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Lent term fourth year > HOLS RBCs > Flashcards

HOLS RBCs Flashcards

1
Q

Where does bone marrow haematopoiesis happen in adult dogs

A

Pelvis, ribs, vertebrae, prox ends of long bones

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2
Q

Where/when does extra-medullary haematopoesis happen

A

when demand for haematopoeitic cells is greater than bone marrow capacity
Spleen, liver (LNs)

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3
Q

Where does EPO come from

A

peritubular interstitial cells in the kidney

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4
Q

What diseases would affect EPO production/action

A

CKD: lower EPO production from kidney
Hypoadrenocorticism/hypothyroidisn: lower EPO activity because activitiy enhanced by thyroid hormone and cortisol

Chronic pulmonary disease: get hypoxia which stimulates extra EPO production

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5
Q

Why is microcytosis seen with haemoglobin deficiency anaemia

A

Because Hb content of cells thought to be a regulator of cell division; so get extra divisions when not enough Hb

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6
Q

What are reticulocytes and in which species it is normal to see them in the blood

A

= immature RBCs; released into blood and mature within 24-48 hours
See as large, polychronatic cells
Normal in dogs/cats/sheep RARE in horses/cows

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7
Q

Erythrocyte life span in different species

A

Cats = 80 days (2.5 months)
Dogs = 110 days (3.5 months)
Horses = 150 days (5 months)

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8
Q

What is different about cat reticulocytes

A

Can group into aggregate AND punctate reticulocytes
Aggregate ones indicate recent regeneration but become punctate within 12 hours
Punctate ones are not polychromatic; look like normal RBCs so need methylene blue staining

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9
Q

Clinical signs of anaemia

A

Due to reduced O2 carrying capacity
Lethargy, weakness, tachypnoea
See pale MMs, tachycardia, systolic heart murmur (due to viscosity changes)

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10
Q

What is the gold standard measure of red cell mass

A

PCV
(HCT should be within 2-3% of this)

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11
Q

What are the definitive signs of a regenerative anaemia

A

1) Increased reticulocyte that MATCHES degree of anaemia
2) Significant polychromasia on blood smear (reticulocytes)
NB: don’t see this in horses because the reticulocytes aren’t released into blood
–> Means at least 7-10/hpf

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12
Q

Supportive signs of regeneration

A

Anisocytosis = variation in erythrocyte size
Macrocytosis = presence of large erythrocytes
Rubricytosis = nucleated red blood cells (likely metarubricytes)
Howel-Jolly bodies (retained dragments of nucleus - see low numbers normally in cats)
Target cells/codocytes = blip of membrane in centre due to increase in rate of membrane:Hb
Basophilis stippling; esp in ruminants

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13
Q

Non-regenerative causes of macrocytosis

A

dyserythrocytosis, erythroleukaemia, FeLV

+ agglutination; in vitro swelling during transport

{few more online]

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14
Q

Non-regenerative causes of microcytosis

A

iron deficiency, portosystemic shunt/hepatic failure
May be normal in some Japanese breeds

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15
Q

What does appropriate rubricytosis mean

A

When presence of nucleated red blood cells is associated with polychromasia/reticulocytosis i.e indicating regenerative response

Vs inappropriate = without this

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16
Q

Causes of inappropriate rubricytosis (without regenerative response)

A

Lead poisoning, marrow damage in heat stroke, erythroleukaemia
+ where not mopped up: splenic contraction, splenectomy

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17
Q

When might be see increased Howell Jolly bodies if not relating to regenerative anaemia

A

With splenectomy

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18
Q

When might we see target cells/codocytes except with regenerative anaemia

A

Fe deficiency
Liver dysfunction (causes increase cell SA)
(related to higher membrane:HB)

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19
Q

What might basophilic stippling mean if not regenerative anaemia

A

Lead poisoning

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20
Q

Classifying anaemia via PCV (/HCT) in dogs

A

Mild: 30-37%
Moderate: 20-29%
Marked: <20%

NB: normal = 35-55%

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21
Q

Classifying anaemia via PCV (/HCT) in cats

A

Mild: 20-26%
Moderate: 15-19%
Marked: <15%

NB: normal = 25-45%

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22
Q

What reticulocytes would match mild vs severe anaemia
and what is normal

A

Normal in dogs = <80x10^9/L; cats 60

Mild: 100x10^9/L
Marked: up to 4x this i.e 400x10^9/L

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23
Q

What changes in MCV and MCHC support regeneration

A

Increased MVC and decreased MCHC

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24
Q

What does high MCHC mean

A

Artefact usually
e.g from lipaemia or haemolysis giving increase haemoglobin value

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25
Q

Causes of decreased MCHC (i.e hypochromic)

A

Regeneration
Iron deficiency
Falsely elevated MCV e.g from in vitro swelling

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26
Q

What if we think it may be regenerative but no reticulocytes etc

A

May be pre-regenerative; in few days after blood loss
- check back in 3-5 days (lag time for RBCs to be made)

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27
Q

Why is regenerative response fairly mild with internal haemorrhage

A

65% erythrocytes and most PPs reabsorbed within 2-3 days
NB: may see leukocytosis due to inflammatory response

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28
Q

Recovery from anaemia in external haemorrhage

A

PP normalises in 1 week
PCV takes 2-3 weeks to normalise; bone marrow production of RBCs

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29
Q

Causes of chronic haemorrhage

A

OFten GI bleeding; may have urinary tract bleeding

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30
Q

Why are clinical signs mild for degree of anaemia in chronic haemorrhage

A

Slow onset gives time for physiological compensation

31
Q

Why might we see a chronic haemorrhage become non-regenerative over time

A

Depletion of iron stores; get a microcytic and hypochromic non-regenerative anaemia

32
Q

General signs that regenerative anaemia is due to haemolysis

A

Low PCV
BUT normal/high plasma protein levels (may be high due to inflammatory response to haemolysis)

33
Q

General signs that a regenerative anaemia is due to haemorrhage

A

Low PCV
Low plasma proteins
(but combine with history etc; remember hydration status important)

34
Q

WHy may we see a more marked regenerative response to haemolytic anaemia vs haemorrhagic

A

Because more Fe available (not losing it to environment)

35
Q

Is intra or extravascular haemolysis associated with more severe anaemia

A

Intravascular haemolysis
+ more rapid onset

36
Q

Signs of extravascular haemolysis

A

Splenomegaly
Hyperbilirubinaemia (jaundice)
Bilirubinuria

37
Q

Signs of intravascular haemolysis

A

Haemoglobinaemia and uria because of Hb release in circulation
+ Liver breakdown of these products may give hyperbilirubinaemia/uria

38
Q

What is the most common type of IMHA in dogs

A

Idiopathic i.e primary

39
Q

What type of IMHA is more common in cats

A

Secondary e.g from drugs

40
Q

Different causes of secondary IMHA

A

Drugs: potentiated sulphonamides, cephalosporins, NSAIDs
Infectious agents
Allloimmune i.e neonatal isoerythrolysis or blood transfusion
Neoplasia

41
Q

Which dog breeds are predisposed to IMHA

A

Females
Cockers/springers
Poodles
irish setter

42
Q

Which infectious agents can cause IMHA in dogs

A

Babesia, anaplasma, ehrlichia, leishmania

43
Q

Which infectious agents can cause IMHA in cats

A

Mycoplasma (=FIA), FeLV

44
Q

What is the definitive test for IMHA

A

Coombs test; detects presence of antibodies on surface of RBCs - NB sensitivity only 60%

45
Q

Signs supporting IMHA diagonsis

A

Regenerative anaemia
Urine: Bilirubinuria/haemoglobinuria
Blood: hyperbilirubinaemia/haemoglobinaemia
Sphereocyte presence in dogs
Ghost cells (indicate intravascular haemolysis)
Autoagglutination

46
Q

How can we confirm is autoagglutination is genuine

A

c/f rouleux
Do in saline agglutination test to disperse rouleaux
NB: negative SAT does not rule out IMHA - need Coombs

47
Q

What are spherocytes

A

Small round, red cells lacking central pallor because part of membrane phagocytosed
Seen in dogs with IMHA

48
Q

Ruling out causes of IMHA

A

Image for neoplasia, check drug history, PCR/serology for infectious agents, bone marrow exam

49
Q

How can haemotrophic mycoplasmas in acts (FIA) cause IMHA

A

M haemofelis etc
Attach to cell membrane and cause extravascular haemolysis
–> This can then induce an antibody response which causes IMHA

50
Q

How does neonatal isoerythrolysis work

A

Mother has anti-erythrocyte antibodies in colostrum; ingested by offspring and RBCs destroyed

51
Q

Blood groups in dogs and natural alloantibodies

A

Most relevant = DEA1.1
NO NATURAL ALLOANTIBODIES
BUT DEA1.1 -ve dogs will develop antibodies against DEA1.1 +ve if they have a transfusion with that blood or birth a DEA1.1 +ve pup

52
Q

Blood groups in cats and natural alloantibodies

A

A: has weak anti-B antibodies
B: has STRONG anti-A antibodies
AB (rare): no natural antibodies

53
Q

Why do we do pre-breeding blood typing in cats

A

Risk of type A kittens being born to type B mother; anti-A antibodies in colostrum will cause haemolytic anaemia in kittens
- Must take away for 48 hours to allow gut to close and avoid ingestion of colostrum

54
Q

Relevant blood groups and natural alloantibodies in horses

A

Those without Aa, Ac and Ca will have antibodies against them
None have anti-Oa antibodies naturally BUT will develop them after birthing an Oa +ve foal

55
Q

Typical blood type of TB horses

A

Aa or Oa

56
Q

2 categories of haemolytic anaemia causes

A

1) Immune mediated
2) Non-immune mediated e.g oxidative damage

57
Q

Most common cause of non-immune mediated haemolytic anaemia

A

Oxidative damage

58
Q

Why do we get Heinz body formation in oxidative damage

A

Oxidation of globin chains cause precipitation of Hb to inside of cell membrane = Heinz body

59
Q

Things associated with Heinz body formation

A

Heinz body anaemia assocaited with: onion, garlic (dogs), paracetamol, zinc (dogs), maple leaves (horses), kale/rape (ruminants
NB: cats normally should <10% of Heinz bodies

+ non-oxidative injury conditions: liver disease, propofol administration, hyperthyroidism, diabetes

60
Q

Signs of oxidative damage causing non-immune mediated haemolysis

A

Heinz body formation
Cell membrane damage (see eccentrocytes)
Methaemaglobin due to oxidation of Fe2+ to Fe3+; causes brown blood

61
Q

Other causes except oxidative damage of non-immune mediated intravascular haemolysis

A

Erythrocyte metabolic disorders with PFK
Severe hypophosphataemia
Haemophagocytic histiocytic sarcoma
Disorders causing RBC fragmentation e.g valvular disease

62
Q

Aplastic anaemia signs

A

Damage to haematopoietic stem cells in marrow so cells replcaed with fat
Affects all lines; see leukopenia and thrombocytopenia FIRST as shorter half life

63
Q

Causes of aplastic anaemia

A

Infections: parvo, FeLV
Drugs: oestrogen from tumour/ecogenous, phenybutazone
Immune mediated

64
Q

What might a macrocytic anaemia in cats be a result of

A

FeLV infection

65
Q

Pure red cell aplasia

A

Due to selective damage to erythroid stem cells in marrow
Usually immune mediated
- Can be secondary to FeLV infection in cats (NB: red cells with be macrocytic)

66
Q

Neoplasia that can cause non-regenerative anaemia

A

Leukaemia: reduction in all lines due to crowding out of stem cells

Other bone marrow neoplasia
- Histiocytic sarcoma
- Metastiasis
- Stage V lymphoma

67
Q

Myelofibrosis causing non-regnerative anaemia

A

Fibroblasts proliferate in marrow and replace normal cells
Marked anaemia without affecting other cell lines
Usually secondary to an underlying cause e/g IMHA from PK deficiency

68
Q

What is the most common secondary cause of non-regenerative anaemia

A

inflammatory disease

69
Q

How does inflammatory disease cause anaemia

A

Must be long standing inflammation
Increased hepicin decreases iron absorption
+ Shortened RBC lifespan
+ less EPO release

See inflammatory leukogram

70
Q

How to diagnose anaemia due to CKD

A

History + increased serum urea and creatinne

71
Q

Most common nutritional deficiency causing non-regenerative anaemia

A

Iron; due to chronic GI haemorrhage rather than dietary deficiencies usually

72
Q

Relative vs absolute erythrocytosis

A

Relative = normal red cell mass but increased erythrocyte concentration e.g dehydration, splenic contraction

Absolute = actual increase in red cell mass i.e more production

73
Q

Primary vs secondary erythroctosis

A

Primary = EPO-independent; neoplastic RBC proliferation

Secondary = EPO-dependent; increased EPO from hypoxia due to right-left shunt or chronic pulmonary disease OR from EPO-secreting renal tumours

Lent term fourth year (38 decks)

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