Equine 7 Flashcards
(96 cards)
1
Q
describe the roles of the liver
A
protein metabolism (plasma proteins and amino acids)
energy metabolism (carbohhydrates and lipids)
detoxification (drug metabolism and bile excretion)
monomuclear phagocyte system (kuppfer cells)
2
Q
when are kuppfer cells active
A
part of the reticulo-endothelial system. active in ethanol induced liver injury but also endotoxin internalisation and activation of subsequent inflammatory cascade
3
Q
what are the common clinical signs of hepatic dysfunction in horses
A
weight loss icterus (hyperbilirubinaemia) hepatic encephalopathy colic - stretching of capsule due to acute hepatocellular swelling or biliary obstruction (choleliths) depression
4
Q
what are the rare signs of hepatic dysfunction in horses
A
photosensitisation diarrhoea (portal hypertension or biliary acid deficiency) bilateral laryngeal paralysis bleeding ascites dependent oedema (hypoalbuminaemia )
5
Q
what are the very rare signs of hepatic dysfunction
A
steatorrhoea tenesmus generalised seborrhoea puritus endotoxic shock polydipsia pigmenturia
6
Q
what are the signs of hepatic encephalopathy
A
circling head pressing ataxia yawning behaviour change seizures (rare) respiratory noise with laryngeal paralysis
7
Q
why do signs occur in hepatic encephalopathy
A
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
8
Q
how is hepatic encephalopathy managed
A
seizure control - sedation - barbiturates - not diazepam supportive care resolve liver issues
9
Q
how does phylloerythrin cause photosensitisation
A
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)
10
Q
how does St John’s wort toxicity lead to photosensitisation
A
hypercin is absorbed by the body and activated by exposure to sunlight causing photosensitivity
liver function is normal
11
Q
describe coagulopathy due to liver disease in horses
A
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
12
Q
which measure indicate liver function in horses
A
bilirubin (ideally conjugated and unconjugated separately)
ammonia
bile acids
dye clearance test - rarely used
13
Q
which measures indicate hepatic insult
A
liver enzymes - SDH (hepatocellular damage) - GGT (biliary damage) - GLDH (hepatocellular damage) less specific - AST - ALP - LDH
14
Q
which prehepatic factors may cause hyperbilirubinaemia
A
increased production due to haemolysis
liver can’t keep up so see increased unconjugated bilirubin
high in foals due to foetal Hb metabolism
15
Q
which intra-hepatic factors may cause hyperbilirubinaemia
A
impaired hepatic uptake - anorexia
see unconjugated bilirubin due to lack of process.
no haemolysis plus increased unconjugated bilirubin = liver problem
16
Q
which post hepatic factors may cause hyperbilirubinaemia
A
impaired excretion
- biliary obstruction (cholangitis, hepatitis)
- normal liver, obstruction further down
mainly see conjugated bilirubin
17
Q
how is ammonia measured and what may it indicate
A
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
18
Q
what is the significance of bile acid testing
A
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
19
Q
what may cause cell necrosis in the liver
A
hepatocellular disease biliary disease drugs hypoxia endotoxaemia
20
Q
how may albumin change in liver disease
A
rarely decreases due to long half-life (20 days)
takes up to three weeks for detectable changes
21
Q
how may liver biopsies help the diagostic process
A
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
22
Q
describe the site and prep for liver biopsy
A
may determine clotting functio n sedation local anaesthesia US guidance 12-14th RIC or 5-8th LIC haemoperitoneum common but not significant
23
Q
how is prognosis of liver disease determined
A
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
24
Q
what may cause focal hepatic injury
A
abscess
neoplasia
zonal hypoxic injury
25
what may cause acute generalised injury
tyzzer's disease
infectious necrotic hepatitis
toxins
(all rare)
26
what may cause chronic generalised injury
biliary hyperplasia and nodular regeneration caused by
inflammation
hypoxia
anti-mitotic agents
27
what toxin does ragwort contain
pyrrolizidine alkaloids
28
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
29
what may be seen on liver histopathology in pyrrolizidine alkaloids toxicity
fibrosis
megalocytes
bile duct proliferation
30
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
31
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
32
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
```
33
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
34
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)
```
35
what is cholangiohepatitis
inflammation of hepatocytes and biliary tree
36
describe primary cholangiohepatitis
Also termed chronic active hepatitis
| Clinical signs often vague and include weight loss, depression, poor performance, anorexia, icterus and fever
37
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
38
what are the causes of secondary cholangiohepatitis
```
cholelithiasis
duodenal inflammation
intestinal obstruction
neoplasia
parasitism
certain toxins
```
39
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
40
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
41
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
42
what specific treatments for cholangiohepatitis are there
Neutrophils predominate on biopsy - Antibiotics
| Plasma cells and lymphocytes predominate on biopsy - steroids
43
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
44
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
```
45
what are the risk factors for hyperlipaemia
```
• Obesity
• Breed
○ Shetland
○ Miniatures
○ Ponies
○ Donkeys
• Gender
○ Female
○ Pregnancy/lactation
• Stress
• Disease
• Anorexia
• Malnutrition
```
46
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
```
47
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
48
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
= Glucose
```
49
how is hyperlipaemia treated
```
treat underlying causes
fluid therapy - 5% dextrose
PPN +/- insulin
enteral nutrition
BCAA supplementation - valine, leucine, isoleucine
```
50
what is the prognosis of hyperlipaemia
poor - 60-100% mortality
| in those that survive, triglycerides normal in 3-10 days
51
how is hyperlipaemia prevented
avoid breeding or transport of obese animals
controlled exercise and feed intake
avoid drastic weight reduction
52
what term is used to describe camelids due to their three chambered forestomach
pseudoruminants
53
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.
54
describe C2 in camelids
connecting tube carrying C1 content through to C3
55
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.
56
how many lips does the oesophageal groove have in camelids
only one (compared to two in cows)
57
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
58
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
59
why is it important to take care if performing flank laparotomy in camelids
thin abdominal musculature
| herniation more likely (need two layer wall closure)
60
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
61
do cameldis have a gall bladder
no - same as a horse
62
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
63
what role do saccules in the ventral regions of C1 play
microfermentation
64
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
65
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
```
66
which colic lesion will cause the most severe signs in camelids
SI lesions > forestomach and LI
67
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
```
68
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
```
69
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
```
70
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)
```
71
what stressors may lead to C3 ulceration
environmental
social
metabolic
72
what proportion of C3 in camelids is glandular
distal 20% - glandular and acid-secreting
| the other 80% is glandular
73
what are the signs of C3 ulceration in camelids
colic
increased heart and resp rate
regurgitation, excessive salivation, copious saliva in mouth (mostly weanlings)
74
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)
75
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
```
76
what are the clinical signs of megaoesophagus in camelids
```
weight loss
respiratory disease
vomiting
ptyalism
choke
stomach ulcers
bad teeth
halitosis
```
77
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.
78
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
79
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
80
what GI parasites affect camelids in the UK
```
• Roundworms
○ Strongyles (eg Haemonchus, Ostertagia and Trichostrongylus)
○ Nematodirus
• Whipworms
○ Trichuris
• Tapeworms
= Moniezia
```
81
what are the clinical signs of parasitic gastroenteritis in camelids
```
• ill-thrift
• weight-loss
• Diarrhoea
• Colic
• Anaemia
• Lethargy
- Anorexia
```
82
how 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
83
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
84
what is the maximum stocking density of camelids
7 alpacas or 5 llamas per acre of pasture
85
which wormers may be used in camelids
BZDs - fenbendazole has high index of safety
pyrantel pamoate
praziquantel
levamisole
86
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
87
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
88
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
89
what are the clinical signs of coccidiosis in camelids
enteritis
diarrhoea (may be haemorrhagic)
tenesmus
90
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
```
91
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
92
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
93
which species of liver fluke affect camelids
fasciola hepatica - more of an issue in the UK especially wetter areas
dicrocoelium dendriticum
94
what are the clinical signs of liver fluke in camelids
acute/chronic/fatal forms
- reduced appetite
- generalised weakness
- recumbency
- anaemia
95
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)
96
how is liver fluke treated in camelids
triclabendazole relatively successful
