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JJ > GI Medicine - Vomiting and Diarrhoea > Flashcards

GI Medicine - Vomiting and Diarrhoea Flashcards

1
Q

what does acute mean?

A

sudden onset

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2
Q

in what animals is acute vomiting and diarrhoea seen commonly?

A

dogs

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3
Q

what may acute vomiting and diarrhoea start with?

A

vomiting and progress through small to large intestinal diarrhoea

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4
Q

how does acute vomiting and diarrhoea often resolve?

A

usually self limiting

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5
Q

define emesis

A

vomiting

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6
Q

define haematoemesis

A

vomiting blood

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7
Q

define haemtochezia

A

fresh blood in/on faeces/diarrhoea (originates in large intestine)

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8
Q

define melaena

A

faecal passage of digested blood (stomach or small intestine origin)

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9
Q

define diarrhoea

A

increase in faecal water content

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10
Q

define tenesmus

A

straining to pass faeces

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11
Q

define dyschezia

A

difficulty passing faeces

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12
Q

define emetic

A

substance which stimulates vomiting

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13
Q

define anti-emetic

A

substance that inhibits vomiting

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14
Q

what is vomiting?

A

a complex, coordinated reflex reaction

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15
Q

what are the events of vomiting coordinated by?

A

the brainstem

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16
Q

does vomiting involve gastric contraction?

A

no

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17
Q

what are the 4 stages of vomiting?

A

prodromal (nausea)
retching
expulsion
relaxation

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18
Q

what occurs in the prodromal phase of vomiting?

A 
nausea 
restlessness and agitation
hypersalivation
gulping 
lip licking
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19
Q

what is inhibited during the retching phase of vomiting?

A

salivation

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20
Q

what happens during the retching phase of vomiting?

A

simultaneous, uncoordinated, spasmodic contractions of respiratory muscles
duodenal retroperistalsis
mixing of gastric contents

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21
Q

what happens during the expulsion phase of vomiting?

A

pyloric contraction and fundic relaxation to move food into upper stomach
relaxation of proximal stomach and lower oesophageal sphincter
airway is protected
abdominal contraction and descent of diaphragm

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22
Q

initially during the expulsion phase of vomiting what is the tone like in the upper oesophageal sphincter?

A

high so that it remains closed

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23
Q

how is the airway protected during the expulsion phase of vomiting?

A

inhibition of breathing

coordinated closure of the glottis and nasopharynx to protect both aspects of the airway

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24
Q

how does abdominal contraction and the descent of the diaphragm lead to vomiting in the expulsion phase of vomiting?

A

stomach is squeezed and vomitus forced up (heaves)
oesophageal retro-peristalsis
reduced upper oesophageal sphincter tone

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25
Q

what muscles relax during the relaxation phase of vomiting?

A

abdominal
diaphragmatic
respiratory

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26
Q

what happens during the relaxation phase of vomiting?

A

muscles relax
glottis and nasopharynx open
breathing returns

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27
Q

describe small intestinal diarrhoea

A 
large volume
watery
normal frequency
normal colour
melaena
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28
Q

describe large intestinal diarrhoea

A 
small volume 
increased urgency and frequency
tenesmus
dyschezia
\+/- mucous
\+/- blood
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29
Q

what does ‘itis mean?

A

inflammation

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30
Q

define gastritis

A

inflammation of the stomach

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31
Q

define enteritis

A

inflammation of the small intestine

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32
Q

define colitis

A

inflammation of the large intestine

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33
Q

define gastro-enteritis

A

inflammation of the stomach and small intestine

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34
Q

define entero-coliitis

A

inflammation of the small and large intestine

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35
Q

define gastro-entero-colitis

A

inflammation of the stomach, small and large intestines

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36
Q

what questions must you ask about vomiting and diarrhoea when completing phone triage?

A 
is vomiting productive or non-productive
frequency - try to gauge fluid loss
foreign body/material risk
haematemesis/melaena
diarrhoea - small or large intestinal
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37
Q

what questions must be asked about the patient generally when completing phone triage?

A

pre exisiting medical or GI disease or medication
worming history (especially with puppies and kittens)
recent change in diet
known scavenger - dietary indiscretion or FB ingestion
clinical demenour
appetite
drinking
other systemic signs

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38
Q

when should you advise a patient receives consultation following phone triage?

A 
unproductive vomiting
large loss of fluid
haematemesis / melaena
suspect FB
inappetant / hypodipsic
other systemic signs
neonate
any other concerns
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39
Q

what are the 3 main categories of acute vomiting and diarrhoea?

A

non fatal, often trivial, may or may not require specific treatment
severe and potentially life threatening
surgical

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40
Q

what are the causes of vomiting and diarrhoea that is non fatal, often trivial and may or may not require specific treatment?

A

dietary indiscretion
parasitism
enteric infection
adverse drug event

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41
Q

what are the causes of vomiting and diarrhoea that is severe and potentially life threatening?

A 
pathogenic and enteric infections (e.g. parvovirus or bacterial)
acute haemorrhagic diarrhoea syndrome
acute pancreatitis
intoxications
surgical disease
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42
Q

what are the causes of vomiting and diarrhoea that are surgical?

A 
intusussception
GDV
incarceration
stricture/partial obstruction
foreign body
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43
Q

what is the major problem seen with surgical GI dieases?

A

vomiting

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44
Q

what is intusussception?

A

telescoping of one intestine loop into another

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45
Q

in what animals is intusussception commonly seen?

A

young rather than old

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46
Q

what must be investigated regarding intusussception?

A

underlying cuase

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47
Q

what is incarceration?

A

loop of intestine becomes strangulated by the mysentry

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48
Q

what are the possible consequences of vomiting and/or diarrhoea?

A

dehydration
hypovolaemia
acid base disturbance
aspiration pneumonia

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49
Q

when is aspiration pneumonia particularly a risk for vomiting patients?

A

if sedated
neuromuscular disease
upper airway incompetency (e.g. laryngeal paralysis)

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50
Q

what are the diagnostic tests used for acute gastroenteritis?

A

history and physical exam
laboratory diagnostics
imaging
response to surgery or symptomatic treatment

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51
Q

what laboratory diagnostics may be used for acute gastroenteritis?

A

bloods - haematology, biochem and electrolytes
faecal - infectious disease testing
specific tests as required (e.g. cPLI or fPLI)

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52
Q

what will a pooled faecal sample test for?

A

parasitology and culture

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53
Q

what will a swab/faecal sample test for?

A

CPV

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54
Q

what is the cornerstone of management of acute vomiting and diarrhoea?

A

maintaining hydration

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55
Q

how may hydration be maintained in acute vomiting and diarrhoea patients?

A

IV fluids

oral rehydration solutions

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56
Q

what fluids are best used to maintain hydration in acute vominting and diarrhoea patients?

A

hartmanns with potassium

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57
Q

what is found within rehydration solutions?

A

glucose, electrolytes and glutamine

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58
Q

when will oral rehydration solutions be used to treat acute V+D patients?

A

if able to manage at home

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59
Q

what is usually sufficent for re-hydrating acute V+D patients if at home?

A

water

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60
Q

what is the dietary advice if acute vomiting is seen?

A

rest the gut (free access to water) for 24-36 hours before reintroducing an bland diet little and often

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61
Q

when should animals with acute vomiting be transferred back onto their normal diet following resting the gut?

A

over 2-5 days once bland diet tolerated

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62
Q

is resting the gut suitable for all patients?

A

no - neonates and diabetics are at risk of hypoglycaemia if they go without food

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63
Q

what is glutamine and why is it useful for acute V+D patients?

A

amino acid which supports enterocytes and helps them to function well

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64
Q

what is the dietary advice if the patient has diarrhoea?

A

feed throughout to nourish enterocytes

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65
Q

what risk is reduced by feeding through diarrhoea?

A

sepsis

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66
Q

what is the issue with needing to feed through diarrhoea in dogs?

A

most have concurrent vomiting

cosmetic issue as will produce more diarrhoea when eating

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67
Q

what is the main supportive/symptomatic management of acute V+D?

A

antiemetics
antispasmodics
antidiarrhoeals

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68
Q

what must be ruled out before anti emetics given?

A

obstruction

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69
Q

how do anti diarrhoeals work?

A

bind toxins and excess water as well as modifiying GI motility and secretions

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70
Q

what is often found in anti-diarrhoeals?

A

clay (kaolin)

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71
Q

how is acute vomiting and diarrhoea treated?

A

anthelmintics
antibiotics rarely indicated
pre and pro biotics

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72
Q

when will anthelmintics be given?

A

if puppy or kitten

if adult and not recently wormed

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73
Q

when should antibiotic use for treatment of acute V+D be considered?

A

if haemorrhagic diarrhoea

if pyrexic

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74
Q

what is the benefit of giving pre and pro biotics?

A

safer than unnecessary antibiotics

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75
Q

what drugs are always contraindicated for patients with vomiting and diarrhoea?

A

NSAIDs

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76
Q

what should happen if patients with acute V+D have pre-exisiting NSAID use?

A

consider that they could be the cause

withhold for the duration of V+D episode and restart when resolved

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77
Q

why are NSAIDs contraindicated for V+D patients?

A

inhibition of prostaglandins which are needed for maintenance of GI mucosal integrity and renal blood flow during hypovolaemic stress

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78
Q

what are prostaglandins required for?

A

maintenance of GI mucosal integrity and renal blood flow during hypovolaemic stress

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79
Q

what are prostaglandins required for?

A

maintenance of GI mucosal integrity and renal blood flow during hypovolaemic stress

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80
Q

when should you consider than the cause of gastroenteritis may be infectious?

A 
neonates
unvaccinated animal
haemorrhagic diarrhoea
pyrexia
raw fed patient
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81
Q

what should happen to potentially infectious patients until any alternative diagnosis confirmed?

A

barrier nurse and isolate

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82
Q

what are the nursing considerations for acute V+D?

A

patient hygiene
environmental hygiene
kennel signage

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83
Q

what are the areas of patient hygiene that must be considered in V+D patients?

A

clean/dry bottom
avoid patient over grooming/rubbing
tail bandage

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84
Q

what are the areas of environment hygiene that must be considered in V+D patients?

A

waste disposed of appropriately
appropriate washing/disinfection of contaminated items
PPE

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85
Q

what are the 2 main types of gastrointestinal foreign body presentations?

A

no obstruction

obstruction

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86
Q

if the foreign body is smooth/small and gastric and not causing obstruction how should it be treated?

A

induce emesis

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87
Q

what drug is used to induce emesis in dogs?

A

Apomorphine

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88
Q

what drug is used to induce emesis in cats?

A

Xylazine

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89
Q

if the foreign body is non obstructive and intestinal how should it be treated?

A

natural passage with radiographic monitoring

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90
Q

if the foreign body is gastric but larger and not smooth but not causing obstruction how should it be treated?

A

endoscopic retrieval or surgery depending on size

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91
Q

what will happen to bones in the stomach?

A

will be dissolved by gastric acid in a few days

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92
Q

what can be done if the FB is a needle in the intestine?

A

feed high fibre diet

monitor for passage

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93
Q

how is an obstructive gastrointestinal FB treated?

A

surgery

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94
Q

what is gastric dilation?

A

acute dilation of the stomach

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95
Q

what is GDV?

A

acute dilation of the stomach with torsion of the stomach and twisted splenic pedicle

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96
Q

what is the effect of GDV?

A

impaired venous return (pressure on caudal vena cava)
compromised gastric mucosa
leading to shock and death

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97
Q

what is a key sign of GDV?

A

unproductive vomiting

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98
Q

how quickly must GDV be treated?

A

ASAP - is life threatening

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99
Q

what dogs are more likely to get GDV?

A

deep chested breeds

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100
Q

what is the cause of GDV?

A 
not really known but may be:
diet
aerophagia
delayed emptying of stomach due to pyloric blockage
timing of exercise very soon after meal
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101
Q

how is GDV treated?

A

aggressive IVFT
immediate decompression of stomach
IV antibiotics
surgical correction

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102
Q

what can a bandage be useful for during GDV treatment?

A

placed between cheek teeth so that the dog can bite on something while having stomach tubed conscious

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103
Q

how is the stomach decompressed in GDV patients?

A

stomach tube if possible

needle paracentesis if not

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104
Q

how long should the stomach tube for GDV treatment be?

A

from tip of nose to last rib

105
Q

what diameter should stomach tubes be?

A

same as would be required for ET tube

106
Q

what surgery is performed on GD or GDV patients?

A

gastropexy

+/- derotation if GDV

107
Q

what is gastropexy?

A

stomach is tied to the abdominal wall in a normal position to prevent reccurance

108
Q

what are the main parasitic causes of acute (or chronic) V+D?

A

roundworms
hookworms
whipworms
cestodes (do not cause GI signs)

109
Q

do roundworms typically cause clinical GI signs?

A

rarely but may do in puppies/kittens

110
Q

what is caused by hookworms?

A

GI bleeding

111
Q

what is caused by whipworms?

A

inflammation and diarrhoea

112
Q

what are the protozoal causes of acute or chronic V+D?

A

coccidia
giardia
Tritrichomonas foetus

113
Q

when is coccidia problematic?

A

only in puppies and kittens

coinfections

114
Q

what GI signs are caused by Giardia?

A

large and small intestine diarrhoea

115
Q

in what animals is Giardia seen?

A

young dogs and cats

116
Q

what is the risk associated with Giardia?

A

can be zoonotic

117
Q

how is Giardia diagnosed?

A

3 pooled faecal sample (SNAP test)

118
Q

in what animals is Tritrichomonas foetus infection seen?

A

young cats (less than 18 months)

119
Q

what can be caused by Tritrichomonas foetus?

A

intractable diarrhoea
peri-anal oedema
faecal incontinence

120
Q

how is Tritrichomonas foetus transmitted?

A

faeco-oral

121
Q

how is Tritrichomonas foetus diagnosed?

A

colonic wash and PCR from sample

122
Q

how is colonic wash performed?

A

10mls sterile saline into colon and then collected through a urinary catheter (usually foley)

123
Q

how is Tritrichomonas foetus treated?

A

poorly responsive to treatment
environmental management to reduce transmission
as maturity reached they have an adequate immune response

124
Q

what causes acute pancreatitis?

A 
idiopathic
dietary indiscretion
hyperlipaemia
impaired perfusion
trauma to pancreas
handling of pancreas in surgery
125
Q

what happens during acute pancreatitis?

A

local release of pancreatic enzymes

pancreatic autodigestion leading to severe local inflammation and pain

126
Q

what can be caused by pancreatitis?

A

systemic inflammation and death

127
Q

what are the systemic signs of acute pancreatitis?

A 
mild to fatal
inappetance 
lethargy
severe abdominal pain
V+D
jaundice
128
Q

why is jaundice caused in acute pancreatitis patients?

A

due to bile duct obstruction if pancreas swells

129
Q

what position may dogs adopt when they have acute pancreatitis?

A

prayer position

130
Q

how is acute pancreatitis diagnosed?

A

history and physical exam
imaging (x ray and ultrasound)
lab evaluation

131
Q

what is involved in the laboratory examination for acute pancreatitis?

A

haematology
biochemistry
pancreatic lipase immunoreactivity (PLI)

132
Q

what tests are available for pancreatic lipase immunoreactivity?

A 
benchside or external lab
species specific (cPLI or fPLI)
133
Q

how is acute pancreatitis treated?

A

IVFT
nutritional support through feeding (oral or tube)
analgesia (NSAIDs contraindicated as V+D)

134
Q

what is the prognosis of acute pancreatitis?

A

variable to guarded

death and recurrence are possible

135
Q

what attitude to feeding pancreatitis patients has overtaken the fasting idea?

A

should be fed well throughout as it improves prognosis

136
Q

when should acute pancreatitis patients be offered water?

A

frequent, small amounts once vomiting is controlled

137
Q

how should food be introduced to acute pancreatitis patients once vomiting is controlled?

A

slowly (little and often)

138
Q

what soft of diet should be fed to acute pancreatitis patients?

A

highly digestible
complex carbohydrate
low fat

139
Q

what does chronic pancreatitis result from?

A

repeated attacks of acute pancreatitis

chronic low grade pancreatitis

140
Q

what are the signs of chronic pancreatitis?

A

chronic, recurrent, grumbling GI signs
inappetance and lethargy
V+D

141
Q

how is chronic pancreatitis managed?

A

at home
modified diet
manage nausea/appetite
analgesia (not NSAIDs)

142
Q

define anorexia

A

a loss of desire to eat despite being physically able to

143
Q

what may anorexia be due to?

A

a variety of GI and systemic disorders

144
Q

define hyporexia

A

reduced appetite

145
Q

define polyphagia

A

excessive appetitie

146
Q

define pica

A

appetite for non-nutritional substrates (e.g. licking concrete or metal)

147
Q

what is pica usually due to?

A

micro-nutrient deficiencies (e.g. iron or B12

148
Q

what secondary complications does prolonged anorexia lead to?

A

weight loss
impaired immune function
increased risk of sepsis
poor wound healing and slow recovery

149
Q

define borborygmi

A

gurgling

150
Q

define flatus

A

passing wind

151
Q

define ileus

A

reduced GI motility

152
Q

when is V+D defined as chronic?

A

when it is greater than 3 weeks in duration

153
Q

what are the main signs and findings of chronic GI disease?

A 
altered appetite (quantity and substrate)
dehydration
vomiting (+/- blood)
diarrhoea (+/- digested or fresh blood)
weight and condition loss
borborygmi/flatus
abdominal discomfort
154
Q

what are the uncommon signs of chronic GI disease?

A

ascites

oedema

155
Q

what are the main causes of chronic V+D?

A

primary GI disease

secondary to extra-GI disease

156
Q

what are the main primary GI diseases that cause chronic V+D?

A

gastric ulceration
dietary intolerance/sensitivity
inflammatory
neoplastic

157
Q

what are the main causes of chronic V+D that are secondary to extra-GI diseases?

A

liver disease
kidney disease
chronic pancreatitis
endocrine disease (hyperthyroid in cats and hypoadrenocorticism in dogs)

158
Q

how is the cause of chronic V+D diagnosed?

A 
history and clinical exam
lab diagnostics to eliminate extra-GI causes
absorption tests
imaging
gastroscopy / laparotomy and biopsy
159
Q

what lab diagnostics will be used to rule out GI disease?

A 
haematology
serum biochem
basal cortisol
total thyroxine
pancreatic tests (f/cPLI and f/cTLI)
faecal analysis
160
Q

what are absorption tests used for?

A

to check amount of vitamin B9 (folate) and B12 (cobalamin) being absorbed from different areas of the GI tract

161
Q

when is contrast radiography performed?

A

when lab results and imaging have not achieved a definite diagnosis and endoscopy is not available

162
Q

what are the issues with contrast studies?

A

messy
time consuming
difficult to interpret
often done poorly

163
Q

what is used for GI contrast studies?

A

barium

164
Q

what are BIPS?

A

barium impregnated polyethylene spheres

165
Q

what is shown by BIPS?

A

spheres vary in size so can give an indication of the size of the obstruction

166
Q

what is the role of ultrasound in diagnosing the cause of chronic V+D?

A

identify masses, intussusceptions and measure GI wall thickness
evaluate lymph nodes for free fluid

167
Q

what are the 2 main ways to perform intestinal biopsy?

A

laparotomy

endoscopy

168
Q

what is the advantage of laparotomy for intestinal biopsy?

A

enables multiple full thickness biopsies (more detail)

169
Q

what is the disadvantage of laparotomy for intestinal biopsy?

A

surgical risk of dehiscence is high (2-12%)

170
Q

what is the advantage of endoscopy for intestinal biopsy?

A

minimally invasive

171
Q

what is the disadvantage of endoscopy for intestinal biopsy?

A

small biopsies only

may not reflect jejunal disease (as scope cannot reach)

172
Q

what are chronic enteropathies?

A

chronic disease of the small intestine

173
Q

what is the most common form of chronic enteropathy?

A

inflammatory bowel disease (IBD) complex

174
Q

what diseases make up the IBD complex?

A

food responsive diarrhoea (FRD)
antibiotic responsive disease (ARD)
true idiopathic inflammatory bowel disease (iIBD)

175
Q

what is food responsive diarrhoea (FRD) caused by?

A

intolerance / hypersensitivity

176
Q

what is antibiotic responsive disease (ARD) caused by?

A

abnormality in the gut flora of the GI tract that interacts poorly with the immune system

177
Q

what breed is antibiotic responsive IBD seen in?

A

GSD

178
Q

what is true idiopathic inflammatory bowel disease (iIBD) caused by?

A

inflammation caused by the immune system within the gut wall launching an auto immune response

179
Q

what is protein losing enteropathy a form of?

A

chronic enteropathy

180
Q

what is protein losing enteropathy?

A

severe (diffuse) SI disease resulting in severe malabsorption and loss of albumin and globulin

181
Q

what are the signs of protein losing enteropathy (PLE)?

A

severe weight loss
oedema
ascites
risk of thromboembolytic events

182
Q

what are the causes of PLE?

A

IBD
lymphangiectasia
alimentary lympho(sarco)ma

183
Q

how is PLE diagnosed?

A

endoscopy

184
Q

how is chronic V+D treated?

A

treat underlying cause

185
Q

what are the commonly used therapies for chronic V+D?

A 
exclusion of parasitism
dietary modification
vitamin B12
steroids
anti-emetics
appetite stimulants
186
Q

how should food intolerance/hypersensitivity be managed?

A

avoidance of allergen

novel or hydrolysed diets

187
Q

what are hydrolysed diets?

A

all food broken down into constituents so that body doesn’t recognise where they originate and so will no launch allergic response

188
Q

what are the general feeding principles for all GI disease?

A

highly digestible
restricted fat - prevent GOR and delayed gastric emptying
supplementary fibre - reduce LI diarrhoea (fermantable or non-fermentable)
little and often (3-4 times per day)

189
Q

what must be considered with inappetant patients?

A

reasons for inappetance that are related and unrelated to GI disease

190
Q

what are the reasons unrelated to GI disease that a patient may be inappetant?

A

pain

stress

191
Q

what are the reasons related to GI disease that a patient may be inappetant?

A 
dehydration
hypokalaemia
hypocobalaminaemic
nausea
delayed gastric emptying making them feel full due to impaired motility
192
Q

what must not be introduced to patients in hospital?

A

new prescription diets

193
Q

how can food intake in hospital be encouraged?

A

warm, wet and smelly food

ask owner about individual preferances

194
Q

what individual eating preferences may patients have?

A 
prefurred foods
environment to eat in
solitary or accompanied eating
hand feeding
owner encouragement . facilitation
195
Q

what are the main aspects of medical therapy for inappetance?

A

control nausea
stimulate appetite
ensure patient is not receiving any drugs that may be supressing appetite

196
Q

what drugs are used to control nausea?

A

maropitant

metaclopromide

197
Q

what drug is used to stimulate appetite?

A

mirtazapine

198
Q

what drugs may suppress patient appetite?

A

opioids - reduce motility

NSAID - contraindicated anyway as cause GI irritation

199
Q

what nutritional support is available if patient is struggling to eat?

A

feeding tubes (N/O, oesophageal, percutaneous endoscopic gastrotomy)

200
Q

what can feeding tubes be used for?

A

microenteral nutrition
liquid or blended feeding
medication admin

201
Q

what is microenteral nutrition?

A

glucose, AA and electrolytes given to support enterocytes as only receive nutrition from intestinal lumen

202
Q

why does cobalamin need to be supplemented?

A

B12 is needed for metabolism in almost all cells

will lead to inappetance and poor enterocyte health

203
Q

how may cobalamin be supplemented?

A

SQ

oral

204
Q

how is cobalamin administered SC?

A

weekly until normalised (4-6 weeks)

recheck serum levels 4-6 weeks after end of course to ensure levels are staying high

205
Q

how is cobalamin administered orally?

A

daily in mage doses

remeasure serum levels after 4-6 weeks

206
Q

what is exocrine pancreas insufficiency?

A

failure of normal exocrine (enzyme) pancreatic secretion

207
Q

what does EPI lead to?

A

maldigestion and malabsorption

208
Q

what may EPI be caused by?

A

pancreatic acinar atrophy (PAA)

recurrent pancreatitis

209
Q

what is pancreatic acinar atrophy?

A

progressive atrophy of pancreas in dogs

210
Q

what breeds in PAA most commonly seen in?

A

GSD

211
Q

at what age does PAA usually begin?

A

young adult

212
Q

why may recurrent pancreatitis cause EPI?

A

scar tissue forms after each bout and so functional aspects are lost

213
Q

what are the key signs of EPI?

A

ravenous appetite
diarrhoea
typically fatty/greasy faeces
severe weight loss

214
Q

why are EPI sufferers faeces usually greasy?

A

lipaze is not produced from the pancreas

215
Q

how is EPI diagnosed?

A

trypsin like immunoreactivity (TLI) serum test (species specific)

216
Q

what are the issues with EPI treatment?

A

expensive

lifelong

217
Q

how is EPI treated?

A

oral pancreatic extract (either capsules or fresh (frozen) pancreas

218
Q

how often should EPI patients be fed per day?

A

2-3 meals per day

219
Q

what must be given with each meal for an EPI patient?

A

enzymes

220
Q

what diet should be fed to EPI patients?

A 
highly digestible
high protein (quality)
not low fat
non-complex carbohydrates
vitamin supplementation (cobalamin)
221
Q

what is colitis?

A

colonic inflammation

222
Q

what is used to treat colitis?

A

Sulphasalazine (Salazopryn)

223
Q

what is Sulphasalazine (Salazopryn) contraindicated for?

A

SI disease

224
Q

how does Sulphasalazine (Salazopryn) work?

A

sulfonamide bound to 5-ASA
link is cleaved by bacteria in colon
leads to local release of 5-ASA which acts as a local anti inflammatory

225
Q

what drug type is Sulphasalazine (Salazopryn)?

A

NSAID

226
Q

what is a major side effect of Sulphasalazine (Salazopryn)?

A

keratoconjunctivitis sicca (KCS) - dry eye

227
Q

what must be measured before and during Sulphasalazine (Salazopryn) administration?

A

schirmer tear test (STT) to confirm normal

228
Q

what is irritable bowel syndrome?

A

large intestinal pattern diarrhoea +/- occasional vomiting

229
Q

in what dogs is IBS usually seen?

A

anxious / nervous small / toy breed dogs (potential for underlying physical or emotional disorder)

230
Q

how is IBS diagnosed?

A

exclusion of all other causes of signs

231
Q

what are some of the reasons that an animal may be vomiting blood that is not of GI origin?

A

coagulopathy

swallowed blood from respiratory tract (oral, nasal or pulmonary)

232
Q

what is seen with gastric or small intestinal bleeding?

A

haematemesis

melaena

233
Q

what is seen with large intestinal bleeding?

A

haematochezia

234
Q

what may partially digested blood in vomit look like?

A

coffee grounds

235
Q

what are the causes of GI ulceration?

A 
drugs (NSAIDS, opioids)
foreign body (direct trauma)
neoplasia
hypoadrenocorticism
kidney or liver disease
other rare causes
236
Q

how are gastric ulcers treated?

A 
evaluate for and remove/treat underlying cause
acid blockers
coating agents
analgesia
Misoprostol
surgery if perforated
237
Q

what are the main acid blockers used to treat gastric ulcers?

A

proton pump inhibitors - omeprazole
histamine receptor agonists
antacids

238
Q

what is the role of misoprostol?

A

given after NSAID overdose as it is a prostaglandin analogue and so will help to overcome defecit

239
Q

what is constipation?

A

impaction of the colon or rectum with faecal material including hair/bones etc

240
Q

what is the consistency of faeces during constipation?

A

excessively dry or hard

241
Q

what does prolonged constipation lead to?

A

irreversible changes to the colon wall which reduces motility an leads to obstipation

242
Q

define obstipation

A

the inability to pass the accumulation of dry hard feces. This can cause impaction of the entire length of the colon and lead to permanent damage

243
Q

what are the signs of constipation?

A 
infrequent defecation
dyschezia
tenesmus
pain associated with defecation (successful or not)
vomiting
anorexia
lethargy
244
Q

what are the causes of constipation?

A 
dietary
dehydration of electrolyte derangement
drug related (reduced motility)
environmental
pain/orthopedic problems making posturing for defecation difficult
spinal / neuromuscular disease
pelvic canal obstruction
perineal/perianal disease
245
Q

what are the environmental causes of constipation?

A

stress
dirty or absent toileting opportunities
lack of exercise

246
Q

how is constipation treated?

A

identify and correct the underlying cause
fluid therapy (with electrolyte correction if needed)
oral laxatives
enemas
motility modification
surgery (case dependent)

247
Q

how is the cause of constipation identified?

A

full history
clinical, neurological, rectal and peri-anal exam
abdominal and pelvic x-rays
lab tests

248
Q

what can be used to clear the colon in a constipated patient?

A

microlax enema
oral laxatives
enema

249
Q

what are the main oral laxatives available?

A

lactulose
lax-a-past
katalax

250
Q

how is an enema performed?

A

warm water
+/- lubricant
digital manipulation and manual evacuation

251
Q

what type of enema must not be used in patients with constipation?

A

phosphate containing

252
Q

how can constipation be prevented?

A 
ensure adequate water intake
control any underlying disease
add fibre into diet
ensure litter tray is in a good location, is clean and is large enough
provide analgesia if needed
increase exercise
increase gut motility
laxatives
253
Q

why should fibre be added to the diet in constipated patients?

A

stimulates colonic motility

254
Q

what drugs are used for motility modification?

A

Cisapride

255
Q

what is megacolon?

A

loss of neuromuscular function of the colon producing weakened colonic contractions and faecal overload

256
Q

what species is megacolon most often seen in?

A

cats

257
Q

what causes megacolon?

A

idiopathic - neuromuscular dysfunction

chronic underlying disease

258
Q

how is megacolon treated?

A

as for constipation - last resort is sub-total colectomy

259
Q

what is the major side effect of a subtotal colectomy?

A

can lead to chronic diarrhoea

JJ (33 decks)

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