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CVSOH 4 > Small Animal Gastrointestinal > Flashcards

Small Animal Gastrointestinal Flashcards

1
Q

Define chelitis, glossitis, gingivitis, stomatitis, gingivomastitis, tonsilitis and pharyngitis.

A

Chelitis – inflammation of the lips

Glossitis – inflammation of the tongue

Gingivitis – inflammation of the gums

Stomatitis – inflammation of the oral mucosa/whole mouth

Gingivostomatitis – inflammation of the gums and oral mucosa

Tonsilitis – inflammation of the tonsils

Pharyngitis – inflammation of the pharynx

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2
Q

What are some primary swallowing disorders?

A
  • Difficulty lapping or forming a bolus
  • Audible noise when swallowing
  • Gulping excessively – persistent and ineffective swallowing
  • Dropping food
  • Gagging, retching
  • Regurgitation food/liquid
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3
Q

What are some secondary swallowing disorders?

A
  • Halitosis
  • Nasal discharge
  • Coughing, dyspnoea
  • Blood tinged saliva
  • Failure to thrive
  • Backing away from food, interested in food but reluctance to eat
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4
Q

What history should be taken when trying to assess regurgitation?

A
  • Regurgitation versus vomiting
  • Oesophageal foreign body likely?
  • Any medications?
  • Recent anaesthesia?
  • Any other gastrointestinal signs?
  • Generalised neuromuscular clinical signs?
  • Coughing or dyspnoea?
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5
Q

Distinguish regurgitation and vomiting.

A

Regurgitation - passive, no abdominal effort, immediate/delayed after eating, neutral pH, brainstem not involved

Vomiting - active, abdominal effort and heaving, delayed after eating, acidic, brainstem involved in neural reflex

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6
Q

What do you assess in full clinical examination of regurgitation cases?

A
  • Generalised vs. localised disease
  • Neurological examination?
  • Hydration/volaemic status
  • Body condition
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7
Q

What do you assess in sedation/GA examination of regurgitation cases?

A
  • Pre-anaesthetic blood tests
  • Difficulty opening mouth
  • Airway obstruction
  • Brachycephalic breeds
  • Reflux and aspiration
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8
Q

What can you examine in an oropharyngeal examination?

A
  • Trauma/foreign bodies
  • Pain on palpation – head and jaw
  • Dental disease
  • Lip folds, mucous membranes and tonsils
  • Muscle mass – generalised/localised with any changes in muscle mass that could indicate a neuromuscular issue
  • Jaw opening
  • Check under tongue – string foreign bodies, masses
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9
Q

What can be present in the oral cavity that could cause swallowing disorders?

A
  • Oral masses and inflammatory
  • Ulceration or burns
  • Salivary gland disease – referral for CT and salivary gland sampling
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10
Q

How do you assess the masticatory muscles?

A
  • Creatinine kinase
  • Anti-2M antibodies for MMM/masticatory muscle myositis
  • AChR antibiodies for myasthenia gravis
  • Muscle biopsy
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11
Q

Distinguish structural and functional dysphagia.

A

Structural – caused by a structural abnormality. Foreign body, mass lesion – inflammatory, cyst, granuloma, abscess, neoplasia

Functional – caused by a functional abnormality. Normal physical exam, neuromuscular issue

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12
Q

Distinguish pseudoptyalism and ptyalism.

A

Pseudoptyalism – physiological in response to food (normal), conformation, dysphagia including obstructive disease

Ptyalism/hypersalivation – bitter taste, drugs, oral disease/ulceration, nausea, acid reflux (GERDs), rabies, hepatic encephalopathy in cats

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13
Q

Name some internal and external causes of halitosis.

A

Internal:
- Respiratory disease
- Gastric disease – poor gastric emptying
- Metabolic disease, such as renal disease

External:
- Peri-anal disease
- Coprophagia

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14
Q

Name 4 differential diagnoses for swallowing disorders.

A

Oral pain
Oral mass
Oral trauma
Neuromuscular disease

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15
Q

What are some structural oesophageal differential diagnoses?

A
  • Luminal
  • Intramural – neoplasia sitting in wall of the oesophagus
  • Extramural – mass nearby the oesophagus, not actually in the wall
  • Strictures
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16
Q

What are some functional oesophageal differential diagnoses?

A
  • Nerves or neuromuscular junctions
  • Muscles
  • Primary disease
  • Secondary disease - metabolic, endocrinopathies (hypothyroidism, hypoadrenocorticism)
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17
Q

Name some congenital and acquired structural oesophageal disease.

A

Congenital – vascular ring anomaly

Acquired – foreign body, neoplasia, gastro-oesophageal intussusception

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18
Q

What is functional gastro-oesophageal reflux?

A
  • Reflux of gastric acid and enzymes into the oesophagus
  • Leads to inflammation
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19
Q

What are some acute and some chronic causes of functional gastro-oesophageal reflux?

A

Acute – during anaesthesia

Chronic – obesity, lower oesophageal sphincter disease

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20
Q

What is GERD?

A

Gastro-oesophageal reflux disease

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21
Q

What are 3 causes of GERD?

A
  • Hiatal hernia: congenital/age-related
  • Lower oesophageal sphincter dysfunction
  • Underlying chronic enteropathy
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22
Q

What are the causes of oesophagitis?

A
  • Peri-anaesthetic reflex
  • Ingestion of caustic chemical, hot liquids/foods, foreign bodies, irritants (doxycycline)
  • Chronic GERD
  • Persistent vomiting
  • Oesophagitis can lead to oesophageal strictures – iatrogenic oesophagitis can also occur after stricture dilation
  • Excessive stomach acid – gastrinoma, mast cell tumour
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23
Q

What are some causes of focal megaoesophagus?

A
  • Vascular ring anomaly – heart-base location in young dog
  • Foreign body
  • Stricture
  • Space occupying lesion
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24
Q

What is a risk of megaoesophagus?

A

Aspiration pneumonia

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25
Q

What are the clinical signs of aspiration pneumonia?

A

Tachypnoea
Pyrexia
Lethargy
Inappetence

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26
Q

Name 7 differential diagnoses for diffuse megaoesophagus and how each of these is diagnosed.

A
  • Idiopathic megaoesophagus - exclude all other differentials
  • Myasthenia gravis - AChR antibodies
  • Diffuse oesophagitis - history, endoscopy
  • Hypoadrenocorticism - ACTH stim test
  • Hypothyroidism - T4/TSH
  • Neuromuscular disease - neuro exam, CK, EMGs
  • Dysautonomia - rare, other signs
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27
Q

What can give false megaoesophagus?

A

Radiograph conscious as some anaesthetic drugs can cause oesophageal dilation, giving a false megaoesophagus.

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28
Q

Which blood tests are used to investigate swallowing disorders?

A
  • Routine haematology and biochemistry
  • Electrolytes
  • cPLi/fPLi – if suspect pancreatitis leading to nausea
  • Pre-anaesthetic profile in older patient if GA needed
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29
Q

How are swallowing disorders investigated with radiogrpahy?

A
  • Dental radiography
  • Whole skull radiography/jaw radiography – bone lysis from osteomyelitis, neoplasia
  • Neck radiography
  • Thoracic radiography – ideally inflated 3 views for metastasis assessment if suspicious about neoplasia
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30
Q

How are swallowing disorders investigated with ultrasonography?

A
  • POCUS (TFAST and AFAST) – trauma and effusions, if patient has breathing problems
  • Assess organs – neoplasia, abnormalities on bloods
  • Ultrasound-guided cystocentesis or FNA
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31
Q

How are swallowing disorders investigated using CT?

A
  • Reveals smaller thoracic metastases
  • 3D skull assessment
  • Cellulitis/abscesses associated with foreign bodies or retrobulbar disease
  • Salivary gland assessment
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32
Q

How is reflex and regurgitation investigated?

A
  • Haematology
  • Serum biochemistry
  • Survey neck and chest radiography
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33
Q

How should we remove an oesophageal foreign body?

A

Surgery can cause oesophageal damage or strictures. Endoscopy

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34
Q

What is a risk of contrast radiography to investigate regurgitation disorders?

A

Barium mixed with food/liquid - high risk of aspiration

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35
Q

What is fluoroscopy?

A

Dynamic conscious x-ray, moving image can watch patient eat and swallowing

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36
Q

What can fluoroscopy diagnose?

A
  • Swallowing – diagnosis of dysphagia/regurgitation
  • Evaluation of intermittent pathology – such as, sliding hiatal hernia
  • Respiratory – diagnosis of airway collapse
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37
Q

When is endoscopy indicated?

A
  • To retrieve foreign body
  • To evaluate for hiatal hernia (after other imaging)
  • To evaluate for/dilate stricture
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38
Q

When is endoscopy contraindicated?

A

If megaoesophagus already shown

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39
Q

How can swallowing disorders be managed?

A
  • Dentistry
  • Specific therapies for masticatory muscle disease
  • Consider nutrition – wet food/slurry? Feeding tubes?
  • Manage nausea
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40
Q

How can regurgitation be managed?

A
  • Correct the underlying disease if possible
  • Positional feeding
  • Medications
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41
Q

How can the underlying diseases of regurgitation be corrected?

A
  • Neuromuscular or endocrine disease – treat as appropriate
  • Hiatal hernias often managed successfully without surgery
  • Myasthenia gravis – anticholinesterase drugs
  • Oesophageal foreign body – endoscopic retrieval
  • Oesophageal stricture – balloon dilation
  • Vascular ring anomaly – surgery
  • BOAS – surgical?
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42
Q

What is positional/postural feeding essential for?

A

Megaoesophagus – until function normal, prokinetics are of no benefit/LES drugs cause harm

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43
Q

How does omeprazole work?

A
  • Proton pump inhibitor
  • Irreversibly binds H + secretion
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44
Q

What is the effect of cisapride?

A
  • Stimulates intestinal 5-HT 4 receptors
  • Increased lower oesophageal sphincter tone
  • Decreased pyloric tone, propulsive peristaltic waves throughout whole GI tract
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45
Q

When is cisapride indicated?

A

GERD
Feline idiopathic megacolon
Pro-motility agent in other species

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46
Q

What is used if cisapride is not tolerated?

A

Metoclopramide – to facilitate gastric emptying may be of value

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47
Q

What is sucralfate?

A
  • Complex of sucrose octasulphate and aluminium hydroxide
  • Precipitates and binds ulcerated tissue (oesophagus, stomach) – chemical diffusion barrier
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48
Q

What should be considered when medicating with sucralfate?

A
  • Avoid direct co-administration with acid blockers (1-2 hours apart)
  • Impedes absorption of quinolones, tetracyclines, digoxin
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49
Q

What is ‘pink lady’?

A

Antacid and lidocaine (referral)

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50
Q

How is GERD managed?

A
  • Postural feeding – little and often
  • Low fat to facilitate gastric emptying
  • Consider hydrolysed diet if concurrent chronic enteropathy
  • Weight management
  • Acid blockers – omeprazole
  • LES drugs – cisapride
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51
Q

How is oesophagitis managed?

A
  • Oesophageal rest – gastrotomy tube?
  • Reintroducing food – soft, bland food, small, frequent meals, low fat diet if gastro-oesophageal reflux
  • Acid blockade – omeprazole
  • Coating agents – sucralfate
  • Improve lower oesophageal sphincter tone – cisapride
  • Facilitate gastric emptying – metoclopramide
  • NSAIDs
  • Weight loss, low fat diet
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52
Q

What are the possible complications of regurgitation?

A
  • Malnutrition
  • Dehydration
  • Anorexia or (perceived) polyphagia
  • Reflux pharyngitis/rhinitis – nasal discharge
  • Aspiration pneumonia – cough, dyspnoea, pyrexia
  • Sometimes swallowing pain
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53
Q

How are the complications of regurgitation managed?

A
  • Diagnose and manage GERD and stricture early
  • Aspiration pneumonia
  • Consider nutritional requirements/management pre-operatively
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54
Q

Outline acute and chronic onset of vomiting and diarrhoea.

A

Acute – most are under 1 week, definitely under 3 weeks

Chronic – over 3 week duration

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55
Q

What are the clinical signs of acute gastrointestinal disease?

A
  • Vomiting
  • Diarrhoea
  • Variable appetite
  • Flatus, borborygmi, bloating, eructation
  • Haematemesis
  • Melaena/fresh blood in faeces
  • Weight loss
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56
Q

Name the 4 stages of vomiting.

A

Prodromal (nausea)
Retching
Expulsion
Relaxation

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57
Q

How can vomiting be classified?

A
  • Active, abdominal effort, brainstem involvement
  • Gastric and upper intestinal content
  • Gastrointestinal or extra-gastrointestinal disease
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58
Q

What are the characteristics of small intestinal diarrhoea?

A

Large volume
Normal frequency
No urgency
With/without other signs of SI disease:
- Malabsorption, weight loss – clinical, laboratory
- Inappetence vs. polyphagia, coprophagia or pica
- Gas production

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59
Q

What are the characteristics of large intestinal diarrhoea?

A
  • Small volume
  • Increased frequency
  • With urgency
  • With straining (tenesmus)
  • With difficulty (dyschezia)
  • With/without blood (haematochezia) or mucus
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60
Q

What is involved in the physical examination of acute gastrointestinal disease?

A
  • Consider PPE/barrier nursing
  • Hydration and fluid status – dehydrated? Hypovolaemic?
  • Assess pain and localise
  • Palpable abnormality?
  • Evidence of systemic disease
  • Rectal examination
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61
Q

What are some primary causes of vomiting and diarrhoea?

A
  • Mass lesions
  • Inflammatory disease
  • Dietary indiscretions/intolerances
  • GI ulceration
  • Obstructive lesions – foreign bodies, torsions, intussusception, stricture,
  • Toxins/drugs
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62
Q

What are some extra-gastrointestinal causes of vomiting and diarrhoea?

A

Pancreatic disease
Renal disease
Hepatic disease
Endocrine disease
Pyometra
Peritonitis
Systemic inflammatory or neoplastic disease
Motion sickness
Vestibular disease
Drugs

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63
Q

What are some examples of aspects of a history that direct us towards primary gastrointestinal disease?

A
  • Known foreign body ingestion
  • Palpable GI mass lesion
  • Haematemesis/melaena
  • Young puppy/kitten with worms in diarrhoea
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64
Q

What are the clinical signs of acute pancreatitis?

A
  • Vomiting
  • Diarrhoea (less common)
  • Inappetence
  • Abdominal pain
  • Pyrexia – sterile inflammatory response
  • Jaundice? Because of where the pancreas sits, it may affect other structures in that area, such as extra-hepatic bile duct obstruction
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65
Q

Distinguish the onsets of acute and chronic pancreatitis.

A

Acute - sudden onset

Chronic - waxing/waning, may be persistently symptomatic or have intermittent episodes

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66
Q

Distinguish the inflammation of acute and chronic pancreatitis.

A

Acute - variable severity

Chronic - progressive inflammatory/fibrosis cycles

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67
Q

Distinguish the prognoses of acute and chronic pancreatitis.

A

Acute - potentially fully reversible

Chronic - end stage can result in EPI/eccrine pancreatic insufficiency or DM/diabetes mellitus

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68
Q

What are the possible triggers of pancreatitis?

A
  • Idiopathic
  • Hyperlipaemia – dietary indiscretion is common, obesity, hyperlipidaemia – too much lipid in the blood, makes blood viscous, reduces oxygenation
  • Miniature Schnauzers breed disposition
  • Blunt abdominal trauma
  • Hypoperfusion – hypovolaemia, lipaemia?
  • Drug related – KBr, phenobarbitone, azathioprine, L-asparaginase, glucocorticoids
  • Immune mediated
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69
Q

What are the local and systemic effects of pancreatitis?

A

Local enzyme release – localised pancreatitis, fat necrosis of fat around the pancreas

Systemic enzyme effects – acute kidney injury, cardiac arrhythmias, effusions, shock, SIRS, DIC, death

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70
Q

What are the possible species causing bacterial enterocolitis?

A

E. coli, Clostridium perfringens, Campylobacter spp. and Salmonella spp. can all be isolated from healthy dogs faeces so how do we know which bacteria are causing clinical signs

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71
Q

What are the risk factors of bacterial enterocolitis?

A

Raw fed
Young
Unsanitary/crowded environment

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72
Q

What are the clinical signs of bacterial enterocolitis?

A

Haemorrhagic vomiting and/or diarrhoea
Pyrexia
Sepsis
With/without abdominal pain
Enterotoxaemia is possible

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73
Q

How can bacterial enterocolitis be diagnosed?

A

Culture to evaluate for parvovirus
PCR to speciate
ELISA for toxins

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74
Q

What are the characteristics of acute haemorrhagic diarrhoea syndrome?

A

Marked haemoconcentration, can have vomiting, bloody gelatinous diarrhoea

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75
Q

What is the pathogenesis of C.perfringes causing acute haemorrhagic diarrhoea syndrome?

A
  • NetF toxin leads to pore formation in enterocytes
  • Fluid leakage into intestines leading to diarrhoea
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76
Q

Which breed is over-represented for acute haemorrhagic gastroenteritis?

A

Miniature Schnauzer

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77
Q

What are the consequences of acute haemorrhagic diarrhoea syndrome?

A
  • Abdominal pain
  • Obtundation
  • Extreme fluid losses into gut lumen – hypovolaemic shock rapidly, marked haemoconcentration
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78
Q

How is acute haemorrhagic diarrhoea syndrome diagnosed?

A
  • Clinical signs
  • Marked elevation in PCV without commensurate increase in proteins
  • Exclude other causes with similar presentations (acute dietary indiscretion/intoxication, acute pancreatitis, hypoadrenocorticism, parvovirus, other bacterial enteritides and intussusception)
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79
Q

What is the epidemiology of parvovirus?

A

Faeco-oral spread – very effective: large quantities shed in diarrhoea, low infective dose, resistant virus – remains infective for up to 1 year

Inactivated by formalin and hypochlorite disinfectants

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80
Q

What are the clinical signs of parvovirus?

A
  • Haemorrhagic diarrhoea – anorexia, depression, abdominal pain, considerable fluid deficits
  • With/without vomiting
  • Neutropenia
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81
Q

What is the consequence queens being infected with feline parvovirus/feline panleukopenia/feline infectious enteritis during pregnancy?

A
  • Can lead to cerebellar hypoplasia in kittens
  • Hypermetric ataxia and intention tremors
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82
Q

What is the signalment of tritchomonas foetus?

A

Kittens, young cats under 12-18months of age, maturity leads to an effective immune response

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83
Q

What are the clinical signs of tritchomonas foetus?

A
  • Asymptomatic – chronic recurrent large intestinal diarrhoea
  • With/without peri-anal oedema
  • With/without faecal incontinence
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84
Q

What are the consequences of acute gastrointestinal disease?

A
  • Dehydration – may lead to pre-renal azotaemia
  • Acid-base disturbance
  • Aspiration pneumonia – especially if sedated/neuromuscular disease/upper airway incompetency
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85
Q

How is there acid-base disturbance from acute gastrointestinal disease?

A
  • Loss of water/electrolytes
  • Fed or fasted state affects acid loss
  • Loss of acid from stomach or loss of bicarbonate from duodenum
  • Pattern depends on whether pylorus is obstructed or non-obstructed
86
Q

What is the consequence of pyloric obstruction?

A

Losing acid > metabolic alkalosis and hypokalaemia

87
Q

How can we differentiate general haemorrhagic diarrhoea from AHDS?

A

PCV

88
Q

What are the further initial tests that can be done investigating acute gastrointestinal disease?

A
  • Acute pancreatitis – cPLI/fPLI
  • Hypoadrenocorticism (dogs) – basal cortisol/ACTH stimulation
  • Hyperthyroidism (cats – usually chronic) – total T4
89
Q

What is PLI?

A

Pancreatic lipase immunoreactivity – species specific (canine and feline):

  • Quantitative monoclonal antibody – spec cPL and spec fPL
  • Qualitative SNAP test – very sensitive, lots of false positives, useful to exclude as getting a negative is more likely to be true
90
Q

What may blood tests reveal about the pancreas in acute gastrointestinal disease?

A
  • Inflammatory changes on haematology
  • Cholestatic hepatopathy
  • Post-hepatic icterus
  • Increased cPLI/fPLI
  • Acute phase protein response – low albumin neg app, high globulin pos app
91
Q

What are the possible indications for diagnostic imaging when investigating acute gastrointestinal disease?

A
  • Perform early in acute vomiting and diarrhoea if palpable abnormality
  • If you suspect structural disease within the abdomen but not palpable e.g. history of foreign body ingestion
  • If abnormalities on bloods
92
Q

How is acute/chronic pancreatitis radiographed?

A
  • Local peritonitis right cranial quadrant – loss of detail, ileus
  • Poor sensitivity/specificity
93
Q

How is acute/chronic pancreatitis imaged on ultrasonography?

A
  • Acute – changes may be seen
  • Chronic – may appear normal
  • Pain on probe-pressure
  • Abnormal size
  • Reduced echogenicity
  • ‘Mass effect’
  • Cyst/abscess/free fluid
94
Q

How is parvovirus diagnosed in puppies?

A
  • Faecal parvovirus antigen ELISA (in house SNAP test) - repeat if suspicious and negative. may get false positives for 4-8 days post live vaccination
  • Send to faecal sample to laboratory for PCR – delayed diagnosis versus in house
  • Post-mortem (various tissues) – useful information for other in-contact dogs/puppies
95
Q

For less severe small intestinal haemorrhagic diarrhoea than parvovirus, how is a diagnosis reached?

A
  • Faecal parasitology – faecal smear
  • Giardia antigen ELISA SNAP test 90% sensitive, 95% specific
  • Giardia oocysts: shedding is intermittent, 3 pooled samples in zinc sulfate floatation = 95% sensitive
  • Colonic wash if suspicion of Tritrichomonas – Tritrichomonas PCR
96
Q

When should bacterial causative agents of acute gastrointestinal disease be considered?

A

Pyrexic
Neutropenic
Septic
Young
Raw fed
Acute haemorrhagic vomiting and/or diarrhoea

97
Q

How are small, soft or non-caustic gastric foreign bodies removed?

A

Attempt emesis

98
Q

When is endoscopy used to manage gastric foreign bodies?

A
  • If had full meal since then do not try to retrieve – see if passes
  • Look for with endoscopy if recent ingestion but look for signs of peritonitis and deterioration, may need to give food to ensure keeps passing along
  • If incidental finding then likely to be embedded in stomach wall – leave alone
99
Q

What should be done about bone gastric foreign bodies?

A

Gastric bones should dissolve

100
Q

How are intestinal foreign bodies treated?

A
  • If obstructed/perforated – surgical resection
  • Small/not obstructed/needle – bread, high fibre diet for bulk to help passage
101
Q

If there are no investigations and patient may not need specific treatment, how is acute gastrointestinal disease managed?

A
  • Short period of starvation if vomiting?
  • Bland easily digestive diet
  • Owners bring back if deterioration or failure to improve in 48 hours
  • Fluid options at home - rehydration solutions, wet/watered down food, little and often
102
Q

What are some treatment options for acute gastrointestinal disease?

A
  • Nutrition
  • Fluid intake
  • Medications
  • Pre/probiotics – limited evidence, used for patients we are not that worried about, makes owner feel better
  • Anti-diarrhoea pastes with kaolin/pectin – cosmetic benefit
103
Q

What medications can be used to treat acute gastrointestinal disease?

A
  • Anti-emetics – exclude obstruction first
  • Appetite stimulants
  • Analgesia?
  • Anthelmintics?
  • Antibiotics only if indicated clinically
  • Buscopan (rarely used, licensing) – spasmolytic
104
Q

Why is bland food given little and often in acute gastrointestinal disease?

A
  • Intestinal cells require nutrients to recover
  • Transition back to normal diet over 2-5 days when gastrointestinal signs improved
105
Q

Which antiemetics are used in dogs with acute gastrointestinal disease?

A
  • Maropitant first line – NK1 receptor antagonist, hepatic metabolism
  • Metoclopramide in addition if needed – D2 receptor antagonist/5-HT 4
  • Ondansetron sometimes used – serotonin antagonist
106
Q

Which antiemetics are used in cats with acute gastrointestinal disease?

A
  • Maropitant most common
  • Ondansetron if maropitant ineffective (uncommon in primary care)
107
Q

When are antiemetics contraindicated?

A

Do not give anti-emetics if suspicion of obstruction

108
Q

When should small animals be wormed against round worms?

A
  • Regular worming of dam during pregnancy
  • Routine anthelmintic puppy/kitten plan
109
Q

What is the effect of the hookworm, Ancylostoma(sub-)tropical, and how is this managed?

A

Considerable GI blood loss with/without anaemia, with/without iron deficiency

Iron supplementation/blood transfusion if needed

110
Q

What is the effect of the hookworm, Uncinaria stenocephal?

A

Penetrates digital skin > migrates > pedal pruritus (itchy feet) with/without diarrhoea

111
Q

What is the effect of whipworms and how is this managed?

A
  • Reside in caecal and colonic
  • LI signs with/without GI blood loss, abdominal pain
  • Need repeated treatments as long PPP
112
Q

How are giardia (protozoa) species managed?

A
  • Fenbendazole - 3 days
  • Metronidazole - 5 days
  • Treat all pets in household
  • Hygiene – zoonotic
113
Q

How is tritrichomonas feotus (protozoa) managed?

A
  • Ronidazole (side effects - neurological signs, teratogenic)
  • Environment – hygiene. Isolate – do not reintroduce? Zoonotic? Faeco-oral and mutual grooming
  • Manage stress
114
Q

What are the effects of probiotics on the gastrointestinal tract?

A
  • Live micro-organisms
  • PO administration
  • Alter intestinal flora
  • Modulate intestinal immune system
  • Proposed beneficial effect on health
115
Q

When are antibiotics used in acute gastrointestinal disease?

A

Treat if systemically ill - haemorrhagic gastroenteritis, pyrexia, inflammatory leukogram

116
Q

How is acute pancreatitis managed?

A
  • Fluid support – IV crystalloids
  • Plasma for systemic inflammatory response
  • Nutritional support
117
Q

What medications are used to treat acute pancreatitis?

A
  • Antiemetics – Maropitant, metoclopramide
  • Appetite stimulant – Mirtazepine
  • Analgesia
118
Q

Why is the prognosis of acute pancreatitis guarded?

A
  • Risk of death or recurrence
  • Possible sequalae – chronic recurrent pancreatitis, exocrine pancreatic insufficiency, diabetes mellitus
119
Q

How is acute haemorrhagic diarrhoea syndrome treated?

A
  • Intravenous crystalloid therapy
  • Amoxicillin clavulanate when indicated – pyrexia or signs of sepsis
120
Q

How is canine parvovirus managed?

A
  • Barrier nursing/disinfection with hypochlorite
  • Naso-oesophageal tube trickle feeding, once vomiting controlled – faster recovery, lower mortality
  • Aggressive fluid therapy – IV crystalloids
121
Q

How is canine parvovirus treated?

A
  • Control emesis – maropitant, metoclopramide, potentially ondansetron
  • Antibiotics – if severe H+ diarrhoea or neutropenic, amoxicillin clavulanate (IV)
  • Faecal microbial transplantation (FMT)?
  • Feline ω-interferon – borderline benefit? Expensive
122
Q

What gastrointestinal diseases are German shepherds predisposed to?

A
  • Chronic enteropathies/antibiotic responsive diarrhoea (ARD)
  • High incidence of EPI/eccrine pancreatic insufficiency
  • Anal furunculosis
123
Q

What may the mucous membranes reveal about gastrointestinal disease?

A
  • Pale – poor perfusion, anaemia
  • Petechiae – mmbs, ventrum and ear pinnae most
  • Primary coagulopathy
124
Q

What are the primary chronic gastrointestinal differential diagnoses?

A

Chronic inflammatory enteropathies (CIEs)/Chronic enteropathy:
- Food responsive diarrhoea (FRD)
- Antibiotic responsive diarrhoea (ARD)
- Idiopathic inflammatory bowel disease (IBD/iIBD)

GI neoplasia

125
Q

What are the chronic extra-gastrointestinal differential diagnoses?

A
  • Exocrine pancreatic insufficiency (EPI)
  • Endocrine disease
  • Renal disease
  • Hepatic disease
  • Sterile inflammatory, such as chronic pancreatitis
126
Q

What are protein losing enteropathies?

A

Severe (diffuse) small intestinal disease. Severe loss of albumin and globulin through the gut, so you get a panhypoproteinaemia (low TP, albumin and globulin on bloods) and sometimes see isolated hypoalbuminaemia. Could be protein leaking into the blood or element of poor absorption.

127
Q

What could cause moderate-severe hypoalbuminaemia?

A
  • Exudative disease
  • Blood loss
  • Liver disease – inadequate production = bile acid stimulation test
  • Intestinal disease – PLE, loss of protein into GIT = B12/folate
  • Kidney/glomerular disease – PLN, excessive renal loss of protein into urine = urine protein:creatinine ration
128
Q

What are the complications of hypoalbuminaemia?

A
  • Hypoalbuminaemia > effusions, oedema
  • Loss of anti-thrombin 3 anticoagulant
129
Q

How is loss of anti-thrombin-3 anticoagulant treated?

A

Thrombi prophylaxis – clopidogrel or aspirin

130
Q

What are the causes of protein losing enteropathies and how are these differentiated?

A

Histopathology

  • IBD
  • Lymphangiectasia
  • Alimentary lymphoma
131
Q

What is the pathogenesis of lymphangiectasia?

A
  • Lymphatic vessels become dilated and rupture
  • Leak lymph into intestinal lumen
  • Loss of proteins and fat
  • Diarrhoea and profound weight loss
132
Q

Which dog breed is predisposed to lymphangiectasia?

A

Norwegian lundehund

133
Q

How is lymphangiectasia treated?

A
  • High quality and easily digestible low-fat diet
  • Anti-inflammatory doses of steroids
  • Clopidogrel or aspirin
  • Supplement fat-soluble vitamins
134
Q

What is triaditis?

A

Inflammation of liver, pancreas and intestines

135
Q

What does chronic pancreatitis result from?

A
  • Repeated attacks of acute pancreatitis
  • Or chronic low-grade pancreatitis
  • Duct-centred fibrosis in Cocker Spaniels
136
Q

What is the consequence of chronic pancreatitis?

A

Progressive destruction and fibrosis

137
Q

What are the clinical signs of chronic pancreatitis?

A
  • Chronic/intermittent inappetence
  • With/without vomiting
  • With/without diarrhoea (large intestinal)
  • With/without abdominal pain
138
Q

Name 2 pancreatitic neoplasias.

A

Ductular and acinar adenocarcinoma
Endocrine neoplasia (very rare)

139
Q

How are ductular and acinar adenocarcinomas characterised?

A
  • Largely incurable, malignant
  • Signs predominantly related pancreatitis with/without pancreatic mass lesion CBD obstruction > cholestasis and post-hepatic jaundice
140
Q

How is endocrine neoplasia characterised?

A

Insulinoma > hypoglycaemia

Gastrinoma > gastric ulceration and diarrhoea

141
Q

What are the clinical signs of chronic gastritis?

A
  • Intermittent chronic vomiting (vague) – periodic early morning vomit with bile (bilious vomiting)
  • Poor appetite
142
Q

What are the consequences of gastric bleeding?

A
  • Haematemesis, melaena
  • Anaemia
143
Q

What is the aetiology of chronic gastritis?

A
  • Dietary sensitivity
  • Idiopathic – part of IBD
  • Spiral bacteria (Helicobacter)?
144
Q

What are 3 causes of upper gastrointestinal haemorrhage?

A

Coagulopathy
Gastrointestinal pathology - primary or extra-gastrointestinal
Swallowed blood

145
Q

What are some extra-gastrointestinal diseases that can cause upper gastrointestinal haemorrhage?

A
  • Renal disease
  • Hepatic disease
  • Hypoadrenocorticism – deficiency in steroid leads to gastric ulceration
  • GI hypoperfusion
  • Hyperacidity syndromes – gastrinoma– produces gastrin leading to stomach acid production, mast cell tumour
146
Q

What are some primary gastrointestinal diseases that can cause upper gastrointestinal haemorrhage?

A
  • Drug induced ulcers – NSAIDs, steroids
  • Foreign body – trauma
  • Neoplasia – gastric carcinoma
  • Inflammatory disease
147
Q

What are some possible complications of gastric ulcers?

A
  • Chronic (external) blood loss – loss of iron, iron-deficiency anaemia
  • Perforation – septic peritonitis, surgical correction needed
148
Q

Which diagnoses can lead to a protein losing enteropathy?

A

Lymphangiectasia, alimentary lymphoma and inflammatory bowel disease

149
Q

How can chronic gastrointestinal disease be investigated with faecal analysis?

A

Faecal screen – faecal parasitology, giardia species antigen ELISA

Colonic wash – tritrichomonas

150
Q

How are bloods used to investigate chronic gastrointestinal disease?

A
  • Exclude hyperthyroidism
  • If considerable azotaemia or underlying hepatopathy, direct investigations to kidneys/liver
  • Malabsorption – hypoalbuminaemia, hypocholesterolaemia
  • Electrolyte derangements - GI fluid and electrolyte losses (vomiting and diarrhoea), hypoadrenocorticism
151
Q

How are further blood tests used to investigate chronic gastrointestinal disease?

A
  • GI investigation blood screens often cover B12 and folate together
  • With/without PLI – SNAP versus quantitative test
  • With/without TLI
152
Q

Why is folate measured in the investigation of chronic gastrointestinal disease?

A
  • B9 absorbed in proximal SI (jejunum) with folate carrier
  • Hypofolataemia – marker of jejunal absorption of micronutrients
153
Q

Why is cobalamin measured in the investigation of chronic gastrointestinal disease?

A

B12 is absorbed in distal small intestine (ileum) – absorption depends on intrinsic factor binding. Pancreatic production only in cat

154
Q

What is hypocobalaminaemia caused by?

A
  • Ileal malabsorption
  • Dysbiosis (some bacteria consume B12)
  • EPI –exclude with TLI
  • Hereditary disorders
155
Q

What is hypercobalaminaemia caused by?

A

Neoplastic and hepatic disease in cats

156
Q

What are the clinical signs of exocrine pancreatic insufficiency?

A

Consider if diarrhoea or considerable weight loss

157
Q

How is exocrine pancreatic insufficiency diagnosed and treated?

A

If TLI low then treat EPI – highly digestible diet, enzyme supplementation, check vitamin B12 levels

158
Q

What happens to electrolytes in atypical addisons?

A

Low sodium and high potassium, ratio of less than 27. Atypical addisons’s can have completely normal electrolytes.

159
Q

Does hypocbalaminaemia indicates pathology in the proximal small intestine?

A

No – folate indicates this

160
Q

Describe diet trials for food intolerance/sensitivity.

A
  1. Novel protein/carbohydrate or hydrolysed protein Specific
  2. Feed exclusively with water for 3-10 weeks
  3. Re-challenge after diet trial
  4. If no improvement, try a different diet
  5. If signs resolved, continue new diet for around 6 months for gut recovery
  6. Then re-challenge by slowly adding back in foods – wait a week each time before adding a new protein or carbohydrate
161
Q

What is done post diet trail for food intolerances/sensitivities?

A
  • Exclude hypoadrenocorticism in dogs – basal cortisol, ACTH stimulation
  • Urinalysis if indicated – pyelonephritis – chronic vomiting
  • BAST if indicated
  • Evaluate FIV/FeLV in cats – FIV antibody ELISA, FeLV antigen ELISA
162
Q

When should you perform diagnostic imaging early when investigating chronic gastrointestinal disease?

A
  • Palpable abdominal abnormality/mass lesion
  • Pain
  • GI haemorrhage
  • Concern for GI perforation
163
Q

Which primary chronic gastrointestinal pathologies can be investigated with diagnostic imaging?

A
  • Altered gastrointestinal wall thickness
  • Loss or change of gastrointestinal wall layering
  • Mass lesions
  • Ulceration
164
Q

Which chronic extra-gastrointestinal pathologies can be investigated with diagnostic imaging?

A
  • Abdominal inflammatory disease
  • Abdominal neoplastic disease
  • Metabolic/endocrine disease
  • Genitourinary disease
165
Q

What are some secondary motility disorders causing functional abnormal delayed gastric emptying?

A
  • Primary GI disease – ulceration, inflammation, neoplasia, malabsorption
  • Local inflammatory abdominal disease (e.g. pancreatitis)
  • Electrolyte disturbance (hypokalaemia, hypercalcaemia)
  • Drugs – especially opioids
  • Pain, stress
166
Q

What are some structural abnormal causes of delayed gastric emptying?

A
  • Pyloric foreign body
  • Pyloric mass lesion – neoplasia, polyp
  • Chronic hypertrophic pylorogastropathy
167
Q

If there are no abnormalities found in diagnostic imaging, what is done?

A
  • Diet trial vs. endoscopy/histopathology
  • Assuming didn’t diet trial at earlier stage
168
Q

If there are extra-gastrointestinal abnormalities found on diagnostic imaging, what is done?

A

Investigate and treat as appropriate

169
Q

If there are primary focal gastrointestinal abnormalities found on diagnostic imaging, what is done?

A

Endoscopy

Surgery required if:
- Chronic foreign body
- Concern for sepsis/perforation
- Focal lesions (excision) – neoplasia, chronic hypertrophic pylorogastropathy

170
Q

If there are primary diffuse gastrointestinal abnormalities found on diagnostic imaging, what is done?

A

Referral for endoscopy with/without biopsies

171
Q

Why are biopsies done last in investigations into chronic gastrointestinal disease?

A
  • Extra-GI disease common
  • Parasitic disease common
  • Some drugs cause GI clinical signs
  • Dietary intolerance – diet trails would resolve
172
Q

What presentations might persuade us to biopsy earlier?

A

Anorexia
Abnormal GI imaging
Hypoalbuminaemia

173
Q

What can be achieved with laparotomy under GA?

A
  • Enables multiple full thickness biopsies from multiple regions of GIT
  • Can sample other organs
  • Surgical risk of dehiscence
174
Q

What can be achieved with endoscopy under GA?

A
  • Minimally invasive
  • Small biopsies – not full thickness
  • May not reflect jejunal disease
175
Q

What are some chronic inflammatory enteropathies that can be diagnosed with biopsy?

A

Structural changes – villus blunting, change to structure of villi

Inflammatory infiltrate
- Lymphoplasmacytic or eosinophilic
- Neutrophilic or histiocytic

176
Q

What is the most common inflammatory infiltrate ion GI biopsies?

A

Lymphoplasmocytic

177
Q

How can dietary management be used for chronic gastrointestinal disease?

A
  • Gastrointestinal veterinary diets
  • Exclusion diet
  • Prescription diets in cats - wean over 1-4 weeks
  • If any nausea – consider anti-emetics
  • Consider appetite stimulants
178
Q

How can cobalamin supplementation be given?

A

Subcutaneous injections - weekly until normalised (4-6 weeks). Re-measure serum cobalamin 4-6 weeks after completion of course

Oral - daily (mega-doses). Re-measure serum cobalamin after 4-6 weeks. Check once stopped 4-6 weeks to ensure holding. Megadoses mean they normalise blood B12 despite ileal malabsorption and low intrinsic factor

179
Q

How is the microbiome medically targeted?

A
  • Probiotics/prebiotics
  • Antibiotics
  • Faecal microbiome transplantation
180
Q

How is chronic gastritis treated?

A
  • Removal of aetiological agent if known
  • Acid blockers – PPIs/proton pump inhibitors (omeprazole) vs. H2 antagonists (cimetidine)
  • Diet - multiple small feedings (late at night?) Low fat diet – stomach will empty faster. Exclusion diet
181
Q

How is chronic pancreatitis treated?

A
  • Avoid risk factors – high fat diet is a risk factor for pancreatitis, easy digestible (not necessarily low fat unless hyperlipaemic) is a good step
  • Weight reduction
  • Opioids if hospitalised, paracetamol (not cats), tramadol, gabapentin
  • Anti-emetics
  • Appetite stimulation
182
Q

How is IBD treated?

A
  • Exclusion diet
  • Immunosuppression with tapering course of corticosteroids
  • Tapering course or long term immunosuppressants
  • With/without adjunct chlorambucil (cats), azathioprine (dogs), cyclosporine (both – cats check toxoplasma gondii status first
  • Monitoring response - demeanour, weight gain and BCS, monitor cobalamin and albumin on bloods prior to tapering
183
Q

What is the prognosis of IBD treatment?

A
  • Cannot predict based on clinical OR histopathological severity
  • May progress to small cell lymphoma in cats
  • Ultimately cautious – guarded
184
Q

How is lymphoplasmocytic colitis treatment?

A
  • Sulphsalazine (Salazopyrin) - cleaved by colonic bacteria > local release of 5-ASA
  • Local anti-inflammatory
185
Q

What are the clinical signs of granulomatous/histiocytic ulcerative colitis?

A

Large intestinal diarrhoea with/without severe weight loss

186
Q

How is granulomatous/histiocytic ulcerative colitis diagnosed?

A
  • Adherent and invasive E.coli
  • Ideally culture and sensitivity as multi-drug resistance
  • Enrofloxacin 6-8 weeks minimum
  • 1 month beyond clinical resolution
  • Enrofloxacin cartilage damage in young dogs
187
Q

What is the pathogenesis constipation?

A

Impaction of the colon or rectum with faecal material – excessively dry/hard faeces, hair, bones

Prolonged constipation > irreversible changes > obstipation

188
Q

What are the clinical signs of constipation?

A
  • Infrequent defecation
  • Passing mucus instead of constipated material or ‘Diarrhoea’
  • Dyschezia; straining to defecate (tenesmus)
  • Pain associated with attempted or successful defecation
  • Anorexia, lethargy
  • Vomiting due to obstruction of faeces and metabolic consequences
189
Q

What are the possible causes of constipation?

A
  • Hair/bone content
  • Chronic disease causing dehydration
    hypokalaemia, hypercalcaemia
  • Drug related
    stress, lack of exercise, dirty/absent toileting opportunities
  • Pain/orthopaedic problems – inability to posture
  • Spinal or neuromuscular disease – disc disease, tail pull, idiopathic megacolon, dysautonomia
  • Obstruction - neoplasia, stricture, foreign body, atresia, fractures, callus, mass lesion
  • Perineal hernia
  • Peri-anal, ano-rectal pain
190
Q

How is constipation managed?

A
  • Fluid therapy with/without electrolyte correction
  • Oral laxatives – mild cases
  • Enemas – colonic irrigation under GA, manual removal of faecal matter
  • Motility modification (cisapride)
  • Surgery - mass lesions, perineal hernia
191
Q

What are the clinical signs of rectal diseases?

A
  • Dyschezia
  • Blood streaks on stools
  • Dragging bottom
  • Acutely overgrooming elsewhere obsessively
192
Q

What are the differential diagnoses for rectal diseases?

A
  • Anal sac infections
  • Foreign bodies
  • Neoplasia
  • Rectal polyps
193
Q

What are rectal polyps and their effects?

A
  • Benign adenomatous growth
  • Affect terminal rectum
  • Causes haematochezia without diarrhoea
  • May transform to carcinoma
194
Q

How are rectal polyps removed?

A

By traction (regrow) or pull out

Rectal polyp with haemorrhage submucosal resection during a rectal

195
Q

How can anal furunculosis/perineal fistulae be treated?

A
  • Immunosuppression/immune-modulation – ciclosporin. Other immunosuppressants less effective
  • Topical treatments can maintain remission – barrier creams, topical immunosuppressant
  • Analgesia – not NSAIDs
  • Antibiotics? If linked to ARD, consider antimicrobial resistance
  • Surgery
196
Q

What are the risks of anal furunculosis surgery?

A

Post-operative infections
Incontinence
Anal stenosis
Recurrence

197
Q

How can constipation and cystitis be differentiated from observation?

A

Constipation – high posture straining to poo

Cystitis – squat lower in cystitis

198
Q

What is the difference between obstipation and megacolon on a radiograph?

A

Maximum diameter of the colon and the length of L5

199
Q

Distinguish iodine and barium use for imaging the gastrointestinal tract.

A

Iodine are radiodense so show up and we can put in IV, body excreted via kidneys to illuminate urinary system. So care with cats and kidney disease and iodine. Barium is per os and shows up GI tract and is excreted in the faeces unchanged

200
Q

Can you use endoscopy for linear foreign bodies?

A

Can use endoscopy but need to make sure it is safe to do so, often worth a try if very recent

201
Q

What determines if you use emesis or not for a gastrointestinal foreign body?

A

FB localisation determines whether or not you can do emesis not amount of time afterwards (confusion about emesis with toxin ingestion)

202
Q

How can red rubber catheters be used to retrieve non-perforating small intestine foreign bodies?

A

Plicated so single enterotomy incisions and get end of linear FB and tie to end of rubber catheter and push this down into the intestine which can be milked out or get FB inside rubber catheter and pull out

203
Q

How much of the small intestine can you remove?

A

Can take out around 80% of small intestine

204
Q

What can peristalsis on a radiograph mimic?

A

Plication

205
Q

How can post operative analgesia have complications from gastrointestinal surgery?

A

Giving lots of opioids after surgery can sometimes may a well animal appear/feel worse and look flat, leading to unnecessarily worry about peristalsis

Cats do not do well on methadone post op, so switch to buprenorphine after surgery. Dogs are opposite

206
Q

What can be done with ileus?

A

Prokinetics post operatively for ileus – especially if small intestinal FB caused obstruction

Abdominal massage in rabbits with ileus – tell owners to do this

207
Q

Which drugs are prokinetic and antiemetic?

A

Cisapride – prokinetic
Lidocaine – prokinetic
Maropitant – antiemetic
Metoclopramide – antiemetic and prokinetic
Ranitidine – prokinetic

208
Q

How is pneumoperitoneum diagnosed from a radiograph?

A

Looking for gas on radiograph that is next to diaphragm that is not in the stomach

209
Q

Which sutures are used in resection and anastamoses surgeries?

A

Inverting sutures will reduce lumen size so avoid for small intestinal R and As, which predisposes to blockages – inverting patterns include Lempert, connel, cushing, Utrecht. 2mm max between these sutures and not too far from incision

210
Q

How soon will you offer food after gastrotomy with no complications?

A

As soon as animal can maintain sternal recumbency and lift head, or 2 hours, 4 hours or wait until 2 hours after vomiting. Younger animals need to be offered food even sooner.

CVSOH 4 (13 decks)

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