagnosed?
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
What exceptions are there of regeneerative IMHA?
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
What are intravascular hosts a sign of?
Intravascular lysis
37
What causes autoagglutination and how does it present?
Antierythrocyte IgM or Very high antierythrocyte IgG Appears as red cells cluster as grapes
38
What is the difference between agglutination of RBC vs Rouleaux formation?
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
What is the purpose of the saline agglutination and how is it done?
Rouleaux disappear and agglutinates stay therefore allowing distinguishing 1 drop of anti coagulated +4 or more drops of saline
40
What is the purpose of the coomb's test and when can it not be done?
Used to detect presence of antiRBC antiboides and complement RBCs using rabbit antisera Cannot be done if agglutionation is already evident
41
How does the alvedia antiglobulin test work and what does it test for?
Immuno-chromatographic technology Detects for presence of immunoglobulin and/or C3 components binding to RBC surface with a colour change
42
What are the possible triggers for secondary IMHA?
Drugs Vaccines Neoplasia Inflammatory diseases Infectious diseases
43
What tests are for IMHA and what further tests can be done?
Smear checking for autoagglutination Saline agglutination test Coomb's test Antiglobulin test Further tests- Biochemistry/urinalysis, Imaging, PCR, PT/aPTT
44
Describe the biochemistry and urinalysis of IMHA?
Biochem: Elevated ALT and AP Hyperbilibrubinaemia Possible azotaemia Urinalysis: Haemoblinuria Billirubinuria Proteinuria
45
What is non-regeneerative anaemia and what are its causes?
Absence of reticulocytes- make sure its not pre-regen Causes- primary marrow disease, other diseases affecting marrow function, lack of erythropoietin
46
What can cause intramarrow disease for non-regeneratvie anaemia?
Idiosyncratic drug reactions Oestrogen toxicity Pure red cell aplasia Aplastic pancytopenia Myelofibrosis/myelosclerosis Myelodysplastic syndromes Bone marrow sample required for confirmation
47
What drugs can give idiosyncratic drug reactions?
Unpredictable individual adverse reactions Implicated: Oestrogen Antibiotics NSAIDs Anticonvulsants Antivirals antifungals methimazole
48
What does oestrogen toxicity cause and how can it be caused?
Causes pancytopenia- thrombocytopenia, neutropenia, anemia Causesd from exogenous oestrogen or endogenous- sertoli cell tumours
49
How is oestrogen toxicity treated?
Bactericial antibiotics Blood/platelet rich transfusions Removal of offending neoplasm Prognosis very poor
50
What is red cell aplasia? What are its causes and treatment?
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
What is aplastic anaemia and how is it treated?
Pancytopenia Treatment- supportive, as in oestrogen toxicity, immunosupression
52
What is myelofibrosis? What is it secondary too? How is it treated?
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
What is anaemia of chronic disease?
Very common Normocytic, normochromic non-regenerative anaemia Mild to rarely moderate Doesn't require specific therapy- should resolve after chronic disease cured
54
What is anaemic of chronic kindey disease?
Normocytic, normochromic, non regenerative anaemia Reduced erythropoietin production Reduced red cell survival Reduced erythropoiesis Haemorrhage- thrombocytopathies, GI ulceration
55
How can anaemia of chronic kidney disease be treated?
Increase EPO concentrations Minimide blood loss- gut protectants, H2 blockers
56
What feline retroviruses can cause non-regenerative anaemia?
FIV- erythroid dysplasia, maturation arrest FeLV- usually non-regen, occasionally macrocytic- multiple mechanisms (red cell aplasia, aplastic anaemia, anaemia of chronic disease)
57
How is IDA treated?
Determine and treat underlying cause Iron supplementation Bloof packed red cell transfusion
58
How can IMHA be treated?
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
What can be used for the immunosuppressive therapy?
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
What are the corticosteroid side effects?
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
When is a second immunosupressant needed for treatment of IMHA?
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
How can immunoglobulins be used to treat IMHA?
Human IVIG Block fc receptors in macrophages and bind/block circulating antibodies Salvage therapy if not responding to 2 immunosupressants
63
How much treatmenr should be used for IMHA and how long for?
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
Why is antithrombotic therapyused for treatment of IMHA?
High risk of thromboembolic disease in IMHA- severe intravascular haemolytics most at risk, anticoagulant/antiplatlet drug
65
What specific drugs are used for antiplatelets and anticoagulants?
Antiplatelets- clopidogrel, asprin Anticoagulants- unfractionate heparin, dalteparine
66
What other supportive therapy can be used for IMHA?
Blood transfusion- base on clinical situation of patient Gastroprotectants- omeprazole
67
What is neontatal isoeryhthrolysis?
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
69
What is microangiopathic haemolytic anaemia? How is it caused?
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
What are schistocytes and what can cause them?
Fragmented RBCs Caused by: DIC Glomerulonephritis Neoplasia esp endothelial tumours Vascular anomalies
71
What are acanthocytes and what can cause their formation?
Multiple rounded projections of variable length- unevenly spaced- on RBCs Liver disease Splenic HSA Lymphoma Glomerulonephritis
72
What can cause oxidative injury in dogs and cats and what does it result in?
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
What are heinz bodies? What causes them? What stain highlights them?
Round pale inclusions on inner surface of RBC membrane Aggregated of denatured haemoglobin New methyl blue stain highlights them
74
What is the treatment for oxidative damage?
Immediate withdrawl of offending cause Supportive care N-acetyl cysteine for paracetamol poisoining
75
What is intrinsic haemolytic anaemia?
Rare inherited metabolic defects Pyruvate kinase deficiency Phosphofructokinase deficency Osmotic fragility
76
What blood parasites are their?
Babesia canis Babesia gonis Ehrlichia Anaplasma Mycoplasma haemofelis
77
What is mycoplasmosis? How is it diagnosed and treated?
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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