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PHYSIOLOGY
- Exocrine
- Endocrine
- 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
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Pancreatic Pathology
Pancreas (simple in terms of pathol)
- Exocrine:
- • Pancreatitis - Acute vs Chronic
- • Tumours – adenocarcinoma (next lecture)
- Endocrine:
- • Diabetes Mellitus
- • Islet cell tumours
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PANCREATITIS
- “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
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PATHOGENESIS of Pancreatitis
- Auto digestion by enzymes
- – inappropriately activated or
- – leaking out of duct into parenchyma
(ie digestive enzs in wrong place)
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AETIOLOGY - (think of oranges and kiwi fruit...)
VITAMIN C
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VITAMIN C
• V Acute ischaemia vascular occlusion, hypotension
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VITAMIN C
Pancreatitis Aeitology
• Infections/inflammation– Viral eg. Mumps, Parasitic infestation (obstruction)
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VITAMIN C
Trauma – Obstruction - Biliary tract disease (gall stones), Ampullary tumour
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VITAMIN C
• Auto immune pancreatitis
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VITAMIN C
Metabolic Alcoholism
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VITAMIN C
Idiopathic/ Iatrogenic - Drugs
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VITAMIN C
Neoplastic - secondary to an ampullary tumour
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VITAMIN C
C Hereditary pancreatitis (How is that C??)
...scorpion bites also.... maybe they're full of Vitamin C?
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MECHANISM
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
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PATHOLOGY
- Damage to acini, fat cells, blood vessels
- • Necrosis
- • Inflammation – complement, kinins, clotting (thrombosis)– chemotaxis of inflammatory cells
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Resolution of pancreatitis
Remove stimulus
- Repair
- – Macrophages remove debris
- – No regeneration– If extensive necrosis then fibrosis/scarring
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SYMPTOMS AND SIGNS
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
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INVESTIGATIONS
Serum amylase and lipase
- Ultrasound or CT:
- Acute - enlarged inflamed pancreas
- Chronic - calcifications in the pancreas
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- ACUTE PANCREATITIS
- Swollen, haemorrhagic and fat necrosis
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CHRONIC PANCREATITIS
Shrunken, hard, pale, fibrous with visible calcification
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LONG TERM COMPLICATIONS
- • Pancreatic pseudocyst (abscess)
- • Pancreatic insufficiency
- – Malabsorption
- – Secondary diabetes
- • Increased risk of carcinoma
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- Pancreatic pseudocyst
- (can see hole where enzs have dissolved pancres)
- shown histologically too
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TREATMENT
- • Correct the cause
- (eg stop drinking or getting bitten by scorpions)
• Rest the pancreas (Tx clotting cascade, resp distress etc)
• Support the patient
• ?Surgery
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CHOLELITHIASIS, CHOLECYSTITIS
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- Function
- • Storage of bile
- • Episodic release into duodenum
- Bile
- • Aids in the digestion of fats
- • Is a vehicle for excretion of some wastes
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Gall Bladder Pathology
• Cholelithiasis and Cholecystitis (Acute and Chronic)• Adenocarcinoma (next lecture)
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CHOLELITHIASIS
“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
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CHOLELITHIASIS Symptoms
• 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
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CHOLECYSTITIS
“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
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Pathology
- • Mucosal damage - ulceration
- • Inflammation - acute/chronic
- • Mucosal regeneration with hyperplasia
- • Fibrosis (repair)
- • Muscle hypertrophy (trying to overcome inability to squirt)
- • Diverticula (Rokitansky-Aschoff sinuses)
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COMPLICATIONS OF CHOLELITHIASIS/CHOLECYSTITIS
• 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
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Tx of Cholelithiasis / Cholecystitis
• Observe with pain relief, nil by mouth
• Surgery– Open or laparoscopic
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