GI and hepatic Flashcards

Question

Chronic vomiting

Answer 1

Chronic vomiting GI Tract – Chronic inflammatory (gastritis, gastroenteritis, colitis, chronic enteropathy), mucosal insult (Dietary intolerance), infectious (bacterial/viral/parasitic) obstructive (pyloric FB, Neoplasia, parasitic, constipation) Cerebral cortex – Neoplasia/SOL, CNS disease Vestibular system – chronic vestibular damage, otitis interna, neoplasia, cerebellar disease CRTZ Endogenous: any systemic metabolic or endocrine disease resulting in chronic changes e.g. diabetes mellitus, Addisons, chronic renal failure, liver failure, chronic pancreatitis, electrolyte disturbances, acid-base disturbances, hyperT4 (cats) Exogenous: Toxins/Drugs less likely

Answer 2

Physiology: Passive expulsion of food from the pharynx or oesophagus. This is a failure of swallowing (Dysphagia) and/or subsequent movement of food down the oesophagus to the stomach. Realistically we should therefore be considering anatomy, particularly muscular and neurological systems involved in eating and swallowing. Oesophagus – proximal and distal sphincters, food moves between them via peristalsis, controlled by the muscular wall (dogs – striated, cats – striated proximally and smooth distally)

Answer 3

Failure to prehend/bite (mouth) and initially swallow (pharynx): Pain – on closing (e.g. dental disease, stomatitis) or on opening (e.g. retrobulbar abscess) or both (fractured jaw, TMJ disease). Failure of neuro-muscular control – cranial nerves disease (V, VII, IX, X, XII), CNS disease, masticatory myositis, Botulism, myasthenia gravis. Obstruction – pharyngeal FB, polyp, neoplasia, abscessation, lymphadenopathy

Answer 4

Failure to pass the oesophagus: Dilatation (megaoesophagus) – may be congenital or occurring via either being active stretch (e.g. a chronic obstruction) or passive stretch (weak muscular wall, dysmotility) or idiopathic. Obstruction – intraluminal (internal), mural (wall) or extramural (external) Intraluminal – foreign body, stricture (e.g. secondary to oesophagitis) Mural – neoplasia, inflammation Extramural – Vascular ring anomaly, Hiatal Hernia, SOL (neoplasia) Neuro-muscular disorder – Myasthenia gravis, botulism, tetanus, distemper, dysautonomia, peripheral neuropathy (e.g. autoimmune), Addisons, Hypothyroidism

Answer 5

speak to the owner. Vomiting is usually associated with retching, abdominal effort and lots of noise! Regurgitation is passive, the food just ‘plops’ out, no retching, less noise. The timing after food can be variable, so not that reliable, but does it look partially digested?

Answer 6

Regurgitation - depends on the cause: Megaoesophagus - Difficult to manage! Omeprazole (PPI) – risk of worsened aspiration. Feed from a height – 5-10 minutes! Small balls rather than big amounts. Could consider a feeding tube. Prognosis is often poor for chronic regurgitation. Treat any concurrent/underlying disease e.g. hypothyroidism, PRAA, etc. Oesophagitis – Pain relief!! Feeding Tube (bypass the oesophagus) Oesophageal Foreign body – remove it, endoscopy, consider referral – rupture -> thoracotomy

Answer 7

Vomiting: Consider the cause and treat the underlying. Be aware – reaching for drugs may just mask the problem e.g. FB. Maropitant – NK1 antagonist -> helps with centrally mediated Nausea e.g. metabolic, CRTZ, Vestibular Metoclopramide – D2 receptor antagonist and 5-HT3 receptor antagonist -> Dual effect, CRTZ and lower oesophageal sphincter, BUT prokinetic so if FB present could rupture the GI Tract Ondansetron – 5HT3 – centrally acting (CRTZ) Nutrition: Especially in chronic cases where BCS is reducing. Consider feeding tubes – bypass the problem if you can; NO/NG tube, O tube, PEG tube. TPN/PPN – parenteral nutrition; ideally a central line is required so not often a routine first opinion approach but it is feasible with good nursing.

Answer 8

Omeprazole – Proton Pump Inhibitor, reduced H+ secretion -> useful for gastric ulceration (and reducing CSF production e.g. Syringomyelia). Long term use -> Dysbiosis. <3-4 weeks. Misoprostol – Prostaglandin analogue – Increases mucosal blood flow and therefore healing e.g. ulcers – DON’T USE IN PREGNANCY – primarily used for NSAID tox H2 Receptor antagonists e.g. cimetidine – reduce acid secretion, effectiveness is questionable, minimal research in small animal and not supportive. Sucralfate – polyionic surfactant (anion) binds to damaged mucosa (positively charged proteins exposed) – weak evidence for use in oesophagitis, probably not helpful in gastric ulceration – use liquid not tablets.

Answer 9

Drinking ability normal if form stomach Poor if from oropharynx,oesophagus No pain on swallowing with stomach pH will be +-<5 if from stomach WIll be immediately after eating if from oropharynx or oesophagus Will be bile if from stomach unless pyloric obstruction

Answer 10

Hypersalivation Lethargy Anorexia Lip smacking Burping

Answer 11

History – Diet, toxin exposure, medications, trauma Clinical exam (peripheral receptors) Non specific/Normal Signs of nausea Abdominal pain Diarrhoea Neurological exam (vomiting centre/vestibular) Normal Bloodwork (CRTZ); haematology, biochemistry, electrolytes, cPli, cortisol, pH Non specific/Normal Dehydration Mild liver parameter elevations Mildly elevated leukogram Specific tests based on localisation Ultrasound, Radiography, Endoscopy

Answer 12

Trauma - foreign body, intussusception Toxin - dietary indiscretion or drugs Inflammatory - acute enteritis - Immune mediated - dietary indiscretion, idiopathic - Infectious - bacterial, viral, parasitic, protozoal Main D/dx: Obstruction (Foreign body or intussusception) Acute enteritis Dietary indiscretion/Toxin Idiopathic lymphocytic/plasmacytic or eosinophilic Infectious

Answer 13

Do I have a foreign body? Scavenger Acute, severe vomiting Abdominal pain or palpable obstruction Pathophysiology Obstruction - Increased pressure - Dilation and compromised perfusion - Inflammation/Necrosis - Vomiting Diagnosis Plain/Contrast Radiography Ultrasonography (CT) (Endoscopy) Treatment Removal

Answer 14

Pathophysiology Vigorous contraction of a segment of intestine into the lumen of the adjacent relaxed segment. Obstruction  Increased pressure  Dilation and compromised perfusion  Inflammation/Necrosis  Vomiting Causes Idiopathic Parasitism Masses Foreign bodies (linear) Diagnosis Ultrasound Treatment Surgery

Answer 15

Treatment Symptomatic Diet IVFT Anti-emetics - maropitant, metoclopramide

Answer 16

Inflammatory Immune mediated chronic enteritis Dietary indiscretion Idiopathic (Lymphocytic Plasmacytic/Eosinophilic) Infectious chronic enteritis - SIBO Neoplastic Adenocarcinoma, Leiomyosarcoma, Mast Cell Tumour, Alimentary Lymphoma Polyp Metabolic Endocrine; Addisons, DM, hyperT4 Hepatic, renal etc Anomalous Lymphangiectasia

Answer 17

Clinical signs: Chronic vomiting Chronic diarrhoea Melaena Haematemesis Weight loss Clinical exam: Lymphadenopathy? Abdominal mass? Abdominal pain? Bloodwork: Often normal Dehydration? Leukocytosis? Hypercalcemia? Anaemia? High urea? (GI bleeding) Gammopathy? Elevated hepatic enzymes? Radiography: Abdominal mass Constricting lesions or filling defects on contrast Ultrasound: Intestinal mass Loss of wall layering Reduced motility Lymphadenopathy Diagnosis Biopsy (surgical or endoscopy) for diagnosis and grading Staging with bloodwork and FNA/biopsy of local lymph nodes +/- spleen/liver Treatment: Surgery Chemotherapy for mast cell tumours Prognosis: Grade dependent but usually 200-300 days 75% have mets at diagnosis Mast cell tumours carry a very poor prognosis

Answer 18

Clinical signs: Chronic vomiting Chronic diarrhoea Melaena Haematemesis Weight loss Clinical exam: Lymphadenopathy? Abdominal mass? Abdominal pain? Bloodwork: Often normal Dehydration? Leukocytosis? Hypercalcemia? Anaemia? High urea? (GI bleeding) Gammopathy? Elevated hepatic enzymes? Radiography: Abdominal mass Constricting lesions or filling defects on contrast Ultrasound: May look similar to enteritis Thickened abdominal wall on ultrasound Loss of intestinal wall layering Reduced motility Lymphadenopathy Diagnosis: Biopsy/FNA for diagnosis or grading Staging with bloodwork and FNA/biopsy of local lymph nodes +/- spleen/liver Treatment: Surgery Chemotherapy (COP, CHOP, LOPP) Prognosis: Grade and lineage dependent (4-18m) Poor in dogs except for colorectal Better in cats

Answer 19

Right and left lobes Closely associated with duodenum and stomach Dogs - 2 ducts – one opens next to common bile duct on major duodenal papilla, other on minor duodenal papilla Cats – Single duct – fuses with bile duct before opening on major duodenal papilla *Design flaw*

Answer 20

Pancreatic acinar cells - secrete digestive enzymes – zymogens – inactive form. Enzyme inhibitors prevent enzymes digesting pancreatic tissue Zymogens secreted into intestinal lumen - cleaved by enterokinase which activates them If enzyme activation happens in pancreas can lead to pancreatitis Endocrine tissue – 1-2% of the pancreas, found in islets of langerhans.

Answer 21

Acute pancreatitis Inflammation of the pancreas Sudden onset Little or no permanent changes after recovery Chronic pancreatitis Continuing inflammatory disease Irreversible morphological changes – fibrosis and atrophy Can lead to permanent impairment of function

Answer 22

Hereditary – Min Schnauzers, Yorkshire Terriers, Boxers, Cocker Spaniels, Poodles and Dachshund. Siamese and Bengal cats. Hyperlipidaemia – Miniature Schnauzers (idiopathic hypertriglyeridaemia) High fat meal? (not in cats) Obesity? (not in cats) Cats – GI disease/vomiting - leading to bile reflux Pancreatic ischaemia and hypoxia shock, severe acute anaemia, dehydration, hypotension during GA, occlusion of venous outflow during abdominal surgery Pancreatic trauma - RARE eg. due to surgical biopsy, surgical manipulation, blunt abdominal trauma Common pathway – decreased secretion of pancreatic juices - premature activation of digestive enzymes – damages the pancreas – inflammation leads to pancreatitis

Answer 23

Acute pancreatitis: Lethargy/weakness Anorexia – suspect pancreatitis in any cat not eating/behaving normally Vomiting Diarrhoea Severe acute pancreatitis: Shock Collapse Abdominal pain Cranial abdominal mass Mild ascites Dehydration Fever Jaundice - uncommon

Answer 24

Changes on CBC, biochem and urinalysis - nos specific and variable Haem - anaemia, haemoconcentration, leukocytosis Biochem - azotemia (prerenal), increase liver enzymes (ALP), hyperbilirubinaemia, hyper or hypoglycaemia, hypoalbuminaemia hypertriglyceridaemia Hypercholesterolaemia Electrolytes Hypokalaemia Hypochloraemia Hyponatraemia Hypocalcaemia cPL and fPL - specific and sensitive test for pancreatitis If need urgent result then run Snap cPL. If negative the dog doesn't have pancreatitis. If positive, send sample away for spec cPL to confirm diagnosis. cTLI and fTLI (trypsin like immunoreactivity) less sensitive and less specific Increase rapidly in early stages of pancreatitis but decline quickly Limited diagnostic utility Amylase and lipase Non-specific assay Influenced by hepatic, renal, intestinal disease and neoplasia Don't use to confirm pancreatitis Radiography: Evidence of pancreatitis rarely seen Useful to rule out other differentials Decreased detail/ground glass appearance cranial abdomen Displacement of abdominal organs Abdominal ultrasound: Enlargement of pancreas Localised peritoneal effusion Decreased echogenicity – pancreatic necrosis Hyperechogenicity – pancreatic fibrosis – chronic pancreatitis Pancreatic duct dilation User-dependent

Answer 25

Correct underlying fluid and electrolyte abnormalities Treat underlying cause Analgesia - buprenorphine, methanone, morphine, fentanyl patch, ketamine, or lidocaine CRI Antiemetics - maropitant, ondanstron, metaclopramide Antibiotics - if infectious cause identified - TMPS, enrofloxacin, metronidazole, clindamycin Steroids Start feeding once vomiting controlled - High carb, low fat Enteral feeding for anorexic cats - NO tube - Oesophagostomy tube Outpatient support of cats: Sub cutaneous fluids – 80-100ml Hartmann’s. Administer via butterfly cannular (from bag or via syringe) Maropitant 1mg/kg s/c or oral (off-license) Mirtazapine – 2mg/cat transdermal Buprenorphine 0.01-0.03mg/kg q 6-8h (sub-lingual or in-clinic im inj)

Answer 26

Signs similar to pancreatitis Significance unclear Fluid of low cellularity Treat medically or surgically

Answer 27

Bacterial infection only rarely present Clin signs and lab abnormalities similar to pancreatitis May palpate mass in cranial abdomen Surgical excision best avoided unless evidence of enlarging mass +/- sepsis and not responding to medical therapy Antimicrobials of questionable value

Answer 28

Avoid high-fat meals Fat restricted diet – if recurrent bouts of pancreatitis Oral pancreatic enzyme supplements Cats with recurrent episodes – trial prednisolone 1mg/kg q 12-24h for 1 week tapering to 0.5mg/kg EOD as needed. Prognosis Unpredictable and varies in severity Difficult to give accurate prognosis Most cases given supportive care respond spontaneously and do well long term Acute pancreatitis can be life-threatening Poor prognosis if continue to refuse food or can't tolerate food Hypocalcaemia with acute necrotizing pancreatitis in cats has poor prognosis

Answer 29

Adenomas, adenocarcinoma, sarcoma adenocarcinoma more common Clinical signs: Similar to chronic pancreatitis; - vomiting, anorexia, diarrhoea, weight loss May have signs associated with metastatic lesions eg lameness, dyspnoea, bone pain Cats - paraneoplasic alopecia – shiny skin disease – alopeica of ventrum, limbs and face. Laboratory abnormalities Lab results may be unremarkable May have neutrophilia, anaemia, hypokalaemia, bilirubinaemia, azotaemia, hyperglycaemia, increased liver enzyme activities Some dogs have very high serum lipase Hypercalcaemia can occur Imaging findings Radiography: - decreased contrast cranial abdomen - may see mass - spleen may be caudally displaced Ultrasonography - soft tissue mass in region of pancreas - if peritoneal effusion present – sample it for cytology - FNA of mass can be attempted – only successful in 25% of cases Diagnosis Often made at ex-lap or at post-mortem Biopsy and histology required to establish definitive diagnosis Treatment Adenomas Benign – only treat if cause clin signs If find mass during ex-lap – partial pancreatectomy to establish diagnosis Adenocarcinomas Often metastatic disease present by time of diagnosis. Sites of metastatic disease – liver, abdominal and thoracic lymph nodes, mesentery, intestines, lungs. If no gross metastatic lesions, surgical resection can be attempted Clean surgical margins rarely achieved Overall prognosis is grave

Answer 30

Nodular hyperplasia Occurs frequently in older cats and dogs Small nodules found throughout exocrine portion of the pancreas No capsule – adenomas have a capsule Doesn't lead to functional change Doesn't cause clinical signs Usually incidental finding

Answer 31

Pancreatitis Oedematous tissue Soft Swollen Fibrinous adhesions Serosanguinous free abdominal fluid Severely affected areas may be liquified Pseudocysts Haemorrhages (pancreas and omentum) Abdominal fat necrosis Histology – multifocal infiltration of neutrophils plus haemorrhage, necrosis, oedema and vessel thrombosis

Answer 32

Disruption to mucosal barrier Gastroparesis Treatment of “Acute gastritis” Time Reduce toxin exposure Fluid therapy if necessary Anti-emetics - Maropitant (Ondansetron) Reduce acid damage Highly digestible diet- Low fat, low fibre, wet OR Hypoallergenic (e.g. Purina HA) fed little and often - Proton pump inhibitors - H2 antagonists - Antacids - Synthetic prostaglandins - Sucralfate Prokinetics - Cisapride/Metoclopramide

Answer 33

Gastroparesis - biochem, US, contrast radiography Disruption to mucosal barrier - Bloods, US, gastroscopy, biopsy Obstruction - Bloods, plain and contrast radiography, US

Answer 34

May be primary and present with any other gastric disease May be secondary: Hypokalaemia Hyper/hypocalcaemia Significant illness Opioid usage Treat with prokinetics (metoclopramide/cisapride)

Answer 35

Chronic Usually a progression of acute gastritis Immune mediated Dietary indiscretion Idiopathic (Lymphocytic Plasmacytic/Eosinophilic and various other terminologies) Infectious Bacterial – Helicobacter? Metabolic disease (e.g. uraemia, hepatic disease) Reduced perfusion and prostaglandin production (e.g. NSAIDs, steroids, post surgery) Neoplasia (MCT, gastrinoma) Clinical signs: Chronic vomiting Haematemesis Clinical exam: Abdominal pain? Bloodwork: Often normal Radiography Unremarkable Ultrasound Thickened gastric wall on ultrasound Reduced motility Lymphadenopathy Endoscopy May look similar to gastric neoplasia Biopsy for definitive diagnosis Treatment: Symptomatic Diet/Antibiotics/Immunosuppressives Prognosis: Usually excellent

Answer 36

Helicobacter Consider if non-responsive to standard medications and diet High prevalence in normal companion animals Pathogenicity unclear in animals but known pathogenicity in human chronic gastritis In man is treated with “triple therapy” Amoxiclav Clarithromycin (metronidazole in veterinary) Proton pump inhibitor/Pepto-Bismol

Answer 37

Gastric Ulceration End point of chronic gastritis Metabolic disease (e.g. uraemia, severe hepatic disease, hypoadrenocorticism) Reduced gastric perfusion (e.g. NSAIDs, steroids, post surgery) Neoplasia (local, MCT, gastrinoma) Clinical signs: Chronic vomiting Haematemesis Melaena Clinical exam: Lymphadenopathy? Abdominal mass? Abdominal pain? Fluid thrill if perforated Bloodwork: Dependent on underlying cause Evidence of GI bleeding Radiography: Loss of detail if perforated Ultrasound: Loss of gastric wall layering Reduced motility Free fluid if perforated Endoscopy: May look similar to neoplasia Biopsy for definitive diagnosis Treatment: Surgical if perforated Medical management as for chronic gastritis Prognosis: Variable

Answer 38

Very common Chronic intermittent bilious vomit Typically early morning on an empty stomach Usually responds to diet alteration

Answer 39

Rare neuroendocrine tumour in pancreas Autonomous gastrin secretion Ulceration/erosion along GIT

Answer 40

Clinical signs: Chronic vomiting Haematemesis Weight loss Clinical exam: Lymphadenopathy? Abdominal mass? Abdominal pain? Bloodwork: Often normal Dehydration? Leukocytosis? Hypercalcemia? Anaemia? High urea? (GI bleeding) Gammopathy? Elevated hepatic enzymes Radiography: Cranial abdominal mass Ultrasound: Thickened gastric wall on ultrasound Reduced motility Lymphadenopathy Loss of gastric wall layering Free fluid if perforated Endoscopy: Biopsy for definitive diagnosis Large mass Deep ulceration at the lesser curvature Treatment: Surgical removal (often difficult) Prognosis: Poor (MST 6m with 74% met rate)

Answer 41

Lymphoma Clinical signs: Chronic vomiting Haematemesis Weight loss Clinical exam: Lymphadenopathy? Abdominal mass? Abdominal pain? Bloodwork: Often normal Dehydration? Leukocytosis? Hypercalcemia? Anaemia? High urea? (GI bleeding) Gammopathy? Elevated hepatic enzymes? Radiography: Cranial abdominal mass Ultrasound: Thickened gastric wall on ultrasound Reduced motility Lymphadenopathy Loss of gastric wall layering Endoscopy: May look similar to gastritis Biopsy for definitive diagnosis Treatment: Chemotherapy (COP, CHOP, LOPP) Prognosis: Grade dependent (4m-18m)

Answer 42

Diagnostic - diagnosis on inspection/palpation, or samples Therapeutic - control bleed, contamination, pain, masses, obstructions, traumatised organs, dystocia, fluids Preventative - gastropexy, enteroplication - intussusception 1. Cranial quadrant 2. Intestinal tract 3. Right paravertebral region 4. Left paravertebral region 5. Caudal quadrant

Answer 43

Reconstruct original anatomy External rectus sheath is critical layer Continuous preferred - even tension distribution, rapid closure, less suture (foreign material) 6 throws - sliding self locking knot and aberdeen knot Absorbable monofilament - Polyglyconate 2/0 dogs, 3/2/0 Restrict exercise for 2-3 weeks monitor incision for redness, swelling, oozing, heat, pain. Reexamine 4-5 days post op Monitor urination, defecation, behaviour, feeding

Answer 44

Oesophageal tube placement Removal of oesophageal FB Partial resection - tumour Tube - clamp down oesophagus - cut across clamp - send tube towards oropharynx, loop round, pull down to place Fingertrap suture

Answer 45

Retching Regurgitation (food & water) Vomiting (?) (can owner differentiate regurgitation from vomiting?) Ptyalism Anorexia Restlessness Cervical pain High index of suspicion from clinical history Plain radiography (in most instances) Endoscopy In most instances, an emergency requiring immediate removal Most can be removed endoscopically using grasping forceps Refer to a centre that has the appropriate equipment and expertise Approximately 10% cannot be removed orally and are pushed into the stomach; bony FBs will then be digested with no requirement for a gastrotomy Medical therapy to reduce likelihood of stricture formation H2 antagonist Proton-pump inhibitor sucralfate Analgesics Feed soft food

Answer 46

Placement of gastric feeding tubes (percutaneous endoscopic gastrostomy (PEG), open gastrostomy, etc.) Gastrotomy for removal of a gastric foreign body Gastropexy to prevent volvulus Correction of gastric dilatation volvulus (GDV) Pyloroplasty to manage gastric outflow disease Partial gastrectomy for resection of a gastric tumour, ulceration, etc.

Answer 47

Minimally invasive, highly effective for dysphagia oesophageal disorders chronic diseases that may require long-term nutritional assistance

Answer 48

Longitudinally between greater and lesser curvature with stay sutures to hold

Answer 49

Full thickness biopsy (e.g., inflammatory bowel disease) Enterotomy for removal of a foreign body Enterectomy (e.g., foreign body, intussusception, tumour, etc.) Enteroplication (potential aspect in the management of intussusception) Cholecystoenterostomy (biliary tract bypass procedure)

Answer 50

Colopexy (e.g., as part of management of perineal hernia) Colotomy (e.g., impaction, foreign body (rarely)) Colectomy (e.g., tumour, polyp) Subtotal colectomy (e.g., megacolon in the cat)

Answer 51

Biopsy - pancreatitis Islet cell tumour – insulinoma Pancreatitis Pancreatic abscess Pancreatic pseudocyst Pancreatic abscess Pancreatic tumour – carcinoma Dog Pancreatic duct - small (absent 8%) Accessory pancreatic duct - large Cat Pancreatic duct - present Accessory pancreatic duct - absent (80%)

Answer 52

Diet – acute gastroenteritis Change, allergy, intolerance, scavenging Food poisoning – suggests infectious agent Toxins – usually through dietary indiscretion Drugs – antimicrobials, chemotherapy etc Infections – viral, bacterial, parasitic Inflammatory disease – CE/IBD, Pancreatitis Metabolic disease – hypoadrenocorticism Anatomic disease – intussusception/FB Neoplasia – peracute lymphoma, paraneoplasia Anomalous - Stress/anxiety – usually mixed/large bowel

Answer 53

Viral, parasitic, bacterial Young, immunocompromised Colonies, kennels Mixed are worse - parasites plus virus Viruses Parvovirus Coronavirus Adenovirus (FeLV, FIV – CHRONIC ENTERITIS, WEIGHT LOSS, lymphoma in FeLV) Rotavirus (Norovirus) Bacteria Salmonella Campylobacter E.coli – ETEC, EHEC, EPEC Clostridium perfingens, C. difficile Shigella Yersinia enterocolitica – rarely reported Mycobacteria in cats – granulomatous enteritis – not acute disease Parasitic Helminths Protozoa - Giardia, Tritrichomonas

Answer 54

Faecal oral transmission Young puppies, older unvaccinated Infects rapidly dividing cells - gut crypts, bone marrow, lymphoid tissue

Answer 55

Faecal oral transmission Young puppies, older unvaccinated Infects rapidly dividing cells - gut crypts, bone marrow, lymphoid tissue Vomiting Haemorrhagic diarrhoea – profuse and foetid, mucosal sloughing Rapid dehydration Panleucopaenia Depressed, anorexic, pyrexic Loss of mucosal barrier – septicaemia/endotoxaemia and shock/DIC Ileus Differentials for CPV: HGE - including neoplasia and idiopathic HGE (AHDS) Salmonella, enteric infections Intussusception FB Hypoadrenocorticism Acute intoxication Diagnosis Signalment and clinical signs strongly supportive Faecal analysis – EM for virus, Ag tests (SNAP) or PCR Haematology and biochemistry – consequences of disease Panleucopenia – consequence of viral replication Azotaemia, acid-base disturbance, electrolyte disturbances, liver enzymes abnormal, possibly low total protein Clotting times may be prolonged if severe systemic consequences present Management Fluid therapy, acid base assessment, whole blood, plasma, colloid Antibiotics - broad spectrum (amoxyclav) due to GI translocation of bacteria Antiemetic - metaclopramide, maropitant Pro-motility - metaclopramide Antacid and ulcer coating -omeprazole Oral fluid and nutrients Prevent with vaccination, cleaning and disinfection (bleach, virkon)

Answer 56

Syndrome of acute haemorrhagic diarrhoea - AHDS Idiopathic in most cases ddx - parvovirus, intussusception, pancreatitis Small breed Vomiting +/- blood Foetid diarrhoea, protein loss Depression, anorexia Haemoconcentration - hypovolaemia, PCV high, TP not high as GI loss, no leukopenia Fluid therapy Whole blood Antimicrobial - potential for clostridial and sepsis - amoxyclav, metronidazole, fluoroquinolone Good prognosis but not severe

Answer 57

Feline parvo Signs as CPV kittens, feral cats, CPV-2 DIagnosis same as CPV Vaccine

Answer 58

Dog - young, highly contagious, villus destruction, subclinical, small bowel. Watery and mucoid D+ IVFT and nutritional support Cat - signs as dog FIP - can mutate to FIP causing coronavirus

Answer 59

Commensal in dogs - potential long term zoonosis Young, immunocompromised Acute enterocollitis - D+ + blood/mucus Vomiting, straining, fever, abdo pain, Diagnosis - faecal culture, stain PCR fluoroquinolone treatment

Answer 60

Young, immunocompromised Commensal in many Can become 1 of 4 Transient asymptomatic diarrhoea Acute Gastroenteritis Carrier state Bacteraemia Can be mild or severe with haemorrhagic diarrhoea, pyrexia, sepsis Only treat if severe sepsis and shock on on basis of culture

Answer 61

C. perfringens, C. difficile – normal anaerobic flora! Diarrhoea generally due to enterotoxin production need trigger – diet change, hospitalisation etc Large intestinal type d+/HGE (AHDS) Manage complications Treat with metronidazole Environmental spores very resistant - hypoclorite

Answer 62

Common gut commensal Histiocytic ulcerative colitis in boxers Strains ETEC - shiga toxin - heat labile and heat stable enterotoxin secretory diarrhoea

Answer 63

Dog - nematodes Toxocara canis Toxoscaris leonina Uncinaria stenocephala Ancylostoma caninum Trichuris vulpus Dog cestodes Taenia hydatigena Taenia pisiformis Taenia ovis Taenia serialis Taenia multiceps Dipylidum caninum Echinococcus granulosis/equinus/multilocularis Cat - nematode Toxocara catis Toxoscaris leonina Ancylostoma tubaeforme Cat - cestode Taenia hydatigena Taenia taeniaeformis Dipylidum caninum

Answer 64

Ascarids Puppies/kittens mostly – adults have low burdens and worm migration patterns are different (adults have mainly somatic migration which generally leads to cyst formation in tissues) Fail to gain weight Pot bellied appearance Vomiting and small bowel diarrhoea Obstruction of GIT if large burdens along with respiratory disease when migrating Hookworms Kennelled dogs most commonly identified Diarrhoea Weight loss Anaemia with Ancylostoma? Interdigital dermatitis/perineal irritation Cestodes D caninum, taenia sp.and echinococcus sp. Signs rare in adults – zoonotic aspect necessitates control Diagnosis Clinical signs and history Faecal examination Treatment Heavy importance for treatment due to public health considerations (VLM and OLM) Toxacara and cestodes Treatment does not remove encysted larvae Occult parasitic infestation should be considered in animals being investigated for IBD This treatment for intestinal parasites should form part of the initial therapy in these cases

Answer 65

Coccidian – faecal-oral Isospora canis – dog (paratenic host?) I. felis, I. rivolta – cat (paratenic host?) Pups/kittens, poor conditions etc lead to most severe clinical signs Diarrhoea in experimental dogs (I canis) suggests primary pathogen Small intestinal location but mixed bowel signs often seen Can seen chronic intermittent shedding by carriers during stress or concomitant disease Can be severe and mortality can occur Dx with faecal exam – direct or flotation for oocysts Tx - mild disease is self-limiting if underlying cause present will resolve when this is resolved Sulphonamides or potentiated sulphonamides Toltrazuril and diclazuril can also be effective Studies however indicate shedding can recur after treatment Highlights the importance of the individual animal/circumstance Cryptosporidium sp – Dogs and cats usually infected by host specific crypto Pups/kittens, poor conditions etc (need to steam clean environment to control) Many animals infected but few develop diarrhoea Malabsorptive and secretory diarrhoea Co-infection with giardia or tritrichomonas increased severity of signs Diagnosis by feacal smear, IFA or PCR Self limiting unless underlying cause Treatment determine underlying cause Dietary manipulation and neutraceuticals Antibiotics of limited benefit – tylosin, azithromycin and paromomycin Zoonotic potential Giardia spp. (felis and canis as well as other sp.) Colony/home problem most commonly or secondary Surface of small bowel: dog (duodenum) and cat (ileum) – faecal-oral transmission, can be subclinical infection in many animals Acute – chronic, usually mild (soft watery with mucus – ie mixed bowel characteristics) (can be present in CE cases and exacerbate background disease - always test for it) Can result in severe, chronic disease with weight loss Via liberation of toxins, development of dysbiosis, induction of IBD, dysmotility, inhibition of enterocyte function Dx – faecal smear evaluation (direct smear evaluation or flotation techniques) also SNAP test (ELISA) available – for faecal antigen along with IFA (this is poorly specific) Tx- Fenbendazole 3-5 days – LICENSED metronidazole, ronidazole and tinidazole fibre may help, unclear benefit of neutraceuticals Tritrichomonas foetus (strictly this is a large intestinal parasite) Cat (rarely dog) Large bowel diarrhoea Colonies/breeders Common (30% of cats with d+?) Often present as secondary pathogen Microscopy, culture, PCR Difficult to treat - ronidazole

Answer 66

Coccidian – faecal-oral Isospora canis – dog (paratenic host?) I. felis, I. rivolta – cat (paratenic host?) Pups/kittens, poor conditions etc lead to most severe clinical signs Diarrhoea in experimental dogs (I canis) suggests primary pathogen Small intestinal location but mixed bowel signs often seen Can seen chronic intermittent shedding by carriers during stress or concomitant disease Can be severe and mortality can occur Dx with faecal exam – direct or flotation for oocysts Tx - mild disease is self-limiting if underlying cause present will resolve when this is resolved Sulphonamides or potentiated sulphonamides Toltrazuril and diclazuril can also be effective Studies however indicate shedding can recur after treatment Highlights the importance of the individual animal/circumstance Cryptosporidium sp – Dogs and cats usually infected by host specific crypto Pups/kittens, poor conditions etc (need to steam clean environment to control) Many animals infected but few develop diarrhoea Malabsorptive and secretory diarrhoea Co-infection with giardia or tritrichomonas increased severity of signs Diagnosis by feacal smear, IFA or PCR Self limiting unless underlying cause Treatment determine underlying cause Dietary manipulation and neutraceuticals Antibiotics of limited benefit – tylosin, azithromycin and paromomycin Zoonotic potential Giardia spp. (felis and canis as well as other sp.) Colony/home problem most commonly or secondary Surface of small bowel: dog (duodenum) and cat (ileum) – faecal-oral transmission, can be subclinical infection in many animals Acute – chronic, usually mild (soft watery with mucus – ie mixed bowel characteristics) (can be present in CE cases and exacerbate background disease - always test for it) Can result in severe, chronic disease with weight loss Via liberation of toxins, development of dysbiosis, induction of IBD, dysmotility, inhibition of enterocyte function Dx – faecal smear evaluation (direct smear evaluation or flotation techniques) also SNAP test (ELISA) available – for faecal antigen along with IFA (this is poorly specific) Tx- Fenbendazole 3-5 days – LICENSED metronidazole, ronidazole and tinidazole fibre may help, unclear benefit of neutraceuticals Tritrichomonas foetus (strictly this is a large intestinal parasite) Cat (rarely dog) Large bowel diarrhoea Colonies/breeders Common (30% of cats with d+?) Often present as secondary pathogen Microscopy, culture, PCR Difficult to treat - ronidazole

Answer 67

Signalment - breed, age (young - infectious, parasitic, congenital) (older - neoplastic, degenerative, inflammatory) Sex - repro history History Vaccination status Worming status Scavenging, diet (ALL aspects), drugs Contact with other animals Environment/travel Health of owners – zoonoses Previous illness/surgeries Other body systems involved Clinical signs Duration Progression Severity Frequency Continuous or intermittent Length of intervening normality Response to treatment and diet Which arose first (ie vomiting or diarrhoea etc) Character of vomiting/regurgitation Bile, food, saliva, blood Character of diarrhoea (small vs large vs mixed) Urgency/Straining (tenesmus) Blood Melaena - digested Haematochezia - fresh Mucus Frequency (>/<3/day) Faecal volume Weight loss Steatorrhoea Flatulence/borborygmi Vomiting Bloating/abdominal discomfort Clinical findings Dehydration/cardiovascular status Evidence for oral ulceration/FB Palpable thyroid in cats/dogs Thoracic auscultation – dull if effusions Cardiac – abnormalities if hypoadrenocorticism/cardiac disease Abdomen – pain, focal mass/intestinal bunching, fluid, faeces Rectal – foreign material, mucosal friability Cutaneous examination – food sensitivity, poor coat condition

Answer 68

Hypertonic water loss often seen Characterised by Increased motility Increased secretion Decreased absorption Loss of sodium (and often bicarbonate) Care as vomiting in conjunction will also lose chloride and H+ which makes acid base status often complex Maintenance of fluid balance Balanced isotonic solution (Hartmann’s – also has buffering capacity) or 0.9% saline Choice should be based on evaluation of electrolytes or acid base status. However SOME fluid is better than no fluid! IVFT rates based on dehydration factor, ongoing losses and maintenance requirements Weigh animals regularly to determine if achieving goals of IVFT or measure ins and outs Adsorbants May reduce diarrhoea Efficacy not proven Kaolin Pectin Chalk Bismuth subsalicylate Magnesium aluminium silicate Activated charcoal Alter intestinal flora/bind flora Coat or protect mucosa Absorb toxins Bind water and possibly antiscretory Probiotics Antimotility drugs - Opiates - No licences spasmolytics Antimicrobials - NOT for routine symptomatic Helicobacter – of questionable significance – triple therapy Definitively diagnosed infectious diarrhoea Loss of GI mucosal integrity and evidence for sepsis Neutropenia/immunosuppression e.g. parvo/post chemotherapy

Answer 69

Faecal analysis – most important sample Faecal – parasites – SNAP Giardia Faecal – virology– SNAP Parvo Faecal for microbiology? Bacteria – Salmonella, Campylobacter, Clostridia (Viruses) Faecal for parasites – OR JUST TREAT? Nematodes Cestodes Giardia – multiple samples?

Answer 70

Food responsive enteropathy (FRE) Dysbiosis (Antibiotic responsive enteropathy) (SIBO/ARE)*** Steroid responsive enteropathy – SRE (IBD?) Non-responsive enteropathy (NRE) PLE – e.g. lymphangiectasia EPI Neoplasia (Irritable bowel disease) (Non-GI causes)

Answer 71

Clinically abnormal response attributed to the ingestion of a food or food additive. Adverse food reactions are categorized as either food allergy or food intolerance reactions. Food allergy reactions - immunologically mediated adverse reaction to food unrelated to any physiological effect of the food or food additive. Relapse when specific antigens from previous diet are reintroduced (distinguishes from intolerance) Food intolerance reactions refer to any abnormal physiologic response to a food that is not believed to be immunologic in nature and may include food poisoning, food idiosyncrasy, pharmacologic reaction, toxicological reaction or metabolic reaction. Abnormal clinical response following ingestion of a food or component thereof Food intolerance (no primary immunologic response) - Food additives and all other causes Food toxicity (poisoning) - Aflatoxins, deoxynivalenol Disturbed microflora - Rapid changes in diet Dysmotility - Types and frequency of feeding Pharmacologic reactions - Methylxanthines, histamine (raw fish) Maldigestion/malabsorption - Undigested components – fermentation and osmotic diarrhoea Physical - Home prepared carcass diet – bone/wool etc irritant effect Non-specific sensitivity - Response to certain formulations of diet – high moisture diets in giant breeds Food hypersensitivity/allergy - Type I and Type IV Usually chronic small bowel diarrhoea Vomiting May be some skin signs Food trial Needs to be accepted by patient and owner Offending antigen excluded For GI disease should be no longer than 3 weeks Signs of improvement noted very quickly compared with skin In cats with ARF most resolved within 7 days Reintroduction of diet should lead to relapse

Answer 72

Major cause/complication of CE Move away from antibiotics to manage CE in dogs and cats Consequences of secondary bacterial overgrowth/dysbiosis - Utilise nutrients/interfere with absorption - Damage epithelium and microvillar enzyme dysfunction - Increase mucosal permeability/fluid loss - Deconjugate bile acids - Hydroxylate fatty acids - Stimulate colonocyte secretion Chronic d+ - small bowel Weight loss/failure to thrive Vomiting/borborygmus/appetite changes Dx History to determine underlying cause MDB, UA, Faecal, imaging and endoscopy For idiopathic ARD screening tests -ve Antibiotic treatment not acceptable now Ancillary approaches – now preferred Dietary manipulation Highly digestable diet Low fat (unclear of efficacy for primary ARD and tylosin responsive disease) Secondary overgrowth leads to hydroxylation of fats and diarrhoea Caution as calorie restriction will reduce weight recovery Prebiotics Alter colonic flora in cats but no current evidence that alter small intestinal numbers in dogs Probiotics Unclear if this improves the outcome in primary or secondary overgrowth – Prokolin enterogenic, YSL3, Vivomixx Cobalamin supplementation Essential to improve recovery rate

Answer 73

Persistent GI signs with histopath evidence for inflammation - Mucosal infiltrations with inflammatory cells - Eosinophillic, lymphocytic plasmocytic, granulomatous, neutrophilic, regional - Gastroenteritis - Enterocolitis - Gastroenterocolitis - Triaditis in cats Middle aged animals mainly Uncommon in dogs <12months Cats of any age are reported but mostly middle aged Suspected to be largely the result of small intestinal IBD though no epidemiological data for this Chronic diarrhoea common SI in character but if prolonged or involving colon can be mixed Vomiting more common in cats can be haemorrhagic (esp cats) May not notice diarrhoea as passed outside Weight loss with more severe mucosal disruption Appetite very variable – increased, decreased, no change Abdominal discomfort – variable and concomitant signs # History and clinical signs Typical breeds, non-specific signs Physical examination Thin, thick gut loops, abd LN palpable? [CAT] Ascites/oedema Rule out chronic FB or intussusception, evaluate wall layering with US - radiograph and US Biopsy - endoscopic or full thickness Eosinophilic enteritis - second most common after LPE - lymphocytic plasmacytic enteritis - GI haemorrhage, bowel perforation, focal mass lesions Treatment - on severity of clinical signs - keep diary Dietary manipulation Antiparasitic - fenbendazole Vitamins - often malabsorption Antibiotics - not recommended - oxytetracycline Probiotics Immunosuppression - prednisolone

Answer 74

Limited response to therapy Consider - non GI disease, neoplasia, dysbiosis, vitamin D deficiency, bile acid diarrhoea

Answer 75

Albumin and globulin low Worse prognosis than other chronic enteropathies Major ddx - Severe inflammatory disease - IBD - Lymphangiectasia - can be with IBD - Neoplasia - lymphoma

Answer 76

Villus lacteal dilation secondary to inflammation of the mucosa due to occlusion of outflow Can be secondary to inflammation, neoplasia, or primary - breed assocaition - Lipogranulomatous changes - centred on lymphatics Can also see secondary to blocked chyli/thoracic duct - R heart failure, liver tumour Outcome is lipid malabsorption - chronic small bowel d+ - PLE, weight loss, protein rich ascites PLE Low albumin and globulin (c.f. liver dz/PLN) Low cholesterol Lymphopenia Low Ca/Mg (exacerbates the effect of hypocalcaemia) Ultrasound – mucosal striations Endoscopy – white spots on villus tips, white nodules or plaques, white fluid Biopsy - endoscopy preferable but problems with depth of samples Treatment Treat any primary cause Neoplasia, IBD, anatomic disease Primary lymphangiectasia Ultra-low fat diet - Previously MCTG – as diets had poor calorific value 0 MCTG not absorbed via lymphatics Fluid therapy particularly if ascitic as dehydrated Albumin/Colloid for hypoproteinaemia - Plasma requires large volume to alter COP and protein concentration - Albumin improves integrity of vascular endothelium Diuretic for effusions - Caution as this can worsen hypovolaemia Fluid withdrawal – not indicated unless causing morbidity - Short term single centesis may be beneficial Immunosuppress if inflammatory component or if lipogranulomas are present

Answer 77

Acinar cell loss – pancreatic acinar atrophy (PAA) in most dogs Can be associated with chronic pancreatitis Possible preceding AI lymphocytic pancreatitis Loss of enzymes Significant reserve – most of gland gone before clinical signs are seen usually seen in young animals (1-4yo) If later in life suspect secondary to chronic pancreatitis Chronic diarrhoea Weight loss – emaciation Poor hair coat History - Weight loss despite normal/increased appetite - Scavenging, coprophagia, pica - Voluminous yellow greasy stool - Often mixed bowel diarrhoea - Increased volume and frequency - Occasionally vomiting - Can see nervousness or aggression suspected to reflect abdominal pain Often mild non-specific changes Liver enzyme elevations Reduction in Cholesterol/triglycerides hypoproteinaemia Amylase/lipase usually normal CBC often unremarkable Can see anaemia due to cobalamin deficiency Low Fat soluble vitamins – especially E and A, maybe K?? Usually no clinical effect noted Pancreatic enzyme supplementation H2 antagonist to reduce the gastric degradation Can use specific diet if response is considered suboptimal Moderate fat, highly digestible, low-fibre diet can help Vitamin supplementation Parenteral cobalamin – weekly, monitor blood levels Prognosis – good with treatment

Answer 78

Lymphoma (LPE as precursor, FeLV -ve) Adenocarcinoma/adenomatous polyps Leiomyoma/leiomyosarcoma Mast cell tumour Fibrosarcoma Haemangiosarcoma Diffuse Chronic small bowel d+ and weight loss Melaena/PLE Vomiting Focal – obstruction/motility change/haemorrhage Palpable on physical? Secondary hypoproteinaemia, anaemia Ultrasound – focal mass/loss of wall architecture or layering Biopsy – endoscopic vs. laparotomy Assess spread - staging

Answer 79

Begin feeding ASAP Water intake Electrolytes Warm and wet food Low fat food - decrease gastric emptying time 15-30% protein dogs 30-40% cats Excess protein to be avoided as strong stimulus of pancreatic secretion Fibre to not exceed 5%

Answer 80

Maintenence 50ml/kg/24hours 2ml/kg/hour Puppy/kitten 3-4ml/kg/hour

Answer 81

Estimate % dehydrated times this by body weight to get fluid defecit Work this out as hour much to give over time you want to give - i.e. 12 hours Add maintenence to this Keep weighing patient Add losses in to this - weigh bedding, catheters, bloods taken etc Hartmanns is alkalotic so is the correct choice as most will be acidotic patients - saline is acidifying Measure albumin

Answer 82

Increased CRT Pale mm Low temp Increased HR Weak pulses Increased RR Vasopressors - create vasoconstriction or increase cardiac contractility - for shock patients Dobutamine Nor-adrenaline Dopamine

Answer 83

Decreased CRT Red mm Pyrexic Increased HR Poor pulse/bounding Increased RR Vasopressors - create vasoconstriction or increase cardiac contractility - for shock patients Dobutamine Nor-adrenaline Dopamine

Answer 84

Lactate <2.0 Blood pressure >60 map - measure every 5 mins PCV/TP

Answer 85

Jaundice/Icterus = Hyperbilirubinemia (>50μmol/l)

Answer 86

Physiology revision: Bilirubin is a product of haemoglobin metabolism. (Hemoglobin -> Heme -> Biliverdin -> Bilirubin) Much of this occurs in the liver, where Bilirubin is conjugated and excreted into the bile. Conjugated bilirubin enters the biliary tree and the GI tract at the duodenal papilla. On reaching the colon – colonic bacteria deconjugate bilirubin into urobilinogen, which then oxidises into urobilin (wee-bilin) and stercobilin (poo-bilin) Urobilin -> reabsorbed and excreted in the urine -> yellow wee Stercobilin -> excreted in the faeces -> brown poo

Answer 87

Pre hepatic - haemoglobin Hepatic - liver and intrahepatic biliary tract Post hepatic - biliary excretion - extrahepatic

Answer 88

Primarily considering an oversupply of precursors (haemoglobin/heme) into the system, essentially flooding the body with bilirubin that cannot be excreted quickly enough. Haemolytic anaemia Acquired defects Hypophosphataemia Oxidative damage E.g. toxic insults – onion/garlic/paracetamol Metabolic disease – hypert4, diabetes mellitus, renal disease Genetic defects Abyssinian and somali cats hereditary haemolysis Non-spherocytic haemolytic anaemia in beagles Phosphofructokinase deficiency in spaniels Immune mediated Primary Secondary - Drugs/toxins - Other immune disease e.g. systemic lupus erythematosus - Infectious – FeLV, Lepto - Neoplasia e.g. lymphoma

Answer 89

Primarily considering an oversupply of precursors (haemoglobin/heme) into the system, essentially flooding the body with bilirubin that cannot be excreted quickly enough. Haemolytic anaemia Acquired defects - Hypophosphataemia - Oxidative damage - E.g. toxic insults – onion/garlic/paracetamol - Metabolic disease – hypert4, diabetes mellitus, renal disease Genetic defects - Abyssinian and somali cats hereditary haemolysis - Non-spherocytic haemolytic anaemia in beagles - Phosphofructokinase deficiency in spaniels Immune mediated Primary Secondary - Drugs/toxins - Other immune disease e.g. systemic lupus erythematosus - Infectious – FeLV, Lepto - Neoplasia e.g. lymphoma Mechanical injury - Turbulent blood flow Neoplasia e.g. haemangiosarcoma DIC Severe myolysis – myoglobin

Answer 90

Looking for haemolysis then underlying causes Haematology Anaemia - Macrocytic, hypochromic, regenerative is classic - Microcytic, normochromic, non-regenerative - chronic disease - liver Blood smear - Spherocytosis - Autoagglutination Saline agglutination test Thrombocytopaenia can develop concurrently in IMHA - evans syndrome Visual inspection of serum - red vs normal Further testing for IMHA - external coombs test Further bloods/infectious disease screening Further history to assess toxin/drug risk Imaging - neoplastic causes of IMHA - Lung and abdo US - CT with contrast

Answer 91

Hepatic disease Infectious (hepatitis) - Bacterial - Fungal - Viral CAV FIV FIP FeLV Inflammatory - Cholangiohepatitis Neoplasia - Lymphoma - MCT - Adenocarcinoma Drugs/Toxins - Paracetamol - NSAIDs - LOTS MORE!!! Degenerative - Amyloidosis - Lipidosis (cats) - Cirrhosis Proximal biliary disease - Cholangitis/cholangiohepatitis

Answer 92

Abnormal liver function is the focus Biochem ALT - found inside liver cells - so elevation are consistent with hepatocellular damage - If cirrhosis - less cells so may be normal level - no cells damaged - focal neoplasia small area so may be normal AST -found n liver and muscle - skeletal and cardia - elevated through venepuncture CK elevations found if due to muscle damage - ALP - widespread but in conc amounts in biliary tree - Small elevations significant in cat - shorter half life compared with dog - Reactive hepatopathies - hyperadrenocorticism, diabetes mellitis, thyroid disease GGT - present in biliary tract cells - Similar to ALP in determining biliary tract disease - Useful in combination In hepatic disease - ALT and ALP likely rise similar degree Urea - end product of protein metabolism and ammonia production - low values - reduced liver function Ammonia - may be high but labile so test quickly Albumin - produced by liver so low values may support disease Clotting factors - all produced by liver - prolonged aPTT and PT Bile acid stim test - assess liver function and biliary flow Enterohepatic recycling - made in liver, released to gallbladder - bile, reabsorbed in GI and return to liver for re release - excellent test of function but poor differentiation between hepatic and post hepatic jaundice Imaging US or CT FNA/biopsy - biopsy risk of bleeding but more likely diagnosis - care with coagulopathy

Answer 93

Intraluminal obstruction - Cholelithiasis (stones) - Gall Bladder Mucocoele (Border Terriers) - Inspissated Bile - Gall bladder polyps - Cysts (Cats) Mural - Inflammatory swelling Cholangitis, cholecystitis, choledochitis Neoplasia Extramural - Pancreatic disease Pancreatitis Pancreatic neoplasia (head of pancreas) Duodenal disease - Infectious - Inflammatory - Neoplastic Porta hepatis stricture - Local inflammatory/infectious/neoplastic disease

Answer 94

Biochemistry: - ALP – cholestatic marker - biliary damage will lead to release into the serum. - GGT in combination with ALP - ALT will probably elevate to a degree also through ascending damage to the liver, but the proportional increase in ALP will be larger. - Cholesterol – usually excreted in the bile, so elevations support biliary obstruction/reduced biliary flow. - Liver function should be largely retained - Urea, Albumin and Clotting times are usually normal. Imaging Ultrasound Gall bladder Biliary tree Pancreas Surrounding mesentery and lymph nodes Gall Bladder FNA for Culture and Sensitivity Exploratory surgery to assess the biliary tree cPLI/fPLI for pancreatitis

Answer 95

History: Signalment Acute vs Chronic Vaccination status Toxin exposure? Trauma (e.g. muscle damage) Urine colour – dark yellow/orange Faeces – bloody diarrhoea? -> exposure to NSAIDs? Coagulopathy? Ataxia/head pressing After feeding Clinical exam: Ecchymoses/bruising – coagulopathy with liver disease? Peripheral oedema – hypoalbuminaemia (liver disease) Pain!!! Neurological exam – deficits -> hepatic encephalopathy (ammonia) BCS – lost in chronic disease Abdominal enlargement – ascites (portal hypertension/hypoalb)/hepatomegaly

Answer 96

Crucial role in many metabolic processes Digestion/metabolism/storage of nutrients including fat/triglycerides protein carbohydrate/glycogen cholesterol vitamins and minerals Waste management e.g. NH3, bilirubin Protein metabolism including albumin synthesis Production and activation of coagulation factors Drug metabolism/detoxification Immunoregulation e.g. Kupffer cells

Answer 97

Coping strategies in the face of disease: massive structural and functional reserve clinical signs not seen until >70% of functional liver mass lost liver failure signs seen earlier in acute disease because less time for adaptation by surviving hepatocytes significant capacity to regenerate Hepatocytes are organized in radial cords forming a six-sided polyhedral prism with portal triads at each of the corners and a single central vein Blood flows from portal triad to central vein (zone 1 to zone 3) Bile is made by zone 3 cells and flows in the opposite direction to blood Hypoxic damage primarily affects zone 3 Metabolic & toxic damage primarily affects zone 1 Fibrosis - repeated injury - nodular regeneration and fibrosis

Answer 98

Non specific signs - Depression/lethargy - Anorexia - Weight loss - V+ D+ - PUPD More specific signs - Jaundice - Hepatic encephalopathy - Ascites - Drug intolerance - Coagulopathy Why these signs? “GI type signs” (anorexia, V/D and weight loss) sometimes due to portal hypertension: leads to vascular stasis and venous congestion  adverse effect on GI tract increases the risk of GI ulceration PU/PD (various reasons suggested)  urea production   medullary solute gradient impaired renal concentrating mechanism  dilute urine & compensatory PD Psychogenic component? Linked to hepatic encephalopathy Reduced hormone metabolism e.g. cortisol Ascites Mechanisms include: Portal hypertension  portal flow  resistance to flow eg cirrhotic liver Hypoalbuminaemia has to be significantly low eg serum albumin < approx. 15 g/l Hepatic encephalopathy – causing neurological signs Ammonia & other encephalopathic toxins originate in the GI tract Normal situation  detoxified in the liver Abnormal  detoxification fails for several reasons: congenital portosystemic shunts (cPSS) toxins bypass the processing plant of the liver fulminant acute liver disease detoxification processes in the liver are compromised and overwhelmed acquired portosystemic shunts chronic fibrotic/cirrhotic liver disease leads to multiple tortuous anastomotic vessels opening up to divert blood from the hepatic portal vein to bypass the liver Neurological signs ie hepatic encephalopathy Waxing and waning non-localising on neuro exam May be associated with feeding Hyperactive &/or depressed/dull/clumsy Circling, pacing, central blindness Salivation, especially cats Seizures ---> coma

Answer 99

GI disease Pancreatitis Endocrine disease - hyperadrenocorticism (very rare in cats) - diabetes mellitus - hypothyroidism (dogs)/hyperthyroidism (cats) Right-sided congestive heart failure Hypoxia e.g. secondary to shock, trauma, anaemia Toxaemia Sepsis/bacteraemia Drug induced in dogs e.g corticosteroids, phenobarbitone

Answer 100

Primary vs. secondary liver disease Focus on careful interpretation of signalment, history, physical exam and results of initial diagnostic investigations avoiding unnecessary testing if the evidence suggests 2ry hepatopathy assessing response to treatment: 2ry disease should resolve with management of the underlying disease

Answer 101

Markers of hepatocellular damage - ALT, AST, GLDH released from hepatocytes following damage cell necrosis or changes in membrane permeability cause enzyme leakage Markers of cholestasis - ALP and GGT found on bile canalicular membrane small amounts normally secreted into bile impaired bile flow increased synthesis and release of enzymes Markers of liver function - non specific - Albumin, urea, glucose, cholesterol, coagulation factors Markers of liver function - specific - bilirubin, bile acids, ammonia Albumin and all the globulins except gamma globulins are synthesised exclusively in the liver Hypoalbuminaemia due to reduced hepatic function is only seen when the liver loses more than 70% of its function Mild anaemia may be seen due to anaemia of inflammatory disease Acanthocytes and target cells can be seen with chronic hepatitis due to alteration in membrane phospholipids

Answer 102

Urine specific gravity often decreased due to various mechanisms causing PU/PD….and 2ry hepatopathy Bilirubinuria normal to find some bilirubin in dog urine but can be increased always abnormal in cat urine Sediment analysis ammonium biurate crystals? identifies dogs at risk of urate urolithiasis

Answer 103

poor sensitivity for detection of liver disease some information about liver size ie normal if contained within the costal arch the caudal border appears angular stomach axis is parallel to the ribs might see choleliths mineralisation consider thoracic radiography if worried about neoplasia

Answer 104

poor sensitivity for detection of liver disease unless mass lesion nodular disease significant change in echotexture gives some information about liver ie normal if moderately and uniformly echoic less echoic than spleen (“kidney, liver, spleen”) coarsely granular parenchyma uniform texture Things to look for any ascites? parenchyma focal/diffuse change? is the margin irregular? can we do a guided biopsy? biliary tract dilation of bile ducts? abnormal gall bladder wall and/or contents? can we get a guided aspirate? vasculature (Doppler) congenital portosystemic shunt? acquired portosystemic shunts?

Answer 105

Toxin/drug induced phenobarbitone carprofen (esp. Labrador retrievers?) potentiated sulphonamides azathioprine paracetamol xylitol environmental toxins e.g. blue green algae, mushrooms Infectious Leptospira Viruses: CAV-1 ; neonatal canine herpes virus bacteria from the GI tract Tyzzer’s disease (clostridium piliformis) Sepsis and endotoxaemia Congenital portosystemic shunt primary portal vein hyperplasia Metabolic Glycogen storage disease Hepatic amyloidosis Non-specific clinical signs include anorexia vomiting/haematemesis diarrhoea/melaena PU/PD jaundice dehydration fever cranial abdominal pain hepatic encephalopathy depression seizures coma hepatomegaly evidence of coagulopathy petechial haemorrhages GI bleeding ascites and portal hypertension? more likely in chronic disease can occur due to hepatocyte swelling

Answer 106

Supportive- very important! intravenous fluid support avoid lactated ringers solution/Hartmanns? liver cannot metabolise lactate as the buffer monitor serum potassium and supplement in iv fluids as necessary monitor blood glucose regularly and supplement if necessary Treat the cause if known, for example: antibiotics for leptospirosis stop hepatotoxic drugs if you are sure they are implicated phenobarb also causes non pathological induction of hepatic enzymes  mild to moderate ↑ ALP/ALT N-acetylcysteine for paracetamol toxicity, may help with xylitol toxicity too Treat hepatic encephalopathy Manage coagulopathy as necessary fresh frozen plasma vitamin K therapy might help Treat any gastrointestinal ulceration GI bleeding can be aggravated by coagulopathy Control vomiting maropitant: may need to use with caution due to hepatic metabolism consider CRI metoclopramide? Diet: short period of starvation while any vomiting is controlled do not starve for > 24-48 hours palatable low fat high quality diet do not restrict protein as this may inhibit hepatocyte regeneration Other symptomatic and supportive therapy: e.g. ursodeoxycholic acid, anti-oxidants (SAMe) Antibiotics: broad spectrum agents safe for use in liver disease include: ampicillin, potentiated amoxicillin, metronidazole (at lower dose) and fluoroquinolones use iv in the acute stages BUT not appropriate unless suspect infectious cause eg lepto in dogs, neutrophilic cholangitis in cats or HE Difficult to predict because varies with extent of damage Full recovery is possible but can progress to chronic disease (hepatitis, fibrosis and cirrhosis) Severe cases can require a high level of intensive care refer to a specialist centre if possible Can take a waxing and waning course despite treatment Negative prognostic indicators include presence of : ascites and splenomegaly suggests portal hypertension has developed can still be reversible in acute disease

Answer 107

Difficult to predict because varies with extent of damage Full recovery is possible but can progress to chronic disease (hepatitis, fibrosis and cirrhosis) Severe cases can require a high level of intensive care refer to a specialist centre if possible Can take a waxing and waning course despite treatment Negative prognostic indicators include presence of : ascites and splenomegaly suggests portal hypertension has developed can still be reversible in acute disease Management of acute HE Identify, remove and treat precipitating causes: gastrointestinal bleeding constipation metabolic alkalosis ….more non ionised NH3 available to enter neuronal cells hypokalaemia.....H+/K+ shifts cause alkalosis and favour non ionised NH3 azotaemia inflammatory disease IVFT crystalloids (avoid lactated ringers (Hartman’s solution) +/- potassium as needed Glucose monitor and supplement as needed Diet: feed a high quality diet little and often ASAP protein/calorie malnutrition will increase NH3 formation by catabolism of body protein Warm water/lactulose enemas: to remove any source of ammonia from the faeces can be followed by a neomycin retention enema Ampicillin iv to protect against bacteraemias Gastroprotectants if evidence of gastrointestinal bleeding omeprazole sucralfate

Answer 108

Management of chronic HE (Common in pups/dogs with congenital PSS) Dietary management is the main strategy: key to the successful management of HE feed normal to slightly increased amounts of protein protein source should be high-quality and highly-digestible feed small amounts of food several times per day Medical therapy: lactulose a disaccharide which passes into the colon to be degraded by bacteria into SCFAs this acidifies the colonic environment trapping NH3 as ammonium ions (NH4+) SCFAs are a preferred energy source for colonic bacteria, causing them to incorporate more ammonia into their own bacterial proteins promotes osmotic diarrhoea decrease time over which colonic contents are acted on by intestinal bacteria Medical therapy: antibiotics if diet alone, or diet + lactulose, are not effective use drugs that are effective against anaerobic organisms: metronidazole amoxicillin Antibiotics effective against gram-negative, urea splitting bacteria e.g. neomycin sulphate may also be used (but resistance develops). Not commonly used.

Answer 109

There are anatomical differences concurrent biliary tract disease, pancreatitis and IBD/(F)CE more common in cats pancreatic duct joins the CBD before reaching the duodenum in most cats “triaditis” or multi organ inflammatory disease There are metabolic differences ineffective glucuronidation pathway reduces ability to metabolise drugs and toxins more susceptible to toxic damage sensitive to many hepatotoxic drugs Cats must eat and they must eat high quality protein in cats hepatic gluconeogenesis relies on protein protein calorie malnutrition occurs if they are fed a low protein diet cats rely on dietary taurine and arginine arginine deficient diet increase NH3 (ie compromises urea cycle) taurine essential for conjugation of bile salts The pathological processes in the liver are different: cats rarely get severe fibrosis and cirrhosis portal hypertension and acquired portosystemic shunts are uncommon cats are especially susceptible to hepatic lipidosis- a severe disease primary hepatic lipidosis is rare in dogs secondary hepatic lipidosis is clinically significant in cats (not in dogs) underlying diseases can include DM, pancreatitis, IBD/FCE anything that stops food intake

Answer 110

Lethargy Change in appetite inappetence? polyphagia Weight loss BCS often reflects duration of disease Vomiting PU/PD Pyrexia Jaundice Hepatomegaly Ascites not very specific other causes not uncommon eg FIP, CHF

Answer 111

Cats are more prone to infiltrative diseases. 1. Neutrophilic cholangitis –infiltration of neutrophils. Is a septic inflammatory disease. 2. Lymphocytic cholangitis – infiltration of lymphocytes. This is usually a chronic disease, suspected to be immune mediated. 3. Hepatic lipidosis – is the result of peripheral fat mobilisation, overwhelming the liver. Severe cholestasis is caused by compression secondary to hepatocyte triglyceride vacuolar distension. Cholangitis Appropriate antibiotic 4-6 week course amoxicillin is a good 1st choice or if no diagnostics Ursodeoxycholic acid choleretic effects anti inflammatory/immune modulating properties Anti oxidants (SAMe, silymarin) Supportive care if sick (can be septic SIRS MODS) IVFT +/- potassium, glucose analgesia especially if triaditis Enteral nutrition to avoid hepatic lipidosis as a complication “IBD/FCE diet” or high protein critical care diet don’t protein restrict Neutrophilic cholangitis Appropriate antibiotic 4-6 week course amoxicillin is a good 1st choice or if no diagnostics Ursodeoxycholic acid choleretic effects anti inflammatory/immune modulating properties Anti oxidants (SAMe, silymarin) Supportive care if sick (can be septic SIRS MODS) IVFT +/- potassium, glucose analgesia especially if triaditis Enteral nutrition to avoid hepatic lipidosis as a complication “IBD/FCE diet” or high protein critical care diet don’t protein restrict Lymphocytic cholangitis

Answer 112

Idiopathic chronic hepatitis: most common liver disease in dogs cause unknown rule out chronic infectious/toxic disease as much as possible several breed predispositions (cocker spaniel, Labrador, Bedlington terrier, springer spaniel, standard poodles) Copper-associated liver disease: associated with some specific breeds Labrador retriever, Dalmatian, Sky terrier, Doberman pinscher WHWT: some (but not all) have copper accumulation True copper storage disease: Bedlington terriers Congenital vascular disease e.g. congenital portosystemic shunts (cPSS) Neoplasia: primary hepatocellular carcinoma (lymphoma) secondary very common site for metastases can be clinically silent can haemorrhage eg met from splenic haemangiosarcoma Biliary tract disease biliary mucoceles neutrophilic cholangitis extrahepatic bile duct obstruction bile duct rupture

Answer 113

Clinical signs of canine chronic hepatitis non specific clinical signs including inappetence weight loss vomiting +/- haematemesis if GI ulceration diarrhoea +/- melaena PU/PD lethargy, depression  true neuro signs/hepatic encephalopathy Early signs can be missed or misdiagnosed as self limiting GI disease dogs present in an “acute” crisis but could be “acute on chronic” disease What do we expect on physical examination? Findings will vary hugely with the stage of disease at presentation often very non-specific Important clinical findings include: poor body condition jaundice ascites These cases remind us of the importance of reviewing a case that is not responding as you expect, for example A dog with repeat visits for V/D not responding to diet management A dog with variable appetite that is now showing weight loss…or abdominal distension?

Answer 114

What drugs might be used to treat chronic liver disease? Destolit (ursodeoxycholic acid) Antioxidants: SAMe, Silybin/silymarin, vitamin E Corticosteroids Antibiotics Diuretics What is the justification for UDA? UDA is a hydrophilic bile acid which displaces more toxic hydrophobic bile acids draws water in to bile ie it has choleretic effects is immune-modulating prevents cells entering the apoptosis pathway increases production of glutathione What is the justification for corticosteroids? Anti-inflammatory Immune-modulating Anti-fibrotic? Main indication: Suspected autoimmune hepatitis What dose might we use? Prednisolone 1-2 mg/kg/SID (ie immune suppressive not just anti inflammatory) Ciclosporine might become the preferred treatment because there are fewer side effects When should we avoid corticosteroids? End-stage/cirrhosis/bridging fibrosis Ascites/GI ulceration (=portal hypertension) Risk of undiagnosed infection (bacterial, viral, fungal) What are the potential adverse effects of corticosteroids? increase protein catabolism can cause or worsen hepatic encephalopathy fluid retention can cause (or worsen) ascites ulcerogenic effects - GI ulceration dexamethasone is more ulcerogenic than prednisolone increased risk of infection or exacerbates existing infections Managing ascites Furosemide with spironolactone if poor response monitor potassium? Peritoneal drainage? only if life threatening because reforms rapidly contributes to dehydration aggravates  albumin

Answer 115

Anomalous connection between the portal and systemic venous systems Can be intrahepatic - joins venacava inside liver Or extraheptaic - joins venacava outside liver

Answer 116

Neurologic Lethargy, ataxia, obtundation, pacing, circling, blindness, seizures, coma Gastrointestinal Vomiting, diarrhoea, anorexia, pica, melaena, haematemesis Urinary – ammonium urate crystals Haematuria, stranguria, pollakiuria, urethral obstruction

Answer 117

Surgical ligation What material? Polyprolene (non-reactive) Silk (reactive) Complete attenuation 50-86% can not tolerate Partial attenuation Second surgical 3-6 months later Ameroid ring Ring of casein surrounded by stainless steel Hygroscopic substance that swells after absorbing fluid Incites a fibrous tissue reaction Cellophane banding Clear non-medical grade cellophane 3- or 4-ply strips sterilised using EO Titanium clips used to hold in place Fibrous tissue reaction leading to gradual occlusion

Answer 118

Primary and secondary (metastatic) disease Metastatic disease is quite common excellent blood and lymphatic supply Primary liver tumours are relatively uncommon in dogs hepatocellular tumours > biliary tumours malignant > benign Tumours can be solitary, nodular or diffuse lymphoma can be nodular or diffuse More likely to be older dogs Primary Hepatocellular carcinoma Hepatocellular adenoma – some now refer to this as low-grade hepatocellular carcinoma Haemangiosarcoma (primary/secondary) Biliary carcinoma Biliary adenoma Lymphoma Neuroendocrine tumours Leiomyosarcoma

Answer 119

Often non-specific clinical signs lethargy, poor appetite Signs may be associated with a complication abdominal bleed if ruptured mass? Palpable mass may be only sign abdominal distension/discomfort? Signs often as for chronic hepatitis Laboratory findings can be similar to chronic hepatitis markers of hepatocellular damage? findings relating to abdominal bleed? Diagnostic imaging radiography ultrasound Definitive diagnosis FNA for cytology? biopsy for histopath Surgery is treatment of choice assess for metastatic disease before major interventions thoracic radiographs R and L lateral +/- DV met checks are best done on inflated chest films ie under GA Chemotherapy only effective for lymphoma

GI and hepatic Flashcards

(143 cards)