Abnormlaities of the erythrom 2 Flashcards

1
Q

How can you test for meleana?

A
  • meat free diet (red meat) for 5d before test or will be positive
  • not always visable blood
  • “feacal occult blood” very sensitive but NOT specific
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2
Q

Causes of increased losses?

A
> haemorrhage (external) 
- meleana
- UT
- Epistaxis
- Post-trauma/surgery
> haemorrhage (internal) 
- bleeding tumour
- trauma
- into tissue (bleeding diathesis) 
- surgery 
> haemolysis 
- ^ internal RBC destruction 
- intra v extravascualr
- normal erythrocytes or abnormal/damaged ?
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3
Q

What is the most common form of haemolyss? Dxx?

A

> IMHA

  • anti-redcell Ab (IgG, IgM, IgA)
  • red cells opsonised -> lysis (IgM) or phagocytosis
  • may agglutinate
  • Coombs test + (for anti RBC Ab)
  • may be severe/rapid, usually strongly regenerative
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4
Q

What is seen microscopically with IMHA? Ddx?

A

> agglutination
- flaky blood macroscopicallly
- grape like bunches of RBC
- in saline agglutination test (screening)
- one drop saline one EDTA anticoagulated blood mix on slide
- look for flecking before starts to dry (will still occour if AGGLUTINATION, will get rid of ROULEUX artefact)
Ddx = Rouleaux artefact
- stack of coins
- high protein stuck on RBC
- gritty, lumpy macroscopically
- but not pathological

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5
Q

What causes intravascular haemolysis? How is this seen?

A

> complement mediated

- ghost cells (barey visable, membrane still present, Hbg gone)

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6
Q

What causes extravascular haemolysis?

A
  • macrophages in liver/spleen
  • takes bites out of lipid bilayer -> spherical cell (spherocytes) as membrane reforms
  • smaller, and very dark (no central pallor)
  • normal volume though diameter will appear less
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7
Q

What else may be found with IMHA? Dxxx

A
  • ^ bilirubin (esp with extravascular breakdown)
  • neutrophilia, monocytosis (marrow upregulation)
  • patelets may also be affected (Evans syndrome IMHA+ platelets)
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8
Q

What parasites may cause haemolysis?

A
> mycoplasma haemofelis and M. haemominutum (formerly haemobartonella) 
- epicellular
- large and small forms 
- ^ fragility and hameolysis
- cyclical 3-8 weeks 
- not in UK 
> Babesia (dogs, USA, mediterranean) 
- tick borne dz
- pyriform bodies INSDIE RBC 
- haemolytic
> Cytauxzoon felis (US) 
- intracellular
- prominant splenic RBC removal
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9
Q

Dx of mycoplasma haemofelis?

A
  • PCR excellent

- blood smear not reliable

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10
Q

Tx babesia?

A
  • Imidocarb
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11
Q

Which animals develop Heinz bodies more readily?

A

Cats

- low number unremarkable in cats

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12
Q

What are heinz bodies and how do they appear?

A
  • denatured/oxidised Hbg

- Little ‘nose’ on cell, same colour of RBC

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13
Q

Causes of Heinz body formation?

A
  • onions
  • paracetamol
  • Vit K
  • propylene glycol
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14
Q

What are eccentrocytes?

A
  • Hbg uneven distribution within the cell -> eccentric distribution
  • oxidative damage to membrane (cf. Heinz - Hbg)
  • seen most commonly in dogs, seen horses with red maple toxicosis
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15
Q

What are schistocytes and keratocytes?

A
  • Shear injury products d/t microangiopathic dmage (tumours w/ narrow vessels eg. angiosarcoma) or organ inflammatory beds (severe hepatitis, DIC) d/t fibrin stranding cutting them in half
  • Clue to underlying disease vs cause
    > schistocytes
  • RBC fragments 2* to shear injury
  • assoc with fibrin deposition in vessels and DIC
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16
Q

What are acanthocytes?

A
  • surface prjections (spicules)
  • variable length, unevenly spacd
  • narrow base and blunted
    > seen with splenic dz
17
Q

Pre-keratocytes and Keratocytes?

A
  • red cells with apposed and sealed membrane
  • helmet shaped cells
  • associated with shearing (intravascular trauma eg. vasculitis, DIC) alongside shistocytes
18
Q

Spherocytes

A
  • extravascular destruction by macrophages taking a bite out -> membrane reforms as a sphere
  • darker and smaller, perfectly round
  • no central pallor
19
Q

Give egs of inherited hemolytic dz

A

> Pyruvate kinase deficiency [Basenjis and Beagles]
- Energy production deficiency
- initially may be very regnerative
- may go on to develop myelofibrosis and acute crisis (death @ 1yr)
- chronic, severe haeolysis
PFK deficiency [English springers]
- RBC sensitive to alkaline ph : low grade haemolysis with severe episodes superimposed
feline porphyria

20
Q

MOst common non-regenerative anemia?

A

> anaemia of inflammatory/chronic disease

  • normocytic, normochromic
  • usually mild and lowly progressive
  • Fe sequestration (bugs want iron)
  • inflam mediators -> shortened erythrocyte survival
21
Q

Causes of non-regenerative anaemia? FINISH

A
  • chronic disease
  • renal
  • endocrine
  • FeLV
22
Q

How does renal anaemia occour? Tx?

A
  • EPO production v
  • normocytic, normochromic, mild - mod
  • impacts quality of life
    > Tx: EPO injections (though human so can => immune response)
    > aim to ^ PCV (though not to normal)
23
Q

Is endocrine anaemia a common problem?

A

Rare

  • hypothyroid and hypoadrenocorticism
  • normocytic, normochromic, mild
  • thyroid hormone and cortisol facultative effect on RBC production
24
Q

How common is FeLV anaemia? How are they linked? What type of anaemia is seen?

A
  • FeLV subgroup C
  • 70% anaemic cats!
  • selective depression of erythropoeisus
  • dyspalstic production
  • myeloproliferative dz ‘crowding out’
    > usually non-specific erythroid hypoplasia
  • may be normocytic/chromic but may be macrocytic
25
Q

Causes of aplastic anaemia

A
  • FeLV, estrogen tox, phenylbutazone, chemotherapy, unknown
26
Q

What is missing with apastic anaemia? What remains? What is needed to dx this?

A
  • ALL precursors (complete non-regenerative marrow)
  • fat, plasma cells and mast cells left
  • need core biopsy otherwise cant tell if youve just got a rubbish sample
27
Q

What is myelodysplasia? What is seen in the marrow?

A
  • type of non-regenerative anaemia (pre-leakaemia)
  • adequate cellularity in marrow but abnormal maturation/proliferation of cells (ineffective haemopoiesis)
  • in the marrow: erythrocyte macrocytosis, binucleates, maturation defects, giant neutrophils, hypersegmented neuts, macroplatelets
  • may progress to leukaemia
28
Q

What is myelopthisis?

A
  • neoplasia crowding out the bone marrow and altering environment
  • usually haematopoetic neoplasia (esp lymphoid)
29
Q

What is myelofibrosis? Dxx?

A
  • response to injury of fibrous elements of marrow -> dry taps
  • may be reactive following prolonged regenerative attempts
  • Need core biopsy: reticulin stains up the fibrous elements
  • osteosclerosis: cortical bone ^
    +- marked extramedullary haematopoiesis
30
Q

Which dz are exeptions to the non-regenerative type thing..

A

> iron deficiency anaemia may -> non-regenerative in the long term
immune mediated attack of RBC precursors no the mature cells -> non-regenerative

31
Q

Why is melena particularly bad?

A
  • LOSS of iron (cf. haemothorax etc. where RBC will be recycled)
32
Q

Main 6 questions to ask wrt anaemia?

A
  • mild mod severe?
  • regenerative/non?
  • macro/microcytic?
  • hypo/normochromic?
  • specific morphology changes?
  • does the sample give you the answer?
33
Q

What is polycythaemia?

A

= erythrocytosis
- ^ HCT, RBC count and Hbg
> may be spurious or relative
- dehydration (volume contraction) most common
- RBC redistribution (splenic contraction) esp in horses

34
Q

Causes and subgroups of absolute erythrocytosis?

A
> 1* (polycythemia vera) neoplasia [ in humans all cell lines, in animals RBC only]
- myeloproliferative disorder of erythroid stem cells 
- EPO level normal/decreased
- PO2 normal 
> 2* (appropriate or innaropriate
- chronic hypoxia
- EPO secreting tumours
- EPO level raised
35
Q

Hyperthyroid cats have ^ RBC - is this pathological?

A
  • technically pathological but normal for the physiological state they are in (higher metabolic rates = higher oxygen demand)
36
Q

What should be submitted alongside EDTA sample? How should this be stored??

A

Fresh blood smear

  • store blood in fridge until analysis (slows changes)
  • store smears at room temperature (NOT IN FRIDGE)