Case 3 - clinical overview of disease of the pancreas Flashcards
what are non specific symptoms of GI discomfort
indigestion
fullness
bloating
nausea
pain
what are the intermittent severe indigestion differentials
gastro-oesophageal reflux disease
Peptic ulceration
Biliary stone disease
Inflammatory bowel disease
Pancreatic disease
what are the dimensions of the pancreas
14-20cm and weighs 100g
how does the pancreas sit in the body
anteriorly faces the lesser sac
the head borders the confluence of SMV and PV
body left border of SMV and the aorta
tail the left border of the aorta to the splenic hilum
what is the SMV
superior mesenteric vein
what is the PV
portal vein
what is the endocrine function of the pancreas
20% by mass
islet cells secrete hormones
blood glucose homeostasis
what is the exocrine function of the pancreas
80% by mass
digestive enzymes
acid buffering
released into duodenum
what reflex is initiated by food ingestion
gastro-colic reflex
what is released into the stomach as a response to food
gastrin leads to HCL and pepsinogen
what is released to act on the pancreas
secretin is released from intestinal mucosa to act on the pancreas
what does secretin do
decreases acid release and gastric motility
what does CCK do
acts on pancreas –> lipase and acts on GB for contractions
what are the positive feedback controls of the exocrine pancreas
ach
VIP
GRP
CCK
secretin
what are the negative feedback controls of the exocrine pancreas
somatostatin
pancreatic polypeptides
what enzymes does the exocrine pancreas produce to facilitate digestion
Lipase
Proteases
Amylase
Nucleases
where are these enzymes released
into the duodenum
what does hydrolysis require presence of
bile acids for emulsification
what does pancreatic lipase do
turns triglyceride into monoglyceride and free fatty acids
what is the pro enzyme involved in protein digestion and where is it stored
chymo-tripsin
what happens to trypsinogen
activated by duodenal enterokinase to trypsin
what does trypsin do
activates pro enzymes
where is amylase secreted from
pancreas and salivary glands
what does amylase digest
starch and glycogen
what does this digestion produce
Produces maltose (disaccharide) and maltriose (trisaccharide)
what do the brush border enzymes do
complete digestion to glucose
what are the causes of acute pancreatitis
idiopathic - 20%
Gallstones - 50%
Microlithasis
Ethanol - 25%
Trauma/tumor
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP
Drugs
what is the pathogenesis of acute pancreatitis
inappropriate intra-pancreatic activation of trpysin leading to acinar auto-digestion and death
what is mild acute pancreatitis
pancreatic inflammation and oedema
what is severe acute pancreatitis
pancreatic necrosis and multi organ failure and death
what are the signs and symptoms of acute pancreatitis
severe abdominal and back pain
Nausea and vomiting
Respiratory distress
Fever
Haemorrhage
Shock
Hypotension
Tachycardia
Oliguric
Cullen’s sign
how is acute pancreatitis diagnosed
severe abdominal pain and enxyme released into bloodstream
CXR - exclude perforation
+
CT - assess for pancreatic necrosis, abscess or fluid collection
what enzymes are released into the bloodstream
amylase (normal in 10%)
Lipase (more sensitive/specific)
what is the Glasgow Imrie criteria for acute pancreatitis
3 or more of the below in the first 48 hrs indicates a severe attack
PaCO2 <8kPa
Age >55 years
Neutrophils >15x10 to the power of 9 /L
Calcium <2mmol/L
Renal Function urea>16mmol/L
Enzymes LDH <600iU/L / AST>2000iU/L
Albumin <32g/L
Sugar. glucose >10mmol/L
what is the altanta classification for acute pancreatitis
Mild - no organ failure, or complication
Moderate - transient organ failure OR complication
Severe - persistent organ dysfunction lasting >48 hours
what are the complications of AP
acute fluid collection
pseudocysts
WON
what are these pseuodcysts
Organised fluid collections line by granulation tissue
Symptoms due to mass effect
May self resolve
Symptoms due to infection
what is WON
waled off pancreatic necrosis (WON)
Dying/non-viable pancreatic tissue
Requires drainage
what poses a risk for pancreatitis
ERCP
what is chronic pancreatitis
chronic, continuous inflammation
Fibrotic changes, loss of tissue, and acinar to ductal metaplasia
Loss of functional unit
impairment of pancreatic function
Exocrine - digestive enzymes
Endocrine - insulin
chronic pain
what are the causes of chronic pancreatitis
idiopathic - 20-30%
Alcohol - 60-70% - but don’t assume
genetic: e.g cystic fibrosis (CFTR), SPINK1, PRSS1
Autoimmune: e.g IgG4
Hyperlipidaemia - hypertriglyceriaemia
what is the pathogenesis of chronic pancreatitis
Increased acinar protein secreted leads to increased viscosity pancreatic duct plugging
Leads to increased acinar atrophy and fibrosis
reduction in NaHCO3 + fluids
Leads to increased viscosity pancreatic duct plugging
Lead to increased acinar atrophy and fibrosis
what does increased cytochrome P450 non-oxidative pathways lead to
reactive oxygen species
cell damage
what are the signs and symptoms of CP
Pain:
epigastric to back
Episodic (relating to ongoing damage)
Malabsorption:
weight loss
Steatorrhoea - fat malabsorption
Diabetes - type 3
Jaundice - due to bile duct obstruction
what kind of pain is there in chronic pancreatitis
pressure in duct or parenchyma causing pancreatic ischaemia
Inflammation and pancreatic fibrosis
Abnormal CNS pain processing
Reduced bicarbonate secretion
what is the malabsorption due to chronic pancreatitis
lipase levels fall before protease and amylase
Fat malabsorption occurs when lipase production is reduced by 90%
what does this result in
steatorrhea (7g faecal/100g diet)
Weight loss
Reduced bicarbonate - acidic environment - reduced bile acid secretion
how is chronic pancreatitis diagnoses
faecal elastase
Endoscopic ultrasound
CT/MRI
what are the possible diagnosis techniques in diagnosing chronic pancreatitis
14CO2 breath test - in use, not in Manchester
PABA (para-amino benzoic acid)
Urine collection
Increasingly uncommon
direct hormonal stimulation (research)
what type of pain management is given to chronic pancreatitis patients
Analgesia:
non steroidal anti inflammatory drugs
Opiates
Neuropathic e.g tricyclic antidepressants
optimise diabetic control
endoscopic therapy
Stone disease/strictures
nerve blocks
surgery - decompression verus resection
how do we treat the malabsoprtion of CP
replacement of pancreatic enzymes - Creon/pancreatin
Combination of protease, lipase and amylase
Capsules/granules taken before and during meals/snacks
Mimicking normal secretion
what is pancreatogenic diabetes - type 3c
5-10% of all diabetes
Independent predictor of mortality
Difficult to manage -
Patient characteristics
Risk of hypoglycaemia
usually low insulin requirements - but brittle
Insulin pumps can be useful
what is the survival rate for CP
70% survival 10 years
40% survival 20 years
what is the common type of cancer in chronic pancreatitis
Adenocarcinoma more common in chronic pancreatitis
5% develop over 20 year period
Increased pain
Weight loss
Obstructive jaundice
Poor prognosis:
surgical management
Chemotherapy
Palliative
give a summary of the exocrine pancreas
vital role in protein, fat and carbohydrate digestion
Cephalic, gastric, intestinal control
Production of enzymes - CCK
Production of bicarbonate - secretin
Release into duodenum
