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Lymphoreticular > Equine Neonatal Dz > Flashcards

Equine Neonatal Dz Flashcards

1
Q

When is colostrum produced?

A

Last 2 weeks pregnancy

- selective secretion of Ig from serum and local production

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2
Q

What soluble compounds are in colostrum?

A
  • Ig (mainly IgG and IgGT, some IgM and IgA)
  • hormones
  • growth factors
  • cytokines
  • lactoferrin
    CD14
  • enzyems/lysozymes
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3
Q

Cellular compounds colostrum

A
  • lymphocytes
  • macrophages
  • neutrophils
  • epithelial cells
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4
Q

Hoe much colostrum should foal drnk?

A

1-2l in first 3h life

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5
Q

How is Ig absorbed?

A

Pinocytosis by specialised enterocytes 12-24hrs after birth

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6
Q

When are Ig levels measured?

A
  • 18-24hrs

detectable in serum @ 4-6hrs, peak 18-24

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7
Q

How long do passive transfer Abs alst? When do foals Igs levels increase?

A

~ a month
- foals Ig reaches adult level ~5-10 months
so nadir around ~1month old

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8
Q

Reasons for FPT?

A 
> maternal 
- lack of colostrum (premature lactation) 
-poor uality low conc IgG (SG  foal 
- contracture of tendons, neonatal asphyxia syndrome, sepsis 
- rejected by mare 
> lack of absorption
- time frame (ingested too late) 
- GIT dz (hypoxic damage)
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9
Q

Consequence of FPT?

A
  • pdf development infectious dz

- sepsis (arthritis, pneumnoia D+, meningitis)

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10
Q

Define complete and partial FPT

A

8g/l

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11
Q

How can FPT be dx ?

A
  • Total protein (Igs are protein)
  • Snap test (ELISA) blood
  • Colostrum SG
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12
Q

Tx FPT

A

> Colostrum NGT
- if under 12hrs
- no signs systemic compromise
- 1-2L equine colostrum SG >1.060
- 200-400ml at a time
- NGT (not syringe) dont waste and may assphyxiate
IV plasma
- 1-2L
- foal >8hrs, 12-18hrs
- signs systemic dz
- if no high quality colostrum available
- commercially available (1L bags, 15-17g/L IgG)
- 1L increases IgG conc by 2-3g/L
1L plasma w/ >25g/L IgG ^ IgG conc by 4-8g/L
NB: if foal sick will use up Abs, repeat

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13
Q

Outline plasma administation

A
  • diazepam sedation
  • monitor for signs of plasma reaction (slowly so signs will e noticed early)
  • 1 drop,sec (3ml/mmin)
  • check HR
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14
Q

Tx plasma reactions?

A
  • stop
  • 1mg/kg flunixin +- IV fluid
  • wait 1-2hrs, restart tansfusion slowly
  • try using different batch/donor (shouldnt react to multiple)
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15
Q

What is neonatal isoerythrolysis? pathogenesis

A
  • IMHA of newborn foal d/t imcompatible bllood types of mare and foal
  • mare put to stallion of different blood group, foal inheits this
  • placenta breached at some point, mare makes immune response to foals blood (1st preg)
  • 2nd preg colostrum full of Abs against its own blood type
  • antibodies coat RBC intra and extra vascaulr haemolysis
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16
Q

What are the main blood antigens in the horse?

A

Aa +/-

Qa +/-

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17
Q

Which species is NI very common in?

A

Mules

- d/t donkey factor!!

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18
Q

Clinical signs of NI?

A
  • normal at first, no FPT, clinical signs up to 12d pp! but usually
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19
Q

Dx NI?

A

> clin path

  • anamia
  • haemaglobinuria
  • haemoglobinaemia
  • ^ unconjugated bilirubin
  • metablic acidosis
  • pre-renal/renal azotaemia
  • toxic hepatopathy / hypoxic hepatocellular necrosis
  • possible despite IgG Haemolytic cross mach
  • ID haemolysis of foals WBC by mares serum with addition of external (Rabbit!) complement
  • evaluate for signs of agglutiation if no compleemnt available but false -ve possible.
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20
Q

Tx NI?

A
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21
Q

NI prevention?

A

> mare w/ hx NI

  • determine blood group of sire
  • test serum for alloAbs
  • prevent any colostrum intake if same sire/other incompatible sire if is used
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22
Q

What is combined immunodeficiency and which foals does it affect?

A
  • Autosomal recessive genetic dz of Arabian foals
  • enzyme defect: Non-functional DNA dependant protein kinase -> no mature functional B or T cells
  • recurrent infections once passive immunity waned
  • associated w/ infection with uncommon agents eg. adenovirus, pnumonia, D+
23
Q

Px and prevention of combined immunodeficiency?

A
  • fatal @ approx 5 mo

- dam and sire must both be carriers of gene - genetic test available

24
Q

Equine specific facts wrt anaemia?

A
  • can compensate with spleen
  • regenerative and non-regenerative can ONLY BE DETERINED ON BM ASPIRATE
  • circulating lifesplan erythrocytes long (140-150d)
  • hroses repsond slowr and take longer to recover from anaemic insult
  • Howell-Jolly bodies normal in equine blood and DO NOT INDICATE RESPONSIVE ANAEMIA
25
Q

CLinical/lab signs of anamia?

A

> indications of inadequate oxygen delivery to tissues
- plasma lactate ^ d/t anaerobic metabolism
- v PvO2 (venous) d/t ^ O2 extractino from blood
PE
- pale mm
- ^HR, RR
-weakness/excercise intolerance/collapse

26
Q

Why may PCV, HCT and RBC not be affected in acute blood loss?

A
  • RBC and plasma both lost so proportion remains the same within blood sample
  • with chronicity interstitial fluid replaces blood volume and RBC conc decreases
27
Q

Classification of anaemia and possible causes during work up?

A

> acute
- external bleeding
- internal bleeding (haemabdomen, haemothorax, broad ligament, kidneys, DIC)
chronic
- regenerative (haemorrhage: GI/renal) (haemolysis: IMHA/infectious/toxic)
- non-regenerative (Fe deficiency, chronic dx, BM suppression)

28
Q

Causes of haemabdomen?

A
  • trauma (ruptureed spleen/liver)
  • ruptured mesenteric vessel
  • uterina a. rupure
  • neoplasia
  • coagulopathy/DIC
  • abdominal abscess
29
Q

Causes of epistaxis

A
  • trauma
  • ethmoid haematoma
  • EIPH
  • neoplasia
  • gutteral pouch mycosis
  • pulmonary haemorrhage
  • coagulopathy/DIC
  • rupture rectus capitis m.
  • sinus abscess/infection
30
Q

Causes of haemothorax?

A
  • trauma (rib fx esp foals, lacerated heart/large vessel)
  • pulmonary haemorhage
  • necrotising pneumonia
  • ruptured pulmonary vessel/embolism
  • ruptured pulmonary abscess
  • coagulopathy/DIC
  • neoplasia
31
Q

Causes of haematuria?

A
  • trauma
  • pyelonephritis
  • cystitis/urothithiasis
  • urethral rent (male)
  • neplasia
  • coagulopathy/DIC
32
Q

Causes of chronic regenerative blood loss?

A 
> GI 
- parasitism 
- neoplasia
- coagulopathy 
- ulceration 
- granulomatous enteritis
- DIC
> haemolysis
- infectious (EIA, piroplasmosis) 
- IMHA
- toxic (redd maple leaf tox USA) 
- iatrogenic
33
Q

Causes of NON-regenerative chronic blood loss?

A 
> Fe deficiency
- chronic haemorrhage
- nutritional deficiency (rare)
- chronic dz
> BM failure
- myelopthisis
- myeloproliferative dz
- toxins (phenylbutazone, chloramphenicol) 
- idiopathic pancytopaenia
> misc
- rhEPO (less common now)
- chronic hepatic/renal dz
34
Q

Tx anaemia?

A

> stabilisation (anaemia itself may not need to be treated)

  • guided by cliical and lab findings (HR, RR, lactate, PvO2) NOT PCV
  • control blood loss if source found
  • IVFT if severe blood loss
35
Q

Presenting complaint and clinical signs of haemabdomen?

A

> colic

  • abdo pain
  • hypovolaemia (^HR, slwo capillary and jugular refill time, ^ lactate)
  • Dx: ultrasonongraphy
36
Q

Px of haemabdomen?

A

depdns on underlying cause, survival ~ 50%

37
Q

What is periparturient haemorrhage and when is it commonly seen?

A
  • haemorrhge from uterine vessels after more commonly than before parturition
  • important cause pp colic and death
  • delivery often uneventful!!
    > mares may be prone to repeated bleeds in future pregnancy
38
Q

What 2 forms of pp haemorrhage may occour?

A
  • into broad ligament

- into abdomen (can be rapidly fatal)

39
Q

Tx pp haemorrhage?

A

CV stabilisation

40
Q

2 forms of IMHA?

A

> 1*
- uncommon: ABs directed against patients RBC ag
2*
- Ab formation precipitated by 1* dz, rug administration, neoplasia, immune mediated dz

41
Q

Dx IMHA?

A

> coombs test can be attempted
- presence of anti-RBC Ab directly (surface of RBC) or indierctly (serum)
- false +/- possible
flow cytometry to demonstrate Abs on RBC

42
Q

Tx haemolytic anaemia?

A
  • tx 1* dz process
  • stop lal meds
  • transfusion IF signs of inadequate oxygen delivery
  • immunosuppressioin (steroids, azathioprine and cyclophosphamide (latter 2 rarely in horse)
43
Q

What is EIA?

A
  • equine infectious anaemia
  • lentivirus
  • transmitted via insects, blood contaminated equipment
  • not present UK, risk from imports
  • persistnet infection - infected horse remains lifelong carrrier
44
Q

3 syndromes of EIA? What is the associated anaemia associated with?

A
  • acute, chronic and inapparent

- anaemia caused by intra and extravascular haemolysis, BM suppression -> thrombocytopenia also common

45
Q

Dx EIA?

A

Coggins test (AGID) or ELISA

46
Q

Px/management of EIA cases?

A
  • euthanasia/lifelng quarantine if horse + as danger to other horses
47
Q

What is seen with haemolytic anaemia d/t oxidatic injury to RBC? WHen may this also be seen?

A

> Heinz Body Formation
- oxidative damage to Hbg precipitates on RBC membrane
- RBC less deformable and rapidly cleared from circulation
D/t
- drugs (phenothiazine, methylene blue)
- plants (onions, Brassica spp. red maple)

48
Q

Pathogenesis of red maple leaf toxicity (not UK)

A
  • wilted leaves

- methaemoglobin results from oxidative change of Hbg Fe to a non usable state for O2 transport

49
Q

Causes of anaemia d/t inadequate erythropoesis?

A 
> most common d/t chronic dz 
- chronic inflam or infection/ neoplasia
- sequestration of iron
- shortened RBC lifespan 
- defective erythropoeitin response
> Iron deficiency 
- can develop with chronic blood loss
- tx Fe supplmentation 
> OTher
- neoplastic process
- +- chronic renal failure
- after adminsitration og hrEPO (cross reacts against endogenous EPO) 
- idiopathic
50
Q

Type of anaemia caused by chronic dz?

A
  • mild - mod
  • normocytic, normochromic
  • non-regnerative
  • not associated with clinical signs (will not present for this)
51
Q

Tx anaemia d/t chronic dz?

A
  • tx 1* disease not anaemia itself
52
Q

Why is anaemia important?

A
  • 98% O2 transported by hbg
  • CaO2 determined by Hbg
    > CaO2 = (1.34xHbxSaO2) + (0.003xPaO2)
53
Q

What is CaO2 and what should this be in a normal horse? How does this differ in the anaemic and hypoxaemic horse?

A

> oxygen content of blood
- CaO2 = 1.34ml/g15g/dl0.99+0.003100mmHg
= ~21ml/dl
Anaemic PCV 10%
- CaO2 = 1.34[[3.3g/dl]]0.99+0.003100mmHg
= 4.7ml/dl (79% decrease)
hypoxaemic
- CaO2 = 1.3415[[0.8]]+0.003*[[45mmHg]]
= 16.2ml/dl (20% decrease)

54
Q

What is the foals immune system like when born? @ what sage of gestation do T and B lymphocytes develop?

A
  • competent but naive and born agammaglobunlinaemic
    ( able of mounting an immune response but hasnt been challenged and no trasnfer of Ig d/t epitheliochorial placenta) Ab protective levels reached @ 2 weeks and presenceo f maternal Abs suppresses foals own Ig production (so wait to vax until after maternal Ab waned)
  • T lymphocytes funcional @ 100d gestation
  • B lymphocytes functional @ 200d gestation
  • complement ~10% adult activity
  • ## phagocytosis and killing some organsims low in newborns

Lymphoreticular (31 decks)

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