GI Medicine Flashcards
1
Q
What are the clinical signs of oropharyngeal disease?
A
Drooling saliva +/- blood (ptyalism vs pseudoptyalism)
Halitosis
Dysphagia +/- odynophagia
2
Q
How do we investigate oral disease?
A
Physical examination (consider feasibility of intubation) Radiographs Minimum database FNA and/or biopsy Special tests
3
Q
What can cause oropharyngeal disease?
A
Oropharyngeal foreign bodies
Oral ulceration/burns
Oropharyngeal inflammatory disease
4
Q
How do we treat oropharyngeal disease?
A
Depends on underlying cause Neoplasia = surgery (/cryosurgery, radiation, chemotherapy) Foreign body = remove Trauma = wound management/surgery Inflammation = anti-inflammatories Bacterial infection = antibiotics
5
Q
What nursing considerations should we have for oral disease?
A
Analgesia (NSAIDs, opioids)
Nutrition - oral feeding (warm/wet/soft) / requirement for bypass/tube feeding
Barrier nursing for infectious aetiologies
6
Q
Why is poor oral/dental hygiene bad?
A
Partially causative e.g. feline gingivostomatitis
Source of ongoing bacteria/oropharyngeal inflammation/infection
7
Q
Describe regurgitation.
A
Passive return of food Hallmark of oesophageal disease Immediate or delayed - undigested food +/- mucus/saliva Neutral pH Solid or liquid Fresh blood if ulcerated
8
Q
What secondary problems can we see with regurgitation?
A
Malnutrition, dehydration
Anorexia or perceived polyphagia
Reflux pharyngitis/rhinitis (nasal discharge)
Aspiration pneumonia (cough, dyspnoea, pyrexia)
Swallowing pain (odynophagia)
9
Q
How do we investigate oesophageal disease?
A
Physical examination
Chest X-rays - conscious!
Lab tests - haematology/serum biochemistry
+/- oesophagoscopy
10
Q
What are the possible pathophysiologies of oesophageal disease?
A
Megaoesophagus
Oesophagitis
Oesophageal obstruction (complete/partial) - intraluminal/intramural/extraluminal
11
Q
Describe megaoesophagus.
A
Oesophageal dilation/dysfunction Generalised (idiopathic, myasthenia gravis) Focal dilation (e.g. vascular ring anomaly)
12
Q
How do we treat megaoesophagus?
A
Idiopathic = no cure
Myasthenia gravis = neostigmine, pyridostigmine
Vascular ring anomaly = surgery
Nursing care/management to minimise impact of oesophageal dysfunction
13
Q
What nursing considerations should we have for megaoesophagus patients?
A
Postural feeding
Stairs/work surface
+/- support, e.g. Bailey chair
Slurry vs textured food
14
Q
What complications can occur for megaoesophagus patients?
A
Aspiration pneumonia - tachypnoea, pyrexia, lethargy, inappetence
Treat with IV antibiotics
Body weight and condition, adjust feeding as necessary
15
Q
Describe oesophagitis.
A
Oesophageal inflammation caused by ingestion (caustics, hot liquids/foods, foreign bodies, irritants e.g. doxycycline) / gastro-oesophageal reflux / persistent vomiting
May cause oesophageal strictures
16
Q
What are the clinical signs of oesophagitis?
A
Regurgitation Hypersalivation Anorexia Pain Weight loss
17
Q
How do we manage oesophagitis?
A
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)
18
Q
What are the causes of gastro-oesophageal reflux?
A
Reflux of gastric acid/enzymes, inflammation
During anaesthesia
Persistent vomiting
Hiatal hernia
GERD (‘heartburn’) - spontaneous reflux (obesity, BOAS)
19
Q
Describe oesophageal foreign bodies.
A
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
20
Q
What is an oesophageal stricture and how do we treat it?
A
Fibrosis after severe ulceration of mucosa
Treatment = dilation with balloon catheter
21
Q
Describe vomiting.
A
A complex, coordinated reflex reaction
Integrated sequence of overlapping events
Does not involve gastric contraction
22
Q
What are the 4 stages of vomiting?
A
Stage 1 = prodromal phase
Stage 2 = retching
Stage 3 = expulsion
Stage 4 = relaxation
23
Q
Describe the prodromal phase of vomiting.
A
Nausea
Restlessness, agitation
Hypersalivation
Gulping, lip-licking/smacking
24
Q
Describe the retching stage of vomiting.
A
Inhibition of saliva
Simultaneous, uncoordinated, spasmodic contractions of respiratory muscles
Duodenal retroperistalsis
Mixing of gastric contents
25
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)
26
Describe the relaxation stage of vomiting.
Muscles - abdominal, diaphragmatic, respiratory
Glottis, nasopharynx
Return of breathing
27
Describe small intestinal diarrhoea.
Large volume, watery
Normal frequency
Often normal colour
+/- malaena
28
Describe large intestinal diarrhoea.
```
Small volume
Increased urgency and frequency
Tenesmus, dyschezia
+/- mucus
+/- blood
```
29
Define -gastritis, -enteritis and -colitis.
- gastritis = stomach
- enteritis = small intestine
- colitis = large intestine
30
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
```
31
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
```
32
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
```
33
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
34
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
```
35
Give some examples of causes of surgical disease v/d.
```
Intussusception (has underlying cause)
Gastric dilation and volvulus
Incarceration
Stricture/partial obstruction
Foreign body
```
36
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)
37
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
38
How can we maintain hydration in a v/d patient?
IV - Hartmann's (+KCl)
| Oral rehydration solutions
39
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
40
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
41
What supportive/symptomatic management can we offer v/d patients?
Antiemetics - exclude obstruction first
Antispasmodics
Anti-diarrhoeals - cosmetic only
42
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
43
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
44
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
```
45
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
46
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
47
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
48
How do we treat GDV?
Aggressive fluid therapy
Immediate decompression
IV antibiotics
Surgical correction (gastropexy +/- derotation)
Transient peri-operative cardiac arrythmias common
49
What infectious causes of v/d exist?
Canine/Feline Parvovirus
Bacterial enterocolitis
Acute Haemorrhagic Diarrhoea Syndrome
50
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)
51
What protozoal causes of acute v/d exist?
Coccidia spp.
Giardia spp.
Tritrichomonas foetus
52
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
53
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
```
54
How do we diagnose acute pancreatitis?
History and physical examination
Imaging (radiography, ultrasound)
Haem/biochem
Pancreatic lipase immunoreactivity (PLI)
55
How do we treat acute pancreatitis?
Fluid support, IV crystalloids
Nutritional support (oral or naso-oesophageal/oesophageal tube)
Analgesia/antiemetics until resolution
56
What is the prognosis for acute pancreatitis?
Highly variable to guarded
Death is possible
Recurrence is possible
57
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)
58
What secondary complications can occur from prolonged anorexia?
Weight loss
Impaired immune function
Increased risk of sepsis
Poor wound healing and slow recovery
59
Define borborygmi, flatus and ileus.
```
Borborygmi = gurgling
Flatus = passing wind
Ileus = reduced gastrointestinal motility
```
60
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
```
61
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
62
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)
63
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
```
64
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
```
65
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
66
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
67
How do we treat chronic v/d?
```
Treat underlying cause
Exclusion of parasitism - fenbendazole course
Dietary modification
Vitamin B12 supplementation
Steroids
Antiemetics
Appetite stimulants
```
68
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)
```
69
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
70
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
```
71
What nutritional support can we provide for inappetant patients?
Feeding tubes - naso/oesophageal, gastric/percutaneous
| For microenteral nutrition, liquid/blending feeding, medication administration
72
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
73
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
74
How can we diagnose exocrine pancreatic insufficiency?
Trypsin-like immunoreactivity (TLI) serum test
| Species specific i.e. cTLI / fTLI
75
How can we treat exocrine pancreatic insufficiency?
Expensive, lifelong
| Oral pancreatic extract
76
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)
```
77
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
78
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
79
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)
80
Describe jaundice.
AKA icterus
Yellow discolouration - hyperbilirubinaemia (increased bilirubin in blood)
Not generally harmful
Marker of possible hepatic disease
81
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
```
82
Describe ascites in liver disease.
Fluid accumulation in abdomen - typically referring to watery (low protein/cellularity) fluid
Leads to abdominal effusion
83
What are the possible reasons for ascites in liver disease?
Hypoalbuminaemia
Portal hypertension
Sodium and water retention
84
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
85
What precipitates hepatic encephalopathy and what makes it worse?
Precipitating events = high protein meal, vomiting/diarrhoea, diuretics
Worse after high protein meal, gastrointestinal haemorrhage
86
How can we diagnose liver disease?
Lab tests - liver enzymes, bilirubin, bile acids, blood glucose, blood clotting parameters
Imaging
Liver cytology/biopsy
87
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)
88
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?
89
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
90
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
```
91
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)
```
92
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
93
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
```
94
Describe gall bladder mucocoeles.
Gall bladder full of inspissated bile and mucus
Kiwi fruit appearance
Asymptomatic / obstructing bile flow / rupture
Medical / surgical management
95
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
```
96
What are the predispositions for feline hepatic lipidosis?
Obesity
High fat/carbohydrate diet
Systemic illness
Diabetes mellitus
97
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
98
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
99
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
100
What are the signs of hepatic neoplasia?
Asymptomatic
Primary hepatic/obstructive signs
Rupture - haemoabdomen
101
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
102
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
103
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
```
104
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
```
105
Describe constipation.
Impaction of the colon/rectum with faecal material +/- hair/bones etc.
Excessively dry/hard faeces
Prolonged constipation = irreversible changes, obstipation (intractable constipation)
106
What are the signs of constipation?
Infrequent defecation
Dyschezia - straining to defecate (tenesmus)
Pain associated with (un)successful defecation
Vomiting
Anorexia, lethargy
107
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
```
108
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?
109
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
```
110
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
