Gastroenterology AI Flashcards
1
Q
What is the difference between regurgitation and expectoration?
A
Regurgitation is the passive expulsion of food or other material from the pharynx or oesophagus, while expectoration is the expulsion of material from the respiratory tract associated with coughing.
2
Q
What is the pathophysiology of regurgitation?
A
The oesophagus is a long tubular organ bordered by the upper oesophageal sphincter and lower oesophageal sphincter. During swallowing, the upper oesophageal sphincter relaxes to allow passage of food or liquid into the proximal oesophagus. Primary and secondary peristaltic waves move the food towards the stomach. Diseases that interrupt this process can result in regurgitation.
3
Q
What are the clinical signs of regurgitation?
A
The regurgitant may include undigested food, digested food, or clear, frothy fluid. Weight loss and polyphagia may occur. Signs of aspiration pneumonia including lethargy, anorexia, cough, or dyspnoea may be present. Cervical oesophagus dilation and neurological abnormalities may also be observed.
4
Q
What are the differential diagnoses for regurgitation?
A
Possible differential diagnoses for regurgitation include oesophageal disorders (megaoesophagus, oesophagitis, obstruction), alimentary disorders (pyloric outflow obstruction, hiatal hernia, gastric dilatation volvulus), neurologic disorders (central nervous system, peripheral neuropathy, dysautonomia), neuromuscular disorders (myasthenia gravis, botulism, tetanus, acetylcholinesterase toxicity), immune-mediated disorders, and endocrine disorders (hypothyroidism, hypoadrenocorticism).
5
Q
What is the primary goal in managing regurgitation?
A
The primary goal is to provide adequate nutrition while managing the underlying disease process. In cases of primary megaoesophagus or oesophageal dysmotility, the management focuses on diet and feeding strategies, as well as potential gastrostomy feeding tube placement.
6
Q
What are the recommended feeding strategies for managing regurgitation?
A
Patients should be fed small, frequent high-calorie meals. The consistency of the food may vary from chunky food or meatballs to a liquefied diet. Adding a tasteless thickening agent to drinking water can be attempted. Keeping the pet upright during and after feedings, using a Bailey chair or manual support, and gentle coupage may help with food movement. Some patients may require gastrostomy feeding tube placement.
7
Q
Which medications are commonly used in the treatment of regurgitation?
A
Prokinetic drugs like cisapride and metoclopramide are controversial in dogs but may be effective in cats. Bethanechol may be effective in some dogs. Gastroprotective therapy to decrease stomach acidity (proton pump inhibitors, H2-receptor antagonists) and mucosal protectants (sucralfate) should be used in all cases.
8
Q
What are the clinical signs of hiatal hernias?
A
The most common clinical signs of hiatal hernias are intermittent regurgitation, vomiting, and hypersalivation, often precipitated by excitement or exercise. Dyspnoea and coughing may occur with severe herniation or aspiration pneumonia.
9
Q
How can hiatal hernias be diagnosed?
A
Survey thoracic radiographs should be obtained in all dogs with suspected hiatal hernia. A dynamic barium procedure (videofluoroscopy) is far more likely to identify intermittent herniation of the stomach and can allow assessment of oesophageal motility. Oesophagoscopy can also be used to diagnose sliding hiatal hernia.
10
Q
What is the recommended medical therapy for hiatal hernias?
A
Proton pump inhibitors such as omeprazole are superior acid suppressants compared to H2-receptor antagonists and should be administered with sucralfate suspension to afford greater mucosal cytoprotection.
11
Q
How can normal hiatal anatomy be restored in dogs with large congenital hiatal hernias?
A
Normal hiatal anatomy can be restored by diaphragmatic crural apposition, oesophagopexy, and left fundic tube gastropexy techniques.
12
Q
What is cricopharyngeal dysphagia and how is it characterized?
A
Cricopharyngeal dysphagia is a rare congenital or acquired neuromuscular disorder of the upper oesophageal sphincter (UOS). It is characterized by achalasia (failure of relaxation) of the UOS or a lack of coordination between relaxation of the UOS relaxation and pharyngeal contraction (asynchrony).
13
Q
What are the clinical signs of cricopharyngeal dysphagia?
A
Affected animals demonstrate progressive dysphagia (typically worse when drinking water) at the time of, or shortly after, weaning. Clinical signs are characterized by repeated attempts to swallow, gagging, retching, and nasal regurgitation due to food or fluid accumulation within the pharynx.
14
Q
How is cricopharyngeal dysphagia diagnosed?
A
Video fluoroscopy is necessary to confirm the diagnosis by demonstrating the reflux of contrast material and the inability of the upper oesophageal sphincter to relax properly.
15
Q
What is the treatment for cricopharyngeal dysphagia?
A
Surgical myotomy or myectomy of the cricopharyngeal muscle is considered as the treatment for cricopharyngeal dysphagia.
16
Q
What are some possible causes of dysphagia in cats?
A
Possible causes of dysphagia in cats include structural abnormalities such as oral tumors, ulcers, or stomatitis, as well as neurologic disorders, neuromuscular disorders, and nervous system diseases like neuropathy.
17
Q
What are some possible causes of dysphagia in dogs?
A
Possible causes of dysphagia in dogs include neurologic disorders, neuromuscular disorders, obstruction by a foreign body, neoplasia, inflammatory conditions, trauma, and pain.
18
Q
What are some differential diagnoses for dysphagia?
A
Some differential diagnoses for dysphagia include obstructive lesion (anatomic or mechanical), foreign bodies, neoplasia, inflammatory conditions, lymphadenopathy, sialocoele, lingual frenulum disorder, cricopharyngeal achalasia/asynchrony, cleft palate, TMJ disorder, trauma, pain, periodontal diseases, stomatitis, glossitis, pharyngitis, and neurologic disorders.
19
Q
What diagnostic tests can be done to evaluate dysphagia?
A
Diagnostic tests that can be done to evaluate dysphagia include history and physical examination, complete blood count and serum chemistry profile, thyroid testing, urinalysis, survey radiographs of the head, neck, and thorax, acetylcholine receptor antibody titre (if myasthenia gravis is suspected), endoscopy, contrast videofluoroscopy motion studies, and muscle biopsy.
20
Q
What is Creatine Kinase (CK) and what does an increase in CK indicate in dysphagia cases?
A
Creatine Kinase (CK) is an intracellular enzyme found in high concentrations in muscle cells and within the brain. An increase in CK in dysphagia cases can indicate the presence of a myopathy.
21
Q
What are some possible complications of dysphagia?
A
Some possible complications of dysphagia include aspiration pneumonia, which should be addressed in the treatment plan.
22
Q
What dietary modifications can be attempted in the treatment of dysphagia?
A
In the treatment of dysphagia, dietary modifications such as changes in food consistency (liquid, solid), meal frequency (smaller, more frequent), and feeding positions (upright) can be attempted.
23
Q
When might placement of a feeding tube become necessary in the treatment of dysphagia?
A
Placement of a feeding tube may become necessary in the treatment of dysphagia if dietary adjustments are not providing adequate caloric intake for the patient.
24
Q
How are smaller foreign bodies best removed?
A
Smaller foreign bodies are best removed with a flexible endoscope and basket, biopsy forceps, or snare retrieving forceps.
25
How can fish-hooks lodged in the proximal to mid-oesophagus be dislodged?
Fish-hooks that are lodged in the proximal to mid-oesophagus can be dislodged with the distal end of a rigid endoscope by inserting the open end of the scope between the shaft and hook portion and pushing aborally.
26
What can be done to temporarily bypass the oesophagus during feedings in animals with severe oesophagitis or necrosis?
A gastrostomy tube can be inserted during foreign body removal in animals with severe oesophagitis or necrosis to temporarily bypass the oesophagus during feedings.
27
What is the specific therapy for oesophagitis after foreign body removal?
Specific therapy for oesophagitis should include sucralfate suspensions and proton pump inhibitors for 7-10 days following removal of the foreign body.
28
When is oesophagotomy indicated during foreign body removal?
Oesophagotomy is indicated if endoscopy fails to remove the foreign body; however, it is preferable to attempt to push the foreign body into the stomach for removal via gastrotomy.
29
What are the clinical signs of a vascular ring anomaly?
Affected puppies and kittens usually present for regurgitation of solid foods at the time of weaning. Weight loss with failure to thrive despite a good appetite is commonly observed. The presence of a moist cough, dyspnoea, and fever suggest aspiration pneumonia. Physical examination often reveals a thin, stunted animal that is otherwise normal. Occasionally, a dilated oesophagus can be observed or palpated in the cervical region.
30
What can focal leftward deviation of the trachea near the cranial border of the heart be caused by in young dogs?
Reliable sign of Persistent right aortic arch (PRAA) in young dogs.
31
How can an oesophagram help in diagnosing vascular ring anomalies?
An oesophagram may be performed to confirm the location of oesophageal obstruction and the severity of oesophageal distension.
32
What is cricopharyngeal achalasia?
Cricopharyngeal achalasia is a condition characterized by dysfunction or inability of the cricopharyngeal muscle to relax, leading to difficulty in swallowing.
33
What are the two approaches for the treatment of cricopharyngeal achalasia?
The two approaches for the treatment of cricopharyngeal achalasia are the standard ventral midline approach with 180° rotation of the larynx and the lateral approach with 90° rotation of the larynx.
34
What is the procedure involved in cricopharyngeal myotomy?
Cricopharyngeal myotomy involves transecting the cricopharyngeal muscle to the level of the pharyngeal mucosa.
35
What is the benefit of using a closed endoscopic CO2 laser cricopharyngeal myotomy?
The closed endoscopic CO2 laser cricopharyngeal myotomy is being increasingly utilized due to reduced anesthesia time and morbidity compared to the traditional transcervical cricopharyngeal myotomy.
36
What is botulinum toxin and how is it used in the temporary management of cricopharyngeal achalasia?
Botulinum toxin is a neurotoxin synthesized from the bacillus Clostridium botulinum. It is injected into the cricopharyngeus muscle in 3 sites using a transbronchial needle. It weakens muscle contraction and provides temporary relief from cricopharyngeal achalasia.
37
What is the limited duration of botulinum toxin's effect?
The effect of botulinum toxin lasts for about 3-4 months.
38
How can the effect of botulinum toxin be used to screen dogs for a permanent surgical myectomy?
The limited duration of botulinum toxin's effect can be used to identify dogs that might benefit from a permanent surgical myectomy. Animals that respond favorably to the toxin should do well with surgical myectomy.
39
What is the purpose of adding commercial food thickeners such as 'Thick-It' in the management of cricopharyngeal achalasia?
Adding commercial food thickeners can help identify the optimal consistency of food and water for dogs with cricopharyngeal achalasia.
40
What are the four main types of dysphagia?
The four main types of dysphagia are oral dysphagia, pharyngeal dysphagia, cricopharyngeal dysphagia, and oesophageal dysphagia.
41
What are the causes of dysphagia?
The causes of dysphagia can be associated with neurological or muscular abnormalities, neoplasms, foreign bodies, strictures, or traumas.
42
What is oral dysphagia characterized by?
Oral dysphagia is characterized by abnormalities with prehension, mastication, lubrication, and transportation of food from the tongue to the pharynx.
43
What are some possible causes of oral dysphagia?
Mechanical interference, foreign bodies, fractures, periodontal disease, stomatitis, gingivitis, tumours, or neurological defects involving the cranial nerves can cause oral dysphagia.
44
What is pharyngeal dysphagia characterized by?
Pharyngeal dysphagia is characterized by the inability to propel the food bolus from the oropharynx, through the hypopharynx, and to the proximal esophagus.
45
What are some common causes of pharyngeal dysphagia?
Common causes of pharyngeal dysphagia include neuropathy of cranial nerves V, VII, or XII, neoplasia, or pharyngeal dysfunction.
46
What is cricopharyngeal dysphagia?
Cricopharyngeal dysphagia is the abnormal transportation of a bolus through the proximal esophageal sphincter, either due to inadequate opening/relaxation or abnormal timing of its opening/relaxation.
47
What are some possible causes of cricopharyngeal dysphagia?
Cricopharyngeal dysphagia can be caused by neuromuscular diseases like myasthenia gravis, hypoadrenocorticism, or hypothyroidism, and it can also be a heritable trait in certain breeds like the Golden Retriever.
48
What are the clinical signs that can help differentiate regurgitation from dysphagia and vomiting?
The clinical signs that can help differentiate regurgitation from dysphagia and vomiting are: oropharyngeal regurgitation, abdominal effort, prodromal nausea, character of food ejected, timing of food ejected, swallow attempts after a single bolus, ability to drink, and pain on swallowing.
49
What should be performed before investigating oesophageal disease?
Before investigating oesophageal disease, a complete history should be taken, followed by a thorough physical examination, neurological examination, routine haematology and biochemistry tests, and plain and contrast radiography.
50
What can be revealed by plain and contrast radiography in patients with oesophageal disease?
Plain and contrast radiography can reveal oesophageal foreign bodies, megaoesophagus, strictures, thoracic masses, hiatal and diaphragmatic hernias. It can also show complications such as aspiration pneumonia or pneumothorax.
51
What is the best method for visualizing intraluminal disorders in the oesophagus?
Endoscopy is the best method for visualizing intraluminal disorders in the oesophagus, including foreign bodies, oesophagitis, strictures, neoplasia, and gastroesophageal reflux.
52
What tests can be considered for diagnosing oesophageal disease?
Tests that can be considered for diagnosing oesophageal disease include ACTH stimulation test, T4/TSH test, acetylcholine receptor antibodies test, and the Tensilon test.
53
What is oesophagitis?
Oesophagitis is an acute or chronic inflammatory disorder of the oesophageal mucosa that can cause a secondary motility disorder and regurgitation.
54
What is the most common cause of high-grade oesophagitis and stricture formation in dogs?
Gastroesophageal reflux during anesthesia represents the most common cause of high-grade oesophagitis and stricture formation in dogs.
55
What are the clinical signs of oesophagitis?
The clinical signs of oesophagitis can include anorexia, dysphagia, odynophagia, regurgitation, hypersalivation, and coughing (with concurrent aspiration pneumonia).
56
What is the chemoreceptor trigger zone (CRTZ) and where is it located?
The CRTZ is a region in the floor of the fourth ventricle and it lacks a blood-brain barrier, allowing it to sample chemical stimuli in the blood.
57
What are the dominant receptors in the CRTZ?
The dominant receptors in the CRTZ are serotonin type 3 (5-HT3) receptors and dopamine type 2 (D2) receptors.
58
Where are the peripheral receptors that initiate vomiting stimuli?
Peripheral receptors that initiate vomiting stimuli are found throughout the body, including in the duodenum, peritoneum, bile ducts, uterus, prostate, and kidneys.
59
What role does vestibular stimulation play in vomiting?
Vestibular stimulation feeds into the CRTZ before activating the emetic centre in dogs, but it appears to act directly on the emetic centre in cats.
60
Which receptors are found on the smooth muscle of the gastrointestinal tract and vagal afferent neurons?
5HT3 and NK1 receptors are found on the smooth muscle of the gastrointestinal tract and vagal afferent neurons.
61
What drug is a potent stimulator of emesis in dogs but has little to no effect in cats?
Apomorphine is a potent stimulator of emesis in dogs but has little to no effect in cats.
62
What type of receptors are more important in emesis in cats?
Alpha2 receptors are more important in emesis in cats, as demonstrated by the effectiveness of xylazine, an alpha2 agonist, as an emetic in cats.
63
What are some possible causes or aetiologies of vomiting?
Possible causes or aetiologies of vomiting include metabolic/endocrine disorders, intoxicants, drugs, abdominal disorders, dietary causes, gastric disorders, disorders of the small intestine, disorders of the large intestine, and central nervous system disease.
64
What is the definitive therapy for Persistent Right Aortic Arch (PRAA)?
The definitive therapy for PRAA is surgical ligation and transection of the ligamentum arteriosum via a left intercostal approach.
65
What is the recommended treatment for animals with severe debilitation from malnutrition due to PRAA?
Animals with severe debilitation from malnutrition will require enteral nutritional support via gastrostomy tube feedings prior to surgery.
66
What is the most common cause of regurgitation in dogs?
Megaoesophagus is the most common cause of regurgitation in dogs.
67
Which breeds are predisposed to congenital idiopathic megaoesophagus in dogs?
Familial predisposition has been suggested in the Irish Setter, Great Dane, German Shepherd, Labrador Retriever, Chinese Shar-Pei, Newfoundland, Miniature Schnauzer, and Fox Terrier breeds.
68
In which breed of cats is congenital megaoesophagus more commonly seen?
Congenital megaoesophagus in cats is rare, although Siamese cats are predisposed.
69
What is the underlying cause of acquired secondary megaoesophagus (ASM)?
The underlying cause of ASM is unknown, but a defect in the afferent neural response leading to reduced responsive to oesophageal distension is suspected.
70
What is the major cause of ASM in dogs?
Myasthenia gravis accounts for 25-30% of ASM in dogs.
71
What are some diseases that could cause an acquired secondary megaoesophagus?
Some diseases that could cause an acquired secondary megaoesophagus include Systemic Lupus Erythematosus (SLE), Polymyopathies, Polyneuropathies, botulism, distemper, neoplasia, severe oesophagitis, Addison’s disease, thymoma, pituitary dwarfism, lead toxicity.
72
What are some distinguishing factors between vomiting and regurgitation?
Some distinguishing factors between vomiting and regurgitation include the presence of prodromal signs of nausea, abdominal contractions (retching), and the presence of bile in vomit episodes.
73
What do owners typically report when their pet regurgitates?
Owners typically report that the animal simply lowers its head and material is expelled during regurgitation.
74
Can bile be present in regurgitation?
In rare instances, bile may be present in regurgitation due to reflux of bile from the stomach into the esophagus prior to regurgitation.
75
What are the distinguishing factors in the material produced during vomiting and regurgitation?
During vomiting, animals may produce undigested food or digested-appearing food. Regurgitation may also involve the regurgitation of digested-appearing food.
76
What should be considered if there is uncertainty in distinguishing vomiting from regurgitation?
If there is uncertainty in distinguishing vomiting from regurgitation based on the episode description alone, the rest of the history and physical examination should be used for further evaluation.
77
What is the timing of the episodes relative to feeding in vomiting and regurgitation?
Both vomiting and regurgitation can occur anytime relative to feeding.
78
What does the dipstick analysis of vomit reveal?
The dipstick analysis of vomit can reveal a pH level of ≤5 or ≥8 and the presence or absence of bile.
79
What is the key difference in abdominal contractions between vomiting and regurgitation?
Abdominal contractions (retching) are usually present during vomiting, while they are not usually present during regurgitation.
80
What is the definitive diagnostic procedure for oesophageal stricture?
Oesophagoscopy
81
What are the clinical signs of oesophageal stricture?
Progressive regurgitation, dysphagia, odynophagia, regurgitation, salivation, anorexia, coughing, and weight loss.
82
How can oesophagitis be diagnosed?
Oesophagitis can be diagnosed through endoscopy and oesophageal biopsy or by observing the appearance of the oesophageal mucosa.
83
What can be used to increase lower oesophageal sphincter pressure and enhance gastric emptying?
Prokinetic agents such as cisapride or metoclopramide.
84
What is the purpose of using proton pump inhibitors (PPIs) in the treatment of oesophagitis?
PPIs are used to suppress gastric acid and have superior acid suppressive effects compared to H2-receptor antagonists.
85
What is the most common cause of oesophageal strictures?
Oesophageal strictures are most commonly caused by Gastro-oesophageal Reflux (GOR) during general anaesthesia.
86
How are benign strictures treated?
Benign strictures are best treated by mechanical dilation using balloon dilation.
87
What is the purpose of sucralfate in managing reflux oesophagitis?
Sucralfate binds to damaged and eroded oesophageal mucosa, providing an effective protective barrier.
88
How is the position of the balloon catheter visualized during the dilation procedure?
The position of the balloon catheter is visualized through the endoscope or via fluoroscopy.
89
What is the purpose of using an inflating device with a manometric pressure gauge during balloon dilation?
The purpose is to slowly increase the pressure to the specified level recommended by the manufacturer.
90
What is the recommended duration for keeping the balloon inflated during the stricture dilation?
The balloon is kept inflated for 60-90 seconds.
91
What are the potential complications of dilatation techniques?
The potential complications include bleeding and the risk of perforation.
92
What is the role of transendoscopic administration of triamcinolone in the stricture dilation procedure?
It has been associated with a reduced rate of re-stricture formation.
93
What technique can be used to administer triamcinolone into the submucosa of the stricture site?
The transbronchial aspiration needle can be threaded down the biopsy channel of the endoscope.
94
Which medication, when applied topically at the stricture site, has been shown to be beneficial for preventing re-stricture?
Topical mitomycin C (5 mg of mitomycin C using a soaked gauze sponge that is placed endoscopically).
95
What is the success rate of treatment by dilation for oesophagitis?
Studies indicate a success rate of 77-88% for treatment by dilation.
96
What diagnostic test should be done to screen for causes of Acquired Secondary Megaoesophagus?
An AChR antibody titre for acquired Myasthenia Gravis
97
When should the AChR antibody titre test be repeated in dogs with an initial titre in the 'grey-zone'?
4-8 weeks later
98
What diagnostic procedures should be considered based on the individual case presentation?
Oesophagoscopy, electromyography, nerve conduction velocity, and muscle and nerve biopsy
99
Is there a proven association between megaoesophagus and hypothyroidism?
No
100
What is the treatment of idiopathic megaoesophagus and acquired forms that fail to respond to specific medical therapy?
Supportive and symptomatic
101
What feeding position should be recommended to assist passage of ingesta into the stomach?
Elevated or upright position (e.g., Bailey chair)
102
What is the most common form of hiatal hernia?
Type I sliding hiatal hernia
103
Which breeds have documented congenital sliding hiatal hernias?
Chinese Shar-Pei, Chow Chow, English Bulldogs, French Bulldogs, Pugs, and Boston Terriers
104
What is the first phase of swallowing called?
Oral preparatory phase
105
Which cranial nerves are involved in the oral phase of swallowing?
Cranial nerves V, VII, and XII
106
What happens during the pharyngeal phase of swallowing?
The soft palate elevates, larynx and hyoid move forward, epiglottis retroflexes, vocal folds close, and muscles of the pharynx contract.
107
Which cranial nerves are involved in the pharyngeal phase of swallowing?
Cranial nerves V, VII, IX, and X
108
What is the last phase of swallowing called?
Oesophageal phase
109
Which cranial nerve is involved in the oesophageal phase of swallowing?
Cranial nerve X
110
What is dysphagia defined as?
Difficulty swallowing
111
What are some potential causes of delayed gastric emptying?
Delayed gastric emptying can be caused by gastric outflow obstruction or gastric hypomotility.
112
What should be included in the dietary history when evaluating a vomiting patient?
A complete dietary history should be obtained, including past and current diets. Recent diet changes or opening a new bag or can of food may be the cause of vomiting.
113
What should be considered when assessing the patient's medication history?
The medication history should include information about drugs, supplements, nutraceuticals, and alternative therapies that could be associated with vomiting.
114
What are some important factors to consider when evaluating the patient's physical examination?
During the physical examination, important factors to consider include patient demeanor, body condition, posture, oral examination, assessment of each body system, vital signs, percentage dehydration, and abdominal palpation for evidence of pain, effusion, or organomegaly.
115
What investigations are usually performed for a vomiting patient with mild clinical signs?
For a vomiting patient with mild clinical signs, a minimalistic approach is usually appropriate. Faecal examination may identify parasitic causes of vomiting. Abdominal radiographs are performed if there is a clinical suspicion of surgical disease or if vomiting does not resolve with initial treatment.
116
What can abdominal radiographs help identify in a vomiting patient?
Abdominal radiographs can help identify surgical diseases such as suspected foreign body ingestion or conditions where vomiting does not resolve with initial treatment.
117
What are some clinical signs of GDV?
Some clinical signs of GDV include anxiety and looking at the abdomen, standing and stretching, drooling, distended abdomen, unproductive retching, weakness, and collapse.
118
What are some common findings on clinical examination of a GDV patient?
Common findings on clinical examination of a GDV patient include tachycardia, pallor of the mucous membranes, weak pulses, and possible abdominal distension.
119
What are the typical hematologic changes seen in a GDV patient?
The hematologic changes in a GDV patient are usually restricted to an increase in packed cell volume associated with hypovolemia, and a stress leukogram may also be present.
120
What acid-base disturbance is commonly seen in a GDV patient?
Metabolic acidosis is the most common acid-base disturbance seen in a GDV patient, and hypokalemia is usually present as well.
121
What are some common clinicopathologic findings on bloodwork of a GDV patient?
Common clinicopathologic findings on bloodwork of a GDV patient include pre-renal azotemia secondary to systemic hypotension, increased serum ALT and AST levels due to hypoxic damage, and elevated total bilirubin levels due to cholestasis.
122
Why is it important to measure plasma lactate in a GDV patient?
Measuring plasma lactate levels in a GDV patient can help determine the presence of gastric necrosis, prognosis, and the need for aggressive therapy. A good finding is a decrease of more than 43-50% within 12 hours.
123
What changes can occur to the coagulation profile in a GDV patient?
As the condition progresses, changes to coagulation factors can occur, including thrombocytopenia, prolonged PT and/or APTT, and increased levels of fibrinogen, which suggest the development of disseminated intravascular coagulation.
124
What imaging technique is used to confirm a GDV and differentiate between torsion and dilation?
Radiography is used to confirm a GDV and differentiate between torsion and dilation. Right lateral radiographs typically reveal a gas-filled fundus and a separate gas-filled structure above the fundus known as the pylorus (appearing as a 'double bubble'). A soft tissue band separating the two gas-filled compartments is highly supportive of GDV.
125
What are the techniques commonly used for gastropexy?
The techniques commonly used for gastropexy are belt-loop gastropexy and incisional gastropexy.
126
What post-operative complications can occur after a splenectomy?
Post-operative complications after a splenectomy can include ventricular dysrhythmias, gastrointestinal hypomotility, electrolyte disturbances (specifically hypokalaemia), aspiration pneumonia, gastritis, peritonitis, reperfusion injury, Disseminated Intravascular Coagulation (DIC), Thromboembolic disease (PTPE), and systemic Inflammatory response Syndrome (SIRS).
127
What should be included in the post-operative management for patients with gastric dilatation-volvulus (GDV)?
The post-operative management for patients with GDV should include intensive nursing care monitoring vitals, urine output, and weight; analgesia with opioids; gastroprotectants; gastric motility enhancers (such as metoclopramide); fluids; feeding with a highly digestible and energy dense product; ECG monitoring; blood pressure monitoring; and electrolyte, haematology, acid base status, and coagulation testing (if concerns over DIC).
128
What is the overall mortality rate of patients with GDV?
The overall mortality rate of patients with GDV is 10-15%.
129
What are the types of gastric neoplasms that can occur in dogs and cats?
The types of gastric neoplasms that can occur in dogs and cats include leiomyosarcoma, lymphoma, fibrosarcoma, rare anaplastic sarcoma, gastric extramedullary plasmacytoma, adenocarcinoma, squamous cell carcinomas, mast cell tumors, gastrointestinal stromal tumors (GIST tumors), polyps, and leiomyomas.
130
What is the most common gastric neoplasm in dogs?
The most common gastric neoplasm in dogs is malignant adenocarcinoma, accounting for 47-72% of all canine gastric malignancies.
131
What is the most common gastrointestinal neoplasm in both cats and dogs?
The most common gastrointestinal neoplasm in both cats and dogs is lymphoma.
132
What is the difference between small-cell lymphoma and large-cell lymphoma in feline gastric lymphoma?
In feline gastric lymphoma, small-cell lymphoma is more localized to the GI tract and carries a better prognosis than large-cell lymphoma.
133
What is the recommended dosage of prednisolone for treating gastritis?
The recommended dosage of prednisolone for treating gastritis is 1 to 2 mg/kg/day PO, tapered to every other day at the lowest dosage that maintains remission over 8 to 12 weeks.
134
When can a combination of a test diet and prednisolone be started in patients with moderate to severe lymphoplasmacytic gastritis?
A combination of a test diet and prednisolone can be started in patients with moderate to severe lymphoplasmacytic gastritis if they are HLO-free and show no evidence of lymphoma on gastric biopsies.
135
What may be instituted if ulceration or erosion is detected in gastritis patients?
Antacids and mucosal protectants may be instituted if ulceration or erosion is detected in gastritis patients.
136
Which medications can be used as adjunctive prokinetic agents for delayed gastric emptying?
Metoclopramide, cisapride, and erythromycin can be used as adjunctive prokinetic agents for delayed gastric emptying.
137
What is the safer alternative to azathioprine in cats for managing inflammatory bowel disease and small-cell lymphoma?
Chlorambucil is a safer alternative to azathioprine in cats for managing inflammatory bowel disease and small-cell lymphoma.
138
How is diffuse eosinophilic gastritis of undefined aetiology usually approached?
Diffuse eosinophilic gastritis of undefined aetiology is usually approached as described for lymphoplasmacytic gastritis.
139
What is the treatment for antral hypertrophy in brachycephalic dogs?
Antral hypertrophy in brachycephalic dogs is treated with surgery.
140
What are some risk factors for developing gastric dilatation and volvulus (GDV)?
Some risk factors for developing GDV include advancing age, lean body condition and deep/narrow thoracic conformation, first-degree relative with a history of GDV, stress and aggressive/fearful behavior, once daily feeding, rapid consumption of dry food, previous splenic disease, and increased gastric ligament laxity. Certain breeds also have a higher risk of GDV.
141
According to the course notes, is there any conclusive evidence to show that one PPI is clinically more effective than another for the treatment of gastric ulceration in dogs or cats?
No, there is no conclusive evidence in dogs and cats to show that one PPI is clinically more effective than another for the treatment of gastric ulceration.
142
Based on evidence from studies in humans and research animals, how often should PPIs be administered for treating acid-related gastric ulceration?
Based on evidence from studies in humans and research animals, PPIs administered twice daily are superior to other gastroprotectants for treating acid-related gastric ulceration.
143
What is the consensus opinion regarding the tapering of PPIs in dogs and cats after prolonged use?
The consensus opinion is that PPIs should be tapered in dogs and cats after prolonged use of >3-4 weeks.
144
According to the course notes, should PPIs be administered concurrently with other agents that require an acid milieu for oral absorption?
According to the course notes, PPIs should not be administered concurrently with other agents that require an acid milieu for oral absorption.
145
What are some of the cytoprotective effects of Misoprostol?
Misoprostol has cytoprotective effects caused by increased bicarbonate secretion, decreased pepsin content of gastric secretion, preservation of tight junctions among epithelial cells, increased mucus layer, increased mucosal blood flow, and improvement of mucosal regenerative capacity.
146
Is Misoprostol effective for preventing GUE associated with the administration of glucocorticoids in dogs and cats, according to the course notes?
According to the course notes, there is no evidence that Misoprostol decreases GUE from glucocorticoids in dogs and cats.
147
What is the mechanism of action of Sucralfate in acid-peptic disease?
The mechanism of action of Sucralfate in acid-peptic disease is multifactorial. It forms stable complexes with protein in damaged mucosa where there is a high concentration of protein.
148
According to the course notes, what is the comparative benefit of using Proton pump inhibitors (PPIs) and Sucralfate for management of GUE?
According to the course notes, Proton pump inhibitors (PPIs) are superior to Sucralfate for management of GUE.
149
What can cause the development of ulcers in the gastric mucosal barrier?
Severe insult to the mucosal barrier from drugs, foreign bodies, or neoplasia.
150
When acid reaches the submucosal layer, what happens?
Mast cells are degranulated and histamine is released.
151
What is the most predictable cause for gastric erosion and ulceration?
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) or glucocorticoids, either alone or in combination with intervertebral disc disease.
152
Which drugs can cause gastric erosions and ulcers in healthy dogs?
Flunixin meglumine, aspirin, and ibuprofen.
153
What are COX-2 selective agents and how are they different from other NSAIDs?
COX-2 selective agents are drugs that block 'inducible' cyclooxygenase (COX-2) and are less ulcerogenic in dogs. They include carprofen, meloxicam, deracoxib, and etodolac.
154
What are some risk factors for gastric erosion or ulceration?
Uraemia, hepatic failure, hypoadrenocorticism, hypotension, and high doses of glucocorticoids.
155
What clinical findings are associated with gastric erosions or ulcers?
Vomiting, haematemesis (frank blood or digested blood with a 'coffee ground' appearance), melaena, abdominal pain, and anaemia.
156
What can be observed in cats and dogs with chronic kidney disease (CKD) related gastric damage?
In dogs and cats with CKD, mucosal oedema, vasculopathy, and mineralization correlated to the degree of azotaemia and calcium phosphorus product can be observed.
157
What are some possible causes of gastritis in dogs and cats?
Possible causes of gastritis in dogs and cats include dietary allergy or intolerance, parasitism, reaction to bacterial antigens, and unknown pathogens.
158
What is the most common form of gastritis in dogs and cats?
The most common form of gastritis in dogs and cats is mild to moderate superficial lymphoplasmacytic gastritis with concomitant lymphoid follicle hyperplasia.
159
What is the prevalence of gastric Helicobacter spp. infection in healthy pet dogs?
Gastric Helicobacter spp. infection is highly prevalent in 67% to 100% of healthy pet dogs.
160
What are the potential pathogenic effects of gastric Helicobacter spp. infection in dogs and cats?
The pathogenicity of gastric Helicobacter species is largely unknown in veterinary medicine.
161
How should symptomatic patients with biopsy-confirmed Helicobacter spp. infection and gastritis be treated?
Symptomatic patients with biopsy-confirmed Helicobacter spp. infection and gastritis should be treated with a combination of metronidazole, amoxicillin, and famotidine.
162
What are the recommended treatments for lymphocytic-plasmacytic gastritis?
Mild lymphoplasmacytic gastritis without follicular hyperplasia and evidence of Helicobacter like organisms (HLO) should be initially treated with diet, including novel protein sources or commercial hydrolysed diets.
163
What substances may be present in diets used to treat lymphocytic-plasmacytic gastritis?
Diets used to treat lymphocytic-plasmacytic gastritis may contain substances such as menhaden fish oil or antioxidants that can potentially alter inflammation.
164
What was the response rate of dogs and cats to treatment with metronidazole, amoxicillin, and famotidine?
In an uncontrolled clinical trial, clinical signs responded to treatment in 90% of 63 dogs and cats, with 74% of the re-endoscoped animals showing no evidence of Helicobacter spp. in gastric biopsies.
165
What are the factors that should be considered when adjusting the rate and volume of fluids during fluid therapy?
The rate and volume of fluids should be adjusted according to patient assessment, including heart rate, pulse quality, mucous membrane colour, and capillary refill time.
166
Why should hypokalaemia be carefully monitored and supplemented appropriately after fluid therapy?
Hypokalaemia is common after fluid therapy and should be carefully monitored and supplemented appropriately.
167
What type of analgesics should be titrated to effect in the case of GDV?
Opiate analgesics should be titrated to effect in the case of GDV.
168
What are the two methods for performing gastric decompression?
Gastric decompression can be performed by orogastric intubation with a well-lubricated stomach tube or a 16-g catheter can be used to trocarise the stomach.
169
What precautions should be taken when passing an orogastric tube for gastric decompression?
When passing an orogastric tube, measure the tube from the patient’s chin to their xiphoid prior to introducing the tube to prevent stomach perforation. Standing the dog on its hindlimbs can aid with placing the orogastric tube.
170
Where should percutaneous gastrocentesis be performed in the abdomen?
If percutaneous gastrocentesis is performed, it should be done on the right-hand side of the abdomen.
171
What are the two most common ECG abnormalities seen with GDV?
The two most common ECG abnormalities seen with GDV are Ventricular tachycardia and Ventricular premature complexes.
172
When should arrhythmias associated with GDV be treated?
Arrhythmias associated with GDV should be treated if associated with weakness, syncope, or heart rates >150 beats per minute.
173
What is the purpose of a homemade non-spicy, fat-restricted, bland diet?
The purpose is to introduce a diet that is easy on the stomach and helps resolve vomiting.
174
What are some examples of food that can be included in a homemade non-spicy, fat-restricted, bland diet?
Boiled chicken and rice, low-fat cottage cheese, and rice in a 1:3 ratio.
175
How should the food be given when introducing a homemade non-spicy, fat-restricted, bland diet?
The food should be given little and often.
176
What agents are often administered to pets with acute vomiting or diarrhea?
Bismuth subsalicylate (Pepto-Bismol), kaolin-pectin, sucralfate, activated charcoal, and magnesium, and aluminium- and barium-containing products.
177
What is the underlying cause for the development of gastric erosions and ulcers?
An imbalance between gastric acid secretion and gastric mucosal barrier protection.
178
What are the four main layers of the stomach?
Serosa, muscular layers, submucosa, and mucosa.
179
What cells can be found in the gastric pits of the fundic area of the stomach?
Parietal cells, chief cells, and mucosal neck cells.
180
What is the role of the pyloric sphincter?
The pyloric sphincter prevents solid food from entering the duodenum.
181
What tests can be done to identify systemic or metabolic diseases?
Complete blood count, serum biochemistry profile, and urinalysis
182
How can obstruction be diagnosed using intestinal radiographs?
Measurements can be taken to help diagnose obstruction by comparing the width of the look of the intestine with the height of the midbody of L5.
183
What discussions should be held with the owner prior to surgery for an obstruction?
Anaesthesia related complications, wound complications, intestinal dehiscence, peritonitis, and death should be discussed.
184
What diagnostic testing should be done for chronic vomiting if a cause is not found?
Ultrasonography, a bile acid profile, pancreatic lipase testing, and ACTH stimulation testing should be considered.
185
What are the clinical manifestations of gastric disease?
Vomiting, haematemesis, melaena, retching, burping, hypersalivation, abdominal distension, abdominal pain, or weight loss.
186
What is the diagnostic approach for primary gastric disease?
The diagnostic approach initially focuses on historical and physical findings, with clinicopathologic testing and diagnostic imaging employed in patients with systemic involvement or chronic signs.
187
How can signalment help in diagnosing gastric disorders?
Age and breed can be helpful in the diagnosis of certain gastric disorders.
188
What clinicopathologic tests can help differentiate primary GI disease from non-GI disease?
Blood and urine samples, rapid evaluation of microhaematocrit (PCV), total solids (TS), blood glucose, blood urea nitrogen (BUN), urine specific gravity, glucose, ketones and protein, and plasma concentrations of sodium (Na) and potassium (K) can help differentiate.
189
How rare are abnormalities in complete blood count (CBC) with primary gastric disease?
Abnormalities in complete blood count (CBC) are infrequent with primary gastric disease.
190
What are some clinical signs of gastric cancer in dogs?
Some clinical signs of gastric cancer in dogs include sudden anorexia, vomiting blood, and weight loss.
191
What are some clinical signs of gastric cancer in cats?
Some clinical signs of gastric cancer in cats include lethargy, anorexia, and rapid weight loss.
192
What physical examination findings may be present in cases of gastric cancer?
In some cases of gastric cancer, mild cranial abdominal discomfort may be present during physical examination.
193
What might be evident in the biochemistry results if ulceration is present?
If ulceration is present, hypoproteinaemia may be evident in the biochemistry results.
194
What imaging techniques can be used to assess gastric cancer?
Radiographs and ultrasound can be used for imaging in cases of gastric cancer.
195
What visual signs may indicate gastric adenocarcinoma during endoscopy and biopsy?
Visual signs of gastric adenocarcinoma during endoscopy and biopsy may include mottled and purple appearance to the mucosa, deep pigmentation of the mucosa, loss of normal stomach landmarks, ulceration, an obvious mass, rigidity, and boarding of the mucosa.
196
What should be done if severe gastritis is suspected during biopsy?
If severe gastritis is suspected during biopsy, multiple samples must be collected to gain representative samples and differentiate it from neoplasia.
197
What is the most common form of treatment for gastric cancer?
Surgery is the most common form of treatment for gastric cancer.
198
What are the possible causes of increased PCV and TS?
Dehydration
199
What is the possible cause of normal PCV and increased TS?
Hyperglobulinaemia
200
What is the possible cause of decreased PCV and normal TS?
Acute haemorrhage
201
What are the possible causes of decreased PCV and decreased TS?
Haemorrhage and anaemia + hypoproteinaemia
202
When are survey radiographs the test of choice?
When initially evaluating gastric disease, vomiting, or abdominal pain.
203
What can radiographs provide information on?
Gastric position and contents, size and shape of liver, kidneys, and spleen, detection of intussusception, peritonitis, pneumoperitoneum, and changes suggestive of pancreatitis.
204
What is the best method for diagnosing primary gastric inflammation, ulceration, or neoplasia?
Endoscopy
205
What is the term for the syndrome marked by vomiting of sudden onset presumed to be due to a gastric mucosal insult or inflammation?
Acute gastritis
206
What are the characteristics of microcytic, hypochromic anaemia?
Microcytic, hypochromic anaemia is associated with iron deficiency and usually indicates chronic bleeding.
207
What are the possible causes of elevated liver enzymes and bilirubin in patients with gastric ulcer?
Possible causes include liver disease or pancreatitis as the primary cause of ulceration.
208
What does hyponatraemia with hyperkalaemia, with or without azotaemia, suggest in relation to gastric ulcer?
It is highly suggestive of hypoadrenocorticism.
209
How can urine analysis be helpful in diagnosing gastric ulcer?
Urine analysis can help rule out urinary causes of anaemia or hypoalbuminemia and provide evidence of renal disease.
210
What imaging modality is recommended to assess gastric wall anatomy?
Ultrasonography is a better imaging modality for evaluating the gastric wall for thickening associated with ulcers or masses.
211
What is the definitive diagnostic aid for detecting a gastric ulcer?
Endoscopy is the definitive diagnostic aid for detection of a gastric ulcer.
212
What should be done when a concurrent gastric pathology is suspected during endoscopy?
Ulcers should be biopsied at the periphery to avoid perforation.
213
What is the recommended treatment for gastric erosions and ulcers?
Treatment is directed at the underlying cause and includes addressing hydration, perfusion, electrolytes, acid-base balance, and managing pain.
214
What are the three methods used to diagnose Giardia?
The three methods used to diagnose Giardia are: 1. Surface of intestinal biopsies, 2. Identification of oocysts in faeces by zinc sulfate flotation, 3. Giardia antigen by faecal ELISA tests.
215
What is the recommended treatment for Giardia?
The recommended treatment for Giardia is Metronidazole 25 mg/kg PO q 12 h for 5 days. Fenbendazole (50 mg/kg PO q 12 h for 3-5 days) can also be combined with Metronidazole.
216
What measures are advised for decontamination to prevent Giardia reinfection?
Decontamination of the patient’s coat by bathing and the patient’s environment by steam cleaning is advised to prevent Giardia reinfection.
217
What information is important to gather from the clinical examination and history taking of an intestinal patient?
From the clinical examination and history taking, it is important to gather information about the animal’s vaccination status, worming status, diet, the characteristics of the diarrhea, and whether the symptoms indicate a systemic or gastrointestinal disease.
218
What tests are used in the work-up of an intestinal patient?
The tests used in the work-up of an intestinal patient include serum biochemistry, hematology, fecal sampling, trypsin-like immunoreactivity (TLI) test, serum folate and cobalamin assay, intestinal ultrasound, abdominal radiography, and biopsy.
219
What conditions are commonly associated with chronic diarrhea?
The conditions commonly associated with chronic diarrhea include Exocrine Pancreatic Insufficiency (EPI), Antibiotic Responsive Diarrhea (ARD), Inflammatory Bowel Disease (IBD), Lymphangiectasia, and Protein Losing Enteropathies.
220
What are the different categories of chronic diarrhea?
The different categories of chronic diarrhea include diet-responsive, antibiotic-responsive, and steroid-responsive diseases.
221
What should be considered if the intestinal biopsy results are normal?
If the intestinal biopsy results are normal, Irritable Bowel Syndrome or Antibiotic Responsive Diarrhea need to be considered.
222
What is the most sensitive and specific test for Exocrine Pancreatic Insufficiency (EPI)?
Serum trypsin–like immunoreactivity (TLI) is the most sensitive and specific test for EPI.
223
What are the common symptoms of EPI?
Common symptoms of EPI include appetite and diarrhea or loosely formed feces that are yellow/grey and appear undigested.
224
What is the most common cause of EPI in dogs and cats?
Chronic pancreatitis is the most common cause of EPI in both dogs and cats, suspected to be the cause of EPI in nearly 100% of cats and in approximately 50% of dogs with EPI.
225
Which dog breeds are almost exclusively prone to pancreatic acinar atrophy, a major cause of EPI in dogs?
German Shepherd dogs, Rough-coated Collies, and Eurasians are almost exclusively prone to pancreatic acinar atrophy, which accounts for approximately 50% of EPI cases in dogs.
226
What are the major causes of non-Protein Losing Enteropathy (PLE) malabsorptive disease in dogs?
The major causes of non-PLE malabsorptive disease in dogs include dietary-responsive disease, antibiotic-responsive disease, and parasitic disease.
227
What are the most common causes of Protein Losing Enteropathy (PLE)?
The most common causes of PLE are lymphangiectasia, lymphoma, fungal infections, and Inflammatory Bowel Disease (IBD).
228
What diagnostic process should be followed in PLE cases?
PLE is a diagnosis of exclusion. If the patient does not have severe cutaneous disease, ruling out hepatic insufficiency and protein-losing nephropathy is necessary to diagnose PLE.
229
What is the next step in diagnostics if a 2- to 3-week therapeutic trial is not an option?
If a therapeutic trial is not possible, aggressive diagnostics should be considered, including abdominal ultrasound, abdominal radiographs, and intestinal biopsy (surgical or endoscopic).
230
What are the most common causes of protein-losing enteropathy (PLE) in adult canines?
The most common causes of PLE in adult canines are severe IBD, lymphangiectasia, and lymphoma.
231
What are the most common causes of protein-losing enteropathy (PLE) in cats?
Although PLE is rare in cats, IBD and lymphoma are the most likely causes.
232
What are the clinical signs of PLE in animals?
The clinical signs of PLE in animals include anorexia, history of chronic diarrhea and vomiting, severe weight loss, and signs of hypoproteinemia (ascites, subcutaneous edema, hydrothorax).
233
What are the possible diagnoses when hypoproteinemia is detected in an animal?
Possible diagnoses when hypoproteinemia is detected in an animal include malnutrition, severe burns, liver disease, renal disease, and protein-losing enteropathy (PLE).
234
What diagnostic procedure is recommended for confirming PLE in animals, and why?
A biopsy is required for a definitive diagnosis of PLE in animals. Low serum albumin levels do not make these patients good surgical candidates, so endoscopic biopsy is the least invasive technique available.
235
What is lymphangectasia?
Lymphangectasia is a condition characterized by dilation of the lymph vessels in the small intestine. It is one of the most common small intestinal diseases that presents with signs of protein-losing enteropathy.
236
What are the primary and secondary causes of lymphangectasia?
The primary cause of lymphangectasia is a congenital disease where the intestinal or systemic lymphatic system fails to develop properly. Secondary causes include intestinal inflammatory diseases (such as IBD), intestinal neoplasia, venous hypertension, congestive heart failure or portal vein thrombosis.
237
What are the clinical signs and diagnostic abnormalities associated with lymphangectasia?
The clinical signs of lymphangectasia include chronic diarrhea, vomiting, and ascites in advanced cases. Laboratory abnormalities include lymphopenia, low albumin, and low cholesterol.
238
What are the two types of dietary modification used in the treatment of IBD?
The two types of dietary modification used in the treatment of IBD are elimination diets using a novel protein and carbohydrate source and hydrolysed diets.
239
Why are hydrolysed diets often reserved for less severely affected cases of IBD?
Hydrolysed diets are often reserved for less severely affected cases of IBD because they have reportedly greater success, even in patients that have failed a trial with an antigen-limited exclusion diet.
240
What is the potential benefit of probiotics or prebiotics in targeting the pathogenesis of IBD?
The potential benefit of probiotics or prebiotics in targeting the pathogenesis of IBD is the modulation of the enteric flora.
241
Which probiotic strain has shown the most effect in the treatment of IBD?
The probiotic strain VSL#3 has shown the most effect in the treatment of IBD.
242
Why can antibiotics be justified in the treatment of IBD?
Antibiotics can be justified in the treatment of IBD partly to treat any secondary small intestinal bacterial overgrowth (SIBO) and partly because of the importance of bacterial antigens in the pathogenesis of IBD.
243
What is the most important treatment modality in idiopathic IBD?
Immunosuppression is the most important treatment modality in idiopathic IBD.
244
What is the recommended initial dosage of prednisolone for severe IBD?
The recommended initial dosage of prednisolone for severe IBD is 1-2 mg/kg PO q 12 h (2-4 mg/kg/day) for 2-4 weeks.
245
What is the purpose of cytotoxic drugs in the treatment of IBD?
Cytotoxic drugs can be added to the treatment of IBD to provide a steroid-sparing effect, especially if clinical signs of IBD recur consistently when the corticosteroid dosage is tapered.
246
What is the recommended dosage of ronidazole for young kittens or cats with hepatopathy?
The recommended dosage of ronidazole for young kittens or cats with hepatopathy is 10mg/kg once daily for two weeks.
247
When should ronidazole be prescribed?
Ronidazole should only be prescribed when there is a proven infection and not as a therapeutic trial.
248
Why should the powder form of ronidazole be placed in capsules prior to administration?
The bitterness of the powder means that it must be placed in capsules prior to administration.
249
What is the recommended duration of giving a probiotic or a synbiotic when treating with ronidazole?
It is recommended to give a probiotic or a synbiotic for four weeks starting on the same day as the ronidazole treatment.
250
Which types of tumors are commonly associated with the large intestine in dogs?
The most common canine colonic tumors are adenocarcinoma, lymphoma, leiomyosarcoma, adenoma, and adenomatous polyp.
251
Which breed(s) are over-represented in the occurrence of canine colonic tumors?
German Shepherds, Collies, and West Highland White Terriers are over-represented in the occurrence of canine colonic tumors.
252
In cats, what is more commonly observed in the large intestine, adenocarcinoma or lymphoma?
In cats, adenocarcinoma is more common (46%) than lymphoma (41%) in the large intestine.
253
What are the clinical signs of ileo-colic intussusception?
The clinical signs of ileo-colic intussusception include intermittent vomiting, loss of appetite, mucoid bloody diarrhea, a cylinder-shaped mass in the cranial abdomen, and abdominal pain.
254
What is megacolon?
Megacolon is a condition where the colon becomes significantly enlarged and loses its normal motility.
255
What are the two main causes of megacolon?
The two main causes of megacolon are colonic inertia (functional obstruction) and outlet obstruction (mechanical obstruction).
256
What is the most common cause of colonic inertia?
The most common cause of colonic inertia is idiopathic megacolon.
257
What is idiopathic megacolon in cats?
Idiopathic megacolon in cats is a disease where the colon loses its normal motility and becomes progressively larger.
258
What is the most common cause of outlet obstruction?
The most common cause of outlet obstruction is obstruction due to poorly healed pelvic fractures.
259
What are some other factors that can contribute to the development of megacolon or constipation?
Tumours, strictures, and hernias of the rectum/anus can also contribute to the development of megacolon or constipation.
260
How is idiopathic megacolon diagnosed?
Idiopathic megacolon is usually diagnosed based on the typical history of clinical signs, physical examination findings (distended colon with firm hard faeces), rectal examination, neurological examination, blood work, and abdominal radiographs.
261
What is the initial medical management for idiopathic megacolon?
The initial medical management for idiopathic megacolon includes hydration, enema, deobstipation, low-residue diet, and medications such as lactulose and cisapride.
262
What can cause damage to enterocytes without histologic damage?
Bacterial toxins, malnutrition, and ischaemia can cause damage to enterocytes without histologic damage.
263
What are the natural causes of decreased epithelial barrier function?
Luminal aggressive factors and endogenous inflammatory mediators are natural causes of decreased epithelial barrier function.
264
What are the consequences of barrier damage?
Barrier damage can lead to entry of antigens, allergic and/or inflammatory reactions, and translocation of bacteria into the circulation.
265
What is one substance that can increase intestinal permeability by damaging the barrier?
Nonsteroidal anti-inflammatory drugs (NSAIDs) can increase intestinal permeability by damaging the barrier.
266
What are the effects of villus atrophy?
Villus atrophy causes loss of intestinal surface area and results in fat malabsorption.
267
Which infectious agents can cause villus atrophy?
Rotavirus infects the villus tip, while coronavirus infects the midvillus, causing cell loss and mild to moderate diarrhea.
268
What can cause complete villus and crypt collapse and severe diarrhea?
Cytotoxic drugs (e.g., vincristine) and parvovirus infection can cause complete villus and crypt collapse and severe diarrhea.
269
What are some potential causes of ileus?
Functional abdominal surgery, ischemia, inflammatory conditions (such as pancreatitis and peritonitis), metabolic disturbances, neuromuscular causes, and physical obstructions can all cause ileus.
270
What are some examples of viral particles that can be identified using electron microscopy?
Some examples of viral particles that can be identified using electron microscopy are rotavirus, coronavirus, and parvovirus.
271
What tests are available for identifying parvovirus?
Faecal ELISA and PCR tests are available for identifying parvovirus.
272
What is hypocobalaminaemia and what is it specific for in dogs?
Hypocobalaminaemia is a condition of low cobalamin (vitamin B12) levels and it is relatively specific for small intestinal disease in dogs.
273
What are the implications of cats and dogs having less capacity to store cobalamin than humans?
Cats and dogs have less capacity to store cobalamin than humans, and cats also lack the binding protein transcobalamin I, leading to rapid loss of cobalamin through enterohepatic recycling.
274
What can severe cobalamin malabsorption do to cobalamin stores in cats?
Severe cobalamin malabsorption can deplete cobalamin stores in cats within a month.
275
Why is concurrent cobalamin supplementation necessary in patients with GI disease and cobalamin deficiency?
Concurrent cobalamin supplementation is necessary in patients with GI disease and cobalamin deficiency because they may not respond appropriately to treatment of the underlying disease process without it.
276
What does the presence of melaena in faeces indicate?
The presence of melaena in faeces, which is dark, tarry, oxidized blood, reflects either swallowed blood or generalized or localized GI bleeding proximal to the large intestine.
277
What can microcytosis with thrombocytosis on a complete blood count suggest?
Microcytosis with thrombocytosis on a complete blood count can suggest iron deficiency secondary to chronic blood loss.
278
What tests can be done to investigate cats with chronic colitis or constipation?
Faecal parasitology, Giardia testing, FeLV and FIV, serum thyroxine
279
In patients with haematochezia, dyschezia, or constipation, what imaging modality can potentially identify obstructions and megacolon?
Plain radiographs of the abdomen and pelvic region
280
What can survey radiographs potentially identify in patients with haematochezia, dyschezia, or constipation?
Radiopaque foreign bodies, faecal impaction, and extra-luminal causes of obstruction such as pelvic canal stenosis or prostatomegaly
281
How can a negative contrast colonogram help in determining the structure of the colon on radiographs?
By insufflating with air when the colon is empty, it can help identify the colon, as well as highlight colonic wall thickening and masses
282
What is the method of choice for visualizing the entire colon and obtaining mucosal biopsies in patients with large intestinal diarrhoea and/or haematochezia?
Flexible endoscopy (colonoscopy)
283
Why is surgery to obtain full-thickness colonic biopsies not recommended?
Because of the risks of wound dehiscence and septic peritonitis
284
What should be avoided when preparing a patient for colonoscopy?
Soap or laxatives as they may induce histological changes in the colonic mucosa
285
How long should dogs and cats ideally be fasted before colonoscopy?
36 to 48 hours
286
What is the name of the syndrome characterized by acute haemorrhagic diarrhoea in dogs?
Haemorrhagic Gastroenteritis (HGE)
287
What is the recently renamed name for Haemorrhagic Gastroenteritis (HGE)?
Acute haemorrhagic diarrhoea syndrome (AHDS)
288
Which breed of dogs is most frequently affected by acute haemorrhagic diarrhoea?
Small-breed dogs and especially Miniature Schnauzers
289
What are the clinical signs observed in dogs with Haemorrhagic Gastroenteritis (HGE)?
Acute haemorrhagic malodorous diarrhoea, sometimes vomiting, depressed mentation, and abdominal discomfort
290
What is the usual treatment for Haemorrhagic Gastroenteritis (HGE)?
Aggressive Intravenous fluid therapy
291
Which viral infections can cause enteritis and subsequent diarrhoea in dogs and cats?
Canine parvovirus infection, Feline parvovirus infection/panleukopenia, Canine and feline coronavirus infections, Feline immunodeficiency virus, Feline leukemia virus, Rotaviruses, Norovirus
292
How do Rotavirus and Coronavirus affect the small intestinal villi?
They cause villus atrophy, resulting in a loss of absorptive capacity for fluids and nutrients
293
What is the most appropriate method to detect bacterial pathogens in dogs and cats with diarrhoea?
Faecal culture
294
What can ultrasound reveal in cases of lymphoma?
Ultrasound may reveal intestinal wall thickening, a loss of layering, and enlarged mesenteric lymph nodes.
295
What diagnostic method can be used to gain biopsy samples in cases of lymphoma?
Endoscopy can be utilized to gain biopsy samples.
296
What is a useful prognostic indicator for cats with lymphoma?
A favorable initial response to chemotherapy is a useful prognostic indicator for cats.
297
In dogs, which type of lymphoma usually responds poorly to treatment?
Apart from rectal lymphoma, dogs usually respond poorly to treatment.
298
Where are adenocarcinomas usually seen in dogs and cats?
Adenocarcinomas are usually seen in the duodenum and colon in dogs, and the jejunum of cats.
299
What are some clinical signs of adenocarcinomas?
Clinical signs of adenocarcinomas include obstruction, melena or fresh blood in the feces, constipation, and diarrhea.
300
What is a characteristic finding in patients with large intestinal disease?
Presence of mucus in the feces is a characteristic finding in patients with large intestinal disease.
301
What other diagnostic should be considered if there is suspicion of pancreatitis in cases of large intestinal disease?
Pancreatic lipase immunoreactivity (PLI) measurement may be indicated if there is any suspicion of pancreatitis.
302
What are the possible diagnoses for small intestinal bacterial overgrowth (SIBO) and idiopathic antibiotic responsive diarrhea (ARD)?
The possible diagnoses for SIBO and ARD are Small Intestinal Bacterial Overgrowth and Idiopathic Antibiotic Responsive Diarrhea.
303
What is small intestinal bacterial overgrowth (SIBO)?
SIBO is an increase in the absolute number of bacteria in the upper small intestine during the fasted state.
304
What is the alternative name for small intestinal bacterial overgrowth (SIBO) in idiopathic cases?
The alternative name for SIBO in idiopathic cases is antibiotic-responsive diarrhea (ARD).
305
What are the clinical signs of idiopathic antibiotic-responsive diarrhea (ARD)?
The clinical signs of ARD include chronic intermittent diarrhea, weight loss, stunted growth, borborygmi, flatus, and vomiting.
306
What is the most reliable diagnostic test for ARD?
The most reliable diagnostic test for ARD is a response to empirical therapy.
307
What antibiotics can be used to control signs in idiopathic ARD?
Antibiotics such as oxytetracycline, metronidazole, and tylosin can be used to control signs in idiopathic ARD.
308
How long is the initial course of antibiotics given for idiopathic ARD?
The initial course of antibiotics is given for 4 to 6 weeks.
309
What is the recommended dose of tylosin for idiopathic ARD?
The recommended dose of tylosin for idiopathic ARD is 20 mg/kg PO q 8-12 h, but a reduced dose of 5 mg/kg has also been shown to be effective.
310
Define diarrhoea.
Diarrhoea is defined as an increase in faecal fluidity, faecal frequency, and in the volume of faeces.
311
What can cause diarrhoea in small intestinal disease?
Small intestinal disease can cause diarrhoea if the material from the ileum exceeds the absorptive capacity of the colon or causes colonic secretion of water.
312
Why does large intestinal disease commonly cause diarrhoea?
Large intestinal disease commonly causes diarrhoea because there is nothing distal to it to absorb water.
313
What is dysbiosis?
Dysbiosis describes the disturbance of the normal microbiome that can occur following infection, antibiotic usage, sudden dietary change, or due to underlying mucosal immuno-incompetence or inflammation.
314
What can result in fat malabsorption?
Interruption of normal enterohepatic circulation and lack of bile salts result in fat malabsorption.
315
What are primary brush border membrane diseases?
Primary brush border membrane diseases are biochemical abnormalities that occur in the absence of structural damage.
316
What is the mechanism of cobalamin deficiency seen in Chinese Shar-Peis with intestinal disease?
The mechanism of cobalamin deficiency has not been elucidated yet, but defects in cobalamin–intrinsic factor uptake in the ileum can be due to a mutation in the receptor molecule cubilin.
317
What can cobalamin malabsorption cause?
Cobalamin malabsorption can cause diarrhoea, as it results in histological abnormalities and dysfunction of the small intestine.
318
What is one limitation of using histology to diagnose dietary-responsive or antibiotic-responsive enteropathies?
Histology is not a good way to diagnose dietary-responsive or antibiotic-responsive enteropathies.
319
What are the cardinal signs of small intestinal disease?
The cardinal sign of small intestinal disease is diarrhea.
320
What are some nonspecific signs of small intestinal dysfunction?
Some nonspecific signs of small intestinal dysfunction include polyphagia, polydipsia, dehydration, peripheral edema, borborygmi, ascites, abdominal pain, coprophagia, pica, and anorexia.
321
What is the initial management approach for acute diarrhea?
The initial management of acute diarrhea is nonspecific and supportive.
322
When are antiemetics indicated in the treatment of acute diarrhea?
Anti-emetics are indicated if the patient is vomiting and an intestinal obstruction has been ruled out.
323
What are some treatment options for cases of acute small intestinal disease?
Some treatment options for cases of acute small intestinal disease include fluid therapy, dietary modifications, checking anti-parasitic history and administering treatment if appropriate, and prescribing antimicrobials when infectious agents have been confirmed.
324
What are prebiotics and probiotics used for in the treatment of small intestinal diseases?
Prebiotics are selective substrates used by 'beneficial' microbial species, while probiotics are microorganisms that encourage the growth of 'beneficial' gut organisms. The combined use of prebiotics with probiotics is known as synbiotics.
325
What is the recommended dietary approach for patients on long-term high dose antibiotics?
Patients should be placed on hydrolysed diets and prebiotics should be considered.
326
What should be periodically done to determine if long-term high dose antibiotic treatment is still required?
The treatment should be periodically stopped.
327
What are the clinical signs of Inflammatory Bowel Disease (IBD)?
Chronic vomiting, chronic diarrhea, weight loss, abdominal discomfort/pain, excessive borborygmi and flatus.
328
What is the most common histologic form of IBD?
Lymphocytic-plasmacytic enteritis (LPE).
329
What is the postulated cause of IBD?
IBD is postulated to be an immune mediated disease where the animal loses tolerance to the normal commensal bacterial species within the gut.
330
What diagnostic procedure is necessary for a diagnosis of intestinal inflammation in IBD?
Intestinal biopsy is necessary for a diagnosis of intestinal inflammation.
331
What diagnostic imaging method is superior to radiography for identifying small intestinal disease in IBD?
Ultrasonographic examination is superior to radiography for identifying small intestinal disease in IBD.
332
What limitations does endoscopy for intestinal biopsies have in diagnosing IBD?
Endoscopic biopsy samples only capture the mucosa, so it is possible to miss deeper lesions.
333
In which patients do colonic ulcers very rarely develop?
Colonic ulcers very rarely develop in patients with acute intervertebral disc disease or after spinal surgery.
334
Where do colonic ulcers tend to occur?
Colonic ulcers tend to occur in the proximal colon, especially at the left colic flexure.
335
What is the mechanism behind the development of colonic ulcers in these patients?
The mechanism is poorly understood, but it is believed that localized ischemia and increased intraluminal pressure of neurogenic origin are involved.
336
What complicates the understanding of the mechanism behind colonic ulcers in these patients?
The fact that many of these patients are also treated with glucocorticoids complicates the understanding of the mechanism.
337
How do glucocorticoids affect the development of colonic ulcers?
Glucocorticoids can reduce mucin production and impair healing, thus contributing to the development of colonic ulcers.
338
What are the initial symptoms of colonic ulceration?
Colonic ulceration initially causes haematochezia, which is the passage of blood through the rectum.
339
What can colonic ulcers eventually lead to?
Colonic ulcers can eventually lead to perforation and septic peritonitis.
340
What is the prognosis for patients with colonic ulcers?
The prognosis is poor for patients with colonic ulcers.
341
What is the definition of chronic diarrhea?
Chronic diarrhea is diarrhea that is not improving within 14 days or occurs over 3-4 weeks.
342
What are the expected symptoms of small bowel disease in chronically diseased patients?
Loss of body weight and/or condition are expected symptoms in small bowel disease.
343
What are the typical symptoms of large bowel disease?
Weight loss, haematochezia, and faecal mucus are typical symptoms in severe large bowel disease.
344
What symptoms may occur if the rectal area is affected?
Tenesmus may occur if the rectal area is affected.
345
When should diarrhea usually be attended to?
Diarrhea should usually be attended to if it has a relatively small set of testable differentials, is a predominant problem, or is likely to cause morbidity or mortality.
346
What initial diagnostics should be performed for a patient with chronic diarrhea?
Complete Blood Count, Biochemistry Profile, and Urinalysis should be performed as initial diagnostics.
347
What additional gastrointestinal specific evaluations may be required if initial tests are normal?
Faecal examination, serology, radiography, ultrasound, endoscopy, or exploratory laparotomy may be required.
348
When is culture of faeces indicated?
Culture of faeces is indicated in animals with haemorrhagic diarrhea or fever, inflammatory leukogram, or neutrophils on rectal cytology.
349
What is the recommended method for diagnosing Campylobacter infection in dogs and cats?
PCR from fresh faeces.
350
Are all Campylobacter species considered pathogenic in humans?
Yes.
351
In healthy animals, when should antimicrobial therapy for Campylobacter infection be reserved?
For cases where there could be contact with immunocompromised humans.
352
What is the zoonotic potential of Salmonella organisms?
Salmonella organisms have a zoonotic potential.
353
What are the clinical signs of a Salmonella infection in dogs?
Acute diarrhea (ranging from mild to severe and bloody), anorexia, fever, abdominal pain, and vomiting.
354
Why is antibiotic treatment not recommended for healthy infected animals or stable animals with just diarrhea caused by Salmonella?
Antibiotic treatment can promote bacterial resistance and a carrier state.
355
When should antibiotic treatment be considered for Salmonella infection in dogs?
In cases with severe hemorrhagic diarrhea, shock, persistent fever, or sepsis.
356
What is the recommended duration of antibiotic therapy for Salmonella infection?
10 days initially, but prolonged therapy can be required.
357
What should be done to ensure the infection has been eliminated after Salmonella treatment?
The faeces should be re-cultured on several occasions.
358
What are some medications used to treat steroid-refractory colonic IBD in canine cases?
Azathioprine and cyclosporine
359
What medication is used to treat refractory or severe feline IBD, combined with prednisolone?
Chlorambucil
360
What is Faecal Microbial Transplant used for?
Treating resistant Clostridium difficile infection in human patients and IBD
361
What is the classic finding in colonic biopsy of dogs with granulomatous colitis?
Numerous periodic-acid Schiff-positive histiocytes in the lamina propria
362
What is the recommended treatment for granulomatous colitis in dogs?
Enrofloxacin for 8 weeks
363
What is Tritrichomonas foetus?
A microscopic single-celled flagellated protozoan parasite
364
What is the most sensitive and specific test for detecting T. foetus infection in cats?
PCR (polymerase chain reaction) test
365
What are some drugs that have efficacy against T. foetus infection in cats?
Ronidazole and tinidazole
366
What are the most common biochemical abnormalities in gallbladder diseases?
The most common biochemical abnormalities in gallbladder diseases are increased liver enzymes (alanine aminotransferase, alkaline phosphatase, and gamma-glutamyl transpeptidase) and hyperbilirubinaemia.
367
What is a mucocele in the context of gallbladder diseases?
A mucocele is an accumulation of the mucus component of the bile, which leads to thickening of the bile.
368
What is the relationship between hyperlipidaemia and gallbladder mucocele in dogs?
Dogs with hypercholesteraemia are nearly 3 times more likely to develop gallbladder mucoceles compared to those without this biochemical abnormality. Furthermore, those with hypertriglyceridaemia are 3.55 times more likely to have gallbladder mucoceles compared to those without hyperlipidaemia.
369
What are common causes of elevated liver enzymes in the absence of primary hepatobiliary disease?
Common causes of elevated liver enzymes in the absence of primary hepatobiliary disease include medication (glucocorticoid therapy, phenobarbital therapy), inflammation/infection (pancreatitis, sepsis), muscle injury, gastrointestinal disorders, systemic infections, and more.
370
What is the significance of hypoglycaemia in liver dysfunction?
Hypoglycaemia only occurs after approximately 75% of hepatic function is lost and is the result of reduction in hepatic glycogen stores, gluconeogenesis, and clearance of insulin. It can also be seen periodically in patients with Portosystemic shunts.
371
What is the relationship between hypoalbuminaemia and severe end stage liver disease?
Hypoalbuminaemia occurs with chronic liver disease once approximately 70% of liver function has been lost. It is a useful prognostic indicator in severe end stage liver disease. Often when the serum albumin concentration is low due to advanced liver disease, the serum concentration of globulins will be normal to increased.
372
What is the function of bile acids and how are they synthesized?
Bile acids are synthesized by the liver exclusively from cholesterol, which is the major route of cholesterol excretion. Bile acids help solubilize dietary lipids and are excreted into the bile and stored in the gallbladder. They are then excreted into the duodenum to help solubilize dietary lipids. They are reabsorbed in the ileum and transported back to the liver via the portal vein, where >95% of the bile acids are removed and the process starts all over again.
373
What can an accumulation of bile acids in the liver lead to?
An accumulation of bile acids in the liver, due to disruption in the enterohepatic circulation caused by liver dysfunction or portosystemic shunting, can result in elevations in serum bile acid concentration. This can be seen with portosystemic shunts, parenchymal hepatic disease, and cholestasis. The bile acids are converted to secondary bile acids, which have a direct toxic effect on hepatocytes.
374
What is the most common cause of primary hepatic disease?
Primary hepatic disease is most commonly caused by cirrhosis or lobular dissecting hepatitis in dogs and chronic inflammatory biliary disease in cats.
375
What are the six types of congenital portosystemic shunts found in dogs and cats?
The six types of congenital portosystemic shunts found in dogs and cats are: intrahepatic portocaval shunts, extrahepatic portocaval shunts, extrahepatic portoazygous shunts, portal vein atresia with resultant multiple portocaval anastomoses, hepatic arteriovenous malformations causing portal hypertension-induced patency of portosystemic anastomoses, and microintrahepatic PSS (formerly known as MVD).
376
What percentage of congenital PSSs are intrahepatic (IHPSSs) in both dogs and cats?
Approximately 25-33% of congenital PSSs are intrahepatic (IHPSSs) in both dogs and cats.
377
Which breeds are commonly associated with portosystemic shunts in dogs?
Portosystemic shunts are commonly seen in the Cairn Terrier, West Highland White Terrier, Yorkshire Terrier, Labrador, and Irish Wolfhound.
378
Which breeds are commonly associated with portosystemic shunts in cats?
In cats, extrahepatic portosystemic shunts (EHPSSs) are more commonly identified. Domestic shorthair, Persian, Siamese, Himalayan, and Burmese breeds are overrepresented.
379
What are the clinical signs of congenital PSSs in animals?
The clinical signs of congenital portosystemic shunts (PSSs) vary but often include failure to thrive, small stature, weight loss, strange behaviors (such as stargazing, head pressing, or random barking), intermittent blindness, and pacing or aggression. Jaundice and ascites are usually not associated with congenital PSSs.
380
What is the difference between congenital PSSs and acquired shunts in regard to ascites?
Congenital PSSs typically do not cause ascites, except in the very rare case of hepatic arteriovenous malformation. Acquired shunts can result in ascites as a consequence of portal hypertension.
381
What are the clinical signs of congenital PSSs in cats?
In cats, the clinical signs of congenital PSSs may be very subtle and include copper-colored irises, ptyalism, and intermittent seizures.
382
What is the purpose of using medical treatment for 3-4 weeks prior to surgery in patients with PSS?
Medical treatment prior to surgery allows partial reversal of the catabolic state of the patient, improves body condition score, albumin levels, and neurological signs.
383
What conditions can precipitate hepatic encephalopathy in animals?
Metabolic alkalosis, hypokalaemia, constipation, gastrointestinal haemorrhage, diets with a high protein/purine/methionine content, azotaemia, hypermetabolic state or fever, and dehydration can precipitate hepatic encephalopathy in animals.
384
What should be done to alleviate severe neurological signs related to hepatic encephalopathy?
Rapid stabilization is required and nothing should be given orally until the animal is alert and aware. Bloods should be obtained for various tests and IV line and fluid therapy to correct dehydration should be initiated. Gastroprotectants may also be administered if there is evidence of GI bleeding.
385
What should be monitored and supplemented if necessary in young puppies and kittens with congenital portosystemic shunts (cPSS)?
Glucose should be monitored regularly and may need to be supplemented intravenously in young puppies and kittens with cPSS, as their glycogen stores and gluconeogenesis are minimal.
386
How can enemas be used in animals with hepatic encephalopathy?
Enemas can be used to decrease the number of urease-producing bacteria in the colon and remove toxic by-products of bacterial metabolism. Warm water enemas may be used during a hepatic encephalopathy crisis until no faecal material is present in the evacuated fluid.
387
What is the role of lactulose in reducing blood ammonia levels in animals with hepatic encephalopathy?
Lactulose, when hydrolyzed by colonic bacteria, leads to a reduction in colonic pH and ammonium ions (NH4+) formation. Ammonium ions are trapped in the colon and excreted with the faeces, while lactulose also inhibits ammonia production by colonic bacteria.
388
What percentage of humans with hepatic encephalopathy show improvement following a warm water enema?
Only 20% of humans with hepatic encephalopathy show improvement following a warm water enema, but 80-90% show benefit from lactulose.
389
What are the main functions of the liver?
The main functions of the liver are: metabolism of carbohydrates, proteins and lipids; production of albumin and some globulin; storage of vitamins and iron; detoxification/excretion of waste products; production of insulin like growth factor (IGF 1); synthesis of clotting factors and vitamin-K dependent factors; production of bile, aiding in the digestion and absorption of fats.
390
What is the source of macrophages in the liver?
The liver is a source of macrophages.
391
How many lobes is the liver divided into?
The liver is divided into multiple lobes, including the left lateral, right lateral, medial, quadrate, and caudate lobes.
392
What are the two major vessels that supply blood to the liver?
The two major vessels that supply blood to the liver are the hepatic artery and the hepatic portal vein.
393
What is the function of Kupffer cells in the liver?
Kupffer cells are a population of macrophages in the liver that phagocytose damaged red blood cells, platelets, bacteria, toxins, viruses, various hormones, neoplastic cells, immunoglobulins, complement, and haemosiderin.
394
What is the fluid-filled space between the sinusoids and the hepatocytes called?
The fluid-filled space between the sinusoids and the hepatocytes is called the space of Disse.
395
What are the three types of fluid found in liver disease?
The three types of fluid found in liver disease are true transudate, modified transudate, and exudate.
396
How is portal hypertension classified based on anatomical location?
Portal hypertension is classified based on anatomical location as pre-hepatic, intrahepatic, or post-hepatic.
397
What are the causes of pre-hepatic portal hypertension?
Pre-hepatic portal hypertension is caused by increased resistance in the extrahepatic portal vein due to obstruction, such as congenital atresia or fibrosis, thrombosis, or neoplasia.
398
What is the most common cause of intrahepatic portal hypertension?
Chronic hepatitis with fibrosis or cirrhosis is the most common cause of intrahepatic portal hypertension.
399
What is the pathogenesis of hepatic encephalopathy in dogs?
The pathogenesis of hepatic encephalopathy in dogs is not fully understood, but hyperammonemia, increased plasma concentrations of endogenous benzodiazepines, hypercortisolism, altered tryptophan metabolism, and altered manganese metabolism have all been implicated.
400
What is the significance of hyperammonemia in hepatic encephalopathy?
Hyperammonemia is considered the most important mediator in hepatic encephalopathy, but its exact role and correlation to the presence and/or severity of HE in dogs are still unclear.
401
What is a common clinical sign of hepatic encephalopathy in cats?
A common clinical sign of hepatic encephalopathy in cats is ptyalism, which is observed in 75% of cases.
402
Which clinical signs may be exhibited by dogs with hepatic encephalopathy?
Dogs with hepatic encephalopathy may exhibit depression, stupor, circling, star gazing, compulsive behaviors, coma, blindness, and seizures.
403
What are the three most common hepatic biopsy techniques?
The three most common hepatic biopsy techniques are core needle biopsy, laparoscopic biopsy, and surgical biopsy.
404
When is general anesthesia required for hepatic biopsy?
General anesthesia is required for surgery and laparoscopy, and may be necessary for some patients undergoing core needle biopsies.
405
What are the limitations of needle biopsies?
Needle biopsies have limitations due to their small sample size.
406
What are the contraindications for performing tru-cut biopsies?
Tru-cut biopsies should not be performed in patients with ascites, microhepatica or suspected cirrhosis. Automatic tru-cut biopsies are contraindicated in cats due to a high fatality rate.
407
When is laparotomy indicated over laparoscopy for liver biopsies?
Laparotomy is indicated over laparoscopy when there is concern over a biliary duct obstruction or vascular anomaly that may require surgical correction in addition to obtaining a liver biopsy, or when the patient is undergoing surgery for an issue unrelated to its hepatobiliary disease.
408
What are the advantages of surgical biopsy over other techniques?
The advantages of surgery include the exposure, ability to manipulate the tissues, ability to obtain a larger sample, and ability to monitor the biopsy site for bleeding.
409
What are the recommended number of biopsies to obtain for histopathology?
It is advisable to obtain at least 4-5 biopsies from different liver lobes for histopathology, one biopsy for aerobic and anaerobic culture, and one for quantification of copper and other heavy metals.
410
What are the common bacteria isolated from bile samples?
The most common bacteria isolated from bile are E. coli, Enterococcus spp., Streptococcus spp., Bacteroides spp., and Clostridium spp.
411
How can liver function be evaluated in terms of enterohepatic circulation?
Liver function can be evaluated by estimation of serum bile acids after a 12-hour fast and two hours after a small meal.
412
What is the sensitivity and specificity of pre and postprandial bile acid elevations in diagnosing PSS in dogs and cats?
Pre and postprandial bile acid elevations have been reported to be 99% sensitive and 95-100% specific for diagnosing PSS in dogs and cats.
413
What is the sensitivity and specificity of fasting bile acids in diagnosing PSS in dogs and cats?
Fasting bile acids have a sensitivity of 93% and specificity of 67% in dogs, and sensitivity of 100% and specificity of 71% in cats for diagnosing PSS.
414
What is the limited value of bile acids in the screening of hepatobiliary diseases?
Bile acids have limited value for screening most hepatobiliary diseases, with a sensitivity of 54-74%.
415
What can cause elevated bile acids in patients with secondary hepatopathies?
Secondary hepatopathies such as hyperadrenocorticism can cause elevated bile acids.
416
What is the effect of cholestasis on coagulation in hepatobiliary disorders?
Cholestasis can cause malabsorption of fat-soluble vitamins, leading to a prolonged prothrombin time. Vitamin K dependent clotting factors can be affected.
417
What laboratory tests are commonly used to assess coagulation status in hepatobiliary disorders?
Common laboratory tests include prothrombin time, activated partial thromboplastin time, fibrinogen, fibrin degradation products, and D-dimers.
418
What is the primary source of ammonia in the investigation of hepatobiliary diseases?
Ammonia is derived primarily from the action of colonic bacteria on the breakdown products of ingested protein.
419
What are some gastrointestinal signs that can occur in dogs with liver disease?
Some gastrointestinal signs that can occur in dogs with liver disease include vomiting, diarrhea, anorexia, pica, GI bleeding, melaena, and haematemesis.
420
How frequent are gastrointestinal signs in cats with liver disease?
Gastrointestinal signs are less frequent in cats compared to dogs with liver disease.
421
What is the diagnostic basis for hepatic encephalopathy?
The diagnosis of hepatic encephalopathy is based on evidence of hepatic dysfunction in a patient with neurological deficits.
422
What are the differential diagnoses for hepatic encephalopathy?
The differential diagnoses for hepatic encephalopathy include other metabolic encephalopathies, brain neoplasia, infectious diseases, toxins, intracranial haemorrhage, and ischaemic events.
423
What is hepatocutaneous syndrome?
Hepatocutaneous syndrome is a form of superficial necrolytic dermatitis that can occur in dogs and cats with liver disease.
424
What are the dermatological signs of hepatocutaneous syndrome in dogs?
In dogs, hepatocutaneous syndrome manifests as hyperkeratosis with subsequent crusting and fissuring of the paw pads.
425
What are the dermatological signs of hepatocutaneous syndrome in cats?
In cats, hepatocutaneous syndrome can manifest as ulceration and crusting of oral mucocutaneous junctions, pinnae, periocular areas, interdigital areas, ventral abdomen, and inguinal areas.
426
Which drugs are specifically toxic to cats?
Diazepam (oral), Methimazole, and Griseofulvin are specifically toxic to cats.
427
What is the difference between hepatic arteriovenous malformation (HAVM) and a hepatic arteriovenous fistula?
HAVM is composed of numerous communications (malformation) while a hepatic arteriovenous fistula is a single communication.
428
What are the signs and symptoms of hepatic arteriovenous malformation (HAVM)?
HAVM is associated with hepatofugal blood flow, arterialization of the portal vein, and often presents with ascites.
429
What is the prognosis for patients with hepatic arteriovenous malformation (HAVM)?
The long-term prognosis for HAVM is generally poor.
430
How is the diagnosis of portosystemic shunts confirmed?
Diagnosis of portosystemic shunts is confirmed through history, physical examination, and laboratory analysis.
431
What changes in haematology and biochemistry are consistent with hepatic dysfunction?
Changes consistent with hepatic dysfunction include microcytic anaemia, hypoalbuminaemia, low urea, hypocholesterolaemia, and hypoglycaemia.
432
What is the most useful screening test in evaluating liver function in animals suspected of having congenital portosystemic shunts (cPSS)?
The bile acid stimulation test is the most useful screening test for evaluating liver function in animals suspected of having cPSS.
433
What diagnostic imaging techniques can be used to identify and locate portosystemic shunts?
Abdominal ultrasonography and computed tomography angiography (CTA) can be used to identify and locate portosystemic shunts.
434
Why should clotting times be measured before any invasive procedure for patients with portosystemic shunts (PSS)?
Severe hepatic dysfunction can result in prolongation of clotting times, so measuring clotting times before invasive procedures is important.
435
What are the functions of stellate cells in the liver?
Stellate cells store lipids including vitamin A and secrete collagen to form fibrous scar tissue in liver disease.
436
What is the purpose of the fibrous scar tissue formed by stellate cells?
The fibrous scar tissue acts as a wall to prevent the spread of damage in liver disease.
437
What is the role of hepatocytes in protein synthesis?
Hepatocytes can stimulate or block protein synthesis.
438
What is the space of Disse?
The space of Disse is the area between hepatocytes and sinusoids where nutrients, ions, toxins, etc. must cross before entering the hepatocyte.
439
Which zone of hepatocytes receives blood rich in oxygen and incoming nutrients?
Zone 1 hepatocytes, which are closest to the portal triad, receive blood rich in oxygen and incoming nutrients.
440
In which zone of hepatocytes does P450 metabolism occur mostly?
P450 metabolism occurs mostly in zone 3 hepatocytes, which are nearest to the central veins.
441
What is the functional reserve capacity of the liver?
The liver has an enormous functional reserve capacity and can regenerate fully numerous times over.
442
When do many diseases of the liver become apparent?
Many diseases of the liver only become apparent when chronic and a large portion of the liver has been lost.
443
What should be considered in dogs with acute signs of abdominal pain and a suspected mucocele on abdominal imaging with free abdominal fluid present?
Gallbladder rupture
444
What additional support for a diagnosis of gallbladder rupture can a comparison of serum to peritoneal fluid bile acids concentrations provide?
Additional support
445
What percentage of blood and oxygen content does the portal vein provide to the liver?
Up to 80% of blood and 50% of oxygen content
446
What are the respective veins that drain blood from the GI tract, spleen, and pancreas?
Their respective veins
447
What are the three branches the portal vein separates into in cats?
Left, central, and right branches
448
What happens when the path of the blood entering the liver is interrupted by an anomalous vessel?
Blood is diverted away from the liver and along the path of least resistance, reaching the systemic circulation
449
What are the two types of congenital shunts associated with hepatic vascular abnormalities?
Intrahepatic portosystemic shunts (IHPSSs) and Extrahepatic portosystemic shunts (EHPSSs)
450
Which imaging modalities can be used to diagnose congenital portosytemic shunts (cPSS) in dogs?
Abdominal ultrasonography, computed tomographic angiography, and direct visualisation or portovenography during coeliotomy
451
What can cause reflux of duodenal juice into the pancreatic and bile duct?
Vomiting
452
What type of bacteria have been found in patients with pancreatitis and hepatic diseases?
Enteric species, such as E.coli
453
What is triaditis in cats?
A combination of pancreatitis, cholangitis, and inflammatory bowel disease (IBD)
454
What percentage of examined cats have been reported to have feline cholangitis or cholangitis with pancreatitis and IBD?
17% - 39%
455
Which cat breed is reported to be over-represented for pancreatitis in some studies?
Siamese cats
456
What is the function of the gallbladder?
To store and concentrate bile produced in the liver
457
Where does the common bile duct enter the duodenum?
At the major duodenal papillae through the sphincter of Oddi on the dorsal surface of the duodenum
458
What are common clinical signs of liver disease?
Depression, vomiting, diarrhea, hyporexia, weight loss, abdominal pain, polydipsia, polyuria, stranguria, pollakiuria, exercise intolerance, icterus, ascites, neurological signs, prolonged bleeding
459
Is there a correlation between the ultrasonographic appearance and the presence of clinical signs?
The nature of the ultrasonographic appearance seems to have no correlation with the presence or absence of clinical signs.
460
What is an incomplete stellate pattern more frequently associated with?
An incomplete stellate pattern is more frequently associated with gallbladder rupture.
461
Is gallbladder wall thickening always associated with gallbladder mucoceles?
Gallbladder wall thickening is not always associated with gallbladder mucoceles.
462
How are gallbladder mucoceles and cholelithiasis commonly found?
Gallbladder mucoceles and cholelithiasis are commonly asymptomatic and are often found incidentally during other clinical investigations.
463
What percentage of gallbladder mucoceles are incidentally found during ultrasound examination?
Up to 44% of gallbladder mucoceles are incidentally found during ultrasound examination.
464
What is the recommended treatment for asymptomatic patients with gallbladder mucoceles?
In asymptomatic patients, medical treatment could be attempted while carefully monitoring the patient with ultrasound.
465
What is the treatment of choice for symptomatic patients with gallbladder mucoceles?
In symptomatic patients, the treatment of choice is cholecystectomy.
466
What imaging modality is most commonly used to assess hepatic size?
Radiography is most commonly used to assess hepatic size.
467
What can cause cholestasis of sepsis?
Cytokines inhibit the expression of hepatocyte transporters necessary for bilirubin transport.
468
What are the liver function tests used to diagnose hepatobiliary disease?
ALT, ALKP, GGT, and AST.
469
How is clinical jaundice detected in the pink mucous membranes?
Values above >35µmol/L.
470
What bilirubin level is required to detect clinical jaundice in the sclera?
Values above >30µmol/L.
471
What test can be used to rule out pancreatitis in dogs and cats?
Canine/feline pancreatic lipase immunoreactivity assay.
472
What are some possible findings in urinalysis of patients with liver disease?
Glucosuria, proteinuria, hyposthenuria, bilirubinuria, and ammonium biurate crystalluria.
473
When should the liver be investigated?
If the patient has persistently high liver enzyme values, significantly elevated bile acids or bilirubin, ascites of unknown cause, hepatomegaly of unknown cause, or bloodwork abnormalities and is a breed known to have associated hepatopathies.
474
What diseases may result in hepatomegaly and what diseases may result in microhepatica?
Acute hepatitis and neoplasia may result in hepatomegaly, while chronic hepatitis and portosystemic shunts tend to result in microhepatica.
475
Which breeds are breed-related to chronic hepatitis and copper storage accumulation in Labradors and Doberman Pinschers?
Labrador Retrievers and Doberman Pinschers
476
Name three breeds in which hepatic amyloidosis has been documented.
Abyssinian cats, Oriental cats, Siamese cats, and Chinese Shar-Pei dogs
477
What are the clinical signs of liver disease?
Many animals with liver disease may have no clinical signs
478
What bilirubin level is necessary to visualise jaundiced serum?
When the bilirubin level exceeds 15µmol/L
479
What size can the liver be in dogs with chronic hepatopathies?
In chronic hepatopathies in dogs, the liver tends to reduce in size
480
What is the most common physical finding in cats with liver disease?
Hepatomegaly
481
What is a stress leukogram?
A stress leukogram is often seen in both acute and chronic hepatitis
482
Which liver enzyme tests are liver specific?
Liver enzyme tests are not all liver specific
483
What are some historical information that should be considered when evaluating a patient with liver disease?
Current medications, exposure to drugs, toxins, nutraceuticals and supplements, environment of the patient including time and supervision outdoors, exposure to environmental toxins and infectious agents, travel history, and vaccination status.
484
What are some clinical symptoms that may raise suspicion for feline hepatic lipidosis (FHL)?
Middle aged, over-conditioned cats with a recent history of weight loss and anorexia.
485
What are some common clinical findings in dogs with hepatopathies?
Vague clinical findings such as apathy and lethargy.
486
Can chronic hepatitis present acutely with jaundice, anorexia, and ascites?
Yes, chronic hepatitis can present acutely with jaundice, anorexia, and ascites.
487
How can impaired bilirubin handling occur?
Impaired bilirubin handling can occur as a pre-hepatic, hepatic, or post-hepatic problem.
488
What are the three types of jaundice?
Pre-hepatic jaundice, hepatic jaundice, and post-hepatic jaundice.
489
What is ascites?
Ascites is the accumulation of free fluid within the abdominal cavity.
490
What are some causes of post-hepatic jaundice?
Common causes include pancreatitis, choleliths, cholecystitis, and neoplasia.
491
What is the recommended protein content in the diet for stable animals with hepatic encephalopathy (HE)?
Moderately restricted in protein (14–17% protein dry matter basis).
492
What should be the protein source in the diet for stable animals with HE?
High quality protein with high levels of branched-chain amino acids compared to aromatic amino acids.
493
Which protein source may be a better option than meat-based protein for dogs with HE?
Soy-based protein.
494
What should be the main caloric source in the diet for animals with HE?
A highly digestible carbohydrate source.
495
What should be closely monitored in patients with severe HE?
Neurological signs, systemic blood pressure, routine laboratory parameters, blood glucose, urine output, and bladder size.
496
Which drugs should be avoided or used cautiously in patients with HE?
Drugs metabolized by the liver and highly protein-bound drugs.
497
What is the prognosis for patients with mild HE?
Fair to good.
498
What is the treatment of choice for symptomatic portosystemic shunts (PSSs)?
Surgical attenuation or ligation.
499
How should a lactulose enema be prepared?
The lactulose should be diluted with warm water (3 parts lactulose to 7 parts warm water).
500
What is the recommended dosage for a lactulose enema?
The dosage is 1-10 ml/kg, and it should be retained in the colon for 20-30 minutes.
