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CVNT2 > Diseases of the Gastrointestinal System > Flashcards

Diseases of the Gastrointestinal System Flashcards

1
Q

what are the clinical signs of oropharyngeal disease?

A

drooling saliva +/- blood
halitosis
dysphagia +/- odynophagia

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2
Q

what is ptyalism?

A

overproduction of saliva

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3
Q

what is pseudoptyalism?

A

normal production of saliva but unable to keep it in mouth/swallow it

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4
Q

what is odynophagia?

A

painful swallowing

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5
Q

how can you investigate oral disease?

A

physical examination - may require sedation/GA

radiographs

minimum database

FNA and/or biopsy

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6
Q

what does chelitis mean?

A

inflammation of the lips

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7
Q

what does glossitis mean?

A

inflammation of the tongue

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8
Q

what does gingivitis mean?

A

inflammation of the gums

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9
Q

what does stomatitis mean?

A

inflammation of the oral mucosa

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10
Q

what is gingivostomatitis?

A

inflammation of the gums and oral mucosa

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11
Q

what types of malignant neoplasia are seen in the mouth?

A

squamous cell carcinoma
malignant melanoma
sarcomas

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12
Q

how is oropharyngeal disease treated?

A 
depends on underlying cause! 
surgery for neoplasia
surgery/wound management for trauma 
foreign body removal 
anti-inflammatories 
antibiotics
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13
Q

what are the nursing considerations for oral disease?

A

specific diagnosis/treatment of underlying disease

analgesia (opioids, NSAIDs)

providing warm/wet/soft food OR considering bypass/tube feeding

barrier nursing for infectious aetiologies

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14
Q

what does odynophagia mean?

A

swallowing pain

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15
Q

what is regurgitation?

A

passive return of food (hallmark of oesophageal disease)

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16
Q

what is vomiting?

A

an active, forceful, reflex ejection of gastric and upper intestinal content
following stimulation of a neural reflex
that has synaptic centres in the brainstem

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17
Q

what does regurgitated material usually consist of?

A

undigested food +/- mucus/saliva covering

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18
Q

what are the possible secondary problems/complications of regurgitation?

A

malnutrition and dehydration

anorexia or (perceived) polyphagia

reflux pharyngitis/rhinitis

aspiration pneumonia

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19
Q

what is reflux pharyngitis/rhinitis?

A

regurgitation contents making their way into the nasal cavity and causing inflammation

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20
Q

how can oesophageal disease be investigated?

A

physical examination

chest x-rays (must be conscious)

lab tests - haematology and serum
biochemistry

oesophagoscopy

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21
Q

what are the 3 types of oesophageal disease?

A

megaoesophagus
oesophagitis
oesophageal obstruction

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22
Q

what are the 3 types of oesophageal obstruction?

A

intraluminal
intramural
extraluminal

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23
Q

what is megaoesophagus?

A

oesophageal dilation and dysfunction

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24
Q

what causes generalised megaoesophagus?

A

usually idiopathic

can be myasthenia gravis

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25
Q

what can cause focal dilation of the oesophagus?

A

vascular ring anomaly

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26
Q

how is megaoesophagus treated?

A

no cure if idiopathic - supportive treatment only

neostigmine and pyridostigmine for myasthenia gravis

surgery for vascular ring anomaly

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27
Q

what is involved in nursing management of megaoesophagus?

A

postural feeding - stairs/work surface, bailey chair

slurry vs. textured food - individual differences

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28
Q

what are the most common complication of megaoesophagus? how is it treated?

A

aspiration pneumonia - tachypnoea, pyrexia, lethargy, inappetence

treat with IV antibiotics

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29
Q

what is oesophagitis?

A

inflammation of the oesophagus?

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30
Q

what can oesophagitis be caused by?

A

caustics

hot liquids/foods

foreign bodies

irritants (e.g. doxycycline stuck in throat)

GOR/persistent vomiting

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31
Q

what can oesophagitis lead to?

A

oesophageal strictures

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32
Q

why might GOR occur?

A

during anaesthesia - relaxing of sphincters

persistent vomiting

hiatal hernia

GERD (heartburn) - spontaneous reflux, possibly due to obesity or BOAS

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33
Q

what are the signs of oesophagitis?

A

regurgitation

hypersalivation

anorexia, weight loss

pain

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34
Q

how is oesophagitis managed?

A

oesophageal rest - soft, bland, low fat food in small amounts

analgesia (topical vs systemic)

liquid antacid gels/coating agents

acid blockers (omeprazole)

drugs to reduce further reflux (metaclopramide, cisapride)

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35
Q

how is an oesophageal foreign body removed?

A

usually endoscopically
fluoroscopically
surgery

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36
Q

how does oesophageal stricture occur?

A

fibrosis after severe ulceration of mucosa

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37
Q

how can oesophageal stricture be treated?

A

balloon dilation

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38
Q

what is emesis?

A

vomiting

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39
Q

what is haematemesis?

A

vomiting blood

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40
Q

what is haematochezia?

A

fresh blood in/on faeces/diarrhoea

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41
Q

what is malaena?

A

faecal passage of undigested blood

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42
Q

what is diarrhoea?

A

increased faecal water content

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43
Q

what is tenesmus?

A

straining to pass faeces

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44
Q

what is dyschezia?

A

difficulty passing faeces

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45
Q

what is an emetic?

A

a substance that stimulates vomiting

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46
Q

what is an anti-emetic?

A

substance that inhibits vomiting

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47
Q

does vomiting involve gastric contraction?

A

no

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48
Q

what are the 4 stages of vomiting?

A
  1. Prodromal (nausea)
  2. Retching
  3. Expulsion
  4. Relaxation
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49
Q

what is involved in the prodromal phase of vomiting?

A 
nausea
restlessness, agitation 
hypersalivation 
gulping
lip-licking/smacking
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50
Q

what is involved in the retching stage of vomiting?

A

inhibition of salivation

simultaneous, uncoordinated, spasmodic
contractions of respiratory muscles

duodenal retroperistalsis

mixing of gastric contents

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51
Q

what is involved in the expulsion phase of vomiting?

A

pyloric contraction and fundic relaxation

relaxation of proximal stomach and lower oesophageal sphincter

protection of airway (closure of glottis and nasopharynx)

abdominal contraction and descent of diaphragm with reduced oesophageal sphincter tone

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52
Q

what is involved in the relaxation phase of vomiting?

A

relaxation of abdominal, diaphragmatic and respiratory muscles

re-opening of the glottis and nasopharynx

return of breathing

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53
Q

how can you identify small intestinal diarrhoea?

A

large volume, watery
normal frequency
often normal colour
+/- melaena

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54
Q

how can you identify large intestinal diarrhoea?

A

small volume
increased urgency and frequency
tenesmus, dyschezia
+/- mucus and/or blood

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55
Q

which part of the GI tract does gastritis refer to?

A

stomach

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56
Q

which part of the GI tract does enteritis refer to?

A

small intestine

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57
Q

which part of the GI tract does colitis refer to?

A

large intestine

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58
Q

which part of the GI tract does gastro-enteritis refer to?

A

stomach and small intestine

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59
Q

which part of the GI tract does entero-colitis refer to?

A

small and large intestine

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60
Q

which parts of the GI tract does gasto-entero-colitis refer to?

A

stomach, small and large intestine

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61
Q

what are the important questions for phone triage for patients with vomiting/diarrhoea?

A

productive/non-productive vomiting

frequency - gauge fluid losses

foreign material

haematemesis/melaena?

small or large intestinal?

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62
Q

when would you advise consultation for diarrhoea/vomiting?

A

unproductive vomiting

large fluid volumes lost

haematemesis/melaena

suspicion for foreign material ingestion

inappetant/hypodipsic

other systemic signs

puppy/kitten

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63
Q

what are the categories of acute vomiting and diarrhoea?

A
  1. non-fatal, often trivial, may or may not require specific treatment
  2. severe and potentially life-threatening
  3. surgical disease
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64
Q

what can cause non-fatal/trivial vomiting and diarrhoea?

A

dietary indiscretion
parasitism
enteric infection
adverse drug event

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65
Q

what can cause severe and potentially life-threatening diarrhoea and vomiting?

A

pathogenic enteric infections (parvo, bacterial)

acute haemorrhagic diarrhoea syndrome

acute pancreatitis

surgical disease

intoxications

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66
Q

what types of surgical disease can cause acute vomiting and diarrhoea?

A 
intusussception 
GDV 
incarceration 
stricture/partial obstruction 
foreign body

(usually vomiting is the major problem in surgical disease)

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67
Q

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

A

dehydration
hypovolaemia
acid-base disturbance
aspiration pneumonia

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68
Q

what diagnostic tests can be done for acute gastroenteritis?

A

history, physical examination

bloods - haematology, biochemistry, electrolytes

faecal infectious disease testing

imaging

response to symptomatic treatment/surgical management

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69
Q

how can you maintain hydration in a V/D animal?

A

IV Hartmann’s in clinic
oral rehydration solutions if at home - glucose/electrolyte/glutamine-containing solutions
water usually sufficient

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70
Q

what dietary advice should be given to owners with vomiting animals?

A

if acute vomiting, rest the gut 24-36hrs but provide free access to water

re-introduce bland diet little and often

transition to normal diet over 2-5 days

not suitable for neonates or diabetic patients

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71
Q

what dietary advice should be given to owners of animals with diarrhoea?

A

feed through diarrhoea - quicker recovery and reduces potential of sepsis

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72
Q

what supportive/symptomatic support is available for V/D patients?

A

antiemetics - exlcude obstruction first
antispasmodics e.g. buscopan
anti-diarrhoeals - cosmetic only (kaolin based)

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73
Q

how can you treat acute vomiting/diarrhoea?

A

antithelmintics if puppy/kitten or is adult and not recently wormed

antibiotics rarely indicated - consider if haemorrhagic diarrhoea +/- pyrexia

pre/probiotics may or may not have effect - safer than unnecessary antibiotics

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74
Q

why can’t NSAIDS be given to V/D patients?

A

prostaglandins required for maintenance of GI mucosal integrity
maintenance of renal blood flow in hypovolaemic states

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75
Q

are NSAIDs contraindicated for V/D use?

A

yes ALWAYS

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76
Q

what nursing considerations should be taken with acute gastroenteritis?

A

patient hygiene - clean/dry bottom, avoid over-grooming, tail bandage

environmental hygiene - appropriate waste disposal, appropriate washing/disinfection of contaminated items

appropriate PPE

barrier nursing if possibly infectious

kennel signage

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77
Q

how can a smooth, small gastric FB be treated?

A

induce emesis

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78
Q

what is used to induce emesis in dogs?

A

apamorphine

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79
Q

what is used to induce emesis in cats?

A

xylazine

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80
Q

how is a non-obstructive intestinal FB treated?

A

wait for natural passage with radiographic monitoring

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81
Q

how is an obstructive FB treated?

A

usually surgery

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82
Q

what is GDV?

A

gastric dilation-volvulus - acute dilation and torsion of the stomach

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83
Q

why is GDV dangerous?

A

can occlude the caudal vena cava which causes impaired venous return and compromised mucosa - leading to shock and death

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84
Q

which dogs are more likely to suffer with GDV?

A

deep-chested breeds

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85
Q

what are the causes of GD/GDV?

A

not completely sure

could be diet, aerophagia, delayed emptying, exercise timing

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86
Q

how is GD/GDV treated?

A

aggressive fluid therapy

immediate decompression via a stomach tube

IV antibiotics if compromised stomach wall

surgical correction (derotation +/- gastropexy)

87
Q

what are the possible parasitic causes of acute/chronic vomiting and/or diarrhoea?

A

roundworms
hookworms
whipworms
cestodes

88
Q

what are the possible protozoal causes of acute vomiting and/or diarrhoea?

A

coccidia spp. - only problematic in puppies/kittens/coinfections

giardia spp. - affects young dogs and cats, possibly zoonotic

Tritrichomonas foetus

89
Q

what is tritrichomonas foetus?

A

protozoal infection of young cats

90
Q

what are the GI signs of tritrichomonas foetus infection?

A

intractable diarrhoea
+/- perianal oedema
+/- faecal incontinence

91
Q

how is tritrichomonas foetus infection diagnosed?

A

colonic wash and PCR

92
Q

how is tritrichomonas foetus treated?

A

poorly responsive to treatment (ronidazole)
environmental management
will mount an effective immune response with maturation

93
Q

what are the pre-disposing features for idiopathic pancreatitis?

A

dietary indescretion
hyperlipaemia
impaired perfusion
trauma/handling

94
Q

how does acute pancreatitis cause disease?

A

local release of pancreatic enzymes leads to pancreatic autodigestion
causes severe local inflammation with pain

95
Q

what are the signs of acute pancreatitis?

A

range from mild to fatal

inappetence, lethargy

severe abdominal pain, vomiting, diarrhoea

+/- jaundice (bile duct obstruction)

dogs may adopt prayer position

96
Q

how is acute pancreatitis diagnosed?

A

history and physical examination

imaging (radiography and ultrasound)

haematology, serum biochemistry

pancreatic lipase immunoreactivity test

97
Q

what is the treatment for acute pancreatitis?

A

fluid support
nutritional support - feeding is beneficial, oral v.s tube feeding
analgesia
antiemetics

98
Q

what is the prognosis for acute pancreatitis?

A

highly variable to guarded
death is possible
recurrence is possible

99
Q

when/ how should pancreatitis patients begin drinking/eating again?

A

frequent, small amounts of water once vomiting controlled

slowly reintroduce highly digestible complex carbohydrate food

low fat food if hyperlipaemic or repeated bouts

100
Q

how does chronic pancreatitis occur?

A

results from repeated attacks of acute pancreatitis

101
Q

what are the signs of chronic pancreatitis?

A

causes chronic, recurrent, grumbling GI signs
inappetence, lethargy
vomiting and/or diarrhoea

102
Q

how is chronic pancreatitis managed?

A

at-home dietary modification
manage nausea/appetite
analgesia (not NSAIDs!)

103
Q

what is anorexia?

A

a loss of desire to eat, despite being physically able to

104
Q

what is hyporexia?

A

reduced appetite?

105
Q

what is polyphagia?

A

excessive appetite

106
Q

what is pica?

A

appetite for non-nutritional substrates e.g. licking concrete/metals

107
Q

what are the secondary complications of prolonged anorexia?

A

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

108
Q

what is borborygmi?

A

gurgling sounds

109
Q

what is flatus?

A

passing wind

110
Q

what is ileus?

A

reduced gastro-intestinal motility

111
Q

what duration is considered chronic vomiting/diarrhoea?

A

> 3 weeks

112
Q

what are the signs and findings with chronic GI disease?

A 
altered appetite 
dehydration 
vomiting +/- blood 
diarrhoea +/- blood 
weight/condition loss 
borborygmi, flatus 
abdominal discomfort
113
Q

what are some possible causes of chronic vomiting and/or diarrhoea under primary GI disease?

A

gastric ulceration

dietary intolerance/sensitivity

inflammatory e.g. IBD

neoplastic e.g. gastric carcinoma, GI lymphoma

114
Q

what are some causes of chronic V/D which are secondary to extra-GI disease?

A

liver disease
kidney disease
pancreatitis (chronic)
endocrine disease (hyperthyroidism in cats, hypoadrenocorticism in dogs)

115
Q

how might chronic V/D be approached diagnostically?

A 
history and clinical examination 
haematology and serum biochemistry 
basal cortisol, total thyroxine 
pancreatic tests 
faecal analysis 
absorption tests (B9 and B12) 
imaging (radiographs and ultrasound) 
gastroscopy/laparotomy and biopsy
116
Q

what is the basal cortisol test?

A

test for adrenal gland function

117
Q

what is the total thyroxine test?

A

test for thyroid gland function

118
Q

what other imaging might be used if endoscopy is unavailable?

A

contrast radiography

119
Q

what are the disadvantages in using contrast radiography for exploring chronic V/D?

A

messy
time-consuming
difficult to interpret
often done poorly

120
Q

what are BIPS? what is it used for?

A

barium impregnated polyethylene spheres

used in place of ingesting/injecting barium powder/fluid

121
Q

why might ultrasound be used for investigating chronic V/D?

A

identifying masses, intussusceptions and measuring GI wall thickness
evaluate lymph nodes for free fluid

122
Q

what are the 2 methods of obtaining an intestinal biopsy?

A

laparotomy - full thickness biopsies

endoscopy - superficial, may not reflect jejunal disease

123
Q

which diseases are part of the inflammatory bowel disease (IBD) complex?

A

food-responsive
antibiotic responsive
true idiopathic inflammatory bowel disease

124
Q

which breed is most likely to suffer from antibiotic responsive disease?

A

german shepherds

125
Q

what are chronic enteropathies?

A

chronic disease of the small intestine

126
Q

what is protein-losing enteropathy?

A

a form of chronic enteropathy

–> severe SI disease resulting in severe malabsorption and loss of albumin and globulin

127
Q

what are the signs of protein-losing enteropathy?

A

severe weight loss

oedema and ascites due to reduced oncotic pressure of blood

risk of thromboembolic events

128
Q

what causes protein-losing enteropathy?

A

various causes - IBD, lymphangiectasia, alimentary lymphosarcoma/lymphoma

129
Q

how is protein-losing enteropathy diagnosed?

A

endoscopy

130
Q

what are the commonly used therapies for supporting chronic V/D?

A

exclusion of parasitism - fenbendazole course

dietary modification

vitamin B12

steroids

anti-emetics
appetite stimulants

131
Q

what are the dietary considerations for those with food intolerances/hypersensitivity?

A

avoidance of allergen

hydrolysed diets

132
Q

what are the general principles re. diet in chronic V/D?

A

highly digestible
restricted fat in GOR/delayed gastric emptying
supplementary fibre
little and often

133
Q

what considerations need to be made regarding inappetent patients?

A 
in pain or stressed?
dehydrated 
hypokalaemic 
hypocobalaminaemic 
nauseous 
delayed gastric emptying
134
Q

how can we encourage food intake in chronic V/D patients?

A

avoid introducing prescription diets in the hospital
warm, wet and odorous food
check with owner about individual preferences
ensure euhydrated with balanced electrolytes

135
Q

what medical therapies are available for inappetence?

A

nausea control - maropitant, metoclopramide

appetite stimulants - mirtazepine

consider effects of other drugs - opioids reduce GI motility, NSAIDs cause GI irritation and erosion

136
Q

how can you supplement cobalamin (B12)?

A

subcutaneous injections weekly for 4-6 weeks until normalised

oral mega-dose
re-measure serum cobalamin after 4-6 weeks

137
Q

what is exocrine pancreatic insufficiency?

A

failure of normal exocrine pancreatic secretion (enzymatic)

138
Q

what causes exocrine pancreatic insufficiency?

A

usually due to pancreatic acinar atrophy (esp german shepherds)

may be due to recurrent pancreatitis (cats)

139
Q

what are the signs of exocrine pancreatic insufficiency?

A

extreme polyphagia
diarrhoea, typically fatty/greasy
severe weight loss

140
Q

how is EPI diagnosed?

A

trypsin-like immunoreactivity serum test (species-specific)

141
Q

how is EPI treated?

A

no cure - expensive and lifelong management

oral pancreatic extract - uncoated powder or fresh frozen pancreas

142
Q

what diet should you feed animals with EPI?

A

2-3 meals a day, always with enzyme

highly digestible food

high protein

non-complex carbohydrates

cobalamin supplementation required in many

143
Q

what is colitis?

A

colonic inflammation resulting in large bowel diarrhoea

144
Q

how is colitis treated?

A

sulphasalazine (contraindicated in SI disease) - local anti-inflammatory

145
Q

what is the major side effect of sulphasalazine?

A

keratoconjunctivitis sicca (dry eyes)

146
Q

what is irritable bowel syndrome?

A

large intestinal pattern diarrhoea +/- occasional vomiting

147
Q

how is IBS diagnosed?

A

by exclusion of other causes of signs

148
Q

what is the treatment for IBS?

A

long-term dietary modification
anti-spasmodics
anti-cholinergics

149
Q

why might there be blood in the faeces or vomit?

A

coagulopathy
swallowed blood
gastric/SI bleeding (haematemesis, melaena)
LI bleeding (haematochezia)

150
Q

what are the possible causes of GI ulceration?

A

drugs (NSAIDs, steroids)

direct trauma from a foreign body

neoplasia (gastric carcinoma)

hypoadrenocorticism

kidney disease
liver disease

151
Q

how should gastric ulcers be treated?

A

evaluate for and remove/treat underlying cause

acid blockers

coating agents (sucralfate)

analgesia

surgery if perforated

152
Q

what types of acid blockers can be used to help treat gastric ulcers?

A

proton pump inhibitors (omeprazole)
histamine receptor agonists
antacids

153
Q

what condition can a perforated gastric ulcer lead to?

A

septic peritonitis

154
Q

what is constipation?

A

impaction of the colon or rectum with faecal material

155
Q

what can prolonged constipation lead to?

A

obstipation

156
Q

what is obstipation?

A

intractable constipation

157
Q

what are the signs of constipation?

A

infrequent defecation

dyschezia and tenesmus

pain associated with unsuccessful defecation

vomiting, anorexia, lethargy

158
Q

what are some of the possible causes of constipation?

A

dietary
dehydration
drug-related

environmental (stress, lack of toileting opportunities)

pain/orthopaedic problems - inability to posture

spinal/neuromuscular disease

pelvic canal obstruction

perineal/perianal disease

159
Q

how can constipation be treated?

A

identify and correct underlying cause

fluid therapy +/- electrolyte correction

oral laxatives, enemas

motility modification

surgery (cause dependent)

160
Q

how can constipation be avoided?

A

ensure adequate water intake

dietary modification (fibre)

litter tray management

increased exercise

motility modification (cisapride) 
laxatives
161
Q

what is megacolon?

A

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

162
Q

which animals most commonly suffer from megacolon?

A

cats - idiopathic

163
Q

how can megacolon be treated?

A

treat as for constipation

last resort is sub-total colectomy

164
Q

what are the main synthesis products of the liver?

A

proteins - albumin, globulin, clotting factors

glucose

cholesterol

165
Q

what kinds of clearance/detoxification are involved in normal hepatic function?

A

encephalopathic toxins (ammonia)
bilirubin
bile acids
enterically absorbed drugs

166
Q

what are some of the possible clinical signs of hepatic dysfunction?

A

inppetance, lethargy, V/D

jaundice

ascites

hepatic synthetic and/or detoxification failure

167
Q

what is icterus?

A

yellow discolouration of the skin/mucous membranes/eyes due to hyperbilirubinaemia

168
Q

what is hyperbilirubinaemia?

A

increased bilirubin in the blood

>10umol/L

169
Q

at what level does tissue deposition of bile pigment become apparent?

A

> 40umol/L

170
Q

what is a pre-hepatic cause of jaundice?

A

haemolysis (moderate-severe)

171
Q

what is a hepatic cause of jaundice?

A

failure of hepatic uptake, conjugation and/or transport of bilirubin

172
Q

what are the possible post-hepatic causes of jaundice?

A

failure of excretion of bile
cholestatic disease
biliary rupture

173
Q

what are the causes of ascites (in terms of liver disease)?

A

hypoalbuminaemia
portal hypertension
sodium and water retention

174
Q

what can hepatic dysfunction/abnormal blood supply to the liver lead to?

A

failure of conversion of ammonia to urea, leading to hyperammonaemia and/or hepatic encephalopathy
failure of drug detoxification

175
Q

what are the signs of forebrain dysfunction?

A 
lethargy 
obtundation 
head pressing 
pacing, walking in circles 
seizures 
coma
176
Q

what can build up in the blood which leads to forebrain dysfunction?

A

encephalopathic toxins

177
Q

after which events will a hepatic encephalopathy be worse?

A

high protein meal

GI haemorrhage

178
Q

what are the precipitating events for hepatic encephalopathy?

A

feeding high protein meal
vomiting, diarrhoea
diuretics

179
Q

what are the laboratory tests for liver disease?

A 
liver enzymes 
bilirubin 
bile acids 
blood glucose 
blood clotting parameters
180
Q

how can liver disease be diagnosed?

A

laboratory testing
imaging
liver cytology/biopsy

181
Q

what are the most common causes of acute liver disease?

A

toxins or infections

182
Q

which ingested toxins can cause acute liver disease?

A

xylitol
mushrooms
blue green algae

183
Q

which drugs can cause acute liver disease?

A 
phenobarbitone 
paracetamol 
azathioprine 
doxycycline 
lomustine
184
Q

which infections can cause acute liver disease?

A

leptospirosis
ascending biliary infection
canine adenovirus

185
Q

what are the main nursing considerations for acute liver disease?

A

management of hepatic encephalopathy

anti-emetics (may be feeling nauseous)

management of hypoglycaemia

may be coagulopathic - consider implications of venepuncture

barrier nursing if infectious cause

186
Q

where should venepuncture be performed in patients with acute liver disease?

A

ideally leg - patient may be coagulopathic and you can’t apply a pressure bandage to the jugular vein

187
Q

how do you manage hepatic encephalopathy?

A

lactulose - oral or retention enema

+/- seizure management

monitor/maintain normal hydration and electrolytes (esp K)

188
Q

what is involved in nutritional management of liver disease?

A

restricted animal protein diet - otherwise hepatic prescription diets
copper restricted
antioxidant supplemented

189
Q

what are the sterile causes of inflammatory liver disease?

A 
chronic hepatitis (dogs) 
lymphocytic cholangitis (cats)
190
Q

what are the infectious causes of inflammatory liver disease?

A

cholangitis/cholangiohepatitis - chronic or acute
chronic/acute leptospirosis (dogs)
feline infectious peritonitis - chronic

191
Q

what are the specific treatments for inflammatory liver disease?

A

de-coppering therapy

antibiotics - only where specifically indicated

192
Q

what are the general treatments for inflammatory liver disease?

A

dietary modification

liver supportive therapies (anti-oxidants)

anti-inflammatories (steroids)

choleretics

hepatic encephalopathy therapies

ascites management (spironolactone)

193
Q

what are choleretics?

A

substances which increase the volume of secretion of bile from the liver as well as the amount of solids secreted

194
Q

what chelating agents are used in de-coppering therapy?

A

D-penicillamine

zinc therapy for longer term use

195
Q

how can copper intake be restricted?

A

dietary - prescription diet, avoid red meat, offal, eggs, cereals

consider water source - copper in old pipes

196
Q

which antioxidants can be used in inflammatory liver disease management?

A

silymarin/silibinin/sylibin (milk thistle)

SAMe

197
Q

which synthetic choleretic is used in inflammatory liver disease management?

A

ursodeoxycholic acid (UDCA)

198
Q

how does UDCA work?

A

stimulates bile flow, modulates inflammatory response in liver

199
Q

what is UDCA?

A

a synthetic, hydrophilic ‘beneficial’ bile salt (choleretic)

200
Q

what is gall bladder mucocoele?

A

where the gall bladder is full of inspissated bile and mucus - can cause blockage

201
Q

what does a gall bladder mucocoele look like?

A

kiwi fruit appearance

202
Q

what is feline hepatic lipidosis?

A

hepatocyte triglyceride deposition - leads to massive intracellular fat accumulation

203
Q

what are the predispositions for feline hepatic lipidosis?

A

obesity
high fat/carbohydrate diet
systemic illness
diabetes mellitus

204
Q

what can feline hepatic lipidosis progress into?

A

liver failure - encephalopathy and coagulopathy

205
Q

how is feline hepatic lipidosis diagnosed?

A

FNA - check clotting first

monitor CVS parameters post-procedures

206
Q

what is the treatment for feline hepatic lipidosis?

A

treat the underlying disease

nutritional support
antioxidants
UDCA
L-carnitine

never force-feed/syringe feed a cat!

207
Q

what are the usual blood findings with a congenital portosystemic shunt?

A

low albumin
low cholesterol
high bile acids
high ammonia

208
Q

how is a portosystemic shunt diagnosed?

A

ultrasound

209
Q

what is a portosystemic shunt?

A

an extra vessel which passes blood from the portal vein straight into the caudal vena cava, bypassing the liver

210
Q

what can occur due to portovascular anomalies?

A

liver dysfunction due to lack of nutrient supply

accumulation of toxins leading to hepatic encephalopathy

211
Q

how can a portosystemic shunt be treated short-term?

A 
ensure well hydrated with normal K levels
restricted protein diet 
lactulose to trap ammonia in colon 
antibiotics 
\+/- anti-seizure therapy
212
Q

what is the ideal long-term solution for a portosystemic shunt?

A

surgical closing of shunted vessel

213
Q

what are the signs of hepatic neoplasia?

A

asymptomatic
primary hepatic/obstructive signs
rupture –> haemoabdomen

214
Q

what are the types of hepatic neoplasia?

A

primary tumours - surgery
infiltrative - chemo
metastatic - no treatment as has already spread from elsewhere

CVNT2 (47 decks)

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