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BVMS 3 > Module 16 Wk 2 > Flashcards

Module 16 Wk 2 Flashcards

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1
Q

(Oropharyngeal problems and cervical swellings)

What is Sialocoele?

A

It is leakage of saliva from gland or duct which can collect submucosally or subcutaneously causing a swelling.

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2
Q

What are the aetiologies of sialocoele?

A
  • Idopathic
  • Trauma
  • Sialoliths
  • Neoplasia
  • Foreign Body
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3
Q

What is sialoliths?

A

Salivary stones which block ducts

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4
Q

How would a patient present when suffering with sialocoele

A

A non-painful fluctuant swelling

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5
Q

Location deterimines the clinical signs of the patient, What will you see clinically if its in the zygomatic glands?

A

Exophthalamus

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6
Q

What is Exophthalamus?

A

a bulging or protruding eyeball or eyeballs

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7
Q

Location deterimines the clinical signs of the patient, What will you see clinically if its in the Pharyngeal glands?

A

Laboured breathing/airway obstruction

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8
Q

Location deterimines the clinical signs of the patient, What will you see clinically if its in the Sublingual glands?

A

Dysphagia + cervical swelling

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9
Q

How can you diagnose sialocoele?

A
  • Clinical signs
  • Aspiration of fluid via cytology and appearence
  • Imaging
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10
Q

What should the cytology and appearence of the aspirated fluid show?

A
  • Cytology - stain for mucin, small amounts of nuertrophils, macrophages, lymphocytes and plasma cells and RBC.
  • For diagnosis fluid should appear viscous and honey coloured
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11
Q

What imaging can you use to diagnose sialocoele?

A
  • sialogram but hard to perform
  • Contract CT
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12
Q

How can you treat a sialocoele?

A
  • Surgery - Sialoadenectomy
  • Conservative management but not reconemended as will most defo recur
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13
Q

What is the main cause of Cenrvical swelling in dogs?

A

Oropharyngeal stick injury

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14
Q

Describe how dog might present with acute oranpharyngeal stick injury?

A
  • Pain
  • dysphagia
  • Bloody saliva
  • Gagging/retching
  • Oronpharyngeal haemorrhage
  • s/c emphysema
  • Pyrexia
  • Pyothorax/mediastinitis
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15
Q

When a dog presents like this what should you proceed to do with the aid of sedation or GA?

A
  • Check sublingual, whole oropharyns, hard and soft palate
  • Can use endoscope to identify and expore tracts
  • Radiograph cervical area and throax
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16
Q

What might the radiographs presenting with acute oropharyngeal stick injury symptoms look like?

A
  • Precence of free gas within cervical tissue planes
  • Pneumothorax
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17
Q

What should occur on surgical exploration of an acute stick injury presentation?

A
  • Explore tract and remove any debris
  • Oral or ventral cervical approach
  • Flush lots to remove debris
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18
Q

Why do dogs present with chronic oranpharyngeal stick injury?

A
  • accute injury was missed
  • occurs after initail treatment being unsuccessful
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19
Q

What are the differentials for cervical swellings?

A
  • abscess
  • cyst
  • granuloma
  • neoplasia
  • lymphadeopathy
  • heamatoma
  • sialocoele
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20
Q

How do you diagnose a chronic oranpharyngeal stick injury?

A
  • Clinical signs and hostory
  • Response to treatment
  • FNA of swelling
  • Orpharyngeal exam
  • Imaging
  • Surgical exploration
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21
Q

What should happen in a surgucal exploration of a chronically presenting oranpharyngeal stick injury?

A
  • Remove foreign material ans infected tissue
  • Debride wound and lavage
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22
Q

What is a cleft palate?

A
  • Congenital lip and palate defect in cats and dogs
  • Acquired due to trauma
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23
Q

What age should a congenitial cleft palate be repaired at?

A

3-4months

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24
Q

What trauma can cause cleft palate?

A
  • Fall from height
  • Electric cord chewing
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25
What usually causes a oronasal fistuala?
Usually occurs due to severe peiodontal disease or tooth extraction.
26
What do you see with chronic nasal fistuala?
Unilateral nasal discharge and sneezing
27
What do you see with acute oronasal fistuala?
nasal bleeding or visualisation of the nasal cavity
28
How can you surgically repail an oronasal fistula?
- Labial flap - Must not be under tension or will fail - May be chronically infected - Consider referral for large chronic defects
29
What are common oral neoplasia found in dogs?
- Malignant melanoma - Squamous cell carcinoma - Fibrosarcoma - Peiodontal ligament tumour - Equlids
30
What are common oral neoplasia in cats?
- Squamous cell carcanoma - Fibrosarcoma
31
What are clinical signs of oral neoplasia?
- Abnormal prehension of food - Blood tinged saliva - Difficulty swallowing - ulceration - halitosis
32
What is halitosis?
HOnking breath
33
How can you treat oral neopasia?
* Surgery * Chemotherapy * Radiotherapy
34
Describe the surgery, Maxillectomy, to treat oral neoplasia
- Removal of part of the upper Jaw - Usually indicated for oral neoplasia - Can have good functional outcome but needs careful case selection
35
Describe the surgery, Maxillectomy, to treat oral neoplasia
- Removal of part of the lower jaw - Usually indicated for oral neoplasia - Good outcome and usually well tolerated
36
(The Oesophagus -regurgitation & dysphagia) What is dyspahgia?
Difficulty swallowing
37
Describe the process of normal swelling?
1. Oral - preparatory (voluntary) - prehension, mastication, prep of food bolus 2. Pharyngeal - pharynx contracts to allow bolus to move into the proximal oesophagus 3. oesophageal
38
Describe the anatomy of the oseophagus?
It runs from the pharynx to the stomach starting dorsal to larynx, running on the left side dorsally to the trachea entering stomach at the cardia
39
What are the two sphinchters called and where are they located at either end of the oesophagus?
- upper and lower oesophagal sphincter - cricopharynx and cardia of stomach
40
What are the layers of the oesophagus?
- Mucosa - Submucosa - Muscularis - Striated muscle (dog) and Striated 1/3 & smooth muscle 2/3 (cat) - Adventitia (no serosa)
41
What is the oesophagus innervated by?
The vagus nerve
42
List the Mechanical oesophageal diseases
- Vascular ringe abnormaly - Foreign body - Stricture (rare) - Hiatal hernia - Perioesophageal obstruction (rare) - Neoplasia (rare) - Gastro-oesophageal intussception (very rare) - Parasitic granuloma (very rare in UK)
43
List the functional oesophageal diseases
- Megaoesophagus (MO) (congenital or acquired) - Idiopathic oesophageal dysmotilit - Oesophagitis - Gastroesophageal reflux - Lower oesophageal sphincter achalasia-like syndrome (rare)
44
What is cricopharyngeal achalasia/asynchrony?
It is the failure of the upper oesophagus sphincter to relax (achalasia) OR Incoordination between pharyngeal contraction and upper oesophageal sphincter relaxation (asynchrony)
45
What are the clinical signs of cricopharyngeal achalasia/asynchrony?
When patient try and swallow repeatedly but gag, retch, struggle to drink and may eject food from mouth immediately after eating
46
How do you treat cricopharyngeal achalasia/asynchrony?
- Myotomy or muyectomy of the cricopharyngeus muscle - Botox
47
What are oral symptoms of dysphagia?
- Abnormal prehension - Dropping food - Halitosis - Ptyalism - Cough
48
What are the pharyngeal symptoms of dysphagia?
- Halithosis, Ptyalisms - Hard/REPETITIVE swallowing whilst eating and/or drinking - Gagging - Coughing
49
What are oesophageal symptoms of dysphagia?
- Usually only 1 swallowing attempt (or repetitive dry swallowing), may or may not be able to drink, may bring up food at any time after eating - Ptyalism - Halitosis - REGURGITATION - Restless - Epigastric pain - Cough
50
Define regurgitation
Passive evacuation of food and/or fluid from the oesophagus resulting from local mechanical events within the oesophagus
51
Aspiration Pneumonia is a complication that can occur due to regurgitation. What is it?
It is food or water aspirated into lungs causing chemical injury followed by secondary infection.
52
What are clinical signs of aspiration pneumonia?
- Soft cough - dyspnoea - tachypnoea - pyrexia - lung crackles - +/- nasal discharge
53
How do you treat aspiration pneumonia?
- O2 therapy - Fluid therapy - Broad spectrum antibiotic - Nebulation - Coupage
54
What is coupage?
Coupage is a technique that can be performed by veterinary staff and pet owners to help clear secretions from the lungs. Coupage is performed by striking the chest gently but firmly with cupped hands.
55
How should you investigate an oesophageal disease?
- Signalment/History - Clinical examination - Clinical pathology - Plain thoracic radiographs - Contrast radiographs - Fluoroscopy - oesophagoscopy - oesophageal surgery
56
On your clinical exam, what abnormalities may you find in a patient suffering from an oesophagal disease?
- hypersalivation - poor BCS - Bulging in neck - could be food ro air - Muscle atrophy/weakness - Resp signs
57
T/F haematology is usually expected with oesophagal disease.
True
58
What might you see on the haematology of a patient with aspiration pneumonia?
- Leucocytosis - Left shift neutrophilia - monocytosis
59
What abnormalities would you see on radiographs of a patient that is suffering with an oesophageal disease?
- Radioopaque FB - Dilation of oesophagus - Hiatal defects - Pulmonary changes - Pneumomediastinum/ mediastinitis/pleural effusion - Peri-oesophageal masses
60
What is contract radiography useful for when it comes to oesophagal diseases?
- Luminal obstruction - Mucosal irregularity - Significant alterations in motility - Hiatal hernia
61
What oesophageal disease might be better evaluated with fluoroscopy?
- Pharyngeal disorders - Subtle oesophageal motility disorders
62
What does an oesophagoscopy allow?
- Assessment of lumen & mucosa for Obstructions, Inflammation, Perforation or Hiatal hernia - Biopsy or cytology sampling (rare) - Foreign body removal - Balloon dilation of strictures
63
T/F oesophageal surgery is often indicated?
False - rarely
64
What are the challenges with oesophageal surgery?
- Risk of AP on induction of GA - Thoracotomy for intrathoracic oesophagus - Risk of contamination of thoracic cavity - Healing challenging - Fixed length
65
What is an oesophagotomy?
Incision into lumen
66
What is an oesophagectomy?
Removal of portion of oesophagus
67
What is oesophagostomy?
Creation of opening for feeding tube
68
What is vascular ring anomaly?
Persistent right aortic arch is the most common, where the right arch becomes a functional aorta instead of the left fourth arch.
69
What does vascular ring anomaly cause and how does it present?
- Causes significant narrowing and obstruction of the oesophagus - Start regurgitating when weaned, often have weight loss and stunting.
70
What breeds are predisposed to vascular ring anomaly?
- GSDs and Irish setters
71
How can you treat vascular ring anomalys?
- Surgery to transect ligamentum arteriosum - Treat aspiration pneumonia and improve BC
72
What are common foreign bodies in small animals that can cause oesophageal disease?
Bones, fish hooks, needles, sticks and toys
73
What are common sites where foreign bodies obstruct?
- Thoracic inlet - Heart base - Just cranial to diaphragm
74
A patient with a foreign body obstructing the oesophagus has what presentation on clinical examination?
- honky breath - Cervical FB maybe be palpable - systemic signs suggest aspiration pneumonia or perforation
75
How should you treat a patient with a foreign body obstruction?
- Stabilise patient - GA - endoscopic removal - If unable to do this, remove endoscopically or large perforation you should do an oesophagotomy or oesophagectomy
76
What are the 3 potential sequelae from a foreign body obstruction of oesophagus?
- stricture - Fistula - Diverticulum
77
What is strictures?
Circular band of scar tissue secondary to severe oesophagitis
78
What are progressive signs of strictures?
- Hungry but loose weight - Better with liquids
79
How do you diagnose Strictures?
- Difficult to see on plain films, so contrast radiography used - Endoscopy to find cause and take biopsy
80
How should you treat strictures?
- Endoscopic balloon dilation - Followed by medical therapy for oesophagitis - +/- steroids to reduce recurrence
81
What are the two main types of hiatal hernia?
- Sliding – distal oesophagus and stomach move into mediastinum through oesophageal hiatus - Perioesophageal – portion of stomach moves into mediastinum through defect adjacent to oesophageal hiatus
82
What are the effects of a hiatus hernia?
- gastroesophageal reflux due to reduction in LES pressure - Oesophagitis - Hypomotility
83
What are the clinical signs of hiatus hernia?
- If it is congenital, it will be soon after weaning - regurgitation, vomiting, hypersalivation, haematemesis, poor BC, dyspnoea, AP
84
How should you treat a hiatus hernia?
Small hernia - Medical management for oesophagitis Large hernia - Surgical management - Narrow oesophageal hiatus - Pexy oesophagus - Pexy fundus of stomach
85
What is a megaoesophagus (MO)
Diffuse oesophageal dilation & aperistalsis Congenital
86
What breeds are predisposed to MO
Irish setter, GSD, Great Danes, Newfoundlands, Labrador retrievers
87
When do clinical signs of congenital MO start?
Clinical signs usually start at weaning
88
What can MO be secondary too?
- Myasthenia gravis - Severe oesophagitis - Generalised myopathy - Generalised neuropathies - Toxins - Hypoadrenocorticism - Hypothyroidism
89
What are the clinical signs of MO?
Regurgitation, dysphagia, +/- hypersalivation, +/- weight loss - +/- respiratory signs - +/- signs of underlyingdisease
90
How do you diagnose MO?
Xray (usually plain) Oesophagoscopy - If suspect secondary to structural problems or oesphagitis
91
How might you look for secondary causes of MO?
- Neuro exam - Haematology/biochemistry - CK/AST - Acetyl choline receptor antibodies - ACTH stimulation test - T4/TSK
92
How should you treat MO?
- Treat underlying cause if secondary - Postural feeding - Ideal food consistency varies - Sildenafil - Treat aspiration pneumonia
93
What is oesophagitis?
Inflamed oesophagus
94
What can oesophagitis be caused by?
- Chronic vomiting - Gastroesophageal reflux - Ingestion of caustic agents - Foreign bodies
95
What are the Clinical signs or oesophagitis?
- Variable (asymptomatic to severe) - Dysphagia, regurgitation, odynophagia, hypersalivation, food avoidance, weight loss
96
How do you Diagnosis Oesophagitis?
- Inflammation seen endoscopically - Biopsy usually unnecessary
97
How do you treat oesophagitis?
- Small, low fat, high protein meals +/- withhold food PO - Sucralfate liquid - Metoclopramide - Gastric acid secretory inhibitors - H2 antagonists or proton pump inhibitors
98
What is Gastroesophageal reflux
Disorder of LES allowing reflux of fluids/ingesta into oesophagus which leads to oesophagitis
99
What is gastroesophageal reflux caused by?
- Chronic vomiting - Gastric emptying disorder - Hiatal hernia - Upper airway obstruction - Anaesthesia
100
How do you go about treating gastroesophageal reflux?
- Avoid high fat diets - Sucralfate suspension - Gastric acid secretory inhibitors - Metoclopramide - Surgery for upper airways in brachycephalic dogs helps
101
How can you diagnose Myasthenia gravis?
- Tensilon test – generalised only, non-specific - Acetyl choline
102
How do you treat myasthenia gravis?
* Pyridostigmine * Consider injectable
103
(Investigation & Management of Vomiting in Dogs & Cats) What may activate the chemoreceptor trigger zone?
- Uraemia - DKA - Cardiac glycoside toxicity - Apomorphine - Chemotherapy
104
What are the receptors found in the chemoreceptor trigger zone?
- D2 (dopamine) - 5HT3 (serotonin) - M1 (cholinergic) - Opioid receptors - Histamine - NK1 (Neurokinin-1 receptor)
105
What may activate the gastro-intestinal tract/peripheral stimuli?
- Chemicals/irritants - Inflammation - Excessive stretch of the GI tract - Peritonitis - Colitis may vomit too due to stretch - Bladder obstruction
106
What are the receptors found in the gastro-intestinal tract?
- 5HT1 (serotonin) - a1-Adrenergic - Nk1 (Neurokinin-1 receptor)
107
What can triggering of the vestibular apparatus cause clinically?
- Motion sickness - Vestibular syndroms
108
What are the receptors that resinate in the vestibular apparatus?
- H1 (histamine) - M1 (cholinergic)
109
Define vomiting
Active and forceful expulsion of gastric and/or duodenal contents
110
Define regurgitation
Passive retrograde expulsion of oesophageal or gastric contents with NO forceful abdominal contractions
111
What are the aetiologies of acute vomiting?
- GI disorders - Non-GI disorders
112
What are GI disorders that will cause vomiting?
- acute gastritis/enteritis - dietary indiscretion - Foreign body - mesenteric torsion - Intussusception - (GDV)
113
What are non-GI disorders that can cause acute vomiting?
- Acute pancreatitis - Acute hepatobiliary disease - Acute renal failure - Peritonitis - Acute neurological insult - Endocrine dysfunction - Toxin ingestion/explore
114
What questions should you ask when taking a history of a patient of acute vomiting?
- Recent dietary changes? - Scavenging? - How frequently is the patient vomiting? - Is the vomiting productive? - Undigested food / partially digested / faecal odour? - Is there blood or coffee grounds in the vomit? - Has there been any recent weight loss? - Concurrent GI Signs? - Is the patient on any medication? - Is the patient systemically unwell? - Appetite?
115
What should you assess on physical examination of a patient with acute vomiting?
- Systemic disease - Demeanour - Pyrexia - Liver disease - Painful abdomen - Assess hydration
116
What investigation should you do on a patient with acute vomiting?
- CBC and serum biochem - Urinalysis - Diagnostic imaging to see if surgery is needed - Abdom US
117
When performing imaging on a patient with acute vomiting, what should you be looking out for?
- GDV - GI FB - Obstructive pattern - GI perforation - Peritonitis
118
When performing an abdominal US what should you be evaluating and looking for?
- Evaluate the whole GI tract - Assessment of the biliary system - Evaluate the pancreas - Evaluate repro system
119
What should you use to address fluid and electrolyte disturbances caused by vomiting?
IVFT with appropriate electrolyte supplementation
120
What should you use to reduce the frequency/stop vomiting?
Anti emetic drugs?
121
What should you use to reduce acid production, particularly if there are concerns for gastro-duodenal ulceration?
Anti-ulcer drugs
122
What should you use to improve gastric emptying?
Prokinetic drugs
123
List the different types of anti emetics seen in practice?
- NK1 pathway inhibitors (Maropitant) - Anti-dopaminergics (Metoclopramide) - Serotonin antagonists (Ondansetron) - Phenothiazines (Chlorpromazine)
124
List the types of anti-ulcer drugs seen in practice?
- Histamine (H2)- blockers (Cimetidine, Ranitidine, Famotidine) - Proton pump inhibitors (Omeprazole) - Sucralfate - Synthetic prostaglandins (Misoprostol)
125
What are the different types of pro-kenetic drugs used in practice?
- Metoclopramide (CRI) - Ranitidine - Cisapride
126
What is the pump inhibitor drug of choice for ant-ulceration therapy?
Drug of choice where gastric or duodenal ulceration is present
127
How are sucralfate anti-ulceration therapy used and how does it work?
- Orally - Binds to gastric ulcers
128
Cimetidine < Ranitidine < Famotidine H2 Blockers Cimetidine is the only veterinary licensed product * Oral preparation only * Causes inhibition of cytochrome P450 enzymes and therefore may interfere with metabolism of other drugs Ranitidine is available as an intravenous product * Prokinetic activity * Care with IV injection as it can cause hypotension bro idek man
still dont know man
129
How should you investigate chronic vomiting?
- CBC - serum biochem - urinalysis
130
What can you use the initail investiagtion tests for?
Use the results to locate where the primary diseases process is - liver, chronic kidney or endocrine.
131
What can you identify in the abdominal US of chronically vomiting patients?
- Chronic FB - GI neoplasia - PYloric outflow obstruction - Chronic pancreatopathy
132
When would you use endoscopic evaluation of a patient with chronic vomiting?
- When primary GI disease is suspected - Investigate haematemesis - Gastric FB removal - Mucosal biopsy for definitive diagnosis
133
What are potential causes of gastritis in chronically vomiting patients?
- parasitic infection (e.g. Ollunlanus in cats) - fungal infection (e.g. pythiosis, rare) - bacterial infection (Helicobacter-associated gastritis*) - Dietary hypersensitivities/intolerance
134
How should you manage chronic gastritis?
- Treat the underlying cause - Diet modification e.g. a hypoallergenic diet - Immunosuppressant medication (prednisolone) - Symptomatic management (anti-emetics)
135
What is helicobacter-assoc gastritis?
Spiral shaped gram –ve bacteria often identified in dogs and cats with chronic gastritis
136
How should you treat Helicobacter-associated gastritis?
Triple therapy - Amoxicillin plus metronidazole plus bismuth +/- famotidine - Amoxicillin plus metronidazole plus omeprazole - Clarithromycin plus metronidazole plus ranitidine
137
(Approach to the Abdomen and GI Surgery) What are the aims of an exploratory laparotomy?
- Be systematic - Assess everything - Recognise normal abdominal anatomy - Recognise abnormal abdominal structures and pathology - Know appropriate action dependant on findings (cystotomy, enterotomy etc)
138
What is in the cranial quadrant of the abdomen?
- Diaphragm - Liver - Gall bladder - Stomach - Spleen - Pancreas (left limb)
139
What is contained in the right quadrant of the abdomen?
- Kidney - Adrenal - Ureter - (ovary) - Right limb of the pancreas - Caudal vena cava
140
What is contained in the left quadrant of the abdomen?
* Kidney * Ureter * Adrenal * (ovary)
141
What is contained in the caudal quadrant of the abdomen?
* Colon * Bladder * Urethra * Prostate * Inguinal canals
142
What is contained in the central compartement of the abdomen?
Intestinal tract * Start at pylorus * Examine entire small and large intestine * Check colour, peristalsis * Check mesenteric LN Check omentum
143
What steps should you take before closing the abdomen?
- Replace organs - Ensure all swabs have been removed
144
What should be included when closing the linea alba?
External rectus sheath provides the strength in linea alba closure so must be included in each bite.
145
What pattern should you use when Closing the abdomen?
Simple cont or interupterd
146
What are two instruments used in Gastrointestinal surgery?
- Bowel clamps - Atraumatic forceps
147
What suture material and needles are used in gastrointestinal surgery?
- Monofilament syntheitic abdorbable material - Taper pointed needle SWAGEDDD ON
148
What suture pattern should you use on the ntestine in gastrointestinal surgery?
Simple interrupted or cont
149
What suture pattern should you used on the stomach different layers in a gastrointestinal surgery?
Mucosal/submucosal layer = simple cont seromuscular layer = inverting (cushing or lambert)
150
What is the priniciples of GI surgery?
* Try to exteriorise portion of GI tract being operated on * Isolate area with moistened swabs * Have a dirty area on your trolley * Handle foreign bodies with instruments and then discard these. * Change gloves at instruments once GI tract is closed * Lavage at the end of surgery (100-200ml/kg)
151
W.hat is omenatal wrap?
Its where you place omental wrap around insicion lines to promote early serosal seals
152
What are the benefits of using omental wrap?
- Speeds up healing - Increases blood supply - Increases drainage - Reduces leakage - Stimulates and augments angiogenesis
153
What is the most common indication for a gastrotomy?
FB that cannot be endoscopically retrieved and emesis is not indicated/appropriate
154
How do you do a gastrotomy?
- Cranial abdominal incision (xiphoid to umbilicus) - Incision between greater and lesser curvatures - Stay sutures used to lift up area and surround with swabs to minimise contamination
155
How many layers for closure in a gastrotomy?
2
156
What are the indiactions for a SI surgery
- obstruction - Enterotomy - Enterectomy
157
What kind of things could be causing an obstruction in the SI?
- Foreign body - Neoplasia - Intussusception - Intestinal Voluvulus/strangulation - Linear FB
158
What is an enterotomy?
Incise into intestine to remove FB
159
What is an enterectomy?
Remove a portion of intestine
160
DEscribe the steps of an enterotomy?
1. Exteriorise area of small intestine 2. Milk intestinal contents away from the segment 3. Place bowel clamps (or assistant fingers) proximal and distal to FB 4. Incise distal to FB (not directly over FB) using a no.15 scalpel blade 5. Make a linear incision on the antimesenteric border of the intestine 6. Extend incision to easily remove Fb without tearing intestine 7. Remove Fb using instruments
161
What suture patterns should you use to close and enterotomy?
Simple interrupted or simple continuous
162
What suture material should you uses when closing up an enterotomy?
Use monofilament absorbable suture material on taperpoint needle
163
How should you perform a leak test after an enterotomy?
- Occlude intestine - Using a 25g needle inject 5mls saline - Apply gentle pressure and look for leakage
164
Describe the steps to perform and enterectomy?
1. Exteriorise section of bowel and pack with moistened swabs 2. Identify area to resect allowing for a healthy margin 3. Double ligate vessels suppling area to be resected incise the mesentery 4. Milk intestinal contents out of the segment 5. Place crushing clamps: portion to excise 6. Place non-crushing clamps (doyen) on the portion to suture 7. Excise the portion of intestine 8. Close with simple interrupted appositional sutures 9. Monofilament absorbable synthetic suture, taperpoint needle 10. Place first suture at mesenteric border 11. Second at antimesenteric border 12. Then 3 o’clock and 9 o’clock 13. Place sutures with 3mm bites and fill in 3mm apart 14. Close the mesentery (simple continuous suture) 15. Leak test and omentalise
165
When might you see intussusception in young animals?
- Heavy worm burden or enteritis - Can occur spontaneously
166
When can you see intussusception in older animals?
seconday to neoplasia
167
What can you use to diagnose intussusception?
- Clinical signs of GI obstruction - Palpation – ‘sausage’ - Radiography - Ultrasound – classic target like mass
168
How can you treat intussusception?
- Reduction - Enterectomy
169
How do you perform an enteroplication?
Suture adjacent loops of SI together on antimesenteric surfaces
170
What are the benefits and cons of enteroplication?
May prevent recurrence but complications can be life threatening so should only be used in recurrent cases where benefit outweighs the risk.
171
What sort of items cause linear foreign bodies in cats?
String or thread
172
How does the string or thread become an issue?
- It becomes anchored around the base of the tongue and is swallowed - Intestines bunch up around the string and become ‘concertina’ - String ‘cheese wires’ mesenteric border of gut. - Can cause perforation and secondary peritonitis.
173
(GDV) What may be the cause of cause in the stomach with GDV?
- Aerophagia - Bacterial proliferation - Failure to eructate or pass gas into the intestine
174
What may cause fluid causing dilation of stomach in GDV?
- Food - Gastric secretions - Transudate from mural venous congestion of the stomach wall
175
What are the 11 risk factors that can contribute to GDV?
1. Breed 2. Deep-chested conformation 3. First degree relative with history of GDV 4. Previous GDV 5. Diet 6. Excercise 7. Stress 8. Age 9. Previous splenectomy 10. Splenic torsion 11. Gastric FB
176
Even though any breed can get GDV what breeds are predisposed?
Great Dane, St Bernard, Standard Poodle, Weimaraner, Gordon Setter, Irish Setter Basset hound
177
What is the pathophysiology of GDV?
Distention and movement of the stomach impact severely on many different body systems
178
What effects does GDV have on the cardivascular system?
- Reduces venous return to the heart - Occludes the portal vein, causing venous congestion of the intestinal tract - Reduces venous return back to the heart and reduces circulating blood volume. - Endotoxic and septic shock due to compromised mucosal barrier - myocardial ischemia
179
What percentage of GDV cases develop ventricular arrythmias within 48hrs?
25%
180
Why might a GDV patient develop cardiac arrythmias?
Due to reduced tissue perfusion...
181
What Respiratory effects can GDV cause?
Dyspnoeic with rapid, shallow breathing
182
What does the dialted stomach putting pressure on diaphragm cause?
Reduces functional reserve capacity of the lungs
183
What is spleen attached to stomach by?
Gastrosplenic ligament
184
How is the spleen effected in GDV?
The spleen gets displaced dorsally anf to the right where it becomes congested due to stretching and twisting of its vessels.
185
With GDV, what does the increased intramuscular intraluminal pressure in the stomach cause?
It prevents blood flow to the gastric wall, causing hypoxia and necrosis of the gastric wall.
186
In GDV what does the stomach do
- Stomach rotates in a clockwise direction (on the longitudinal axis) (usually, can rotate both ways) - 90 to 360 degree rotation - Pylorus moves ventrally and to the left - Fundus moves to the right
187
What are the clinical signs of GDV?
- Retching - Unproductive vomiting - Cranial abdominal distension - Circulatory collapse (weak pulses and tachycardic) - Hypersalivation - Dyspnoea
188
When physical exam on a patient with GDV what can you expect to find?
- Distended painful abdomen (hyper resonant on percussion) - Tachycardic - Tachypnoeic - Pale - Slow CRT - Collapse
189
How do you diagnose GDV?
- Clinical signs - physical exam - history - Abdominal radiography will confirm
190
What will you see on abdominal radiograph of a patient suffering with GDV?
- Gas filled distended stomach - Compartmentalisation lines (‘inverted c’) - Can’t see fluid filled pylorus
191
T/F Emergency stabilisation should be started BEFORE imaging suspected GDV patients
True obvs
192
How should you go about stabilising a GDV patient?
- Fluid therapy - Gastric decompression
193
How should you go about fluid therapy in the GDV patient?
- Place 2 cephalic catheters (as large bore as possible) - Shock fluid bolus = 90ml/kg/hr over 15mins then reassess and Repeat up to 4 times
194
Orogastric intubation (stomach tubing) * Wide bore stomach tube is measured from nose to 11th rib * Lubricated the tube * Patient should be sitting * Place 7.5cm coflex bandage roll in mouth (hollow centre) and tape mouth closed in improvised gag * Pass stomach tube down the core of the roll * DO NOT FORCE * Once passed decompress then gastric lavage * Cannot always pass tube
195
Percutaneous decompression * 14, 16 or 18g over the needle catheter * Clipped prepped area of tympanic right flank * Try orogastric intubation first * May be able to pass orogastric tube after needle decompression (reduced pressure at gastro-oesophageal junction)
196
What is further stabilisation you could do in the GDV patient?
- IV antibiosis - O2 therapy - Anti arrythmics - Analgesics
197
What are surgical goals for GDV patients?
- Reposition stomach - Assess stomach for necrosis - Perform gastropexy
198
Do all patients with GDV require surgery?
Oui
199
Step by step how do you reposition the stomach in a GDV case?
1. Midline ventral laparotomy 2. Establish direction of rotation before derotating 3. re-position with care 6. Find duodenum and follow it to pylorus 7. Pylorus is gently lifted across to the right and fundus pushed down and to the left 8. Check cardia to ensure untwisted
200
What is the most common type of rotation with GDV and how can you tell if the stomach has rotated like that?
- 180o clockwise rotation most common - Greater omentum covering the stomach suggests clockwise
201
What should a normal gastric wall look like when assessing for viability?
- Pink, blanches and rapidly recolours. - Peristalsis. - Active haemorrhage from the cut surface.
202
If the gastric wall is compromised how might you describe it and what does this mean?
Erythematous - redness of the skin or mucous membranes caused by increased blood flow to the capillaries
203
If the gastric wall is necrotic what colours might you see?
green blu purp and bla
204
What should you do with necrotic areas of the gastric wall?
Perform a partial gastrectomy or gastric invagination
205
What is an incisional gastropexy?
Incisional gastropexy is a surgery where the stomach is attached to the abdominal wall using small cuts and stitches. This helps stop the stomach from twisting, which can cause a serious condition called bloat.
206
How do you perform an incisional gastropexy?
- Vertical incision 4-6cm is made in the right body wall (transverse abdominus) behind the last rib, 5cm from the linea alba - A similar incision is made on the pyloric antrim between the greater and lesser curvatures through the seromuscular layer. - The edges of the stomach wall are sutured to the edges of the body wall doing the cranial incisions first.
207
(Investigation & Management of Diarrhoea in Dogs & Cats) What would your differential diagnosis list be when presented with a dog or cat with diarrhoea?
- Dietary issue - Infectious cause - Neoplasia - Inflammation - Extra-intestinal disorder - Miscellaneous - Drugs or toxins
208
What dietary things could cause diarrhoea?
- Abrupt dietary change - Dietary indiscretion - Dietary intolerance/allergy
209
How could be diarrhoea be cause by an infectious agent?
Parasitic, Viral, bacterial or fungal
210
What kind of neplasms could cause diahhorea to occur?
- Alimentary lymphoma - Intestinal carcinoma - Leiomyosarcoma - Mast cell tumour
211
What inflammatory conditions can result in diarrhoea?
- Inflammatory Bowel Disease - Colitis - Lymphangiectasia
212
What extra-intestinal disorders result in diarrhoea?
- Exocrine pancreatic insufficiency - Hydroadrenocortism (addi) - Liver disease - Pancreatitis - Peritonitis
213
What questions should you ask about the onset of the diarrhoea?
- Is the diarrhoea acute or chronic? Chronic is more than 2 weeks - Is the diarrhoea constant or intermittent?
214
What question can you ask owner to try determine if its a small or large intestinal disease causing the diarrhoea?
Ask them about the characteristics of the diarrhoea
215
What other two things should you ask owner about in a consultation about a dog with diarrhoea?
- in contact animals - anthelmintic history and vaccination
216
What are the characteristics that it is a small intestine causing diarrhoea?
- Normal to large volume - Frequency of defaecation is normal to mildly increased - Melaena - Concurrent weight loss** - Concurrent vomiting - Ascites if associated with protein-losing enteropathy (PLE)
217
What are the characteristics that it is a large intestine causing the diarrhoea?
- Variable but often small volume - Increased frequency of defaecation often associated with urgency - Mucus - Haematochezia (fresh blood) - Faecal tenesmus - Dyschezia (pain associated with defaecation)
218
On clinical examination of a patient with diarrhoea, what might pyrexia indicate?
An infectious cause or maybe a systemic complication of the underlying disorder.
219
On clinical examination of a patient with diarrhoea, what might Malnutrition indicate?
Chronic maldigestion or malabsorptive disorder
220
On clinical examination of a patient with diarrhoea, what might presence of ascites indicate?
May suggest protein losing patient
221
What is you DDx for acute haemorrhagic diarrhoea?
- parvo - coronavirus - samonella - campylobactor - E.coli - clostridial diarrhoea - Clostridium perfringens-assoc diarrhoea - acute heam diarrhoea syndrom - abdominial castrophe
222
What is abdominal castrophe?
peritonitis from a visceral source
223
How would you diagnose parvo as the cause of acute diarrhoea?
- Feacal antigen test - serology from anti-CPV antibodies - haemagglutination inhibition test - PCR on feaces - IFA on tissue specimans at PM
224
How would you diagnose Entero-pathogenic bacteria as the cause of acute
- standard feacal culture - Feacal culture for characteristics of specific bacteris using PCR - ELISA - Screening for giardia
225
How can you diagnose extra-intestinal causes for the acute diarrhoea?
- Heam + biochem - Cortisol to exclude addisons - Diagnostic imaging
226
How should you go about managing acute diarrhoea that is thought to be caused by dietary indiscretion?
- Dietry modification - Supportive IVFT if required (severy dehydrated) - Probiotics
227
How should you go about managing parvoviral enteritis?
- You should perform heam and biochem - Venous blood gas management - coagulation profile
228
Why would you perform the a heam and biochem on a patient who has parvoviral enteritis?
- Heam and biochem - would do this because neutropenia may influence whether to give antibiotics or not, and electrolyte deficiency will influence IVFT.
229
Why would you perform a venous blood gas analysis on a patient suffering from parvoviral enteritis?
Acid-base derangements may impact the choice of fluid therapy and aggressiveness of fluid therapy.
230
Why would you perform a coagulation profile on a patient suffering from parvoviral enteritis?
Parvoviral enteritis is sometimes associated with DIC and may influence desicion to administer plasma
231
How should you treat a patient with parvoviral enteritis
- IVFT - IV antibiotics if neutropenic - Anti-emetics - Early nutritional support - Interferon
232
What kind of Fluids would you use in a patient with parvociral enteritis?
Crystalloids +/- colloids and plasma
233
T/F the management of acute haemorrhagic diarrhoea syndeom is the same as parvoviral enteritis apart from interferon?
True
234
What is your DDx for chronic diarrhoea?
- Dietary - Neoplastic - Inflammatory
235
What investigation tests should you use when diagnosing chronic diarrhoea
- Faecal analysis - Heam and serum biochem - Diagnostic imaging - Endoscopic assessment of GI mucosa - Histopathology
236
Why would you perform a faecalrformal analysis on a patient with chronic diarrhoea?
- feacl parasitology - Faecal dysbiosis index
237
What non-GI disorders are you looking for on heam and bio chem of a patient with chronic diarrhoea?
- Liver, endocrine diseases - pancreatic disorders - renal disease
238
Why would you use diagnostic imagaing on a patient with chronic diarrhoea?
- To identify or rule out neoplastic processes or disorders such as partial bowel obstruction - To inform decision-making about whether endoscopy or exploratory coeliotomy should be performed to obtain a diagnosis
239
Why would you do histopathology on a patient with chronic diarrhoea?
- neoplastic vs non-nesoplastic
240
How would you treat chronic diarrhoea that has been caused by protazoa?
anti-protozoal agent
241
How would you treat a patient with chronic diarrhoea that has been caused by EPI?
Enzyme replacement therapy
242
How would you treat a patient with chronic diarrhoea caused by hypoadrenocortism?
Hormone replacement therapy
243
How would you treat a patient with chronic diarrhoea caused by intesntinal lymphoma
chemo
244
What is faecal tenesmus?
Straining to defecate
245
What is dyschezia?
Difficult or painful defaecation
246
Is Diarrhoea a alarge or small intestinal characteristic?
Large
247
What is haemoatochezia?
Passage of fresh blood on faeces
248
What are the causes of tenesmus and Dyschezia?
- Colorectal disease - perianal and perineal disease - Prostatic disease - Urogenital disease - Miscellaneous
249
What investigations should you perform on a patient with feacal tenemus/dyschexia plus diarrhoea and what for?
- Feacal parasitology and culture for giardia. Trichuris, Ancylostoma, Tritrichomonas - Rectal cytology for infectious agents like fungal elements - Diagnostic imaging to rule out extraluminal disease and intussusception and to identify lymphadenopathy and mural thickening - colonoscopy and mucosal biopsy
250
What might idiopathic inflammation of the colon occur concurrent with?
May occur concurrently with IBD affecting the small intestine
251
How do you diagnose idiopathic colitis?
Exculsion plus compatible histopathological chnages
252
How should you manage idiopathic colitis diet wise?
Hydrolysed protein diets or supplememtal fibre
253
What antibiotic would you use when treating idiopathic colitis?
Metronidazole
254
What anti-inflammatory drug should you use when treating idiopathic colitis?
Sulfasalazine
255
What immunosuppressive drugs can you use when treating idiopathic colitis
- Prednisolone (1st line immunosuppressive agent) - Azathioprine (2nd line immunosuppressive agent in dogs) - Cyclosporine (2nd line immunosuppressive agent in dogs) - Chlorambucil (2nd line immunosuppressive agent in cats)
256
What antibiotic should you use to treat granulomatous colitis
Fluoroquinolones
257
How do Fluoroquinolones work?
They work by inhibiting bacterial DNA replication, specifically targeting enzymes called DNA gyrase and topoisomerase IV, which are essential for bacterial cell survival and reproduction.
258
How would you describe idiopathic large intestinal diarrhoea in dogs?
Intermittent diarrhoea is characterised by increasing frequency, faecal mucus, hematochezia and tenesum
259
What does trichomonas foetus infection cause in cats?
Mild to mod lymphpplasmacytic and neutrophilic colitis
260
What are diagnostic tests for tritrichomonas foetus? and what are their sensitivities?
- Feacal wet prep - less than 20% - In-pouch culture - 65% - PCR for trich DNA - 97%
261
How should you go about treating a patient with Tritichomonas foetus infection?
- International Cat Care website for up-to-date information - High High-fibrefibre diet - Ronidazole - Probiotics - Treatment of concurrent infections?
262
What mechanical obstruction cause constipation?
- Intraluminal - Impaction with bones/hair, rectal stricture, perineal hernia (diverticulum) - Intramural - Neoplasia - Extramural - Pelvic fractures/stenosis, neoplasia, prostatic disease
263
What neuromuscular dysfunctions can cause constipation?
- lumbosacral disease - Hypogastric or Pelvis nerve disorders - colonic smooth muscle dysfunction
264
What metabolic/endocrine doseases can lead to constripation?
- Dehydration - Hypokalaemia - Hypercalcaemia - Hypothyroidism - Obesity
265
What inflammatory processes may cause constripation?
- Anal sac disease - Anal furunculosis/Perianal fistula
266
What enviromantal impacts could cause constripation?
- soiled litter tray - inactivity/HospitalisationW
267
What kind of drugs could induce constipation?
- opiods - anticholingerics
268
If a cat presents with constipation, obstipation and megacolon what might be the patients history?
Typically there is a chronic history of reduced production of faeces +/- faecal tenemus and dyschezia
269
If a cat presents with constipation, obstipation and megacolon what might be their clinical presentation?
- Intermittent haematochezia and mucoid diarrhoea - Systemic signs of inappetance, malaise, vomiting, weight loss - May be a history of RTA/pelvic trauma
270
What is the main cause of obstipation in cats?
- Idiopathic megacolon - pelvic canal stenosis - Nerve injury or sacral deformity
271
What should you do to exculed other causes of obstipation?
- serum biochem - T4 - Abdominal radiography +/- US - colonoscopy
272
What are the aims of therapy of feline constipation?
- Chieve normal hydration - remove impacted faeces - increase dietry fibre - pharmalogic manipulation of clonic function
273
How can you remove impacted faeces?
Enemas and manual evacuation
274
What diet should you put a patient on that is suffering with constipation?
High fibre for mild constipation and low residue diets for obstripation?megacolon
275
What are cosequences of chronic obstipation and megacolon
- mucosal ulceration and inflammation - clonic perforatio - sub to total colectomy +/- pelvic osteotomy
276
When would you perform a pelvic osteostomy on a patient with chronic obistiapation and megacolon?
If the megacolon is secondary to pelvic canal stenosis
277
What is anal furunculsosis/Perinanal fistula?
Chronic inflammatory disease resulting in ulceration and fistulous tracts in the nal and perianal areas.
278
What breed is predisposed to anal furunculosis and perinanal fistula?
GSDs
279
What might anal furunculosis/Periananla Fistula be concurrent with?
Idiopathic colitis
280
How would you non-specifically treat anal furunculosis/Perinanal fistula?
- Clean to reduce bacterial contamination - Antibiotics to treat secondary infection - Analgesia - stool softners
281
what immunosupressive therapy can be used to treat anal furunculosis/perianal fistula?
ciclospornin orally +/- ketoconazole Tacrolimus topicallu
282
What is perianal hernial a common cause of?
Straining to defeacate
283
What is a perineal hernia?
It is a perineal swelling where there is a loss of lateral support to rectum and deviation of rectum into subcut hernia
284
What kind of dogs are more likekly to suffer with perineal hernias?
older male entire dogs
285
For sphincter faecal incontinence, can you treat it?
- Usually permanent and untreatable - Loperamide may be useful in the management of mild faecal incontinence
286
What does Loperamide do?
(increases the anal canal pressure and attenuates the rectosphincteric relaxation reflex)
287
🐶 (Patterns of hepatobiliary and pancreatic disease in dogs and cats) What are the functions of the liver?
- Bilirubin metabolism - Bile acid metabolism - Carbohydrate metabolism - Lipid metabolism - Xenobiotic metabolism - Protein synthesis - Immune function
288
Describe the process of bilirubin metabolism
1. Senescent erythrocytes 2. Phagocytosed by macrophages in spleen, bone marrow, and liver 3. Globin portion degraded within macrophages (constituents returned to the amino acid pool) 4. Heme Fe transferred to Fe-binding proteins such as transferrin for recycling 5. Remaining portion of heme 6. Biliverdin (circulating bound to albumin) 7. Uptake by hepatocytes and glucuronydation 8. Bile excretion
289
What are the two types of congenitial shunts?
Extrahepatic shunts Intrahepatic shunts
290
What are extrahepatic shunts?
Shunting from portal vein or major trubuataries to caudal vena cava or azygos vein
291
What breed of dogs are more likely to suffer with extrahepatic shunts?
Smaller breeds of dogs and cats
292
What are intrahepatic shunts?
They are located in the left hepatic division where there is a persistant patent fetal ductus venosus
293
When are intrahepatic shunts typically seen?
In larger breeds of dogs
294
What is the pathogenesis of aquired shunts?
1. chronic liver disease 2. portal fibrosis 3. Portal hypertension
295
What is the clinical presentation of a juvenile patient with a congenital shunt?
Failure to thrive
296
What is the clinical presentation of a patient with a congenital shunt?
Small liver Neurological signs (hepatic encephalopathy -history of depression, convulsions, and other nervous signs exacerbated by a high-protein diet, and may be alleviated by dietary control)
297
What are the clinical presentation of a patient with an aquired shunt?
- Chronic liver disease resulting in portal hypertension - Possible ascites - 1l liver enzyme serum levels
298
What causes canine infectious hepatitis?
Canine adenovirus 1
299
What is canine adenovirus 1?
It is a DNA virus with tropism for endothelium, mesothelium and hepatocytes.
300
Whta is the clinical presentation of a patient with canine infectious hepatitis?
- Fever, abdominal pain, vomiting and melena (in severe cases) - Corneal opacity (oedema; "blue eye") in chronic cases (possible spontaneous resolution) - Rare peracute cases → sudden death without clinical manifestations
301
Describe the gross pathology of canine infectious hepatitis?
- Petechial to ecchymotic haemorrhages in serosa and organs - Enlarged and friable (necrotic) liver - Fibrin strands on liver surface, particularly between lobes - Thickening of gall bladder wall (oedema) - Small amounts of blood-tinged ascites
302
Descibe the histology of Canine infectious hepatitis
- Hepatocellular necrosis - Hepatocellular and endothelial intranuclear inclusion bodies
303
What can chronic hepatitis in dogs be caused by?
Infectious causes like viruses, bacteria, fungi, parasites or toxic causes.
304
although infectious agents and toxins can cause chronic hepatitis in dogs what are most cases usually considered?
Idiopathic or breed related
305
* Presumed immune-mediated /autoimmune mechanisms * Copper implicated in progressive necro-inflammatory canine liver disease, with breed-related susceptibility * Inflammatory infiltrates dominated by T-cells * Hepatocellular necrosis and loss * Progression to parenchymal collapse and fibrosis
306
307
What is the cm=linical presentation of chronic hepatitis in the english springer spaniel?
Lethargy, decreased appetite, vomiting, weight loss, diarrhoea, polydipsia
308
On physical examination of a english springer spaniel with chrinic hepatitis what might you find?
Icterus, hyperthermia, poor body condition, ascites, abdominal pain
309
Describe the clinical pathology of chronic hepatitis in the english springer spaniel
- I WBC count (most cases) | - 1 ALT and ALP - I AST, GGT, bilirubin and resting bile acids - U Albumin and Urea (some cases) | - 1 PT and PTT (some cases)
310
What is copper essential for?
Copper (Cu) is essential cofactor for enzymes & cellular functions
311
Where is coppers main uptake?
Uptake in the gastrointestinal tract
312
How does copper distribute throughout the body?
Distribution through the body bound to ceruloplasmin and albumin
313
Where is copper stored? and what is it bound too?
Storage mainly in liver and kidney and bound to metallothionine.
314
Where is copper mainly excreted?
Excretion mainly in the bile
315
What does free copper ions result in?
Generation of hydroxyl radicals
316
What clinical signs seen in copper-associated liver disease in dogs?
Exercise intolerance, depression, anorexia, vomiting, weight loss, icterus
317
What is the only breed you see heamolysis as a clinical sign of copper associated hepatic disease?
Bedlington terrier
318
How do you diagnose copper associated liver disease?
Increased liver enzymes copper levels in fresh liver sample histopathology
319
With copper associated liver disease what liver enzyme is more increased?
ALT is more increased than ALP
320
What us a idiosyncratic reaction?
An idiosyncratic reaction is an unpredictable, rare response to a drug or substance, unrelated to the dose. It may result from genetic factors or metabolic issues and can range from mild to severe, including allergic reactions or organ damage.
321
What does more xylitol in toxin dosage cause?
centrolobular to massive necrosis with haemorrhage of liver
322
What are the two main causes of steroid-induced hepatopathy?
latrogenic: Sustained therapeutic administration of corticosteroids. Endogenous: Cushing's syndrome due to hyperadrenocorticism (e.g., ACTH-secreting pituitary tumour).
323
What happens to hepatocytes in steroid-induced hepatopathy?
Intracytoplasmic accumulation of glycogen and fluid influx leads to marked hepatocellular swelling and vacuolation.
324
Does steroid-induced hepatopathy affect normal liver function?
No, normal liver function is maintained.
325
Which serum enzyme level is elevated in steroid-induced hepatopathy?
Glucocorticoid-inducible alkaline phosphatase (ALP).
326
What happens to serum ALT levels in steroid-induced hepatopathy?
Serum ALT levels show only a minor or negligible increase.
327
Which species is most commonly affected by suppurative cholangitis/-hepatitis?
Cats are typically affected; it is uncommon in dogs.
328
Suppurative cholangitis/-hepatitis often occurs concurrently with which other conditions?
Pancreatic and intestinal diseases (triaditis).
329
What does suppurative cholangitis/-hepatitis lead to?
Inflammation and degeneration of biliary and bile ducts, progressing to hepatic fibrosis.
330
What is the pathogenesis of suppurative cholangitis/-hepatitis?
Bile and biliary tract inflammation is associated with ascending bacterial infection. Escherichia coli is the most common bacterial isolate.
331
Which other bacteria have been reported in suppurative cholangitis/-hepatitis?
Bacteroides, haemolytic Streptococcus, and Clostridia.
332
What type of cholangitis commonly affects cats over 4 years of age?
Lymphocytic cholangitis/-hepatitis.
333
What are the clinical features of lymphocytic cholangitis in early stages?
Clinically silent in the initial stages.
334
What are the progressive features of lymphocytic cholangitis?
Prominent fibrosis, cholestasis, and possible icterus.
335
What is the presumed cause of lymphocytic cholangitis?
Immune-mediated aetiopathogenesis.
336
What condition may lymphocytic cholangitis be difficult to distinguish from?
Well-differentiated lymphoma.
337
What is gallbladder mucocele?
Gallbladder distension with accumulated mucoid secretion, which may progress to semisolid material.
338
What complications can gallbladder mucocele cause?
Variable extrahepatic biliary obstruction, possible ischaemic necrosis, and rupture.
339
What are the presumed causes of gallbladder mucocele?
Decreased gallbladder motility. Bile stasis. Altered bile composition and viscosity.
340
What are the functions of the exocrine pancreas?
Production and secretion of digestive enzymes. Production of intrinsic factor (required for Vitamin B12 absorption).
341
Which pancreatic enzymes are secreted as inactive proenzymes?
Trypsin, chymotrypsin, collagenase, phospholipase, elastase, carboxypeptidases.
342
Which pancreatic enzymes are secreted as active enzymes?
Amylase and lipase.
343
What causes EPI in dogs and cats?
Dogs: Juvenile pancreatic atrophy. Cats: Chronic pancreatitis.
344
At what point does EPI become clinically apparent?
Upon loss of 85-90% of secretory capacity.
345
How is EPI diagnosed?
By measuring serum Trypsin-Like Immunoreactivity (TLI).
346
What are the clinical features of EPI?
Diarrhoea, chronic weight loss despite voracious appetite, possible steatorrhea, and malassimilation of nutrients.
347
What breed is most commonly affected by juvenile pancreatic atrophy?
German Shepherds (autosomal recessive inheritance).
348
Which other breeds show familial predisposition to juvenile pancreatic atrophy?
Rough-Coated Collies and suspected in English Setters.
349
What is the primary cause of juvenile pancreatic atrophy in dogs?
It is presumed to be an autoimmune process against the acinar cells, preceded by intense inflammatory cell infiltration dominated by CD8+ T-lymphocytes.
350
What is the key event in the pathogenesis of acute pancreatitis?
The activation of trypsinogen to trypsin within acinar cells, which leads to the activation of pancreatic proenzymes and autodigestion of the organ.
351
What are the three major mechanisms of acute pancreatic necrosis?
Obstruction of duct(s) Direct injury to acinar cells Disturbances of enzyme trafficking within acinar cells
352
What is the outcome of acute pancreatic necrosis?
The resolution is generally incomplete, with a recurrent necrotising process that may lead to the complete destruction of pancreatic tissue.
353
What are the local effects of trypsin activation in acute pancreatitis?
Tripsin activates phospholipase A and elastase, leading to damage of local blood vessels, oedema, haemorrhage, and thrombosis.
354
What are the systemic effects of acute pancreatitis?
Release of activated enzymes, inflammatory mediators, and embolic debris into systemic circulation, which may cause hypotension, hypovolaemic shock, DIC, multiple organ failure, and other complications.
355
What are some risk factors for acute pancreatitis in dogs?
Middle-aged to old dogs Females > males Overweight or obese dogs Breeds like Miniature Schnauzer, Yorkshire/Silky Terriers, Miniature Poodles, Cocker Spaniels Conditions like hyperadrenocorticism, hypothyroidism, and hypercalcaemia.
356
What are the main risk factors for pancreatitis in cats?
Abdominal trauma (e.g. falling from height), acute hypercalcaemia, ductal reflux of duodenal contents, and organophosphate poisoning.
357
What is chronic pancreatitis characterised by?
Fibrosis and pancreatic atrophy, often following acute pancreatitis, and typically does not cause significant insufficiency.
358
What is the diagnostic cut-off value for canine pancreas-specific lipase (cPSL) in acute pancreatitis?
400 µg/L.
359
What is the diagnostic cut-off value for canine pancreatic elastase-1 (cPE-1) in pancreatic disease?
Serum cPE-1 > 17.24 ng/ml.
360
What is triaditis in cats?
A concurrent inflammation of the pancreas, liver, and small intestine, often triggered by intestinal inflammation leading to bacterial reflux.
361
What are common clinical signs of triaditis in cats?
Anorexia, weight and muscle mass loss, diarrhoea, vomiting, icterus, hepatomegaly, abdominal pain, and shock.
362
What are some clinical pathology abnormalities in cats with triaditis?
Increased liver enzymes (ALT, AST, GGT, ALP) and bilirubin Increased pancreatic lipase levels Decreased cobalamin, folate, and albumin
363
🐶 (Investigating Canine and Feline Liver Disease) How many lobes doe sthe liver consist of?
Six
364
What are the components of the liver's dual blood supply?
- Hepatic Artery – Supplies 25% of blood (oxygenated). - Portal Vein – Supplies 75% of blood (nutrient-rich, deoxygenated).
365
where does the portal vein collect blood from?
The portal vein collects blood from: - Gastrointestinal Tract (GIT) - Gallbladder (GB) - Pancreas - Spleen
366
What are the functions of hepatocytes?
They have metabolic and detoxifying functions
367
At what point does liver failure develop in terms of functional capacity loss?
Liver failure does not occur until more than 70% of functional capacity is lost
368
What is the structure of the biliary system?
A branched network that transports bile from individual hepatocytes.
369
What is the role of the gallbladder in the biliary system?
The gallbladder is the storage site for bile.
370
How does the biliary system connect to the duodenum?
Via the common bile duct.
371
what is the anatomic difference in the pancreatic duct between cats and dogs?
Cats and dogs have variations in the structure of the pancreatic duct.
372
What are the two primary functions of bile?
Emulsifies fats and neutralises stomach acid.
373
What is primary liver disease?
Disease originating in the liver itself.
374
What is secondary liver disease?
Disease caused by factors outside the liver leading to: - Non-specific reactions by liver cells. - Increased liver enzymes +/- ultrasound or histopathology changes.
375
What hypoxia or hypotension-related conditions can cause secondary hepatopathy?
Shock Surgery Seizures Anaemia
376
What cardiac conditions can lead to secondary hepatopathy?
Right-sided congestive heart failure (CHF) Pericardial effusion
377
Which non-hepatic inflammatory diseases can cause secondary hepatopathy?
Gastrointestinal (GI) disease Pancreatitis Sepsis Toxaemia
378
Which drugs can cause secondary hepatopathy in dogs?
Glucocorticoids and Phenobarbital.
379
How can metastatic neoplasia affect the liver?
Metastatic neoplasia can lead to secondary hepatopathy.
380
Which endocrinopathies can cause secondary hepatopathy?
Cushing's disease Addison's disease Diabetes mellitus Hyperthyroidism (cats) Hypothyroidism (dogs) Hyperlipidaemia (Miniature Schnauzers)
381
What does the severity of clinical signs of liver disease depend on?
speed of disease or amount of liver damage.
382
Which breeds are associated with chronic hepatitis?
Springer Spaniels Dobermans Cocker Spaniels Labradors
383
Which breeds are prone to copper storage disease?
Bedlington Terriers Labradors (USA)
384
Which breeds are prone to gall bladder mucoceles?
Shetland Sheepdogs Border Terriers
385
Which condition is common in overweight cats with recent anorexia?
Feline hepatic lipidosis.
386
What congenital abnormalities are associated with young cats and dogs?
Portosystemic shunt (PSS) Portal vein hypoplasia
387
When you are taking a history of a patient with suspected acute liver disease what you asking?
- Patient healthy until recently? - Recent toxin exposure? - Drug administration?
388
When you are taking a history of a patient with suspected chronic liver disease what you asking?
- Patient has often had weeks or months of non-specific signs - weight loss?
389
What are hepatotoxic drugs that can cause acute hepatic disease?
- NSAIDs - Paracetamol (cats) - Azathioprine - TMPS antibiotics (dogs) - Diazepam (cats) - Lomustine - Carbimazole/methimazole
390
What infectious diseases can cause acute hepatic disease?
- Leptospirosis - CAV-1 - Bacterial hepatitis - Bacterial cholangiohepatitis/cholangitis
391
What metabolic condition can cause acute hepatic disease in cats?
Hepatic lipidosis
392
Name toxins that can cause acute hepatic disease
Xylitol (found in chewing gum) Mycotoxins (e.g., aflatoxicosis) Amanita mushrooms Cyanobacteria (blue-green algae, microcystin toxicosis)
393
Name a type of neoplasia that can cause acute hepatic disease.
Diffuse infiltration, such as lymphoma.
394
What is an idiopathic cause of acute hepatic disease?
The cause is unknown (idiopathic).
395
What are the biochemical indicators of liver damage?
ALT and AST.
396
What are the biochemical indicators of cholestasis?
ALP GGT Bilirubin
397
What are the biochemical indicators of liver function?
Bile acids* Ammonia* Bilirubin Glucose Urea Albumin Cholesterol (*Bile acids and ammonia are more specific indicators.)
398
what do hepatocellular “leakage enzymes” indicate?
Hepatocellular membrane damage.
399
Which intracellular markers are hepatocellular leakage enzymes?
Alanine Aminotransferase (ALT) Aspartate Aminotransferase (AST)
400
What is ALT specific for, and what are its half-lives in cats and dogs?
Specific for: Liver damage. Half-life: 3–4 hours in cats 60 hours in dogs
401
where else is AST found besides the liver?
Skeletal muscle, cardiac myocytes, kidneys.
402
What do membrane-bound markers indicate, and where are they located?
ndicate impaired bile flow (“cholestasis”). Located at the bile canalicular surface.
403
What are the membrane-bound markers, and how specific are they?
Alkaline Phosphatase (ALP or ALKP): Least specific. Gamma Glutamyl Transferase (GGT): More specific for hepatobiliary disease but less sensitive.
404
What are the half-lives of ALP in dogs and cats?
77 hours in dogs 6 hours in cats
405
What are the isoforms of ALP, and when can steroid-induced ALP be seen in dogs?
soforms: Liver ALP Bone ALP (from osteoblasts, young animals, or bone neoplasia) Steroid-induced ALP. Steroid-induced ALP causes: Exogenous: Corticosteroid medication (topical or systemic). Endogenous: Cushing’s Disease.
406
If there is elevated liver enzymes with no clinical signs, when might they need re-evaluated?
2-4weeks
407
What do liver enzyme levels not tell you?
* Cause is primary or secondary * Function of the liver * Prognosis
408
What is biirubin?
Yellow pigment produced from haem catabolism
409
What si the primary source of bilirubin?
RBC
410
Describe the process of billirubin to bile.
Bilirubin is transported to the liver and conjugated, secreted into bile.
411
Where is bile stored and excreted?
It is stored in the gall bladder and excreted via ducts.
412
What is jaundice?
It is yellow staining of tissue from excess bilirubin
413
What is the cause of pre-hepatic jaundice?
Excess bilirubin production from haemolysis (e.g. haemolytic anaemia).
414
What is the cause of hepatic jaundice?
Defective bilirubin processing in the liver due to Abnormal uptake, Impaired conjugation or Defective excretion.
415
What is the cause of post-hepatic jaundice?
Obstruction of bile flow due to: Pancreatitis. Neoplasia. Choleliths. Cholecystitis. Bile duct rupture.
416
What biomolecules are made in the liver?
Glucose, Urea, Albumin, Cholesterol.
417
When do biomolecules decrease in liver disease?
Decrease with >70% liver dysfunction.
418
What are the clinical signs of biomolecule decrease due to liver dysfunction?
Ascites: Albumin <15 g/l. Hypoglycaemia: Ataxia, tremors, seizures.
419
What are non-liver causes of albumin decrease?
PLE (protein-losing enteropathy). PLN (protein-losing nephropathy).
420
What are non-liver causes of glucose decrease?
Addison’s, sepsis, insulinoma, xylitol toxicity
421
What are non-liver causes of urea decrease?
Low-protein diet, PUPD (polyuria-polydipsia)
422
What are non-liver causes of cholesterol decrease?
Malabsorption, malassimilation.
423
What causes high bile acids?
Reduction in hepatocellular mass. Impaired hepatocyte function. Disturbed enterohepatic circulation.
424
What disrupts enterohepatic circulation?
Portal blood flow disruption to the liver. Obstruction of biliary flow from the liver.
425
What are the differential diagnoses for high bile acids?
Portosystemic shunt. Diffuse hepatic disease. Biliary stasis.
426
What is the most sensitive liver function test for non-jaundiced dogs?
Bile acid stimulation test.
427
What is the procedure for a bile acid stimulation test?
Starve the patient for 12 hours (pre-prandial sample). Feed the patient, then take a post-prandial sample 2 hours later.
428
Why does the post-prandial bile acid level increase?
Feeding causes gall bladder contraction, releasing bile acids.
429
What are the normal bile acid levels?
Pre-prandial: 0–10 μmol/l. Post-prandial: 0–20 μmol/l.
430
What bile acid level indicates hepatic dysfunction?
>40 μmol/l indicates hepatic dysfunction.
431
What are “grey zone” bile acid results?
20–40 μmol/l. Can occur with secondary hepatopathies.
432
What are the limitations of the bile acid test?
Does not determine specific aetiology. Not helpful if the patient is jaundiced.
433
Why is a bile acid test not useful in jaundiced patients?
Bile acid increase occurs before jaundice in hepatobiliary disease. Cannot differentiate hepatic from post-hepatic jaundice.
434
What does hyperammonaemia indicate?
Abnormal portal blood flow. Hepatic dysfunction. Rare urea cycle abnormality.
435
What coagulation factors are produced by the liver?
All except factor VIII and von Willebrand factor (vWF).
436
What happens to coagulation in severe liver damage?
Blood coagulation may be impaired.
437
When should coagulation be checked?
Before surgery, liver FNAs, abdominal taps, or cystocentesis.
438
What haematological changes occur with liver disease?
Mild anaemia: Chronic disease, GI bleeding, or coagulopathy. Microcytic, hypochromic anaemia: Portosystemic shunts.
439
What findings on urinalysis suggest liver disease?
Low specific gravity (polydipsia). Bilirubinuria. Ammonium urate crystals.
440
What can radiography evaluate in liver disease?
Liver shape and size. Presence of choleliths. Ascites limits usefulness.
441
What is the role of ultrasound in liver disease?
Assess hepatic parenchyma and portal vein branches Investigate biliary tract for post-hepatic jaundice. Identify nodules, masses, or abdominal effusion.
442
What causes ascites in liver disease?
Decreased oncotic pressure (hypoalbuminaemia). Increased hydrostatic pressure (portal hypertension).
443
What causes portal hypertension?
Cirrhosis or fibrosis obstructing blood flow. Vascular obstruction (e.g., thrombus or neoplasia).
444
What is chronic hepatitis?
Inflammation of hepatic parenchyma. Commonly idiopathic.
445
What breeds are prone to chronic hepatitis?
Labrador Retrievers. English Springer Spaniels. Cocker Spaniels. Dobermans.
446
What is lymphocytic cholangitis?
Inflammation with lymphocytes in the portal region. Associated with immune-mediated disease.
447
What causes vacuolar hepatopathy?
Hepatocytes distended with glycogen. Linked to glucocorticoids or hyperadrenocorticism.
448
What is gall bladder mucocele?
Gall bladder distended with thick mucus. Requires surgical cholecystectomy.
449
What is bile peritonitis?
Inflammatory response to free bile in the abdominal cavity. Caused by trauma, chronic inflammation, or neoplasia.
450
🐶 (Pancreatitis and Exocrine Pancreatic Insufficiency in the Dog and Cat) What do pancreatic acinar cells produce and secrete?
Produce and secrete proteolytic enzyme precursors (zymogens), amylases & lipases (hydrolases).
451
What do the pancreastic duct cells produce and secrete?
Produce and secrete bicarbonate-rich fluid to help neutralise stomach acid as it enters the small intestine.
452
Dogs vs Cats: Pancreatic Ducts
Dogs: Two ducts: Pancreatic duct (smaller) Accessory duct → Opens at the minor duodenal papilla, distal to the common bile duct (CBD). Cats: One duct: Pancreatic duct merges with the CBD before opening at the major duodenal papilla.
453
What is the intrinsic factpre that the pancreas produces essential for?
Absorption of cobalamin (vitamin B12)
454
Why in cats with pancreatic disease will the VitB12 be lower?
Due to intrinsic factor depletion whihc is what they mainly rely on to get their VitB12
455
What is acute pancreatitis?
Acute pancreatitis in dogs is sudden pancreatic inflammation caused by premature activation of zymogens within the pancreas, leading to self-digestion, pain, and inflammation.
456
What are zymogens?
inactive digestive enzymes
457
What are proteolytic enzymes synthesised as?
Inactive zymogens
458
How are the zymogens kept seperate from the proteolytic processes?
By being packaged into granules
459
What is incorporated into the zymogen granules and why?
Pancreatic seceretory trypsin inhibitor to prevent premature activation of trypsin.
460
Pathogenesis of Acute Pancreatitis in Dogs
Lysosomes & zymogen granules fuse to form vacuoles Lysosomal enzymes activate trypsinogen to trypsin Vacuoles rupture releasing active enzymes into cell Other zymogens then activated Causes cell necrosis & pancreatic autodigestion Inflammatory mediators & cytokines etc cause cell necrosis & inflammation
461
What are risk factors for acute pancreatitis in dogs?
- Hypertriglyceridaemia - Genetic predispositions in Miniature Schnauzers & Yorkshire Terriers - Drugs e.g. KBr - Hypotension/ischaemia/trauma - Hypercalcaemia - Underlying neoplasia
462
What are risk factors for acute pancreatitis in cats?
- Biliary Tract Disease - Inflammatory Bowel Disease - Ischaemia - Infection: toxoplasmosis, FIP - O-P toxicity - Trauma
463
Describe the clinical presentation of acute pancreatitis in dogs and cats?
- anorexia - vomiting - weakness/lethargy - diarrhoea - dehydration - abdominal pain - fever - Icterus
464
What 3 clinical signs are less common in cats with acute pancreatitis?
- vomiting - abdominal pain - icterus
465
How do you diagnose a dog or cat with acute pancreatitis?
- Clinical Presentation - Haematology & Serum -Biochemistry - Serum amylase and lipase - Trypsin-like immunoreactivity (TLI) - Pancreas Specific Lipase (PLI) - Diagnostic Imaging - Cytology & Pancreatic Biopsy
466
When doing heamatology on a patient who is suspected to have acute pancreatitis what are you looking for?
Inflammatory leucogram
467
When doing serum biochem on a patient who is suspected to have acute pancreatitis what are you looking for?
- Elevations in ALT, AP - Hyperbilirubinaemia - Hypocalcaemia - Azotaemia & electrolyte disturbances
468
Do levels of serum amylase and standard lipase increase or decrease in acute pancreatitis?
Increase
469
Even though serum amylase and standard lipase levels increase in acute pacreatitis what are the downsides that make it less releaible as a diagnosise.
- Lack sensitivity and specificity - Levels are influenced by GFR and therefore increase in dehydrated patients - Originate from extra-pancreatic tissue e.g. gastric/intestinal mucosa - In dogs serum lipase may be increased with neoplastic, hepatic and renal disease, or following steroid administration
470
Even though serum trypsin-like immunoreactivity increases with acute pancreatitis what is its downsides?
It increases early in acute pancreatitis but the half-life is very short and levels fall rapidly resulting in poor sensitivity of the test. There can also be a delay in obtaining results as its an external test.
471
What are the two tests for canine pancreas specific lipase?
SNAP cPLTM - in house Spec cPL - external lab
472
What should you do if the in house snap test for canine PLI is positive or negative?
If negative? unlikely to have acute pancreatitis If positive? send away for quantitative test
473
Describe the meaning of the results of a Spec test for canine PSI?
<200 ug/L – negative 200 – 399 ug/l – equivocal zone >400 ug/L – positive
474
What mighta false positive be due to on a Spec cPL?
Potential false +ve if renal disease or steroid administration
475
What could you see on an abdominal radiograph of a patient with acute pancreatitis?
- Low sensitivity - Loss of serosal detail or an increase in opacity in the R cranial quadrant - Displacement of duodenum and/or transverse colon - Dilated gas-filled duodenum - R/O other causes of clinical presentation esp FB
476
What could you see on an abdominal ultrasound of a patient with acute pancreatitis?
- Enlarged or ill-defined hypoechoic to complex mass - Functional ileus of the duodenum - Hyperechoic tissues around the pancreas - focal peritonitis
477
How should you go about managing a patient with acute pancreatitis?
Supportive and symptomatic management - Fluid and electrolyte balance - Analgesia - Anti-emetic and Anti-ulcer therapy - Anticoagulant therapy (heparin) if thrombosis suspected - Nutritional support - Management of complications
478
Why would you use plasma in acute pancreatitis?
Provides α-2 macroglobulin (enzyme inhibitor)
479
How does pancreatic extract help with acute pancreatitis?
Decreases pancreatic stimulation
480
When should you consider antbiotics as part of the treatment for acute pancreatitis?
Consider if pyrexia, GI ulceration, pancreatic abscess
481
When should you consider corticosteroids as part of the treatment for acute pancreatitis?
Counteract almost all pathways of inflammation
482
What might occur an episode of acute pancreatitis?
- Pancreatic abscess formation - Necrotic masses - Pancreatic pseudocysts - Duodenal perforation/septic peritonitis - Biliary tract obstruction
483
What can chronic pancreatitis be cause by?
May be due to progression from acute disease May present due to progressive loss of exocrine & endocrine function
484
When should you suspect chronic pancreatitis?
- Intermittent, low-grade clinical signs - Recurrent acute episodes of pancreatitis - Exocrine pancreatic insufficiency - Diabetes mellitus (PUPD, weight loss, polyphagia) – more common in the cat but not really common at all
485
How are you going to diagnose chronic pancreatitis?
- Biopsy if having surgery for another reason (changes may be patchy) - Ultrasound - PLI: insensitive due to loss of pancreatic mass
486
For intermittent/low-grade relapsing presentation what should you treatment plan look like?
- Analgesia (e.g. gabapentin) - Low-fat diet (particularly if hyperlipidaemia is a trigger) - Vitamin B12 injections - if low - Consider appetite stimulants (cats; e.g. mirtazapine) - Treat EPI if present or if chronic weight loss - Treat DM if present
487
Exocrine Pancreatic Insufficiency (EPI) - When do clinical signs develop?
Clinical signs develop when 90% of pancreatic secretory capacity is lost.
488
What is EPI?
Exocrine Pancreatic Insufficiency - A decrease in pancreatic secretory capacity
489
What is the most common cause of EPI in cats?
Chronic pancreatitis.
490
What is the end-stage autoimmune cause of EPI in dogs?
Pancreatic acinar atrophy
491
Which breeds are predisposed to pancreatic acinar atrophy due to an autosomal recessive condition?
German Shepherd Dogs (GSDs) and Rough Collies.
492
What is pancreatic aplasia?
A congenital condition where the pancreas fails to develop properly, leading to EPI.
493
What is the relationship between chronic pancreatitis and diabetes mellitus?
Chronic pancreatitis may lead to concurrent diabetes mellitus.
494
At what age does pancreatic acinar atrophy typically present in dogs?
In young dogs.
495
What are the key clinical signs of EPI in dogs and cats?
- Weight loss despite a good appetite (polyphagia) - Chronic diarrhoea (often voluminous, pale, and greasy stools) - Flatulence - Poor coat condition - Increased faecal volume
496
How do you diagnose EPI?
- Measure Trypsin-like Immunoreactivity (TLI) - This blood test is highly sensitive and very specific for EPI - Sample after 12h fast
497
How do you go about managing EPI interms of enzyme supplementation?
- Powder or granules (not unopened capsules) - Enteric coated? – controversial - Give with every meal – mix with food - Can be unpalatable for cats
498
How do you go about managing EPI interms of diet?
- Individual variation - May be able to continue original diet - No single best diet - Highly digestible, low fibre, moderate fat diet may help? - Little & often?
499
How do you go about managing EPI interms of Cobalamin supplementation?
- Cbl deficiency common (82%) in dogs and cats with EPI - IF deficiency plus Small Intestinal Bacterial Overgrowth (SIBO) - Affects prognosis - Supplementation essential by SQ injection
500
how do you treat EPI?
- Dysregulation of GI flora via Antibiotic responsive diarrhoea = Metronidazole, tylosin, tetracyclines The effect of gastric pH * Consider H2-antagonists or proton pump inhibitors Diet change - Fat restriction? Consider concurrent SI disease * Chronic inflammatory enteropathy * Dysbiosis * Concurrent intestinal parasitism e.g. chronic giardiasis May need further investigations BROOOOOOO idk
501
(Advanced fluid therapy for the small animal patient) Why give fluids?
To treat dehydration, shock, electrolyte imbalances, maintain oncotic pressure, and promote diuresis.
502
What is the normal maintenance fluid requirement for dogs and cats?
50 ml/kg/day (likely overestimated for large dogs and underestimated for small dogs/cats)
503
What are the major causes of decreased fluid intake?
Anorexia and starvation.
504
What are pathological causes of fluid loss?
Vomiting, diarrhoea, renal disease, panting (pyrexia), wound exudation, and third-space losses.
505
Definition of dehydration
A deficit in total body water, often used to refer to isotonic and hypotonic losses.
506
Common clinical signs of dehydration
Dry mucous membranes, prolonged skin tenting, sunken eyes, tachycardia, and weak pulses.
507
What happens to PCV/TP in dehydration?
Both increase, but baseline values may be unknown.
508
Why is weight loss an unreliable dehydration marker in dogs?
Normal starting weight is often unknown, and weight loss does not always correlate with fluid loss.
509
What type of fluids are used for dehydration correction?
Isotonic crystalloids (e.g. Hartmann’s, Ringer’s, 0.9% NaCl).
510
What is the main exception for not using isotonic crystalloids?
When there are dramatic sodium concentration abnormalities.
511
What is the most common route of fluid administration?
Intravenous (IV).
512
When might subcutaneous (SC) or oral fluids be used?
In cases of mild dehydration.
513
How is the fluid deficit calculated?
% dehydration × body weight (kg) × 1000 = deficit in ml.
514
How is the total daily fluid requirement calculated?
Deficit + maintenance + ongoing losses.
515
Why is continuous re-evaluation of fluid therapy necessary?
To account for ongoing losses and reassess hydration status.
516
A 10kg dog is 10% dehydrated. How much fluid does it need in 24 hours?
Deficit: 10% × 10,000ml = 1000ml Maintenance: 50ml/kg/day × 10 = 500ml Total = 1500ml (or 62ml/hr).
517
A 4kg cat is 8% dehydrated. How much fluid does it need in 24 hours?
Deficit: 8% × 4000ml = 320ml Maintenance: 50ml/kg/day × 4 = 200ml Total = 520ml (or 22ml/hr).
518
What might cause ongoing fluid losses?
Vomiting, diarrhoea, renal polyuria, third-space losses, wound drainage, panting, and salivation.
519
How can ongoing losses be estimated?
Indwelling urinary catheter, weighing towels, measuring vomitus/diarrhoea output
520
How often should fluid therapy be reassessed?
Usually every 12-24 hours but as frequently as every 4 hours in critical cases
521
What is the main emergency electrolyte disturbance?
Hyperkalaemia.
522
What are symptoms of hypokalaemia?
Muscle weakness, polyuria, polydipsia.
523
Causes of hypokalaemia?
Decreased intake, translocation (ECF → ICF), increased loss.
524
How is hypokalaemia managed?
Potassium supplementation in fluids (NaCl or Hartmann’s).
525
What is the main cause of hypernatraemia?
Hypotonic fluid loss or salt intoxication.
526
Why must chronic hypernatraemia be corrected slowly?
To avoid osmotic demyelination syndrome (≤0.5 mmol/l/hr change).
527
What is a common cause of hyponatraemia?
GI disease with hypertonic volume losses.
528
What are risks of rapidly correcting chronic hyponatraemia?
Osmotic demyelination (myelinosis).
529
Causes of hypoalbuminaemia?
Hepatic disease, protein-losing enteropathy/nephropathy, inflammatory effusions.
530
At what albumin level is intervention critical?
<15 g/L.
531
What is used to support oncotic pressure in hypoalbuminaemic patients?
Synthetic colloids (20ml/kg/day), albumin transfusion, or plasma.
532
What are potential side effects of colloids?
Coagulopathy, renal damage, anaphylaxis.
533
Diarrhoea-related electrolyte changes?
Hypokalaemia, metabolic acidosis, variable sodium levels.
534
Why is Hartmann’s preferred in diarrhoea cases?
It provides a balanced electrolyte solution.
535
How does pre-pyloric vomiting affect electrolytes?
Hypokalaemia, hyponatraemia, hypochloraemic metabolic alkalosis.
536
What is paradoxical aciduria?
Acidic urine despite extracellular alkalosis.
537
Fluid therapy considerations in pancreatitis?
Correct dehydration, possibly use fresh frozen plasma in severe cases.
538
What happens with fluid loss in bowel obstruction?
Marked sodium, potassium, and albumin loss, leading to metabolic acidosis.
539
Why avoid Hartmann’s in severe liver disease?
Impaired lactate metabolism.
540
Why is hypoalbuminaemia common in liver disease?
Decreased hepatic production.
541
Why might ascitic patients need adjusted fluids?
To prevent worsening third-spacing.
542
Who requires only maintenance fluids?
Comatose patients or those with feeding tubes.
543
How do maintenance fluids differ from replacement fluids?
Lower sodium (40-60 mmol/l), higher potassium (15-30 mmol/l).
544
Why is glucose added to maintenance fluids?
To prevent haemolysis and make them isotonic.
545
Why is 5% dextrose not suitable for calorific support?
Massive volumes are needed to meet metabolic energy requirements.
546
Why should 5% dextrose not be used for shock treatment?
It metabolises quickly, leaving a hypotonic fluid that doesn’t stay in the vascular space.
547
Why is 5% dextrose not useful for dehydration treatment?
Dehydrated patients need electrolytes, which it lacks.
548
Signs of fluid overload?
Chemosis, nasal discharge, tachypnoea, restlessness, peripheral oedema, polyuria.
549
Which patients are at high risk of fluid overload?
Those with renal disease, cardiac disease, hypoalbuminaemia, pulmonary contusions.
550
What are catheter-related fluid therapy complications?
Infection, thrombophlebitis, catheter blockage or displacement.

BVMS 3 (23 decks)

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