GI Medicine Flashcards
What are the clinical signs of oropharyngeal disease?
Drooling saliva +/- blood (ptyalism vs pseudoptyalism)
Halitosis
Dysphagia +/- odynophagia
How do we investigate oral disease?
Physical examination (consider feasibility of intubation) Radiographs Minimum database FNA and/or biopsy Special tests
What can cause oropharyngeal disease?
Oropharyngeal foreign bodies
Oral ulceration/burns
Oropharyngeal inflammatory disease
How do we treat oropharyngeal disease?
Depends on underlying cause Neoplasia = surgery (/cryosurgery, radiation, chemotherapy) Foreign body = remove Trauma = wound management/surgery Inflammation = anti-inflammatories Bacterial infection = antibiotics
What nursing considerations should we have for oral disease?
Analgesia (NSAIDs, opioids)
Nutrition - oral feeding (warm/wet/soft) / requirement for bypass/tube feeding
Barrier nursing for infectious aetiologies
Why is poor oral/dental hygiene bad?
Partially causative e.g. feline gingivostomatitis
Source of ongoing bacteria/oropharyngeal inflammation/infection
Describe regurgitation.
Passive return of food Hallmark of oesophageal disease Immediate or delayed - undigested food +/- mucus/saliva Neutral pH Solid or liquid Fresh blood if ulcerated
What secondary problems can we see with regurgitation?
Malnutrition, dehydration
Anorexia or perceived polyphagia
Reflux pharyngitis/rhinitis (nasal discharge)
Aspiration pneumonia (cough, dyspnoea, pyrexia)
Swallowing pain (odynophagia)
How do we investigate oesophageal disease?
Physical examination
Chest X-rays - conscious!
Lab tests - haematology/serum biochemistry
+/- oesophagoscopy
What are the possible pathophysiologies of oesophageal disease?
Megaoesophagus
Oesophagitis
Oesophageal obstruction (complete/partial) - intraluminal/intramural/extraluminal
Describe megaoesophagus.
Oesophageal dilation/dysfunction Generalised (idiopathic, myasthenia gravis) Focal dilation (e.g. vascular ring anomaly)
How do we treat megaoesophagus?
Idiopathic = no cure
Myasthenia gravis = neostigmine, pyridostigmine
Vascular ring anomaly = surgery
Nursing care/management to minimise impact of oesophageal dysfunction
What nursing considerations should we have for megaoesophagus patients?
Postural feeding
Stairs/work surface
+/- support, e.g. Bailey chair
Slurry vs textured food
What complications can occur for megaoesophagus patients?
Aspiration pneumonia - tachypnoea, pyrexia, lethargy, inappetence
Treat with IV antibiotics
Body weight and condition, adjust feeding as necessary
Describe oesophagitis.
Oesophageal inflammation caused by ingestion (caustics, hot liquids/foods, foreign bodies, irritants e.g. doxycycline) / gastro-oesophageal reflux / persistent vomiting
May cause oesophageal strictures
What are the clinical signs of oesophagitis?
Regurgitation Hypersalivation Anorexia Pain Weight loss
How do we manage oesophagitis?
Oesophageal rest (+/- gastrotomy feeding, soft/bland food small + frequent)
Analgesia
Liquid antacid gels/coating agents
Acid blockers (omeprazole)
Drugs to reduce further reflux (metoclopramide, cisapride)
What are the causes of gastro-oesophageal reflux?
Reflux of gastric acid/enzymes, inflammation
During anaesthesia
Persistent vomiting
Hiatal hernia
GERD (‘heartburn’) - spontaneous reflux (obesity, BOAS)
Describe oesophageal foreign bodies.
E.g. bones, sticks, needles, fish-hooks, rawhide chews
Can lodge anywhere - obstruction/regurgitation, may be able to drink
Raw/bone feeding = risk
Remove endoscopically/fluoroscopically +/- surgery
What is an oesophageal stricture and how do we treat it?
Fibrosis after severe ulceration of mucosa
Treatment = dilation with balloon catheter
Describe vomiting.
A complex, coordinated reflex reaction
Integrated sequence of overlapping events
Does not involve gastric contraction
What are the 4 stages of vomiting?
Stage 1 = prodromal phase
Stage 2 = retching
Stage 3 = expulsion
Stage 4 = relaxation
Describe the prodromal phase of vomiting.
Nausea
Restlessness, agitation
Hypersalivation
Gulping, lip-licking/smacking
Describe the retching stage of vomiting.
Inhibition of saliva
Simultaneous, uncoordinated, spasmodic contractions of respiratory muscles
Duodenal retroperistalsis
Mixing of gastric contents
Describe the expulsion stage of vomiting.
Pyloric contraction, fundic relaxation
Relaxation of proximal stomach and lower oesophageal sphincter
Initially high tone in upper oesophageal sphincter
Protection of airway (inhibition of breathing, coordinated closure of glottis and nasopharynx)
Abdominal contraction and descent of diaphragm (stomach squeezed and vomitus forced up, oesophageal retroperistalsis, reduced upper oesophageal sphincter tone)
Describe the relaxation stage of vomiting.
Muscles - abdominal, diaphragmatic, respiratory
Glottis, nasopharynx
Return of breathing
Describe small intestinal diarrhoea.
Large volume, watery
Normal frequency
Often normal colour
+/- malaena
Describe large intestinal diarrhoea.
Small volume Increased urgency and frequency Tenesmus, dyschezia \+/- mucus \+/- blood
Define -gastritis, -enteritis and -colitis.
- gastritis = stomach
- enteritis = small intestine
- colitis = large intestine
What are the main phone triage questions we should ask for a vomiting/diarrhoea patient?
Vomit - productive/non-productive Frequency - fluid losses Foreign material Haematemesis/melaena? Diarrhoea - small/large intestinal
What other questions should we ask in a phone triage for a v/d patient?
Pre-existing medical disease/medications (e.g. NSAIDs) Pre-existing gastrointestinal disease Worming history (especially puppies/kittens) Recent dietary change? Known scavenger? Clinical demeanour Appetite, drinking Other systemic signs
When should we advise consultation for a v/d patient?
Unproductive vomiting Large fluid volumes lost Haematemesis/melaena Suspicion for foreign material ingestion Inappetent/hypodipsic Other systemic signs Puppy/kitten Any other concerns
Give some examples of causes of non-fatal, often trivial acute v/d.
Dietary indiscretion
Parasitism (e.g. roundworms, whipworms, protozoal)
Enteric infection
Adverse drug event
Give some examples of causes of severe and potentially life-threatening v/d.
Pathogenic enteric infections (parvovirus, bacterial) Acute Haemorrhagic Diarrhoea Syndrome Acute pancreatitis Surgical disease Intoxications
Give some examples of causes of surgical disease v/d.
Intussusception (has underlying cause) Gastric dilation and volvulus Incarceration Stricture/partial obstruction Foreign body
What are the possible consequences of vomiting and/or diarrhoea?
Dehydration
Hypovolaemia
Acid-base disturbances (loss of electrolytes)
Aspiration pneumonia (especially if sedated/neuromuscular/upper airway incompetency)
What are the diagnostic tests for acute gastroenteritis?
History, physical examination
Bloods - haem/biochem/electrolytes
Faecal - infectious disease testing (pooled sample/swab or faecal sample)
Imaging
+/- response to symptomatic treatment/surgical management
How can we maintain hydration in a v/d patient?
IV - Hartmann’s (+KCl)
Oral rehydration solutions
What dietary advice can we give for a vomiting patient?
Rest the gut - free access to water
So starve for 24-36hrs
Re-introduce bland diet, little and often
Then transition to normal diet over 2-5 days
What dietary advice can we give for a diarrhoea patient?
Feed through diarrhoea
Reduces potential of sepsis
Cosmetic problem in dogs, but usually concurrent vomiting
What supportive/symptomatic management can we offer v/d patients?
Antiemetics - exclude obstruction first
Antispasmodics
Anti-diarrhoeals - cosmetic only
How do we treat acute v/d?
Anthelmintics (if puppy/kitten or not recently wormed)
Antibiotics rarely indicated - consider if haemorrhagic diarrhoea +/- pyrexic
Pre/probiotics
How do we use NSAIDs in v/d patients?
Absolutely contraindicated!
Pre-existing use - withhold for duration
Prostaglandins required for maintenance of GI mucosal integrity/renal blood flow in hypovolaemic states
When should we consider an infectious cause of acute gastroenteritis?
Puppy/kitten Unvaccinated animals Haemorrhagic diarrhoea Pyrexia Raw-fed patient Barrier nurse/isolate until diagnosis confirmed
What nursing considerations should we have for acute gastroenteritis patients?
Patient hygiene - clean/dry bottom, avoid patient over-grooming, tail bandage
Environmental hygiene - appropriate waste disposal. washing/disinfection of contaminated items, PPE
Kennel signage
How do we treat gastrointestinal foreign bodies?
Non-obstructive:
Small and gastric = induce emesis
Intestinal = natural passage / radiographic passage
Other gastric = endoscopic retrieval/surgery
Obstruction = surgery
Describe Gastric Dilation and Volvulus (GDV).
Acute dilation of stomach + volvulus
Torsion of the stomach +/- twisted splenic pedicle
Impaired venous return, compromised gastric mucosa
Leads to shock and death
Deep-chested breeds
How do we treat GDV?
Aggressive fluid therapy
Immediate decompression
IV antibiotics
Surgical correction (gastropexy +/- derotation)
Transient peri-operative cardiac arrythmias common
What infectious causes of v/d exist?
Canine/Feline Parvovirus
Bacterial enterocolitis
Acute Haemorrhagic Diarrhoea Syndrome
What parasitic causes of v/d exist?
Roundworms (rarely cause clinical signs) - zoonotic risk, can be passed transplacental/transmammary
Hookworms
Whipworms
Cestodes (do not cause GI signs)
What protozoal causes of acute v/d exist?
Coccidia spp.
Giardia spp.
Tritrichomonas foetus
Describe acute pancreatitis.
Idiopathic/secondary to predisposing feature (hyperlipaemia, dietary indiscretion, impaired perfusion, trauma/handling)
Causes local release of pancreatic enzymes, pancreatic autodigestion, severe local inflammation with pain
May cause severe systemic inflammation and death
What are the clinical signs of acute pancreatitis?
Range from mild to fatal Inappetence, lethargy Severe abdominal pain, v/d \+/- jaundice (bile duct obstruciton) Dogs may adopt 'prayer' position
How do we diagnose acute pancreatitis?
History and physical examination
Imaging (radiography, ultrasound)
Haem/biochem
Pancreatic lipase immunoreactivity (PLI)
How do we treat acute pancreatitis?
Fluid support, IV crystalloids
Nutritional support (oral or naso-oesophageal/oesophageal tube)
Analgesia/antiemetics until resolution
What is the prognosis for acute pancreatitis?
Highly variable to guarded
Death is possible
Recurrence is possible
Describe chronic pancreatitis.
Causes chronic, recurrent, grumbling GI signs
Inappetence, lethargy
Vomiting and/or diarrhoea
At-home dietary modification, manage nausea/appetite, analgesia (not NSAIDs)
What secondary complications can occur from prolonged anorexia?
Weight loss
Impaired immune function
Increased risk of sepsis
Poor wound healing and slow recovery
Define borborygmi, flatus and ileus.
Borborygmi = gurgling Flatus = passing wind Ileus = reduced gastrointestinal motility
What are the clinical signs of chronic GI disease?
Altered appetite Dehydration Vomiting +/- blood Diarrhoea +/- digested/fresh blood Weight/condition loss Borborygmi, flatus Abdominal discomfort
What are some primary GI disease causes of chronic v/d?
Gastric ulceration
Dietary intolerance/sensitivity
Inflammatory e.g. inflammatory bowel disease
Neoplastic e.g. gastric carcinoma, GI lymphoma
What are some extra-gastrointestinal disease causes of chronic v/d?
Liver disease
Kidney disease
Pancreatitis (chronic)
Endocrine disease e.g. hyperthyroidism (cats), hypoadrenocorticism (dogs)
How can we diagnose an underlying cause of chronic v/d?
History and clinical examination Haem/biochem/PLI/faecal analysis Absorption tests (vitamin B9 and B12) Imaging (abdominal radiographs, ultrasound) Gastroscopy/laparotomy and biopsy
What are the differences between laparotomy and endoscopy?
Laparotomy = enables full thickness biopsies, surgical risk of dehiscence Endoscopy = minimally invasive, small biopsies, may not reflect jejunal disease
Describe chronic enteropathies.
Chronic disease of the small intestine
Common
Inflammatory bowel disease complex - food responsive diarrhoea, antibiotic responsive disease, true idiopathic inflammatory bowel disease
Describe protein-losing enteropathy (PLE).
A form of chronic enteropathy
Severe diffuse small intestinal disease resulting in severe malabsorption and loss of albumin/globulin
Severe weight loss, oedema, ascites, risk of thromboembolic events
Various causes - inflammatory bowel disease, lymphangiectasia, alimentary lympho(sarco)ma
Diagnosis = endoscopy
How do we treat chronic v/d?
Treat underlying cause Exclusion of parasitism - fenbendazole course Dietary modification Vitamin B12 supplementation Steroids Antiemetics Appetite stimulants
What dietary considerations should we have for chronic enteropathy patients?
Avoidance of allergen, novel vs hydrolysed diets Highly digestible Restricted fat Supplementary fibre Little and often (3-4 times/day)
How can we encourage food intake in inappetant patients?
Avoid introducing prescription diets in the hospital
Warm, wet, smelly
Individual preferences - food, environment, solitary/hand/owner feeding
Ensure euhydrated, balanced electrolytes
What medical therapy can we provide for inappetant patients?
Control nausea (maropitant, metoclopramide) Stimulate appetite (mirtazapine) Patient receiving any drugs that may suppress appetite? - opioids - reduced GI motility, NSAIDs contraindicated
What nutritional support can we provide for inappetant patients?
Feeding tubes - naso/oesophageal, gastric/percutaneous
For microenteral nutrition, liquid/blending feeding, medication administration
In what two ways can we supplement cobalamin (vitamin B12)?
Subcut injections - weekly until normalised (4-6 weeks), re-measure serum cobalamin 4-6 weeks after completion of course
Oral - daily (mega-doses), re-measure serum cobalamin after 4-6 weeks
Describe exocrine pancreatic insufficiency (EPI).
Failure of normal exocrine (enzyme) pancreatic secretion
Causes maldigestion/malabsorption
Usually due to pancreatic acinar atrophy - young adult onset
May be due to recurrent pancreatitis
How can we diagnose exocrine pancreatic insufficiency?
Trypsin-like immunoreactivity (TLI) serum test
Species specific i.e. cTLI / fTLI
How can we treat exocrine pancreatic insufficiency?
Expensive, lifelong
Oral pancreatic extract
What diet should we give to exocrine pancreatic insufficiency patients?
2-3 meals a day, enzyme with every meal! Highly digestible High protein, good quality Not low fat Non-complex carbohydrate Vitamin supplementation (cobalamin)
Describe colitis.
Colonic inflammation
Treated with sulphasalzine - sulfonamide bound to 5-ASA, local anti-inflammatory
Major side effect if keratoconjunctivitis sicca (KCS) - measure Schirmer Tear Test (STT) before and during treatment
Describe irritable bowel syndrome.
Large intestinal pattern diarrhoea +/- occasional vomiting
Typically anxious small breed dogs
Diagnose by exclusion of other causes of signs
Treatment = long-term dietary modification, anti-spasmodics, anti-cholinergics
What are the clinical signs of hepatic dysfunction?
Inappetence, lethargy
Vomiting, diarrhoea
Jaundice
Ascites
Hepatic synthetic failure (proteins/carbohydrates/fats/clotting factors)
Hepatic detoxification failure (hepatic encephalopathy/persistent drug activity)
Describe jaundice.
AKA icterus
Yellow discolouration - hyperbilirubinaemia (increased bilirubin in blood)
Not generally harmful
Marker of possible hepatic disease
What are the possible causes of jaundice?
Pre-hepatic = haemolysis (moderate-severe) Hepatic = failure of hepatic uptake, conjugation and/or transport of bilirubin Post-hepatic = failure of excretion of bile, cholestatic disease/biliary rupture
Describe ascites in liver disease.
Fluid accumulation in abdomen - typically referring to watery (low protein/cellularity) fluid
Leads to abdominal effusion
What are the possible reasons for ascites in liver disease?
Hypoalbuminaemia
Portal hypertension
Sodium and water retention
Describe failure of detoxification of the liver.
Hepatic dysfunction and/or abnormal blood supply
Failure of conversion of ammonia to urea (hyperammonaemia, hepatic encephalopathy)
Failure of drug detoxification (anaesthetic agents)
Encephalopathic toxins
Forebrain dysfunction
What precipitates hepatic encephalopathy and what makes it worse?
Precipitating events = high protein meal, vomiting/diarrhoea, diuretics
Worse after high protein meal, gastrointestinal haemorrhage
How can we diagnose liver disease?
Lab tests - liver enzymes, bilirubin, bile acids, blood glucose, blood clotting parameters
Imaging
Liver cytology/biopsy
What are the most common causes of acute liver disease?
Toxins e.g. xylitol, mushrooms, phenobarbitone, paracetamol, doxycycline
Infections e.g. leptospirosis, ascending biliary infection, canine adenovirus (rare)
What nursing considerations should we have for acute liver disease patients?
Management of hepatic encephalopathy (lactulose, +/- seizure management, maintain normal hydration/electrolytes especially K)
Anti-emetics
Management of hypoglycaemia (glucose infusion/complex carbohydrates little + often)
May be coagulopathic - consider venepuncture
Specific therapies - antioxidants, antibiotics, barrier nursing?
How do we nutritionally manage acute liver disease patients?
Restricted animal protein - ideally replete protein/plant-based, or hepatic/renal prescription diets
Copper restricted
Antioxidant supplemented
What are the causes of chronic inflammatory liver disease?
Sterile = chronic hepatitis (dogs - idiopathic/copper/other), lymphocytic cholangitis (cats) Infectious = chronic/acute cholangitis/cholangiohepatitis, chronic/acute leptospirosis (dogs), chronic feline infectious peritonitis
How do we treat chronic inflammatory liver disease?
De-coppering therapy Antibiotics - only where specifically indicated Dietary modification Liver supportive therapies (antioxidants) Anti-inflammatory therapies (steroids) Choleretics Hepatic encephalopathy therapies Ascites management (spironolactone)
Describe de-coppering therapy for inflammatory liver disease.
Chelating agent = D-penicillamine / Longer-term zinc therapy (not with D-pen)
Restrict copper intake - prescription diet, avoid red meat/offal/eggs/cereals
What is ursodeoxycholic acid (UDCA)?
Hydrophilic, 'beneficial' bile salt Used in liver disease patients Synthetically derived Mechanism = stimulates bile flow, modulates inflammatory response in liver Efficacy not yet proven Not safe in rabbits
Describe gall bladder mucocoeles.
Gall bladder full of inspissated bile and mucus
Kiwi fruit appearance
Asymptomatic / obstructing bile flow / rupture
Medical / surgical management
Describe feline hepatic lipidosis.
Hepatocyte triglyceride deposition Primary / secondary disease Massive intra-cellular fat accumulation Liver failure - encephalopathy, coagulopathy (diagnose by FNA, check clotting, give vitamin K therapy, monitor cardiovascular parameters post-procedures) Death
What are the predispositions for feline hepatic lipidosis?
Obesity
High fat/carbohydrate diet
Systemic illness
Diabetes mellitus
How do we treat feline hepatic lipidosis?
Secondary = treat underlying disease
Nutritional support (tube feeding, appropriate protein content)
Antioxidants
UCDA
L-carnitine?
Owner commitment crucial - often requires 6-8 weeks of at-home tube feeding
Describe a portosystemic shunt.
Blood from GI tract bypasses liver, straight to systemic circulation
Lack of nutrient supply to liver = liver dysfunction
Blood from GI tract not filtered by liver, accumulation of toxins
Hepatic encephalopathy, brain dysfunction
How do we treat a portosystemic shunt?
Well hydrated, normal blood potassium
Restricted protein (or plant-based protein) diet
Lactulose - traps ammonia in colon
Antibiotics
+/- anti-seizure therapy
Longer-term, ideally surgically close shunting vessel
What are the signs of hepatic neoplasia?
Asymptomatic
Primary hepatic/obstructive signs
Rupture - haemoabdomen
What are the types of hepatic neoplasia and how is each treated?
Primary tumours = surgery
Infiltrative (e.g. lymphoma) = chemotherapy
Metastatic (e.g. carcinomas) = no treatment
Describe the different presentations of GI bleeding.
Coagulopathy
Swallowed blood - oral, nasal (epistaxis), pulmonary (haemoptysis)
Gastric/small intestinal bleeding - haematemesis, melaena
Large intestinal bleeding - haematochezia
What are the causes of GI ulceration?
Drugs e.g. NSAIDs, steroids Foreign body/direct trauma Neoplasia e.g. gastric carcinoma Hypoadrenocorticism Kidney/liver disease
How do we treat GI ulcers?
Evaluate for and treat underlying cause Acid blockers - proton pump inhibitors (omeprazole) Coating agents (sucralfate) Analgesia Surgery if perforated
Describe constipation.
Impaction of the colon/rectum with faecal material +/- hair/bones etc.
Excessively dry/hard faeces
Prolonged constipation = irreversible changes, obstipation (intractable constipation)
What are the signs of constipation?
Infrequent defecation
Dyschezia - straining to defecate (tenesmus)
Pain associated with (un)successful defecation
Vomiting
Anorexia, lethargy
What are the causes of constipation?
Dietary e.g. hair/bone content Dehydration/electrolyte derangements Drug-related e.g. opioids Environmental (stress, dirty/absent toilet, lack of exercise) Pain/orthopaedic problems - inability to posture Spinal/neuromuscular disease Pelvic canal blockage Perineal/perianal disease
How do we treat contispation?
Identify and correct underlying cause (full history + clinical exam, abdominal/pelvic radiographs, lab testing)
Fluid therapy +/- electrolyte correction
Oral laxatives
Enemas - colonic irrigation/manual removal of faecal matter
Motility modification (drugs)
Surgery?
How do we manage/prevent chronic constipation?
Ensure adequate water intake, control underlying disease Dietary modification - add fibre Litter tray management Increased exercise Motility modification (cisapride) Laxatives
Describe megacolon.
Loss of neuromuscular function of colon, producing weakened colonic contractions and faecal overload
Most common in cats
Idiopathic - neuromuscular dysfunction / chronic underlying disease
Treat as for constipation
Last resort is sub-total colectomy
