Anaemia Flashcards

1
Q

Define anaemia

A

Reduction in the erythron mass based upon PCV (Htc), haemoglobin and RBC count

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2
Q

What is the clinical consequence of anaemia?

A

Inadequate oxygen carrying capacity in the blood

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3
Q

What is the physiological response to anaemia?

A
  • Increased RBC 2,3-DPG - lowers Hb-o2 affinity - allows better o2 delivery to peripheral tissues
  • Cats - Variety of Hbs which have different o2 affinities
  • Increased EPO - alters tissue perfusion
  • Behaviour alteration
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4
Q

What are the physiological causes of anaemia?

A
  • Increased RBC loss
  • Increased RBC destruction - IMHA
  • Inadequate bone marrow production of RBC
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5
Q

What clinical signs are associated with anaemia?

A
  • Pallor/ weakness
  • CRT
  • Tachy and bounding/weak pulses
  • Tachypnoea, dyspnoea
  • Haemic murmur - results from low blood viscosity
  • Jaundice
  • Petechia
  • Pyrexia
  • Lymphandenopathy
  • Abdominal pain
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6
Q

Outline the normal response to decreased O2.

A

Reduced O2 levels in the blood EPO release from the kidney Stimulates Red bone marrow to produce RBCs Increased O2 carrying capacity of the blood

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7
Q

What is regenerative anaemia?

A

The regenerative response is due to the bone marrow trying to compensate increasing erythropoiesis by releasing juvenile RBCs (reticulocytes)Leads to polychromasia

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8
Q

What is meant by pre-regenerative?

A

A smear visualised before the release of reticulocytes has taken place - need 3-4 days before seeing an increase in juvenile RBCs

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9
Q

What is non-regenerative anaemia?

A

When the bone marrow is unable to compensate due either to primary bone marrow disease or no endocrine (EPO) response to reduced O2 carrying capacity

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10
Q

At which days post insult is the regenerative response at its peak?

A

4-7 daysCharacterised by polychromasia and reticulocytes

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11
Q

What is the difference between an aggregate and punctate reticulocyte?

A

Aggregate contain large amounts of RNA and last only 24 hours.Punctate contain small amounts of RNA and last up to 10 days.

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12
Q

Which type of reticulocyte reflect current/ ongoing regenerative response in cats?

A

Aggregate

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13
Q

What is the observe response to acute haemorrhage?Describe and explain the haemocrit values observed immediately following haemorrhage and 24 hours later.

A
  • Proportional loss of all blood components, fluid moves into the vascular space, decreased PCV and TP Hct
  • Immediately - PCV 45% due to compensatory splenic contraction
  • 24 hrs - PCV 40% due to interstitial fluid moving into the vascular space
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14
Q

How would an animal with acute haemorrhage present in practice?

A

Would present as hypovolaemic shock:

  • Pallor
  • Tachycardia
  • Weak peripheral pulses Poor peripheral perfusion
  • > CRT
  • Cold extremities
  • Increased lactate
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15
Q

What finding is most suggestive of acute blood loss as a cause?

  • Hypochromasia and microcytosis on smear
  • Decreased TP
  • Thrombocytopenia
  • Polychromasia
  • Decreased MCHC
A

3

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16
Q

How can chronic blood loss lead to iron deficiency anaemia?How is IDA characterised on a blood smear?

A

Leads to consumption of irons stores.

  • Hypochromasia
  • Microcytic RBCs
  • May be regenerative (once erythropoiesis slows) or non-regenerative
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17
Q

How long does it take for IDA to develop in adults and why?

A

Takes about one month of chronic bleeding to develop due to abundant stores of iron in adults

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18
Q

What is the most common cause of IDA?

A

GI haemorrhage - may be due to NSAIDs, steroids, neoplasiaCan also be:

  • Urinary
  • Skin
  • Resp
  • Congenital defects
  • Parasitic infestations
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19
Q

How can IDA be treated?

  • Treating IDA
  • Treating underlying GI haemorrhage
A

IDA

  • Blood transfusion
  • Iron supplementation - oral ferrous sulphate, IM iron dextran GI haemorrhage
  • Sucralfate - acid buffer
  • H2 antagonist
  • H+ pump inhibitor
  • PGE analogue
20
Q

IMHA

A

Production od Abs against RBCs.Causes haemolysis and removal by macrophages and complement

21
Q

How does extravascular haemolysis cause jaundice?

A

Bilirubin is produced in haemolysis of RBCs.It is conjugated by the liver and excreted with bile.If liver capacity is overwhelmed hyperbilirubinaemia occurs leading to jaundice

22
Q

How does intravascular haemolysis lead to haemoglobinuria/ jaundice?

A

Haemoglobinuria

  • Free haemoglobin in the vascular space
  • Haptoglobin saturation
  • Hb dissociates in dimers which passes freely through the kidneys Jaundice
  • Free Hb
  • Binds haptoglobin and metabolised in the liver
  • If liver is overwhelmed = jaundice
23
Q

Which RBC shape abnormality is strongly supportive of IMHA?

A

SpherocytesDue to macrophage pitting the membrane portion which contains the Ab-Ag complex.

24
Q

Cell ghost

A

Very pale staining RBCs which are indicative of direct membrane damage by complement

25
Q

What is cold agglutinin disease?

A

An autoimmunediseasecharacterized by the presence of high concentrations of circulating antibodies, usually IgM, directed against red blood cells.Leads to:

  • Capillary blockage
  • Ischemia
  • Extremity necrosis
26
Q

What is the Coombs test?

A

Test for IMHAAn antiglobulin test

27
Q

Which tests are used in diagnosis of IMHA?

A
  • Clin signs Haematology
  • Autoagglutination - RBC grape clusters - persists if RBCs are washed
  • Regeneration
  • Spherocytes
  • Leukocytosis
  • Positive coombs test - used with caution - tests for Ab and complement
28
Q

What situations can cause false positive and false negative results from a coombs test?

A

False positive

  • Previous blood transfusion
  • Bystander complement and Ab effect Negative
  • Antisera at wrong concentration
  • Glucocorticoid therapy
29
Q

Name three haemic parasites.

A
  • Mycoplasma haemofelis
  • Anaplasma
  • Babesia
  • Ehrlichia
30
Q

Outline a treatment plan for IMHA.

A
Immunosupression	
* Corticosteroids	
* Cytotoxics - azathioprine	
* Cyclosporin
Start the dose high and gradually reduce to effect (two weeks between dose reductions - may be on treatment for life
31
Q

How do corticosteroids reduce IMHA?

A

Reduction in Fc receptor mediated RBC destructionInhibits complement activationReducing circulating cytokines

32
Q

Outline five side effects which may result from corticosteroid use.

A
  • PUPD
  • Polyphagia - obesity
  • Muscle wastage, poor exercise tolerence Gi
  • gastritis
  • ulceration
  • pancreatitis
  • Other organ damage long term
33
Q

What is the mechanism of action of azathioprine and Cyclophosphamide?

A
  • Suppress T cell and dependent B cell responses (from helper T cells)
  • Reduce lymphocytenumbers
  • Reduced Ab production
  • Affects macrophage function - cyclo
34
Q

How does cyclosporin work?

A
  • Suppressed CMI

* Secondary reduction in Ab production

35
Q

Neonatal isoerythrolysis

A

Destruction of neonatal erythrocytes by materal antibody

36
Q

IMHA may be associated with all, except…

  • IDA
  • Thromboembolic disease
  • DIC
  • Hypoxia & hypoperfusion
  • Neutrophilia and left shift
A

5 - associated with monocytosis and left shift

37
Q

Mechanical damage/ fragmentation as RBCs pass through fibrin meshwork in microvasculate.

A

Microangiopathic haemolysis

38
Q

How can mechanical damage to RBCs occur in the vasculature?

A
  • Altered vasculature - haemangiosarcoma
  • Fibrin nets - DIC
  • Glomeronephritis
  • Congenital defects
39
Q

Which RBC shape abnormalities are typical of microangiopathic haemolysis?Describe each.

A

Schistocytes

  • fragmented RBCs Acanthocytes
  • rounded projections of variable length from the RBCs surface
40
Q

Oxidative damage of RBCs occurs due to…The disease processresults in..

A

Increased free radicals in the blood leading to cell damage

  • Heinz body formation - denatured Hb within RBCs
  • Methaemoglobinaemia
  • Membrane oxidation
41
Q

What is a Howell Jolly body?

A

A nuclear remnant - NOT indicative of oxidative damage

42
Q

Intoxication of which substance in cats can lead to oxidative damage..

A

Paracetamol

43
Q

What can cause non-regenerative anaemia?

A

Primary marrow disease Drug reaction

  • NSAIDS, phenobarb, oestrogen (endo/exog)
  • Neoplasia
  • Pure red cell aplasia - immune mediated
  • A plastic anaemia
  • Lack of EPO - renal disease
44
Q

Describe anaemia of chronic kidney disease.

A
  • Normocytic
  • Normochromic
  • Non-regen
  • Reduced EPO
  • Haemorrhage
  • Reduced red cell survival/ erythropoiesis
45
Q

Outline some infectious causes of anaemia.

A
  • Feline retroviruses - FeLV, FIV Rickettsial
  • Ehrlichia
  • Leishmania
  • Babesia
  • Mycoplasma haemofelis