Equine 7 Flashcards
describe the roles of the liver
protein metabolism (plasma proteins and amino acids)
energy metabolism (carbohhydrates and lipids)
detoxification (drug metabolism and bile excretion)
monomuclear phagocyte system (kuppfer cells)
when are kuppfer cells active
part of the reticulo-endothelial system. active in ethanol induced liver injury but also endotoxin internalisation and activation of subsequent inflammatory cascade
what are the common clinical signs of hepatic dysfunction in horses
weight loss icterus (hyperbilirubinaemia) hepatic encephalopathy colic - stretching of capsule due to acute hepatocellular swelling or biliary obstruction (choleliths) depression
what are the rare signs of hepatic dysfunction in horses
photosensitisation diarrhoea (portal hypertension or biliary acid deficiency) bilateral laryngeal paralysis bleeding ascites dependent oedema (hypoalbuminaemia )
what are the very rare signs of hepatic dysfunction
steatorrhoea tenesmus generalised seborrhoea puritus endotoxic shock polydipsia pigmenturia
what are the signs of hepatic encephalopathy
circling head pressing ataxia yawning behaviour change seizures (rare) respiratory noise with laryngeal paralysis
why do signs occur in hepatic encephalopathy
GI derived neurotoxins (decreased breakdown in liver and excess production in GI disease)
false neurotransmission (ammonia and GABA)
increased BBB permeability
impaired CNS energy metabolism
altered BCAA:AAA ratio
increased manganese
how is hepatic encephalopathy managed
seizure control - sedation - barbiturates - not diazepam supportive care resolve liver issues
how does phylloerythrin cause photosensitisation
gut derived breakdown product of chlorophyll which is usually metabolised by the liver. this doesn’t occur in liver disease.
UV light leads to oxidative cascade causing inflammation and skin sloughing (mainly unpigmented skin)
how does St John’s wort toxicity lead to photosensitisation
hypercin is absorbed by the body and activated by exposure to sunlight causing photosensitivity
liver function is normal
describe coagulopathy due to liver disease in horses
rare
liver synthesises many clotting proteins (factors II, VII, IX, X, protein C). the extrinsic pathway is the first to show prolongation duet to short half life of factor VII.
may do clotting profile before biopsy
which measure indicate liver function in horses
bilirubin (ideally conjugated and unconjugated separately)
ammonia
bile acids
dye clearance test - rarely used
which measures indicate hepatic insult
liver enzymes - SDH (hepatocellular damage) - GGT (biliary damage) - GLDH (hepatocellular damage) less specific - AST - ALP - LDH
which prehepatic factors may cause hyperbilirubinaemia
increased production due to haemolysis
liver can’t keep up so see increased unconjugated bilirubin
high in foals due to foetal Hb metabolism
which intra-hepatic factors may cause hyperbilirubinaemia
impaired hepatic uptake - anorexia
see unconjugated bilirubin due to lack of process.
no haemolysis plus increased unconjugated bilirubin = liver problem
which post hepatic factors may cause hyperbilirubinaemia
impaired excretion
- biliary obstruction (cholangitis, hepatitis)
- normal liver, obstruction further down
mainly see conjugated bilirubin
how is ammonia measured and what may it indicate
required citrated sample
assay within 1 hour
ideally control from an animal on the same diet should be assessed
relationship between presence of ammonia and hepatic encephalopathy but no relation between level of ammonia and severity
what is the significance of bile acid testing
mostly removed by the liver from circulation
may increase with chronic starvation
highly specific for liver disease/dysfunction especially if chronic
pre-and post-prandial sample not important in horses
what may cause cell necrosis in the liver
hepatocellular disease biliary disease drugs hypoxia endotoxaemia
how may albumin change in liver disease
rarely decreases due to long half-life (20 days)
takes up to three weeks for detectable changes
how may liver biopsies help the diagostic process
indicated after biochem suggests liver disease
target therapy
formulate prognosis
- animals with abnormal liver function
- animals with structural pathology
- animals with persistently increased serum enzyme activity
describe the site and prep for liver biopsy
may determine clotting functio n sedation local anaesthesia US guidance 12-14th RIC or 5-8th LIC haemoperitoneum common but not significant
how is prognosis of liver disease determined
difficult - extent of damage may not correlate with function
histopathology may be useful
biopsy scoring system - works under assumption the liver is uniformly affected
- fibrosis
- irreversible cytopathology (necrosis, megalocytosis)
- inflammatory infiltrate
- haemosiderin accumulation
- biliary hyperplasia
what may cause focal hepatic injury
abscess
neoplasia
zonal hypoxic injury
what may cause acute generalised injury
tyzzer’s disease
infectious necrotic hepatitis
toxins
(all rare)
what may cause chronic generalised injury
biliary hyperplasia and nodular regeneration caused by
inflammation
hypoxia
anti-mitotic agents
what toxin does ragwort contain
pyrrolizidine alkaloids
how do pyrrolizidine alkaloids cause liver damage
metabolised by mircosomal enzymes of the hepatocyte to pyrroles. they cross-link double stranded DNA preventing mitosis and resulting in megalocytes. as cells die they are replaced by fibrous tissue
what may be seen on liver histopathology in pyrrolizidine alkaloids toxicity
fibrosis
megalocytes
bile duct proliferation
what is clinical presentation of pyrrolizidine alkaloids toxicity
1-6months after ingestion as damage is cumulative
weight loss
laryngeal paralysis
increased plasma activities of liver derived enzymes
how is pyrrolizidine alkaloids diagnosed and treated and how is prognosis determined
diagnose on histology
no specific antidote
supportive therapy - high protein, palatable diet
poor prognosis: serum bile acid >50umol/l or extensive fibrosis on histopathology
what is tyzzer’s disease
clostridium piliforme (soil living) affects foals between 6 and 44 days old leading to acute death. liver swollen with 1-5mm white foci throughout the parenchyma and coagulative necrosis
what is infectious necrotis hepatitis
clostridium novyi type B (black disease)
progressive, acute clinical signs for 24-72 hours leading to death.
treat with penicillin but no reported survivors
which toxins may cause acute liver damage
iron injection - neonatal foals - some survive but often acutely fatal centrolobular necrosis - Arsenic (pesticide) - Carbon tetrachloride (fumigant) - Chlorinated hydrocarbons (insecticide) - Monensin (ionophore) - cardiotoxic - Phenol (wood preservative, disinfectant) - Paraquat - herbicide Periportal changes - Phosphorous (fertiliser)
what is cholangiohepatitis
inflammation of hepatocytes and biliary tree
describe primary cholangiohepatitis
Also termed chronic active hepatitis
Clinical signs often vague and include weight loss, depression, poor performance, anorexia, icterus and fever
how is primary cholangiohepatitis diagnosed
Hepatocellular and biliary enzymes are elevated
Diagnosis made on liver histopathology
- Evidence of hepatocellular necrosis, acute inflammation and fibrosis
- Lymphocytic/plasmacytic inflammation - cause unknown but a similar condition in humans is autoimmune
- Neutrophilic inflammation - cause believed to be bacterial infectio
what are the causes of secondary cholangiohepatitis
cholelithiasis duodenal inflammation intestinal obstruction neoplasia parasitism certain toxins
describe cholelithiasis
more common than hepatic lithiasis in horses
nidus for infection likely from ascending biliary inflammation or infection
choleliths composed of bilirubin, esters of bile acids and cholesterol and calcium phosphate
see anorexia, intermittent colic, icterus and pyrexia
ultrasound for diagnosis
difficult to treat
how is liver disease managed
dextose IV - reduce ammonia and enteric production of toxins
highly palatable, high carbohydrate, low protein diet
B vitamins and folic acid
supplement ADEK
describe some specific liver disease treatments
- Lactulose 80-120ml PO every 6 hours - decreases ammonia absorption (hepatic encephalopathy)
- Metronidazole or neomycin PO - decreased GI production of NH3 (clostridia)
- DMSO reduce cerebral oedema (hepatic encephalopathy)
- No basis for flumazenil (GABA receptor antagonist for hepatic encephalopathy) in the horse - inconsistent results in other species
what specific treatments for cholangiohepatitis are there
Neutrophils predominate on biopsy - Antibiotics
Plasma cells and lymphocytes predominate on biopsy - steroids
describe specific treatments for cholelithiasis
TMPS, penicillin, gentamicin for ascending infection
Treat for 2 weeks after clinical signs resolve - DMSO may help to dissolve choleliths
what are the clinical signs of hyperlipaemia
initial - anorexia - lethargy - weakness progression - reluctance to move -in-coordination - dysphagia - head pressing, circling - recumbency, paddling of legs, nystagmus - convulsions - profound depression, coma
what are the risk factors for hyperlipaemia
• Obesity • Breed ○ Shetland ○ Miniatures ○ Ponies ○ Donkeys • Gender ○ Female ○ Pregnancy/lactation • Stress • Disease • Anorexia • Malnutrition
which disease are associated with hyperlipaemia
• Intestinal parasitism • Enteritis/colitis • Gastric/large colon impactions • Dysphagia • Lymphosarcoma • Equine hyperadrenocorticism • Peritonitis • Metritis Anything that causes negative energy balance
describe the pathophysiologgy of liver disease
Negative energy balance
- -> uncontrolled breakdown of lipid stores. In fat animals there is excessive storage of NEFA which are then mobilised to face the energy demand. Release of larger VLDLs and lipoprotein lipase cannot keep up with increase in NEFA production
- -> hyperlipaemia
how is hyperlipaemia diagnosed
• Plasma triglyceride
○ >5mmol/L = hyperlipaemia
○ 1.5-5mmol/L = at risk, hyperlipidaemia
• Other abnormalities - liver markers elevated
○ GGT
○ ALP
○ SDH
○ Bile acids
= Glucosehow is hyperlipaemia treated
treat underlying causes fluid therapy - 5% dextrose PPN +/- insulin enteral nutrition BCAA supplementation - valine, leucine, isoleucine
what is the prognosis of hyperlipaemia
poor - 60-100% mortality
in those that survive, triglycerides normal in 3-10 days
how is hyperlipaemia prevented
avoid breeding or transport of obese animals
controlled exercise and feed intake
avoid drastic weight reduction
what term is used to describe camelids due to their three chambered forestomach
pseudoruminants
describe C1 in camelids
Occupies much of the left side of the abdomen. The cranial and caudal sacs are weakly divided by a horizontal pillar. It is relatively thin-walled and does not have papillae lining its surface. Instead it has rows of saccules along its ventromedial aspect. There is no reticular structure.
similar function to the rumen, water and VFAs absorbed here.
describe C2 in camelids
connecting tube carrying C1 content through to C3
describe C3 in camelids
more like the equine stomach than the abomasums of ruminants. The proximal 80% of C3 is non-glandular and the distal 20% is glandular, secreting acid. C3 is tubular in shape and curves around the medial aspect of C1 on the right side of the midventral abdomen, lying caudoventral to the liver.
how many lips does the oesophageal groove have in camelids
only one (compared to two in cows)
what shape is the camelid colon and what problems may occur
spiral - makes them efficient at re-absorbing water from the intestinal content.
faecoliths relatively common cause of colic
volvulus around root of mesentery may occur
describe the caecum and omentum in camelids
caecum - small
omentum not well developed so have a reduced ability to wall off pockets of infection, stomach ulcers and abscesses. no omental sling so crucial to flush the abdomen and not leave blood/fibrin clots in the abdomen that may cause adhesinos during surgery
why is it important to take care if performing flank laparotomy in camelids
thin abdominal musculature
herniation more likely (need two layer wall closure)
describe the liver in camelids
located in the right side of the abdomen mostly under the ribcage although the caudal border extends beyond the last rib. US second to last rib space.
caudal border fimbriated
do cameldis have a gall bladder
no - same as a horse
how is function of C1 assessed
analyse sample of fluid via stomach tube collection (don’t expect more than 10ml)
protozoa - microscopy
bacteria - new methylene blue stain
pH - may appear alkaline due to saliva contamination
chloride concentrations if GI obstruction suspected
what role do saccules in the ventral regions of C1 play
microfermentation
where do ulcers generally develop in camelids
lesser curvature of the third compartment at the junction of the glandular and non-glandular mucosa and duodenum
what is the most important tool in camelid GI medicine
ultrasound - cannot easily palpate abdomen - signs often similar despite cause - physical exam often similar despite cause bloodwork next step
which colic lesion will cause the most severe signs in camelids
SI lesions > forestomach and LI
what are the clinical signs of colic in camelids
separation from herd inappetent flare nostrils roll/sit with legs out to the side shift position regularly kick at belly elevated resp rate may not be a consistently increased heart rate reduced gut sounds OR increased in gastrooenteritis
what are the causes of colic in camelids
intestinal lesion - spiral colon impaction - upper intestinal lesion - hairballs - mesenteric torsion/volvulus gastroenteritis C3 ulceration --> rupture distended stomachs urethral blockage uterine torsion dystocia pregnancy toxaemia less common - epiploic foramen entrapment - ruptured rectum
what diagnostic steps are used in colic in camelids
thorough physical exam - check rectum for faecal quantity and character ultrasound exam - distended intestine loops - motility - free fluid - ulceration/rupture - size of bladder/other organs blood work - hydration - electrolytes - other systemic disease peritoneal tap if considering surgery
what are the indications for abdominal surgery in camelids
continuous/intractable pain persistent low grade discomfort despite supportive therapy abnormal rectal findings abnormal peritoneal fluid failure to pass faeces >24 hours failure to urinate >6-8 hours positive US findings increased chloride in C1 fluid hypochloraemic, hypokalaemic metabolic alkalosis (GI obstruction)
what stressors may lead to C3 ulceration
environmental
social
metabolic
what proportion of C3 in camelids is glandular
distal 20% - glandular and acid-secreting
the other 80% is glandular
what are the signs of C3 ulceration in camelids
colic
increased heart and resp rate
regurgitation, excessive salivation, copious saliva in mouth (mostly weanlings)
how are C3 ulcers diagnosed in camelids
clinical exam
rule out surgical colic
faecal occult blood testing unreliable
US - some ileus, thickening and oedema of C3. severe cases may have increase in free peritoneal fluid locally between C3 and the liver.
peritoneal tap - if ruptured may have flocculent fluid
bloodwork - inflammatory changes on haematology (leucocytosis or leucopenia with left shift)
how are C3 ulcers treated in camelids
peracute cases - surgical closure of discrete ulceration followed by thorough abdominal lavage and ICU care in general - remove initial cause of stress - sucralfate - ranitidine - parenteral omeprazole (oral not effective) - antibiotics - IVFT
what are the clinical signs of megaoesophagus in camelids
weight loss respiratory disease vomiting ptyalism choke stomach ulcers bad teeth halitosis
what are the potential causes of megaoesophagus in camelids
• persistent right aortic arch
- OP toxicity
- severe muscle wasting as a result of gastrointestinal parasitism
• abdominal disorders such as peritonitis and gastric ulcers
• Pleuritis
• Hypothyroidism
• iron deficiency
• high titres to Toxoplasma gondii
• gastric atony from OP toxicity
• vagus trauma (or oesophageal trauma and scarring) as a result of jugular venous interference.
how is megaoesophagus diagnosed in camelids
radiographs
- Normally the mega-oesophagus is identified in the thoracic region
- Strictures further cranially could result in a more focal mega-oesophagus in the cervical region.
- Usually be seen without contrast although barium may be given in equivocal cases.
- Evaluate the chest at the same time for aspiration pneumonia. This may affect the prognosis.
blood work to investigate underlying cause
how is megaoesophagus treated in camelids
feed frequent small portions of highly digestible, easily swallowed food from an elevated position
owners often build a ramp
prognosis depends on how successful management is
what GI parasites affect camelids in the UK
• Roundworms
○ Strongyles (eg Haemonchus, Ostertagia and Trichostrongylus)
○ Nematodirus
• Whipworms
○ Trichuris
• Tapeworms
= Monieziawhat are the clinical signs of parasitic gastroenteritis in camelids
• ill-thrift
• weight-loss
• Diarrhoea
• Colic
• Anaemia
• Lethargy
- Anorexiahow is parasitism diagnosed in camelids
faecal examination
- standard McMasters test
- centrifugation of samples to enhance sensitivity
- concentrated sugar solution used for flotation
- modified stolls test better at recovering eggs
how are GI parasites treated in camelids
some only require dosing 2x a year, other every 2 months depending on stocking density and management practices
dose individually depending on weight
- underdosing –> drug resistance
- overdosing –> unwanted side effects with some drugs
what is the maximum stocking density of camelids
7 alpacas or 5 llamas per acre of pasture
which wormers may be used in camelids
BZDs - fenbendazole has high index of safety
pyrantel pamoate
praziquantel
levamisole
which drugs are contraindicated in camelids
avermectins not effective against nematodirus, whipworms and tapeworms. not effective used as oral drenches or pourons as not absorbed sufficiently
moxidectin - extremely long half-life so not recommended
which ages of camelids are most susceptible to coccidiosis
neonates and juveniles.
adults more resistance due to mature immune systems and prior exposure
associated with overcrowding and poor hygiene
decribe the life cycle of coccidia
ingestion of sporulated oocysts
sporozoites released which penetrate epithelial cells in the small intestine (motile stage)
sporozoites undergo both sexual and asexual reproductive stages producing oocysts
oocysts shed in faeces. also cause direct damage to the epithelial mucosa of the SI
what are the clinical signs of coccidiosis in camelids
enteritis
diarrhoea (may be haemorrhagic)
tenesmus
which species of Eimeria have been identified in camelids
lamae alpacae macusaniensis - oocyst much larger than the other species (81-107um) and very thick wall ivitaensis punoensis peruviana
how is coccidiosis treated in camelids
diclazuril (Vecoxan, Janssen Animal Health) or toltrazuril (Baycox, Bayer) in the UK.
Clinically affected animals should be isolated and treated.
Unaffected animals from the same pen should also be treated since they will
how is coccidiosis prevented in camelids
good management practices and maintenance of hygienic facilities for young animals
strategic use of anticoccidial drugs
prophylactic anticoccidials in wetter months
preventative measures before and during stressful events - decoquinate in feed
which species of liver fluke affect camelids
fasciola hepatica - more of an issue in the UK especially wetter areas
dicrocoelium dendriticum
what are the clinical signs of liver fluke in camelids
acute/chronic/fatal forms
- reduced appetite
- generalised weakness
- recumbency
- anaemia
how is liver fluke diagnosed in camelids
- detection of fluke eggs is challenging
- sedimentation procedure for F hepatica
- biochemistry - liver damage, evidence of cholestasis (increased GGT)
how is liver fluke treated in camelids
triclabendazole relatively successful
