Regenerative Anaemia

Question 1

What are the clin path findings of regenerative anaemia?

Answer 1

High MCV
High RDW
Low MCHC
Polychromasia

Question 2

What is the stain for counting reticulocytes?

Answer 2

new methylene blue

Do an absolute count as this is more representative

Question 3

Outline the process of blood loss

Answer 3

Either from a bleeding tumour, trauma, or coagulopathy
Low TP before low PCV (as lose both and then get splenic contraction)
If has been going of for a few days you get thrombocytosis
If chronic, see low MCHC and MCV

Question 4

What are the breed dispositions for clotting facotr deficiencies

Answer 4

PFK - Abysinnian and spaniels

PK - pugs and basenjis

Question 5

How do you diagnose IMHA?

Answer 5

Regenerative anaemia and one of:
Spherocytes
+ve in saline agglutination (6 drops of saline and 1 of blood)
Direct AB test - coombs - only needed if saline test is -ve

Question 6

What is the likely signalment of an IMHA patient?

Answer 6

Breeds - cocker and springer spaniels, OESD, Collies, Mini schnauzers, Poodles, Bichons
4-7 years
No sex
Possibly some seasonal distribution in the US

Question 7

What are some of the less common findings with IMHA

Answer 7

Can be chronic Hx
Coagulopathies
Extremity necrosis
Hepatosplenomegaly

Question 8

What may you see on clin path with IMHA?

Answer 8

Leukocytosis
Thrombocytopaenia in up to 70% cases
(need to differentiate between this and DIC/ evans)
high Bili in 60-85%
high ALKP - 80-90
High ALT - 60
AST - up to 70
Changes in HCT (therefore changes in RBC indeices) as the agglutination affects reading

Question 9

What are possible immunogenic targets in IMHA?

Answer 9

Innocent bystnader
Alloimmune
Modified self
Exposed crytpic antigen
Auto immune

Question 10

What happens in IMHA only including IgG?

Answer 10

Predominantly extravascualr haemolysis
Binding of Fc fragment on macrophages
Mainly occurs in spleen, also liver
Total or partial phagocytosis - spherocytes formed

Question 11

What happens in IMHA including both IgG and IgM?

Answer 11

more IgM - more IV h+ - leads to jaundics
Destruction of RBCs via the classical complement pathway
More aggressive

Question 12

What should you do to see if IMHA is primary or secondary

Answer 12

Check for Hx of travel or drugs
PE - check lymphadenopahty for evidence of myelo-proliferative disease
imaging - neoplasia, thromboembolic dz, FBs
Infections or inflammatory dz - PCR/ serology
BM biopsy

Question 13

Compare IMHA in dogs and cats

Answer 13

Dogs - normally primary, cats secondary
Cats - often non regenerative at presentation, and more severe anaemia
Lymphocytosis more common, neutrophilia less so
neutropaenia and thrombocytopaenia commonly seen with non regenerative
IV haemolysis less common in cats, but can still see jaundice
Must test of FIV, FeLV and mycoplasma, ideally also toxoplasma and assess for evidence of FIP
Apparently can be caused by severe hypophosphatemia in cats

Question 14

What are the possible secondary causes of IMHA in animals?

Answer 14

Infectious diseases
• Mycoplasma species, Babesia, Ehrlichia/Anaplasma, Leishmania, (Ricketssia + various others), FeLV, FIV, FIP

Recent medications / drugs / vaccination
• TMPS’s, penicillins, methimazole

Neoplasia
• Especially lymphoid and myeloproliferative diseases

Inflammatory disease

Question 15

neonatal iso erythrolysis occur?

Answer 15

Allo-immune haemolysis
Type A or AB kittens ingesting anti A Abs from a Type B queen
Clinical signs varibale, kittens can appear fine at first, the progress to reluctance to feed
Sometimes taking off the mum for a few days whilst intestinal barrier strengthens is all that is needed.

Question 16

What are the differentials for thrombocytopaenia

Answer 16

Decreased production
– Myelopthisis, drugs / toxic, infectious, Hereditary (e.g. Cavalier King Charles Spaniel)

Destruction
– Primary IMT, secondary IMT (drugs / toxins, infections/ inflammation, neoplasia, SLE)

Use
– Bleeding, DIC, vasculitis, sepsis / inflammation

Sequestration
– Hepatic / splenomegaly, sepsis

Question 17

What levels of platelets help you to rule in / out different things

Answer 17

Won’t be lower than 50 just from bleeding
Won’t be lower than 100 just from sequestration
Spontaneous bleeding uncommon less than 30
N.B cavity bleeding more secondary haemostasis issue

Question 18

What possible imaging may you wish to do for IMTP?

Answer 18

Haem, BM sampling, antiplatelet antibodies, tick expsoure checks including PCR/ serology, culture of anything infected (e.g. urine)

Question 19

How sick are IMTP patients at presentation?

Answer 19

Normally fairly well

If v sick - consider DIC (check clotting)

Question 20

What are the main types of haemoplasma?

Answer 20

Mycoplasma haemofelis is the most pathogenic species, able to cause anaemia in immunocompetant cats, while ‘Candidatus Mycoplasma haemominutum’ and ‘Candidatus Mycoplasma turicensis’ are less pathogenic and generally only result in anaemia if concurrent disease is present

Question 21

Outline paracetemol toxicity in cats

Answer 21

Cats are particularly sensitive to paracetamol toxicity due to their relative deficiency in activity of the enzyme glucuronyl transferase; methaemoglobinaemia and Heinz body formation can occur with paracetamol doses as low as 10 mg/kg, and the rapid formation of Heinz bodies can lead to significant anaemia. Other signs include depression, vocalisation, salivation, facial oedema, vomiting, hyperventilation, icterus and cyanosis.
Laboratory evidence of hepatotoxicity generally develops 24 to 36 hours after ingestion

Question 22

How do you treat paracetemol toxicity in cats?

Answer 22

acetylcysteine, cimetidine and vitamin C treatment, although limiting absorption and inducing vomiting is indicated if treatment can be started within two to four hours of ingestion. Blood transfusions, oxygen and fluid support may be required. SAMe treatment may also be beneficial. Prognosis is guarded for paracetamol toxicity unless rapid treatment is started.

Question 23

Outline PK deficiency

Answer 23

Pyruvate kinase (PK) is an enzyme critical to RBC energy metabolism, and PK deficiency leads to RBC haemolysis.
autosomal recessive inherited trait in Abyssinians and Somalis, also recently been found in the Bengal and Singapura breeds.
Genetic molecular screening tests are now available to identify affected and carrier cats,
Over half of those affected show anaemia associated with PK-induced haemolysis, and around 25 per cent will die due to the disease, with most showing anaemia and/or splenomegaly by three years of age.
Chronic haemolysis can lead to the formation of bilirubin choleliths, which can cause biliary tract obstruction. Management options include avoiding stress which may precipitate haemolytic crises, splenectomy and glucocorticoids (to reduce haemolysis via the macrophage phagocytic system), and blood transfusions.