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
What are the 2 main types of lymphocytes?
``` -Reactive= involved in IR and recently vaccinated animals Granular= have pink granules in 1 area of cytoplasm ```
26
What can spleen contraction and Addisons both cause?
Lymphocytosis (also caused by young animals in new environment)
27
What can cause lymphopenia?
Stress by steroids, acute inflammation, lymphoma
28
What can cause monocytosis?
Chronic inflammation or steroids and stress
29
How do acute and chronic inflammatino cause different leucograms?
Acute causes lymphopenia and chronic causes monocytosis
30
What can parasites, hypersensitivities and allergic reaction all cause? (leucogram)
Eosinophilia
31
Describe the classic stress leucogram
++ neutrophilia +eosinophilia +lymphopenia -+monocytosis
32
What does a high neutrophil count and high lymphocyte count indicate?
Excitement leucogram
33
Briefly describe leukaemia
- 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)
34
Describe the difference between acute and chronic leukaemia
- 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
35
Describe the cytopenia seen in acute leukaemia
- Neutrophils dissaapear first (hours) - Platelets (days) - RBCs (months)
36
Describe the difference between lymphoma that involves the BM and acute lymphomblastic leukaemia
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
37
What stage of lymphoma can involve the BM?
Stage 5
38
What are the examples of immunophenotyping in leukaemia?
- Histology of BM | - Biopsies
39
What is lymphocyte clonality PCR?
PARR- PCR for antigen receptor rearrangments | Uses T cell and B cell primers to diffrentiate between.
40
List some types of lymphadenopathy
- Reactive hyperplasia - Lymphadenitis - Metastatic neoplasia - Lymphoma
41
How can you diagnose lympahdenopathy?
FNA or fine need capilallary sample | Do it before steroids
42
Whats the difference between lymphadenitis and lympadenopathy?
``` Lymphadenopathy= enlragement of LNs Lymphadenitis= inflammation ```
43
What does a normal lymph node FNA contain?
-80/90% small lymphocytes -Lymphoblasts -Macrophages -Plasma cells Reactive hyperplasia is cytologicaly indistinguishable from normal LNs.
44
Briefly describe the cytology of lymphadenitis
-Increased neutrophils and oesinophils -More macrophages (incl multinucleate giant cells in granulomatous inflammation) -
45
What tumours would you expect to metastasise to LNs?
Carcinoma Myeloproliferative disorders Mast cells Melanomas
46
How do you diagnose lymphoma?
- Incr % of large immature lymphocytes - More mitoses - Histology is usually required for confident diagnosis
47
Presented with lymphadenopathy. Cytology slide of lymph node FNA shows mainly small lymphocytes. Reactive or neoplastic?
Reactive
48
How is anaemia defined?
NOT a diagnosis but defined by: - PCV - Hg - RBCC
49
What are the clinical signs of anaemia?
-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*
50
When would you consider a high PCV normal?
- In sighthounds - In thoroughbreds - Stress/ excitement (cause splenic contraction)
51
When would you consider a low PCV normal?
- Puppies/ kittens <6-12months - ACP (relaxes spleen) - Late gestation
52
What are the basic tests for anaemia?
- PCV - TS - Blood smear
53
Briefly describe the PCV and TS test for anaemia
-Combining TS and PCV gives you indication of hydration status (add 2 to TP gives you estimate of TS)
54
How does dehydration affect haematocrit reading?
Causes concentrated plasma giving higher PCV
55
What are the causes of non regenerative and regenerative anaemia?
- Regen: haemolysis and blood loss (haemorrhage) | - Non regen: suppression of erythropoeisis (either intramarrow or extramarrow)
56
What you expect to see on the haem profile of regenerative anaemia?
- Reticulocytes - Anisocytosis - Poikilocytosis - Basophilic stippling - Incr Howel-Jolly bodies (nucelar remnants) - Incr Heinz bodies (damaged Hg)
57
What type of anaemia can oxidative damage cause?
Regenerative
58
What can chronic blood loss lead to in terms of type of anaemia?
-Leads to iron deficiency causing non regenerative anaemia.
59
What clinical sign will you see with haemolysis ? | hint mm
Icterus
60
Describe non regenerative anaemia
- 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
What must you bear in mind when interpretating anaemia results?
- 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
What haematology tests would you run for anaemia? | What biochem tests would you run for anaemia?
``` -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
What marker is most useful clinically when dealing with anaemia in horses?
``` Serial PCV (should incr by 1-2% every 2-3 days) -Circulating reticulocytes are never present ```
64
Briefly describe giving a blood transfusion in horses
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
List some causes of haemolysis in horses
- Immune mediated dxs (Lupus erythematous) - Clostridia - Drug reaction (not relevant to question but remember PPID can cause non regen anaemia in horses)
66
What are the different CS of primary/ secondary haemostasis?
Primary: petechiae, ecchymoses, gingival bleeding, retinal bleeding Secondary: deep/ cavity bleeding, haematomas
67
What are the causes of primary haemostasis?
- Thrombocytopenia - Thrombocytopathia - vWF deficiency
68
Describe causes of thrombocytopenia
- 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
Describe some of the tests for primary haemostasis
- 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
What is the most common cause of thrombocytopneia?
IMTP- immune mediated destruction of PLTs
71
Briefly describe IMTP
-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
What is thrombocytopathia? How do you diagnose it? How do you treat it?
- 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
What are the causes of thrombocytopathia?
- Drug induced (NSAIDs) | - Platelet dysplasia (myeloproliferative dx/ neoplasia)
74
What can cause thrombocytopenia in cattle?
- Bovine panleucocytopenia - BVDV - Bracken poisoning
75
Describe vWF deficiency (disease)
-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
In what sort of haemostasis is epistaxis common?
Secondary
77
Describe the 2 types of haemostasis
``` Congenital= haemophilia Acquired= Vit K antagonism or Hepatic dx ```
78
Describe haemophilia
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
Briefly describe vitamin K antagonism
- 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
Why does hepatic disease cause haemostatic problems?
Because clotting factors are produced in the liver. If liver disease causes haemostatic problems then you know the liver dx is advanced.
81
Describe how to diagnose hepatic dx as the cause of secondary haemostasis
- 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
Describe the tests for tertiary haemostasis
``` -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
What is involved in virchows triangle?
3 things that affect thrombosis - Endothelial injury - Hypercoagubility - Abnormal blood flow
84
What 3 diseases are linked with thrombosis imparticular?
-Feline thromboembolic disease Protein losing nephropathy HAC
85
Describe how DIC is a dynamic process
-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
What can trigger DIC?
- Endothelial damage: heat stroke/ sepsis - Platelet activation: mainly viral (FIP), endotoxaemia - Release of tissue procoagulants: traums, pancreatitis, bacterial infections, EM
87
Common DIC triggers in the dog
- Haemangiosarcoma - Sepsis - Pancreatitis - IMHA - Metsastases - EM - Angiostronglylus vasorum
88
What are the common DIC triggers in a cat
- Liver lymphoma - Pancreatic adenocarcinoma - Sepsis - Hepatic lipidosis
89
How do you diagnose DIC?
-Combination of haemostatic abnormalities: Thrombocytopenia, prolonged clotting times, D-dimers raised. -Presence of shistocytes
90
How do you treat DIC?
With heparin as long as sufficient antithrombin 3 present | -Have to ID and treat underlying trigger cause!
91
What % of blood loss causes shock and death?
>50%
92
What % of blood loss causes peripheral vasconstriction and tachycardia?
<20%
93
What % of blood loss causes decr cardiac output, hypotension and collapse?
30-40%
94
Why are high shock fluid rates no longer recommended?
-Can dilute clotting factors are rapid increase in BP can dislodge primary haemostatic plugs
95
What can cause haemolysis?
``` IMHA Neonatal isoerythrolysis Infection (Babesia, Mycoplasma haemofelis) Cu toxicity Oxidative damage ```
96
Describe Mycoplasma Haemofelis
``` - 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
What are the adverse effects of doxyxycline and enroflaxacin in cats?
``` Doxycycline= oesopahgeal stricture Enroflaxacine= retinal degeneration/ blindness ```
98
What disease do farmers often call Red water?
Babesia- causes haemoglobinuria
99
Describe babesia
- Intracellular protozoan - Tick vector= dermacentor - CS= haemolytic anaemia and haemoglobinuria - Diagnosis= microscopy, PCR, incr liver enzymes, incr bilirubin - Tx= imidocarb or doxycycline
100
Name 1 d/d for babecsia
IMHA
101
What is imidocarb?
Urea derivative antiprotozoal drug
102
Describe oxidative damage
-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
Briefly describe copper toxicity
-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
What are the causes of aplastic anaemia?
Canine/ feline parvovirus | Ehrlichia canis
105
List some intra marrow causes of anaemia
- Primary disorders Iron deficiency Aplastic anaemias (E.canis, canine/ feline parvo) RBC anaemia- immune mediated
106
Briefly describe iron deficiency anaemia
- CHONIC blood loss - Longterm tx needed to help BM recover - Normo/microcytic hypochromic - NON regenerative
107
What is anaplasmosis also known as?
Ehrlichia canis
108
What infection would you suspect if you found bacteria inside monocytes/ macrophages in an anaemic animal?
Anaplasmosis
109
Briefly describe Ehrlichia canis infection
- Rickettsia bacteria - Infects monocytes/ macrophages - Tick vector=Rhipicephalus - Diagnosis= Microscopy and PCR - Tx= Doxycycline. Prevent with flurolaner
110
List some causes of extra marrow anaemia
CKD (reduced renal EPO production) Oestrogen induced BM suppression (ferrets or ssertoli cells) FeLV-C
111
What can IMHA be secondary to in cats?
FeLV FIP Mycoplasmaa haemofelis Chronic bacterial infections
112
What sort of hypersensitivity is involved in IMHA or IMTP?
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
How does IMHA lead to formation of spherocytes?
-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
How can a blood smear be used to diagnose IMHA?
Presence of spherocytes
115
Describe the signalment of IMHA
Dogs: young/ middle ages (6yo), cockers, old english, bichon, schnauzers Cats: less common than in dogs, 2yo, males more than females
116
List some CS of IMHA
- Hepatomegaly/ splenomegaly - Tachycardia - Tachypnoea - Pyrexia - Pale mm
117
How do you diagnose IMHA?
``` 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
What is the signalment for IMTP?
Dogs= any age Cockers, poodles, Old English More common in females
119
What are the IMTP clinical signs?
``` Sudden bruising Epistaxis Meleana Hypovolaemic Weak pulses Tachycardia ```
120
How do you diagnose IMTP?
Blood sample from cephalic vein - Confirm thrombocytopenia - Confirm anaemia =PCV and TS both low - Rule out other causes
121
Describe the action of Prednisolone
-Direct T cell suppression -Inhibits phagocytic activity -Reduces Ag processing All act to suppress immune response.
122
What are the second line immunosuppressive drugs for dogs and cats?
Dogs=cyclosporine, azathioprine Cats=cyclosporine, chlorambucil (vincristine for IMTP dogs)
123
What is the main reason IMHA patients die?
Embolism disease
124
Explain neonatal isoerythrolysis in cats and horses
-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
What is Arab horse SCID?
Can't produce functional B or T lymphocytes.