Anaemia Flashcards

1
Q

Define anaemia

A

Clinical presentation defined by reduction in PCV, red blood cell count, haemoglobin

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2
Q

Give examples of normal variations that may lead to increased PCV

A
  • Greyhounds and other sighthounds often naturally have higher PCV (>50)
  • Stress/excitement causing splenic contraction, temporary increase in circulating RBCs
  • Anabolic steroids
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3
Q

Give examples of normal variations that may lead to decreased PCV

A
  • Age: puppies and kittens <6-12 months have lower normal range
  • ACP (relaxes splenic capsule)
  • Reproductive status (late pregnancy)
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4
Q

What are teh potential aetiologies of anaemia?

A

Loss of blood cells via blood loss, reduced production or haemolysis

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5
Q

What are the potential causes of a regenerative anaemia?

A
  • Haemorrhage

- Haemolysis

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6
Q

List potential causes of haemorrhage

A
  • Internal loss or external loss
  • Trauma
  • Coagulopathy
  • Endo or ectoparasites
  • GI blood loss (tumours, ulcers)
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7
Q

List the potential causes of haemolysis

A
  • Erythrocytes removed from circulation by macrophages in spleen, liver, bone marrow (extravascular haemolysis) because they or the system are abnormal
  • Destruction of erythrocytes in vascular space
  • Immune mediated diseases
  • Infection
  • Oxidative damage
  • Rare genetic disorders
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8
Q

Give examples of infections that lead to haemolysis

A
  • Babesia spp..

- Mycoplasma haemofelis

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9
Q

Give examples pf oxidants that lead to haemolysis

A
  • Heavy metals
  • Onion
  • Garlic
  • rape
  • Kale
    Cabbages
  • Drugs e.g. paracetamol
  • Phenothiazine in horses
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10
Q

Compare the toxic dose of paracetamol in cats and dogs

A
  • Cats: much lower, 10-40mg/kg

- Dogs: 100mg/kg

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11
Q

Explain how oxidants cause haemolysis

A

Oxidation of haem iron to form methaemoglobin and/or oxidation of haemoglobin to form Heinz bodies

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12
Q

List genetic disorders that may cause haemolysis

A
  • Hereditary non-spherocytic haemolytic anaemia
  • Pyruvate kinase deficiency
  • Phosphodructokinase deficiency
  • Feline porphyra
  • Haemolysis in Abyssinian and Somali cats
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13
Q

List potential causes for intra-marrow suppression of erythropoiesis leading to non-regenerative anaemia

A
  • Primary disorders of erythropoiesis
  • iron deficiency
  • Aplastic anaemia (damage to haemopoietic stem cells)
  • Pure red cell aplasia (only red cells not produced)
  • Myelofirbosis
  • Myelodysplastic syndromes
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14
Q

Describe myelofibrosis

A
  • Scarring in bone marrow, can no longer produce cells
  • Replacement of marrow with fibroblasts and collagen
  • May be primary or secondary following IMHA, neoplasia for example
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15
Q

What may cause aplastic anaemia?

A
  • Ehrlichia canis
  • Canine and feline parvo
  • Idiopathic
  • Drugs incl. chemo
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16
Q

Describe pure red cell aplasia

A
  • Only red cells not produced

- Can be immune mediated, FeLV-C

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17
Q

Describe myelodusplastic syndromes

A
  • Stem cells not forming properly, usually some form of neoplasia
  • Includes Refractory Anaemia (RA), Refractory Anaemia with Excess Blasts (RAEB) and others
  • Slow form of leukaemia
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18
Q

List potential causes for extra-marrow suppression of erythropoiesis leading to non-regenerative anaemia

A
  • Anaemia of chronic disease
  • Anaemia of chronic renal failure
  • Secondary to endocrine disorders
  • Oestrogen induced bone marrow suppression
  • FeLV (additionally to specific disease of FeLV - C)

(secondary disorder of erythropoiesis)

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19
Q

What type of anaemia are the following blood smear features indicative of?

  • reticulocytes >5%
  • Anisocytosis
  • Poikilocytosis
  • Normoblastosis
  • Howell-Jolly bodies elevated
  • Heinz bodies elevated
  • Reactive leukocytoosis
A

Regenerative anaemia

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20
Q

Describe the blood smear characteristics of non-regnerative anaemia

A
  • No atempt to produce new cells
  • No reticulocites/polychromasia, anisocytosis, poikilocytosis, normoblastosis (unless damage to bone marrow stroma or in MPD), Howell-Jolly bodies, Heinz bodies or reactive leukocytosis
  • I..e normocytic, normochromic cells
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21
Q

What is a potential consequence of longstanding chronic bleeding?

A

Iron deficiency anaemia

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22
Q

What conditions are indicated by macrocytic, normochronic red blood cells?

A
  • FeLV
  • Myeloproliferative disease
  • Vit B12 and folic acid deficiency
  • Chemotherapy e.g. with methotrexate
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23
Q

Compare the clinical signs of acute and chronic anaemia

A

Often absent in chronic due to adaptation

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24
Q

Describe the clinical signs of anaemia

A
  • Pale mucous membranes
  • Lethargy, exercise intolerance
  • Tachypnoea, tachycardia (lack of oxygen dist.)
  • Poor pulse quality
  • Flow murmur
  • Pica (esp. mineral based material)
  • +/- signs related to underlying pathology e.g. splenomegaly, lymphadenopathy, pain, icterus, melaena
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25
Q

What does icterus suggest in anaemia?

A

Haemolysis

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26
Q

What are the main differentials for anaemia?

A
  • Cardiovascular disease

- Liver disease

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27
Q

List clinical signs that may indicate haemolysis

A
  • Haemoglobinuria
  • Haemoglobinaemia
  • Icterus (seen earlier in serum vs mucous membranes/sclera)
28
Q

How would you interpret an acute haemorrhage with smear showing it as non-regenerative?

A

Probably not non-regenerative, regenerative response lags 2-4 days behind anaemia

29
Q

How would you interpret a cause of severe anaemia with mild clinical signs?

A

Suggests chronic disease, and increased O2 carrying capacity of the remaining RBCs

30
Q

Identify tests that are useful in the investigation of anaemia

A
  • Haematology
  • Herum biochem
  • Urinalysis
  • Virology
  • Faecal analysis
  • Coomb’s test
  • Coagulation profile
  • Imaging
  • Bone marrow biopsy
  • Microhaematocrit
31
Q

Discuss the use of PCV in the investigation of anaemia

A
  • May have operator error
  • Patient side Hb testing is an alternative
  • Interpret with total solids
  • Acute blood loss may not result in changes in PCV or total solids for some hours
32
Q

What may high total solids indicate and how does this relate to anaemia?

A

Indicates dehydration, can mask severity of anaemia

33
Q

What do normal total solids in relation to anaemia indicate?

A

Non-regenerative anaemia or haemolysis

34
Q

What do low total solids in relation to anaemia indicate?

A

Blood loss

35
Q

What do the following values indicate regarding the severity of anaemia (and from that, the most likely underlying cause):

  • PCV (%): 15
  • RBCC (x10^12/l): 2.0
  • Hb (g/dl): 4.5
A

Severe

Suggests: haemolysis, bone marrow disease

36
Q

What do the following values indicate regarding the severity of anaemia:

  • PCV (%): 23
  • RBCC (x10^12/l): 3.5
  • Hb (g/dl): 7.5
A

Moderate

37
Q

What do the following values indicate regarding the severity of anaemia (and from that, most likely cause):

  • PCV (%): 30
  • RBCC (x10^12/l): 4.8
  • Hb (g/dl): 10.0
A

Mild: anaemia of chronic disease, acute blood loss

38
Q

What are the aims of management of severe anaemia?

A
  • Reduce oxygen expenditure
  • Increase oxygen carrying capacity
  • Allow time to diagnose and address cause of anaemia
39
Q

What are the consequences of >20% blood volume loss?

A

Peripheral vasoconstriction, tachycardia

40
Q

What are the consequences of >30-40% blood volume loss?

A

Decreased cardiac output, hypotension, collapse

41
Q

What are the consequences of >50% blood volume loss?

A

Shock and death

42
Q

Outline the management of acute haemorrhage

A
  • Prevent further bleeding: look for source, apply pressure
  • Fluid replacement
  • Blood transfusion support
  • Treatment of underlying disorder
43
Q

What is most significant to address in acute haemorrhage?

A

Immediate effects of volume depletion, loss of circulating RBCs can be sorted out later

44
Q

Describe the clinical signs of Mycoplasma haemofelis

A
  • Variable related to haemolytic anaemia
  • Regenreative anaemia
  • Jaundice
  • Pale mucous membranes
  • Pyrexia, depression, weakness, anorexia, weight loss
  • Severity varies from mild to fatal
45
Q

Which groups of cats are more severely affected by Mycoplasma haemofelis?

A

Young or immunosuppressed (FIV)

46
Q

How is Mycoplasma haemofelis transmitted?

A

Fleas, ticks, and vertically

47
Q

How is Mycoplasma haemofelis diagnosed?

A
  • Blood smear with Romanowsky or acridine orange stain sampled when cat is sick and before treatment
  • Quantitative PCR
48
Q

What is the main disadvantage of diagnosing Mycoplasma haemofelis based on blood smears?

A

Cyclical parasitaemia on red blood cells means they may be missed (false negatives)

49
Q

Describe the treatment of Mycoplasma haemofelis

A
  • Doxycycline first choice (10mg/kg SID) before or with food
  • Enrofloxacin second choice (5mg/kg SID)
  • Treat for 2-8 weeks
  • Repeat PCR (cure rather than remission may be difficult)
  • Supportive treatment e.g. transfusion may be necessary
50
Q

Describe the occurence of Babeisa in UK dogs

A
  • Not endemic to UK, but sporadic cases in travelling dogs
  • Tick borne
  • Endemic in cattle
51
Q

Describe the presentation of Babesia

A

Signs of haemolytic anaemia

52
Q

Describe the presentation of Ehrlichia canis

A
  • Acute phase: malaise and bleeding, difficult to identify

- Chronic: complete bone marrow failure, intra marrow non-regenerative anaemia, white cell problems

53
Q

Outline the prevention of Babesia and Ehrlichia

A
  • Both tick transmission, avoid tick habitats, check dogs daily and use acaricides
  • Vaccine for Babesia available, prevents severe disease but not infection
54
Q

Outline the treatment for oxidant anaemia

A
  • Immediate removal of oxidative agent (emesis <4hr)
  • Activated charcoal
  • Supportive care
  • Monitor haematological parameters, may need transufsion
  • For paracetamol: acetyl cysteine (dogs and cats) and ascorbic acid (cats only) reverse oxidate effects
55
Q

How do acetyl cysteine and ascorbic acid work in the treatment of paracetamol intoxication?

A
  • Acetyl cysteine increases elimination of toxic metabolites

- Ascorbic acid resolves methaemoglobinaemia by returning to oxyhaemoglobin

56
Q

How does copper poisoning occur?

A

Capacity for Cu storage in liver exceeded, sudden release of Cu stores into circulation, leading to haemolysis and liver damage (icterus)

57
Q

Give examples of sheep feeds high in copper

A
  • Silage where pig or chicken manure has been used

- Brewer’s mash from copper stills

58
Q

Describe the clinical signs of copper poisoning in sheep

A
  • Lethargy, anaemia, teeth grinding, polydipsia
  • Pale, icteric MMs, haemoglobinuria
  • Death 1-2 days after onset of signs
  • At PM, tissues pale to dark yellow, kidneys very dark
59
Q

Outline the treatment and prognosis of copper poisoning in sheep

A
  • Oral or injectable ammonoium tetrathiomolybdate
  • Addition of copper binders to feed e.g. sulphur
  • Expensive
  • Poor prognosis if severe
60
Q

Identify the potential aetiologies of iron deficiency anaemia

A
  • Late feature of chronic blood loss

- Bone marrow stores deplete before anaemia develops

61
Q

describe the diagnosis of iron deficiency anaemia

A
  • Normo to microcytic, hypochromic
  • Non-regenerative
  • Increased platelet count
  • Red cells fragile, schistocytes, keratocytes and target cells seen
62
Q

Outline the treatment of iron deficiency anaemia

A

Long term treatment required to replenish bone marrow

63
Q

Outline how anaemia of chronic disease occurs and the treatment

A
  • Generally mild, non-regenerative anaemia
  • Bone marrow responds less well to EPO
  • Reduced iron stores, reduced RBC survival
  • Endocrine disorders
  • Need to treat the underlying condition
64
Q

Outline how oestrogen induced bone marrow suppression occurs and leads to anaemia

A
  • Persistent oestrus in ferrets

- Oestrogen damages haemopoietic stem cells

65
Q

Outline how anaemia of chronic kidney disease occurs and outline the treatment

A
  • Reduced renal EPO production
  • Check for other sources of blood loss e.g. GI ulcers which can also occur with kidney disease
  • Treat with recombinant human EPO (becomes less effective in cats over time due to antibody production, expensive)