Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name 4 differential diagnoses for swallowing disorders.

A

Oral pain
Oral mass
Oral trauma
Neuromuscular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some functional oesophageal differential diagnoses?

A
  • Nerves or neuromuscular junctions
  • Muscles
  • Primary disease
  • Secondary disease - metabolic, endocrinopathies (hypothyroidism, hypoadrenocorticism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name some congenital and acquired structural oesophageal disease.

A

Congenital – vascular ring anomaly

Acquired – foreign body, neoplasia, gastro-oesophageal intussusception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is functional gastro-oesophageal reflux?

A
  • Reflux of gastric acid and enzymes into the oesophagus
  • Leads to inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is GERD?

A

Gastro-oesophageal reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are 3 causes of GERD?

A
  • Hiatal hernia: congenital/age-related
  • Lower oesophageal sphincter dysfunction
  • Underlying chronic enteropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a risk of megaoesophagus?

A

Aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the clinical signs of aspiration pneumonia?

A

Tachypnoea
Pyrexia
Lethargy
Inappetence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What can give false megaoesophagus?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is reflex and regurgitation investigated?

A
  • Haematology
  • Serum biochemistry
  • Survey neck and chest radiography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How should we remove an oesophageal foreign body?

A

Surgery can cause oesophageal damage or strictures. Endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A

Barium mixed with food/liquid - high risk of aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is fluoroscopy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

When is endoscopy indicated?

A
  • To retrieve foreign body
  • To evaluate for hiatal hernia (after other imaging)
  • To evaluate for/dilate stricture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When is endoscopy contraindicated?

A

If megaoesophagus already shown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How can regurgitation be managed?

A
  • Correct the underlying disease if possible
  • Positional feeding
  • Medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is positional/postural feeding essential for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does omeprazole work?

A
  • Proton pump inhibitor
  • Irreversibly binds H + secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When is cisapride indicated?

A

GERD
Feline idiopathic megacolon
Pro-motility agent in other species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is used if cisapride is not tolerated?

A

Metoclopramide – to facilitate gastric emptying may be of value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is sucralfate?

A
  • Complex of sucrose octasulphate and aluminium hydroxide
  • Precipitates and binds ulcerated tissue (oesophagus, stomach) – chemical diffusion barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is ‘pink lady’?

A

Antacid and lidocaine (referral)

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
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
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
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
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

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
56
Q

Name the 4 stages of vomiting.

A

Prodromal (nausea)
Retching
Expulsion
Relaxation

57
Q

How can vomiting be classified?

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

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
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
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
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

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
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
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

66
Q

Distinguish the inflammation of acute and chronic pancreatitis.

A

Acute - variable severity

Chronic - progressive inflammatory/fibrosis cycles

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

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
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

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

71
Q

What are the risk factors of bacterial enterocolitis?

A

Raw fed
Young
Unsanitary/crowded environment

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

73
Q

How can bacterial enterocolitis be diagnosed?

A

Culture to evaluate for parvovirus
PCR to speciate
ELISA for toxins

74
Q

What are the characteristics of acute haemorrhagic diarrhoea syndrome?

A

Marked haemoconcentration, can have vomiting, bloody gelatinous diarrhoea

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
76
Q

Which breed is over-represented for acute haemorrhagic gastroenteritis?

A

Miniature Schnauzer

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
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)
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

80
Q

What are the clinical signs of parvovirus?

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

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
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
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

CVSOH 4 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions