PATH 17 PANCREATITIS

• Exocrine
• • acini - manufacture & secrete digestive enzs as proenzymes
• • enzs activate once in ducts
• • ducts transport activated enzymes

• Endocrine
• • islet cells secrete hormones into blood stream eg insulin

Pancreas (simple in terms of pathol)

•  Exocrine:
• • Pancreatitis - Acute vs Chronic
• • Tumours – adenocarcinoma (next lecture)

• Endocrine:
• • Diabetes Mellitus
• • Islet cell tumours

• “Inflammation of the pancreas”
• Variable time course and severity
• Convention divides pancreatitis into:
• • Acute
• • Chronic (continuous or relapsing)
• It is the same disease process and the distinction is blurred

• Auto digestion by enzymes
• – inappropriately activated or
• – leaking out of duct into parenchyma

(ie digestive enzs in wrong place)

VITAMIN C

• V Acute ischaemia vascular occlusion, hypotension

• Infections/inflammation– Viral eg. Mumps, Parasitic infestation (obstruction)

Trauma – Obstruction - Biliary tract disease (gall stones), Ampullary tumour

• Auto immune pancreatitis

Metabolic Alcoholism

Idiopathic/ Iatrogenic - Drugs

Neoplastic - secondary to an ampullary tumour

C Hereditary pancreatitis  (How is that C??)

...scorpion bites also.... maybe they're full of Vitamin C?

What is the initiating event?

• Defective intracellular transport of proenzymes within the acinar cell

• Primary injury to the acinar cell -oxidative stress - free radicals

• Altered secretion of proteins

• Duct obstruction, raised pressure

• Fibrosis - distorts architecture, interferes with blood flow and secretion flow

• Damage to acini, fat cells, blood vessels
• • Necrosis
• • Inflammation – complement, kinins, clotting (thrombosis)– chemotaxis of inflammatory cells

Remove stimulus

• Repair
• – Macrophages remove debris
• – No regeneration– If extensive necrosis then fibrosis/scarring

Inflammation:- pain / swelling (oedema) / redness / heat (temperature

An “acute” abdomen

Abdominal pain - severe and constant, through to the back

Abdominal tenderness - “board like” (rigidity)

In chronic pancreatitis - unremitting or repeated attacks of pain

Systemic effects secondary to activation of complement, kinins, clotting:

• • DIC (diffuse intravascular coagulation) 
• • Shock, multiorgan failure (ARDS, ARF)
• • Death

• If there is bile duct obstruction ---> jaundice 
• • Due to tissue oedema

Serum amylase and lipase

• Ultrasound or CT:
• Acute - enlarged inflamed pancreas
• Chronic - calcifications in the pancreas

• ACUTE PANCREATITIS
• Swollen, haemorrhagic and fat necrosis

CHRONIC PANCREATITIS 

Shrunken, hard, pale, fibrous with visible calcification

• • Pancreatic pseudocyst (abscess)
• • Pancreatic insufficiency
• – Malabsorption
• – Secondary diabetes
• • Increased risk of carcinoma

• Pancreatic pseudocyst 
• (can see hole where enzs have dissolved pancres)
• shown histologically too

• • Correct the cause
• (eg stop drinking or getting bitten by scorpions) 

• Rest the pancreas (Tx clotting cascade, resp distress etc)

• Support the patient

• ?Surgery

= gall stones

• Function
• • Storage of bile
• • Episodic release into duodenum

• Bile
• • Aids in the digestion of fats
• • Is a vehicle for excretion of some wastes

• Cholelithiasis and Cholecystitis (Acute and Chronic)• Adenocarcinoma (next lecture)

“Gall stones”

• Pathogenesis -  
• Formation is due to an imbalance between bile salts, cholesterol and lecithins.

• • Stones classified as cholesterol or pigment (bilirubin/calcium salts)
• Form slowly over time

• Asymptomatic, picked up on ultrasound

• Pain – constant or colicky(ie waxes and wanes) (cholecystitis)

Thought to be due to contraction of gall bladder attempting to pass stone into cystic duct

“Inflammation of the gall bladder”

• • Usu assocd w gall stones (obstruction at the neck)
• • Mechl damage of mucosa
• • Chemical irritation
• • Ischaemia (cystic artery inflamed leading to thrombosis)
• • Can get superadded bacterial infection

• • Mucosal damage - ulceration
• • Inflammation - acute/chronic
• • Mucosal regeneration with hyperplasia
• • Fibrosis (repair)
• • Muscle hypertrophy (trying to overcome inability to squirt)
• • Diverticula (Rokitansky-Aschoff sinuses)

• Superadded bacterial infection– empyaema/generalized sepsis

• • Stone in biliary tree
• – Obstructive jaundice or pancreatitis
• – Infection in biliary tree (- cholangitis)

• • GB perforation
• – abscess formation
• – peritonitis
• – fistulas

• Increased risk of carcinoma

• Observe with pain relief, nil by mouth

• Surgery– Open or laparoscopic