19) acute and chronic pancreatitis, exocrine pancreas insufficiency in dogs and cats Flashcards
common diseases of the exocrine pancreas
o Pancreatitis – acute & chronic
o Problem with digestive enzyme production
o Exocrine pancreatic insufficiency (EPI)
o Exocrine pancreatic neoplasia → ADENOCARCINOMA
o Nodular hyperplasia
Physiology:
o Digestive enzymes: o Production, storage, release o a -amylase, lipase → intact molecule o Proteases → zymogens, inactive enzymes ▪ TRYPSINOGEN, chymotrypsinogen, proelastase, procarboxypeptidase, prophospholipase ▪ Activated in the gut
o Defences against autodigestion
o Multi-level defence
o Enzymes are stored in inactive zymogenes → if TRYPSIN is still activated → pancreas secretory trypsin inhibitor (PSTI) bind it reversibly [in the pancreas]→ if it is not enough and trypsin is still activated → [in the plasma]:
o α1- proteinase inhibitor bind it reversibly
o Macroglobulins make a complex with it irreversibly
o Macrophages phagocyte the complex
pancreatitis classification
- Acute – chronic – recurrent
- Mild – severe – fatal
- Acute serous – acute haemorrhagic-necrotising (AHNP) – purulent
acute pancreatitis - pathogenesis
Problem with the defences against autodigestion
I. Pathologic activation of trypsin in pancreas
▪ Abnormal IC fusion of lysosomes + zymogens
▪ Oxidative stress, hypotension, acidosis
II. +Ineffective defence mechanisms
▪ PSTI, anti-trypsins, macrophages
III. Cascade-like activation ↑↑↑/proteases, cytokines, free radicals, neutrophil migration → inflammation, circulatory failure
IV. Local & regional & multisystemic effects
▪ Local effects: oedema, inflammation, haemorrhage, necrosis → acute fluid accumulation, (formerly: sterile abscess or pseudocyst)
▪ Regional effects: damage of adjacent organs:
• Cholestasis, EHBO
• Duodenitis, colitis
• Local peritonitis
▪ Systemic effects: damage of distant organs
• SIRS (systemic inflammatory response syndrome)
• MODS (multiple organ dysfunction syndrome)
• Acute renal failure (ARF/AKI)
• Respiratory complications: ARDS/ALI, pleuritis
• Cardiac complications: arrhythmia cordis
• Intestines: ischaemia, inflammation
• DIC, septicaemia
• Coagulation, fibrinolysis, complement, kallikrein-kinin, cytokines, free radicals
diagnosis of acute pancreatitis
o Signalment, history, clinical findings
o Diagnostic imaging
o Routine laboratory tests
o Pancreas-specific laboratory tests
aetiology of pancreatitis
o Alcohol use
o Gallstones
o Hereditary
o Idiopathic
nationale
o Breed: miniature schnauzer, terriers (e.g. Yorkshire), dachshund, poodle
o Age: middle-aged, older
o Condition: obese
nationale
o Breed: miniature schnauzer, terriers (e.g. Yorkshire), dachshund, poodle
o Age: middle-aged, older
o Condition: obese
history - risk factors
o Genetics – e.g. miniature schnauzer: PSTI defect
o Food – high fat diets, ‘garbage consumption’
o Hyperlipidaemia – obesity, endocrine disorders (DM, Cushing’s + polyphagia)
o Drugs – KBr, phenobarbital, azathioprine, sulphonamides, tetracyclines, furosemide
o Toxin – organophosphates, zinc
o Pathogens
o Babesiosis, Leishmania
o Pancreatic trauma
o Abdominal surgery/ e.g. adrenalectomy
o Ischemia, perfusion ↓
o Duodenal reflux, ductal hypertension
clinical findings
• Vomiting (water also!) (90%) • Anorexia, lethargy (90%) • Abdominal pain (58%) • Rarely: fever (32%), diarrhoea (33%), jaundice, dyspnoea • → Dehydration, shock: o ♥↑, R ↑, CRT ↑, dry MM
diagnostic imaging
• Abdominal radiography (non-specific)
• Abdominal US (specific)
o Decreased echogenicity → pancreatic necrosis
o Peripancreatic region: increased echogenicity → localised peritonitis
• (Computer tomography – CT)
• (Laparoscopy)
• (Endoscopic US – EUS)
Haematology in acute pancreatits
I. PCV ↔↑ a. Dehydration, hypovolaemia II. WBC ↑ + CRP ↑ a. Leucocytosis b. ‘Left shift’ III. Thrombocytes ↔↓ IV. APTT, PTT, D-dimer V. Plasma a. Icteric b. Lipemic
different things we can test in the blood in acute pancreatitis
o Blood glucose, electrolytes, acid-base status (non-specific
diagnosis summary acute pancreatitis
o Relevant clinical signs and history
▪ Vomiting, abdominal pain, anorexia, risk factors
o + Abdominal US
▪ Machine: high-quality, operator, skilful
o + Lab test
▪ Spec cPL/fPL or Snap cPL pet-side test
• Negative → not pancreatitis
• Positive → confirm with spec cPL
▪ (Significant/multiple increase of amylase & lipase)
o Definitive diagnosis: biopsy and histology [NOT practical]
therapy of acute pancreatitis
- Fluid Therapy – essential!
o Pancreas particularly susceptible to hypovolemia
o Aim: homeostasis+ pancreas microcirculation ↑
• Crystalloids/LR
• Oncotic therapy with colloids/HAES
o Plasma transfusion
▪ Suggested in DIC
▪ Replacement of antiproteases (?) - Analgesia – even if abdominal pain is not evident!
o Opioids:
▪ Butorphanol → buprenorphine → fentanyl
▪ FLK (fentanyl-ketamine-lidocaine) CRI
o Fentanyl patch: delayed onset (12-24h)
▪ NSAID: not suggested, ulcerogenic, renal damage - Antiemetics
o Initially even if there is no vomiting
I. Maropitant: first choice decreases visceral pain
II. Ondansetron
III. Metoclopramide prokinetic, dopamine antagonists - Manage complications
o Gastric acid suppressants (gastric ulcer, oesophagitis)
I. Omeprazole: first choice → proton pump blockers
II. Pantoprazole
III. Ranitidine, famotidine → H2-receptor antagonists
o Antibiotics – infected necrosis, bacterial translocation (intestinal bleeding, prolonged starvation, hypovolaemia), sepsis
o Amoxiclav, fluorokin+metron, cefalosp. (3rd gen)
o Corticosteroids – CIRCI [critical illness-related corticosteroid insufficiency]
o Low dose in critical illness
o Hypotension, non-responder to fluid therapy
o Surgical intervention – if unavoidable
o Complete bile duct obstruction
o Pancreatic abscess, if ab + percutan drainage not effective - Special nutrition
o Aim: to prevent malnutrition, feed enterocytes and keep pancreas at rest
o Feed asap, high digestible low-fat diet
I. Mild pancreatitis
o Short (48-72h) fasting period
o Vomiting Ø water CH easy-to-digest protein
o Small amount several times, Ø fat: low-fat intestinal diet
II. Severe pancreatitis
o Parenteral or enteral feeding?
o Ø long fasting period
chronic pancreatitis
• Recent studies more common (fe > ca)
• Cont. inflammation exocrine +- endocrine damage
• Definitive dx.: histology (?) not practical
o Irreversible morphological damage
o Fibrosis, atrophia, lymphocytic infiltration
• Diagnosis = symptoms + lab work + US/diagn value< AP
• Middle age, older
• Types:
o Idiopathic
▪ Toy breeds; terriers
▪ Spaniels
▪ Chavalier King Charles, cocker
▪ Collie, boxer, sled-dogs
o Autoimmune
▪ Cocker sp, ♂>♀
▪ 50% DM and/or EPI
▪ + other AI-diseases: KCS, GN
▪ Immunosuppr. (steroids) may be beneficial
• Symptoms:
o For months – years
o Recurrent postprandial pain, appetite Ø, vomiting, haematochezia/colitis
o Recc. acute episodes ≈ severe AP
o Most common cause of EHBO
o End stage DM, EPI
• Diagnosis:
o Challenging: diagn value of tests ↓ ~ AP; cPLI = best
o US varied: norm. ≈ severe AP; mass-like (cocker sp)
▪ < 60% sensitivity
• Treatment diet, analgesics, replace of functional deficiency
o Low fat diet, life-long
o Analgesics if needed, orally ≈ AP
o Treatment of acute flare up ≈ severe AP
o EPI, DM-treatment
feline pancreatitis
• Acute (necrotic/suppurative) < chronic – subclinical
• Cause: trauma, ischemia + concurrent disorders (92%)
o +IBD + cholangitis (triaditis), DM, lipidosis hep.
• Aetiology(?):
o 1) Bact. translocation, hematogen spreading acute, severe
o 2) IBD immuno mediated chronic
• Symptoms/ACUTE – NON-SPECIFIC
o >7 year
o Vomiting, abd. pain < dog
o Anorexia, lethargy, hypothermia
o + Diarrhoea, dehydration, icterus, dyspnoea
• Symptoms/CHRONIC
o Even LESS characteristic – weight loss
o Signs of concurrent disorders (92%!)
• Diagnosis:
o Blood work: see dog+ Ca++ ↓ (prognostic value)
o Spec fPL, detect concurrent disorders also!
o US sensitivity ↓ (24-67%)
• Treatment
o Acute ~ dog+ ab ↑ (more often reasonable) + Noe feeding tube!
o Chronic: acute +
▪ Improve appetite (mirtazapine), B12
▪ +-steroids? ‒ in anti-inflammatory dose
▪ SAME – antioxidant
• S-adenosyl methionine
EXOCRINE PANCREAS INSUFFICIENCY (EPI)
symptoms and aetiology
• Progressive loss of pancreatic acinar cells (>90%) maldigestion + malabsorption • Aetiology: o Pancreatic acinar atrophy (PAA) ▪ German shepherd - 60% of EPI-patients ▪ Collie, Chow-chow, Eurasia dog ▪ Autoimmune cause ▪ Young adult ▪ NO diabetes mellitus o Chronic pancreatitis ▪ Cats, spaniels ‒ end-stage CP → DM possible ▪ Older animals • Symptoms: o Chronic disease o Alert, good general state o Polyphagia ↔ weight loss, cachexia o Pasty diarrhoea: clay-like faeces, yellowish ▪ Undigested particles (steatorrhea) ▪ Large volumes and increased daily defecation episodes o Other signs ▪ Rough hair, scaling skin (seborrhoea) ▪ Dysphagia, coprophagic; flatulence
