19) acute and chronic pancreatitis, exocrine pancreas insufficiency in dogs and cats

Question 1

common diseases of the exocrine pancreas

Answer 1

o Pancreatitis – acute & chronic
o Problem with digestive enzyme production
o Exocrine pancreatic insufficiency (EPI)
o Exocrine pancreatic neoplasia → ADENOCARCINOMA
o Nodular hyperplasia

Question 2

Physiology:

Answer 2

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

Question 3

pancreatitis classification

Answer 3

• Acute – chronic – recurrent
• Mild – severe – fatal
• Acute serous – acute haemorrhagic-necrotising (AHNP) – purulent

Question 4

acute pancreatitis - pathogenesis

Answer 4

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

Question 5

diagnosis of acute pancreatitis

Answer 5

o Signalment, history, clinical findings
o Diagnostic imaging
o Routine laboratory tests
o Pancreas-specific laboratory tests

Question 6

aetiology of pancreatitis

Answer 6

o Alcohol use
o Gallstones
o Hereditary
o Idiopathic

Question 7

nationale

Answer 7

o Breed: miniature schnauzer, terriers (e.g. Yorkshire), dachshund, poodle
o Age: middle-aged, older
o Condition: obese

Question 7

nationale

Answer 7

o Breed: miniature schnauzer, terriers (e.g. Yorkshire), dachshund, poodle
o Age: middle-aged, older
o Condition: obese

Question 8

history - risk factors

Answer 8

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

Question 9

clinical findings

Answer 9

• Vomiting (water also!) (90%)
• Anorexia, lethargy (90%)
• Abdominal pain (58%)
• Rarely: fever (32%), diarrhoea (33%), jaundice, dyspnoea
• → Dehydration, shock:
o ♥↑, R ↑, CRT ↑, dry MM

Question 10

diagnostic imaging

Answer 10

• 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)

Question 11

Haematology in acute pancreatits

Answer 11

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

Question 12

different things we can test in the blood in acute pancreatitis

Answer 12

o Blood glucose, electrolytes, acid-base status (non-specific

Question 13

diagnosis summary acute pancreatitis

Answer 13

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]

Question 14

therapy of acute pancreatitis

Answer 14

1. 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 (?)
2. 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
3. Antiemetics
   o Initially even if there is no vomiting
   I. Maropitant: first choice decreases visceral pain
   II. Ondansetron
   III. Metoclopramide prokinetic, dopamine antagonists
4. 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
5. 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

Question 15

chronic pancreatitis

Answer 15

• 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

Question 16

feline pancreatitis

Answer 16

• 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

Question 17

EXOCRINE PANCREAS INSUFFICIENCY (EPI)

symptoms and aetiology

Answer 17

• 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