Gastroenterology Flashcards
Cause of vomiting
motion sickness, ingestion of emetogenic substances, GI obstruction, abdominal inflammation/irritation and extra-gastrointestinal tract disease that may stimulate medullary vomiting centre region, CNS, behaviour
definition of vomiting
active, forceful process of ejection of gastric/intestinal content with prodromal signs
signs of vomiting
vomiting
dehydration
abnormal behaviour
diagnosis for vomiting
History (acute onset of vomiting in unvaccinated puppy could be infectious),
signalment, CBC, biochemistry, pH would be less than 5 (showing gastric acid),
gastroduodenoscopy and biopsy (colonoileoscopy in cats),
faecal exam (parasites),
x-ray and ultrasonography,
cats (FeLV, FIV, hyperthyroidism)
treatment for vomiting
Fasting, fluids, antiemetic agent, antiemetic agents, anti-secretory agents, prokinetics
- if animal is stable with vomiting, then symptomatic treatment for 1st 1-2 days
cause of diarrhoea
Acute
- caused by diet, parasites or infectious diseases
Chronic
- small intestinal: maldigestion (EPI), nonprotein-losing malabsorptive and protein-losing enteropathy
pathogenesis of diarrhoea
Osmotic diarrhoea
- unusually large amounts of poorly absorbable osmotically active solutes in the intestinal lumen
- occurs with malabsorptive disorders where nutrients are maldigested or mal-absorbed, remain within the intestinal lumen and osmotically attract water. EPI is example
Secretory diarrhoea
- abnormal ion transport in intestinal epithelial cells.
Increased mucosal permeability
- causes loss of fluids, electrolytes, proteins and RBC into intestinal lumen
- erosive or ulcerative enteropathies, IBD or neoplastic disorders
Deranged motility
- abnormal ileal and colonic motility patterns may contribute to clinical symptomatology of IBD
- suppression of contractions and stimulation of giant migrating contractions
definition of diarrhoea
increase in frequency, fluidity or volume of faeces
signs of diarrhoea
weight loss, polyphagia, frequency of bowel movements, volume of faeces, blood in faeces, mucus in faeces, tenesmus, maybe vomiting
diagnosis of diarrhoea
signalment, history, FIV, FeLV, faecal panel, radiography, Ultrasound
CBC
- eosinophilia ? secondary to endoparasitism, eosinophilic enteritis, mast cell neoplasia
- anaemia ? from enteric blood loss
- neutrophilia ? stress, inflammation or infection
- lymphopenia is relatively common finding in dogs with intestinal lymphangiectasia
Serum chemistry
- BUN can be increased from dehydration or gastrointestinal bleeding
- panhypoproteinemia, hypocholesterolaemia – protein losing enteropathy
Specialised gastrointestinal function tests
- serum trypsin-like immunoreactivity – exocrine pancreatic insufficiency
- serum cobalamin and folate: measurement of serum Vit B12 and folate concentrations – absorptive function of ileum and jejunum, decreased in IBD or lymphoma
Chronic
- Parasite test (giardia, tritrichomonas – ELISA, snap test but IFA is gold standard)
- failure to lose weight/body condition despite chronic diarrhoea indicates large bowel disease
- weight loss usually indicates small bowel disease
treatment for diarrhoea
: dietary therapy (highly digestible, moderately fat-restricted food), antimicrobials (metronidazole 10-15mg/kg q12h), oral protectants (activated charcoal), fluids, motility modifier (iopermaide 0.1-0.2mg/kg q8-12dog, q12 cat), probiotics,
- chronic diarrhoea: oral corticosteroids (for IBD)
differentials for diarrhoea
Dietary, inflammatory, infectious, pancreatitis, obstruction, neoplasia, drugs + toxins
when is diarrhoea acute/chronic
acute if lasts for less than 14 days, chronic if longer than 14 days
cause of dysphagia
results from oral pain, masses, foreign objects, trauma, neuromuscular dysfunction or combination
what is dysphagia
difficulty swallowing
signs of dysphagia
difficulty of prehension of water and food, drooling, nasal discharge
- repeated, often unproductive attempts to swallow with extension oof the head and neck during swallowing, often accompanied by gagging, retching, odynophagia and ptyalism
diagnosis of dysphagia
complete examination of pharynx, X-rays (positive contrast)
how do you differentiate between dysphagia and regurgitation
localisation of disease
- oesophageal dysphagic and salivation must be differentiated from oropharyngeal dysphagia and salivary gland diseases (sialadenitis or Sialoadenosis)
what is regurgitation
Expulsion of material from the mouth, pharynx or oesophagus whereas vomiting is expulsion from the stomach and/or intestines
cause of regurgitation
obstruction and muscular weakness
pathogenesis of regurgitation
passive process that occurs without prodromal signs
signs of regurgitation
expelling material from mouth, pharynx or oesophagus
diagnosis of regurgitation
watch the animal eating, fluoroscopic evaluation of swallowing barium to differentiate pharyngeal from cricopharyngeal dysfunction
- plain radiograph and later barium contrast
treatment of regurgitation
depending on cause: foreign body (surgery), weakness (supportive therapy)
haematemesis
- vomiting of blood (fresh/digested)
- damage in the oesophagus, stomach or duodenum
- ingestion of blood from mouth, nose, respiratory tract
- check haematocrit and plasma total protein concentration to see if blood transfusion needed
melena
- “black stool” digested blood
- food
- bismuth compounds
- upper GI bleeding/respiratory tract bleeding
- cause: hookworm, GUE, ingested blood
haematochezia
- fresh blood in stool
- disease of large intestine: colitis, proctitis, large intestine tumour, anal sac disease
- if has haematochezia and diarrhoea – problem approached in same manner as large bowel diarrhoea
- acute haematochezia may result from trauma (passing a foreign body)
- digital rectal exam necessary – express each anal sac repeatedly and examine the contents, biopsy/colonoscopy recommended if unhelpful digital rectal exam
- barium enema isn’t recommended
tenesmus
- straining to defecate vocalisation, painful defecation – dyschezia
- cause: perineal inflammation/pain, rectal inflammation/pain, colonic/rectal obstruction in cat (urethral obstruction, rectal obstruction or constipation)
predisposition for faecal incontinence
older more than younger
cause of faecal incontinence
injuries to spine/tail, anal gland disease and/or intestinal disorder
pathogenesis of faecal incontinence
inability to retain faeces in the colon and rectum leading to uncontrolled leakage of faecal material at times other than during conscious defecation
signs of faecal incontinence
scooting on floor, defecating in atypical areas, bloated abdomen, tenderness or aversion to being touched near tail, loss of tone and voluntary movement of the tail, weight
weight loss, vomiting, spasms of urogenital diaphragm
diagnosis of faecal incontinence
history, CBC, biochemistry, urinary and faecal analysis (infection or parasite)
treatment of faecal incontinence
- changes in diet (low residue diets), warm water enemas, maybe surgical reconstruction
- anti-inflammatory agents, opiates
- motility-modifying drugs shouldn’t be used if infectious or toxic cause is suspected and opiates never used with patients with respiratory disease
cause of stomatitis
physical insults, uraemia, inadequate host responses to pathogen, renal failure, trauma, immune-mediated disease, upper respiratory, tooth root abscess, etc
pathogenesis of stomatitis
Inflammation of the oral tissue that usually begins in the periodontium or the oropharyngeal area
signs of stomatitis
decreased appetite, ptyalism, oral haemorrhage, difficulty prehending or chewing food, blood tinged saliva, oral pain, nasal discharge, facial swelling, ulceration of the lips, oral inflammation
- thick, ropey saliva, severe halitosis, and/or anorexia caused by pain
diagnosis of stomatitis
- hemogram and serum chemistry
- FeLV/FIV testing – all cats with stomatitis
- oral and dental radiographs
- tissue biopsy and histopathology – rule out neoplasm
treatment of stomatitis
symptomatic and specific
- thorough teeth cleaning and aggressive antibacterial therapy, maybe extracting teeth
- bovine lactoferrin = suggested to ameliorate otherwise resistant lesions in cats
cause of feline lymphocytic plasmacytic gingivitis
idiopathic, maybe: feline calicivirus, bortonella henselae, immunodeficiency from FeLV or FIV
signs of feline lymphocytic plasmacytic gingivitis
red gingiva around the teeth and/or posterior pillars of the pharynx. Dental neck lesion often accompanies the gingivitis
diagnosis of feline lymphocytic plasmacytic gingivitis
biopsy of affected gingiva
- histologic evaluation reveals lymphocytic plasmacytic infiltration
- serum globulins can be increased
treatment of Feline lymphocytic plasmacytic gingivitis/
no reliable therapy, proper cleaning and polishing of teeth, ATB, high-dose corticosteroid therapy
prognosis of Feline lymphocytic plasmacytic gingivitis
guarded
sialodenitis definition
inflammation of the salivary gland
predisposition of sialodenitis
rarely clinical problem in dogs and cats
cause of sialodenitis
unknown, has occurred as idiopathic event, secondary to chronic vomiting/regurgitation, trauma from penetrating wounds/systemic infection affecting salivary glands, rabies, distemper
signs of sialodenitis
painless enlargement of one or more salivary glands. Animals may be dysphagic, fever, depression, reluctance to open mouth and eat
diagnosis of sialodenitis
Biopsy, cytology/ histopathology confirm that the mass is salivary tissue and determines whether inflammation or necrosis is present
treatment of sialodenitis
if substantial inflammation and pain, surgical removal, if vomiting (treat cause)
- developed abscess should be drained through overlying skin – systemic antibiotics
prognosis of sialodenitis
excellent
sialdenosis
sialdenosis is a non-inflammatory, non-neoplastic, usually bilateral enlargement of the mandibular salivary gland, associated with regional swelling and exophthalmos but no apparent pain
predisposition of nasopharyngeal stenosis
uncommon in cats, quite rare in dog
cause of nasopharyngeal stenosis
congenital malformation, response to inflammation from chronic upper respiratory disease or regurgitation into the nasopharynx, foreign body/ any irritant contacting affected area
pathogenesis of nasopharyngeal stenosis
pathologic narrowing of the nasopharynx due to the formation of a web of scar tissue which leads to upper airway obstruction
signs of nasopharyngeal stenosis
dyspnoea, gagging, sneezing, stridor, retching, vomiting, regurgitation, anorexia, oculonasal discharge
diagnosis of nasopharyngeal stenosis
CT or MRI, nasopharyngeal endoscopy (passing a catheter through the ventral nasal meatus)
treatment of nasopharyngeal stenosis
surgical options (nasopharyngeal stenosis include excision of the scar tissue, balloon dilation or stent placement)
predisposition of laryngeal paralysis
common in dogs, rare in cats
- middle – older, large and giant breeds (Lab, Irish setters, Great Danes)
cause of laryngeal paralysis
tumours or lesions in neck or chest, trauma to the throat, hormonal disorders (hypothyroidism and Cushing’s)
pathogenesis of laryngeal paralysis
Failure of arytenoid cartilages to abduct during inspiration. Congenital, acquired, unilateral and bilateral forms
vocal fold is narrowed
signs of laryngeal paralysis
dynamic upper airway obstruction
dry cough, voice changes, noisy breathing, stridor, collapse, regurgitation and vomiting may occur
diagnosis of laryngeal paralysis
based on clinical signs, laryngoscopy (under light LA for confirmation), radiographs are not diagnostic
- direct or endoscopic laryngoscopy in shallow anaesthesia
- disease of larynx with same symptoms:
o Laryngeal neoplasia, obstructive laryngitis, foreign body, trauma, laryngeal collapse, extraluminal masses around the larynx and acute laryngitis
o Palpation of the area – x-ray
o Thyroid hormones
o Acetylcholine receptor antibody test
o Chest x-ray – aspiration pneumonia?
treatment of laryngeal paralysis
relieving signs of airway obstruction
- corticosteroids effected temporarily in mild cases
- severe obstruction may require tracheotomy
complications of laryneal paralysis
aspiration pneumonia 8-25% of dogs post op
differentials for laryngeal paralysis
myositis, recurrent laryngeal/vagal nerve tumour, inflammation, myasthenia gravis, severe hypothyroidism, trauma
definition of laryngitis
inflammation of the mucosa or cartilages of the larynx
predisposition of laryngitis
primary occurs more in cats than dogs and secondary more common than primary in both
cause of layrngitis
some infections, aspiration of food, inhalation of irritating vapours, barking, trauma. Acute laryngitis can develop into chronic laryngitis, trauma from intubation, infections
pathogenesis of laryngitis
inflammation/irritation of the laryngeal mucosa often characterised by edema and hypervascularisation
signs of laryngitis
dry short cough, vocal changes, stridor, halitosis, animal may stand with its head lowered and mouth open, swallowing is difficult and painful, bad breath, bluish gums
diagnosis of laryngitis
based on clinical signs and laryngoscopy, auscultation
treatment of laryngitis
steroids or NSAIDs, oxygen therapy, intubation/ventilation if needed, systemic antibiotics
prognosis of laryngitis
earlier the treatment, the better the outcome, if the larynx or any surrounding cartilage areas in the airway include chronic damage, the prognosis is worse
predisposition of laryngeal neoplasia
rare in dogs and cats
cause of laryngeal neoplasia
genetics, infection, cell malformation, age, environmental pollutants, chronic inflammation
pathogenesis of laryngeal neoplasia
- found on wall of the larynx and can cause respiratory obstruction
- laryngeal oncocytomas occur most often with young dogs
- chondrosarcomas of the larynx are mostly of malignant sort and develop in CT of the larynx
- SCC of the larynx can form in the upper, middle or lower area
signs of laryngeal neoplasia
weakness, regurgitation of undigested food/blood, vomiting after eating, dysphagia, dyspnoea, change in tone, respiratory distress, cyanosis, coughing, lethargy, depression, weight loss, halitosis
diagnosis of laryngeal neoplasia
- CBC, biochemistry and urinalysis
- radiographs of neck and chest, CT
- FNA on lymph notes
- endoscopy
treatment of laryngeal neoplasia
surgery, chemo
what are the most common neoplasia in dogs and cats
- Most common in dogs: rhabdomyoma, SCC and oncocytoma
- Most common in cats: lymphoma, SCC and adenocarcinoma
oesphagitis definition
inflammation of the MM and/or deeper layers of the oesophagus
cause of oesophagitis
GER, foreign body, chemical damage, structural abnormalities, chronic vomiting, invasion by larvae, NSAIDs
signs of oesophagitis
regurgitation, increased salivation, painful swallowing, inappetence
diagnosis of oesophagitis
haematology, biochemistry, X-ray + contrast, endoscopy
treatment for oesophagitis
- mild form: diet
- moderate to severe: sucralfate, metoclopramide, antisecretory drugs, ATB
- hospitalisation of dogs with aspiration pneumonia and cachexia
- complications – strictures of the oesophagus
GER predisposition
dogs that have abdominal surgery
cause of GER
incompetence of cardiac sphinter, GA
pathogenesis of GER
reflux of gastric contents into oesophagus
signs of GER
mucous lesions – prolonged contact with gastric acid, decreased appetite, difficulty swallowing, licking the lips, change in bark, chronic cough, appearance of generalised discomfort, pacing/ restlessness at night
diagnosis of GER
Endoscopy, caudal sphincter pressure measurement and 24-hour intraluminal pH determination
- physical exam: localise pain and feel for abdominal mass, obstructions etc
- CBC, biochemistry and urinalysis
- Xray and ultrasound
- diagnosed on endoscopy – shows oesophageal inflammation
treatment of GER
fat restrictive. mucosal protectors (sucralfate), PPI (omeprazole/esomeprazole), H2 blockers (ranitidine/ famotidine) and prokinetics (metoclopramide)
predisposition of oesophageal FB
: most common in small dogs, less common in cats
cause of oesophageal FB
food boluses, toys, hairballs, ETC
pathogenesis of oesophageal FB
most common localisation: in front of the aperture thoracis cranialis, the thoracic oesophagus above the base of the heart or cranially from the lower oesophageal sphincter
symptoms of oesophageal FB
increased salivation, difficulty swallowing, straining, regurgitation, lethargy, loss of appetite.
diagnosis of oesophageal FB
x-ray immediately before endoscopy
treatment of oesophageal FB
- endoscopic removal of a foreign body
- “pushing” foreign body into the stomach
- surgery
- post FB removal: PPI and prokinetic drugs
prognosis of oesophageal FB
without perforation usually good, perforation = guarded
oesophageal stricture definition
severe, deep inflammation of the oesophagus
cause of oesophageal stricture
any cause, especially foreign bodies or severe gastroesophageal reflux
pathogenesis of oesophageal strictures
circular narrowing occurs as secondary pathological change due to inflammation of the deeper layers of the oesophageal mucosa
signs of oesophageal strictures
regurgitation, hypersalivation, dysphagia, choking, gagging and weight loss, hyporexic
diagnosis of oesophageal strictures
intraluminal and extraluminal masses. Contrast x-ray: precision in revealing the exact position, number and extent of change on the oesophagus. Endoscopy
treatment of oesophageal strictures
Surgery, balloon catheter dilation, bougienage, stent placement
prognosis of oesophageal strictures
very chronic strictures have more guarded prognosis
mega oesophagus predisposition
GSD, golden retriever’s, and irish setters
cause of mega oesophagus
- Congenital oesophageal weakness is unknown
- acquired in dogs: neuropathy, myopathy or myasthenia gravis
- cats: may be a cause of acquired oesophageal weakness
- primary: idiopathic and can be congenital or acquired
- congenital defects: vascular ring anomalies, oesophageal diverticular, congenital myasthenia gravis, idiopathic congenital megaoesophagus
pathogenesis of megaoesophagus
severe diffuse oesophageal hypomotility and flaccid dilation of the oesophagus
signs of megaesophagus
regurgitation, aspiration pneumonia as a complication
diagnosis of megaoesophagus
survey radiographs or barium contrast oesophagram
treatment of megaoesophaugs
- congenital: cannot be cured or resolved by medically therapy
- acquired: treat underlying disease
- surgery for vascular ring anomalies
- frequent small meals and feeding from an elevated position
prognosis of mega oesophagus
guarded
hiatal hernia def
Diaphragmatic abnormality that allows part of the stomach to prolapse into thoracic cavity
predisposition of hiatal hernia
brachycephalic breeds
causes of hiatal hernia
can be congenital or acquired in origin
pathogenesis of hiatal hernia
protrusion of the oesophagus, lower oesophageal sphincter (LES), and/or part of stomach through oesophageal hiatus into the thoracic cavity
signs of hiatal hernia
regurgitation primary symptoms, some are asymptomatic
diagnosis of hiatal hernia
Plain radiographs/positive contrast
treatment of hiatal hernia
surgery, if signs appear later in life, aggressive medical management of GER (cisapride, omeprazole) sometimes sufficient, if not surgery
prognosis of hiatal hernia
often food after surgical repair (congenital cases) or aggressive medical management (acquired)
predisposition of gastroesophageal intussusception
more common in dogs, especially young, very rare in cats
- rare condition of young dogs (< 3 months)
cause of gastroesophageal intussusception
many have pre-existing oesophageal disease (idiopathic megaoesophagus)
pathogenesis of gastroesophageal intussusception
rare hiatal disorder resulting from invagination of the stomach into the lumen of the oesophagus; other abdominal organs may or may not invaginate as well
signs of Gastroesophageal intussusception
regurgitation, vomiting, dyspnoea and collapse
diagnosis of Gastroesophageal intussusception
histoy
physical exam
X-ray of neck and chest
treatment Gastroesophageal intussusception
endoscopic or surgical reduction
prognosis of Gastroesophageal intussusception
guarded, successuful oucome if prompt diagnosis and intervention
predisposition of acute haemorrhagic diarrhoeal syndrome
smaller breeds (yorkies, schnauzers, mini pinschers, Maltese)
cause of acute harmorrhagic diarrhoeal syndrome
unknown, maybe C. perfringens
signs of acute haemorrhagic diarrhoeal syndrome
more severe than acute g. Profuse haematemesis and/or haematochezia. Rapidly critically ill: severe dehydration, DIC and renal injury
diagnosis of acute haemorrhagic diarrhoeal syndrome
History
pcv (most have increased)
thrombocytopenia
treatment of acute haemorrhagic diarroeal syndrome
fluid therapy: aggressive fluid therapy IV (to prevent shock, DIC, renal failure) crystalloids
- same as in acute gastritis, ATB, synthetic colloids, plasma
- antimicrobial therapy has not been found beneficial
prognosis of acute haemorrhagic diarrhoea sydnrome
good for most animals that are presented on time and receive aggressive fluid treatment on time
predisposition for acute gastritis
dogs more likely than cats
cause for acute gastritis
dietary or intolerance, foreign bodies, drugs and toxins. Systemic disease, parasites, bacteria and virus, NSAIDs
pathogenesis of acute gastrtis
syndrome marked by vomiting of sudden onset presumed to be due to a gastric mucosal insult or inflammation
signs of acute gastritis
acute onset of vomiting (food and bile), uninterested in food, nauseous, fever uncommon, abdominal pain uncommon
diagnosis of acute gastritis
history, physical exam, signalment (young animal, often foreign body), response to symptomatic treatment, abdominal imaging, lab testing, US
treatment of acute gastritis
- fluid therapy: orally, SC (rare), or IV, diet restriction (24h), 1st give water if no vomiting, small amounts of food, bland diet
- drugs only if necessary
- adsorbents (activates charcoal, kaolin-pectin)
- central-acting antiemetics (maropitant)
- ACID reducing drugs (H2 blockers, PPI)
- ATB – rarely indicated
- foreign bodies: endoscopy, can give emetic (H2O2 per os in dogs, but need to know what foreign body is, if has sharp edges don’t do it)
prognosis of actue gastritis
for uncomplicated acute gastritis: usually complete recover
- excellent as long as fluid and electrolyte balance is maintained
predisposition of GUE
more common in dogs
cause of GUE
metabolic/ endocrine (hypoadrenocorticism, uraemia), inflammatory (uraemic), neoplastic (leiomyoma), drug induced (NSAIDs), hypotension (shock, sepsis), idiopathic (stress, spinal surgery, exercise- induced)
pathogenesis of GUE
associated with number of primary gastric and non-gastric disorders
signs of GUE
hyporexia, vomiting, haematemesis, melena, pale MM, weakness, abdo pain, hypersalivation, ulcer performation: signs of septic peritonitis
diagnosis of GUE
history (finding evidence of GI blood loss), physical exam
- CBC: anaemia, thrombocytosis, decreased iron saturation, eosinophilia, neutrophilic leucocytosis)
- biochemistry and urinalysis (acidic urine)
- serum gastrin and gastric pH
- coagulations
- abdominal imaging, ultrasound (detects gastric thickening), endoscopy (+biopsy)
treatment of GUE
- patient status, underlying cause
- fluid therapy: IV fluids – rate: hydration/perfusion status
- treatment of dehydration: over 4-24hr
- fluid deficit (% dehydration x body weight kg)
- daily physiologic requirements (30xBW/kg)
same as you would use for ulcer (PPI etc)
prognosis of GUE
favourable if the underlying cause can be controlled and if therapy prevents perforation of the ulcer
predisposition of GDV
large deep chested dogs, easting once a day, male
cause of GDV
- hepatic portal vein/caudal cava obstruction
- impair venous return to the heart
- hypovolemic shock
- devitalisation of the gastric wall
- splenic torsion or avulsion
- congestion of abdominal viscera
- endotoxemia
pathogeensis of GDV
caused by poor gastric emptying of solids produce some degree of chronic gastric distention subsequent stretching of hepato-gastric and duodeno-gastric ligaments
signs of GDV
non-productive retching, salivation, abdominal distension, abdominal pain “restlessness”, weakness, collapse
abdominal distension and tympany, tachycardia, mucosal pallor, hypothermia, depression, coma
diagnosis of GDV
history, physical examination, abdominal imaging after decompression and shock stabilisation
- lab testing: increased PCV, acido-base and electrolyte abnormalities, increase plasma lactate
- ECG
treatment of GDV
- fluid therapy: aggressive, IV fluids, aggressive monitor, potassium
- decompression: trocarisation: 12-16g catheter, orogastric tube, warm water lavage
- drugs: broad spectrum ATB-IV, arrhythmia
- surgery: as soon as animal constitutes an acceptable anaesthetic risk
- post-surgery: monitor the patient
predisposition for chronic gastritis
common in dogs: 35% of dogs with chronic vomiting, 26-48% asymptomatic dogs
- more common in cats than dogs
cause of chronic gastritis
immune, H.pylori, ollulanus tricuspis (cause granulomatous gastritis in cats)
types of chronic gastritis
- lymphocytic plasmacytic (immune and/or inflammatory reaction to variety of antigens)
- eosinophilic (allergic reaction probably to food antigens)
- atrophic (chronic gastric inflammatory disease and/or immune mechanism)
signs of chronic gastritis
hyporeixa and vomiting
diagnosis of chronic gastritis
histologic exam of gastric biopsies, US
treatment for chronic gastritis
- lymphocytic plasmacytic = sometimes responds to dietary therapy, if inadequate = prednisolone
- canine eosinophilic gastritis = responds well to strict elimination diet if not prednisolone
- atrophic = difficult to treat, diets low in fat and fibre might help, also might respond to anti-inflammatory, antacid and/or prokinetic therapy
prognosis of chronic gastritis
often good
cause of acute enteritis
parasites, virus, fungus, IBD, ingestion of toxins, neoplasia, boarding at a kennel, scavenger
def of acute enteritis
inflammation of SI
signs of actue enteritis
Diarrhoea of unknown cause (common, especially in puppies and kittens), vomiting, dehydration, fever, anorexia, depression, crying and/or abdominal pain
diagnosis of actue enteritis
- history, physical and faecal examinations (faecal flotation and direct faecal exam)
- if animal febrile, has haemorrhagic stool and part of outbreak enteritis = CBC (to identify neutropenia), faecal ELISA (parvo), serological analysis (FeLV, FIV), blood glucose (hypoglycaemia), serum electrolyte (hypokalaemia)
- abdominal imaging
treatment of acute enteritis
- symptomatic therapy
- opiates most effective antidiarrheals
- bismuth subsalicylate – useful for diarrhoea in dogs with mild to moderate enteritis
prognosis of actue enteritis
depends on animal’s condition
- very young/emaciated animals and those with SIRS or intestinal parasites are more guarded
- if intussusception occurs secondary to acute enteritis, the prognosis is guarded
predisposition of colitis
Middle-aged dogs, no sex predilection. Cats: middle aged and more commonly purebred
- granulomatous colitis is rare, breed- specific IBV of young boxers and French bull dogs
- eosinophilic colitis tends to be in animals younger
cause of colitiis
Food intolerance, ingestion of toxins/foreign bodies, bacterial infections, uncontrolled drug therapy, ATB, IBD, neoplasia, changes in bowel position, IBS
pathogenesis of colitis
often presents as chronic, large bowel diarrhoea of unknown origin
signs of colitis
diarrhoea (mucus, haematochezia, tenesmus and occasionally pain), increased urgency and frequency of defecation, weight loss and vomiting occur but are uncommon
diagnosis of colitis
history + clinical examination, faeces, x-ray (contrast), CBC and biochemistry, endoscopy and rectal examination
- excluding other infectious disease
treatment of colitis
- rehydration
- diet – easily digestible, fibre-rich food (colitis), probiotics
- symptomatic – antiemetics, electrolyte correction, analgesia
- ATB: metronidazole (6-10mg/kg BID), amoxicillin (10-20mg/kg BID/TID), tylosine (10-20mg/kg SID/BID/ 3-6 months), enrolxacin (5mg/kg SID)
- sulfasalazine – colitis
prognosis of colitis
short term is good, long term for complete resolution without relapse appears poor
- idiopathic lymphocytic plasmacytic colitis respond to dietary and medical changes
- stricture formation and extensive fibrosis = more guarded
- eosinophilic colitis in dogs – good, in cats more guarded
- hypereosinohpilic syndrome is progressive, fatal and has no effective treatment in animals
- histiocytic colitis of boxers - grave
predisposition of ileus
- most common in young (about 70% less than 1 yr old)
- neoplasia more in middle-aged to old
- intestinal torsion (volvulis) – large breeds
cause of ileus
foreign bodies, bowel invagination, mesenteric torsion and neoplasia
pathogenesis of ileus
temporary arrest of intestinal peristalsis, temporary and reversible obstruction in the intestines
- intraluminal (foreign body), mural (neoplasia, abscess), extramural (adhesion, hernia, neoplasia)
- proximal to the site of the obstruction is the extension of the intestinal segment and the accumulation of gas and liquid content
- paralytic ileus: consequence of primary disease, electrolyte imbalance or anaesthesia
signs of ileus
- depends on location, severity and cause of the obstruction
- acute vomiting (or chronic cases = faecal vomiting)
- sometimes no defecation, sometimes watery to bloody diarrhoea
- dehydration, hypovolemia, shock, bowel necrosis, sepsis and death
diagnosis of ileus
- history and palpation of the abdomen, x-ray and ultrasound
treatment of ileus
surgery (removing the cause of obstruction/bowel resection), rehydration, ATB, analgesic, motility promoters (metoclopramide EXCLUSIVELY WITH PARALYTICAL ILEUS)
predisopisiotn of constipation/obstipation
older, overweight cats with chronic kidney disease or previous episodes of constipation are at increased risk of constipation
constipation + obstipation definitiation
Constipation: infrequent or difficult evacuation of stool from the rectum or colon
Obstipation: intractable constipation refractory to control or cure; implies a permanent loss of colonic function
cause of constiaption
dehydration, neuromuscular control (spinal damage, electrolytes, opioids), consequence of other diseases (colitis, perineal hernia, disease of spine, prostate hypertrophy)
signs of constipation
absent or painful defecation for days – week, anorexia, vomiting and weight loss, watery or mucus material from the rectum
diagnosis of constipation
- colon can be palpated distended with faeces
- digital rectal examination – can detect strictures, foreign bodies, pelvic trauma etc
- serum biochemistry panel – serum T4 level
- radiography or endoscopy
- neurological examination
treatment of constipation
- rehydration
- removal of impacted faeces is required to reduce toxic and inflammatory stress on the bowel wall
- enemas are used to remove impacted faeces
- laxatives and prokinetic agents, lactulose, paraffin oil, bisacodyl
predisposition of mega colon
common in cats and less in dogs
cause of mega colon
idiopathic dilated megacolon and hypertrophic megacolon
Idiopathic dilated megacolon
- functional disturbance of the colonic smooth muscle followed by a more permanent loss of colonic function
- in cats, behavioural or environmental factors (stress and poor litter box hygiene)
Hypertrophic colon
- develops as a sequela of an obstructive lesion
pathogenesis of mega colon
persistent colonic dilatation and hypomotility , colon becomes chronically nelarged
signs of mega colon
chronic constipation or obstipation, weight loss, vomiting, anorexia, tenesmus, lethargy, dehydration
diagnosis of mega colon
abdominal x-ray, in cases of megacolon, colon will be 1.5x length of L7
treatment of mega colon
fluid therapy, clear out colon, adequate exercise, high fibre diet, nutritional supplements, subtotal colectomy, laxative (lactulose) and prokinetic agents (cisapride)
prognosis of mega colon
50% recurrence rate. Prognosis with surgery in cats excellent
definitions of tenesmus
frequent attempts or straining to pass faeces. Occurs with urinary problems and shouldn’t be confused with constipation
pathogenesis of tenesmus
if faecal material isn’t passed, it becomes extremely desiccated, making it more difficult to be passed and more likely to obstruct the colon and rectum
signs of tenesmus
constipation can lead to absorption of toxic intestinal products
predisposition of IBD
GSD, German boxier, yorkies, cocker spaniel, purebred cats, dogs 2-7 years
cause of IBD
adverse reactions to food, idiopathic IBD and ATB responsive diarrhoea, environmental factors, food, immune system, genetics
pathogenesis of IBD
in dogs: small and large intestine, cats: small intestine (triaditis)
signs of IBD
chronic vomiting and diarrhoea
Clinical diagnosis of IBD is considered only if affected animals have:
- Persistent - >3 weeks in duration, gastrointestinal signs (anorexia, vomiting, weight loss, diarrhoea, haematochezia, mucous faeces)
- Failure to respond to symptomatic therapies (parasiticides, ATB, gastrointestinal protectants alone)
- failure to document other causes of gastroenterocolitis by thorough diagnostic evaluation
- histologic diagnosis of benign intestinal inflammation
diagnosis of IBD
- thickened bowel loops may be detected during abdominal palpation if the small bowel is concurrently involved
- digital examination of the anorectum may evoke pain or reveal irregular mucosa, and blood pigments and mucous may be evident on the exam glove
- CBC, biochemistry, urinalysis are often normal in mild cases of large bowel IBD
- elimination of known digestive symptoms: history, exam, bloods, faecal analysis, cobalamin
- x-ray, US, endoscopic examination
classification of IBD
- lymphocytic plasmacytic enteritis
- chronic lymphocytic-plasmacytic colitis
- immunoproliferative enteropathy in basenji
- diarrhoea syndrome in Norwegian elkhound (lunde hund)
- eosinophilic form of IBD
- histiocytic ulcerative colitis
- granulomatous enterocolitis
treatment of IBD
- dietary therapy: dietary modification
- glucocorticoids:
o prednisolone In dogs after failed dietary management,
o sulfasalazine/metronidazole: adjunctive therapy to dietary modification in feline
o dose of glucocorticoids may be reduced by 25% at 1-2 weeks intervals - azathioprine:
o purine analogue that inhibits lymphocyte activation and proliferation
o used as adjunctive therapy with glucocorticoids
o cats need to be monitored for side effects, including myelosuppression, hepatic diseases and APN - cyclosporine: in some cases of refractory IBD
- chlorambucil: in some difficult or refractory cases of feline IBD
- sulpasalazine:
o highly effective prostaglandin synthestase inhibitor – dog - ATB: metronidazole: mild-moderate IBD in both dogs and cats. Side effects: anorexia, hypersalivation, vomiting
- probiotics, anti-diarrhoeal agents, restoration of normal motility, exercise, behavioural modification
- additional therapy: physical therapy
prognosis of IBD
short term, good to excellent. Prognosis for cure is poor and relapses should be anticipated
IBD in cats
triaditis” cholangitis, pancreatitis and IBD in cats
liver, pancreas and small intestines
differentials of IBD
- allergy or intolerance to certain ingredients in foods
- gastrointestinal parasites
- intestinal dysbacteriosis
- hyperthyroidism in cats
- infectious peritonitis in cats FeLV, FIV
- fungi
- neoplastic diseases: lymphoma, adenocarcinoma
- EPI
cause of liver failure
sudden injury, poisoning and infection, endocrine imbalance
pathogeneis sof liver failure
sudden loss of liver function, often associated with neurologic signs and clotting abnormalities
signs of liver failure
ascites, digestive ulcers, lack of blood coagulation, HE
vomiting, excessive thirst, frequent urination, bloody diarrhoea, jaundice, ulcers, aggression, poor coordination, blindness, seizure
diagnosis of liver failure
- lab work: blood and urinalysis
- X-rays and ultrasound: hepatomegaly and diagnosis of cancer, cysts or vascular abnormalities
- medical history
treatment of liver failure
treat underlying cause, fluids, diet changes, antibiotics
- diuretics, Vitamin K
prognosis of liver failure
dependent on diagnosis, some conditions are good
what is heaptic fibrosis
When scar tissue forms and continuously replaces the normal tissue. Not associated with an underlying condition. Characterised by decrease in the size of the liver and particular condition can show changes in blood vessels between the intestines and liver
predisposition of hepatic fibrosis
young dogs, under 2 years
cause of hepatic fibrosis
activation of myofibroblasts can cause hepatic fibrosis – causes inflammation, oxidative stress
signs of hepatic firbosis
ascites, abdominal distension, weight loss, diarrhoea, jaundice, PUPD
diagnosis of hepatic firbosis
- physical exam: urinalysis, stool sample
- blood: bilirubin and cholesterol should be abnormal and liver enzymes, anaemia, and WBC high
- radiographs
- abdominocentesis
treatment of hepatic firbosis
no proven treatments, address the underlying cause, when cause is unknown: anti-inflammatory or immunosuppressive agents, low protein diet
- colchicine: inhibits microtubule polymerisation: inhibits inflammation and fibrosis: dogs: few case reports + significant GI side effects
prognosis of hepatic fibrosis
cannot be cured, so dependent on compliance of owner
what is HE
Neurological dysfunction in patients with liver disease
cause of HE
Pss
cirrhosis
hepatic lipidosis
pathogeensis of HE
- ammonia crosses the BBB
- brain is very sensitive to toxic effects of ammonia, but doesn’t possess urea cycle, so NH3 is detoxified by conversion to glutamine by astrocytes
- excessive NH3 and glutamine build up results in osmotic stress of astrocytes with cell swelling and cerebral oedema
signs of HE
- subtle, non-specific signs: anorexia, depression, weight loss, lethargy, nausea, fever, hypersalivation (especially in cats)
- CNS signs: non-localising, trembling, ataxia, hysteria, dementia, circling, head pressing
diagnsosi of HE
based on symptoms (history and physical examination)
- blood (maybe anaemic)
- biochemistry: elevated liver values, high bilirubin, high kidney, low albumin, low glucose and electrolyte abnormalities
- urinalysis – abnormally dilute urine
- bile acid test if liver disease
- X-ray: to see for enlarged: liver, spleen, tumours
- US, CT or MRI
treatment of HE
supportive therapy and non-meat protein-based diets and lactulose + metronidazole
- mannitol (reduce swelling on brain), L-ornithine L-aspartate (LOLA) to decrease ammonia levels
- seizures: anticonvulsant (diazepam, levetiracetam or phenobarbital)
- enema may be used to reduce colon bacteria
cause of ascites
organ failure or low protein levels (nephrotic syndrome), CHF, right heart failure, chronic liver failure, portal hypertension, kidney failure, malnutrition, hypoalbuminaemia, lymphoma, peritonitis
pathogenesis of ascites
fluid and blood can leak back into abdominal cavity from diseases organs, from parasitic migration, from leaks in the tricuspid valve in the heart, or from blocked blood vessels due to high blood pressure so It then accumulates
signs of ascites
distension of abdomen, lack of appetite, difficulty breathing, abdominal discomfort + pain, lethargy, coughing
diagnosis of ascites
- fluid thrill test – palpating the abdomen which may reveal the presence of fluid wave
- CT and ultrasound
- abdominocentesis
- faecal exam, urinalysis, X-ray, ECG, echo, biopsies
treatment of ascites
- spironolactone 2mg/kg PO q24 (can be increased to 4mg/kg PO q 24)
- furosemide – 1-2mg/kg PO q12
- mild restriction of sodium
- abdominocentesis should be avoided
prognosis of ascites
with concurrent treatment, can be reduced and managed but it can return if cause not resolved
predisposition of acute hepatitis
less common than chronic hepatitis
cause of actue hepatisis
infectious or toxic (leptospirosis, E.canis, clostridium, drugs, idiopathic), aflatoxin
signs of acute hepatitis
acute onset of: anorexia, vomiting, PUPD, dehydration, HE with depression, jaundice, fever, cranial abdominal pain, ascites and splenomegaly
diagnosis of actue hepatitis
history, clinical signs and findings
- liver histopathology confirms but often not obtained until recovery or post-mortem
- marked increased in ALT and AST
- jaundice and increased in markers of cholestasis
- hyperbilirubinemia, hypoglycaemia and hypokalaemia
treatment of acute hepatitis
supportive measures and allowing liver to recover, corticosteroids aren’t indicated and may worsen prognosis, plasma transfusion
prognosis of acute hepaitits
poor, if they recover from acute phase have a good chance of complete recovery
differentials for acute hepatitis
CAV-1 and Leptospira
predisopsition of corhinc hepatitis
Cocker spaniels, dalmatian, Doberman pinschers, springer spaniels, great Dane, labs, Samoyed, standard poodle, young-middle aged
cause of chronic ahepatitis
mutation of gene involved with copper storage disease, mostly idiopathic
pathogenesis of chronic hepatitis
relates to the loss of hepatic mass resulting in loss of function and late in disease process, development of portal hypertension
signs of chronic hepatitis
no clinical signs until late in the disease process
diagnosis of chronci hepatitis
take liver biopsy, diagnostic imaging and aspiration of bile and culture
- persistently elevated liver enzymes
treatment of chronic hepaitis
treating underlying cause, supportive liver function and animals nutritional and metabolic needs
- with idiopathic hepatitis = nonspecific and attempts to slow progression of clinical signs
- choleretics: ursodiol – modulates bile acid pool in biliary stasis
- antioxidants: Vitamin E
- glucocorticoids/ other immunosuppressive drugs
- antifibrotics/antibiotics
predisposition of feline inflammatory infectious hepatic disease
any cat, any age sex or species
cause Feline inflammatory infectious hepatic disease
viral, bacterial, fungal, parasites, poisoning, gall stones, stress, environmental cause, dietary, immune system, certain medications
signs of Feline inflammatory infectious hepatic disease
lethargy, vomiting, weight loss (unspecific signs), fever, abdominal swelling, jaundice, increased thirst, increased urination, dark urine, changes in behaviour, grey/white faeces
diagnosis of Feline inflammatory infectious hepatic disease
FNA, abdo US, biopsy, blood, urinalysis, faecal exam, bile acids
Feline inflammatory infectious hepatic diseasetreatment of
ATB according to culture (ampicillin, amoxicillin and clavulanate), NSAIDs, IV fluids, feeding therapy and supplementation and nutritional support
prognosis of Feline inflammatory infectious hepatic disease
poor if advanced
predisposition of lymphocytic hepatitis
older cats with history of hyperthyroidism
cause of lymphocytic hepatiis
related to thyroid disease or immune system dysfunction
signs of lymphocytic hepatitis
unspecific signs: nausea, inappetence, lethargy, vomiting and jaundice, diarrhoea
diagnosis of lymphocytic hepaitis
X-rays, ultrasound, liver biopsy, CBC, biochemistry, urinalysis
treatment of lymphocytic hepatitis
ATB while awaiting culture results, prednisolone, supportive
predisposition of infectious feline hepatobiliary disease
young-middle aged cats
cause of infectious feline hepatobiliary disease
micro and macro hepatic abscesses, polymicrobial growth in >50% cats
bacterial infections: secondary to ascending intestinal bacteria: klebsiella, listeria, salmonella, brucella, yersinia…
- viral infections: FeLV, FCV, FIP and FIV
- liver flukes: platinosomum spp
signs of infectious feline hepatobiliary disease
acute vomiting, diarrhoea, anorexia and lethargy, abdominal pain, fever, icterus
diagnosis of infecitious feline hepatobiliary disease
iver biopsy (tru-cut-type/ FNA)to differentiate from effusive FIP, increased ALT, AST, GGT and ALP
treatmetn of infectious feline hepatobiliary disease
ATB at least 6 weeks
predisposition of hepatic vascular anomalies - PSS
mostly young animals before 1-2 yr. and acquired 3 year. More common in dogs than cats
- Persian and Himalayan cats
- extrahepatic: terriers, maltese, mini schnauzers
- intrahepatic: irish wolf hound
pathogenesis of PSS
acquired (multiple extrahepatic, secondary to fibrosis, secondary to arteriovenous malformations)
congenital: macrovascular PSS (intrahepatic – large breeds, extrahepatic- small), primary portal vein hypoplasia, disturbances in outflow
Extrahepatic PSS
- abnormal communications between portal vein or one of its contributors and the caudal vena cava
Intrahepatic PSS
- may be left sides: persistence of the fetal ductus venosus after birth
- right sided/centrally located in the liver” anomalous vessels
signs of PSS
HE, vomiting, anorexia, pica, diarrhoea, ptyalism (cats), melena, haematemesis, pollakiuria, ascites, anaemic, neurologic
smaller in structure, failure to gain weight, copper coloured irises (cats)
diagnosis of PSS
- based on neurological signs
- blood: anaemia, microcytosis,
o low: albumin, glucose, cholesterol urea,
o high: serum liver enzyme activities - urinalysis: low USG, ammonium biurate crystalluria, proteinuria
- serum bile acids
- ammonia and ammonia tolerance test
- Xray, US, scintigraphy, CT (liver atrophy)
treatment of PSS
medical (supportive, prognostic 50% euthanised within 10Mo) surgical (shunt attenuation: ligation, aneroid constrictors, cellophane bands)
predisposition of feline hepatic lipidosis
cats prone to mild to moderate steatosis when anorexia and in response to toxic insults
- younger to middle age female cats and obese
cause of feline hepatic lipidosis
obesity, anorexia and stress, environmental differences
- Secondary hepatic lipidosis is seen in cats that are not obese, usually due to neuroendocrine responses to stress
pathogenesis of feline hepatic lipidosis
massive accumulation of fat in hepatocytes leading to acute loss of hepatocyte function
- excessive peripheral lipid mobilisation to the liver, deficiency of dietary proteins and other nutrients that would usually allow fat metabolism and transport out of the liver
signs of feline hepatic lipidosis
- primary: after 6-7 weeks of anorexia and/or loss of more than 25% BW
- secondary: cholangitis, pancreatitis, IBD, neoplasia, DM, hyperthyroidism
- acute loss of hepatocyte function and hepatocyte swelling
- cats usually jaundiced and have intermittent vomiting and dehydration
- depression, ptyalism
diagnosis of feline hepatic lipidosis
- palpable hepatomegaly on physical exam
- biochemical: increased BHB, increased circulating triglycerides, NEFA and VLDL
- lab (GGT normal, hypokalaemia, hyperglycaemia)
- histopathology of a wedge biopsy
- use FNA
treatment of feline hepatic lipidosis
early intensive feeding, high protein diet, rapid institution of tube feeding, treat any concurrent inflammatory disease, fluids (to address electrolyte abnormalities)
prognosis of feline hepatic lipidosis
good as long as feeding is rapidly and effectively instituted
- older age was a poor prognostic indicator
- secondary hepatic lipidosis may do slightly worse than primary
predisposition of liver tumour
Primary liver tumours: rare to infrequent (older animals), dogs: meta changes much more frequent, uncommon in cats,
- unlike in cats, malignant tumours are more common than benign, with metastases – spleen, pancreas and GI
cause of liver tumour
no predisposing factors have been identified, except maybe primary copper storage
signs of lvier tumour
- primary malignant tumours of liver are usually seen in older cats (10-12yrs) and no obvious gender predisposition
- lethargy, vomiting, weight loss, ascites or jaundice
- 50% of cats with liver tumours are asymptomatic
diagnosis of liver tumour
- diagnostic imaging (hepatomegaly), cytology and histology
- high liver enzyme activity and bile acid concentration and mild anaemia and neutrophilia are common but non-specific findings
treatment of liver tumour
primary tumour relies on surgical removal if they are resectable
- primary hepatic tumours generally have a poor response to chemotherapy
- radiotherapy isn’t wise as normal liver tissue is very radiosensitive
rognosis of liver tumour
benign tumours is good after resection but poor for cats with any type of malignant liver tumour. However, most cats with lymphoma of the liver respond to chemotherapy
predisposition of acute pancreatitis
terriers, schnauzers, domestic short hair, middle aged dogs and cats
cause of acute pancreatitis
mutations of trypsin which can predispose to pancreatitis
pathogenesis of acute pancreatitis
inappropriate early activation of trypsinogen inn the pancreas as a result of increased autoactivation of trypsinogen
signs of acute pancreatitis
vomiting, anorexia, diarrhoea, abdominal pain, lethargy, dehydration, hypovolemic shock, DIC, MODS, mild abdominal pain, jaundice
diagnosis of acute pancreatitis
presence of typical clinical signs, elimination of possible diff. dg, elevated PLI, typical ultrasound lesions, histopathology, fluid analysis (abdominal effusion)
- routine lab: CBC, electrolytes and urinalysis doesn’t help but helps with information and treatment
- TLI (trypsin like immunoreactivity) and PLI (pancreatic lipase immunoreactivity)
treatment of acute pancreatitis
fluid, electrolytes, analgesia (fentanyl patch, tramadol) , food, antiemetics (maropitant, ondansetron, thiethylperazine), gastroprotection’s (H2 blockers: famotidine, ranitidine, PPI: omeprazole, sucralfate), ATB (cefotaxime, ciprofloxacin, metronidazole, clindaymycin), insulin, surgery
prognosis of acute pancreatitis
mild with moderate pancreatitis: proper treatment, prognosis is favourable, severe: bad
predisposition of chronic pancreatitis
rare and not that important in dogs, but most common form of pancreatitis in cats
- idiopathic: most common middle-aged dog, king Charles, cockers, collie or boxers, domestic short hairs mostly affected
- autoimmune: English cocker spaniels
pathogenesis of chronic pacnreatitis
characterised by destruction parenchyma, irreversible changes. Leads to progressive/permanent impairment of exocrine and endocrine
signs of chronic pancreatitis
vomiting, inappetence, colitic diarrhoea, pain on palpation, may develop jaundice
diagnosis of chronic pancreatitis
clinical signs unclear or identical to AP, other tests be aware CP as possible D pathohistology
- gold standard: histology
- ultrasound lower sensitivity because there’s less oedema than in acute pancreatitis
- measure serum Vitamin B12 – supplemented if low
treatment of chronic pancreatitis
analgesia, food, immunosuppressants
prognosis of chronic pancreatitis
depends on successful neutralisation of pain as well as treatment of both DM and EPI
predisposition of EPI
both dogs and cats, young GSH, rough collies
cause of EPI
pancreatic acinar cell atrophy or destruction due to pancreatitis, can be autoimmune
pathogensis of EPI
unctional diagnosis that results from lack of pancreatic enzymes. Approx 85-90% of the exocrine secretory pancreas must be non-functioning before signs of EPI are evident
- primary to pancreatic acinar atrophy (D): young GSD, autoimmune, rough collies and English setters
- secondary to end stage chronic pancreatitis (C,D): cats, middle aged/older small breed dogs (Charles, cockers)
signs of EPI
voluminous faeces, often pale and steatorrhea, high defaecation frequency, weight loss, hyperphagic, chronic small intestinal diarrhoea, ravenous appetite, cats (hyporexia and lethargy)
diagnosis of EPI
- CBC, biochemical profile, urinalysis
- TLI – trypsin like immunoreactivity
o dog <2.5 ug/L and compatible clinical signs
o cat < 8 ug/L - Cobolamine (decreased B12), folate
- ELISA faecal elastase test
treatment of eEPI
Specific
- exogenous enzymes: powdered pancreatic extracts, rarw chopped pancreas
- diet: low on fibre, restricted fat, vitamin supplementation B12
supportive
- antacid therapy
- treatment of concurrent disease
prognosis of EPI
- quite good, especially in dogs which respond well to initial therapy > 5 years
- complicated EPI or recurrent acute phases of acute pancreatitis, prognosis is reduced
- +DM the treatment is becoming more challenging and more expensive
vascular ring anomaly
Congenital malformations of the great vessels and their branches that entrap the intrathoracic oesophagus and other intrathoracic structures
Cause: persistent right aortic arch – ligamentum arteriosum continues to develop from the left side and forms a fibrous band that crosses over the oesophagus to connect the main pulmonary artery and anomalous aorta
Signs: cause clinical signs of oesophageal obstruction
Diagnosis: survey thoracic x-ray shows severe dilation of oesophagus
gastric neoplasia
Predisposition: uncommon in dogs and cats, dogs 6-9 years, cats 10-12, gastric leiomyoma tend to occur in older dogs, slight predominance for male dogs and cats to develop GI neoplasia
- most common in dogs: adenocarcinomas
- most common in cats: lymphosarcoma
Signs: vomiting, haematemesis, melena, anorexia, weight loss
Diagnosis:
- routine lab testing helps exclude non-gastrointestinal origins
- anaemia
- x-ray, ultrasound, endoscopy
- definitive diagnosis is based on cytological or histology demonstration of neoplastic cells – FNA
Treatment: chemotherapy, surgical resection
Prognosis: poor to grave
delayed gastric emptying
- most commonly recognised manifestation of gastric motility disorders
Cause: by outflow obstruction (congenital stenosis, FB, neoplasia granuloma, polyps)or defective propulsion (gastric disorders, gastritis, ulcer, neoplasia, peritonitis, pancreatitis)
Signs:
- vomiting (projectile – with pyloric stenosis)
- abdominal distension, weight loss, melena, abdominal discomfort, distension, bloating and anorexia
Diagnosis: suspect DGE when a pet vomits food at least 8 hours, often 10-16 hours after a meal
- dependent of the cause
- Lab: CBC, Biochem, serum gastrin and gastric pH
- abdominal imaging: plain and contrast
- ultrasonography
- endoscopy (before barium contrast)
Treatment:
- directed at underlying cause
- diet: food that facilitates gastric emptying, small amounts, frequent intervals, semi-liquid, protein and fat restricted
- prokinetic drugs: cisapride, erythromycin, metoclopramide)
