Module 8 - Blood Flashcards Preview

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Flashcards in Module 8 - Blood Deck (56):

What is CBC, what does it test for & what kind of sample is need to perform it?

complete blood count - numerical count of cells in blood (RBCs, WBCs, platelets) also Hct/PCV (RBC % in blood). Performed on serum


Define anaemia & polycythaemia...?

anaemia -> low RBC count
polycythaemia -> high RBC count


Describe what happens when animal is anaemic...? What are the different ypes of anaemia?

low RBCs or [Hb] in blood -> decreased O2-carrying capacity
- Fe-defiency anaemia
- Pernicious anaemia
- haemorrhagic anaemia
- haemolytic anaemia
- Thalassaemia
- Aplastic anaemia


Describe Fe-deficiency anaemia...? Which animal is it common in & why?

low absorption of Fe
Excessive loss of Fe
increased Fe requirement
Insufficient intake of Fe
common in piglets because of rapid growth & lack of Fe in sows milk


Describe pernicious anaemia...?

insufficient haemopoiesis from inability of stomach to produce intrinsic factor


Describe haemorrhagic anaemia...?

Excessive RBC loss thru bleeding (from large wounds, gastric ulcers)


Describe haemolytic anaemia...?

RBC plasma membrane ruptures prematurely -> haemoglobin in plasma -> may damage glomeruli in kidneys
May result from: INCOMPATIBLE TRANSFUSED BLOOD, inherited defects (abnormal RBC enzymes), parasites, toxins (eg paracetamol),


Describe thalassaemia...?

Primarily in pop's from countries bordering Mediterranean Sea
deficient synthesis of haemoglobin
group of hereditary haemolytic anaemias in humans
consists of alpha-thalassaemia & beta-thalassaemia


Describe aplastic anaemia...?

destruction of red bone marrow
usually acquired (some unusual inherited forms)
Acquired immune mediated - autoreactive lymphocytes -> destruction of haemopoietic stem cells
Causes: mostly idiopathic and sometimes drugs, viruses & toxins
Treated with allogenic bone-marrow transplantation & immunosuppression


Describe polycythaemia...?

high RBC mass (opposite to anaemia)
relative - increased RBC mass & decreased plasma volume (shock & dehydration & animals treated with heart meds or diuretics)
absolute - increase RBC mass WITHOUT decreased plasma volume
Rare, but described in cats & dogs & cattle


What blood test would you run if you suspect an infection? Why? What are the paramaters & what do they tell us?

CBC - as it includes a % & absolute number (always more important number) of WBCs (leukocytes) -> may indicate, infection (high WBC) or autoimmune & blood diseases (low)


A high/low neutrophil count would most likely indicate what?

high -> bacterial infection
low -> increased risk of infection


A high/low lymphocyte count would most likely indicate what?

high -> viral infections
low -> hepatitis & lymphoma


A high eosinophil count would most likely indicate what?

high -> allergies or parasitic infection


A high monocyte count would most likely indicate what?

high -> blood diseases, certain infections, or auto-immune diseases


A high basophil count would most likely indicate what?

blood diseases


What does a total protein (TP) test involve & indicate?

includes albumin & globulins
high -> dehydration or immune system stimulated -> lots of Ab's
low -> damaged liver or intestine or abnormal immune sys -> cannot produce Ab's


What does an albumin test involve & indicate?

albumin - small protein produced by LIVER
low -> damaged liver or lost thru damaged intestine or in urine in kidney disease
high -> dehydration


What does a alkaline phosphatase test involve & indicate?

originates from many tissues in body
increased [phosphatase] -> most commonly caused by liver disease, bone disease, increased cortisol levels due to drugs given (pred) or Cushing's disease
Cats - high -> due to liver & bone disease


What does a blood urea nitrogen (BUN) test involve & indicate?

influenced by liver, kidneys & dehydration
low -> liver disease
high -> kidney disease (75% damage -> before increase in BUN), severely dehydrated


What does a blood glucose (BG) test involve & indicate?

high - cats & dogs with diabetes mellitus
mildly increased in dogs with Cushing's
low [BG] -> pancreatic cancer or sepsis -> depression or seizures
also, low [BG] if sample incorrectly handled
RBC use glucose so typically plasma or serum used for test


Blood groups in horses...?

>30 blood groups
8 major systems - 7 internationally recognised
A, C, D, K, P, Q, U
One of research interest T


Blood groups in dogs...?

categorised by DEA (Dog Erythrocyte Antigen) system
A system - DEA 1.1, 1.2 & 1.3
Also contains DEA 3, DEA 4, DEA 5, DEA 6, DEA 7, DEA 8
incidence of DEA 1.1 ~45%, 1.2 ~20% (US data)
DEA 1.3 common in GSDs & reported only in Aus
DEA 1.1 - strongest antigen in the dog
typing sera produced by canine alloimmunisation in - 1.1, 1.2, 3, 4, 5 & 7


Blood groups in cats...?

3 recognised groups - A, B & AB
group A most common
B common in some (British Shorthair & Ragdoll), rare in others (Manx & Norwegian Forest)
AB rare in all breeds


Blood groups in cattle...?

11 major groups
A, B, C, F, J, L, M, R, S, T, Z
B group >60 different antigens -> difficult to match donor & recipient
J antigen is lipid found in body fluids -> absorbed onto erythrocytes -> not a 'true' antigen


Blood groups in sheep...?

7 groups (A, B, C, D, M, R, X)
B system - highly polymorphic (many forms)
R system similar to J system in cattle - antigen soluble
M-L system -> red cell K transport


Blood groups in goats...?

similar to those in sheep
5 major systems (A, B, C, M, J)
same reagents used to type both spp.


Is an animals blood group permanent? Briefly explain.

Usually same blood group for life
may change with addition or suppression of antigen (infection, malignancy, autoimmune disease)
bone marrow transplant


Explain blood group incompatibility...?

If exposed to blood group antigen not recognised as self (foreign), immune system -> Ab that binds to foreign antigen -> immunological memory against that antigen -> individual sensitised to that blood group antigen
These Ab's -> bind to surfacer of transfused RBCs -> destruction of cell by recruitment of immune sys. components


How can blood group incompatibility arise? (2 ways)

- via blood transfusion
- neonatal isoerythrolysis


Describe transfusion reactions in dogs... Include which blood groups are used & any problems that may arise during these processes. Also name some breeds with different blood groups.

Significant DEA -> 1.1 & 1.2
1.1 -> extremely antigenic & antigen that is routinely determined in patients & donors
- DEA 1.1-negative dogs exposed -> DEA 1.1-positive -> sensitised -> anti-DEA 1.1 Ab -> acute haemolytic transfusion reaction in sensitised 1.1-ve dog
- serious haemolytic transfusion reaction in DEA 4-negative dog from exposure to DEA 4-positive RBC donor
Greyhounds -ve for DEA 1.1
Most labs +ve for DEA 1.1


A bit about blood transfusions in horses...? Include recipient & donor.

- allogenic blood transfusions potential to introduce foreign Ag's into recipient
- universal equine donor -> is -ve for Aa & Qa (include Quarter Horses & Standardbred)


Describe some transfusion reactions in cats

- if type A blood given to type B cat -> life-threatening acute haemolytic transfusion reactions occurs because of strong presence of anti-A alloantibodies in type B cats
- if type AB or B blood given to type A cats -> risk of acute mild transfusion reaction & premature RBC destruction
- if type A or B blood given to type AB cats -> no apparent clinical transfusion reaction


A bit about neonatal isoerythrolysis (NI) in general...?

- disease of humans & domestic animals - pigs, horses, dogs, cats, cows (PhDCC)
- neonatal isoerythrolysis differs in domestic animals & humans (post-partum - animals, embryogenesis - humans)


What is NI caused by...?

maternal alloantibodies -> ingested via collostrum & passively absorbed from GIT -> attach to neonatal RBCs -> precipitate haemolytic crisis via direct cell lysis and/or agglutination -> destruction of neonatal RBCs


Describe equine NI - (antigens involves & incidences in breeds)

90% NI caused by Aa or Qa antigen
other Ag's include Ab, Qb, Qc...
incidence of clinical NI estimated ~< 1% thoroughbreds; <2% Standardbreds, however sub-clinical NI probably does occur


Describe, in detail, the process of equine NI...

alloantibodies develop when mare bred to stallion that has RBC Ag mare does not share -> foal inherits Ag
alloantibodies produced by mare when exposed to Ag via transplacental haemorrhage late in gestation or parturition
may also be sensitised thru transfusion or immunisation of products from blood or placental abnormalities during gestation
initial immunisation -> low titres of alloAb's (late in gestation or parturition) -> low chance foal develop clinical NI
foals with same RBC Ag in subsequent preg's -> much more likely develop NI -> severe life-threatening


What actions should be taken on foals with severe NI?

- RBC transfusion with Aa- &/or Qa-negative donor free of agglutinins & haemolysing Ab
- if NI not due to Aa or Qa Ab's -> donor herd should have complete blood typing done & be -ve for all major blood types associated with NI such as Aa, Qa, Pa, Ab, Dc, Ua


Describe NI in mules...

reported incidence ~10%
many differences in blood group factors in horses & donkeys
RBC Ag identified using Ab's in serum from mare that produced foal with NI
Ag detected different to horse RBC alloAg -> may be xenoantigen (present in all d's & m's but not horses) -> thus all mule preg's potential risk of NI -> thrombocytopenia (low platelet count) & anaemia


Describe feline NI... Why is it a major problem & breeds affected...

significant cause of death in kittens of certain type B breeds - BRITISH SHORTHAIR, RAGDOLL, DEVON REX...
affects A or AB blood type kitten born from B type mother by getting anti-A Ab's during suckling


Describe, in detail, the process of feline NI...

Ab's recognise antigenic determinants in kitten RBC surface -> intra- or extravascular (spleen/liver) haemolysis -> anaemia, nephropathy or disseminated intravascular coag.
occurs after colostrum ingestion -> clinical signs (few hours or days) -> some die without clinical signs other stop suckling & fade


What are the key diagnostic signs of feline NI? How should it be treated?

primary - dark red-brown urine
weakness with death within 1st week
secondary - pale MM, lethargy tachycardia, collapse, death. Also hypoglycaemia & metabolic acidosis
Treatment - aggressive & immediate!
type A or AB kitten removed from mum (16-24 hours)
kittens fed with milk replacer, previously frozen mother's milk, or placed with type A blood foster
If severe anaemia -> blood transfusion (2-3ml previously washed blood cells during 1st 3 days of life)


NI in cattle...

not naturally occuring
reported in lambs administered bovine colostrum (due to Ab in bovine colostrum to sheep RBCs)


Bleeding disorders introduction...

may be congenital (present at birth) or occur later
platelet defects -> superficial bruises, nosebleeds, black faeces (bleeding into LI), prolonged bleeding at injection & surgery sites
blood clotting protein defects -> delayed bleeding & bruising in deep tissues


Describe the characteristics of thrombocytopathies

DISORDERS OF THE BLOOD PLATELET & abnormal functioning of platelets
presenting animals typically have normal platelet counts on examination, but have spontaneous or excessive bleeding due to failure of platelets clotting normally
Common signs - bleeding from MM, nose, mouth, ears, anus
may first become apparent in young animals -> excessive bleeding with loss of deciduous teeth
can be acquired or hereditary
affects main functions of platelets: activation, adhesion, aggregation -> severe bleeding even from smallest wound
Animals with low platelets + thrombocyto. = more bleeding than animals with just thrombocyto.


Describe acquired thrombocytopathy...?

may occur in response to some drugs eg. painkillers, ABs, NSAIDS
- secondary to systemic disease - kidney & liver, inflamm of pancreas


What is the most common hereditary blood clotting disorder in dogs? Include breeds and how it is caused...

Von Willebrand disease
- high frequency in: GSD, Golden Retrievers, Standard Poodles
- deficiency of von Willebrand Factor (vWF) - adhesive glycoprotein in blood required for normal platelet binding (clotting) at sites of small blood vessels
IN ADDITION - vWF carrier protein for coag. Factor VIII (necessary for clotting) thus lack of vWF -> impairs platelet stickiness & clumping


Characteristics of haemophilia A...

Factor VIII deficiency
inherited deficiency Factor VIII -> haemophilia (humans, cats, dogs, cattle, horses (S, T, QH))
most common inherited bleeding disorder in cats & dogs
arises from mutation in factor VIII gene on X-chromosome (recessive) -> males usually affected while females asymptomatic carriers


Describe canine haemophilia A...

clinical signs depend on degree of deficiency
severely affected ( most severe bleeding symptoms, moderate (1-5% activity), mild (5-30% activity)
in affected puppies -> prolonged bleeding in umbilical cord after birth, gums during teething
dogs lameness due to bleeding into joint, sudden clot formation
treatment - repeated whole blood or plasma transfusions until bleeding controlled


Describe haemophilia A in other species (feline & equine)...

feline: associated with spontaneous haematomas but usually prolonged haemorrhage only after trauma or sx
equine: affected colts usually die during or after birth with severe haemorrhage


Characteristics of haemophilia B...

Factor IX deficiency
less common than haemophilia A although similar signs
animals with low low factor IX levels ( suddenly dev. blood clots, bleeding in joints or organ bleeding
treatment - transfusion fresh or fresh-frozen plasma
spp & breeds: purebred dogs, siamese cats, British Short-haired cats


How do rodenticides affect coagulation? Give example of a first & second generation rodenticide. Antidote?

inhibit enzyme vit. K epoxide reductase -> accumulation of inactive vit. K form -> unable to activate clotting factors (eg. VII, IX, X) -> coagulopathy & haemorrhage
1st gen. - warfarin
2nd gen. (more toxic & last longer) - brodifacoum
antidote - administration of vit. K1


Blood lab analysis for anticoagulant rodenticides...?

haematological abnormalities - anaemia, low haematocrit, thrombocytopenia etc.


How & why is snake venom a danger to animals?

can activate/inactivate most factors involved in coag. or fibrinolysis
classified as: act on coag. factors (eg. prothrombin)
or anti-coag. factors (eg. thrombin inhibitors) or those acting on fibrinolytic enzymes


A bit on Aus' venomous snakes...

Aus elapid snakes among most venomous
venom contains components targeting BLOOD HAEMOSTASIS, neuromuscular signalling & CV system
2 types - 1. procoagulant & 2. anticoagulant


How does snake venom affect haemostasis?

Procoagulants - contain prothrombin activators -> cleave prothrombin -> thrombin -> consumption of fibrinogen -> complete defibrination -> resulting bleeding & coagulopathy may be prolonged (eg. brown, tiger snakes)
Anticoagulants - may cause rapidly reversible coagulopathy without defibrination (king brown)