Cats and dogs 15 Flashcards

1
Q

What to do with a sick dog chronic vomiting with albumin <20g/L

A

○ Start with all 3 -> immune suppression, modify microbiome, diet
§ BUT NOT FMT or probiotics in a sick dog
§ May need a supportive diet at the start
○ Taper off according to dog
§ 1. antibiotics, 2. immune suppression 3. diet

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2
Q

What approach for chronic SI diarrhea in a cat

A
  • SAME AS FOR VOMITING
  • Rule out metabolic disease, out on diet trial
  • Diagnosis
    ○ Ultrasound
    ○ Biopsy of gut
    ○ Vitamin B12
    Usually need lifelong immune suppression - prednisolone
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3
Q

What is the role of the LI

A
  • Physiological barrier (mucus)
  • Large commensal bacterial population:
    ○ Produce short chain fatty acids (SCFA)
    ○ Contributes up to 10% energy requirements
    ○ Dogs majority anaerobes, cats 50%
    ○ If not well developed flora excess sugars not metabolised to SCFA and results in osmotic diarrhoea
  • MAJOR WATER RESERVOIR
  • NO DIGESTIVE ROLE
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4
Q

What are the main signs of LI disease

A
  • Mucoid faeces
  • Haematochezia (fresh blood)
  • Tenesmus (straining to defecate
  • Dyschezia (pain on defecation)
  • Very occasionally weight loss/vomiting
  • Constipation
    Rectal prolapse/perineal swelling
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5
Q

Differentials for colitis what main in australia, mainly causing haematochezia, really sick

A
COMMON IN AUS
- Fibre-responsive (idiopathic) 
- IBD -
○ Lymphocytic-plasmacytic 
○ Histiocytic ulcerative (granulomatous) colitis in boxers 
- C perfingens overgrowth 
- Trichuris vulpis (whipworm) - cat 
HAEMATOCHEZIA
- Neoplasia 
○ Lymphoma 
○ Adenocarcinoma
REALLY SICK
- Uraemic colitis
- Pancreatitis
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6
Q

What is the clinical approach to LI diarrhoea in dogs

A
  • Initially must:
    ○ Establish whether any signs of weight loss, systemic illness or signs of diffuse diarrhoea
    ○ Do a thorough rectal examination - 360 degree examination
  • If animal is well, a breed other than boxer and no palpable rectal abnormality - non-specific treatment trial
  • Investigate if
    ○ A boxer or French bulldog
    ○ Weight loss
    ○ Diffuse diarrhoea
    ○ Systemically unwell
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7
Q

What are the 2 main things within non-specific treatment trial in LI diarrhoea for dogs and what should do with different results

A

Non-specific treatment trial
- Faecal analysis OR fenbendazole 50mg/kg sid 5 days - FOR WHIPWORM
- Fibre supplementation
○ Add Psyllium (soluble) OR low-residue diet
Result
- If good response taper/discontinue fibre or diet if desired after 2-3 months
- If poor response or SICK dog then investigate further
a. Faecal analysis
b. Metabolic screening
c. Biopsy

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8
Q

Biopsy of LI in dogs what are the 2 ways and compare

A
  • Full-thickness biopsies inherently risky in diseased colon
    1. Colonoscopy: required preparation, can exam the entire LI and ileo-colic valve
    2. Proctoscopy: rigid scope -> only seeing descending colon -> enema and 24 hours of fasting only
  • Colonoscopy vs proctoscopy
    ○ Most LI conditions can be diagnosed with rigid proctoscopy except:
    § Occult trichyriasis, ileocolic or caecocolic intussusception, typhlitis or neoplasia that is localised to the transverse or ascending colon
    ○ The main complication of colonoscopy -> perforation of the colon
    § Can occur upon introduction of the instrument, when the colon is insufflate with air, or when biopsies are taken
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9
Q

Biopsy of LI in dogs what preparation is needed for colonscopy

A

○ Fast for 24 hours
○ Go lytely (osmotic cathartic solution)
§ Stomach tube 3 doses of 33mL/kg minimum 3-4 hours apart
§ Naso-oesophageal tube 100mL/kg over 6-8 hours
○ Warm water enemas
§ Evening before and morning of (not within 2 hours)

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10
Q

Cats with LI disease what is less common than in dogs and what is the order of investigation

A
  • Idiopathic disease and clostridial overgrowth LESS COMMON than in dogs
  • Investigation is recommended in following order:
    ○ Faecal analysis - for Trichuris
    ○ Trial treatment with fenbendazole and diet
    ○ Metabolic screening (including T4, FeLV, FIV)
    ○ Ultrasound - higher possibly for lymphoma
    ○ Colonic biopsies if no response to treatment after initial work-up
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11
Q

List the 3 main types of colitis

A
  1. L-P (lymphocytic-plasmacytic) colitis
  2. Clostridial growth (dysbiosis - of clostridia)
  3. Granulomatous (histiocytic ulcerative colitis)
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12
Q

L-P (lymphocytic-plasmacytic) colitis what may also have, diagnosis and treatment

A

○ May have concurrent upper GI sins (may be clinically silent)
○ Biopsy confirmation
○ Try hypoallergenic diet and fibre first then
§ Immunosuppression 6-8 weeks if moderate signs
○ Sulfasalazine (or derviateives) if only LI disease - SIDE EFFECTs

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13
Q

Clostridial growth (dysbiosis) how generally occur, diagnosis and treatment

A

○ Often stress triggered -> generally dysbiosis then causes stress -> goes back to cycle
○ Difficult to diagnose - spores in healthy dogs
○ Treat with fibre
○ Antimicrobials not necessary unless very poor response or concerned about translocation

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14
Q

Granulomatous (histiocytic ulcerative colitis) what does it lead to, breed mainly wihtin and presentation

A

○ Form of colitis with severe mucosal ulceration
○ Predominantly affects boxer dogs, although has been reported in other breeds
Presentation
§ Usually young (<2 yo) at presentation
§ Severe clinical signs
□ Profound haematochezia
□ Often weight loss and poor growth - KNOW IS SEVERE AS NOT COMMON IN LI
§ Also french bulldogs

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15
Q

Granulomatous (histiocytic ulcerative colitis) diagnosis and prognosis with what treatment

A
○ Diagnosis 
- Endoscopically severe ulceration 
- Histologically a mucosal infiltrate of plasma cells, lymphocytes and PAS-positive macrophages 
□ Severe mucosal ulceration 
□ Patchy distribution 
- Culture for E. coli 
- IF SUSCEPT THEN CALL C. MANSIFELD
○ Prognosis 
- Several reports of cures with enrofloxacin 
□ 8 weeks at 5mg/kg sid
□ Long-term remission (>4.5 years)
□ Genetic defect in bacterial killing of E.coli - destroy bacteria with antibiotics
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16
Q

Tritrichomonas foetus what species within, how prevalent and where mainly found

A
CATS 
- World-wide distribution in cats 
○ Australia does not have as high prevalence as US or Europe 
- Mainly cat breeders and shelters 
○ Bengals pre-disposed 
○ Up to 30%
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17
Q

Tritrichomonas foetus clinical signs

A

○ Colitis when increased frequency of defaecation
○ The anus may become inflamed and painful, +/- faecal incontinence
○ Majority under 12 months of age
Most affected cats are otherwise well, and show significant weight loss

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18
Q

Tritrichomonas foetus diagnosis and prognosis

A
  • Diagnosis
    ○ Looking for moving parasites in fresh faecal smears - positive 5/36 cats (not very sensitive)
    ○ Using a specific culture system -> positive 20/36 cats
    ○ Be detection of T-foetus DNA using PCR - positive 34/36 cats
    ○ Faecal sample - should get deep sample not voided
  • Place tube within rectum with syringe -> sedation
  • Prognosis
    ○ Some cats will recover spontaneously by 2 years of age
    ○ However, many will have very severe clinical signs
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19
Q

Tritrichomonas foetus treatment

A
○ Resistant to fenbendazole 
○ Ronidazole more effective 
- Some neurological side effects - is treatment worse than disease
- Not licensed for use in cats
- Bitter taste (so put in capsules) 
- 30mg/kg sid 2 weeks 
- Decrease dose in young cats
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20
Q

Irritable bowel syndrome how defined, what pets, characterised by

A
- Poorly defined disease 
○ Altered bowl motility 
○ Visceral hypersensitivity 
○ Psychosocial factors 
○ Neurotransmitter imbalance 
○ Mucosal inflammatory cytokine 
- Pocket puppies 
- Is it a real disease or symptomatic issues 
- Characterised by diarrhoea (usually LI) vomiting and abdominal cramping
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21
Q

Irritable bowel syndrome diagnosis and treatment

A
  • Diagnosis of exclusion
    ○ Main DDx is IBD with associated pain
  • Treatment
    ○ Empirical treatment with anti-cholinergic and fibre supplementation
    § NB careful with altering motility without histology
    ○ Reduce stresses
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22
Q

if mainly Haematochezia what should do and main differentials

A
  • Main differentials if eliminate metabolic disease, infectious disease (parvovirus, HE) and colitis
    ○ Rectal adenocarcinoma
    ○ Rectal polyp
    ○ INCREASE INDEX OF SUSPESSION
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23
Q

Adenocarcinoma in LI what can result in, diagnosis and treatment

A
  • Infiltrative and cause narrowing of rectum so often also tenesmus
    ○ Metastasise to Sub-lumbar lymph nodes can be huge and then lead to tenesmus
  • Diagnose on rectal examination most of the time, may need biopsy and proctoscopy
  • Older dogs
  • Surgery ideal
  • Piroxicam for palliation
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24
Q

Polyps in LI does it cause obstruction, when diagnosis, treatment and prognosis

A
  • Rarely cause obstruction
  • Usually pedunculated on rectal exam
  • Solitary or multiple
  • Need good sample size for confirmation with histology
  • Surgical excision or anti-inflammatories if indicated
  • Good prognosis
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25
Q

What is animal present with dyschezia/tenesmus what does that indicate and differentials

A
  • OBSTRUCTION TO DEFECATION
  • Perineal fistulae
  • Prostatic disease
  • Pelvic fractures
  • Perineal hernias
  • Perianal gland tumours
  • AG tumours
  • Abscess (cat)
  • Constipation
    Rectal stricture
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26
Q

Anal sacculitis what occurs, general presentation, what needed and treatment

A
  • Anal sac becomes infected (may cause cellulitis)
  • Older, small dogs
  • Very painful
    ○ Sedation or GA often required to examine adequately
  • Treatment
    ○ Expression
    ○ Lavage with saline and instil antibiotic solution
    ○ Higher fibre food to increase defecation and therefore expression
    ○ Removal if recurrent NOT IF RUPTURED
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27
Q

Anal sac adenocarcinoma what sex, what associated with, diagnosis, treatment and prognosis

A
  • Older females
  • Associated with paraneoplastic hypercalcaemia - PU/PD - generally why present no the LI signs
  • Need careful rectal palpation
  • Assess SL lymph nodes
  • Surgical excision (+/- palliative chemo)
  • Guarded prognosis
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28
Q

What is animal present with straining and no result what indicate and differentials

A
CONSTIPATION AND OBSTIPATION 
- Differential as for tenesmus/dyschezia as well as:
○ Poor colonic motility 
§ Idiopathic megacolon
§ Systemic disease (low K, Ca, low T4)
§ Neuromuscular disease high 
○ Obstruction 
○ Dehydration 
○ Dietary (especially bones) 
○ Drug-induced
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29
Q

If animal present with straining without result what is the diagnostic approach

A
  • Evaluate for systemic signs and any rectal/perineal disease
  • IV fluids if dehydrated
  • Abdominal radiographs (pelvic #)
  • Evacuation of faeces (enema)
  • +/- ultrasound or barium enema
  • +/- proctoscopy
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30
Q

Enema when use and how done

A

colitis, impaction

  • Use lukewarm water
  • Don’t use hypertonic enemas if bone impaction
  • Break down impacted faeces with sponge forceps or hose attachment
  • GENTLY - can take hours
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31
Q

Idiopathic megacolon what is it a major cause of, why occurs, differentials and diagnosis

A
  • Major cause of constipation in cats
  • Smooth muscle functional defect
  • Rule out pelvic stenosis, neurological disease, neoplasia and metabolic disease
  • Abdominal radiographs essential
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32
Q

What is the normal radiographic appearance of the oesophagus and what is needed for investigation

A

NORMALLY - cannot see it because it is collapsed and is of the same opacity as the soft tissue within the cervical region and mediastinum
Examinations using contrast media are usually necessary to investigate suspected oesophageal disorders

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33
Q

How to use and which contrast use for contrast studies of oesophagus

A
  • Radiographs must be taken prior to any contrast study
  • Positive contrast used in evaluation of oesophageal lesions and motility disorders
  • Dynamic fluoroscopic examination is usually necessary to evaluate functional abnormalities
  • Barium used to evaluate the mucosa and lumen and can be mixed with food
  • Risk of aspiration -> small volume barium is usually benign but should be still be avoided
  • Use non-ionic iodinated contrast medium
    ○ Swallowing disorders -> best evaluated fluoroscopically as dynamic diseases
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34
Q

megaoesophagus radiographic appearance and what can look like this

A

Air within the oesophagus gives contrast (able to see soft tissue opacity of the walls of oesophagus)
- Dogs when stressed may swallow air see focal area of air within (will not be focal like this)

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35
Q

Tracheooesophageal strip sign what used for and what see when present

A

Helps determine whether air within oesophagus

  • NORMALLY DON’T SEE DORSAL ASPECT OF THE DORSAL WALL OF TRACHEA
  • Seeing Dorsal wall of trachea (ventral and dorsal aspect of this wall)
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36
Q

Megaoesophagus what does it indicate and causes

A
  • Indicates enlargement of oesophagus which may be segmental or generalised, congenital, hereditary or acquired
    ○ Acquired -> neuromuscular, endocrine, inflammatory or obstructive disorders
    ○ Most idiopathic
    ○ May occur cranial to obstruction or associated with oesophagitis
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37
Q

Oesophageal strictures when occur and possible radiographic finding

A
  • Stricture formation may occur with deep oesophageal due to oesophagitis, neoplasia, trauma, FB
  • Oesophagus often normal on survey radiograph
  • Dilation of the oesophagus proximal to the stricture is an inconsistent finding
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38
Q

What are the 3 further imaging tests for the oesophagus

A
  1. Fluoroscopy: Dynamic evaluation of swallowing and oesophageal motility with fluoroscopy important in mild, intermittent or segmental disease.
  2. Ultrasound: Wall layering, relationship to other cervical and abdominal organs
  3. Cross-sectional Imaging - (Computed Tomography, Magnetic Resonance Imaging): Relationship with other organs
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39
Q

assessing the stomach radiographically what is important to assess and what is normal

A
- Assess size 
○ No greater than 3 intercostal spaces wide
○ Fundus typically 2 x wide as pylorus
- Contents - ideally fasted 12-24 hours before exam 
- Position
○ Cranial to 12thrib
○ Axis should be parallel to the ribs 
- Is this a surgical abdomen?
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40
Q

what causes a displacement of gastric silouette caudally and cranially and contrast studies within stomach, what indicate and timing

A

Displacement of the gastric silhouette caudally -> hepatic enlargement
Displacement cranially -> reduction in size of liver
Contrast studies
- Will indicate delayed gastric emptying
○ Normal stomach empty within 1-4 hours after barium administration
○ Retention within 3-4 hours after indicates pyloric obstructive disease
- Fluoroscopy assessment best way to diagnose pyloric obstructive disease

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41
Q

gastric neoplasia which most common in dog and cat, where found and radiographic finding

A
  • Adenocarcinoma most commonly seen in pyloric region
  • Lymphosarcoma most common in cat
  • Filling defect in the contrast caused by neoplastic lesion projecting into the lumen
    Ultrasound or endoscopy is better to diagnosis
42
Q

Ultrasound of the stomach what looking for and what is normal

A
  • Attempt to look at fundus moving into pylorus
  • Is it contracting (should contract 4-5 contractions per minute), Is there peristalsis
  • Stomach wall thickness -> 3-5mm in dogs, cat up to 4mm within normal ranges
43
Q

Small intestines radiograph what assess and where is the cranial duodenal flexure

A
  • Assess distribution
  • Assess contents and degree of distension
  • Is ileus suspected -> is there gas present?
  • The big question-Is this a surgical abdomen?
    Cranial duodenal flexure -> fixed along the caudal surface of the right side of the liver by the hepatoduodenal ligament
44
Q

What are the 3 main rules in dogs and 2 main ones in cats for small intestinal radiographs

A

Dogs
1) Ratio of greatest SI diameter to body of L5 no > 1.6 - most useful
2) No more than twice the width of a rib - overestimates - not really used
3) No loop greater than twice the width of others
Cats
1) No greater than 12 mm in diameter
2) No greater than twice the height of L4

45
Q

what parts of the GI tract should contain granular material on radiograph and gas

A
  • Only the stomach and colon should contain granular material, the contents of the small intestine should be an homogenous soft tissue radiopacity
  • GAS - colon, stomach and caecum
46
Q

ileus what are the 2 main causes and what indicates on radiograph

A
  • Mechanical-due to obstruction - foreign body, mass, stricture
    ○ May lead to functional ileus
  • Functional-due to cessation of peristalsis
    ○ Gastroenteritis
    Single dilated loop (sentinel loop) indicate mechanical obstruction or functional ileus
47
Q

functional ileus what results from and what are the 3 radiogrpahic differences between functional and mechanical

A
  • Peristaltic contractions of bowel cease due to neuromuscular or vascular abnormalities to mechanical
  • Difference between mechanical obstruction and functional
    ○ Mechanically obstructed usually larger diameter than functional
    ○ Both gas and fluid typically are in the lumen of mechanically obstructed where function tends to be more gas or completely gas filled
    ○ Mechanical have some bowel segment normal, functional generalised involvement
48
Q

foreign bodies within GI on radiograph what are the 2 types, what result on ultrasound and what need to assess for

A
  • May be radiolucent or radiopaque
  • On ultrasound typically cause acoustic shadowing
  • Assess for intestinal distension
    ○ Partial vs complete
    § Mass or foreign body
    ○ Ileus mechanical/functional
49
Q

what are some radiogrpahic changes to intestines that suggest linear FB

A

1) C-shaped looped of small intestines -> GENERALLY NO OVERDISTENTION
2) Plicated or pleated appearance as waves of peristalsis climb the FB as gas becomes trapped in the pockets of the SI formed giving rounded, tapered, short tubular C-shape gas opacity
3) Distention/gas within intestines, Stacking of intestines, hairpin turns (sharp turns of intestines)
4) Straight lines in the abdomen are NOT NORMAL so their presence alert to a FB
5) Serosal to serosal measurement >1.5 cm is suggestive
of foreign body obstruction

50
Q

normal ultrasound of small intestines what assist and what makes difficult

A
  • Can assess thickness of the wall layers
  • Cannot be done if lots of food, ingesta or gas present (why ultrasound before endoscope as introduces gas)
    ○ However can assess the contractions and movement of the ingesta within
51
Q

Intussusception what is the typical sonographic appearance

A

“loop within a loop” giving a bulls eye appearance

52
Q

What sonographic changes see with neoplasia and what can do

A
  • Loss of layering
  • Size of lesion can be variable
  • Usually asymmetrical
  • Aspiration via ultrasound - IDEAL
53
Q

Radiogrpahic appearance of colon what assess, normal and what indicates constipation

A
  • Assess position
  • Assess contents
  • Assess size
    ○ Diameter should be < the length of the body of L7
    § Not used as such
    Faeces become more opaque as sit in colon
  • Can help determine whether constipation or normal
54
Q

so if vomiting case and taking radiopgrahs what to do if normal, clearly abnormal or unsure

A
  • Normal radiograph -> supportive treatment
  • Clearly abnormal large distention -> straight to surgery - exploratory laparotomy
  • Unsure????? Multiple options
    ○ Re-radiograph in 12-24 hours?
    ○ Supportive treatment
    ○ Abdominal ultrasound
    ○ Exploratory laparotomy
55
Q

what is the normal radiographic appearance of the pancreas and where sits

A
  • Normal cannot be seen radiographically
    Lies dorsal and medial to the duodenum
    Locate the pancreaticoduodenal vein
  • Normal is mildly hypoechoic to the surrounding fat and triangular in the transverse plane
56
Q

pancreatitis what result radiographically

A

decreased serosal detail within right cranial abdomen, occasionally mass lesion
○ Not great correlation between sonographic findings and clinical severity
- Enlargement of the pancreas leads to increase in the gastric duodenal angle (should be on the left but is on the right)

57
Q

list 6 GIT conditions that need surgery

A
  1. GIT foreign bodies (oesophageal, gastric, intestinal)
  2. Delayed gastric emptying
  3. Gastric dilatation-volvulus (GDV) and gastropexy
  4. Intestinal intussusception
  5. Neoplasia of the GIT (oral, oesophageal, gastric, intestinal, colonic)
  6. Subtotal colectomy for idiopathic megacolon
58
Q

Oesophageal foreign bodies what are the 4 common sites and the main types that get stuck

A
- Four common sites of lodgement:
○ Crico-oesophagus
○ Thoracic inlet
○ Base of heart
○ Diaphragm
- Bones, hooks
- Fish hooks 
○ Do not pull on line out of mouth
○ Do not cut, Keep line long, may be useful
○ Rubber tube over line
○ Endoscopy
○ Surgery if required
§ Push through
59
Q

Oesophageal and gastric FB what are the options for retrieval

A

1) Most oesophageal FBs can be removed with endoscopy
- If cannot remove and FB is mobile can try and push FB in to stomach (not pointy ones)
2) Gastrotomy preferred to 3) oesophagotomy

60
Q

Gastrotomy for the removal of FB what are the 4 main steps and things within

A

1) Isolate Stomach (Moistened Lap Sponges)
2) Stay sutures
3) Longitudinal incision in ventral wall between greater and lesser curvature in relatively avascular area
® Long axis vs short axis
® Position influenced by indication
4) Closure
® Synthetic monofilament absorbable materials are preferred: (3/0 –4/0)
◊ Reduced tissue trauma from tissue drag
◊ Reduced wicking
® Taper point needle –smaller holes vs cutting
® 2-layer simple continuous appositional closure:
◊ Mucosa/Submucosa
◊ Serosa/muscularis

61
Q

Oesophagotomy for removal of oesophageal FB what is important anatomy, where done and the 6 steps

A

□ Oesophagus has segmental blood supply and no serosal layer
□ Cervical oesophagus if possible
1) Intercostal right thoracotomy for access to thoracic oesophagus
2) Trans diaphragmatic approach and manipulate to stomach and gastrotomy if in caudal oesophagus
3) Pack surgical site off carefully with lap sponges
4) Linear longitudinal incision in healthy tissue
5) 2 layer closure
6) Bring omentum through diaphragm if needed

62
Q

Gastric foreign bodies what are the main clinical signs in what age and what are the 2 ways to remove

A
- Clinical signs 
○ Acute or chronic vomiting 2oto gastric obstruction (usually pyloric) → loss of gastric acid and a metabolic alkalosis
○ Often young dogs
1. Endoscopic retrieval
2. Gastrotomy - as above 
○ If FB too large to be removed
63
Q

intestinal foreign bodies solid what are common examples, what cause and treatment

A

–bones, balls, plastic, clothing
○ Cause complete or partial obstruction
○ Electrolyte abnormalities ↓ Na/K/Cl
○ Enterotomy –anti-mesenteric, aborad in healthy bowel
§ Single layer, appositional
○ Resection and anastomosis
§ Sutured - Simple interrupted vs. continuous

64
Q

Linear foreign bodies examples, species what generally occurs

A

Wool, string, fishing line, carpet
○ Cats especially
○ Anchor orad –base of tongue (cats), stomach (pylorus) or duodenum (dogs)
○ Peristaltic movement stretches the foreign body aborally and then causes the intestines to plicate along the object
§ Cause sawing action on mesenteric surface - necrosis along mesenteric side and perforation occurs
□ With time peritonitis may ensue as perforation of the intestinal wall occurs

65
Q

Treatment for linear foreign bodies

A

§ Release foreign body first via cutting at base of tongue, gastrotomy, duodenotomy(proximal release)
□ Several enterotomies and a gastrotomy may be required to remove a linear foreign body
§ Catheter/feeding tube technique (single enterotomy) -> pass through intestines

66
Q

Delayed gastric emptying what are the 2 causes and causes within and main bred

A
  • Congenital
    ○ Pyloric stenosis -pyloric muscular hypertrophy
    ○ Boxer, Boston terrier and Bulldog
  • Acquired
    ○ Chronic hypertrophic gastritis or neoplasia
    ○ Mucosal hypertrophy
    ○ Lhasa apso, shih tzu, Pekingese, and poodle
67
Q

Delayed gastric emptying main clinical signs, diagnosis and 2 surgical procedures

A
  • Vomiting associated with delayed gastric emptying
  • Diagnosis -> Endoscopy to see gastric outflow obstruction
  • Pyloroplasty procedures - making the pylorus wider - specialist level
    a. Transverse pyloroplasty
    Y-U antral pyloroplasty - most common -> Y shaped incision, advance the top part to make U shaped incision
68
Q

Gastric dilation volvulus what is the breed predisposition and main clinical signs

A
- Breed predisposition
○ Deep-chested dogs
○ Medium to large breed dogs:
○ Great Danes, German shepherds, standard poodles, Weimaraners, Saint Bernards, Gordon setters, Irish setters, bassett hounds, Airedale terriers, Irish wolfhounds, borzois, bloodhounds, Akitas, and bull mastiffs
- Clinical signs of GDV
○ Restlessness
○ Bloated / tympanic abdomen, +/-Abdominal pain
○ Drooling
○ Repeated unproductive retching
○ Collapse
○ Weak femoral pulses, increase HR
○ Pale gums, Cold extremities
69
Q

Gastric dilation volvulus diagnosis and pathophysiology

A
  • Diagnosis -> often made from the history, signalment and physical examination
  • Pathophysiology
    a. Rotation of the stomach (clockwise 180 degrees most common) - pylorus ventral and to right
    b. Decrease venous return to the heart, compression of portal vein and CVC
    c. Obstructive shock, collapse, impaired breathing
    d. Stomach necrosis, sepsis then death
70
Q

Gastric dilation volvulus what is survival based upon and important stabilisation techniques

A

○ Survival determined by early and appropriate pre-surgical management rather than surgery
Decompression and shock therapy concurrently
1) Decompression / Gastric lavage
□ Single most important factor in reversing CV effects in patients with GDV-relieve respiratory embarrassment and increase venous return
□ Gastrocentesis R flank ( percutaneous) 16 or 18 G needle - ping area to ensure spleen not underneath
□ Gastric lavage -> with warm water after tube passed or gastrostomy performed - assess stomach contents
ii. Gastric trocarization+/- Orogastric tubing are associated with low complication and high success rates
□ Stomach tube (orogastric) - measure to last rib - generally don’t need to sedate
2) Shock therapy
IV fluids -> place in front legs NOT BACK

71
Q

GDV surgery what is prognostic and the 4 steps

A

○ Perform as soon as patient is stabilized
○ The severity of the presentation is indicator of survival for the patients
-> Dogs presented B&A and walking have better Px than dogs that lateral recumbent ALSO lactate concentration after stabilisation
1) Derotation / correct malpositioning
2) Assess viability of stomach/spleen
3) Gastropexy (prevent recurrence)
4) splenectomy - maybe

72
Q

What is a common finding with GDV surgery and how to reposition the stomach

A

§ See omentum draped over body and fundus instead of stomach and intestines -> pathognomonic
§ Haemoabdomen is common finding while within
MOVEMENT
§ Can occur spontaneously with decompression
§ May need further decompression with gastrocentesis before derotation accomplished if can’t pass stomach tube to decompress
§ Exteriorizing spleen may facilitate derotation
§ Grasp pylorus and pull up with right hand as well as pressing down on the fundus with flattened left hand -cross armed technique

73
Q

what is involved with assess viability for GDV and what can also perform if bad

A

§ Short gastric vessels arise from splenic artery and supply greater curvature-rupture common and may give rise to blood loss, gastric infarction, necrosis
§ 2nd look if can’t decide whether viable or not, can’t decide margins
§ Partial gastrectomy
□ 2 layered closure
□ GIA staples faster and less contamination
□ Can resect up to 60% of the stomach

74
Q

Gastropexy during GDV surgery why done and the 2 types

A

§ Gastropexy -prevents re-volvulus
§ Recurrence rate 73% without gastropexy
§ Types
1) Incisional gastropexy
® Incision through seromuscular layer of stomach parallel to lesser curvature
® Two continuous suture lines to corresponding incision on abdominal wall parallel to last rib and to level of transverse abdominis muscle
2) Belt loop gastropexy

75
Q

Splenectomy during GDV surgery when indicated why controversy

A

§ Splenectomy is indicated if thrombosis of the splenic artery is present
§ Not routinely removed
§ Controversy:
□ The odds of GDV in dogs with a history of previous splenectomy in were 5.3 times those of dogs without a history of previous splenectomy
□ Prophylactic gastropexy in dogs undergoing a splenectomy, particularly if other risk factors for GDV are present.
□ Newer study shows no risk above general population

76
Q

post operative management of GDV how long for and what monitoring

A

○ 3-4 days of intensive monitoring
○ Fluid therapy
○ Monitor TPR, pcv, TPP, electrolyte, fluid, AB status, urine output
○ ECG monitoring -Ventricular arrhythmias are common (~50%) after GDV surgery
○ Rx with lidocaine bolus or CRI –if persistent and affecting cardiac output

77
Q

Prognosis for GDV when good and bad and mortality

A
○ Good if treated early and intensive pre and post op management
○ Negative prognostic factors include:
§ Gastric necrosis
§ Gastric resection
§ Splenectomy
§ Pre-operative cardiac arrhythmias
○ Lactate at presentation >5 especially if not normalising with appropriate emergency treatment
→ mortality > 30%
78
Q

prophylactic gastropexy when recommended, what time done and two ways it can be done

A

○ Prophylactic in GDV susceptible dogs
§ Deep chested breeds
○ Often done at time of desexing
○ Laparoscopic versus open abdomen

79
Q

Intestinal intussusception what age, causes, clinical signs, physical exam, common site, 2 treatment and recurrence

A
  • Young animals Hxof GI upset, parasitism, viral enteritis, FB, tumour, idiopathic
  • Diarrhoea usually more common than vomiting
  • Palpable distended viscus ‘sausage’ -painful
  • Ileocolic junction the most common site
  • Manual reduction-80% require resection and anastomosis
  • Enteroplication
    Recurrence ~25%
80
Q

gastric neoplasia how common and what are the common types

A

rare
○ Adenocarcinoma-most common, 60-70% of malignant tumors
○ Leiomyoma
○ Leiomyosarcoma
○ Lymphosarcoma (LSA)-most common tumor in the cat
○ Adenomatous polyps
○ Carcinoids

81
Q

Intestinal and colorectal neoplasia most common, where arise, second most common, treatment and palliative options

A

Adenomatous polyps (intramural, intraluminal-most common benign tumour in the rectum of dogs)
○ Arise from rectal mucosa
§ Malignant transformation in 25%
○ Adenocarcinoma (most common malignant tumour in dogs) then leiomyosarcoma
○ In cats adenocarcinomas most common LI tumor then lymphomas and MCT
○ Treatment: Surgical excision with 3-5 cm margins
○ Palliative: colonic stenting

82
Q

Feline idiopathic megacolon clinical signs and the medial therapy

A
- Clinical signs
○ Progressive intractable constipation
○ Constipation 
○ Faces with mucus and blood
○ Anorexia
○ Vomiting
○ Weight loss
- Medical Therapy
○ Fluid therapy
○ Enemas
○ Diet -> High fiber, canned pumpkin
○ Fecal softeners
○ Motility modifiers
§ Cisapride1mg/kg TID (or 1.5mg/kg BID)
○ Generally not good long term Px
83
Q

Feline idiopathic megacolon what is the best option for treatment and what is involved, complications and prognosis

A
best option - SURGERY
○ Subtotal colectomy - removing entire colon 
§ Either observe ileocecal valve or ileocolic anastomoses -> have luminal disparity as described other lecture 
□ Sutured anastomosis
□ Stapled anastomosis
□ BAR anastomosis
□ Terminal ileum adapts
® to increase fluid absorption
□ Complications:
® Loose stool, stricture, dehiscence
□ Excellent prognosis
84
Q

If was sent 6 week old Labrador with no vaccination history and Vomiting, diarrhoea, fever what would you do

A

TEST FIRST -> parvo -> out in the car park if possible

85
Q

Cat with low ablubin and globulin and both adominal and pleural effusion what thinking differential, most likely and how to differentiate

A
○ Increase hydrostatic pressure (congestive heart failure), decrease oncotic pressure (low albumin - protein-losing)
○ NOT LIKELY to be congestive as low albumin and globulin 
○ DECREASE IN ONCOTIC PRESSURE likely 
§ Protein-losing enteropathy 
§ Protein-losing glomerulo-nephropathy  
§ TO DIFFERENTIATE 
□ Thoracocentesis to analyse the fluid 
□ Ultrasound guided cystocentesis
86
Q
Problem list 
- Vomiting (5 days)
- Abdominal pain 
- Dehydration 
- Tachycardia (likely second to dehydration) 
- Overweight 
- anorexic
what 4 main differentials and then diagnostic approach
A
Top differential diagnosis 
- Pancreatitis (sore, nausea don't want to eat) 
- GI obstruction 
- GI neoplasia - older so can be there, 
- Metabolic disease -> no pre-existing sign 
Diagnosis 
- bloods CBC - rule out metabolic
- radiograph 
- ultrasound if need
- exploratory laparatomy
87
Q
  • Seven year old female border collie, neutered
    Azathioprine and prednisolone for IMHA
  • Markedly obese, dull and weak, increased temperature, tachycardia, weak pulses, pale mucous membrane
    what is the likely differential and why
A
  • Pancreatitis - leads to multi organ issues

○ Obesity and also azathioprine

88
Q

what does a low glucose generally indicate

A

sepsis or hepatic insufficiency - in this case sepsis

89
Q

what is the common biochmeistry finding for pylorus gastric outflow obstruction

A

○ VERY low chloride -> chronic vomiting and pooling of chloride (sequestration) in the stomach
○ High potassium -> pooling in the stomach
Metabolic alkalosis

90
Q

dog and cat what called when develop and what dentition called

A
  • Dogs & cats – 2 sets of teeth (Diphyodont)
    ○ PRIMARY or DECIDUOUS
    ○ SECONDARY or PERMANENT
  • Primary develops during embryonic & foetal stages
  • Permanent develops during foetal & neonatal
  • Cats & Dogs have heterodont dentition
91
Q

when do teeth start to develop, what occurs and what are the stages called

A
  • Approx. day 25 of gestation
    ○ Thickening of embryonic oral epithelium – known as dental lamina
    ○ Invaginations of epithelium à formation of primordial tooth structure referred to as enamel organ or dental organ
  • Dental organ progresses through a series or stages
    1. bud stage
    2. cap stage
    3. bell stage
92
Q

What occurs at the bud, cap and bell stage of tooth development

A

○ Bud stage
§ Initial coalescence of dental lamina forming buds corresponding with future site of deciduous teeth
§ Cap stage begins when the bud develops a concavity on its deep surface
○ Cap Stage
§ At this stage dental organ is comprised of three layers
□ Outer enamel epithelium
□ Inner enamel epithelium
□ Stellate reticulum
§ Addition of 4th layer (stratum intermedium) marks beginning of bell stage
○ Bell Stage
§ Deciduous dentition buds develop extensions called successional laminae.
□ These progress through bud, cap, bell stage and form permanent dentition

93
Q

enamel characteristics what produced by, are there cells present and what occurs after eruption of tooth

A
  • Hardest tissue in the body – high mineral content arranged in rods of densely packed calcium hydroxyapatite crystals
  • Ameloblasts produce enamel but mature enamel is ACELLULAR
  • After eruption of tooth, ameloblasts are lost which means enamel cannot be repaired or regenerated
94
Q

Dentin how much of the tooth, how long produced for, composition and main characteristic

A
  • Makes up majority of adult tooth
  • CONTINUALLY produced throughout life of a vital tooth
  • 70% mineral, 20% lipid/protein & 10% H20
  • POROUS – approx. 45,000 dentinal tubules/mm2
95
Q

what are the 3 main types of dentin, when produced, what by and how

A
  • 3 main types – primary, secondary & tertiary/reparative
    ○ Primary – produced during development of tooth
    ○ Secondary Dentin – produced throughout life of vital tooth (This causes pulp cavity to progressively become narrower)
    ○ Tertiary – produced in response to injury or irritation
  • Produced by ODONTOBLASTS that line periphery of pulp cavity
    ○ Odontoblastic processes extend down dentinal tubules (some tubules also contain nerve fibres)
    ○ Tooth pain may come from fluid shifts or nerve stimulation
  • Odontoblasts produce tertiary dentin in rapid, disorganised fashion (if they survive initial insult)
96
Q

what is the pulp of the tooth and what are the 2 types of direct stimulated pain

A
  • Pulp comprised of major vessels, nerves and connective tissue
  • Direct stimulation of pulp – sharp localisable pain (myelinated A-delta fibres) + dull throbbing pain (unmyelinated C fibres)
97
Q

Peridontium what are they and the 4 components

A
  • Supporting apparatus of the tooth
  • 4 components
    a. Gingiva
    b. peridontal ligament
    c. cementum
    d. alveolar bone
98
Q

gingiva what are the 2 main areas and the normal sulcus depth in dogs and cats

A

§ Gingival attachment to tooth – junctional epithelium
§ Gingival sulcus – space between tooth and gingiva
§ Normal sulcus depth in cats <1mm and in dogs <3mm

99
Q

what is the structure of a periodontal ligament and alveolar bone

A

b. Periodontal ligament
§ Dense, fibrous connective tissue
§ Supports tooth and attaches it to the alveolus
d. Alveolar bone
§ Consists of two plates of cortical bone separated by spongy bone

100
Q

periodontal disease prevalence and what are the 2 stages

A
  • 70% of cats and 80% of dogs affected by some form of periodontal disease by 2 years of age
  • Two stages
    ○ Gingivitis – reversible inflammation of the gingiva
    ○ Periodontitis – inflammation and irreversible destruction of the periodontium (gingiva, cementum, alveolar bone, periodontal ligament)
    § Initially thought to be caused by irritation of gingiva from calculus