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Equine (fourth year) > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

what are the four mechanisms that cause weight loss?

A

reduced intake
reduced digestion, absorption or assimilation
increased losses
increased requirements

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2
Q

what are the three most common causes of weight loss?

A

dental disorder
parasitism
inadequate diet

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3
Q

what are some possible reasons for malabsorption and protein losing enteropathy?

A

idiopathic, parasites, infiltrative bowel disease, neoplasia

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4
Q

what % of body weight should a horse be consuming in hay?

A

2.5%

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5
Q

what is chronic colic?

A

colic signs of varying intensity lasting more than 48 hours

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6
Q

what is recurrent colic?

A

shorter periods of colic pain with recur at variable intervals

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7
Q

what are the four types of intestinal pain?

A

stretch
inflammation
ischaemia
muscle spasm

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8
Q

what are the two main locations colics can be split into?

A

GI or non-intestinal

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9
Q

what should be investigated/questioned in cases of colic?

A

number/nature of previous colics
faecal output
diet (water/feed access…)
worming history
dental disease and quidding
crib biting/wind sucking
sand??

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10
Q

what can running bloods help to rule in/out of chronic colic cases?

A

specific organ disease (enzymes, bile…)
inflammatory process (WBC, fibrinogen, globulins…)
protein loss (albumin…)

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11
Q

what causes verminous arteritis?

A

strongyles vulgaris (mesenteric artery)

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12
Q

what can mask a possible decrease in total protein?

A

concurrent dehydration

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13
Q

what are the four possible causes of hypoalbunminaemia?

A

protein losing nephropathy
protein losing enteropathy
effusions (peritoneal/pleural)
liver disease

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14
Q

how does albumin change in response to chronic inflammation?

A

goes down (negative acute phase protein)

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15
Q

what are the two main positive acute phase proteins?

A

fibrinogen
serum amyloid A

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16
Q

what are the three general causes of hyperfibrinogenaemia?

A

infection
inflammation
neoplasia

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17
Q

how should peritoneal fluid appear?

A

clear and light yellow

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18
Q

if peritoneal fluid appears red (serosanguinous) with acute colic present, what does this suggest?

A

diapedesis is occurring (blood moving into peritoneal cavity) which usually suggests a strangulating colic

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19
Q

what can neutrophils tell us about the nature of a peritonitis?

A

whether it is septic or not

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20
Q

if there are more degenerate neutrophils present in a peritonitis case, what can be suggested about the nature of this?

A

it is septic (caused by bacteria)

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21
Q

how do neutrophils appear in cases of non-septic peritonitis?

A

hyper-segmented mature nuclei

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22
Q

what can be assessed on intestinal ultrasound?

A

wall thickness
lumen diameter
motility
anatomy

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23
Q

what is the most common reason for increased wall thickness of the GI tract?

A

inflammation

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24
Q

what structures are found on the right hand side of the abdomen?

A

large intestine - caecum, right dorsal colon, right ventral colon

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25
Q

what part of the colon does the caecum empty into?

A

right ventral colon

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26
Q

what is the majority of the left side of the abdomen taken up by?

A

spleen

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27
Q

why is the pelvic flexure a common site for impaction?

A

it is a narrow bend

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28
Q

how many intercostal spaces should the stomach take up?

A

no more than 5 (suggests its enlarged/distended if its more than this)

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29
Q

where will small intestines be found if filled with fluid?

A

bottom of the abdomen

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30
Q

what can be done to test absorption of nutrients in horses?

A

glucose absorption test - give a set amount of glucose and see how much the small intestine absorbs (greater than 85%)

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31
Q

what parts of the GI tract can be biopsied rectally?

A

rectum and duodenum

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32
Q

what are the categories of inflammatory/infiltrative bowel disease?

A

granulomatous enteritis
lymphocytic-plasmacytic enteritis
eosinophilic enteritis

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33
Q

what is multi systemic eosinophilic epitheliotropic disease?

A

eosinophils attack anything with epithelial lining - coronary band, pancreas, skin, liver…

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34
Q

what neoplasia can be strongly associated with weight loss?

A

lymphoma

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35
Q

what are some paraneoplastic syndromes associated with lymphoma?

A

hypercalcaemia
haemolytic anaemia
cachexia

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36
Q

what is the treatment of inflammatory bowel disease?

A

prednisolone
dexamethasone

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37
Q

what needs to be monitored when giving dexamethasone to horses?

A

laminitis

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38
Q

what is a common cause of chronic bacterial colic?

A

bastard strangles (and other abscesses…)

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39
Q

what are the functions of the equine liver?

A

digestive/secretory (bile salts)
metabolic (CHO, protein, fat)
detoxification/excretory
synthetic (clotting factors, proteins)
storage (vitamins, minerals)

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40
Q

what is the first stage of testing when suspecting liver disease?

A

blood analysis (confirms liver disease/damage)

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41
Q

what is needed to determine the severity of pathology and prognosis of liver disease?

A

liver biopsy, blood analysis, clinical signs

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42
Q

how much of the liver function has to be lost for them to show signs of failure?

A

> 70%

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43
Q

what is jaundice?

A

retention of bilirubin (yellow staining of tissue)

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44
Q

what are the three main differentials for jaundice?

A

anorexia (usually mild)
haemolysis
liver failure

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45
Q

what are some clinical signs of liver disease?

A

jaundice
weight loss
depression/CNS signs
skin lesions
haemorrhage
colic (stretching of liver)
oedema
diarrhoea
bilateral laryngeal paralysis

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46
Q

what are some possible CNS signs of liver disease?

A

quiet/dull
yawning
somnolence (sleepy)
central blindness
head pressing
compulsive walking
sham chewing

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47
Q

why does liver disease cause CNS signs?

A

toxins build up

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48
Q

what is the most common skin lesion associated with liver disease?

A

photosensitisation
(can cause pruritus and coronitis)

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49
Q

what can cause hepatic photosensitisation?

A

phylloerythrin accumulation
primary - tetracyclines, st johns wart
immune mediated vasculitis

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50
Q

what are the most common sites of photosensitisation?

A

depigmented skin exposed to sunlight

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51
Q

why can liver disease cause bilateral laryngeal paralysis?

A

recurrent laryngeal nerve is very long (longest axon in body) - more susceptible to damage

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52
Q

what is tested for in blood to show liver damage?

A

liver enzymes

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53
Q

what liver enzymes are specific to the liver?

A

GGT, SDH, GLDH

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54
Q

what is the origin of GGT in the liver?

A

biliary

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55
Q

what is the origin of the SDH and GLDH in the liver?

A

hepatocellular

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56
Q

what liver enzymes are of biliary origin?

A

biliary

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57
Q

what are the other sources of ALP? (other than liver)

A

bone, intestine, kidney, placenta

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58
Q

what do liver enzymes in blood indicate?

A

degree of damage/disease not the function

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59
Q

what does increased GGT and ALP indicate about the type of liver disease?

A

biliary

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60
Q

what does increased AST, GLDH and LDH indicate about the type of liver disease?

A

hepatocellular

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61
Q

what is the most useful test to determine liver function?

A

bile acids

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62
Q

what happens to the majority of secreted bile acids?

A

reabsorbed in SI and return via enterohepatic circulation

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63
Q

what are the three forms bilirubin can be measured in?

A

total
conjugated
unconjugated

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64
Q

where does most bilirubin originate from?

A

RBC and haemoglobin breakdown

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65
Q

what produces unconjugated bilirubin?

A

macrophages breaking down RBCs

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66
Q

what does the liver do to bilirubin?

A

conjugate it which is then excreted into the intestine

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67
Q

what are some causes of increased unconjugated bilirubin?

A

liver failure, haemolysis, anorexia, intestinal obstruction, Gilberts syndrome

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68
Q

what can cause an increase in conjugated bilirubin?

A

cholestasis and hepatocellular failure

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69
Q

why is ammonia difficult to measure?

A

very volatile (evaporates rapidly from sample)
RBCs produce ammonia so will increase as sample stands

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70
Q

why does poor liver function cause an increase in ammonia?

A

liver turns ammonia to urea which is excreted, poor function means this doesn’t occur

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71
Q

what are some non-specific changes on blood analysis that points towards liver disease?

A

decreased urea
increased globulins
increased triglycerides
decreased protein synthesis

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72
Q

how should the liver appear compared to the spleen on ultrasound?

A

liver should be darker (hypoechoic)
if same greyness, liver has been infiltrated by fibrous tissue…

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73
Q

what are some possible complications of liver biopsy? (these are rare)

A

haemorrhage
inappropriate sample (focal lesions)
infection

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74
Q

what can liver biopsy be used to predict?

A

prognostic outcome

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75
Q

what is the toxin in ragwort?

A

pyrrolizidine alkaloid

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76
Q

what makes ragwort palatable?

A

when it is dried in hay (horses rarely eat when at pasture)

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77
Q

how does ragwort poisoning mainly present?

A

signs of liver failure (weight loss, behavioural change, anorexia)

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78
Q

should ragwort poisoning be treated?

A

not if bile acids >50 mol/L

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79
Q

how can ragwort be treated?

A

supportive - fluids, glucose, endotoxaemia treatment
low protein diet (reduce hepatic encephalopathy)

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80
Q

how does the liver usually present in cases of cholangiohepatitis and cholelithiasis?

A

swollen

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81
Q

what is the main treatment of chronic active hepatitis?

A

corticosteroids (immunosuppressive medication)

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82
Q

what should the diet of a horse with liver disease consist of?

A

carbohydrate based
moderate amounts of high quality protein
fat soluble vitamin supplement

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83
Q

how will hyperlipaemia present in a blood tube?

A

dense, white, cloudy serum (looks like fat in severe cases)

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84
Q

what are the risk factors for hyperlipaemia?

A

breed
obesity
females
age (insulin sensitivity)
underlying disease
stress/transport
starvation

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85
Q

why does starvation cause hyperlipaemia?

A

horse in negative energy balance so begin breaking down fat into blood (horses can’t produce ketones)

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86
Q

what animal do we worry about hyperlipaemia most in?

A

donkeys

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87
Q

what are the clinical signs of hyperlipaemia?

A

non-specific (anorexia, lethargy, weakness) - not eating then makes the hyperlipaemia worse

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88
Q

what is done to treat hyperlipaemia?

A

treat underlying disease
get in positive energy balance
correct dehydration, electrolytes and acidosis
insulin therapy (laminitis risk)

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89
Q

what is the prognosis of hyperlipidaemia?

A

guarded (especially in donkeys) - worse in females

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90
Q

what is colic?

A

a clinical sign of abdominal pain

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91
Q

what are some horse level risk factors for colic?

A

some specific colic have a age/sex predilection
stereotypies - wind sucking…

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92
Q

what age horses are predisposed to pedunculate lipoma?

A

older horses

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93
Q

what types of colic do crib-biting/wind-sucking predispose to?

A

epiploic foramen entrapment
simple colonic obstruction
recurrent colic

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94
Q

what are some management level risk factors for colic?

A

geography - sand, grass sickness…
season - housing…
feed types/practices - concentrates, changes…
increased stabling
dental disease
parasites and anthelmintics
water access
transport

95
Q

why is it important to provide advice to owners about colic when their animal has it?

A

reoccurrence is common so management may need to be altered

96
Q

what is the most common site for a pedunculate lipoma?

A

small intestine

97
Q

what are the predisposing factors for pedunculate lipoma strangulation?

A

older horses
more common in ponies than horses
more common in geldings than mares

98
Q

what are the risk factors for large colon volvulus?

A

mares post foaling
larger horses
increased stabling
dental disease
changes in feed

99
Q

what are the risk factors for large colon impaction?

A

stabling (autumn/winter) - box rest
straw bedding

100
Q

what are some risk factors for epiploic foramen entrapment?

A

increased stabling (seasonal)
crib biting and wind sucking

101
Q

what are good factors for predicting mortality in colic cases?

A

reaction length
PCV and heart rate
duration of surgery
post operative complications

102
Q

what are some possible post-operative complications (and colic) for colic cases?

A

ileus, surgical site infection, jugular thrombosis

103
Q

what is equine grass sickness also known as?

A

equine dysautonomia

104
Q

what do clinical signs of equine grass sickness relate to?

A

neuronal degeneration of autonomic and enteric nervous system

105
Q

what are the signs of acute equine grass sickness?

A

colic, reflux, tachycardia, SI distention, sweating, salivation, swallowing difficulty, ptosis

106
Q

what is ptosis?

A

drooping of upper eyelid

107
Q

what are the clinical signs of chronic equine grass sickness?

A

weight loss, dysphagia, tachycardia, patchy sweating, muscle fasciculation, rhinitis sicca
‘elephant on a barrel’ stance

108
Q

what age horses is grass sickness most commonly seen in?

A

2-7 years old

109
Q

what time of year is equine grass sickness seen?

A

spring (April/May)
also peaks in Autumn sometimes

110
Q

what does space-time clustering o0f grass sickness mean?

A

when you see a case you are more likely to see another case close by at a similar time

111
Q

what is the prognosis for grass sickness?

A

often fatal

112
Q

what are the management risk factors for grass sickness?

A

access to grass
recent pasture change
pasture disturbance

113
Q

what are the indications that a colic can be treated medically?

A

mild-moderate pain
good response to analgesia
HR <50
improving GI motility
no net reflux
resolving/no abdominal distention
normal peritoneal fluid
normal PCs and lactate

114
Q

what are the two main principles of medically treating colic?

A

analgesia and fluids

115
Q

what needs to be considered about an analgesic in colic cases?

A

potency
duration of action
other effects (wanted and unwanted)

116
Q

what are the main categories of analgesics for colic?

A

NSAIDs
alpha 2 agonists
opiates

117
Q

what NSAIDs are available for colic cases?

A

phenylbutazone
flunixin meglumine
metimazole
ketoprofen
meloxicam

118
Q

how potent is phenylbutazone when treating colic?

A

moderate (12 hour duration)

119
Q

what pain severity colic would phenylbutazone be used for?

A

mild/moderate (good first line)

120
Q

why should care betaken when giving flunixin meglumine to treat mild/moderate colic pain?

A

can mask increased HR caused by SIRS (endotoxaemia) - horse could be developing a strangulation etc.

121
Q

how strong of an analgesic is flunixin meglumine?

A

very potent

122
Q

what are the alpha 2 agonists available for analgesia of colic?

A

xylazine
romifidine
detomidine

123
Q

what colic cases is xylazine useful for?

A

very painful when wanting to assess patient (short duration of action)

124
Q

what is romifidine usually combined with in colic cases?

A

butorphanol (opiate)

125
Q

what colic cases would romifidine be a useful analgesic?

A

if horse is needle shy (IM administration)
moderate-severe pain

126
Q

what is detomidine usually combined with in colic cases?

A

butorphanol (opiate)

127
Q

what opiates are available for colic cases?

A

butorphanol
pethidine
morphine

128
Q

what colic pain is butorphanol used to treat?

A

moderate-severe

129
Q

when should morphine not be used in colic cases?

A

in first opinion practice

130
Q

what is the effect of butylscopolamine?

A

smooth muscle relaxant

131
Q

what types of colic is butylscopolamine indicated for?

A

spasmodic colic with mild pain
(useful when performing rectal - minimise risk of tear)

132
Q

why may the use of flunixin for colic cases not be recommended?

A

it masks colic pain and the effects of SIRS making assessment of colic difficult (if has got SIRS want to treat ASAP)

133
Q

when is flunixin use for colic cases acceptable?

A

referral not an option and horse has moderate/severe pain (otherwise euthanised)
when exact diagnosis is known

134
Q

how much water/electrolyte should be administered orally to a horse with colic?

A

4-6L (500kg horse) every 4 hours

135
Q

what type of colic can oral fluid aid to assist the resolution of?

A

large colon impaction (hydrate ingesta)

136
Q

when are IV fluids indicated for colic?

A

reflux obtained on nasogastric intubation
severe systemic compromise

137
Q

what is used to effectively treat most cases of spasmodic colic?

A

butylscopolamine and NSAID (metimazole)

138
Q

what causes the pain in spasmodic colic cases?

A

intestinal spasm

139
Q

how severe is pain associated with large colon impaction?

A

mild/moderate

140
Q

what is the classical finding when rectalling a horse with large colon impaction?

A

doughy, firm structure on left of caudal abdomen

141
Q

what is the classic epidemiological clue that the horse presenting with colic has large colon impaction?

A

recent increase in stabling (injury, weather…)

142
Q

how are large colon impactions treated?

A

oral fluids every 4 hours until faeces are passed (magnesium sulphate)
analgesia - flunixin meglumine
can require surgery - clinical parameters, progress…

143
Q

how can gastric impaction be confirmed?

A

gastroscopy

144
Q

how are gastric impactions treated?

A

medically or surgically depending on severity and clinical presentation
IV fluids and carbonated drinks

145
Q

when can a large intestinal displacement/distention be managed medically?

A

normal CV parameters
mild/moderate pain
no marked gaseous distention of large colon

146
Q

what is the initial medical therapy used to treat large intestinal displacement/distention?

A

analgesia
light walk/trot
oral fluid
feed withheld until passing faeces

147
Q

what is left dorsal displacement of the large intestine also known as?

A

nephrosplenic entrapment

148
Q

how can nephrosplenic entrapment be diagnosed?

A

rectal
ultrasound - failure to image left kidney/spleen due to gas

149
Q

what is usually the initial treatment for nephrosplenic entrapment? and why?

A

phenylephrine infusion - shrinks spleen to try get gut to move

150
Q

how can sand cause colic?

A

irritation of colon mucosa (diarrhoea and mild recurrent colic)
colonic impaction

151
Q

how can sand colic be diagnosed?

A

sand in faeces
seashore sound on auscultation
ultrasound/radiography

152
Q

what is not a good way of differentiating if a neonatal colic is medical or surgical?

A

pain (foals are wimps)

153
Q

what are the most likely causes of neonatal colic?

A

meconium impaction
enteritis
SI volvulus
congenital abnormalities

154
Q

how is meconium impaction colic treated?

A

enema

155
Q

what are the most common colics associated with donkeys?

A

colonic impaction

156
Q

what advice would you give to an owner after you have been to look/treat a horse with colic?

A

remove feed and provide water
ask for update in 2 hours (unless signs worsen)
offer small amounts of feed once faeces passed

157
Q

what advice would you give to an owner regarding colic prevention?

A

parasite testing/control
dental exam/treatment
general management - feed, stabling…

158
Q

when would euthanasia be considered an option in colic cases?

A

uncontrollable pain
severe CV compromise (HR> 90, PCV >60, purple MM)
GI rupture - brown/red ingesta in peritoneal fluid

159
Q

what are the signs of GI rupture in horses?

A

marked increase in HR, PCV and MM deterioration
dark red/brown peritoneal fluid with ingesta in

160
Q

what are the indications for surgery in colic cases?

A

severe, unrelenting pain
recurrance of pain even with moderate/potent analgesia (most important)
HR >60bpm
net reflux >2L
deteriorating CV parameters
reduced intestinal motility
increased abdominal distention
deteriorating peritoneal fluid values

161
Q

what are the indications for surgery in colic cases?

A

severe, unrelenting pain
recurrence of pain even with moderate/potent analgesia (most important)
HR >60bpm
net reflux >2L
deteriorating CV parameters
reduced intestinal motility
increased abdominal distention
deteriorating peritoneal fluid values

162
Q

what are common types of small intestinal surgical colics?

A

pedunculated lipoma
epiploic foramen entrapment

163
Q

what are common types of large intestinal surgical colics?

A

large colon displacement
large colon torsion

164
Q

what is the order of doing initial exploration for colic using a midline abdominal excision?

A

exteriorise caecum then trace to ileum
exteriorise SI
exteriorise large colon (palpate RVC and RDC)
exteriorise small colon (palpate down to rectum)

165
Q

what are some possible complications of small intestinal resection?

A

leakage
mesenteric rent
lumen too narrow

166
Q

does a jejuna-caecostomy have a better or worse prognosis than small intestinal anastomosis?

A

worse

167
Q

what is a common cause of cecal colic?

A

high tapeworm burden causing ileal impaction and caecal intussusception

168
Q

how is caecal intussusception treated?

A

surgical resection of caecum

169
Q

what are common primary colic lesions of the large colon?

A

impaction, displacement, torsion, enteroliths

170
Q

what is the most common site for enterotomy?

A

pelvic flexure

171
Q

why is pelvic flexure enterotomy useful?

A

assists correction of torsions/displacement and can confirm sand colic

172
Q

where is the incision for pelvic flexure enterotomy made?

A

immediately cranial to flexure (minimise lumen narrowing at the flexure)

173
Q

what is the most commonly used analgesia for post-operative colic management?

A

flunixin meglumine

174
Q

why is passing a stomach tube in post-operative colic cases important?

A

they can’t vomit - will rupture

175
Q

what is the nutritional management of large intestinal displacements post operatively?

A

offer water within 3 hours
offer feed from 6-12 hours

176
Q

what is an extremely important part of post-operative colic management?

A

walking horse (exercise and grass)

177
Q

what are some possible post-operative complications of colic surgery?

A

surgical site infection, dehiscence, colic, adhesions, SIRS…

178
Q

what is a common place for calculus build up in horses?

A

canines and corner incisors

179
Q

who can perform category one dental procedures?

A

anyone (includes examination, rasping, removing calculus…)

180
Q

who can perform category two dental procedures?

A

equine dentists (includes extraction of poorly attached teeth, wolf teeth (with vet supervision)…)

181
Q

what is the most likely cause of quidding (balling up)?

A

periodontal disease due to diastema

182
Q

what is the peridontium?

A

attachments of the tooth, gum and periodontal ligament

183
Q

what is periodontal disease most commonly caused by?

A

food trapping in diastema

184
Q

what age horse will typically have some caps coming loose and possibly causing periodontal disease?

A

2-4 years old

185
Q

what is oesophageal obstruction also known as?

A

choke

186
Q

what is the most common place for feed to become impacted in the oesophagus?

A

proximal cervical region
distal cervical region (thoracic inlet)

187
Q

what side of the neck does the oesophagus usually sit on?

A

left

188
Q

what are the clinical signs of choke?

A

sudden onset
coughing
ptyalism
dysphagia
extension/flexion of the neck

189
Q

what is ptyalism?

A

overproduction of saliva

190
Q

how is choke treated?

A

most will clear spontaneously (take all feed and water away)
if needed sedate (alpha 2) and pass a nasogastric tube to lavage the oesophagus

191
Q

what aftercare may be required in choke cases?

A

antimicrobials if risk of inhalation pneumonia
water and gradual reintroduce soft feed
check for underlying conditions
endoscope if recurrent

192
Q

what is done if an oesophageal food obstruction cannot be cleared?

A

leave alone for a bit and repeat lavage 8 hours later

193
Q

what is the prognosis of oesophageal tears/perforations?

A

poor/guarded

194
Q

what is essential to the treatment of carbohydrate overload?

A

early and aggressive treatment (not allowing fermentations and endotoxin absorption)

195
Q

what are two possible causes of disease associated with horses breaking into feed stores?

A

carbohydrate overload
additives (poultry - monensin…)

196
Q

what can be done to treat the early stages of carbohydrate overload?

A

lavage gastric content (within 2 hours of ingestion)
activated charcoal
flunixin
cryotherapy/ice feet (prevent laminitis)

197
Q

what can carbohydrate overload lead to that requires intense treatment?

A

SIRS

198
Q

what is dysphagia?

A

difficulty swallowing (or eating)

199
Q

what are the three main groups causing dysphagia?

A

pain, neurology, obstructive

200
Q

what are some causes of dysphagia relating to pain?

A

abscess, dental pathology, trauma, foreign body, masseter myositis…

201
Q

what are some causes of dysphagia relating to neurology?

A

lead, pharyngeal paralysis, head trauma, botulism, equine viral encephalitis…

202
Q

why do lip lacerations often heal very well?

A

very good blood supply (but can dehisce)

203
Q

what is the best way of suturing lip lacerations?

A

using multiple layers of sutures (at least 2)

204
Q

how are mandibular fractures treated?

A

sedate, nerve block and wire

205
Q

what are some possible causes of rectal prolapses?

A

diarrhoea, colic, heavy parasite burden, mass in rectum, dystocia…

206
Q

how are grade I, II or III rectal prolapses treated?

A

reduce prolpase and address underlying cause

207
Q

how are grade IV rectal prolapses treated?

A

surgical management

208
Q

what can cause haemabdomen?

A

abdominal trauma - splenic rupture/tears…

209
Q

what is the initial treatment used for incisional hernias?

A

conservative - prolonged box rest and hernia belt

210
Q

why are horses at increased risk of colic after anthelmintic administration?

A

high parasite burden being killed causing inflammation of mucosa (can give steroids in some cases to help with this)

211
Q

what colics can cyanthostominosis cause?

A

intussusceptions (caecocaecal or caecocolic) - due to altered motility

212
Q

what colics is anoplocephala perfoliata associated with?

A

spasmodic colic
ileal impaction
caecal intussusceptions

213
Q

what type of parasite is Anoplocephala perfoliata?

A

tapeworm

214
Q

why do ascarids cause colic?

A

large worms that cause blockages

215
Q

what is the name for pinworm?

A

Oxyuris equi

216
Q

how clinically significant are Gasterophilus intestinalis?

A

very little (usually)

217
Q

why is control of parasites to prevent risk of disease important in horses?

A

they tolerate worm burdens very well and often only show signs with very high burdens when disease is imminent

218
Q

what is the aim of parasite control strategies?

A

reduce transmission of parasites to prevent high levels of infection and hence the incidence of disease

219
Q

what are the four drugs used for worming horses?

A

fenbendazole, pyrantel, ivermectin, moxidectin

220
Q

how can pasture be managed to reduce worm burden?

A

correct stocking density
faecal collection (>twice a week)
dung heaps away from grazing area
rotate and graze with ruminants

221
Q

what age horses are effected by ascarids?

A

foals (first few months of grazing)

222
Q

what is the ascarid of horses?

A

Parascaris equorum

223
Q

what can the migration of Parascaris equorum cause in foals?

A

respiratory disease - coughing

224
Q

how can Strongyle infection be diagnosed?

A

FEC

225
Q

what can be used and when to treat Strongyles in foals?

A

moxidectin in autumn/winter

226
Q

what is used to treat tapeworm in horses?

A

praziquantel

227
Q

what can be used to treat ascarids in foals?

A

fenbendazole and pyrantel

228
Q

what worm do you not need to worry about in older horses?

A

ascarids (immunity develops)

229
Q

how do FEC of youngstock compare to adult horses?

A

almost always higher

230
Q

what diagnostic tool is recommended for cyathostomins?

A

FEC for adults
small red worm blood test - inform on whether moxidectin treatment is worth it

231
Q

what diagnostic tools are available for tapeworm?

A

FEC
ELISA - good for studs/herds
saliva antigen test (ELISA)

232
Q

what should be the quarantine procedure for horses in terms of worm control?

A

FEC and diagnostics
moxidectin and praziquantel usually recommended
house for 3 days to eliminate shedding post treatment

233
Q

what anthelmintic is Parascaris equorum most commonly resistant to?

A

ivermectin

234
Q

what drugs are strongyles resistant to?

A

benzimadazoles (pyrantel to lesser extent)

Equine (fourth year) (11 decks)

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