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ASC111 Final exam topics > Blood - truncated > Flashcards

Blood - truncated Flashcards

1
Q

Describe polycythaemia…?

A

high RBC mass (opposite to anaemia)
may be RELATIVE or ABSOLUTE
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

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2
Q

Blood groups in horses…?

A

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

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3
Q

Blood groups in dogs…?

A

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

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4
Q

Blood groups in cats…?

A

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

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5
Q

Blood groups in cattle…?

A

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

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6
Q

Blood groups in sheep…?

A

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

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7
Q

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

A
  • disease of humans & domestic animals - pigs, horses, dogs, cats, cows (PhDCC)
  • IMMUNE DESTRUCTION OF RBCs
  • neonatal isoerythrolysis differs in domestic animals & humans (post-partum - animals, embryogenesis - humans)
  • NATURAL OCCURANCE OF NI RECOGNISED IN HORSES, CATS & HUMANS
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8
Q

What is NI caused by…?

A

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

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9
Q

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

A

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

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10
Q

Describe, in detail, the process of equine NI…

A

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

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11
Q

What actions should be taken on foals with severe NI?

A
  • 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
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12
Q

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

A

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

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13
Q

Characteristics of haemophilia A…

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

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14
Q

Describe canine haemophilia A…

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
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15
Q

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

A

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

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16
Q

Blood lab analysis for anticoagulant rodenticides…?

A

haematological abnormalities - anaemia, low haematocrit, thrombocytopenia etc.

17
Q

How does snake venom affect haemostasis?

A

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)

18
Q

What are some different types of anaemia?

A
  • Fe-defiency anaemia
  • Pernicious anaemia
  • haemorrhagic anaemia
  • haemolytic anaemia
19
Q

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

A 
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
20
Q

Describe pernicious anaemia…?

A

insufficient haemopoiesis from inability of stomach to produce intrinsic factor

21
Q

Describe haemorrhagic anaemia…?

A

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

22
Q

Describe haemolytic anaemia…? Name a type of haemolytic anaemia

A

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)
thalassaemia

23
Q

Describe thalassaemia…?

A

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

24
Q

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

A

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

25
Q

Describe, in detail, the process of feline NI…

A

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

26
Q

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

A

primary - dark red-brown urine
jaundice
anaemia
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)

27
Q

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

A

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

28
Q

Blood lab analysis for anticoagulant rodenticides…?

A

haematological abnormalities - anaemia, low haematocrit, thrombocytopenia etc.

29
Q

How & why is snake venom a danger to animals?

A

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

30
Q

A bit on Aus’ venomous snakes…

A

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

31
Q

How does snake venom affect haemostasis?

A

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)

ASC111 Final exam topics (8 decks)

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