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SA GI disease Flashcards

1
Q

Signs of oropharyngeal and oesophageal disease?

A 
Dysphagia
Drooling saliva
Halitosis
Odynophagia
Regurgitation
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2
Q

Signs of dysphagia?

A 
Difficulty lapping or forming bolus
Excessive jaw or head motion
Dropping food from mouth
Drooling saliva/foaming at mouth
Persistent, ineffective swallowing
Nasal discharge
Gagging
Coughing
Failure to thrive
Reluctance to eat or pain
Halitosis
Blood tinged saliva
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3
Q

Causes of dysphagia?

A 
Functional neuromuscular dysphagia:
- cricopharyngeal chalasia/achalasia
- myasthenia gravis
- brainstem disease
- peripheral neuropathy
- polymyopathy
- hypothyroidism
- botulism
Morphological dysphagia:
- oropharyngeal inflammation
oropharyngeal trauma
- foreign bodies
- neoplasia
- congenital/developmental (hare-lip, lip fold deformities, cleft palate, malocclusion, craniomandibular osteopathy, temporomandibular dysplasia)
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4
Q

Causes of halitosis?

A 
Oropharyngeal disease - inflammation, neoplasia, foreign body
Oesophageal disease
Dietary associated
Malabsorption
Dental disease
Nasal cavity and sinus disease
Uraemia
Liver disease
Anal sac disease
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5
Q

Define pseudoptyalism and ptyalism?

A 
Pseudoptyalism = failure to swallow normal volume of saliva
Ptyalism = increased saliva production
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6
Q

How to differentiate between vomiting and regurgitation?

A

Vomiting (active) - salivation, heaving, digested food

Regurgitation (passive) - head down and food comes out, undigested food covered by mucus/saliva

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7
Q

Secondary signs of oesophageal and oropharyngeal disease?

A

Malnutrition/dehydration
Anorexia/polyphagia
Aspiration pneumonia/tracheal compression - cough, dysphagia

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8
Q

Radiography for swallowing problems/vomigurgitation?

A

Survey radiographs - head, neck, thorax
Barium oesophagram +/- fluoroscopy - barium mixed with food, iodine contrast if perforation suspected
‘Met check’

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9
Q

Lab investigations for swallowing problems/vomigurgitation?

A 
Haematology
Serum biochemistry and urinalysis
Virology (cats especially)
'Special' tests
- Anti-ACh receptor antibody (myaesthenia gravis)
- 2-M antibodies (polymyositis)
- ACTH stimulation test (hypoadrenocorticism)
- Thyroid testing?
- Toxicological tests?
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10
Q

Investigations for swallowing problems/vomigurgitation?

A 
History and physical exam
Diagnostic imaging
Endoscopy
Lab investigations
FNA
Biopsy
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11
Q

Major disease syndromes of the oesophagus?

A

Motility - megaoesophagus, dysautonomia, hiatal hernia
Obstruction - vascular ring, stricture, foreign body, neoplasia
Inflammation - oesophagi’s, reflux, hiatal hernia
Misc - diverticulum, broncho-oesophageal fistula

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12
Q

Definition of megaoesophagus?

A

Oesophageal dilation with functional paralysis

-> Failure of progressive peristalsis

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13
Q

Diagnosis of megaoesophagus?

A

Radiography +/- contrast
- uniformly dilated, gas and/or fluid filled
- ventral displacement of trachea
- secondary aspiration pneumonia
Fluoroscopy occasionally essential - oesophageal dysmotility

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14
Q

One example of each cause of secondary megaoesophagus?

A

Neuromuscular - myaesthenia gravis
Oesophageal - oesophagitis
Neuropathies - dysautonomia
CNS - distemper

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15
Q

Treatment and prognosis of idiopathic megaoesophagus?

A 
Feeding from a height - bailey chair
Slurry, textured food, meatballs?
Bethanecol?
Metaclopramide, cisapride?
Prognosis - guarded, danger of aspiration pneumonia, spontaneous recovery in some
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16
Q

Causes of oesophagitis?

A

Ingestion of caustics and irritants
Foreign bodies
Acute and persistent vomiting
Gastric reflux

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17
Q

Clinical signs of oesophagitis?

A 
Anorexia
Dysphagia
Odynophagia
Regurgitation
Hypersalivation
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18
Q

Diagnosis and treatment of oesophagitis?

A

Diagnosis - clinical signs, endoscopy, response to empirical treatment?
Symptomatic treatment - frequent small feeds, antibiotics, liquid antacids, local anaesthetics, gastrostomy tube feeding
Specific treatment - sucralfate, antacids, metaclopramide

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19
Q

Types/causes of oesophageal obstruction?

A

Intraluminal - foreign body, neoplasm, stricture, granuloma

Extraluminal - thyroid, thyme/mediastinum, vascular ring

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20
Q

Aetiology of oesophageal stricture?

A

Fibrosis after ulceration of mucosa by:

  • foreign body
  • caustic material
  • severe oesophagitis
  • gastric reflux esp. pooled secretions during GA
  • drug therapy e.g. doxycycline in cats
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21
Q

Treatment of oesophageal stricture?

A

Bougienage - increased risk of perforation, longitudinal shear
Balloon dilatation - radial stretch (less traumatic), stationary force, less risk of perforation
Inject steroid around the lesion (triamcinolone acetonide)

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22
Q

Signalment of oesophageal foreign body?

A

Usually young animals
Common in greedy dogs eating chop bones esp terriers
Rare in cats

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23
Q

Diagnosis of oesophageal foreign body?

A

Radiography - don’t give barium! - visible foreign body, mediastinitis, abscess
Oesophagoscopy

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24
Q

Treatment for oesophageal foreign body?

A 
Perforal approach:
- flexible or rigid endoscope
- preferably pull FB to mouth
- or push to stomach for gastrostomy
- check for oesophageal tear
Surgical removal:
- last resort
- essential if large laceration
Post removal: radiographs, PEG tube, omeprazole, sucralfate
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25
Q

Vomit reflex?

A 
Contract pylorus
Relax stomach and LOS
Contract abdominal muscles
Thorax vs closed glottis
Open UOS
Antiperistalsis
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26
Q

Differentials for chronic vomiting, secondary to systemic/metabolis disease?

A 
Infections - distemper, lepto
Pyometra
Renal failure
Hepatic disease
Drugs - digoxin, erythromycin, morphine
Ketoacidic DM
Hypoadrenocorticism
CNS disease - motion sickness, vestibular disease
Neoplasia
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27
Q

Differentials for chronic vomiting, secondary to intestinal/peritoneal disease?

A

Inflammatory bowel disease
Intestinal neoplasia
Small intestinal obstruction
Pancreatitis

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28
Q

Differentials for chronic vomiting due to primary gastric diseases?

A 
Chronic gastritis
Gastric retention disorders
Gastric ulcers
Gastric neoplasia
Diffuse GI disease involving stomach - inflammatory bowel disease, alimentary lymphoma
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29
Q

Signs of gastric disease?

A

Vomiting
Haematemesis
Nausea - hypersalivation, retching, anorexia
Melaena
Miscellaneous - belching, bloating, borborygmi, weight loss

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30
Q

Pathophysiology of gastric disease?

A

Gastric outflow obstruction
Gastroparesis
Disruption of mucosal barrier

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31
Q

Diagnosis of chronic vomiting?

A

Distinguish vomiting vs regurgitation
Eliminate secondary causes - Hx, PE, lab analysis, imaging
Abdominal imaging - plain radiography, contrast radiography, ultrasonography
Gastroscopy/coeliotomy
Symptomatic treatment

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32
Q

Physical exam for chronic vomiting?

A

Oral exam - ulcers, linear foreign body
Abdominal palpation - pain, foreign body, intra-abdominal mass, distended stomach or bowel
Rectal exam - diarrhoea, melaena

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33
Q

Lab evaluation for chronic vomiting?

A

Haematology
Biochemistry
Urinalysis - no pathognomic changes, more used to rule out systemic disease, also can assess hydration status

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34
Q

Radiography and ultrasonography for chronic vomiting - what can be checked for?

A 
Radiography: survey abdominal radiograph
- foreign body
- abdominal mass
- intestinal obstuction
- peritonitis
- GDV
Ultrasonography:
- foreign bodies
- ulcers
- thickening of gastric mucosa
- loss of layering (suggests infiltration)
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35
Q

Indication for endoscopy (gastroscopy) for chronic vomiting and what is done?

A

If clinical or radiographic signs of gastric disease
Inspection and biopsy (even if grossly normal)
Foreign body removal

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36
Q

Causes of chronic gastritis?

A 
Aetiology usually unknown
Sometimes generalised IBD
Chronic gastric parasitism 
Hairballs in cats?
Spiral bacteria - Helicobacter?
Immune mediated?
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37
Q

Clinical signs of chronic gastritis?

A

Intermittent chronic vomiting (vague)
+/- periodic early morning vomit with bile
+/- poor appetite
+/- gastric bleeding

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38
Q

Diagnosis of chronic gastritis?

A

Lab changes often non specific
Imagining findings non specific
Gastroscopy and biopsy

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39
Q

Treatment for chronic gastritis?

A

Removal of etiologic agent if known
Diet - multiple small meals, low fat diet (fatty foods stay in stomach longer), hypoallergenic diet (novel protein source, hydrolysed protein)
Acid blocker
Corticosteroids?

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40
Q

What are gastric retention disorders? Types?

A

Retention of food for >8h causing delayed vomiting of food
Anatomical flow obstruction
Functional disorder
- primary motility disorder
- inflammatory disease (IBD, gastric ulcer)

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41
Q

Anatomical outflow obstructions causing a gastric retention disorder?

A

Pyloric stenosis
Neoplasia, polyp
CHPG
Foreign body

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42
Q

Bilious vomiting?

A

Often occurs in dogs fed once daily (especially if fed in the morning)
Vomiting occurs overnight or in the morning
Vomitus often bile stained fluid, not food
Presumably reflects abnormal …
Diagnosis - rule out other causes of vomiting, treatment trial
Treatment - feed more often focussing on late meal, pro kinetics (ranitidine or metaclopramide)

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43
Q

Pyloric stenosis - breeds/species associations? Treatment?

A

Congenital in brachycephalic breeds
Association with megaoesophagus in cats
Treatment: pylorotomy/pyloroplasty

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44
Q

What is chronic hypertrophic pylorogastropathy (CHPG)?

A

Idiopathic mucosal hypertrophy
May cause outflow obstruction
Most common in toy breeds
Treatment - surgery

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45
Q

Treatment for functional causes of gastric retention?

A

Treat underlying inflammatory disease
Prokinetics
- metaclopramide: stimulates normal gastric peristalsis
- ranitidine: H2 antagonist plus pro kinetic action
- erythromycin: low dose stimulates motilin receptors

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46
Q

Causes of haematemesis?

A 
Generalised bleeding
Swallowed blood - oropharyngeal, nasal, pulmonary
Severe gastritis
Gastric ulcer
Gastric neoplasia
Duodenal disease
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47
Q

Signs of gastric ulcers?

A 
Haematemesis
Melaena
Anaemia
Weight loss
Pain
Peritonitis etc if perforated
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48
Q

Aetiology of gastric ulcers?

A 
Drugs - NSAIDs, corticosteroids
Head and spinal injuries - in combination with corticosteroids, also colonic ulcers/perforations
Gastritis
Metabolic - liver disease, uraemia
Bile reflux?
Mastocytosis
Gastrinoma (Zollinger-Ellison)
Spiral bacteria - Helicobacter?
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49
Q

Helicobacter species? Cause disease?

A 
H felis
H heilmannii
H bizzozeroni
others
High prevalence (~100%) - seen on biopsy
Evidence of recognition by host - Ab response, lymphoid follicles
Often no evidence of clinical disease
But a cause of chronic gastritis?
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50
Q

Treatment for gastric ulcers?

A 
Treat identifiable primary cause
Sucralfate
Acid blockers - antacids, H2 antagonists (cimetidine licensed but poss poor efficacy and side effects, ranitidine can be used for motility disorders under cascade), proton pump inhibitors (omeprazole)
Antibiotics?
Triple therapy?
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51
Q

Prevention of gastric ulcers?

A

Limited protective effect: H2 antagonists, PPis, sucralfate

Protective: synthetic PGE (misoprostol)

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52
Q

Triple therapy for Helicobacter?

A

2 antibiotics plus an acid blocker e.g. amoxicillin, metronidazole and omeprazole
Or 3 antibiotics e.g. amoxicillin, metronidazole and clarithromycin (works on luminal and intracellular)

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53
Q

Gastric adenocarcinoma - what do they do? When to suspect?

A 
Infiltrate gastric wall - fibrosis/thickening, ulceration
Often lesser curvature/distal stomach
Metastasis to local LN and liver
Predisposition in Belgian shepherds, collies, bull terriers
Suspect in older animal with:
- chronic vomiting
- anorexia and weight loss
- haematemesis and melaena
- anaemia
- drooling saliva
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54
Q

Gastric neoplasias?

A 
Primary neoplasia infrequent
Middle age/older male dogs > cats
Dogs:
- adenocarcinoma (75%)
- lymphoma
- polyps
- leiomyoma/leiomyosarcoma
Cats:
- lymphoma
- adenocarcinoma
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55
Q

Diagnosis of gastric adenocarcinoma?

A

Contrast radiography
Endoscopic biopsy - often to superficial
Full thickness biopsy

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56
Q

Treatment and prognosis for gastric adenocarcinomas?

A

Surgical resection (palliative, rarely curative)
Grave/hopeless prognosis - probably painful
‘Leather-bottle’ stomach

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57
Q

Advantages and disadvantages of abdominal radiography?

A 
Advs:
- quick
- allows global overview
- assessment of thorax and spine
 - allows differentiation of gas/mineralisation
Disadvs:
- superimposition
- lack of contrast
- soft tissue/fluid same opacity
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58
Q

Technique for abdominal radiography?

A

Take on expiration
Low kVp, high MAS
Grid if >10cm
Projections: VD, right lateral, +/- left lateral

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59
Q

Advs and disadvantages of contrast radiography?

A 
Advs:
- improves sensitivity
- identification of anatomy not seen on plain radiographs (e.g. urethra or ureters, blood vessels)
- allows assessment of internal structure
- some info on function
Disadvs:
- time consuming
- expensive
- complications
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60
Q

Techniques for contrast radiography?

A

Appropriate patient restraint (Ga often required)
Requires food patient preparation - enemas (LUT, LI studies)
Take plain images first
Obtain enough images - genuine lesions are consistent and reproducible

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61
Q

What negative contrast medias are used for radiography? When? Advs/disadvs?

A 
Air, N20, CO2
Used for bladder and gastric studies
Cheap, simple and minimal risk
Air embolus reported, poor mucosal detail
Reduce exposure
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62
Q

What are positive contrast medias for radiography?

A 
Radiopaque (higher atomic number)
Water soluble (iodine based)
Non soluble (barium)
Iodine based agents divided into:
- ionic and non-ionic
- high osmolar and low osmolar
Increase exposure
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63
Q

Advs and disadvs of abdominal ultrasonography?

A 
Advs:
- assessment of internal architecture
- assessment of vasculature
- better soft tissue contrast
- guided biopsy
- accurate measurement
- real time assessment motility
Disadvs:
- limited field of view
- difficult if large amounts of gas
- operator and equipment dependent
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64
Q

Indications for abdominal CT?

A 
Surgical planning
Tumour staging
Retroperitoneal disease
Parenchymal organs (larger dogs)
Vascular malformations
Ureters
Insulinoma (esp large dogs)
Pelvic canal
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65
Q

When is abdominal CT not useful?

A

GIT
Small dogs/cats
Severe renal disease - need IV contrast

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66
Q

Things to do/check for US guided FNA/biopsy of an abdominal lesion?

A

Identify if lesion accessible
Allows visualisation of needle
21-22G
Assess coagulation times and platelets if perform Tru-cut biopsy
Avoid FNA bladder tumours
Avoid crossing body cavities
Catheter biopsy for bladder/urethral masses

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67
Q

Radiological assessment?

A

Check extra-abdominal structures
Assess boundaries of abdomen
Assess serosal detail - relies upon fat between organs
Assess each organ system
5 opacities
Roentgen signs - size, shape, margination, opacity etc

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68
Q

What can reduced serosal detail of an abdominal radiograph indicate?

A

Reduced fat - check body condition

Effacement by fluid/ST (ascites, peritonitis)

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69
Q

Appearance of ascites on US? Where to look?

A 
Fluid anechoic
Need to sample to determine type
Look adjacent to liver and bladder
Assess hepatic veins
Dilation HV - right sided heart disease
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70
Q

What does free gas in the peritoneum look like on radiography? Is it significant? What does it indicate?

A

Large volumes relatively easy to detect - caudal to diaphragm, around stomach/serosal surfaces
Smaller volumes present as gas bubbles outside of GIT
Always significant (unless recent ex-lap)
Indicates rupture of hollow virus (gas producing peritonitis/penetrating trauma)
Usually fluid present also

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71
Q

What is in the retroperitoneum? What to look for radiographically?

A

Space of fat opacity
Primarily kidneys but also Lns, great vessels, adrenals
Swelling and masses - increased soft tissue ventral to spine replacing/obscuring fat, ventral displacement of colon, assess ventral spine carefully
LNs - ventral to L6/7 (not normally visible), may displace and compress colon/rectum - drain pelvic canal and pelvic canal and pelvic limbs (look for anal sac, bladder, prostatic disease, pelvic limb masses)

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72
Q

Normal appearance of adrenal glands on radiography?

A

Not normally visible (may mineralise in cats)
Large masses may displace kidneys ventrolaterally
neoplastic disease may mineralise in dogs

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73
Q

Where are the adrenal glands found on US? Shape?

A 
Left renal artery and CVC landwarks
Left adrenal is monkey nut shaped
Right adrenal is arrow shaped
May invade vessels
incidental nodules common
Still need endocrine testing
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74
Q

Differentials for organomegaly?

A

Focal enlargement - neoplasia, granuloma, abscess, cyst

Diffuse enlargement - inflammation, metabolic disease, infiltrative neoplasia, congestion

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75
Q

Significance of reduced organ size?

A

Usually chronic disease
Mineralisation common
Often irregular
Poor correlation with function

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76
Q

Significance of organ shape changes?

A

More sensitive than size changes
Often non specific - neoplasia, cysts, haematomas, granuloma
No information on function

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77
Q

Significance and causes of abdominal mineralisation?

A 
Often incidental
Dystrophic - secondary to damaged tissue
Metastatic - secondary to abnormal Ca/P
Calculi
Ingesta
Neoplasia
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78
Q

What to assess about the liver on radiography?

A

Position relative to costal arch
Shape of caudal margins (should be sharp)
Caudoventral border sharp triangle
Gastric axis perpendicular to spine - parallel to ribs

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79
Q

Appearance of hepatic masses on radiography?

A

Mass effect of cranial abdomen
Caudal displacement of stomach especially
Focal enlargements - masses, cysts, abscess/granuloma

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80
Q

Appearance of micro hepatica on radiography? Causes?

A

Cranial displacement/rotation of gastric axis
Portosystemic shunts
Cirrhosis
Herniation

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81
Q

Liver on US? Assessing liver disease?

A

Portal veins echogenic walls
Hepatic veins thin walled
Lung/diaphragm interface hyperechoic
Difficult to evaluate diffuse disease on US - may see change in echogenicity compared to spleen
Easier to appreciate multifocal hepatic disease - metastatic tumour, lymphoma, nodular hyperplasia, granuloma, necrosis (FNA/biospy required)

82
Q

How may hepatobiliary disease due to obstruction appear on US? Normal width of common bile duct?

A

Gall bladder size too variable to be helpful
Dilation of common bile duct (normally <3mm in dogs, 4mm in cats)
May see obstructing material along duct or at papilla
Dilation of intrahepatic bile ducts if chronic (7d)

83
Q

Normal appearance of spleen on radiography?

A

Strap like
Head of spleen attached to stomach, caudal to gastric fungus and craniolateral to left kidney (DV view)
Tail mobile
Size variable

84
Q

Splenomegaly on radiography? Causes?

A

Requires subjective evaluation - rounded margins, shape changes (margins)
Causes: GA/sedation in dogs (ACP/Thio), infiltration, inflammatory disease

85
Q

Splenic masses on radiography - what can be seen?

A

Lesions involving tail east to see, especially if no peritoneal fluid
Mid-ventral abdomen (caudal to stomach)
(Caudo)dorsal displacement of small intestine
Lesions involving head better seen on VD projection
Size no indication of malignancy

86
Q

Splenic nodules on ultrasound?

A

Very common on US
Often benign nodular hyperplasia/extramedullary haematopoiesis
Hyperechoic modules - myleolipoma
FNA

87
Q

Problems with contrast studies for GIT imaging?

A

Interpretation can be difficult
Must be carried our properly e.g. good patient preparation
Time consuming, cost intensive, low diagnostic yield
Complication if GI perforation
So superseded by combining radiography with US

88
Q

Parts of the oesophagus?

A

Cervical part - dorsal to left lateral to the tracheal

Thoracic part - within mediastinum, returns to dorsal to the trachea and passes right to the aortic arch

89
Q

What is a redundant oesophagus? Appearance on radiography?

A

Variation of normal oesophagus
Brachycephalic breeds
Contributes to increased opacity and width of the cranial mediastinal region
Often not clinically significant

90
Q

Appearance of megaoesophagus on radiography?

A

Segmental or generalised dilation
May cause ventral deviation of the trachea and widening of the mediastinum
Tracheo-oesophageal stripe sign (summation of tracheal wall and oesophageal wall) is normal

91
Q

Predelection sites for foreign bodies in the oesophagus? Appearance on radiography? What to do?

A

Thoracic inlet, heart base and cranial to the diaphragm/cardia
Often mixed opacity, dorsally and ventrally well defined mass lesion in the region of the oesophagus (need orthogonal views)
Endoscopy or non-ionic contrast

92
Q

How can gas be used to highlight intraluminal structures/lesions?

A

Positional radiography useful (right and left view and VD +/- DV) as gas will move to the non dependent side within hollow viscus
SO po

93
Q

Stomach compartments?

A 
Cardia
Fundus
Body
Pyloric antrum
Pylorus
94
Q

Where is the stomach on radiography?

A

Positioned within the costal arch in the cranial abdomen, directly caudal to the liver

95
Q

What are the 5 layers of the stomach? Appearance on ultrasound?

A

Serosa, muscularis, submucosa, mucosa, luminal surface
Muscularis and mucosa are hypoechoic
Rugal folds are visible in fungus and body (esp in cats)
Gas in fungus often impairs assessment
Pylorus is a thick muscular structure relatively hyperechoic with seemingly blurred layering

96
Q

How may a stomach foreign body appear on radiography and US?

A

Radiography:
- easy to identify if mineral or metallic opacity
- gas may be trapped in textile or botanical FB or toys -> bizarre gas patterns
- may cause partial or complete obstruction e.g gastric distension with fluid in anorexic animals, ‘gravel sign’
US:
- not always easy to discern from food
- often hyperechoic surface and strong distal shadowing
- more difficult if texture or absorptive material and very difficult if linear FB

97
Q

Causes of gastric dilation? Appearance on radiography?

A

Gas dilation - aerophagia, GD, DDG - dark opacity
Fluid and gas dilation - pyloric outflow obstruction (functional ileum, obstruction) - mainly soft tissue opacity with gas opacity floating on top

98
Q

What happens with GDV?

A

Marked gas dilation and rotation around longitudinal axis
Most commonly clockwise rotation:
- pylorus shifts dorsally, cranially and to the left
- body shifts towards the right
- fundus displaced ventrally and to the right
- spleen follows greater curvature towards the right (gastrosplenic ligament)

99
Q

Appearance of GDV on radiography?

A

All parts of stomach markedly gas distended
Fundus displaced caudoventrally and right
Pyloric antrum displaced craniodorsal and left
Compartamentalisation with a dividing soft tissue band (‘shelf’)
Mass effect on other abdominal organs

100
Q

Appearance of gastric wall abnormalities on radiography/US?

A

e.g. neoplasia, haemorrhage, oedema
Often not visible on plain radiographs
US useful
Localised or diffuse wall thickening (has to be substantial before can be reliably detected)
Irregularly marginated gas content
Delayed gas emptying due to partial/complete obstruction
Imaging insensitive for ulceration

101
Q

Normal appearance of small intestines of radiography?

A

Normally smoothly marginated band/tube or as circular/ovoid ST opacity when viewed end on
Usually of ST opacity with some segments being mildly homogenously gas filled in dogs
Little to no gas filling in cats

102
Q

Small intestinal diameter and wall thickness on radiography? Problems?

A

Dilation with gas or fluid of SI associated with obstruction, but increased overall size may be due to diffuse wall thickening (hard to assess)
No one loop more than 2x diameter of any other loops
Dog: 2x width of a rib or 1.6x height of L5 at its narrowest point
Cat: 12mm or 2x height of mid L4 or <2x height of endplate of L2
Wall thickness cannot be reliably assessed on plain radiographs - ‘wall’ is summation of true wall and intestinal luminal fluid - fluid and ST indistinguishable, requires contrast or ultrasonography

103
Q

Wall thickness of SI on US?

A

Mucosa is thickest layer
Duodenum thickest wall of SI segment (5mm in dogs, 3-4mm in cats)
Submucosa is thicker in the ileum and flower-like/wheel-like appearance on transverse images

104
Q

Causes of small intestinal dilation?

A 
Functional ileus secondary to:
- severe inflammation (e.g. parvo)
- peritonitis
- recent surgery
- drugs
- thrombosis
- mesenteric volvulus
Mechanical or obstructive ileum secondary to:
- obstruction (FB, intussusception)
105
Q

Define ileus

A

Failure of intestinal contents to pass normally

106
Q

What does an obstructive pattern of the SI look like on radiography?

A

Fluid and/or gas dilation proximal to the obstruction
Creates two populations of intestine - one abnormal proximal and one normal distal to obstruction (may not see 2 populations if obstruction very proximal or very distal)

107
Q

What are gravel signs in the SI?

A

When partial obstruction
Accumulation of many small mineralised particles proximal to the partial obstruction
Typically little dilation
Can also be seen in the stomach with pyloric/proximal duodenal obstruction

108
Q

What may be seen on US with SI obstruction?

A

Secondary changes depending on level of obstruction:
- fluid dilation proximal to FB and to-and-fro movement
- normal intestines caudal to obstruction
Foreign body
- hyperechoic, irregular or artificially symmetrical shape
- usually strong distal shadowing
- focally dilating the SI/thin wall

109
Q

Appearance of a linear foreign body in SI on US?

A

Usually cause plication/hair-pin bends/bunching and triangular/tear-drop shaped gas bubbles
+/- Localised peritonitis (loss of serosal detail, streaky appearance)
Signs of obstruction (often less severe)

110
Q

Appearance of intussusception on radiography?

A

Ovoid/elongated ST mass/dilation
Possibly crescent shaped gas opacity between intussusceptum (inner) and intussuscipiens (outer)
No ‘normal’ caecal gas, shortened colon

111
Q

Appearance of intussception on ultrasound?

A

Easily diagnosed on US
Onion ring/bullseye appearance on transverse images
Intestinal walls identified within intestinal lumen
Also vessels/blood flow within lumen

112
Q

Imaging for intestinal inflammatory disease?

A

Often normal
Radiography not useful
Ultrasound may show:
- altered mucosal echogenicity
- muscularis thickening (cats ddx: lymphoma)
- normal to mildly thickened overall wall thickness
- preserved layering

113
Q

Imaging for SI neoplasia?

A

Needs to be substantial size for plain radiography
Signs secondary to obstruction may be seen
Care not to over interpret ‘wall thickening’
Large masses may not be possible to determine origin
Localised masses, irregular gas filling/ccontrast column
US very useful
- loss of wall layering, often circumferential, hypo echoic or heterogeneous
- may be very large with central gas containing lumen
- may see signs of obstruction
- assess local LNs

114
Q

Location and appearance of caecum on radiography?

A

Located in right dorsal aspect of abdominal cavity, often level of left kidney
Small in cats, rarely contains gas and normally not visible or comma shaped
In dogs appears as semicircular snail-shell gas filled structure

115
Q

Appearance of colon on radiography?

A

Divided into ascending, transverse and descending colon
Thin walled, distensible tube
‘Question mark’ shaped in DV projection

116
Q

Appearance of constipation/obstipation/megacolon on radiography? Causes?

A

Large intestinal dilation with increasingly more opaque (dehydrated) faecal material
Dog: < length of L7 vertebral body
Cat: megacolon > 1.48x length L5 or 2.8x cranial endplate of L2
Idiopathic, neurogenic (spinal disease, dysautonomia), chronic constipation, chronic inflammation

117
Q

Normal pancreas on radiography? Position?

A

Not seen in normal plain radiographs
Medial to duodenum, between gastric body and transverse colon, medial to spleen and cranial to left kidney
US more useful

118
Q

Significance of pancreatic enlargement? Signs on radiography?

A

Pancreatitis or neoplasia
Lateral displacement of the duodenum and caudal displacement of the colon
Increased ST opacity in the craniodorsal to mid abdomen
Localised loss of serosal detail
Functional ileus may lead to gas filling of the duodenum with pancreatitis

119
Q

Appearance of acute pancreatitis on US?

A 
Enlarged hypoechoic pancreas
Irregular margination
Heterogeneous appearance
Steatitis/hyperechoic mesentery
\+/- biliary obstruction
Corrugation of duodenum
120
Q

Differential diagnoses for chronic diarrhoea?

A 
Adverse reactions to food
IBD
Antibiotic responsive diarrhoea (dogs)
Lymphangiectasia
Lymphoma/tumours
Infectious diarrhoea
Obstructions
Liver disease
Renal disease
Pancreatic disease
Endocrine disease - Addison's, DM, hyperthyroidism
121
Q

What is diarrhoea originating from the SI typically like?

A 
Increased volume
Colour change
Normal to slight increase in frequency
\+/- weight loss
\+/- flatulence, borborygmi, halitosis
122
Q

What diarrhoea originating from the LI typically like?

A 
Decreased volume
Increased frequency
Urgency and tenesmus
Mucus and haematochezia
Dyschezia
Constipation +/- variable consistency
No weight loss?
123
Q

What does melaena indicate?

A

= digested blood so a sign of upper GI disease (stomach or SI bleeding)

124
Q

Preparation required for colonoscopy?

A

Starve for 48h
Polyethylene glycol (laxative) - 3 doses 4h apart with stomach tube
Followed by 2 x warm water enemas

125
Q

Laboratory tests for chronic diarrhoea?

A
  1. Faecal analysis
    - parasites (Giardia, Cryptosporidia, Tritrichomonas foetus-cats)
    - bacteria? (Salmonella, Campylobacter) - although may not be cause
  2. Haematology, serum biochemistry and urinalysis - to rule out systemic diseases (liver/kidney disease etc)
  3. Endocrine tests
    - ACTH stim test/basal cortisol (hypoadrenocorticism)
    - total thyroxine (hyperthyroidism)
    - trypsin-like immunoreactivity (TLI) (exocrine pancreatic insufficiency)
    - total lipase or pancreatic lipase (possible pancreatitis)
    - folate and cobalamin (malabsorption)
126
Q

Typical presentation of Tritrichomonas foetus in cats? Diagnosis?

A 
Multi cat environment
Poor body condition
Chronic diarrhoea
Large intestinal signs
Diagnosis - faecal prep in saline, culture, PCR (best)
127
Q

What does a finding of hypocobalaminaemia (fit B12) mean for chronic diarrhoea?

A

Negative prognostic indicator

Needs treating with cobalamin - SC injection (needed in some dogs with problem absorbing cobalamin) or oral

128
Q

Advantages and disadvantages of endoscopy and coeliotimy for intestinal biopsies?

A

Endoscopy:
- minimally invasive and direct examination
- requires equipment and expertise
- small superficial samples from a limited region
Coeliotomy:
- can get multiple full thickness biopsies
- surgical risk
- best for cats (more likely to miss disease with endoscopy)

129
Q

Possible diagnoses for chronic diarrhoea that can be found by a biopsy?

A 
Non specific normal/mild inflammation:
- adverse reaction to food- antibiotic-responsiveness diarrhoea etc
- IBD (chronic enteropathy)
Moderate-severe inflammation:
- IBD (chronic enteropathy)
Lymphoma
Lacteal dilation:
- lymphangiectasia
- secondary to another disease
130
Q

What treatment trials can be used for chronic diarrhoea after faecal and lab tests and biopsy etc?

A

Diet - food responsive?
Antibacterials - antibiotic responsive?
Steroids - IBD?
Cytotoxics - severe IBD or lymphoma?

131
Q

Definition of constipation?

A

Difficult, incomplete or infrequent evacuation of dry hardened faeces from the bowel

132
Q

Causes of constipation?

A

Dietary - ingested foreign material, low residue diet
Neuromuscular - spinal cord disease (lumbosacral), idiopathic megacolon
Environmental - obesity, hospitalisation, change in routine, inactivity
Colonic obstruction - stricture, pelvic trauma, neoplasia, foreign body
Electrolyte imbalance - dehydration, hypokalaemia
Drug-induced - opiates, phenothiazines, anticholinergics

133
Q

Most useful diagnostic tool for constipation?

A

Radiography

134
Q

Treatment for constipation?

A

Remove underlying cause if possible e.g. surgery for fracture
Oral laxatives - lactulose, polyethylene glycol
(Cisapride) - not licensed
Enemas
Gentle manual evacuation under anaesthetic
Surgery if megacolon
Dietart management - high fibre

135
Q

What is feline triaditis?

A

Inflammatory disease of intestines, pancreas and liver

136
Q

Pathogenesis of pancreatitis?

A

Normally trypsin only activated in SI
Aetiological factors triggers early activation in pancreas
Activated trypsin triggers activation of other proteases
Results in autodigestion of pancreas - direct tissue damage
Cascade initiation:
- coagulation
- fibrinolysis
- complement
- kallikrein-kinin

137
Q

Predisposing factors for acute pancreatitis?

A 
(mostly idiopathic)
Breed - spaniels and terriers
Gender - females, neutered
Obesity
Drugs
Concurrent diseases
Dietary factors
- hypelipidaemia predisposes to obesity and diabetes mellitus, primary hyperlipidaemia in miniature schnauzers (not proven)
- high dietary fat
- dietary indiscretion
138
Q

What disease associations are often found with feline pancreatitis?

A

Cholangitis
IBD
Hepatic lipidosis
Diabetes mellitus

139
Q

Possible clinical signs in order of most common with pancreatitis in dogs?

A 
Dehydration (97%)
Anorexia (91%)
Vomiting (90%)
Weakness (79%)
Abdominal pain (58%) - prayer position
Diarrhoea (33%)
Jaundice (32%)
140
Q

Possible clinical signs in order of most common with pancreatitis in cats?

A 
Lethargy (100%)
Anorexia (93%)
Vomiting (35%)
Abdominal pain (25%)
Diarrhoea (15%)
141
Q

Steps for investigation of chronic diarrhoea, constipation and acute pancreatitis?

A

History/physical exam
Lab tests
Diagnostic imaging
Biopsy

142
Q

Lab tests for pancreatitis?

A 
Haematology and biochemistry
- increased WBCs
- increased glucose/decreased calcium
- increased liver enzymes
- jaundice (increased bilirubin)
Pancreatic enzyme tests
- total amylase and lipase
- pancreatic lipase (more specific but still not perfect, SNAP test)
Results less consistent in cats
143
Q

Imaging for pancreatitis?

A

Radiography - to rule out other disease

Ultrasound - hyperechoic/hypoechoic, enlargement and swelling, mesenteric changes (hyperechoic)

144
Q

Treatment for pancreatitis?

A

Nutritional support
- feed as soon as V+ stops with feeding tube
- move onto interim diet: first small amounts of water, then start food cautiously (low fat diet, small frequent meals)
Pancreatic enzymes as long as doesn’t affect appetite
- reduces pancreatic secretion to poss reduce post-prandial pain (no evidence of efficacy)
- long term diet from 3 weeks onwards, pancreatic/weight management diet if obese
Fluid therapy
Analgesia
- avoid NSAIDs
- buprenorphine
- paracetamol (dogs only)
- tramadol
- gabapentin
Anti-emetics if V+
- allows early enteral nutrition
Antibacterials
- most cases are sterile
- but intestinal wall ‘leaky’ -> bacteraemia so consider prophylactic use
Steroids?
Surgery?

145
Q

Aetiology of exocrine pancreatic insufficiency (EPI)? Which breeds most commonly affected?

A
  1. Pancreatic acinar atrophy
    - most common in dogs
    - possibly heritable in GSD and rough collies (66% are GSDs)
    - lymphocytic infiltration so immune mediated? But only see cases when already atrophy so immuno-suppressives not effective treatment
  2. Pancreatic hypoplasia
    - rare congenital (<6mo)
    - associated juvenile DM
  3. Chronic pancreatitis
    - most common in cats (still rare)
    Rare in cats
146
Q

EPI clinical signs in dogs?

A

Faecal changes - large volumes, foul smelling, greasy (steatorrhoea), putty-like to overt diarrhoea
Appetite changes - polyphagia, coprophagia, pica
Vomiting
Poor coat condition
Poorly muscled/weight loss

147
Q

EPI diagnosis?

A

Trypsin like immunoreactivity:

  • Blood test
  • Best test
  • Normal dog TLI >5ug/L
  • Dogs with EPI <2.5ug/L
  • Equvocal 2.5-5ug/L (repeat in 4 weeks)
  • Subclinical EPI? repeatedly 2.5-5ug/L
148
Q

Treatment of EPI?

A 
Pancreatic enzyme
- uncoated dry powder
- enteric coated granules
- fresh-frozen pancreas
- mix with each meal and feed
Feed highly digestible diet
- no need to fat restrict
- not high fibre
- exclusion diet not necessary
- ensure adequate food intake (2xM for ideal weight)
Cobalamin supplementation if deficient
- pancreas does not produce intrinsic factor
- poor prognostic indicator
Antibacterials for bacterial overgrowths?
Acid blockers?
Treat other diseases in cats (often other diseases present)!
Good prognosis if treated correctly
149
Q

EPI clinical signs in cats?

A

Very similar to dogs
Weight loss (or poor growth)
Diarrhoea
Polyphagia, coprophagia, anorexia, flatulence
Vomiting
Signs of any concurrent disease - lethargy, hair loss, PUPD, weakness

150
Q

What does an exclusion diet involve?

A 
Novel protein source
Sole dietary intake
Minimum 2 weeks
Occasionally 10-12 weeks
Then ideally re-challenge
151
Q

Causes of protein losing enteropathy?

A

IBD
Lymphangiectasia
Alimentary lymphoma

152
Q

Prognosis and treatment for PLE?

A

Poor prognosis - survival may only be few months without appropriate therapy
Go straight to immunosuppression
- prednisolone (2-4 weeks, reduce over 2-3 months)
- cytotoxic (chlorambucil best first choice)

153
Q

Causes of pre-hepatic, hepatic and post-hepatic jaundice?

A

Pre-hepatic - haemolysis
Hepatic - hepatocyte dysfunction, intrahepatic cholestasis
Post-hepatic - extra-hepatic cholestasis

154
Q

Signs of hepatic metabolic dysfunction?

A

Non specific signs - loss of condition, weight loss
Hypoglycaemia
Hypoalbuminaemia - only in chronic disease, can contribute to ascites

155
Q

Why can liver disease cause ascites?

A

Hypoalbuminaemia
Portal hypertension
Sodium and water retention

156
Q

Features of acquired portosystemic shunts - what develops? What do the shunts develop from

A

Usually multiple
Develop secondary to liver disease - juvenile fibrosis, cirrhosis, portal hypertension
Shunts develop from redundant vessels between portal vein and caudal vena cava
Portal hypertension often leads to ascites

157
Q

What is the main problem with portosystemic shunts?

A 
Hepatic encephalopathy
Defective urea formation from NH3
Increased blood NH3 (and other toxins)
Leads to altered CNS function
CNS signs:
- anorexia, v+d, PUPD
- dullness, aggression, staggering, blindness, head pressing, seizures
- worse if high protein meal, GI bleed, dehydration or acid-base imbalance
- increased sensitivity to anaesthetics
158
Q

What can copper-coloured irises in cats be due to?

A

Portosystemic shunt

159
Q

Why can liver disease cause bleeding?

A

Defective production and storage of clotting factors
Vitamin K malabsorption
Portal hypertension -> GI bleeding

160
Q

Liver disease clinical signs?

A 
Icterus
Faecal changes - grey, melaena
Hepatic encephalopathy Drug intolerance
Ascites
Stunted growth (if young)
Vomiting and diarrhoea
Polyuria &amp; polydipsia
Non-specific signs
• Anorexia
• Weight loss
• Weakness
• Poor coat and skin condition
161
Q

Classification of hepatopathies?

A

Primary
- Infectious inflammatory diseases
- Non infectious inflammatory diseases
- Non infectious non inflammatory diseases
Secondary (reactive) - most common, reversible

162
Q

What general causes are there of secondary hepatic disease?

A 
Anoxia
Toxaemia
Nutritional imbalance
Metabolic changes
Infection
163
Q

Reactive hepatopathies?

A 
IBD
Bacterial infections
Periodontal disease
Acute pancreatitis
DM
HAC
Hyperthyroidism
Shock
Septicaemia
etc
164
Q

Causes of primary infectious inflammatory hepatopathies?

A 
Bacterial
- Leptospirosis
- Bacterial cholangiohepatitis
Viral
- Infectious canine hepatitis
- Canine herpes virus
- FIP
Protozoal
- Toxoplasma
165
Q

Causes of primary non infectious inflammatory hepatopathies?

A 
Toxic hepatic disease
Drug induced hepatic disease
All forms of chronic hepatitis
- canine chronic hepatitis
- feline lymphocytic cholangitis
166
Q

Causes of primary non inflammatory non infectious hepatopathies?

A 
Congenital portosytemic shunt
Juvenile hepatic fibrosis
Feline hepatic lipidosis
Neoplasia
Telangiectasis and Peliosis
Surgical 
- trauma
- liver lobe torsion - entrapment
167
Q

Why are there feline hepatic idiosyncrasies? Examples of causes? Consequences?

A

Relative deficiency of glucoronyl transferase
So difficulty conjugating toxins (glucoronidation)
Aspirin, paracetamol, phenols, pine tars, morphine, benzenes, alcohols, barbiturates
Results in methaemoglobinaemia
- haemolytic aneamia (depression, dyspnoea)
- facial oedema
- hepatocellular damage (liver failure and icterus)

168
Q

Treatment for paracetamol toxicity in cats?

A 
N-acetylcysteine
S-adenosyl methionine?
IV fluids
Antibiotics
Activated charcoal if recent ingestion
169
Q

Clinical signs of liver disease in cats?

A

Anorexia and weight loss most common
Icterus relatively common
PUPD - less severe
Hepatoencephalopathy -> hypersalivation
Microhepatica and cirrhosis rarely seen
Pyrexia common in suppurative cholangitis
Chorioretinitis or uveitis (FIP, toxoplasmosis)

170
Q

Differential diagnoses for feline icterus?

A 
Cholangitis complex
FIP (dry form)
Lymphoma
Toxoplasmosis
Lipidosis
Pancreatitis
Haemolytic anaemia
Toxic hepatopathy
Panleucopenia
Neoplasia
Biliary obstruction/bile duct rupture
171
Q

Which liver enzymes are hepatocellular markers and cholestatic markers in small animals?

A

Hepatocellular markers: ALT, AST

Cholestatic markers: ALP, GGT

172
Q

When do serum biochemistry liver tests generally vary from normal?

A

ALT and ALP - early hepatitis
Bile acids - chronic hepatitis, most sensitive test of function
Albumin and bilirubin - cirrhosis
Clotting factors and glucose - end stage

173
Q

How is the gastric axis affected by hepatomegaly and micro hepatica?

A

Normal: gastric axis parallel to ribs
Hepatomegaly: gastric axis tilted caudally
Microhepatica: gastric axis tilted cranially

174
Q

What features of the liver can be assessed by ultrasonography?

A 
Liver size
Heterogenous parenchymal disease
Biliary obstruction
Biliary calculi
Masses
Vasculature - portosystemic shunts, arteriovenous fistulas
175
Q

Indications for liver biopsies?

A

Persistent increases in liver enzymes
Altered liver size
Monitoring progressive liver disease
To evaluate response to treatment

176
Q

Technique options for liver biopsy?

A

‘Blind’ percutaneous
Ultrasound guided percutaneous (‘Tru-cut’ technique)
Laparoscopy
Coeliotomy

177
Q

Contraindications for percutaneous liver biopsy?

A 
Lack of operator experience
Small liver, unless ultrasound available
Focal disease
Extrahepatic cholestasis
Bleeding disorder
Severe anaemia
178
Q

Pathology of juvenile hepatic fibrosis?

A 
Acquired
Progressive fibrosis
Minimal inflammatory reaction
Central vein fibrosis and occlusion most common
Young GSD, Rottweiler
179
Q

How to differentiate between a congenital portosystemic shunt and juvenile hepatic fibrosis with secondary acquired shunts?

A

Ascites with the acquired shunts following hepatic fibrosis, and mostly GSD, Rottweiler
Ascites rare in congenital portosystemic shunts

180
Q

What are the forms of canine chronic hepatitis?

A

Idiopathic chronic hepatitis
Lobular dissecting hepatitis
Drug-induced chronic hepatitis
Copper-associated hepatitis

181
Q

Negative prognostic indicators for shorter survival of dogs with chronic hepatitis?

A

Hypoalbuminaemia
Severity of necrosis and fibrosis in the biopsy
Bridging fibrosis

182
Q

What is hepatic portal hypoplasia?

A

Aka microvascular dysplasia
Microscopic intra-hepatic shunting
Often have no clinical signs or like PSS
Small terrier breeds Increased bile acids

183
Q

What is Feline cholangitis complex?

A

Suppurative or lymphocytic cholangitis (or mix)

Sclerosing cholangitis - end stage

184
Q

What does idiopathic hepatic lipidoses lead to in cats?

A

Biliary stasis
Liver failure
Anorexia
Death

185
Q

Clinical signs of hepatic neoplasia?

A

Similar to inflammatory liver disease

Hepatomegaly - can be irregular shape

186
Q

Primary hepatic neoplasia?

A

Hepatocytes - hepatocellular carcinoma, hepatoma
Biliary - cholangiocarcinoma
Connective tissue - fibroma/sarcoma, haemangioma/haemoangiosarcoma

187
Q

Treatments for liver disease?

A

Dietary modification
Ursodeoxycholic acid (UDCA)
Anti-oxidant drugs and glutathione donors
Treatment of complications
Antibiotics if neutrophils on biopsy or positive bacterial culture
Immunosuppressives if lymphocytes (immune mediated process) on biopsy - prednisolone +/- azathioprine
Anti-fibrotics if fibrosis on biopsy - prednisolone +/- diet/UDCA
Decoppering drugs if copper accumulation on biopsy - penicillamine, tridentine, Zn

188
Q

Diet management for hepatic encephalopathy?

A

Aim to minimise ammonia production
Protein restriction
High biological value - dairy, vegetable

189
Q

Diet management for chronic active inflammation of liver?

A

Aim to reduce inflammation and prevent copper accumulation
Alter mineral balance - low copper and high zinc
Fat soluble vitamins - A, D, E, K, C?
Taurine and L-carnitine for cats
Protein restriction rarely required - feed as much protein as will tolerate, add cottage cheese to a standard ‘hepatic diet’
Anti-oxidants

190
Q

Antibacterial therapy for hepatic encephalopathy and bacterial cholangiohepatitis?

A

Hepatic encephalopathy - use empirically based on clinical picture - ampicillin or metronidazole
Bacterial cholangiohepatitis - documented infection, need culture and sensitivity (bile and tissue)

191
Q

Glucocorticoid advantages and disadvantages for chronic active inflammation of the liver and hepatic fibrosis?

A 
Advs:
- improved well being
- appetite stimulation
- anti-inflammatory
- immunosuppression
- anti-fibrotic
Disadvs:
- steroid hepatopathy
- predisposes to infection
- fluid retention
- catabolic
192
Q

Breeds affected by copper associated hepatopathies?

A 
Bedlington terrier
WHWT
Skye Terrier
Dalmatian
Labrador
Doberman
193
Q

What decoppering agents are there for copper associated hepatopathies?

A 
Copper chelators:
- D-penicillamine
- 2,2,2-tetramine
Copper absorption blocker:
- oral zinc (high zinc in commercial diets or use zinc supplement 1h before feeding)
194
Q

Advantages and disadvantages of adjunctive therapies for liver disease?

A 
Advs:
- don't need biopsy results
- broad spectrum of activity
- wide safety margin
- combination therapy used
Disadvs:
- cost
- worse compliance if give many drugs?
195
Q

Adjunctive therapies for liver disease?

A

Ursodeoxycholic acid (UDCA)
- = hydrophilic bile salt
- alters bile composition (decreases hydrophobic bile acids)
- stimulates bile flow (contraindicated if complete biliary obstruction)
- modulates inflammatory/immune response
- limited evidence available in animals
S-Adenosyl methionine (SAMe)
- ‘glutathione donor’ for hepatic metabolism and detoxification
- no clear evidence as a treatment in animals
- might be useful for paracetamol toxicity in dogs
- might help to reduce effects of chemotherapy or steroids
Milk thistle
- active agents: silychristine, silydianin, silybin
- free radical scavneger
- inhibits inflammation
- inhibits lipid peroxidase
- inhibits collagen deposition
- increases glutathione
- advs: wide safety margin, no absolute contraindications, broad spectrum of activity
- disadvs: cost, no evidence of efficacy
Vitamin E

196
Q

Complications of liver disease? What to do?

A

Hepatic encephalopathy and coma
- identify and treat precipitating cause (dehydration, diuretics, alkalosis, hypokalaemia, GI bleeding)
- reduce ammonia concentrations (low protein diet, lactulose, antibiotics)
- lactulose retention enema if coma
Ascites and oedema
- low sodium diet
- diuretics (spironolactone first choice, occasionally add furosemide)
- paracentesis (drain minimal volume for patient comfort, could worsen bodyside protein status)
Haemorrhage and anaemia
- vitamin K injections
- fresh blood transfusions
- B vitamin injections
- H2 blockers if GI haemorrhage?

197
Q

Diagnose: A 7-year-old neutered female Yorkshire terrier. The owner presents their dog to you reporting watery diarrhoea and weight loss over 2 weeks. On physical examination, the dog is slightly underweight (BCS 4/9), and there is abdominal distension with a fluid thrill. Pulse rate is 120 beats per minute. No other abnormalities are evident.

A

Lymphangiectasia

198
Q

Diagnose: A 5 year-old neutered male cocker spaniel dog. The dog presents with a 4-week history of lethargy and occasional vomiting. On physical examination, the dog is underweight (BCS 3/9), and has icteric mucous membranes and sclera. Pulse rate is 140 beats per minute. No other abnormalities are evident.

A

Pancreatitis

199
Q

Diagnose: A 1 year-old entire female German shepherd dog. The dog presents with a 6-week history of diarrhoea and polyphagia. On physical examination, the dog is underweight (BCS 2/9) and has a poor coat condition, pulse rate 80 beats per minute. No other abnormalities are evident.

A

Exocrine pancreatic insufficiency (EPI)

200
Q

Diagnose: A 7 year old male German Shepherd Dog presents with a history of intermittent melaena and variable appetite over the last 2 weeks, with a gradual deterioration over the last 72 hours such that the dog is now very dull, not eating and has vomited several times. The dog was previously examined at the practice 4 weeks ago prior to receiving a repeat prescription of meloxicam for treatment of coxofemoral osteoarthritis and a clinical examination was unremarkable at this time. His rectal temperature is 38.4C, heart rate and pulse 120, congested and tacky oral mucous membranes, capillary refill time is 1 second and he is uncomfortable/resentful of abdominal palpation.

A

Septic peritonitis

Small animal (19 decks)

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