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Cat & Dog > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Define dysphagia

A

Difficulty eating and/or swallowing

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2
Q

Define pseudoanorexia

A

The animal is hungry, but pathology prevents it from eating

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3
Q

List 5 possible physical causes for dysphagia in the oral cavity

A
  1. Stomatitis
  2. Growths
  3. Foreign body
  4. Cleft palate
  5. Traumatic injury
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4
Q

List 5 possible functional causes of dysphagia

A

Masticatory myositis, rabies, tetnus, trigeminus neuritis, facial paralysis

All are neuromuscular conditions

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5
Q

Define regurgitation

A

A passive process, with no heaving or abdominal muscle contraction, and no prodromal signs (incl. nausea, hypersalivation and pacing)

It basically just falls out of the oesophagus

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6
Q

From where in the oseophagus can regurg originate?

3 places

A

Luminal (inside), intramural (in the wall) and extramural (outside the wall)

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7
Q

List 3 possible causes of luminal regurg

A
  1. FB
  2. Neoplasia
  3. Granuloma (inflammatory response)
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8
Q

List 3 possible causes of intramural regurg

A
  1. Megaoesophagus
  2. Oseophagitis
  3. Dysmotility
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9
Q

In which breeds would you most likely see regurg due to intramural oesophageal dysmotility?

Why?

A

Brachycephalics
The negative pressure in their chest (caused by difficulty breathing) pulls the oseophagus in different directions

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10
Q

List 3 possible causes of extramural regurg

A
  1. Vascular ring anomaly (PRAA - aortic arch wraps around the oesophagus)
  2. Mediastinal mass
  3. Hiatial hernia (stomach pushes up into chest through the hiatus in the diaphragm)
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11
Q

List 4 clinical signs of oseophageal foreign bodies

A
  1. Regurgitation
  2. Anorexia
  3. Drooling
  4. Pain with swallowing
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12
Q

How would you treat an oesophageal foreign body?

A

Pull it out or push it through

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13
Q

Define oseophageal stricture

A

An abnormal narrowing of the oesophageal lumen

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14
Q

List 4 common mediastinal masses

A
  1. Lymphomas
  2. Thyomas
  3. Mesotheliomas
  4. Carcinomas
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15
Q

Which is more common, a mediastinal or oesophageal mass?

A

Mediastinal

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16
Q

What are the two general groups of differentials for megaoesophagus?

A

Local disease and systemic disease

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17
Q

What condition is secondary to local/idiopathic megaoesophagus?

A

Oesophagitis (inflammation)

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18
Q

List 2 systemic disease differentials for megaoesophagus

A
  1. Myasthenia gravis
  2. Paraneoplastic syndromes (ex. mediastinal mass)
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19
Q

What would you test for if you’re suspicious an animal has myasthenia graivs?

A

AchR-antibodies

MA is when Abs target AchR on the postsynaptic terminal

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20
Q

Describe the management for idiopathic/congenital megaoesophagus

A

Start with a course of stomach protectants/antacids to treat oesophagitis, then move onto feeding management (make sure they are fed upright)

Sildanafil - new treat to help w opening of LES

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21
Q

What is the treatment for megaoesophagus caused by myasthenia gravis?

A

Acetlycholine esterase blockers

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22
Q

How would you generally go about finding a cause for and treating megaoesophagus?

A

Test for a number of specific differentials (MG, neoplasms, hypothyroidism, lead intoxication etc.), and if you can’t find anything specific then start a trial treatment for oesophagitis/MG and manage feeding

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23
Q

List 4 clinical signs of GI dysfunction

A
  1. Vomiting
  2. Diarrhoea/melena
  3. Weight loss
  4. Abdominal pain
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24
Q

You are presented with a dog with acute vomiting, what are some possible differentials?

A
  1. Shock
  2. GDV
  3. Foreign body
  4. Infectious enteritis
  5. Drug reactions
  6. Extra-GI pathology (look at the other organs)
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25
Q

List 4 reasons for vomiting originating from inside the GI tract

A
  1. Food intolerance
  2. Infectious agent
  3. Foreign body
  4. Toxin
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26
Q

List 8 possible questions you would ask on a Hx when presented with an animal with GI problems

A
  1. Breed & age
  2. Is it vomiting or regurg?
  3. Vx and worming status
  4. Past medical Hx
  5. Dietary Hx
  6. Environmental Hx
  7. Treatments
  8. Other body systems (Resp., PU/PD)
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27
Q

What would be your diagnostic approach when presented with acutely or chroncially vomiting animal that looks very ill?

A
  1. Haematology & biochem
  2. Imaging
  3. Basal cortisol & canine pancreatic lipase in dogs
  4. Thyroid, feline pancreatic lipase, FELV/FIV in cats
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28
Q

What would be your diagnositc approach when presented with a chronically vomiting animal that does not appear very ill?

A
  1. Supportive therapies
  2. Diet trials
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29
Q

List 4 GI causes for haematemesis

A
  1. Drugs (NSAIDs; gastric ulcers)
  2. Gastric Neoplasia
  3. Foregin bodies
  4. Chronic enteropathy
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30
Q

List 4 extra-GI causes for haematemesis

A
  1. Liver, kidney or pancreas dysfunction
  2. Neoplasia
  3. Sepsis/shock
  4. Heat stroke
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31
Q

What is a primary cause of haematemesis and/or melena in cats

A

GIT tumours (lymphoma, polyps, or adenocarcinomas)

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32
Q

How would you manage a patient that presents GI issues with no haematemesis and is otherwise clinically well?

A
  1. Anti-emetic (maropitant)
  2. Nutrition (blended or elim. diet)
  3. Gastro-protectant (sucralfate)
  4. Probiotics
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33
Q

How would you manage a patient that presents GI issues with haematemesis and is otherwise clinically well?

A
  1. Anti-emetic (maropitant)
  2. Nutrition (blended or elim. diet)
  3. Gastro-protectant (sucralfate)
  4. Probiotics
  5. Antacids (omeprazole - proton pump inhibitor to decrease acid production in the stomach)
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34
Q

What are your options for managing a patient that presents with GI issues and is clinically unwell?

A
  1. IV fluids
  2. Blood transfusion
  3. Surgery to repair ulcers if needed
  4. Endoscopy
  5. Feeding tube
  6. Parenteral feeding
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35
Q

You are presented with a dog with chronic vomiting, what are some possible differentials?

A
  1. Chronic enteropathy/IBD
  2. Recurrent pancreatitis
  3. Parasitic infection
  4. Gastric neoplasia
  5. Chronic renal disease
  6. Chronic colitis
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36
Q

You are presented with a young dog with diarrhoea, what is the most likely cause?

A

An infectious agent

Ex. Parvo or Distemper

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37
Q

List 5 points from a Hx that would suggest an animal is infected with an infectious agent?

A
  1. Young animal
  2. Unvaccinated
  3. Recent boarding at a kennel
  4. Poor husbandry
  5. Pyrexia
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38
Q

If an animal presents with acute diarrhoea, but is otherwise clinically well, what are two ddx?

A
  1. Dietary indiscretion
  2. Parasitic infection (nematodes or protozoa)
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39
Q

How would you treat a clinically well patient presenting with acute diarrhoea?

A
  1. Fluids
  2. Electrolytes
  3. Anti-emetic

Possibly anti-diarrhoea or acid-base balance

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40
Q

List 3 indications with acute dirrahoea that warrant Ab treatment

A
  1. Fever and neutropenia
  2. Aspiration pneumonia
  3. Suspected sepsis
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41
Q

Why would you consider Abs for parvo, but not for other causes for acute diarrhoea?

A

In parvo, animals are febrile and present with severe neutropenia

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42
Q

List 5 parameters you want to monitor in a patient with parvo virus

A
  1. Hydration
  2. Body weight
  3. PCV and TP
  4. Glucose and potassium
  5. WBCs
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43
Q

Differentiate between the clinical signs for SI vs LI disorder

Appetite

A

SI: decreased
LI: no change

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44
Q

Differentiate between the clinical signs for SI vs LI disorder

Abdominal discomfort

A

Moderate for both

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45
Q

Differentiate between the clinical signs for SI vs LI disorder

Weight loss

A

SI: significant (if chronic)
LI: mild

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46
Q

Differentiate between the clinical signs for SI vs LI disorder

Vomiting

A

SI: moderate/severe
LI: mild

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47
Q

When is diarrhoea considered chronic?

A

After 3 weeks

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48
Q

Differentiate between the clinical signs for SI vs LI diarrhoea

Mucus

A

SI: not present
LI: present

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49
Q

Differentiate between the clinical signs for SI vs LI diarrhoea

Frequency

A

SI: less frequent
LI: very frequent

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50
Q

Differentiate between the clinical signs for SI vs LI diarrhoea

Tenesmus & dyschezia

Need to defecate even when bowel is empty and straining to poop

A

SI: no
LI: yes

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51
Q

Differentiate between the clinical signs for SI vs LI diarrhoea

Presence of blood

A

SI: melena
LI: haematochezia

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52
Q

List 4 potential causes of diarrhoea

A
  1. Infectious
  2. Parasitic
  3. Diet
  4. Additives/chemicals
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53
Q

When presented with a clinically well dog with acute diarrhoea, what are your top 3 differentials?

A
  1. Dietary indiscretion/change
  2. Nematodes (roundworms and hookworms)
  3. Protozoa (isospora, crypto, giardia)
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54
Q

Which protozoal parasite is a common cause of diarrhoea in puppies and kittens?

A

Isospora

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55
Q

What are 2 treatment options for an animal presenting with a parasitc infection causing acute diarrhoea?

A
  1. Pyrantel/praziquantel (drontal)
  2. Moxidectin/imidacloprid (advocate)
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56
Q

How would you rule out a parasitic infection as a cause of acute diarrhoea?

A
  1. Treatment trial with drontal or advocate
  2. Faecal smear
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57
Q

What are your options for treating a clinically well patient with acute diarrhoea?

A
  1. Fluids
  2. Electrolytes
  3. Anti-emetics (short course)

Possibly acid-base balancers and anti-diarrhoeal’s, but generally no

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58
Q

Suggest a possible diet plan for an animal recovering from acute diarrhoea

A

Small, frequent meals consisting of low fat, high fibre foods
Can be boiled chicken, rice, potatoes or pumpkin

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59
Q

What are your options for treating a clinically unwell patient with acute diarrhoea?

A

Same as clinically well (fluids, anti-emetics and electrolytes), but you can also consider appetite stimulants, an anti-diarrheal, and oral protectants

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60
Q

What is the risk associated with anti-diarrheal’s?

A

They increase the animal’s risk of toxin absorption and bacterial proliferation
SO, if you’re going to use them only use for a couple of days

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61
Q

Describe the signalment of parvovirus in 4-12 week puppies

A

Anorexia and vomiting in the first 1-2 days, then diarrhoea and haematochezia

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62
Q

List 5 treatment options for a patient with parvovirus

A
  1. Fluids
  2. Correct electrolyte imbalances
  3. Anti-emetics
  4. Feeding !!!
  5. Faecal transplant

Abx only if febrile & severe neutropenia

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63
Q

In which breeds is acute haemorrhagic diarrhoeal syndrome more common?

A

Small and toy breeds (middle age)

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64
Q

What is the clinical presentation of an animal with AHDS?

A
  1. Acute onset haematochezia
  2. Maybe vomiting
  3. Maybe anorexia
  4. Dehydration/hypovolaemia
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65
Q

How would you treat an animal with AHDS?

A

Fluids and potassium as needed

No Abs if uncomplicated

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66
Q

List 3 bacterial agents that can cause bacterial enteritis in the SI and LI

A
  1. Campylobacter
  2. Clostridia
  3. Salmonella
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67
Q

What anti-parasitic would you use to treat a dog with a suspected parasitic infection?

Presents as clinically well with acute diarrhoae

A

Fenbendazole

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68
Q

Bacterial enteritis is rare, what would be some of your other ddx’s?

A
  1. Parvo
  2. Parasites
  3. Dietary indiscretion
  4. AHDS
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69
Q

What diagnostic tools are available to diagnose the cause of diarrhoea?

A

SNAP tests, PCR, haematology, biochemistry, radiology (more severe cases)

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70
Q

What are 5 hallmarks of chronic enteropathy (diarrhoea)

A
  1. Lasts more than 3 weeks
  2. Diarrhoea
  3. Vomiting
  4. Weight loss
  5. Abdominal pain
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71
Q

What is your primary ddx when presented with an animal with chronic enteropathy?

A

There is a dietary problem

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72
Q

After you’ve ruled out extra-intestinal disease as a cause of chronic diarrhoea, what is your pyramid of ddx’s?

A
  1. Food-responsive enteropathy (treat w diet)
  2. Microbiota-modifying enteropathy (used to be Abs - really try not to though)
  3. Immuno-modulator pathology (try immunosuppresives)
  4. Non-responsive
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73
Q

Prior to starting a diet trial, what do you want to rule out? How?

A

Rule out extra-intestinal disease with a faecal smear and deworming (fenbendazole)

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74
Q

What is the primary allergen listed in dogs and cats?

A

Beef

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75
Q

How quickly are you expecting an improvement with a diet trial?

A

Within 2 weeks

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76
Q

What are the advantages of a home-cooked diet vs a commerical one in a diet trial?

A

Home cooked has no preservatives and cross contamination is unlikely

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77
Q

How long should you continue a diet trial for if you see an improvement after 2 weeks?

A

6 weeks

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78
Q

If you try a diet trial for an animal with chronic enteropathy and it doesn’t work, what are your next steps?

A
  1. Haematology, biochem, and urinalysis
  2. Faecal flotation +/ PCR
  3. Check TT4 for cats (indicator of hyperparathyroidism)
  4. Check TLI (indicator of pancreatitis or EPI)
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79
Q

What is a possible dddx for a dog with chronic enteropathy and a low basal cortisol (<40nmol/L)?

What else would you see on the haematology?

A

Addisions disease

High eosinophils and low cholesterol

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80
Q

Where is folate absorbed?

A

In the proximal SI

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81
Q

Where is cobalamin absorbed?

A

In the distal SI

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82
Q

How long should you orally supplement B12?

A

12 weeks (recheck concentrations 1 week after finishing)

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83
Q

How long should you supplement B12 SQ?

A

6 weeks (recheck concentrations 1 month after finishing)

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84
Q

If you have a patient with chronic enteropathy that is not responsive (bottom of the pyramid), what can be your next steps?

A

Radiographs (thoracic and abdominal), ultrasound or biopsy

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85
Q

How would you biopsy a section of the intestine if there is a lesion vs no lesion?

A

Lesion: biopsy the site and around it
No lesion: multiple biopsies

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86
Q

What is a specific ddx for cats presenting with chronic diarrhoea?

A

Tritrichomonas foetus

More infectious in cats than dogs - could also think FIP or salmonella

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87
Q

Which groups of cats are most at risk to tritrichomonas foetus?

A

Young pedigree, multi household cats

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88
Q

How would you treat tritrichomonas foetus in cats?

What do you want to be careful of?

A

Ronidazole

CNS signs

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89
Q

What are 3 forms of protein losing enteropathy?

A
  1. Primary (congential) lymphangiectasia
  2. Secondary (acquired) lymphangiectasia bc of inflammation
  3. Secondary (acquired) lymphangiectasia bc of neoplasia
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90
Q

What is most important to rule out as a cause of PLE?

A

Intestinal lymphoma

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91
Q

Describe the pathogenesis of primary (congential) lymphagiectasia

A

Lymph leakage from lymphatic problems causes inflammation (but it is hard to differentiate cause from effect)

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92
Q

Describe the pathogenesis of secondary (acquired) lymphangiectasia due to inflammation

A

Inflammation leads to lymphatic obstruction, and they burst and leak
This causes more inflammation (cascade)

93
Q

Describe the pathogenesis of secondary (acquired) lymphangiectasia due to neoplasia

A

Neoplastic infiltration disrupts the normal architecture of the lymphatics causing leakage

Most often a lymphoma

94
Q

How would you treat PLE?

A

Diet and immunosuppression, and supplement with cobalamin if needed

95
Q

List 5 clinical signs associated with caudal (rectal-anal) intestinal disease

A
  1. Faecal incontinence
  2. Dyschezia
  3. Haematochezia
  4. Tenesmus
  5. Constipation/scooting
96
Q

What do you want to palpate on a rectal exam in a dog?

A
  1. Perineal glands/pouches
  2. Rectal mucosa
  3. Sublumbar lymph nodes
  4. Prostate gland
  5. Urethra
97
Q

List 3 examples of local/external recto-anal disease

A
  1. Anal gland disease (impacation, inflammation or neoplasia)
  2. Anal furunculosis
  3. Perineal hernia
98
Q

What are your treatment options for anal gland disease?

A

Flush, Abs, or Sx removal

99
Q

What are your treatment options for anal furunculosis?

A

Cyclosporine or topical tacrolimus, and a hydrolyzed protein diet

100
Q

What is your treatment option for a perineal hernia?

A

Surgical repair

101
Q

What is a perianal fistula / anal furunculosis?

A

Tunnel-like formations in the skin and deeper tissues

They usually start small

102
Q

Which breed is most prone to anal furunculosis?

A

German shepards

103
Q

List the 4 categories of ddx’s for internal recto-anal disease

A
  1. Abnormal content (FB)
  2. Rectal/colonic muscosal disease (strictures)
  3. Surrounding soft tissue disease (prostate)
  4. Surrounding boney structure abnormalities (pelvic fracture)
104
Q

If you have a M/N dog with an enlarged prostate, what is your immediate ddx?

Are you as concenred if it is entire?

A

Neoplasia

No, could be benign hyperplasia

105
Q

How would you diagnose a large intestinal stricture or rectal mass?

A

Endoscopy and biopsies

106
Q

Which human condition is anal furunculosis most similar to?

107
Q

How you would treat a large intestinal stricture?

A

Balloon dilation (if benign) or chemo/RT (if malignant)

108
Q

How you would treat a rectal mass?

A

Minimally invasive removal, or Sx, and send for histology

109
Q

Define colitis

A

Large intestinal diarrhoea

110
Q

Define gastric dilation and volvulus

A

Enlargement of the stomach associated with rotation on its mesenteric axis

111
Q

Define a simple dilation of the stomach

A

A stomach that is engorged with air or froth but not malpositioned

112
Q

What two things does the stomach fill with rapidly following GDV?

A

Gas (aerophagia) and fluid

113
Q

Describe how the stomach rotates during a GDV

A

Clockwise, 90-360 degrees
The pylorus moves ventrally and to the left, the fundus moves to the right

114
Q

Where does the spleen displace in a GDV?

A

Right dorsal

115
Q

List 2 effects on the spleen following a GDV

A

Congestion because of stretching of the splenic vessels, and ischaemia because of infarction of the splenic vessels

116
Q

Describe the local effects of increased gastric pressure following a GDV

A

There is venous and arterial compression, causing venous congestion, transudation of fluid, and eventually mucosal hypoxia and tissue ischaemia

Basically the blood supply is cut off

117
Q

Describe the cardiovascular effects of a GDV

A

There is reduced venous return to the heart, so less circulating blood volume, causing cardiac arrythmias and eventually shock (endotoxic and septic)

118
Q

Describe the respiratory effects of a GDV

A

The stomach pushes up on the diaphragm, compressing it and stopping the lungs from fully expanding, meaning the animal is hypo-oxygenating

119
Q

How can an animals diet be a risk factor for GDV?

A

If the diet is single source, they are only fed once a day, or it is highly processed

BUT no diet can reduce the risk of GDV

120
Q

List 5 recommendations for owners with dogs at high risk fo GDV

A
  1. Feed several small meals a day
  2. Avoid stress during feeding
  3. Restrict exercise before and after meals
  4. Do not breed from dogs with a genetic disposition for GDV
  5. Consider a prophylactic gastropexy
121
Q

Describe the presentation of a dog with GDV

A
  • Rapid onset of persistently comiting fluid
  • Tympanic abdomen
  • Collapse
122
Q

How could you confirm the diagnosis of a GDV radiographically?

A

You cannot identify the pylorus on a right lateral, or the ‘double bubble’

123
Q

What are the first two steps in patient stabilisation for a GDV?

A
  1. Fluid resuscitation
  2. Gastric decompression
124
Q

Why do you use the jugular or cephalic vein (NOT the saphenous vein) to administer fluids in a GDV?

A

Because the caudal vena cava is occluded, so nothing coming in through it will be able to get to the heart

125
Q

How much fluid do you want to give, and what type, for emergency treatment of a GDV?

A

90+mL/kg/hour to effect of crystalloid fluids

126
Q

List 2 ways you can decompress the stomach

A
  1. Orogastric intubation
  2. Percutaneous decompression
127
Q

What is the main risk of doing a percutaneous decompression of the stomach

A

That the stomach contents can leak into the abdomen

But, you can fix this in Sx

128
Q

How would you stabilisize a patient with a GDV?

A
  1. Fluid resusictation
  2. Gastric decompression (these 2 first)
  3. IV antibiotics (always)
  4. Oxygen therapy
  5. Therapy for arrhythmias
  6. Analgesia
129
Q

When should you surgically intervene for a GDV?

A

Within an hour or two

130
Q

What are the 3 goals of a GDV surgery?

A
  1. Decompress & reposition the stomach
  2. Assess the stomach and spleen for necrosis
  3. Prevent recurrence (gastropexy)
131
Q

What would you to do remove non-viable/questionable areas of the stomach following a GDV?

A

Non-viable: partial gastrectomy
Questionable: gastric wall invagination

132
Q

Describe non-viable and comprimised gastric tissue

A

Non-viable: wall thinning, green, grey/black
Compromised: avulsed vessels, red, haemorrhagic

133
Q

What is the most common site for necrosis in a GDV? Why?

A

The greater curvature of the stomach
This is the part that gets stretched the most

134
Q

When would you consider a splenectomy following a GDV?

3 things

A
  1. Persistent congestion after 10 minutes of repositioning
  2. Avulsion or infarcion of vessels
  3. Gross necrosis
135
Q

In how many cases will a GDV reoccur?

136
Q

Describe how an incisional gastropexy stops the reoccurance of GDV (i.e., where do you stick the stomach)

A

Adhesions form between the pyloric antrum and the right body wall, behind the last rib

137
Q

Which 2 muscle layers do you stick together in an incisional gastropexy?

A

Part of the stomach wall (not all the way through) and part of the transversus abdominus muscle

138
Q

What is the application of a gastrostomy tube placed in the pylorus?

A

It will act as a form of gastropexy for a GDV

139
Q

What is the application of a gastrostomy tube placed in the fundus?

A

It will be used as a stomach tube for feeding

140
Q

Describe how you would place a gastrostomy tube

A

Make a stab incision through the cranial midline of the left body wall and pull tube through the tunnel. Make a purse string suture in the stomach and a stab incision in the centre, then feed the tube into the gastric lumen and tighten the purse strings. Then place pexy sutures to the body wall (TA muscle). Finally, secure the tube to the body wall using a chinese finger trap suture.

141
Q

How long do you have to keep an gastrostomy tube in for? Why?

A

Minimum of 7 days to encourage adhesion formation
Otherwise risk peritonitis

142
Q

List 4 gastropexy techniques

A
  1. Incisional
  2. Belt loop
  3. Circumcostal
  4. Tube
143
Q

Describe an incorporating gastropexy

What is the risk of doing this?

A

The fundus is incorporated into the abdominal wall for closure

You risk entering the stomach during future abdominal Sx

144
Q

List 2 early post-op and long term complications following GDV

A

Early: cardiac arrhythmias, peritonitis
Long term: gastric hypomotility, recurrence (5-10%)

145
Q

What is the prognosis of a dog with GDV and the gastric wall is intact?

A

90-95% survival

146
Q

What is the prognosis of a dog with GDV if there is gastric necrosis?

A

66% survival

147
Q

Colitis (large intestine diarrhoea) can be either infectious or non-infectious, list 2 specific examples of both

A

Infectious: giardia (parasite) or clostridia (bacteria)
Non-infectious: neoplasia (non-inflammatory) or chronic enteropathy/IBD (inflammatory)

148
Q

How is granulomatous colitis classified?

A

Non-infectious, inflammatory large intestinal diarrhoea

149
Q

Describe the pathogenesis of granulomatous colitis in boxers and french bulldogs

A

There is genetic mutation that stops the macrophages from being able to rid of the e. coli that is naturally present in the gut. The e. coli invade the mucosal epithelium and cause inflammation

150
Q

How would you treat granulomatous colitis?

A

Fluoroquinolone (Abx)
You want to get rid of the e. coli

151
Q

List 3 ddx for constipation

1 for each luminal, intramural and extramural

A
  1. Obstruction (FB or neoplasia)
  2. Stricture (intramural)
  3. Pelvic fracture (extramural)
152
Q

Why is constipation a common problem in animals with renal disease?

A

Because of general dehydration and electrolyte imbalances

153
Q

How would you treat mild/first occurance constipation?

A

Increase fibre in the diet

154
Q

How would you treat moderate/recurrent constipation?

A

Enemas, with or without oral laxatives

155
Q

How would you treat severe constipation?

A

Rehydrate, enema and oral laxatives
Manual extraction may be necessary

156
Q

What are your 2 primary considerations when doing an enema on a cat?

A
  1. Always do under GA and intubation (risk of aspiration)
  2. Never use phosphate containing products (hyperphosphataemia is lethal)
157
Q

How would you administer large volume laxatives in cats?

A

Via an NG tube at a rate of 6-10ml/kg/hour over 6-18 hours

158
Q

Describe the mechanism of osmostic laxatives and give 2 commonly used examples

A

They pull water in to the stool to make it easier to pass
Ex. Lactulose and PEG

159
Q

Where do you want an oesophageal feeding tube to sit once placed, and why?

A

At the base of the oesophagus (not in the stomach), bc if in stomach you risk acid coming back up and causing oesophagitis

160
Q

What are the 2 most important aspects of a physical exam when presented with an animal with large intestinal disease

A
  1. Rectal exam
  2. Neurological exam
161
Q

How would you treat large intestinal diarrhoea with no strucutal abnormalities?

Think tx similar to another condition

A

Treat like CE/IBD

162
Q

List 2 ways in which emetics cause vomiting

A
  1. Gastric irritation
  2. Stimulation of the CNS chemoreceptor trigger zone
163
Q

When are emetics most effective

A

1-2 hours after ingestion

164
Q

Describe how hydrogen peroxide works as an emetic (for owners to do at home)

A

It stimulates the pharynx & stomach by damaging the mucosa, which stimulates the chemoreceptor trigger zone and induces vomiting

165
Q

How do apomorphine and xylazine induce vomiting?

A

They act on the chemoreceptor trigger zone directly

166
Q

Which emetic would you choose for a dog? How would you reverse it?

A

Apomorphine - reverse with metoclopramide

167
Q

Which emetic would you choose for a cat? How would you reverse it?

A

Xylazine - reverse with atipamezole or yohimbine

168
Q

What toxin binder/decontamination method would you use for an unconscious/seizuring patient?

A

Gastric lavage

169
Q

What toxin binder/decontamination method would you use for a conscious patient?

A

Activated charcoal

170
Q

Which 2 anti-emetics are licensed for use in the UK?

A

Maropitant and metoclopramide

171
Q

How often can you give it, how much, and what can go wrong?

Maropitant

A

Once a day
1 mg/kg SQ/Oral
Pain with SQ injection

172
Q

How often can you give it, how much, and what can go wrong?

Ondansetron

A

Every 8-12 hours
0.1-0.2 mg/kg IV (more orally)
Diarrhea

173
Q

How often can you give it, how much, and what can go wrong?

Metoclopramide

A

Every 6-12 hours, usually as a CRI
1-2 mg/kg/day
Constipation

174
Q

If you really want to reduce the acidity in the stomach, which drug do you want to use and why?

How often do you give it?

A

Omeprazole - it is a proton pump inhibitor

2x a day

175
Q

What are the 2 primary classes of drugs we use to reduce the acidity in the stomach?

Which is prefered?

A

Proton pump inhibitors (omeprazole) and H2 (histamine receptor) anatagonists (famotidin)

Omeprazole is preferred

176
Q

What does sucralfate do?

A

It lines the stomach (like a bandaid)

177
Q

What pH does sucralfate need to work?

A

An acidic/low pH

178
Q

What happens if you give a proton pump inhibitor with sucralfate?

A

PPIs work to reduce acid production in the stomach, and scralfate needs an acidic environment to work - so you make the sucralfate ineffective and the sucralfate will reduce the PPIs absorption

They work against each other

179
Q

How do prokinetics work?

A

They act on receptors in the eneteric nervous system (most important is 5-HT4 serotonin receptors) to induce or modify motility

180
Q

What are the 2 primary prokinetics we use in practice?

A

Cisapride and metoclopramide

181
Q

When/why would you choose cisapride over metoclopramide?

A

Cisapride works on the colon, metoclop does not

This is a go to drug in cats with abnormal colon movement

182
Q

Why do you want to limit the use of anti-diarrhoeals?

A

Diarrhea is a protective mechanism of the body, so you want to treat the consequences first and wait for it to self resolve

183
Q

What do you want to be careful of when administering loperamide (anti-diarrhoeal) to collies?

A

They are prone to having an MDR1 genetic defect, which makes them really sensetive to this drug (and other drugs)

184
Q

List 3 uses for dietary fibre

A
  1. Bulking agents/laxatives
  2. Prokinetics for the colon
  3. Increase SCFA production (anti-inflammatories)
185
Q

What is a natural source of psyllium?

A

Pumpkin or wheat bran

186
Q

How does lactulose act as a stool softener, and increase GI motility?

A

Stool softener: cannot be metabolized by enterocytes
Increase motility: it is fermented into SCFA

187
Q

How to SCFA increase GI motility?

A

They stimulate the release of 5-HT (serotonin), which stimulates the peristaltic reflex

Serotonin is a parasympathomemetic - so it stimulates rest and digest

188
Q

How does PEG act as a stool softener?

A

It forms hydrogen bonds with water, preventing its reabsorption and making the stool more watery

189
Q

What is the primary glucocorticoid we use for GI disease?

A

Prednisolone

190
Q

Why do you want to give a lower does of pred in large dogs, compared to small dogs?

A

They don’t clear the drug the same way

191
Q

What is your first line drug for anal furunculosis?

A

Cyclosporine (anti-inflammatory)

192
Q

In which cases is the use of sulfasalazine indicated?

A

Uncomplicated cases of colitis

193
Q

Dogs are more prone to __ pancreatitis

194
Q

Cats are more prone to __ pancreatitis

195
Q

What is the etiology/pathogenesis of acute pancreatitis?

A

Usually idiopathic
Premature activation of trypsinogen causes autodigestion of pancreatic proteins and more trypsinogen to be released, causing the release of pro-inflammatory cytokines and pancreatic enzymes

196
Q

What is the etiology/pathogenesis of chronic pancreatitis?

A

There is progressive fibroinflammatory disease (extension of acute or just constant low level inflammation)
This can lead to exocrine pancreatic insufficiency and/or diabetes

197
Q

Give 3 examples of risk factors for acute pancreatitis

A
  1. Obesity
  2. Hypertriglyceridaemia (mini schnauzer’s especially)
  3. Endocrine disease (diabetes)
198
Q

A combination of acute vomiting and abdominal pain would make you suspicous of what condition?

A

Acute pancreatitis

199
Q

List the suspected condition based on the biochemistry

  1. Elevated liver enzymes
  2. Elevated bilirubin and bile acids
  3. Hypocalcaemia
  4. Azotaemia
A

Acute pancreatitis

200
Q

What neutrophils changes will you see in SIRS associated with acute pancreatitis, and why?

A

Neutrophilia with left shift / degenerative left shift because there is a lot of inflammation
OR neutropenia because the pancreas is eating them

201
Q

List the suspected condition based on the haematology

  1. Neutrophilia or neutropenia
  2. Prolonged aPTT
  3. Thrombocytopenia
A

Acute pancreatitis

202
Q

Give 3 specific diagnostic tests for pancreatitis

A
  1. Serum amylase/lipase
  2. Abdominal ultrasound
  3. Canine/feline pancreatic specific lipase (quantitative)
203
Q

When would abx be indicated for tx of pancreatitis?

A

If the animal is neutropaenic (otherwise no)

204
Q

What are your tx options for acute pancreatitis?

A

Supportive tx - anti-emetics, stomach protectants, fluids, pain management, nutritional support

NOT anti-inflammatorys for the acute phase

205
Q

What do you specifically want to treat in an animal with chronic pancreatitis?

A

You want to provide supportive therapy, but also prevent predisposing factors, treat hypertryglyceridaemia if present (predisposing factor), and replace drugs that may increase risk

206
Q

What is the primary cause of EPI in dogs?

A

Pancreatic acinar atrophy

207
Q

What is the primary cause of EPI in cats?

A

Chronic pancreatitis

208
Q

Which dog breed is most predisposed to EPI?

A

German shepherd’s

209
Q

What is the triad of clinical signs of EPI?

A
  1. Weight loss
  2. Polyphagia (constantly eating)
  3. Chronic diarrhoea (really fatty)

The animal is trying to digest its food but can’t, it goes through

210
Q

What is the best test for diagnosis of EPI?

A

Trypsin-like immunoreactivity (TLI)

211
Q

What would you expect your TLI to be in an animal with EPI, why?

A

Low
Because trypsinogen is not being activated into trypsin

Basically the animal is not making digestive enzymes

212
Q

What would you expect your TLI to be in an animal with pancreatitis, why?

A

High
Because there is over activity/pre-mature activation of digestive enzymes, including trypsin

213
Q

What are you tx options for EPI?

A
  1. Substitute pancreatic enzymes
  2. Supplement cobalamin if low
214
Q

Give 6 clinical signs of liver disease

A
  1. Vomiting (most common)
  2. Jaundice (not common but kinda specific)
  3. Pale mucous membranes/bleeding (bc dysfunctional clotting factors)
  4. Hyperthermia or pyrexia (infection)
  5. Acholic (white) feces (biliary obstruction)
  6. Hepatic encephalopathy/CNS signs (build up of ammonia or toxins)
215
Q

List 3 clinical signs of hepatic encephalopathy

A
  1. Obtundation
  2. Head pressing
  3. Blindness

Ammonia makes you stupid

216
Q

What is hepatic encephalopathy?

A

Failure of the liver to clear ammonia and other toxins causes a build up of these in the blood and they can affect the brain

217
Q

Where are ALT and AST located, and what do elevated levels of these enzymes tell us?

A

In the hepatocellular cytoplasm
Elevated levels means theres damage and the cells are leaking

218
Q

Where is GLDH located, and what does an elevated level of this enzyme tell us?

A

In the hepatocellular mitochondria
Elevated levels tell us the cell has died

219
Q

Where are AP and GGT located, and what do elevated levels of these enzymes tell us?

A

In the biliary epithelium
Elevated levels tells us there is cholestasis

220
Q

Which enzyme, as measured as a parameter of hepatocellular damage, is the most liver specific?

A

ALT

But not very specific

221
Q

List 5 parameters you can meausre to assess liver function

Think about what the liver does

A
  1. Glucose (makes from cards)
  2. Cholesterol (makes from fat)
  3. Urea (makes from protein)
  4. Albumin (makes from protein)
  5. Ammonia (turns into urea)
222
Q

How can you test for liver dysfunction (or shunt disease)?

A

A bile acid stimulation test (BAST)

Increased value indicates pathology

223
Q

Why do you expect your clotting time to be elevated with severe liver dysfunction?

A

Because there is decreased circulation of vitamin K factors and decreased production of clotting factors

224
Q

If you have an isolated elevation in clotting time and you don’t have any suspicion of liver disease, what is your primary ddx?

A

Rodenticide intoxication

225
Q

List parameters you expect to be elevated with liver dysfuction

A

1.Bile acids
2.Ammonia

226
Q

What is the primary cause of pre-hepatic jaundice?

A

Haemolysis
The liver is metabolizing too much hemoglobin into bilirubin that they turn yellow (but also pale from anaemia)

227
Q

What is the primary cause of hepatic jaundice?

A

Severe parenchymal liver disease

228
Q

What is the primary cause of post-hepatic jaundice?

A

There is a build up of bile acids in the liver (they can’t get out bc of obstruction)

Could also be the gall bladder or pancreatitis

229
Q

What is the primary risk of a tru-cut biopsy of the liver?

A

There is a risk of bleeding - and since is US guided you wouldn’t be in there to fix it (may have to go to Sx)

Not the biopsy of choice

Cat & Dog (7 decks)

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