Acute & chronic pancreatitis Flashcards
1
Q
Describe the anatomy of the pancreas
A
- retroperitoneal
- lies between aorta and stomach
- 5 parts: head, neck, body, tail, uncinate process
- head lies in ‘C’ shape of duodenum
- superior mesenteric artery sits posterior to pancreas
- superior mesenteric artery + v pass between head and uncinate process of pancreas + give off branches that enter small bowel mesentery
- tail is in contact w/ the spleen
2
Q
What is the blood supply to the pancreas?
A
airses from coeliac axis (foregut) and superior mesenteric artery (midgut)
- superior pancreatico-duodenal artery (arises from gastroduodenal artery which is a branch of the common hepatic artery which rises from coeliac trunk)
- inferior pancreatico-duodenal artery (arises from SMA)
- pancreatic branches of splenic artery supply neck, body and tail: largest of these is called the arteria pancreatic magna (aka the gr8 pancreatic artery)
3
Q
What is the exocrine function of the pancreas?
A
- acinar cells -> produce digestive enzymes and bicarbonate
4
Q
What is the endocrine function of the pancreas?
A
Islets of Langerhans contain 4 main cell types:
- alpha cells - glucagon
- beta cells - insulin
- delta cells - somatostatin
- PP cells - pancreatic polypeptide
5
Q
What is the difference between acute and chronic pancreatitis?
A
- acute pancreatitis: process that occurs on the back-ground of a previously normal pancreas and can return to normal after resolution of the episode
- chronic pancreatitis: continuing inflammation with irreversible structural changes
6
Q
What are the causes of acute pancreatitis?
A
I GET SMASHED
- Idiopathic
- Gallstones (most common)
- Ethanol (most common)
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion venom
- Hypothermia, hypercalcaemia, hypertriglyceridaemia
- ERCP
- Drugs (SAND: steroids + sulphonamides, azothioprine, NSAIDs, diuretics (loop/thiazide))
7
Q
What is the pathogenesis of acute pancreatitis?
A
- inflammation is secondary to premature + exaggerated activation of digestive enzymes within pancreas
- acute rise in intracellular calcium initiates
- leading to early activation of typsinogen -> trypsin
- impairment of trypsin degradation by chymotrypsin C
- these activated enzymes -> cellular necrosis + autolysis
- gallstones: occlude pancreatic drainage at level of ampulla -> pancreatic ductular hypertension -> inc cytosolic free ionised Ca2+
- alcohol interferes w/ Ca2+ homeostasis in pancreatic acinar cells
8
Q
What are the symptoms of acute pancreatitis?
A
- nausea
- vomiting
- anorexia
- epigastric pain (+ back pain)
9
Q
What are the possible clinical signs of pancreatitis?
A
- tachycardia, hypotension, oliguric
- Grey-Turner’s sign - bilateral flank bruising
- Cullen’s sign - peri-umbilical bruising
- Fox’s sign - ecchymosis over inguinal area
- upper abdominal tenderness
- ileus
- low-grade fever
- if gallstone aetiology: jaundice or cholangitis
10
Q
What are differentials for epigastric pain?
A
- gastric ulcer
- acute cholecystitis
- acute pancreatitis
- chronic pancreatitis
- abdominal aortic aneurysm
- achalasia
- oesophageal rupture
- inferior MI
- intestinal obstruction
11
Q
What are the necessary investigations for acute pancreatitis?
A
- serum lipase -> x3 increased
- serum amylase -> x3 increased
- AST/ALT -> gallstone disease if inc
- FBC -> leukocytosis
- CRP -> increased
- arterial blood gas -> hypoxaemia + disturbances
- AXR -> sentinel loop
- CXR -> atelectasis + pleural effusion (left)
- transabdominal USS
- CT scan 48-72 hrs after dx
- MRCP
- ERCP
12
Q
How do you assess severity of acute pancreatitis?
A
13
Q
What is the management of acute pancreatitis?
A
- ABC
- 4 principles:
- fluid resuscitation (IVF, catheter, strict FB monitoring)
- analgesia
- pancreatic rest (+/- nutritional support - NJ/TPN)
- determining underlying cause
- 95% settle w/ conservative management
- if severe pancreatitis -> HDU
- antibiotics controversial -> commence if necrotic/infected necrosis (Imipenem), but not routinely
- surgery only v rarely required
14
Q
What is the pathogenesis of chronic pancreatitis?
A
- increase in activated trypsin within pancreas
- result of inc/premature activation of trypsinogen
- or by impaired inactivation of activated enzyme from pancreas
- leads to precipitation of proteins within duct umen in form of plugs
- these then form a nidus for calcification
- also cause of ductal obstruction -> ductal hypertension + panc damage
- alcohol impairs calcium regulation -> promote trypsinogen activation
- alcohol only factor interacting w/ env +/- genetic influences
15
Q
What are the clinical features of chronic pancreatitis?
A
- chronic upper abdominal pain (type B)
- steatorrhoea (fat malabsorption)
- anorexia
- diabetes
- malabsorption (-> weight loss)
