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103 Cards in this Set
- Front
- Back
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Dysphagia:
Differentials? |
-sialocoele
-oral neoplasia -MM myostitis (main differentials) |
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Dysphagia:
clinical approach (summarised) |
1.History-concurrent signs? precipitating event?
2. PE-palpation, assess mouth (FB? masses?), CN function (3. rads) (4. U/S/ CT=retrobulbar lesions) |
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Sialocoele:
1. History/Signalment? 2. Diagnosis? 3. Treatment? |
1. large, soft, painless ST swelling under tongue or jaw
-GSD and poodles predisposed -dogs 2. FNA=fluid consistent with saliva, some neutrophils -can do contrast rads to determine responsible gland 3. Treatment=drainage and surgical removal of gland |
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Oral Neoplasia
1. Most common in cats? 2. Most common in dogs? |
1. SCC
2. Malignant Melanoma |
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Oral Neoplasia-Malignant Melanoma
1. Signalment 2. Increased malignancy at_______ |
1. old, middle sized dogs
2. mucocutaneous junction |
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Oral Neoplasia-SCC
1. Signalment/Appearance 2. invasive? 3. treatment-dogs? cats? |
1. cats-tongue; typically ulcerative
2. locally invasive (esp. bone) 3. dogs-resection +/- radiation cats-chemotherapy (carboplatin) |
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Oral Fibrosarcoma
1. Signalment/Appearance 2. Treatment |
1. large breed dogs-golden retrievers
-firm and smooth, may have surface ulceration 2. surgical resection (ideally radiation prior to) |
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Masticatory Muscle Myostitis
1. Signalment 2. Clinical Signs-Acute? Chronic? 3. Diagnosis? 4. Treatment |
1. dogs-any breed (GSD, retrievers, dobermans-other large breeds predisposed); young or middle-aged
2.Acute: painful swelling of MM -excessive salivation, dysphagia -resist opening mouth (painful) Chronic: -atrophy of MM -systemically well-cannot open mouth to eat -(retraction of globes) 3. Dx: clinical signs -positive serum 2M antibodies -histo 4. Tx: prednisolone |
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Differentiate Regurgitation from vomiting.
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Regurgitation:
-passive -no nausea -no retching -no bile in vomitus -+/- distension of cervical oesophagus Vomiting: -usually nausea -usually retching -vomitus=digested or undigested food -+/- bile in vomitus -no distension of cervical oesophagus |
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DDx for Regurgitation?
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-oesophageal strictures
-vascular ring anomaly -oesophageal FB -oesophagitis -magaoesophagus -dysautonomia |
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Diagnostic Approach to Regurgitation?
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1. History-other clinical signs? signalment
2. PE-full neuro exam, thoracic auscultaton 3.Thoracic rads-3 views 4. contrast studies |
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Oesophageal Strictures:
1. Clinical Signs 2. Diagnosis 3. Treatment |
1. CS: regurgitation
-(lethargy) -dysphagia, hypersalivation, pain on swalloeing -signs of aspiration pneumonia (if present)-dyspnoea, soft cough 2. Dx: history, contrast oesophagrams + endoscopy 3. Tx: balloon dilation, supportive care: -Nutrition-PEG tube -antibiotic and adjunctive therapy (aspiration pneumonia) |
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Oesophageal FB
1. Clinical Signs 2. Diagnosis 3. Treatment |
1. CS: history
-regurgitation, reluctance to eat -uncomfortable 2. Dx: plain rads 3. Tx: removal-endoscopic ideal (can push into stomach); thoracotomy (if endoscopy unsuccessful) |
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Megaoesophagus (Congenital)
1. Signalment/Timing 2. CS 3. Tx |
1. miniature schnauzers, wirehaired fox terriers, large breeds
-becomes apparent shortly after weaning (DDx: vascular ring anomaly) -diagnosis via history 2. CS: regurgitation of solid food (may see signs of aspiration pneumonia-poor condition, soft cough) 3. No specific treatment-may resolve spontaneously (rare); feed from height |
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Megaoesophagus (Acquired)
1. Causes 2. Diagnosis 3. Treatment |
1. systemic lupu erythmatosus
-hypoadrenocorticism -tymoma -(focal) myasthenia gravis 2. rule out underlying disease: -full physical exam (+ neuro) -CBC, biochem, electrolytes, urinalysis -thoracic rads (cr. mediastinal mass) -ACTH stim test -ANA titre -thyroid fxn 3. Tx: -treat underlying cause (MG=long acting anticholinesterase and immune suppression) -nutrition-PEG tube -treat complications (oesophagitis and aspiration pneumonia) -decrease frequency of regurgitation: feed from height; change food consistency |
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Oesophagitis:
1. Common causes 2. CS 3. Treatment |
1. Chronic vomiting, (hiatal hernias), chronic reflux, caustic substances
2. regurgitation +/- dysphagia, hypersalivation, pain on swallowing -resp signs if asp. pneumonia -(decreased oesophageal motility) 3. Tx: reduce gastric acidity: ranitidine, omeprazole, (sucralfate) improve LOS fxn: cisapride |
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DDx Acute vomiting +/- diarrhoea?
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-uncomplicated parasitism
-pancreatitis (V>>D) -Haemorrhagic Gastroenteritis -Intestinal obstruction (V>D; FB, intussusception, volvulus) |
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Acute vomiting and diarrhoea clinical approach?
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1. History: -preexisting PD, weight loss, anorexia (underlying/ serious GI disease)
-environmental + dietary history -frequency of vomiting/ progression? 2. PE-all body systems evaluated -evidence of systemic illness or dehydration noted 3. Systemically unwell: -CBC, biochem, electrolytes, urinalysis -rads (FB!!!) |
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Antiemetics-indications for use?
Contraindications? |
Indications:
-vomiting causing fluid, electrolyte or acid-base disturbances -prevent vomiting w/ specific treatments Contraindications: -GI obstruction -GI toxicity -systemic hypotension |
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Name a:
1. anti-emetic 2. prokinetic -include MOA |
1. metaclopramide (Dopaminergic agonist)
2. cisapride (seratonergic) |
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Prokinetics:
-indications? |
-profound ileus/ delayed gastric emptying
-suboptimal emptying (e.g. megacolon in cats) |
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Canine Haemorrhagic Enteritis
1.Signalment 2. Clinical Signs 3. Dx? 4. Tx |
1. toy and miniature predisposed
2. sudden onset of vomiting +/- blood -vomiting may precede diarrhoea by a few hours -severe bloody diarrhoea with foetid odour - depression and shock 3. Dx: CS, -elevated PCV, normal skin turgor -NAD: WBC, abd. rads, biochem 4. Tx: prompt aggressive IV fluids -plasma (hypoproteinemia) -parenteral broad-spectrum antibiotics |
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Canine Haemorrhagic Enteritis
DDx? |
-intussusception
-infectious disease (salmonellosis, campylobacter, parvo) -toxicities |
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Intestinal Obstruction-Clinical Signs?
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-abdominal pain
-fluid proximal to obstruction -vomiting (matabolic alkalosis and dehydration) -reduced/absent intestinal sounds -intestinal distension -hypovolemia, acid/base and electrolyte disturbances -(abdominal distension) -failure to pass faeces and gas |
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Intestinal Obstruction-Simple
1. Appearance 2. Causes and Signalment 3. Clinical Signs 4. Dx 5. Tx |
1. lumen obstructed but no bowel devitalisation;
common in dogs> due to FB, neoplasia 3. vomiting*** 4. abdominal palpation, plain radiography (U/S if partial obstruction) 5. Tx: exploratory laparotomy, treat dehydration, a/b abnormalitits>>Sx resection |
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Linear foreign bodies
1. Signalment 2. CS 3. Dx 4.Tx |
1. cats (string), dogs (stockings)
2. vomiting, depression -cats may present with anorexia only 3. bunched intestine on palpation -rarely visible on rads 4. attempt to cut if fixed around tongue and see if passes normally; Surgery if: object fixed in pylorus, doesn't pass after being cut, unwell after 48 hrs |
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Intusussception
1. Common sites 2. CS 3. Dx 4. Tx |
1. ileocolic, jejeunojejunal
2. small amounts of bloody diarrhoae -vomiting -abdominal pain -palpable abdominal mass (weight loss, hypoproteinaemia-chronic) 3. US!!! -bullseye lesions 4. Surgical resection and anastamosis |
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Acute abdominal pain:
clinical approach? |
1. History-post trauma=ruptured UT; concurrent vomiting=pancreatitis, septic peritonitis
2. PE-analgesia (opioids), palpation, jaundice? anaemia? oral ulceration? prostatomegaly? hydration status 3. Abdominal rads 4. Clin path 5. Abdominal U/S 6. Exploratory laparotomy-only if therapeutic |
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Acute Abdominal pain:
DDx? |
Peritonitis (septic/non-septic)
organ distension/dilation pancreatitis intestinal spasm |
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Peritonitis (septic)
1. Signalment 2. Cause 3. CS 4. Dx 5. Tx |
1. dogs>cats
2. ruptured intestine following FB perforation (secondary to surgical dehiscence, neoplasia, ulceration) 3. moribund +/- pyrexia, low volume abdominal effusion 4. bacteria and degenerate neutrophils in peritoneal fluid 5. thourough Sx exploration + BIOPSY adjacent intestin if no FB -lavage abdomen -drainage -systemic antibiotics (ampicillin + enrofloxacin + metronidazole) |
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Pancreatitis-canine acute
1. Signalment 2. CS 3. Complications? |
1. middle aged, obese dogs
2. **depression **anorexia **vomiting Other signs: -pyrexia -dehydration -abdominal pain -haemorrhagic diarrhoea 3. **jaundice **hypovolemic shock |
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Pancreatitis-canine acute (cont'd)
4. DDx? 5. Dx? |
4. Intestinal obstruction
-septic peritonitis -gastroenteritis -uraemia -other metabolic diseases (hypercalcaemia) 5. Dx: serum lipase + amylase elevated (non-specific); canine pancreas-lipase immunoreactivit -Rads-localised peritonitis -U/S-hypoechoic areas, ID pseudocysts/abscesses -histo exam of pancreas (laparotomy/oscopy) |
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Pancreatitis-canine acute (cont'd
6. Tx? |
6. a) assess nutrition: severe=microenteral nutrition via naso-oesophageal tube; anorexia >3 days=TPN
b) correct fluid/ electrolyte imbalances-Hartmann's c) shock/ DIC=transfusion of fresh/fresh frozen plasma d) analgesia (opioids) e) gastric protectants if haematamesis |
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Feline Pancreatitis
-name the other diseases in triaditis |
-cholangiohepatitis
-IBD -interstitial nephritis |
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Feline Pancreatitis-CS?
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-lethargy**
-anorexia -dehydration -Other signs: hypothermia, vomiting, abdominal pain, palpable abdominal mass, diarrhoea, dyspnoea, ataxia |
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Feline Pancreatitis-Dx
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-increased liver enzymes
-bilirubinaemia (cholestasis) -(increased lipase/amylase) -imaging (difficult) **exploratory laparotomy + BIOPSIES |
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Feline pancreatitis-Tx
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-supportive fluids, antibiotics, antiemetics
-enteral nutrition early -treat any underlying disease |
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Acute abdominal distension
-what two things do we worry about most? |
-fluid
-flatus |
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Acute abdominal distension-DDx?
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-GDV
-Haemabdomen (ruptured haemangiosarcoma; coagulopathy; post trauma) -Peritonitis -bladder dilation due to LUT obstruction -intestinal obstruction (rarely dramatic) |
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GDV-Signalment
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-deep chested dogs
-fed from heigh once a day -familial |
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GDV-Dx
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-presentation
-Rads: dilation-tissue shelf -requires surgical intervention |
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GDV-Preop Tx?
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-resuscitative IV fluids (shock rates) for 30-60 min, then maintenence at 20ml/kg/hr
-PCV/TS, TPR, ECG monitoring -stomach tube (propofol): gastric decompression; if unsuccessful can decompress with large bore needle (trocharisation) |
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GDV Postop Tx?
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-continue IV fluids at 2-3 x maintenence
-analgesia -plasma + colloids if DIC or shock -water day 2 -parenteral antibiotics if necrosis |
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Chronic (2-3 weeks) vomiting indicates _______?
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gastric disease
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Chronic vomiting-clinical approach
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1. History:
-rule out regurgitation -signs of DGE -persist despite fasting? -signs of systemic disease? 2. PE-complete -abdominal palpation and rectal exam -treat symptomatically unless: steatorrhea, polyphagia, weight loss, palpable abnormality, geriatric, hypoproteinemeia, unwell, dehydrated, failure to respond to previous symptomatic therapy |
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Chronic Vomiting-DDx
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-Adverse food reactions
-Gastritis -IBD -Hyperthyroidism (cats) -Pancreatic disease (pancreatitis, neoplasia) |
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Name the stomach's 7 intrinsic mechanisms against gastric digestion
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1. intact apical cell membranes and tight junctions
2. bicarb secretion 3. mucus production 4. microvasculature' 5. cell renewal 6 surface active phospholipids 7. prostaglandins |
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Gastric Ulceration-DDx
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gastritis
neoplasia (esp. gastric carcinoma) gastric hyperacidity (drug induced) DIC liver disease |
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Chronic Gastritis
1. CS 2. Dx 3. Tx |
1. persistent intermittent vomiting that is worsened by eating or drinking
2. mixed inflammatory cell infiltrate in the gastric mucosa 3. hypoallergenic/ hydrolysed diet for 2-4 weeks; rechallenge to Dx food intolerance -sucralfate -ranitidine/omeprazole if haematemesis -moderate/severe infiltrate/poor response=prednisolone |
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Delayed Gastric Emptying
1. CS 2. Cause 3. Dx 4. Tx |
1. vomiting undigested food more than 12h after ingestion
2. outflow obstruction, motility disorders, combo-FB, neoplasia 3. History, rule out metabolic disease, -plain rads -U/S-dynamic -Endoscopy -Exploratory laparotomy-full thickness biopsy of gastric wall 4. Treat underlying disease (if none ID then trial prokinetic) |
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Define Osmotic diarrhoea
Give Examples |
osmolarity of gut lumen increased=water excretion; large volumes watery diarrhoea
-resolves when food witheld 24-48h Eg. dietary overload, malabsorption (EPI, bile deficiency, duodenal mucosal disease, brush border enzyme deficiency, inramural disease, systemic circulatory disease) |
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Chronic Diarrhoea- DDx
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Maldigestion-EPI
Malabsorption: -IBD -neoplasia -lymphangectasia -antibiotic-responsive diarrhoea -breed-specific enteropathies |
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Approach to chronic diarrhoea
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1. History
-vaccination status -worming prophylaxis -small or large bowel origin? 2. PE-abdominal, rectal palpation 3. Further investigation (if suspect systemic disease): -imaging (U/S, rads) -faecal analysis -serum folate and cobalamin |
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List the advantages and disadvantages of both endoscopy and laparotomy for intestinal sampling.
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Endoscopy:
adv=minimally invasive -visualization and biopsy of focal lesions -multiple biopsies -minimal adverse reactions -allows steroid started early Disadv: -requires GA -only duodenum (and distal ileum?) -small, superficial, crushed biopsies -expensive equipment -technically demanding Laparotomy: Adv: -multiple site biopsies -large, full-thickness biopsies -inspection of other organs -potential for corrective surgery Disadv: -requires GA -surgical risk -convalescence -delay for steroid admin |
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IBD
1. Characterised by? 2. causes? 3. What should you try before invasive methods (endoscopy/laparotomy) implemented? |
1. persistent CS of GI disease associated with histological evidence of inflammation in the small and large intestine
2.-chronic infection -food allergy -lymphoma -lymphangiectasia -bacterial overgrowth 3. trial with diet and fenbendazole |
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Lymphocytic-plasmacytic enteritis
Dogs: 1. CS |
-vomiting +/- SI diarrhoea >4 weeks
-weight loss, borborygmus -cyclical course -stress-induced |
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Lymphocytic-plasmacytic enteritis
-Dx |
-faecal analysis and metabolic screening
-endoscopy + BIOPSY -exploratory laparotomy (neoplasia, inacessible site) |
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Lymphocytic-plasmacytic enteritis
-Tx |
1. Dietary management
-selected protein, highly digestible 2. metronidazole-see if improves (if yes, hold off on immunosuppression and change diet) 3. prednisolone |
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Antibiotic responsive enteropathy
1.signalment 2. Dx 3. Tx |
1. cats (more bacteria)
2. quantitative duodenal cultures -breath hydrogen analysis -serum folate and cobalamin -serum unconjugated bile acids 3. treat to see if responds: -metronidazole -oxytetracycline -tylosin |
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Weight Loss-DDx
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Malnutrition:
-food competition, poor quality/contaminated food, anorexia, dysphagia, regurgitation/vomiting Maldigestion: -EPI Malabsorption SI diseases Malutilisation cachexia, liver disease, renal failure, hypoadrenocorticism Increased Metabolic demands |
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Protein losing enteropathy
1. Causes 2. Treatment |
1. IBD
Intestinal neoplasia intestinal lymphangectasia chronic intusussception GI haemorrhage/ulceration Parasitic infections Viral infections 2. azathioprine + prednisolone |
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GI Lymphoma (cats)
1. CS 2. Dx 3. Tx |
1. weight loss, anorexia, vomiting, diarrhoea, PU/PD (may be anorexia +/- weigth loss only)
2. Ultrasound: -thickening of gastric/intestinal wall -loss of normal intestinal wall layering -localised mass -regional hypomotility -mesenteric lymphadenopathy FNA Endoscopy 3. Surgical resection Chemotherapy |
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List the 5 functions of the exocrine pancreas.
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1. Secretion of digestive enzymes to help break down lipids, proteins and polysaccharides in proximal duodenum
2. secretion of bicarb to neutralise gastric acid 3. co-factors to enhance cobalamin and zinc absorption 4, antibacterial factors 5. protection against autodigestion |
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EPI
1. Pathophysiology |
-lack of pancreatic digestive enzymes=maldigestion
-osmotic diarrhoea due to undigested food -bacterial overgrowth -micronutrient deficiency -may get concurrent inflammatory bowel |
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EPI
2. CS |
-steatorrhea
-variable faecal consistency -weight loss, otherwise systemically well -polyphagia, coprophagia -occasionally vomit -dry scruffy coat |
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EPI
3. Dx |
Serum TLI (fasting) <2.5 ug/L=diagnostic
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EPI
4.Tx |
-expensive and lifelong (does not regain function)
-oral pancreatic extract -Diet: highly digestible good quality commercial dog food; higher fat diet -vitamin supplementation: B12, K, E |
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List the Hallmark signs of Distal GI disease
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-mucoid faeces
-haematochezia -tenesmus -constipation/obstipation -dyschezia (weight loss; vomiting [cats]) |
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Define colitis
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LI inflammation and subsequent diarrhoea
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List the most common CS of colitis
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-mucoid faeces
-tenesmus -haematochezia (weight loss; vomiting [cats]) |
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LI diarrhoea-DDx
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-IBD
-neoplasia -clostridial overgrowth -Trichuris vulpis (whipworm) infection |
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Clinical Approach to Colitis
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1. accurate history
2. thorough PE (RECTAL) 3. faecal analysis, metabolic screening, colonoscopy, proctoscopy, biopsy **ensure adequate parasite prophylaxis before colonoscopy*** |
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Lymphocytic-plasmacytic colitis
1. Dx 2. Tx |
1. histopath
2. Dietary: hypoallergenic/ hydrolysed w/ omega-3 (poor response=add fibre, change to low residue) Immunosuppression: prednisolone Sulfasalazine |
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Rectal adenocarcinoma
1. Signalment 2. CS 3. Dx 4. Tx. |
1. older dogs (7-11yo)
2. tenesmus** 3. palpation, proctoscopy, biopsy, differentiate from polyps 4. Sx (difficult access); piroxicam and fibre (if Sx not feasible) |
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Perineal hernia
1. CS 2. Dx 3. Tx |
1. dyschezia, constipation
-perineal swelling -severe signs with bladder herniation 2. rectal exam, imaging 3. surgery (w/ castration) |
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Anal sacculitis
1. CS 2.Tx |
1. painful, swollen anal gland
2. expression, lavage of sac and intralesional antibiotics |
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Idiopathic megacolon
1. Signalment/CS 2. Dx 3.Tx |
1. cats, constipation
2. rule out metabolic/other causes; abdominal rads 3. depends on severity |
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Liver-small and smooth (Tom Cruise)
DDx |
PSS
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Liver-small and bumpy (AFL player)-DDx
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-end-stage liver
-cirrhosis -fibrosis |
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Liver-Big and Smooth (Tom Jones)
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-infiltrative: lymphoma, amyloidosis
-lipidosis -acute hepatitis -vacuolar hepatopathy |
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Liver-Big and Bumpy (Rod Stewart)
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-Neoplasia (Adenoma, metastatic)
-nodular hyperplasia -abscess/cysts |
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Hepatic Encepalopathy-CS
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-ptyalism (cats)
-head pressine -disorientation -seizures -circling -agitation -personality changes -ataxia |
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Name the 5 general treatment principles of liver disease
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1. Immune modifiers-prednisolone
2.Antioxidants-Vit E/C, SAMe, milk thistle 3. Anti-fibrotic agents-colchicine 4. Anti copper medications-D-penicillamine, zinc salts 5. USDA (ursodeoxycholic acid)-natural bile acid (contraindicated in bile duct obstruction) |
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What breeds of dog are predisposed to Extrahepatic PSS? Intrahepatic?
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Extrahepatic: Yorkshire terriers, shih tzu, lhasa apso, mini schnauzer
Intrahepatic: Australian cattle dog, irish wolfhound, retrievers |
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PSS-CS
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-Neuro (~to HE)
-GI-non specific (vomiting, diarrhoea, pica) -Urolithiasis and recurrent UTI -PD -Anaesthetic intolerance -Poor growth -recurrent bacterial infections |
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PSS-Dx
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1. PE: small animal, bilateral renomegaly, poor hair coat
Clinpath: microcytic anaemia -normal liver enzymes -decreased cholesterol -low glucose -low albumin -low urea -dilute urine +/- urate crystals Elevated pre/post prandial bile acids Imaging=U/S, portography, scintigraphy |
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PSS-Tx
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-Medically (same as HE)
-specialis Sx procedure |
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General treatment of chronic HE?
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1. Diet:
-moderately restricted protein (protein must be high quality) -high quality complex carbohydrate -fibre=prevent constipation 2. Lactulose -hastens gut transit time, lowers colonic pH, alters colonic bacteria (gets rid of ammonia) 3. Antimicrobials-Amoxicillin, metronidazole, neomycin 4. Control precipitating factors 5. Treat other complications (coagulopathy, GI ulceration, etc.) |
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Acute hepatopathies/hepatitis
-causes? |
1. Infectious
-viral (adenovirus) -bacterial (septicaemia) -rickettsial -protozoal (neospora) -algae -parasitic 2. Toxins 3, Drugs (e.g. paracetamol (cats), diazepam (cats), carprofen (dogs)) 4. Misc: -DIC -neoplasia -pancreatitis -IBD -GDV -Haemolytic anaemia |
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Causes of Hepatocellular injury?
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-tissue ischaemia and hypoxia
-free radicals and oxidative injury -membrane lipid peroxidation and interactions with phospholipids -depletion of intracellular compounds of co-factors -cellular injury derived from binding of toxins to cell proteins, RNA, DNA -cholestatic injury -microbial endotoxins -injury to hepatocyte plasma membrane |
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Hepatic Injury-CS
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-variable
-Severe=acute onset of vomiting, depression, jaundice -increased ALT and AST -lesser increases of ALP (not cholestatic) -(hyperbilirubinaemia/uria) -abnormal hepatic fxn tests (e.g. bile acids) -Biopsy=hepatic degeneration and necrosis) |
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Acute HE Tx?
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1. Establish data-base (electrolytes, blood gas, glucose, coagulation time)
2. Determine primary cause and treat appropriately 3. Reduce circulating toxins (enemas, cleansing>>retention) 4, Correct acid-base and electrolyte abnormalities (IV fluids-0.9% saline; diuresis; potassium) 5. Control sepsis (systemic antibiotics, aseptic catheter technique) 6. Control concurrent signs 7. Avoid potentiating factors: -stored blood transfusions -medication requiring hepatic metabolism -benzodiazepines -hypokalemia -hypotension -metabolic alkalosis -nutritional support containing amino acids |
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Name the two major types of chronic inflammatory liver diseases in cats
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-Suppurative cholangitis/cholangiohepatitis
-lymphocytic portal hepatitis |
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Chronic liver disease (cats)-CS (none pathognomonic)
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Anorexia, weight loss, pyrexia, jaundice, hepatomegaly, ascites
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Chronic liver disease (cats)-Dx
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1. Clinpath:
-left shift neutrophillia (acute CCH) -mild/moderate increase in bilirubin/ALT -SBA increase 2. Imaging: -rads: assess liver size -U/S other abdominal disease, liver parenchyma 3. Cytology/histopath (get coagulation profile first) 4. Exploratory Laparotomy (biopsy intestins, pancreas, mesenteric lymph node and liver) |
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Chronic liver disease (cats)-Tx
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CCH:
-correct fluid/electrolyte deficits -nutrition if anorectic (oesophagostomy tube) -Antibiotics initially -Sx (if choleliths or complete biliary obstruction) -prednisolone (if no response to antibiotics) |
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Hepatic Lipidosis-CS
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-illness preceded by anorexia of prolonged period
-depression, intermittent vomiting -jaundice - (HE) On PE: hepatomegaly, poor body condition |
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Hepatic Lipidosis-Dx
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-history
-Biochem: hyperbilirubinaemia, large increase in ALP, ALT and AST increased, normal CBC but may see poikilocytosis -Imaging: Rads=hepatomegaly U/S=diffuse hyperechoic hepatomegaly -Cytology: cytoplasmic vacuolisation in hepatocytes -histopath (only after coagulation profile) |
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Hepatic Lipidosis-Tx
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1. Correct dehydration and elecrolyte supplementation (avoid glucose containing solutions)
2. Injectable B vitamins and Vitamin K1 3. Parenteral antibiotics (amoxicillin, enrofloxacin) 4. Nutrition as soon as possible (oesophagostomy, gastrostomy) 5. monitor for hypophosphatemia 6. treat vomiting (if interfering with nutrition) |
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Idiopathic hepatic nodular hyperplasia
1. Signalment/Appearance 2. Dx |
1. older dogs, benign discrete accumulation of hyperplastic hepatocytes that form nodules
2. abnormal ALP (increased), check for underlying disease (e.g. Addison's) U/S=~to hepatic adenomas Wedge biopsy for definitive Dx |
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Hepatic Neoplasia
1. Signalment 2. Common types 3. CS 4. Dx 5. Tx |
1. older dogs
2. Primary: -adenoma, hepatocellular carcinoma, bile duct carcinoma, primary sarcomas Metastatic: haemangiosarcoma, lymphoma, pancreatic tumours 3. non-specific, often asymmetric hepatomegaly 4. percutaneous biopsies, U/S 5. Exploratory laparotomy and lobectomy (if cicrumscribed, benign) |
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List the disorders associated with 'chronic hepatitis' in dogs
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-relapsing pancreatitis/ IBD
-bile duct obstruction -cholecystitis -cholangitis, cholangiohepatitis -cholelithiasis -granulomatous inflammation -leptospirosis -canine adenovirus -chronic toxin ingestion -idiosyncratic drug toxicity -breed related disorders -autoimmune disease -idiopathic |
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Chronic Canine hepatopathies-Tx
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1. Identify and treat underlying initiating process
2. Medical management of metabolic consequences of decreased hepatic function 3. recognition of altered pharmacokinetics of drugs metabolised in the liver 4. immunomodulators 5. anti-collage, copper chelation and/or anti-fibrotic drugs 6. anti oxidants 7. modification of bile acid milieu |
