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VetMed Year 4- Term 1 > w/c 23/June/14 > Flashcards

w/c 23/June/14 Flashcards

1
Q

Immune mediated disease can be organ specific or non-organ specific. Examples of each

A

Organ specific: Myasthesia gravis, IM neutropenia Non-Organ specific: Systemic Lupus Erythematosus

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2
Q

Role of infection in immune-mediated disease

A

Infection is thought to influence autoimmune disease at several levels. -> Break-down of vascular or cellular barriers, allowing exposure of self-antigens. -> Promotion of cell death by necrosis causing inflame = bystander activation -> Molecular mimicry = cross reactivity

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3
Q

What is by stander activation

A

Promotion of cell death by necrosis, causing inflammation

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4
Q

Vasculitis often characterises what type of IM disease

A

Non organ specific

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5
Q

Blood smear of 5 YO Neutered female dog that presents with lethargy and PCV of 20%

A

PCV for dog should be 37-55%

Blood smear shows Spherocytes (extra vascular haemolysis)

Ghost cells (intravascular haemolysis)

Polychromatosaia = reticulocytes = regenerative

= IMMUNE-MEDIATED HAEMOLYTIC ANAEMIA

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6
Q

Coombes Test

  • primary reagents
  • problems with test
A

If acute IMHA is suspected

Normally sent away test.

Primary Reagent: Polyvalent anti-dog or anti-cat IgG, IgM and C3 antiserum (direct antiglobulin test)

FALSE NEGATIVES AND FALSE POSITIVES CAN OCCUR

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7
Q

If ulcer that you suspect is due to underlying IM disease. Appropriate test =

A

Biopsy ACROSS inteface with normal tissue not just middle of ulcer/

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8
Q

Antinuclear antibody test =

A

Indirect immunofluorescence or immuno-peroxidase test.

Hep-2 cells

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9
Q

Which vinca alkaloid is sometimes used for the treatment of IM thrombocytopenia

A

Vincristine and Vinblastin are Vinca alkaloids that bind to tubulin, blocking polymerisation also break down newly formed microtubules- increased release of PLTs from megakaryocytes.

WATCH TOXICITY: GI, neurological

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10
Q

In which part of the cell cycle do the following drugs work a) vinca alkaloids b) calcineurin c) corticosteroids

A

a) Vinca Alkaloids: M phase
b) Calcineurin: G1
c) Steroids: S phase

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11
Q

Azothiaprine summary

A

Greater decrease of cellular than humoral immuinity.

Hepatic metabolism

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12
Q

Therapeutic index of Chlorambucil

A

Narrow therapeutic in cats.

Slowest acting, least toxic of all alkalating agents.

Administered without food.

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13
Q

Start off treatment for IM disease as prednislone, if IMHA or aggressive IM disease consider what adjuvant treatment?

A

Rickettsial/Protozoal infection: Doxacycline

If aggressive IM / IMHA consider adjuvant azothiaprine in dogs, chlorambucil in cats.

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14
Q

If dog with IMHA is on prednisalone and chlorambucil how do you go about tapering dose down

A

CBC and UA should be monitored every 7-14 days.

Corticosteroids should be tapered over 3-4 month period following remission.

20% decrease every 4 weeks.

DO NOT ALTER ADJUNCTIVE Rx at same time!!

Steroids may be stopped all together if clinical remission persists.

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15
Q

What is different about RBC in camelids?

A

Camelids have ellipital RBC’s.

Anucleate in mammals but nucleated in birds and reptiles

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16
Q

RBC sites of production

A

Liver/ Spleen in foetus

Swaps to bone marrow in neonates

Growing animals: Marrow of all bones

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17
Q

Life span of Erythrocyte in a) dog b) cat c) horse/cow

A

a) dog: 100 days
b) Cat: 70 days
c) Dog/Horse: 150 days

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18
Q

What is the difference between haematocrit and PCV

A

Both same information but Haematocrit (HCT) calculated by machine.

Hamatocrit is less acurrate.

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19
Q

Microcytic rbc’s indicitive of

A

PSS, Fe deficiency, hepatic failure.

AKITAS

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20
Q

Macrocytic RBC

A

In regeneration- polychromatophils.

Some poodles

Also in FeLV affected cats

Myelodysplasia

Common artifact in stored blood

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21
Q

Difference between reticulocytes and polychromatophils

A

These are the same cells.

Reticulocytes: Stained with New Methylene Blue, RNA precipitates forming aggregates

Polychromatophils: Diff-quick stain= larger bluer cells

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22
Q

Why should reticulocyte count be corrected

A

The same number of reticulocytes will take up a larger percentage in a very anaemic animal.

Reticu % x patient PCV/normal PCV

Regenerative if >1% corre in dog.

>0.4% corec in cat

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23
Q

Can do faecal occult blood test if Melena is not obvious. What do you need to do to avoid false positives

A

Meat free diet for 5 days otherwise test will be positive.

High sensitive, not very specific.

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24
Q

Immune mediated haemolysis pathogenesis

A

Anti red cell antibodies (IgM, IgG, IgA)

Lysis of red cells more common with IgM but IgG and IgA = phagocysed.

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25
Q

How to differentiate Rouleaux from Agglutination

A

Royleaux: Start repelling each other = ‘stack of coins’ - normal finding due to shape of RBC. Can be due to disease

Agglutaintion= Grape lke structure (1 drop saline + 1 drop EDTA)

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26
Q

Ghost cells

A

Repnants of RBC that have lost haemoglobin.

Membrane only.

Associated with deposition of complement and intravascular haemolysis

i.e. red plasma = indicitive of intravascular haemolysis

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27
Q

Spherocytes identification

A

Central pallor is normal due to biconcave shape.

Spherocytes are smaller in diameter and darker (lots of Hb)

Indicitive of extravascular haemolysis

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28
Q

Increased bilirubin is more indicitive of intra/extra vascular haemolysis?

A

Inc bilibubin is more indicitive of extravascular haemoylysis

May have neutrophillia/monocytosis (due to marrow upreg)

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29
Q

Diagnosisd of Mycoplasma haemofelis

A

Diagnosis: PCR- excellent

Blood smear: NOT RELIABLE/

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30
Q

Babesia pathogenesis

A

USA>UK

Tick borne disease

Pyriform bodies in red cells.

Treatment: Imidocarb.

V. severe if not diagnosis

TRAVEL HISTORY?

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31
Q

Heinz body formation

A

Denatured haemoglobin = Heinz body.

Cats more vunerable than dogs.

Low Numbers UNREMARKABLE IN CATS.

Oxidative injury (onion, paracetamol, prop glycol, vit K)

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32
Q

When would you expect horses to have Eccentrocytes

A

Haemoglobin has uneven distribution within the cell = eccentric distribution.

Seen most in dogs but due to oxidative damage

HORSES WITH RED MAPLE TOXICOSIS

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33
Q

Schistocyte

A

Shear injury product: Schistocytes/Keratocytes

i.e. Tumours (narrow vessel)

Haemangiosarcoma

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34
Q

Acanthocytes

A

Surface projections of variable length.

Projections are uneven spaced on surface.

Associated with splenic disease (haemangiosarcoma)

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35
Q

Causes of non regen anaemia

A

Kidneys: Norm produce EPO (CRF = Decreased production)

EPO injections (may develop antibodies)

Endocrine (hypothyr, hypoadren)

FeLV (70% anaemic cats)- subgroup C

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36
Q

Aplatic Anaemia

A

All precursors wiped out = ALL CELL LINES. platelts, granulocytes etc

Fat, plasma cells, mast cells are left.

Need core biopsy.

OESTROGEN TOXICITY? Testicu tumour

Phenobutazone

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37
Q

Leydig cell tumour =

A

Think derm (alopecia) as release +++ oestrogen

Also non regen anaemia due to oestradiol tox on bone marrow

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38
Q

How does storage of blood and smears differ?

A

Blood= store in fridge until anaylsis

SMERARS= STORED AT ROOM TEMP

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39
Q

How does the Signalment help refine cause of anaemia

A

Young animal: Lower PCV than adults anyway but more like parasitic

Old animal: Bleeding tumours?

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40
Q

How long does it take to develop a regenerative anaemia

A

3-5 days.

Check for polychrosia (diff quick) , corrected reticulocyte (new methyle blue, RNA precipitate) count

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41
Q

If Haemorrhage is susepected as the cause for the regenerative anaemia then what further tests would you do

A

Platelet count (manual)

Diagnostic imaging (thoracic/abdo)

Faecal lungworm

ACTH stim tests (if melena)

Abdo/ Pleural fluid sampling

42
Q

Why would you do a ACTH stim test for cases where you suspect haemorrgage (e.g. melena)

A

Gastrointestinal hemorrhage. Melena and/or
hematemesis have been reported in both typical
and atypical Addison’s cases. Gastrointestinal
ulcers may form as a result of the hypovolemia
due to aldosterone deficiency (poor perfusion
and vascular stasis within the intestines)

43
Q

If Haemolysis is suspected what further tests (for cases of regen anaemia)

A

Urinalysis - bilirubin? Haemoglobinura (with intra vascular haemoylsis may cause renal damage)

  1. Screen for tick bourne disease, Mycoplasia (cats)
44
Q

When would bone marrow biopsy be most indicated

A

Bone marrow aspirate / core biopsy are most indicated if no underlying cause has been found and there is moderate->severe anaemia

OR if more than one cell line affected

45
Q

Poor prognostic indicates for IMHA are…

A

Young to middle aged Cockers, Springers, Bearded collies.

Females >Males

Prog Guarded, esp if haemoglobinaemia.

Pulmonary thromboembolism occur as complication.

CAN occur secondary to neoplasia, infec, drug treatment.

Primary INHA in cats is rare but can occur.

46
Q

Decrease in what element can cause haemolysis

A

Hypophosphatemia can cause haemolysis.

Also shear injury

47
Q

Meylophtiasis

A

Neoplasia.

Bone marrow is crowded out by neoplastic cell lines such as lymphoma, multiple myeloma, leukaemias, mast cell tumours.

48
Q

Intravascular haemolysis is normally Ig_ mediated

Extravascular haemolysis is normally Ig_mediated

A

Intravascular: IgM (poss IgG)

Extravascular: IgG

49
Q

Examples of Inherited haemolytic anaemias

A

Pyruvatekinase (PK) deficiency

Phosphofructokinase (PFK) deficiency

50
Q

Why would you consider asprin/clopridogel in combination with prednisalone + azothiaprine (NOT CATS) in dog with IMHA?

A

Pulmonary thromboembolism is a common cause of death/ sudden onset dyspnoea in dogs.

Cats: use chlorambucil instead of azothiaprine

51
Q

Common aetiology and sequalae for hypophosphataemia

A

Diabetic ketoacidosis

Leads to haemolysis and heamorrhage.

More common in cats.

52
Q

Ideal weight for donor cat and dog

A

Cat: >4.5kg

Dog >25kg

Full biochem and haem repeated monthly

PCV/Total protein each donation

Vaccination but not <14 days before donation

Should not have previously had a transfusion themselves

53
Q

Volume of blood taken for tranfusion (cats/dogs)

A

15-20% of estimated blood volume

Estimate blood volume: Dog: 80-90ml/kg

Cat: 55-65ml/kg

Dogs can donate every 3 weeks but analyse serum iron.

54
Q

Canine donation procedure

A

12 hour fast in case of sedation and to decrease likelihood of lipaemic serum

Pre donation PCV/TP

Jugular

Try to collect over 5-10 minutes.

Max volume 525g (greater = risk of clot formation)

55
Q

Feline donation procedure

A

12 hour fast in case of sedation and reduce risk of lipaemic serum

Pre donation PCV/TP

Sedation: Ketamine/Midazolam

56
Q

Dog blood types, which one do we test for

A

Dog erythrocyte antigen 1,3,4,5,7

Test for DEA 1 as if DEA 1 +VE blood given to DEA 1 -VE patient sensitisation occurs (antibodies form) within 1-2 weeks

Can result in transfusion reaction

Can happen with all blood types but DEA 1 = most serious

57
Q

Feline blood types

A

Type A, B or AB (RARE)

Cats have naturally occuring proteins to blood proteins they don’t have.

58
Q

Why is testing ALL feline blood prior to transfusion more important than testing dog blood

A

Rare for dogs to have naturally occuring antibodies

Cats naturally have antibodies against alloantibodies to blood proteins they don’t have (A,B, AB)

Type AB cats can get either (but ideally AB, then A if not avaliable)

59
Q

Most serious blood tranfusion reaction in cats occurs when

A

Type B cats recieving type B or AB blood = peracute sometimes fatal

Type A cats recieving type B blood = similar reaction in DEA-1 negative sensitised dogs

60
Q

When is dog blood cross matching required

A

When recepient has been transfused mroe than 4 days previously.

There is a history of a transfusion raction

Receipients transfusion history unknown

61
Q

Test for agglutination (blood typing)

A

Used in emergencys

Take serum + EDTA samples from donor AND recipient

Centrifuge for 5 min then seperate serum and plasma

Have 4 slides (donar control, major cross match, minor cross match, recipient control)

Positive agglutination = INCOMPATIBILITY

Negative agglutination = NOT A GUARENTEE BUT MAJOR REACTION UNLIKELY

62
Q

Major / Minor crossing

A

Major cross: recipient antibodies to donon erythrocyte antigen

Minor cross; recipient antigen to donar antibodies

63
Q

Volume of blood required to raise the recipient PCV by 1%

A

2ml/kg of blood raises the recipient PCV by approx 1%.

64
Q

What anticoag is not used for auto-transfusion

A

Auto-transfusion is a last result.

Heparin should not be used as an anticoag as it has a long half life and causes platelet activation

65
Q

Why should plasma not be frozen in a dometic freezer?

A

Needs to be at -30

Max for 12 months then factors start deterorating

If dometic freezer will start deterorating immediately

66
Q

Only indication for plasma is ..

A

Provision of clotting factors (assessed using PT or PTT times)

Animals at risk of bleeding diathesis.

Used pre operatively in animals with inherited coagulopathies such as haemophillia A or Von Willebrands (USE CRYOPRECIPITATE- concentrated fraction of plasma)

Patients suffering rodenticide poisoning

67
Q

Difference between Cryoprecipitate and Cryosupernatant

A

Cryoprecipitate: Conc fraction of plasma containing von Willebrand factor, factor VIII, XI and XII, fibrinogen.

Cryosupernatant: Contains vit K depedent clotting factors, albumin and antithrombin.

Rodenticide tox, vit K defi, hypoalbuminae

68
Q

Blood products should be administered at what rate

A

Over 4-6 hour period.

NOT WITH HARTMANNS/SEPERATE CATHETER as calcium leads to crystal formation.

RATE: 0.5-1ML/KG/HR FOR first 30 mins then increased if no reaction

69
Q

Most common transfusion reaction to FOREIGN PLASMA PROTEINS

A

Swelling of the face = angiodema.

Can also cause urticaria and erythema of the skin.

Tx: Antihistamine drops (chlorpheamine IV)

If worsens= steroids.

If rectal temp rises by 1 degree = stop transfusion

70
Q

If compatible red cells are given the transfusion should last approx

A

4-6 weeks.

71
Q

Example of a non-immunological transfusion reaction

A

Volume overload.

Most commonly cats as they have underdiagnosed cardiac abnormalities.

Seen as tachypnoea and crackles.

Jugular distension or detection of a new mumur.

Tx: oxygen and furosamide

72
Q

TPR should be preformed every ___ minutes for the first hour of tranfusion and then

A

TPR every 15 minutes for first hour of tranfusion and then every hour afterwards

73
Q

What endocrine condition do we need to monitor for if large volumes of blood are given

A

+++ CITRATE WILL CAUSE HYPOCALCAEMIA

74
Q

Causes of haemorrage in horses (external blood loss)

A
  1. External wound involving large artery (prox/distal limb)
  2. Guttural pouch mycosis (erodes int. carotid artery)
  3. Post surgical haemorrhage (e.g. castration, can be internal haemorrhage but rare)
  4. GI parasitism (S. vulgaris)
  5. Haematuria (pyolonephritis, cystitis)
75
Q

Which artery can sometimes rupture before, or more commonly after parturition in the horse (more common in older mares)

A

Uterine artery rupture- normally middle uterine artery.

Clinical signs: Sweating, colic, tachycardia.

Blood either lost into abdo cavity or retained within broad ligament

76
Q

Immune mediated haemolytic anaemia in horses, pathogenesis

A

Primary: Uncommon autoimmune process

Secondary: Antibodies attach to RBC membrane because of alterations in RBC membrane because of primary infection, neoplasatic, or other immune medaited process.

Drugs

77
Q

Treatment of of immune-mediated haemolytic anaemia

A

Discontinue all treatments if possible (consider feed supplements/additives)

Blood transfusion may be nec.

Immunosuppression (most commonly dextamethasone, prednisalone)

78
Q

Red maple toxicity presentation

A

Horses= oxidative damage= Heinz body formation (precipitations of oxidatively denatured haemoglobin on RBC membrane)

Toxin found in wilted leaves can cause intravascular and extravascular haemolysis and methaemaglobinaemia (chocolate brown)

79
Q

Treatment of Equine infectious anaemia

A

Exotic to the UK.

Caused by equine infectious anaemia virus (Lentivirus)

Persistant infection = no treatment.

Horses remain life long carriers

80
Q

Anaemia due to chronic disease pathogenesis (3 things)

A
  1. Iron sequestration ‘anti-bacterial’ mechanism
  2. Defective erythropoeitin response
  3. Decreased RBC life span

TREAT PRIMARY DISEASE

81
Q

Colostrum is mainly comprised of

A

Mainly IgG, some IgA and IgM.

Normal foals suckle within 1-3 hours after birth and consume 1-2Litres.

<4g/L of IgG = Failure of Passive Transfer

4-8g/L of IgG = Partial Failure Passive Transfer

82
Q

Treatment of Failure of Passive Transfer

A

<4g/L = fpt 4-8g/l = Partial FPT

If foals less than 12-18 hrs of age = oral colostrum unless disease.

If foal is >12-18 hours old = IV plasma often 2L required

83
Q

Neonatal erythrolysis can occur in what mares

A

Normally multiparous mares that have been sensitised to foals RBC’s antigens during preg.

CAN ALSO OCCUR IN MAIDEN MARES

  • Foal inherits red cell antigens from sire, different from mare.
  • Red cell must be strongly antigenic (Aa, Qa)
  • Commonly mule foals (donkey sire x horse dam)
84
Q

How must the mare be exposed to foals red cell antigen to for neonatal isoerythrolysis to occur?

A
  • Transplacental haemorrhage
  • Prior blood tranfusion
  • During parurtiion

Antibodies against foals RBC are contained in mares colostrum

Foals develop signs first 4 days of life.

85
Q

Treatment of neonatal isoerthrolysis

A

If 24-48 hours of age: Prevent further colostrum ingestion, plasma transfusion to establish plasma transfer of immunity (<4g/L = FPT 4-8g/L = Partial FPT_

Blood transfusion: Mare’s WASHED red cells (NOT PLASMA)

86
Q

Normal PCV for a) Cattle b) Sheep

A

a) Cow: 24-46
b) Sheep: 27-45

87
Q

Cause of haemolytic anaemia in farm animals

A

Leptospirosis

Postpaturient haemoglobinuria

Bacillary haemoglobinura

Protozoa

Chronic Cu poisoning

Cold water ingestion

Brassica poisoning (rape, kale, cabbage)

Autoimmune haemolytic anaemia

Drug induced

88
Q

Causes of depressed erythrocyte production in farm animals

A

Deficiency of Cobalt or Cu

Iron def

Acute bracken posioning (enzootic haematuria)

Fasciolosis

Lymphosarcoma

Renal disease

Anamia of inflamm disease

89
Q

Enzootic haematuria in farm animal

A

Acute braken poisoning.

= Depressed erythrocyte production

90
Q

How does the type of Anaemia differ between a) Copper b) Cobalt ingestion

A

Chronic copper poisoning: Haemolytic anaemia

Copper and Cobalt DEFICIENCY = Depressed erythocyte production

91
Q

Blood transfusion of adult cow

A

First transfusion should be safe.

5L required.

92
Q

How to differentiate braken poisoning from pyelonephritis

A

Both cause haemtouria in cattle.

Enzootic haemturia= braken poisoning = most common cause in cattle.

Braken posioning will cause anaemia but pylenephritis may not cause anaemia

93
Q

Causes of Abomasal ulcer

A

Sand

Displaced abomasum

Stress

Occult blood in faeces/ black dung

Free air in abdomen

Abdominal pain

94
Q

Most susceptible breeds for chronic poisoning

A

Sheep more susceptible than adult cattle.

Calves moderately susceptible.

Texels and Suffolk most susceptible

Causes haemolytic anaemia

c.f. copper deficiency leads to decreased erythrocyte produ

95
Q

Copper store

A

Texels/Suffolk most susceptible.

Copper is stored and accumulates in liver.

Some centrilobular necrosis occurs as liver copper conc rises.

At some point there is a sudden release of copper from liver into blood = acute fatal syndrome develops

96
Q

Pathogenesis of Chronic copper poisoning

A

Chronic copper poisoning is an acute disease (sudden release from liver store) following chronic absorption and accumulation of copper.

97
Q

Cause of Chronic Copper poisoning

A

The diet: Concentrates, Phytogenous (pasture), hepatogenous (liver damaged by PA)

-Accidental overdose (more likely ACUTE poisoning)

Levels >4 are required

Levels >12 may be dangerous dependent on breed (texels/suffolk parti predisposed)

CATTLE PIG FEEDS EXCEED THIS THEFORE CARE

98
Q

Why should cattle and pig feeds NOT be fed to ewes

A

Chronic Copper poisoning

Levels >4 ppm required for normal health

Levels >12 ppm may be dangerous

Clinical signs: Jaundice, pallor, haemoglobinura

99
Q

How should you test for imminent copper poisoning

A

Blood Cu levels only elevated after release from liver (following continual storage)

BIOPSY LIVER

Necropsy: Swollen yellow liver, gunmental kidneys, jaundice everywhere.

100
Q

Treatment of Cu poisoning

A

Ammonium tetrathiomolybdate (ATM)

Somulose 10ml iv

Sodium Calcium Edetate

PREVENTION: kEEP Dietary Copper <10ppm

Cu absorption inhibitors (Mo,Zn, Fe and soil)

Avoid prolonged feeding of conc

Never feed cow/pig concentratates to sheep

101
Q
A

VetMed Year 4- Term 1 (12 decks)

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