SA GI disease Flashcards

1
Q

Signs of oropharyngeal and oesophageal disease?

A
Dysphagia
Drooling saliva
Halitosis
Odynophagia
Regurgitation
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2
Q

Signs of dysphagia?

A
Difficulty lapping or forming bolus
Excessive jaw or head motion
Dropping food from mouth
Drooling saliva/foaming at mouth
Persistent, ineffective swallowing
Nasal discharge
Gagging
Coughing
Failure to thrive
Reluctance to eat or pain
Halitosis
Blood tinged saliva
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3
Q

Causes of dysphagia?

A
Functional neuromuscular dysphagia:
- cricopharyngeal chalasia/achalasia
- myasthenia gravis
- brainstem disease
- peripheral neuropathy
- polymyopathy
- hypothyroidism
- botulism
Morphological dysphagia:
- oropharyngeal inflammation
oropharyngeal trauma
- foreign bodies
- neoplasia
- congenital/developmental (hare-lip, lip fold deformities, cleft palate, malocclusion, craniomandibular osteopathy, temporomandibular dysplasia)
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4
Q

Causes of halitosis?

A
Oropharyngeal disease - inflammation, neoplasia, foreign body
Oesophageal disease
Dietary associated
Malabsorption
Dental disease
Nasal cavity and sinus disease
Uraemia
Liver disease
Anal sac disease
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5
Q

Define pseudoptyalism and ptyalism?

A
Pseudoptyalism = failure to swallow normal volume of saliva
Ptyalism = increased saliva production
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6
Q

How to differentiate between vomiting and regurgitation?

A

Vomiting (active) - salivation, heaving, digested food

Regurgitation (passive) - head down and food comes out, undigested food covered by mucus/saliva

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7
Q

Secondary signs of oesophageal and oropharyngeal disease?

A

Malnutrition/dehydration
Anorexia/polyphagia
Aspiration pneumonia/tracheal compression - cough, dysphagia

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8
Q

Radiography for swallowing problems/vomigurgitation?

A

Survey radiographs - head, neck, thorax
Barium oesophagram +/- fluoroscopy - barium mixed with food, iodine contrast if perforation suspected
‘Met check’

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9
Q

Lab investigations for swallowing problems/vomigurgitation?

A
Haematology
Serum biochemistry and urinalysis
Virology (cats especially)
'Special' tests
- Anti-ACh receptor antibody (myaesthenia gravis)
- 2-M antibodies (polymyositis)
- ACTH stimulation test (hypoadrenocorticism)
- Thyroid testing?
- Toxicological tests?
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10
Q

Investigations for swallowing problems/vomigurgitation?

A
History and physical exam
Diagnostic imaging
Endoscopy
Lab investigations
FNA
Biopsy
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11
Q

Major disease syndromes of the oesophagus?

A

Motility - megaoesophagus, dysautonomia, hiatal hernia
Obstruction - vascular ring, stricture, foreign body, neoplasia
Inflammation - oesophagi’s, reflux, hiatal hernia
Misc - diverticulum, broncho-oesophageal fistula

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12
Q

Definition of megaoesophagus?

A

Oesophageal dilation with functional paralysis

-> Failure of progressive peristalsis

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13
Q

Diagnosis of megaoesophagus?

A

Radiography +/- contrast
- uniformly dilated, gas and/or fluid filled
- ventral displacement of trachea
- secondary aspiration pneumonia
Fluoroscopy occasionally essential - oesophageal dysmotility

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14
Q

One example of each cause of secondary megaoesophagus?

A

Neuromuscular - myaesthenia gravis
Oesophageal - oesophagitis
Neuropathies - dysautonomia
CNS - distemper

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15
Q

Treatment and prognosis of idiopathic megaoesophagus?

A
Feeding from a height - bailey chair
Slurry, textured food, meatballs?
Bethanecol?
Metaclopramide, cisapride?
Prognosis - guarded, danger of aspiration pneumonia, spontaneous recovery in some
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16
Q

Causes of oesophagitis?

A

Ingestion of caustics and irritants
Foreign bodies
Acute and persistent vomiting
Gastric reflux

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17
Q

Clinical signs of oesophagitis?

A
Anorexia
Dysphagia
Odynophagia
Regurgitation
Hypersalivation
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18
Q

Diagnosis and treatment of oesophagitis?

A

Diagnosis - clinical signs, endoscopy, response to empirical treatment?
Symptomatic treatment - frequent small feeds, antibiotics, liquid antacids, local anaesthetics, gastrostomy tube feeding
Specific treatment - sucralfate, antacids, metaclopramide

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19
Q

Types/causes of oesophageal obstruction?

A

Intraluminal - foreign body, neoplasm, stricture, granuloma

Extraluminal - thyroid, thyme/mediastinum, vascular ring

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20
Q

Aetiology of oesophageal stricture?

A

Fibrosis after ulceration of mucosa by:

  • foreign body
  • caustic material
  • severe oesophagitis
  • gastric reflux esp. pooled secretions during GA
  • drug therapy e.g. doxycycline in cats
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21
Q

Treatment of oesophageal stricture?

A

Bougienage - increased risk of perforation, longitudinal shear
Balloon dilatation - radial stretch (less traumatic), stationary force, less risk of perforation
Inject steroid around the lesion (triamcinolone acetonide)

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22
Q

Signalment of oesophageal foreign body?

A

Usually young animals
Common in greedy dogs eating chop bones esp terriers
Rare in cats

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23
Q

Diagnosis of oesophageal foreign body?

A

Radiography - don’t give barium! - visible foreign body, mediastinitis, abscess
Oesophagoscopy

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24
Q

Treatment for oesophageal foreign body?

A
Perforal approach:
- flexible or rigid endoscope
- preferably pull FB to mouth
- or push to stomach for gastrostomy
- check for oesophageal tear
Surgical removal:
- last resort
- essential if large laceration
Post removal: radiographs, PEG tube, omeprazole, sucralfate
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25
Vomit reflex?
``` Contract pylorus Relax stomach and LOS Contract abdominal muscles Thorax vs closed glottis Open UOS Antiperistalsis ```
26
Differentials for chronic vomiting, secondary to systemic/metabolis disease?
``` Infections - distemper, lepto Pyometra Renal failure Hepatic disease Drugs - digoxin, erythromycin, morphine Ketoacidic DM Hypoadrenocorticism CNS disease - motion sickness, vestibular disease Neoplasia ```
27
Differentials for chronic vomiting, secondary to intestinal/peritoneal disease?
Inflammatory bowel disease Intestinal neoplasia Small intestinal obstruction Pancreatitis
28
Differentials for chronic vomiting due to primary gastric diseases?
``` Chronic gastritis Gastric retention disorders Gastric ulcers Gastric neoplasia Diffuse GI disease involving stomach - inflammatory bowel disease, alimentary lymphoma ```
29
Signs of gastric disease?
Vomiting Haematemesis Nausea - hypersalivation, retching, anorexia Melaena Miscellaneous - belching, bloating, borborygmi, weight loss
30
Pathophysiology of gastric disease?
Gastric outflow obstruction Gastroparesis Disruption of mucosal barrier
31
Diagnosis of chronic vomiting?
Distinguish vomiting vs regurgitation Eliminate secondary causes - Hx, PE, lab analysis, imaging Abdominal imaging - plain radiography, contrast radiography, ultrasonography Gastroscopy/coeliotomy Symptomatic treatment
32
Physical exam for chronic vomiting?
Oral exam - ulcers, linear foreign body Abdominal palpation - pain, foreign body, intra-abdominal mass, distended stomach or bowel Rectal exam - diarrhoea, melaena
33
Lab evaluation for chronic vomiting?
Haematology Biochemistry Urinalysis - no pathognomic changes, more used to rule out systemic disease, also can assess hydration status
34
Radiography and ultrasonography for chronic vomiting - what can be checked for?
``` Radiography: survey abdominal radiograph - foreign body - abdominal mass - intestinal obstuction - peritonitis - GDV Ultrasonography: - foreign bodies - ulcers - thickening of gastric mucosa - loss of layering (suggests infiltration) ```
35
Indication for endoscopy (gastroscopy) for chronic vomiting and what is done?
If clinical or radiographic signs of gastric disease Inspection and biopsy (even if grossly normal) Foreign body removal
36
Causes of chronic gastritis?
``` Aetiology usually unknown Sometimes generalised IBD Chronic gastric parasitism Hairballs in cats? Spiral bacteria - Helicobacter? Immune mediated? ```
37
Clinical signs of chronic gastritis?
Intermittent chronic vomiting (vague) +/- periodic early morning vomit with bile +/- poor appetite +/- gastric bleeding
38
Diagnosis of chronic gastritis?
Lab changes often non specific Imagining findings non specific Gastroscopy and biopsy
39
Treatment for chronic gastritis?
Removal of etiologic agent if known Diet - multiple small meals, low fat diet (fatty foods stay in stomach longer), hypoallergenic diet (novel protein source, hydrolysed protein) Acid blocker Corticosteroids?
40
What are gastric retention disorders? Types?
Retention of food for >8h causing delayed vomiting of food Anatomical flow obstruction Functional disorder - primary motility disorder - inflammatory disease (IBD, gastric ulcer)
41
Anatomical outflow obstructions causing a gastric retention disorder?
Pyloric stenosis Neoplasia, polyp CHPG Foreign body
42
Bilious vomiting?
Often occurs in dogs fed once daily (especially if fed in the morning) Vomiting occurs overnight or in the morning Vomitus often bile stained fluid, not food Presumably reflects abnormal ... Diagnosis - rule out other causes of vomiting, treatment trial Treatment - feed more often focussing on late meal, pro kinetics (ranitidine or metaclopramide)
43
Pyloric stenosis - breeds/species associations? Treatment?
Congenital in brachycephalic breeds Association with megaoesophagus in cats Treatment: pylorotomy/pyloroplasty
44
What is chronic hypertrophic pylorogastropathy (CHPG)?
Idiopathic mucosal hypertrophy May cause outflow obstruction Most common in toy breeds Treatment - surgery
45
Treatment for functional causes of gastric retention?
Treat underlying inflammatory disease Prokinetics - metaclopramide: stimulates normal gastric peristalsis - ranitidine: H2 antagonist plus pro kinetic action - erythromycin: low dose stimulates motilin receptors
46
Causes of haematemesis?
``` Generalised bleeding Swallowed blood - oropharyngeal, nasal, pulmonary Severe gastritis Gastric ulcer Gastric neoplasia Duodenal disease ```
47
Signs of gastric ulcers?
``` Haematemesis Melaena Anaemia Weight loss Pain Peritonitis etc if perforated ```
48
Aetiology of gastric ulcers?
``` Drugs - NSAIDs, corticosteroids Head and spinal injuries - in combination with corticosteroids, also colonic ulcers/perforations Gastritis Metabolic - liver disease, uraemia Bile reflux? Mastocytosis Gastrinoma (Zollinger-Ellison) Spiral bacteria - Helicobacter? ```
49
Helicobacter species? Cause disease?
``` H felis H heilmannii H bizzozeroni others High prevalence (~100%) - seen on biopsy Evidence of recognition by host - Ab response, lymphoid follicles Often no evidence of clinical disease But a cause of chronic gastritis? ```
50
Treatment for gastric ulcers?
``` Treat identifiable primary cause Sucralfate Acid blockers - antacids, H2 antagonists (cimetidine licensed but poss poor efficacy and side effects, ranitidine can be used for motility disorders under cascade), proton pump inhibitors (omeprazole) Antibiotics? Triple therapy? ```
51
Prevention of gastric ulcers?
Limited protective effect: H2 antagonists, PPis, sucralfate | Protective: synthetic PGE (misoprostol)
52
Triple therapy for Helicobacter?
2 antibiotics plus an acid blocker e.g. amoxicillin, metronidazole and omeprazole Or 3 antibiotics e.g. amoxicillin, metronidazole and clarithromycin (works on luminal and intracellular)
53
Gastric adenocarcinoma - what do they do? When to suspect?
``` Infiltrate gastric wall - fibrosis/thickening, ulceration Often lesser curvature/distal stomach Metastasis to local LN and liver Predisposition in Belgian shepherds, collies, bull terriers Suspect in older animal with: - chronic vomiting - anorexia and weight loss - haematemesis and melaena - anaemia - drooling saliva ```
54
Gastric neoplasias?
``` Primary neoplasia infrequent Middle age/older male dogs > cats Dogs: - adenocarcinoma (75%) - lymphoma - polyps - leiomyoma/leiomyosarcoma Cats: - lymphoma - adenocarcinoma ```
55
Diagnosis of gastric adenocarcinoma?
Contrast radiography Endoscopic biopsy - often to superficial Full thickness biopsy
56
Treatment and prognosis for gastric adenocarcinomas?
Surgical resection (palliative, rarely curative) Grave/hopeless prognosis - probably painful 'Leather-bottle' stomach
57
Advantages and disadvantages of abdominal radiography?
``` Advs: - quick - allows global overview - assessment of thorax and spine - allows differentiation of gas/mineralisation Disadvs: - superimposition - lack of contrast - soft tissue/fluid same opacity ```
58
Technique for abdominal radiography?
Take on expiration Low kVp, high MAS Grid if >10cm Projections: VD, right lateral, +/- left lateral
59
Advs and disadvantages of contrast radiography?
``` Advs: - improves sensitivity - identification of anatomy not seen on plain radiographs (e.g. urethra or ureters, blood vessels) - allows assessment of internal structure - some info on function Disadvs: - time consuming - expensive - complications ```
60
Techniques for contrast radiography?
Appropriate patient restraint (Ga often required) Requires food patient preparation - enemas (LUT, LI studies) Take plain images first Obtain enough images - genuine lesions are consistent and reproducible
61
What negative contrast medias are used for radiography? When? Advs/disadvs?
``` Air, N20, CO2 Used for bladder and gastric studies Cheap, simple and minimal risk Air embolus reported, poor mucosal detail Reduce exposure ```
62
What are positive contrast medias for radiography?
``` Radiopaque (higher atomic number) Water soluble (iodine based) Non soluble (barium) Iodine based agents divided into: - ionic and non-ionic - high osmolar and low osmolar Increase exposure ```
63
Advs and disadvs of abdominal ultrasonography?
``` Advs: - assessment of internal architecture - assessment of vasculature - better soft tissue contrast - guided biopsy - accurate measurement - real time assessment motility Disadvs: - limited field of view - difficult if large amounts of gas - operator and equipment dependent ```
64
Indications for abdominal CT?
``` Surgical planning Tumour staging Retroperitoneal disease Parenchymal organs (larger dogs) Vascular malformations Ureters Insulinoma (esp large dogs) Pelvic canal ```
65
When is abdominal CT not useful?
GIT Small dogs/cats Severe renal disease - need IV contrast
66
Things to do/check for US guided FNA/biopsy of an abdominal lesion?
Identify if lesion accessible Allows visualisation of needle 21-22G Assess coagulation times and platelets if perform Tru-cut biopsy Avoid FNA bladder tumours Avoid crossing body cavities Catheter biopsy for bladder/urethral masses
67
Radiological assessment?
Check extra-abdominal structures Assess boundaries of abdomen Assess serosal detail - relies upon fat between organs Assess each organ system 5 opacities Roentgen signs - size, shape, margination, opacity etc
68
What can reduced serosal detail of an abdominal radiograph indicate?
Reduced fat - check body condition | Effacement by fluid/ST (ascites, peritonitis)
69
Appearance of ascites on US? Where to look?
``` Fluid anechoic Need to sample to determine type Look adjacent to liver and bladder Assess hepatic veins Dilation HV - right sided heart disease ```
70
What does free gas in the peritoneum look like on radiography? Is it significant? What does it indicate?
Large volumes relatively easy to detect - caudal to diaphragm, around stomach/serosal surfaces Smaller volumes present as gas bubbles outside of GIT Always significant (unless recent ex-lap) Indicates rupture of hollow virus (gas producing peritonitis/penetrating trauma) Usually fluid present also
71
What is in the retroperitoneum? What to look for radiographically?
Space of fat opacity Primarily kidneys but also Lns, great vessels, adrenals Swelling and masses - increased soft tissue ventral to spine replacing/obscuring fat, ventral displacement of colon, assess ventral spine carefully LNs - ventral to L6/7 (not normally visible), may displace and compress colon/rectum - drain pelvic canal and pelvic canal and pelvic limbs (look for anal sac, bladder, prostatic disease, pelvic limb masses)
72
Normal appearance of adrenal glands on radiography?
Not normally visible (may mineralise in cats) Large masses may displace kidneys ventrolaterally neoplastic disease may mineralise in dogs
73
Where are the adrenal glands found on US? Shape?
``` Left renal artery and CVC landwarks Left adrenal is monkey nut shaped Right adrenal is arrow shaped May invade vessels incidental nodules common Still need endocrine testing ```
74
Differentials for organomegaly?
Focal enlargement - neoplasia, granuloma, abscess, cyst | Diffuse enlargement - inflammation, metabolic disease, infiltrative neoplasia, congestion
75
Significance of reduced organ size?
Usually chronic disease Mineralisation common Often irregular Poor correlation with function
76
Significance of organ shape changes?
More sensitive than size changes Often non specific - neoplasia, cysts, haematomas, granuloma No information on function
77
Significance and causes of abdominal mineralisation?
``` Often incidental Dystrophic - secondary to damaged tissue Metastatic - secondary to abnormal Ca/P Calculi Ingesta Neoplasia ```
78
What to assess about the liver on radiography?
Position relative to costal arch Shape of caudal margins (should be sharp) Caudoventral border sharp triangle Gastric axis perpendicular to spine - parallel to ribs
79
Appearance of hepatic masses on radiography?
Mass effect of cranial abdomen Caudal displacement of stomach especially Focal enlargements - masses, cysts, abscess/granuloma
80
Appearance of micro hepatica on radiography? Causes?
Cranial displacement/rotation of gastric axis Portosystemic shunts Cirrhosis Herniation
81
Liver on US? Assessing liver disease?
Portal veins echogenic walls Hepatic veins thin walled Lung/diaphragm interface hyperechoic Difficult to evaluate diffuse disease on US - may see change in echogenicity compared to spleen Easier to appreciate multifocal hepatic disease - metastatic tumour, lymphoma, nodular hyperplasia, granuloma, necrosis (FNA/biospy required)
82
How may hepatobiliary disease due to obstruction appear on US?
Gall bladder size too variable to be helpful Dilation of common bile duct (normally <3mm in dogs, 4mm in cats) May see obstructing material along duct or at papilla Dilation of intrahepatic bile ducts if chronic (7d)
83
Normal appearance of spleen on radiography?
Strap like Head of spleen attached to stomach, caudal to gastric fungus and craniolateral to left kidney (DV view) Tail mobile Size variable
84
Splenomegaly on radiography? Causes?
Requires subjective evaluation - rounded margins, shape changes (margins) Causes: GA/sedation in dogs (ACP/Thio), infiltration, inflammatory disease
85
Splenic masses on radiography - what can be seen?
Lesions involving tail east to see, especially if no peritoneal fluid Mid-ventral abdomen (caudal to stomach) (Caudo)dorsal displacement of small intestine Lesions involving head better seen on VD projection Size no indication of malignancy
86
Splenic nodules on ultrasound?
Very common on US Often benign nodular hyperplasia/extramedullary haematopoiesis Hyperechoic modules - myleolipoma FNA
87
Problems with contrast studies for GIT imaging?
Interpretation can be difficult Must be carried our properly e.g. good patient preparation Time consuming, cost intensive, low diagnostic yield Complication if GI perforation So superseded by combining radiography with US
88
Parts of the oesophagus?
Cervical part - dorsal to left lateral to the tracheal | Thoracic part - within mediastinum, returns to dorsal to the trachea and passes right to the aortic arch
89
What is a redundant oesophagus? Appearance on radiography?
Variation of normal oesophagus Brachycephalic breeds Contributes to increased opacity and width of the cranial mediastinal region Often not clinically significant
90
Appearance of megaoesophagus on radiography?
Segmental or generalised dilation May cause ventral deviation of the trachea and widening of the mediastinum Tracheo-oesophageal stripe sign (summation of tracheal wall and oesophageal wall) is normal
91
Predelection sites for foreign bodies in the oesophagus? Appearance on radiography? What to do?
Thoracic inlet, heart base and cranial to the diaphragm/cardia Often mixed opacity, dorsally and ventrally well defined mass lesion in the region of the oesophagus (need orthogonal views) Endoscopy or non-ionic contrast
92
How can gas be used to highlight intraluminal structures/lesions?
Positional radiography useful (right and left view and VD +/- DV) as gas will move to the non dependent side within hollow viscus SO po
93
Stomach compartments?
``` Cardia Fundus Body Pyloric antrum Pylorus ```
94
Where is the stomach on radiography?
Positioned within the costal arch in the cranial abdomen, directly caudal to the liver
95
What are the 5 layers of the stomach? Appearance on ultrasound?
Serosa, muscularis, submucosa, mucosa, luminal surface Muscularis and mucosa are hyperechoic Rugal folds are visible in fungus and body (esp in cats) Gas in fungus often impairs assessment Pylorus is a thick muscular structure relatively hyperechoic with seemingly blurred layering
96
How may a stomach foreign body appear on radiography and US?
Radiography: - easy to identify if mineral or metallic opacity - gas may be trapped in textile or botanical FB or toys -> bizarre gas patterns - may cause partial or complete obstruction e.g gastric distension with fluid in anorexic animals, 'gravel sign' US: - not always easy to discern from food - often hyperechoic surface and strong distal shadowing - more difficult if texture or absorptive material and very difficult if linear FB
97
Causes of gastric dilation? Appearance on radiography?
Gas dilation - aerophagia, GD, DDG - dark opacity Fluid and gas dilation - pyloric outflow obstruction (functional ileum, obstruction) - mainly soft tissue opacity with gas opacity floating on top
98
What happens with GDV?
Marked gas dilation and rotation around longitudinal axis Most commonly clockwise rotation: - pylorus shifts dorsally, cranially and to the left - body shifts towards the right - fundus displaced ventrally and to the right - spleen follows greater curvature towards the right (gastrosplenic ligament)
99
Appearance of GDV on radiography?
All parts of stomach markedly gas distended Fundus displaced caudoventrally and right Pyloric antrum displaced craniodorsal and left Compartamentalisation with a dividing soft tissue band ('shelf') Mass effect on other abdominal organs
100
Appearance of gastric wall abnormalities on radiography/US?
e.g. neoplasia, haemorrhage, oedema Often not visible on plain radiographs US useful Localised or diffuse wall thickening (has to be substantial before can be reliably detected) Irregularly marginated gas content Delayed gas emptying due to partial/complete obstruction Imaging insensitive for ulceration
101
Normal appearance of small intestines of radiography?
Normally smoothly marginated band/tube or as circular/ovoid ST opacity when viewed end on Usually of ST opacity with some segments being mildly homogenously gas filled in dogs Little to no gas filling in cats
102
Small intestinal diameter and wall thickness on radiography? Problems?
Dilation with gas or fluid of SI associated with obstruction, but increased overall size may be due to diffuse wall thickening (hard to assess) No one loop more than 2x diameter of any other loops Dog: 2x width of a rib or 1.6x height of L5 at its narrowest point Cat: 12mm or 2x height of mid L4 or <2x height of endplate of L2 Wall thickness cannot be reliably assessed on plain radiographs - 'wall' is summation of true wall and intestinal luminal fluid - fluid and ST indistinguishable, requires contrast or ultrasonography
103
Wall thickness of SI on US?
Mucosa is thickest layer Duodenum thickest wall of SI segment (5mm in dogs, 3-4mm in cats) Submucosa is thicker in the ileum and flower-like/wheel-like appearance on transverse images
104
Causes of small intestinal dilation?
``` Functional ileus secondary to: - severe inflammation (e.g. parvo) - peritonitis - recent surgery - drugs - thrombosis - mesenteric volvulus Mechanical or obstructive ileum secondary to: - obstruction (FB, intussusception) ```
105
Define ileus
Failure of intestinal contents to pass normally
106
What does an obstructive pattern of the SI look like on radiography?
Fluid and/or gas dilation proximal to the obstruction Creates two populations of intestine - one abnormal proximal and one normal distal to obstruction (may not see 2 populations if obstruction very proximal or very distal)
107
What are gravel signs in the SI?
When partial obstruction Accumulation of many small mineralised particles proximal to the partial obstruction Typically little dilation Can also be seen in the stomach with pyloric/proximal duodenal obstruction
108
What may be seen on US with SI obstruction?
Secondary changes depending on level of obstruction: - fluid dilation proximal to FB and to-and-fro movement - normal intestines caudal to obstruction Foreign body - hyperechoic, irregular or artificially symmetrical shape - usually strong distal shadowing - focally dilating the SI/thin wall
109
Appearance of a linear foreign body in SI on US?
Usually cause plication/hair-pin bends/bunching and triangular/tear-drop shaped gas bubbles +/- Localised peritonitis (loss of serosal detail, streaky appearance) Signs of obstruction (often less severe)
110
Appearance of intussusception on radiography?
Ovoid/elongated ST mass/dilation Possibly crescent shaped gas opacity between intussusceptum (inner) and intussuscipiens (outer) No 'normal' caecal gas, shortened colon
111
Appearance of intussception on ultrasound?
Easily diagnosed on US Onion ring/bullseye appearance on transverse images Intestinal walls identified within intestinal lumen Also vessels/blood flow within lumen
112
Imaging for intestinal inflammatory disease?
Often normal Radiography not useful Ultrasound may show: - altered mucosal echogenicity - muscularis thickening (cats ddx: lymphoma) - normal to mildly thickened overall wall thickness - preserved layering
113
Imaging for SI neoplasia?
Needs to be substantial size for plain radiography Signs secondary to obstruction may be seen Care not to over interpret 'wall thickening' Large masses may not be possible to determine origin Localised masses, irregular gas filling/ccontrast column US very useful - loss of wall layering, often circumferential, hypo echoic or heterogeneous - may be very large with central gas containing lumen - may see signs of obstruction - assess local LNs
114
Location and appearance of caecum on radiography?
Located in right dorsal aspect of abdominal cavity, often level of left kidney Small in cats, rarely contains gas and normally not visible or comma shaped In dogs appears as semicircular snail-shell gas filled structure
115
Appearance of colon on radiography?
Divided into ascending, transverse and descending colon Thin walled, distensible tube 'Question mark' shaped in DV projection
116
Appearance of constipation/obstipation/megacolon on radiography? Causes?
Large intestinal dilation with increasingly more opaque (dehydrated) faecal material Dog: < length of L7 vertebral body Cat: megacolon > 1.48x length L5 or 2.8x cranial endplate of L2 Idiopathic, neurogenic (spinal disease, dysautonomia), chronic constipation, chronic inflammation
117
Normal pancreas on radiography? Position?
Not seen in normal plain radiographs Medial to duodenum, between gastric body and transverse colon, medial to spleen and cranial to left kidney US more useful
118
Significance of pancreatic enlargement? Signs on radiography?
Pancreatitis or neoplasia Lateral displacement of the duodenum and caudal displacement of the colon Increased ST opacity in the craniodorsal to mid abdomen Localised loss of serosal detail Functional ileus may lead to gas filling of the duodenum with pancreatitis
119
Appearance of acute pancreatitis on US?
``` Enlarged hypoechoic pancreas Irregular margination Heterogeneous appearance Steatitis/hyperechoic mesentery +/- biliary obstruction Corrugation of duodenum ```
120
Differential diagnoses for chronic diarrhoea?
``` Adverse reactions to food IBD Antibiotic responsive diarrhoea (dogs) Lymphangiectasia Lymphoma/tumours Infectious diarrhoea Obstructions Liver disease Renal disease Pancreatic disease Endocrine disease - Addison's, DM, hyperthyroidism ```
121
What is diarrhoea originating from the SI typically like?
``` Increased volume Colour change Normal to slight increase in frequency +/- weight loss +/- flatulence, borborygmi, halitosis ```
122
What diarrhoea originating from the LI typically like?
``` Decreased volume Increased frequency Urgency and tenesmus Mucus and haematochezia Dyschezia Constipation +/- variable consistency No weight loss? ```
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What does melaena indicate?
= digested blood so a sign of upper GI disease (stomach or SI bleeding)
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Preparation required for colonoscopy?
Starve for 48h Polyethylene glycol (laxative) - 3 doses 4h apart with stomach tube Followed by 2 x warm water enemas
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Laboratory tests for chronic diarrhoea?
1. Faecal analysis - parasites (Giardia, Cryptosporidia, Tritrichomonas foetus-cats) - bacteria? (Salmonella, Campylobacter) - although may not be cause 2. Haematology, serum biochemistry and urinalysis - to rule out systemic diseases (liver/kidney disease etc) 3. Endocrine tests - ACTH stim test/basal cortisol (hypoadrenocorticism) - total thyroxine (hyperthyroidism) - trypsin-like immunoreactivity (TLI) (exocrine pancreatic insufficiency) - total lipase or pancreatic lipase (possible pancreatitis) - folate and cobalamin (malabsorption)
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Typical presentation of Tritrichomonas foetus in cats? Diagnosis?
``` Multi cat environment Poor body condition Chronic diarrhoea Large intestinal signs Diagnosis - faecal prep in saline, culture, PCR (best) ```
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What does a finding of hypocobalaminaemia (fit B12) mean for chronic diarrhoea?
Negative prognostic indicator | Needs treating with cobalamin - SC injection (needed in some dogs with problem absorbing cobalamin) or oral
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Advantages and disadvantages of endoscopy and coeliotimy for intestinal biopsies?
Endoscopy: - minimally invasive and direct examination - requires equipment and expertise - small superficial samples from a limited region Coeliotomy: - can get multiple full thickness biopsies - surgical risk - best for cats (more likely to miss disease with endoscopy)
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Possible diagnoses for chronic diarrhoea that can be found by a biopsy?
``` Non specific normal/mild inflammation: - adverse reaction to food- antibiotic-responsiveness diarrhoea etc - IBD (chronic enteropathy) Moderate-severe inflammation: - IBD (chronic enteropathy) Lymphoma Lacteal dilation: - lymphangiectasia - secondary to another disease ```
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What treatment trials can be used for chronic diarrhoea after faecal and lab tests and biopsy etc?
Diet - food responsive? Antibacterials - antibiotic responsive? Steroids - IBD? Cytotoxics - severe IBD or lymphoma?
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Definition of constipation?
Difficult, incomplete or infrequent evacuation of dry hardened faeces from the bowel
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Causes of constipation?
Dietary - ingested foreign material, low residue diet Neuromuscular - spinal cord disease (lumbosacral), idiopathic megacolon Environmental - obesity, hospitalisation, change in routine, inactivity Colonic obstruction - stricture, pelvic trauma, neoplasia, foreign body Electrolyte imbalance - dehydration, hypokalaemia Drug-induced - opiates, phenothiazines, anticholinergics
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Most useful diagnostic tool for constipation?
Radiography
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Treatment for constipation?
Remove underlying cause if possible e.g. surgery for fracture Oral laxatives - lactulose, polyethylene glycol (Cisapride) - not licensed Enemas Gentle manual evacuation under anaesthetic Surgery if megacolon Dietart management - high fibre
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What is feline triaditis?
Inflammatory disease of intestines, pancreas and liver
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Pathogenesis of pancreatitis?
Normally trypsin only activated in SI Aetiological factors triggers early activation in pancreas Activated trypsin triggers activation of other proteases Results in autodigestion of pancreas - direct tissue damage Cascade initiation: - coagulation - fibrinolysis - complement - kallikrein-kinin
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Predisposing factors for acute pancreatitis?
``` (mostly idiopathic) Breed - spaniels and terriers Gender - females, neutered Obesity Drugs Concurrent diseases Dietary factors - hypelipidaemia predisposes to obesity and diabetes mellitus, primary hyperlipidaemia in miniature schnauzers (not proven) - high dietary fat - dietary indiscretion ```
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What disease associations are often found with feline pancreatitis?
Cholangitis IBD Hepatic lipidosis Diabetes mellitus
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Possible clinical signs in order of most common with pancreatitis in dogs?
``` Dehydration (97%) Anorexia (91%) Vomiting (90%) Weakness (79%) Abdominal pain (58%) - prayer position Diarrhoea (33%) Jaundice (32%) ```
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Possible clinical signs in order of most common with pancreatitis in cats?
``` Lethargy (100%) Anorexia (93%) Vomiting (35%) Abdominal pain (25%) Diarrhoea (15%) ```
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Steps for investigation of chronic diarrhoea, constipation and acute pancreatitis?
History/physical exam Lab tests Diagnostic imaging Biopsy
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Lab tests for pancreatitis?
``` Haematology and biochemistry - increased WBCs - increased glucose/decreased calcium - increased liver enzymes - jaundice (increased bilirubin) Pancreatic enzyme tests - total amylase and lipase - pancreatic lipase (more specific but still not perfect, SNAP test) Results less consistent in cats ```
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Imaging for pancreatitis?
Radiography - to rule out other disease | Ultrasound - hyperechoic/hypoechoic, enlargement and swelling, mesenteric changes (hyperechoic)
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Treatment for pancreatitis?
Nutritional support - feed as soon as V+ stops with feeding tube - move onto interim diet: first small amounts of water, then start food cautiously (low fat diet, small frequent meals) Pancreatic enzymes as long as doesn't affect appetite - reduces pancreatic secretion to poss reduce post-prandial pain (no evidence of efficacy) - long term diet from 3 weeks onwards, pancreatic/weight management diet if obese Fluid therapy Analgesia - avoid NSAIDs - buprenorphine - paracetamol (dogs only) - tramadol - gabapentin Anti-emetics if V+ - allows early enteral nutrition Antibacterials - most cases are sterile - but intestinal wall 'leaky' -> bacteraemia so consider prophylactic use Steroids? Surgery?
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Aetiology of exocrine pancreatic insufficiency (EPI)? Which breeds most commonly affected?
1. Pancreatic acinar atrophy - most common in dogs - possibly heritable in GSD and rough collies (66% are GSDs) - lymphocytic infiltration so immune mediated? But only see cases when already atrophy so immuno-suppressives not effective treatment 2. Pancreatic hypoplasia - rare congenital (<6mo) - associated juvenile DM 3. Chronic pancreatitis - most common in cats (still rare) Rare in cats
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EPI clinical signs in dogs?
Faecal changes - large volumes, foul smelling, greasy (steatorrhoea), putty-like to overt diarrhoea Appetite changes - polyphagia, coprophagia, pica Vomiting Poor coat condition Poorly muscled/weight loss
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EPI diagnosis?
Trypsin like immunoreactivity: - Blood test - Best test - Normal dog TLI >5ug/L - Dogs with EPI <2.5ug/L - Equvocal 2.5-5ug/L (repeat in 4 weeks) - Subclinical EPI? repeatedly 2.5-5ug/L
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Treatment of EPI?
``` Pancreatic enzyme - uncoated dry powder - enteric coated granules - fresh-frozen pancreas - mix with each meal and feed Feed highly digestible diet - no need to fat restrict - not high fibre - exclusion diet not necessary - ensure adequate food intake (2xM for ideal weight) Cobalamin supplementation if deficient - pancreas does not produce intrinsic factor - poor prognostic indicator Antibacterials for bacterial overgrowths? Acid blockers? Treat other diseases in cats (often other diseases present)! Good prognosis if treated correctly ```
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EPI clinical signs in cats?
Very similar to dogs Weight loss (or poor growth) Diarrhoea Polyphagia, coprophagia, anorexia, flatulence Vomiting Signs of any concurrent disease - lethargy, hair loss, PUPD, weakness
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What does an exclusion diet involve?
``` Novel protein source Sole dietary intake Minimum 2 weeks Occasionally 10-12 weeks Then ideally re-challenge ```
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Causes of protein losing enteropathy?
IBD Lymphangiectasia Alimentary lymphoma
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Prognosis and treatment for PLE?
Poor prognosis - survival may only be few months without appropriate therapy Go straight to immunosuppression - prednisolone (2-4 weeks, reduce over 2-3 months) - cytotoxic (chlorambucil best first choice)
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Causes of pre-hepatic, hepatic and post-hepatic jaundice?
Pre-hepatic - haemolysis Hepatic - hepatocyte dysfunction, intrahepatic cholestasis Post-hepatic - extra-hepatic cholestasis
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Signs of hepatic metabolic dysfunction?
Non specific signs - loss of condition, weight loss Hypoglycaemia Hypoalbuminaemia - only in chronic disease, can contribute to ascites
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Why can liver disease cause ascites?
Hypoalbuminaemia Portal hypertension Sodium and water retention
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Features of acquired portosystemic shunts - what develops? What do the shunts develop from
Usually multiple Develop secondary to liver disease - juvenile fibrosis, cirrhosis, portal hypertension Shunts develop from redundant vessels between portal vein and caudal vena cava Portal hypertension often leads to ascites
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What is the main problem with portosystemic shunts?
``` Hepatic encephalopathy Defective urea formation from NH3 Increased blood NH3 (and other toxins) Leads to altered CNS function CNS signs: - anorexia, v+d, PUPD - dullness, aggression, staggering, blindness, head pressing, seizures - worse if high protein meal, GI bleed, dehydration or acid-base imbalance - increased sensitivity to anaesthetics ```
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What can copper-coloured irises in cats be due to?
Portosystemic shunt
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Why can liver disease cause bleeding?
Defective production and storage of clotting factors Vitamin K malabsorption Portal hypertension -> GI bleeding
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Liver disease clinical signs?
``` Icterus Faecal changes - grey, melaena Hepatic encephalopathy Drug intolerance Ascites Stunted growth (if young) Vomiting and diarrhoea Polyuria & polydipsia Non-specific signs • Anorexia • Weight loss • Weakness • Poor coat and skin condition ```
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Classification of hepatopathies?
Primary - Infectious inflammatory diseases - Non infectious inflammatory diseases - Non infectious non inflammatory diseases Secondary (reactive) - most common, reversible
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What general causes are there of secondary hepatic disease?
``` Anoxia Toxaemia Nutritional imbalance Metabolic changes Infection ```
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Reactive hepatopathies?
``` IBD Bacterial infections Periodontal disease Acute pancreatitis DM HAC Hyperthyroidism Shock Septicaemia etc ```
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Causes of primary infectious inflammatory hepatopathies?
``` Bacterial - Leptospirosis - Bacterial cholangiohepatitis Viral - Infectious canine hepatitis - Canine herpes virus - FIP Protozoal - Toxoplasma ```
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Causes of primary non infectious inflammatory hepatopathies?
``` Toxic hepatic disease Drug induced hepatic disease All forms of chronic hepatitis - canine chronic hepatitis - feline lymphocytic cholangitis ```
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Causes of primary non inflammatory non infectious hepatopathies?
``` Congenital portosytemic shunt Juvenile hepatic fibrosis Feline hepatic lipidosis Neoplasia Telangiectasis and Peliosis Surgical - trauma - liver lobe torsion - entrapment ```
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Why are there feline hepatic idiosyncrasies? Examples of causes? Consequences?
Relative deficiency of glucoronyl transferase So difficulty conjugating toxins (glucoronidation) Aspirin, paracetamol, phenols, pine tars, morphine, benzenes, alcohols, barbiturates Results in methaemoglobinaemia - haemolytic aneamia (depression, dyspnoea) - facial oedema - hepatocellular damage (liver failure and icterus)
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Treatment for paracetamol toxicity in cats?
``` N-acetylcysteine S-adenosyl methionine? IV fluids Antibiotics Activated charcoal if recent ingestion ```
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Clinical signs of liver disease in cats?
Anorexia and weight loss most common Icterus relatively common PUPD - less severe Hepatoencephalopathy -> hypersalivation Microhepatica and cirrhosis rarely seen Pyrexia common in suppurative cholangitis Chorioretinitis or uveitis (FIP, toxoplasmosis)
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Differential diagnoses for feline icterus?
``` Cholangitis complex FIP (dry form) Lymphoma Toxoplasmosis Lipidosis Pancreatitis Haemolytic anaemia Toxic hepatopathy Panleucopenia Neoplasia Biliary obstruction/bile duct rupture ```
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Which liver enzymes are hepatocellular markers and cholestatic markers in small animals?
Hepatocellular markers: ALT, AST | Cholestatic markers: ALP, GGT
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When do serum biochemistry liver tests generally vary from normal?
ALT and ALP - early hepatitis Bile acids - chronic hepatitis, most sensitive test of function Albumin and bilirubin - cirrhosis Clotting factors and glucose - end stage
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How is the gastric axis affected by hepatomegaly and micro hepatica?
Normal: gastric axis parallel to ribs Hepatomegaly: gastric axis tilted caudally Microhepatica: gastric axis tilted cranially
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What features of the liver can be assessed by ultrasonography?
``` Liver size Heterogenous parenchymal disease Biliary obstruction Biliary calculi Masses Vasculature - portosystemic shunts, arteriovenous fistulas ```
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Indications for liver biopsies?
Persistent increases in liver enzymes Altered liver size Monitoring progressive liver disease To evaluate response to treatment
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Technique options for liver biopsy?
'Blind' percutaneous Ultrasound guided percutaneous ('Tru-cut' technique) Laparoscopy Coeliotomy
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Contraindications for percutaneous liver biopsy?
``` Lack of operator experience Small liver, unless ultrasound available Focal disease Extrahepatic cholestasis Bleeding disorder Severe anaemia ```
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Pathology of juvenile hepatic fibrosis?
``` Acquired Progressive fibrosis Minimal inflammatory reaction Central vein fibrosis and occlusion most common Young GSD, Rottweiler ```
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How to differentiate between a congenital portosystemic shunt and juvenile hepatic fibrosis with secondary acquired shunts?
Ascites with the acquired shunts following hepatic fibrosis, and mostly GSD, Rottweiler Ascites rare in congenital portosystemic shunts
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What are the forms of canine chronic hepatitis?
Idiopathic chronic hepatitis Lobular dissecting hepatitis Drug-induced chronic hepatitis Copper-associated hepatitis
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Negative prognostic indicators for shorter survival of dogs with chronic hepatitis?
Hypoalbuminaemia Severity of necrosis and fibrosis in the biopsy Bridging fibrosis
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What is hepatic portal hypoplasia?
Aka microvascular dysplasia Microscopic intra-hepatic shunting Often have no clinical signs or like PSS Small terrier breeds Increased bile acids
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What is Feline cholangitis complex?
Suppurative or lymphocytic cholangitis (or mix) | Sclerosing cholangitis - end stage
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What does idiopathic hepatic lipidoses lead to in cats?
Biliary stasis Liver failure Anorexia Death
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Clinical signs of hepatic neoplasia?
Similar to inflammatory liver disease | Hepatomegaly - can be irregular shape
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Primary hepatic neoplasia?
Hepatocytes - hepatocellular carcinoma, hepatoma Biliary - cholangiocarcinoma Connective tissue - fibroma/sarcoma, haemangioma/haemoangiosarcoma
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Treatments for liver disease?
Dietary modification Ursodeoxycholic acid (UDCA) Anti-oxidant drugs and glutathione donors Treatment of complications Antibiotics if neutrophils on biopsy or positive bacterial culture Immunosuppressives if lymphocytes (immune mediated process) on biopsy - prednisolone +/- azathioprine Anti-fibrotics if fibrosis on biopsy - prednisolone +/- diet/UDCA Decoppering drugs if copper accumulation on biopsy - penicillamine, tridentine, Zn
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DIet management for hepatic encephalopathy?
Aim to minimise ammonia production Protein restriction High biological value - dairy, vegetable
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Diet management for chronic active inflammation of liver?
Aim to reduce inflammation and prevent copper accumulation Alter mineral balance - low copper and high zinc Fat soluble vitamins - A, D, E, K, C? Taurine and L-carnitine for cats Protein restriction rarely required - feed as much protein as will tolerate, add cottage cheese to a standard 'hepatic diet' Anti-oxidants
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Antibacterial therapy for hepatic encephalopathy and bacterial cholangiohepatitis?
Hepatic encephalopathy - use empirically based on clinical picture - ampicillin or metronidazole Bacterial cholangiohepatitis - documented infection, need culture and sensitivity (bile and tissue)
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Glucocorticoid advantages and disadvantages for chronic active inflammation of the liver and hepatic fibrosis?
``` Advs: - improved well being - appetite stimulation - anti-inflammatory - immunosuppression - anti-fibrotic Disadvs: - steroid hepatopathy - predisposes to infection - fluid retention - catabolic ```
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Breeds affected by copper associated hepatopathies?
``` Bedlington terrier WHWT Skye Terrier Dalmatian Labrador Doberman ```
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What decoppering agents are there for copper associated hepatopathies?
``` Copper chelators: - D-penicillamine - 2,2,2-tetramine Copper absorption blocker: - oral zinc (high zinc in commercial diets or use zinc supplement 1h before feeding) ```
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Advantages and disadvantages of adjunctive therapies for liver disease?
``` Advs: - don't need biopsy results - broad spectrum of activity - wide safety margin - combination therapy used Disadvs: - cost - worse compliance if give many drugs? ```
195
Adjunctive therapies for liver disease?
Ursodeoxycholic acid (UDCA) - = hydrophilic bile salt - alters bile composition (decreases hydrophobic bile acids) - stimulates bile flow (contraindicated if complete biliary obstruction) - modulates inflammatory/immune response - limited evidence available in animals S-Adenosyl methionine (SAMe) - 'glutathione donor' for hepatic metabolism and detoxification - no clear evidence as a treatment in animals - might be useful for paracetamol toxicity in dogs - might help to reduce effects of chemotherapy or steroids Milk thistle - active agents: silychristine, silydianin, silybin - free radical scavneger - inhibits inflammation - inhibits lipid peroxidase - inhibits collagen deposition - increases glutathione - advs: wide safety margin, no absolute contraindications, broad spectrum of activity - disadvs: cost, no evidence of efficacy Vitamin E
196
Complications of liver disease? What to do?
Hepatic encephalopathy and coma - identify and treat precipitating cause (dehydration, diuretics, alkalosis, hypokalaemia, GI bleeding) - reduce ammonia concentrations (low protein diet, lactulose, antibiotics) - lactulose retention enema if coma Ascites and oedema - low sodium diet - diuretics (spironolactone first choice, occasionally add furosemide) - paracentesis (drain minimal volume for patient comfort, could worsen bodyside protein status) Haemorrhage and anaemia - vitamin K injections - fresh blood transfusions - B vitamin injections - H2 blockers if GI haemorrhage?