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Year 4 LCB > Year 4 LCB > Flashcards

Year 4 LCB Flashcards

1
Q

What can you use to differentiate between regenerative and non regenerative anaemia?

A

Reticulocytes

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2
Q

What are the values of reticulocytes in dogs and cats with regenerative anaemia?

A

Dogs >60 (x10^9/l)

Cats >50(x10^9/l) (only count the aggregate type)

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3
Q

What haematology oddity is normal for akitas?

A

-Microcytic erythrocytes and high potassium

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4
Q

Describe Heinz bodies

A
  • Caused by oxidative damage, low number are normal in cats

- High numbers in cats with hyperT4, lymphoma and DM

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5
Q

When do you see basophilic stippling?

A

Regenerative anaemia and lead poisoning

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6
Q

When do you nucleated red blood cells?

A

-Regenerative anaemia OR if the animal isn’t anaemia then show poor spleen function and marrow damage

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7
Q

How do you differentiate between rouleux formation and agglutination? When do both of these form?

A

-By mixing 1 drop blood wth 1 drop saline. Rouleux will disperse.
(Rouleux shows inflammation in SA)
(agglutination occurs in IMHA or mismatched transfusions)

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8
Q

What does normochromic normocytic anaemia suggest?

A

Pre regenerative phase or non regenerative anaemia

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9
Q

What does macrocytic hypochromic anaemia suggest?

A

Regenerative anaemia

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10
Q

What does microcytic hypochromic anaemia suggest?

A

Fe deficiency anaemia`

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11
Q

How do you calculate PCV?

How do you calculate MCV?

A

PCV= MCVx RBCC

MCV=PCV x1000/ RBCC

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12
Q

When do you see macrocytosis?

A

Regenerative anaemia of FeLV infection

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13
Q

What do you see microcytosis?

A

Iron deficiency

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14
Q

What causes an increase in RDW?

A

Anisocytosis

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15
Q

Describe codocytes and when you’d see them

A
  • AKA target cells, have a bulls eye appearance

- Due to Fe deficiency or liver disease

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16
Q

Describe schistocytes and when you’d see them

A
  • Caused by trauma to circulating RBCs

- Seen with DIC, thrombosis, IMHA or congestive heart failure

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17
Q

Describe spherocytes and when you’d see them

A
  • Small, densely stained

- See in IMHA or animals that have received a transfusion

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18
Q

Describe acanthocytes and when you’d see them

A
  • Sight spiky (not as spiky as burr)
  • Caused by increase in membrane cholesterol or associated RBC fragmentation
  • Seen in liver dx, splenic haemangiosarcoma and Portosystemic shunts
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19
Q

What abnormally shaped RBC is normal to see in ruminants?

A

Crenation or burr

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20
Q

Describe the effect of steroids on neutrophils

A
  • Suppress release from bone marrow
  • Demargination (release from BV walls) and decreaase in extravasation
  • Results in more neutrophils in circulation
  • Results in right shift (mature cells in circulation due to BM neutrophil suppression)
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21
Q

Whats the difference between regenerative and degenerative left shift?

A
  • Regenerative= mostly mature cells released into circulation
  • Degenerative= mostly immature released
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22
Q

What is neutrophil toxic change?

A

Rapid neutropoeisis
Usually due to severe bacterial infection
Results in foamy cytoplasm Dohle bodies and diffuse cytoplasm basophilia

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23
Q

What can cause neutrophilia?

A

FeLV infection
Neoplasia
Parvo
Chemo

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24
Q

What haematology value is a marker for RBC colour?

A

MCHC

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25
Q

What are the 2 main types of lymphocytes?

A 
-Reactive= involved in IR and recently vaccinated animals
Granular= have pink granules in 1 area of cytoplasm
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26
Q

What can spleen contraction and Addisons both cause?

A

Lymphocytosis (also caused by young animals in new environment)

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27
Q

What can cause lymphopenia?

A

Stress by steroids, acute inflammation, lymphoma

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28
Q

What can cause monocytosis?

A

Chronic inflammation or steroids and stress

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29
Q

How do acute and chronic inflammatino cause different leucograms?

A

Acute causes lymphopenia and chronic causes monocytosis

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30
Q

What can parasites, hypersensitivities and allergic reaction all cause? (leucogram)

A

Eosinophilia

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31
Q

Describe the classic stress leucogram

A

++ neutrophilia
+eosinophilia
+lymphopenia
-+monocytosis

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32
Q

What does a high neutrophil count and high lymphocyte count indicate?

A

Excitement leucogram

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33
Q

Briefly describe leukaemia

A
  • Bone marrow neoplasia or lymphoid or non lymphoid origin
  • Can infiltrate other organs e.g. spleen and liver
  • AML= acute myeloproliferative leukaemia (non lymphoid origin e.g. RBC) (also get CML, CLL, ALL)
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34
Q

Describe the difference between acute and chronic leukaemia

A
  • Acute: neoplastic changes occurred DURING stem cell proliferation, this means you get high number of blast (undifferentiated) cells, aggressive and rapid disease, CYTOPENIA common
  • Chronic: neoplastic changes occur AFTER differentiation so you get lots of mature cells, slow, progressive disease, cytopenia rare
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35
Q

Describe the cytopenia seen in acute leukaemia

A
  • Neutrophils dissaapear first (hours)
  • Platelets (days)
  • RBCs (months)
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36
Q

Describe the difference between lymphoma that involves the BM and acute lymphomblastic leukaemia

A

Lymphoma with BM involvement: <25% blast cells in BM, cytopenia is rare, Massive LYMPHADENOPATHY, might not be systemically ill
Lymphoid leukaemia: >25% blast cells in BM, more circulating blast cells, severe cytopenia, mild or moderate lymphadenopathy, usually systemically ill

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37
Q

What stage of lymphoma can involve the BM?

A

Stage 5

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38
Q

What are the examples of immunophenotyping in leukaemia?

A
  • Histology of BM

- Biopsies

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39
Q

What is lymphocyte clonality PCR?

A

PARR- PCR for antigen receptor rearrangments

Uses T cell and B cell primers to diffrentiate between.

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40
Q

List some types of lymphadenopathy

A
  • Reactive hyperplasia
  • Lymphadenitis
  • Metastatic neoplasia
  • Lymphoma
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41
Q

How can you diagnose lympahdenopathy?

A

FNA or fine need capilallary sample

Do it before steroids

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42
Q

Whats the difference between lymphadenitis and lympadenopathy?

A 
Lymphadenopathy= enlragement of LNs
Lymphadenitis= inflammation
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43
Q

What does a normal lymph node FNA contain?

A

-80/90% small lymphocytes
-Lymphoblasts
-Macrophages
-Plasma cells
Reactive hyperplasia is cytologicaly indistinguishable from normal LNs.

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44
Q

Briefly describe the cytology of lymphadenitis

A

-Increased neutrophils and oesinophils
-More macrophages (incl multinucleate giant cells in granulomatous inflammation)
-

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45
Q

What tumours would you expect to metastasise to LNs?

A

Carcinoma
Myeloproliferative disorders
Mast cells
Melanomas

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46
Q

How do you diagnose lymphoma?

A
  • Incr % of large immature lymphocytes
  • More mitoses
  • Histology is usually required for confident diagnosis
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47
Q

Presented with lymphadenopathy. Cytology slide of lymph node FNA shows mainly small lymphocytes. Reactive or neoplastic?

A

Reactive

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48
Q

How is anaemia defined?

A

NOT a diagnosis but defined by:

  • PCV
  • Hg
  • RBCC
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49
Q

What are the clinical signs of anaemia?

A

-Pale mm
-Lethargy
-Poor pulse quality
-Compensatory mechanisms: tachycardia, tachypnoea
D/d for pale mm= hypotension

remember severity of CS reflect the chronicity of anaemia NOT the degree of anaemia

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50
Q

When would you consider a high PCV normal?

A
  • In sighthounds
  • In thoroughbreds
  • Stress/ excitement (cause splenic contraction)
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51
Q

When would you consider a low PCV normal?

A
  • Puppies/ kittens <6-12months
  • ACP (relaxes spleen)
  • Late gestation
52
Q

What are the basic tests for anaemia?

A
  • PCV
  • TS
  • Blood smear
53
Q

Briefly describe the PCV and TS test for anaemia

A

-Combining TS and PCV gives you indication of hydration status
(add 2 to TP gives you estimate of TS)

54
Q

How does dehydration affect haematocrit reading?

A

Causes concentrated plasma giving higher PCV

55
Q

What are the causes of non regenerative and regenerative anaemia?

A
  • Regen: haemolysis and blood loss (haemorrhage)

- Non regen: suppression of erythropoeisis (either intramarrow or extramarrow)

56
Q

What you expect to see on the haem profile of regenerative anaemia?

A
  • Reticulocytes
  • Anisocytosis
  • Poikilocytosis
  • Basophilic stippling
  • Incr Howel-Jolly bodies (nucelar remnants)
  • Incr Heinz bodies (damaged Hg)
57
Q

What type of anaemia can oxidative damage cause?

A

Regenerative

58
Q

What can chronic blood loss lead to in terms of type of anaemia?

A

-Leads to iron deficiency causing non regenerative anaemia.

59
Q

What clinical sign will you see with haemolysis ?

hint mm

A

Icterus

60
Q

Describe non regenerative anaemia

A
  • More common presentation than regenerative
  • Have absent/ v low reticulocyte count
  • Intra marrow: problem with the BM e..g infection, chronic damage, neoplasia, iron deficiency
  • Extra marrow: inappropriate signalling (CKD, excess oestrogen) or FeLV
61
Q

What must you bear in mind when interpretating anaemia results?

A
  • Reticulocyte response takes 2-4 days so may be in pre regenerative phase
  • Horses/ cattle= poor reticulocyte response
  • Chronic bleeding leads to non regen anaemia
  • Severe anaemia with mild CS usually chronic.
62
Q

What haematology tests would you run for anaemia?

What biochem tests would you run for anaemia?

A 
-Haem: 
PCV, TS, Hb, MCV
Reticulocyte count
Blood smears (look for blood parasites and RBC morphology)
-Biochem:
Urinalysis
Virology (FeLV)
Coagulation profile (chronic blood loss?)
BM biopsy (intramarrow?)
63
Q

What marker is most useful clinically when dealing with anaemia in horses?

A 
Serial PCV (should incr by 1-2% every 2-3 days)
-Circulating reticulocytes are never present
64
Q

Briefly describe giving a blood transfusion in horses

A

Blood volume= 7% BW (35L in 500kg horse)
Give a transfusion when >20% circulatin vol lost
OR if PCV <18%
(Normal PCV= 33-45% -TB’s naturally higher)

65
Q

List some causes of haemolysis in horses

A
  • Immune mediated dxs (Lupus erythematous)
  • Clostridia
  • Drug reaction

(not relevant to question but remember PPID can cause non regen anaemia in horses)

66
Q

What are the different CS of primary/ secondary haemostasis?

A

Primary: petechiae, ecchymoses, gingival bleeding, retinal bleeding
Secondary: deep/ cavity bleeding, haematomas

67
Q

What are the causes of primary haemostasis?

A
  • Thrombocytopenia
  • Thrombocytopathia
  • vWF deficiency
68
Q

Describe causes of thrombocytopenia

A
  • Decr PLT production: (BM neoplasia, drug or toxin induced BM suppression)
  • Incr PLT removal (IMTP, DIC)
  • PLT sequestiaation/ loss (vascular pooling/ splenomegaly or acute ongoing haemorrhage)
69
Q

Describe some of the tests for primary haemostasis

A
  • PLT count (EDTA sample, do it quickly or they’ll clump, check for clumps before starting count)
  • BMBT (hard to do, don’t do before PLT count, >1.7-3.3 mind in dog, >3.3mins in anaesthetised cat)
  • TEM (thromboelastometry-PLT function assay)
70
Q

What is the most common cause of thrombocytopneia?

A

IMTP- immune mediated destruction of PLTs

71
Q

Briefly describe IMTP

A

-Common acquired primary haemiostasis defect in dogs
-PLTs destroyed»>PLTs made
-Young/middle aged females
-Cockers, mini poodles, Old English
-Tx= Immune suppression e.g. Prednisolone
MUST HANDLE CAREFULLY can make them bleed intracranially

72
Q

What is thrombocytopathia? How do you diagnose it? How do you treat it?

A
  • Where the patient has normal platelets but they don’t function correctly.
  • Diagnosed with PLT function tests or normal PLT count and prolonged BMBT would make you suspicious
  • No specific tx: symptomatic blood transfusions, remove any drug that might be causing it
73
Q

What are the causes of thrombocytopathia?

A
  • Drug induced (NSAIDs)

- Platelet dysplasia (myeloproliferative dx/ neoplasia)

74
Q

What can cause thrombocytopenia in cattle?

A
  • Bovine panleucocytopenia
  • BVDV
  • Bracken poisoning
75
Q

Describe vWF deficiency (disease)

A

-Most common inheritied bleeding dx in dogs
-3 types:
decr vWF conc in plasma= mild
Structurally abnormal vWF= severe
NO plasma vWF= severe (diagnose with ELISA)
-Common in Dobermans, GSDs, Corgis, Goldies
-Diagnosis
Normal PLT count
BMBT >5-10mins= mild type 1, >12mins= severe
Tx= give plasma to help short term, giving desmopressin to donor dog makes them release more vWF from endothelial cells.

76
Q

In what sort of haemostasis is epistaxis common?

A

Secondary

77
Q

Describe the 2 types of haemostasis

A 
Congenital= haemophilia
Acquired= Vit K antagonism or Hepatic dx
78
Q

Describe haemophilia

A

3 types:
C-factor XI
B- factor IX
A- factor VIII (most common)
-Seen in males, young dogs (bruises/ haematomas)
-DON’T GIVE S/C or IM injections and ensure gentle handling
-Tx= analgesia, gentle physio, fresh plasma transfusion for short term blood loss control.

79
Q

Briefly describe vitamin K antagonism

A
  • AKA coumarin poisoning
  • Vit K dependant clotting factors= 2,7,9,10
  • Carboxylase enzymes activates the clotting factors BUT this enzyme needs vit K to activate.
  • Factor 7 will be lost first (also recovers first)
  • Tx= gastric lavage or activated charcoal, give vitamin K (either s/c or i/m. DO NOT GIVE IV= causes systemic histamine release and anaphylaxis)
80
Q

Why does hepatic disease cause haemostatic problems?

A

Because clotting factors are produced in the liver. If liver disease causes haemostatic problems then you know the liver dx is advanced.

81
Q

Describe how to diagnose hepatic dx as the cause of secondary haemostasis

A
  • APTT and OSPT tests: will both be elevated
  • Incr liver enzymes, incr bile acid, +- jaundice
  • If take a liver biopsy and bleeding is prolonged can give vit K to help.
82
Q

Describe the tests for tertiary haemostasis

A 
-Test for fibrinolysis
FDP (fibrinogen degredation products
D-dimers (must be very marked)
-Test for inhibitors 
Antithrombin (AT3): if <50% at risk of thrombosis
83
Q

What is involved in virchows triangle?

A

3 things that affect thrombosis

  • Endothelial injury
  • Hypercoagubility
  • Abnormal blood flow
84
Q

What 3 diseases are linked with thrombosis imparticular?

A

-Feline thromboembolic disease
Protein losing nephropathy
HAC

85
Q

Describe how DIC is a dynamic process

A

-Microthombosis occurs in multiple organs due to primary/ secondary plugs simultaenously forming in multiple small vessels
(leads to ischaemic necrosis and organ failure
-Then due to consumption of PLTs (thrombocytopenia), clotting factors and anticoagulants also consumed
-Fibrinolysis starts: inactivatin of clotting factors and FDPs inhibit PLT
-Results in bleeding

86
Q

What can trigger DIC?

A
  • Endothelial damage: heat stroke/ sepsis
  • Platelet activation: mainly viral (FIP), endotoxaemia
  • Release of tissue procoagulants: traums, pancreatitis, bacterial infections, EM
87
Q

Common DIC triggers in the dog

A
  • Haemangiosarcoma
  • Sepsis
  • Pancreatitis
  • IMHA
  • Metsastases
  • EM
  • Angiostronglylus vasorum
88
Q

What are the common DIC triggers in a cat

A
  • Liver lymphoma
  • Pancreatic adenocarcinoma
  • Sepsis
  • Hepatic lipidosis
89
Q

How do you diagnose DIC?

A

-Combination of haemostatic abnormalities:
Thrombocytopenia, prolonged clotting times, D-dimers raised.
-Presence of shistocytes

90
Q

How do you treat DIC?

A

With heparin as long as sufficient antithrombin 3 present

-Have to ID and treat underlying trigger cause!

91
Q

What % of blood loss causes shock and death?

A

> 50%

92
Q

What % of blood loss causes peripheral vasconstriction and tachycardia?

A

<20%

93
Q

What % of blood loss causes decr cardiac output, hypotension and collapse?

A

30-40%

94
Q

Why are high shock fluid rates no longer recommended?

A

-Can dilute clotting factors are rapid increase in BP can dislodge primary haemostatic plugs

95
Q

What can cause haemolysis?

A 
IMHA
Neonatal isoerythrolysis
Infection (Babesia, Mycoplasma haemofelis)
Cu toxicity
Oxidative damage
96
Q

Describe Mycoplasma Haemofelis

A 
- CS:
Regernerative anaemia
Jaundice
Pale mm
Pyrexia
Weakness
Weight loss
Lethargy
-Signalment: young/ immunosuppressed (FIV)
-Diagnosis: blood smear with Romanovsky and PCR
-Tx: Doxycylcine SID 2-8wks, 2nd choice= Enroflaxacin SID
Then you repeat PCR to ensure cure
97
Q

What are the adverse effects of doxyxycline and enroflaxacin in cats?

A 
Doxycycline= oesopahgeal stricture
Enroflaxacine= retinal degeneration/ blindness
98
Q

What disease do farmers often call Red water?

A

Babesia- causes haemoglobinuria

99
Q

Describe babesia

A
  • Intracellular protozoan
  • Tick vector= dermacentor
  • CS= haemolytic anaemia and haemoglobinuria
  • Diagnosis= microscopy, PCR, incr liver enzymes, incr bilirubin
  • Tx= imidocarb or doxycycline
100
Q

Name 1 d/d for babecsia

A

IMHA

101
Q

What is imidocarb?

A

Urea derivative antiprotozoal drug

102
Q

Describe oxidative damage

A

-Causes secondary haemolytic anaemia
-Alliums, heavy metals (Zn, Cu), paracetamol all cause it
- Incr Heinz bodies
-Tx: gastric lavage ,4hr, transfusion?, antioxidants
Paracetamol only: acetyl cysteine in dogs or ascorbic acid in cats

103
Q

Briefly describe copper toxicity

A

-Accumulates in liver, sudden release results in RBC lysis
-Lethargy, anaemia, bruxism, PD, pale/ icteric mm
-Usually fatal, dark kidneys on PM
Tx= oral or injectible tetrathiomolybdate and copper binders e.g. sulphur

104
Q

What are the causes of aplastic anaemia?

A

Canine/ feline parvovirus

Ehrlichia canis

105
Q

List some intra marrow causes of anaemia

A
  • Primary disorders
    Iron deficiency
    Aplastic anaemias (E.canis, canine/ feline parvo)
    RBC anaemia- immune mediated
106
Q

Briefly describe iron deficiency anaemia

A
  • CHONIC blood loss
  • Longterm tx needed to help BM recover
  • Normo/microcytic hypochromic
  • NON regenerative
107
Q

What is anaplasmosis also known as?

A

Ehrlichia canis

108
Q

What infection would you suspect if you found bacteria inside monocytes/ macrophages in an anaemic animal?

A

Anaplasmosis

109
Q

Briefly describe Ehrlichia canis infection

A
  • Rickettsia bacteria
  • Infects monocytes/ macrophages
  • Tick vector=Rhipicephalus
  • Diagnosis= Microscopy and PCR
  • Tx= Doxycycline. Prevent with flurolaner
110
Q

List some causes of extra marrow anaemia

A

CKD (reduced renal EPO production)
Oestrogen induced BM suppression (ferrets or ssertoli cells)
FeLV-C

111
Q

What can IMHA be secondary to in cats?

A

FeLV
FIP
Mycoplasmaa haemofelis
Chronic bacterial infections

112
Q

What sort of hypersensitivity is involved in IMHA or IMTP?

A

Type 2 (cytotoxic)- Ab binds to specific cell surface molecule
Damages RBCs by:
-Autoantibody to Ag on RBC surface
-Alloantibody (after blood transfusion, neonatal isoerythrolysis)
-Cross reacting Ab against infectious agent
-Ab against drug on RBC surface
-Idiopathic

113
Q

How does IMHA lead to formation of spherocytes?

A

-Can cause extravascular haemolysis: Ab binds to RBC and complex is phagocytised by mononuclear cells in liver or spleen. If only partially phagocytised this form spherocytes.

114
Q

How can a blood smear be used to diagnose IMHA?

A

Presence of spherocytes

115
Q

Describe the signalment of IMHA

A

Dogs: young/ middle ages (6yo), cockers, old english, bichon, schnauzers
Cats: less common than in dogs, 2yo, males more than females

116
Q

List some CS of IMHA

A
  • Hepatomegaly/ splenomegaly
  • Tachycardia
  • Tachypnoea
  • Pyrexia
  • Pale mm
117
Q

How do you diagnose IMHA?

A 
Confirm anaemia and its regenerative
Do a blood smear looking for spherocytes
Haem profile= left shift neutrophilia
Biochem= incr liver enzymes (ALT+ALP)
Incr bilirubin, low PCV + anaemia= pre hepatic jaundice
118
Q

What is the signalment for IMTP?

A

Dogs= any age
Cockers, poodles, Old English
More common in females

119
Q

What are the IMTP clinical signs?

A 
Sudden bruising
Epistaxis
Meleana
Hypovolaemic
Weak pulses
Tachycardia
120
Q

How do you diagnose IMTP?

A

Blood sample from cephalic vein

  • Confirm thrombocytopenia
  • Confirm anaemia =PCV and TS both low
  • Rule out other causes
121
Q

Describe the action of Prednisolone

A

-Direct T cell suppression
-Inhibits phagocytic activity
-Reduces Ag processing
All act to suppress immune response.

122
Q

What are the second line immunosuppressive drugs for dogs and cats?

A

Dogs=cyclosporine, azathioprine
Cats=cyclosporine, chlorambucil
(vincristine for IMTP dogs)

123
Q

What is the main reason IMHA patients die?

A

Embolism disease

124
Q

Explain neonatal isoerythrolysis in cats and horses

A

-Cats: naturally produce alloantibodies
Queen type B mates with Tom type A. Passes on antiA antibodies on in colostrum
Type A and AB kittens produced: haemolytic anaemia
-Horses: mare sensitised to stallions RBC Ags, blood passes through placenta and she produces alloantibodies
1st foal is ok but each time she carries with same stallion it gets worse.
CS= lethargy, weakness, pallor, jaundice, tacychardia, tachypnoea

125
Q

What is Arab horse SCID?

A

Can’t produce functional B or T lymphocytes.

Year 4 LCB (1 decks)

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