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GI2 > Equine 7 > Flashcards

Equine 7 Flashcards

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)

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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

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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
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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 )
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5
Q

what are the very rare signs of hepatic dysfunction

A 
steatorrhoea 
tenesmus 
generalised seborrhoea 
puritus 
endotoxic shock 
polydipsia 
pigmenturia
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6
Q

what are the signs of hepatic encephalopathy

A 
circling 
head pressing 
ataxia 
yawning 
behaviour change 
seizures (rare)
respiratory noise with laryngeal paralysis
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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

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8
Q

how is hepatic encephalopathy managed

A 
seizure control 
- sedation 
- barbiturates 
- not diazepam 
supportive care 
resolve liver issues
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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)

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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

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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

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12
Q

which measure indicate liver function in horses

A

bilirubin (ideally conjugated and unconjugated separately)
ammonia
bile acids
dye clearance test - rarely used

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13
Q

which measures indicate hepatic insult

A 
liver enzymes 
- SDH (hepatocellular damage)
- GGT (biliary damage) 
- GLDH (hepatocellular damage)
less specific 
- AST
- ALP
- LDH
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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

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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

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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

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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

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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

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19
Q

what may cause cell necrosis in the liver

A 
hepatocellular disease 
biliary disease 
drugs 
hypoxia 
endotoxaemia
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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

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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

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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
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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

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24
Q

what may cause focal hepatic injury

A

abscess
neoplasia
zonal hypoxic injury

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25
Q

what may cause acute generalised injury

A

tyzzer’s disease
infectious necrotic hepatitis
toxins
(all rare)

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26
Q

what may cause chronic generalised injury

A

biliary hyperplasia and nodular regeneration caused by
inflammation
hypoxia
anti-mitotic agents

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27
Q

what toxin does ragwort contain

A

pyrrolizidine alkaloids

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28
Q

how do pyrrolizidine alkaloids cause liver damage

A

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

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29
Q

what may be seen on liver histopathology in pyrrolizidine alkaloids toxicity

A

fibrosis
megalocytes
bile duct proliferation

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30
Q

what is clinical presentation of pyrrolizidine alkaloids toxicity

A

1-6months after ingestion as damage is cumulative
weight loss
laryngeal paralysis
increased plasma activities of liver derived enzymes

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31
Q

how is pyrrolizidine alkaloids diagnosed and treated and how is prognosis determined

A

diagnose on histology
no specific antidote
supportive therapy - high protein, palatable diet
poor prognosis: serum bile acid >50umol/l or extensive fibrosis on histopathology

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32
Q

what is tyzzer’s disease

A 
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
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33
Q

what is infectious necrotis hepatitis

A

clostridium novyi type B (black disease)
progressive, acute clinical signs for 24-72 hours leading to death.
treat with penicillin but no reported survivors

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34
Q

which toxins may cause acute liver damage

A 
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)
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35
Q

what is cholangiohepatitis

A

inflammation of hepatocytes and biliary tree

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36
Q

describe primary cholangiohepatitis

A

Also termed chronic active hepatitis

Clinical signs often vague and include weight loss, depression, poor performance, anorexia, icterus and fever

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37
Q

how is primary cholangiohepatitis diagnosed

A

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

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38
Q

what are the causes of secondary cholangiohepatitis

A 
cholelithiasis 
duodenal inflammation 
intestinal obstruction 
neoplasia 
parasitism 
certain toxins
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39
Q

describe cholelithiasis

A

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
Q

how is liver disease managed

A

dextose IV - reduce ammonia and enteric production of toxins
highly palatable, high carbohydrate, low protein diet
B vitamins and folic acid
supplement ADEK

41
Q

describe some specific liver disease treatments

A
  • 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
Q

what specific treatments for cholangiohepatitis are there

A

Neutrophils predominate on biopsy - Antibiotics

Plasma cells and lymphocytes predominate on biopsy - steroids

43
Q

describe specific treatments for cholelithiasis

A

TMPS, penicillin, gentamicin for ascending infection

Treat for 2 weeks after clinical signs resolve - DMSO may help to dissolve choleliths

44
Q

what are the clinical signs of hyperlipaemia

A 
initial 
- anorexia 
- lethargy 
- weakness 
progression 
- reluctance to move 
-in-coordination 
- dysphagia 
- head pressing, circling 
- recumbency, paddling of legs, nystagmus 
- convulsions 
- profound depression, coma
45
Q

what are the risk factors for hyperlipaemia

A 
• Obesity 
	• Breed 
		○ Shetland
		○ Miniatures 
		○ Ponies 
		○ Donkeys 
	• Gender 
		○ Female 
		○ Pregnancy/lactation 
	• Stress
	• Disease
	• Anorexia 
	• Malnutrition
46
Q

which disease are associated with hyperlipaemia

A 
• Intestinal parasitism 
	• Enteritis/colitis 
	• Gastric/large colon impactions 
	• Dysphagia 
	• Lymphosarcoma 
	• Equine hyperadrenocorticism 
	• Peritonitis 
	• Metritis 
Anything that causes negative energy balance
47
Q

describe the pathophysiologgy of liver disease

A

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
Q

how is hyperlipaemia diagnosed

A 
• Plasma triglyceride 
		○ >5mmol/L = hyperlipaemia 
		○ 1.5-5mmol/L = at risk, hyperlipidaemia 
	• Other abnormalities - liver markers elevated 
		○ GGT
		○ ALP
		○ SDH
		○ Bile acids 
                = Glucose
49
Q

how is hyperlipaemia treated

A 
treat underlying causes 
fluid therapy - 5% dextrose 
PPN +/- insulin 
enteral nutrition 
BCAA supplementation - valine, leucine, isoleucine
50
Q

what is the prognosis of hyperlipaemia

A

poor - 60-100% mortality

in those that survive, triglycerides normal in 3-10 days

51
Q

how is hyperlipaemia prevented

A

avoid breeding or transport of obese animals
controlled exercise and feed intake
avoid drastic weight reduction

52
Q

what term is used to describe camelids due to their three chambered forestomach

A

pseudoruminants

53
Q

describe C1 in camelids

A

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
Q

describe C2 in camelids

A

connecting tube carrying C1 content through to C3

55
Q

describe C3 in camelids

A

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
Q

how many lips does the oesophageal groove have in camelids

A

only one (compared to two in cows)

57
Q

what shape is the camelid colon and what problems may occur

A

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
Q

describe the caecum and omentum in camelids

A

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
Q

why is it important to take care if performing flank laparotomy in camelids

A

thin abdominal musculature

herniation more likely (need two layer wall closure)

60
Q

describe the liver in camelids

A

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
Q

do cameldis have a gall bladder

A

no - same as a horse

62
Q

how is function of C1 assessed

A

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
Q

what role do saccules in the ventral regions of C1 play

A

microfermentation

64
Q

where do ulcers generally develop in camelids

A

lesser curvature of the third compartment at the junction of the glandular and non-glandular mucosa and duodenum

65
Q

what is the most important tool in camelid GI medicine

A 
ultrasound 
- cannot easily palpate abdomen 
- signs often similar despite cause 
- physical exam often similar despite cause 
bloodwork next step
66
Q

which colic lesion will cause the most severe signs in camelids

A

SI lesions > forestomach and LI

67
Q

what are the clinical signs of colic in camelids

A 
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
Q

what are the causes of colic in camelids

A 
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
Q

what diagnostic steps are used in colic in camelids

A 
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
Q

what are the indications for abdominal surgery in camelids

A 
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
Q

what stressors may lead to C3 ulceration

A

environmental
social
metabolic

72
Q

what proportion of C3 in camelids is glandular

A

distal 20% - glandular and acid-secreting

the other 80% is glandular

73
Q

what are the signs of C3 ulceration in camelids

A

colic
increased heart and resp rate
regurgitation, excessive salivation, copious saliva in mouth (mostly weanlings)

74
Q

how are C3 ulcers diagnosed in camelids

A

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
Q

how are C3 ulcers treated in camelids

A 
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
Q

what are the clinical signs of megaoesophagus in camelids

A 
weight loss 
respiratory disease 
vomiting 
ptyalism 
choke 
stomach ulcers 
bad teeth 
halitosis
77
Q

what are the potential causes of megaoesophagus in camelids

A

• 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
Q

how is megaoesophagus diagnosed in camelids

A

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
Q

how is megaoesophagus treated in camelids

A

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
Q

what GI parasites affect camelids in the UK

A 
• Roundworms 
		○ Strongyles (eg Haemonchus, Ostertagia and Trichostrongylus) 
		○ Nematodirus 
	• Whipworms 
		○ Trichuris 
	• Tapeworms 
                = Moniezia
81
Q

what are the clinical signs of parasitic gastroenteritis in camelids

A 
• ill-thrift
	• weight-loss
	• Diarrhoea
	• Colic
	• Anaemia
	• Lethargy
        - Anorexia
82
Q

how is parasitism diagnosed in camelids

A

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
Q

how are GI parasites treated in camelids

A

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
Q

what is the maximum stocking density of camelids

A

7 alpacas or 5 llamas per acre of pasture

85
Q

which wormers may be used in camelids

A

BZDs - fenbendazole has high index of safety
pyrantel pamoate
praziquantel
levamisole

86
Q

which drugs are contraindicated in camelids

A

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
Q

which ages of camelids are most susceptible to coccidiosis

A

neonates and juveniles.
adults more resistance due to mature immune systems and prior exposure
associated with overcrowding and poor hygiene

88
Q

decribe the life cycle of coccidia

A

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
Q

what are the clinical signs of coccidiosis in camelids

A

enteritis
diarrhoea (may be haemorrhagic)
tenesmus

90
Q

which species of Eimeria have been identified in camelids

A 
lamae
alpacae
 macusaniensis - oocyst much larger than the other species (81-107um) and very thick wall 
ivitaensis
punoensis 
peruviana
91
Q

how is coccidiosis treated in camelids

A

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
Q

how is coccidiosis prevented in camelids

A

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
Q

which species of liver fluke affect camelids

A

fasciola hepatica - more of an issue in the UK especially wetter areas
dicrocoelium dendriticum

94
Q

what are the clinical signs of liver fluke in camelids

A

acute/chronic/fatal forms

  • reduced appetite
  • generalised weakness
  • recumbency
  • anaemia
95
Q

how is liver fluke diagnosed in camelids

A
  • detection of fluke eggs is challenging
  • sedimentation procedure for F hepatica
  • biochemistry - liver damage, evidence of cholestasis (increased GGT)
96
Q

how is liver fluke treated in camelids

A

triclabendazole relatively successful

GI2 (27 decks)

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