This document summarizes information about various pancreatic disorders including acute and chronic pancreatitis, autoimmune pancreatitis, and pancreatic cancer. It covers causes, pathophysiology, clinical features, investigations, and management of each condition. For acute pancreatitis, it describes predictors of severe disease and complications like pseudocysts. Management involves early resuscitation, nutritional support, treating underlying causes, and draining infected necrosis. Chronic pancreatitis is often due to alcohol and results in pain, malabsorption, and diabetes. Investigations aim to diagnose chronic pancreatitis and assess function and anatomy. Management focuses on alcohol cessation, pain relief, treating malabsorption, and complications. Autoimmune pancreatitis resembles cancer but responds to steroids

1. Pancreatic disorders

2. Acute pancreatitis:
 3% of all cases of abd pain admitted to hospital.
 Affects 2–28/100 000,increasing in incidence.
 A potentially serious condition with an overall mortality of 10%.
 About 80% of all cases are mild with favourable outcome.
 Approximately 98% of deaths occur in the 20% of patients with severe
disease& about 1/3 within the first week, usually from multi-organ failure.
 After this time, the majority of deaths result from sepsis, especially that
complicating infected necrosis.
 At admission, it is possible to predict patients at risk of complications.
 Individuals who are predicted to have severe pancreatitis&those with
necrosis or other complications should be managed in a specialist centre
with an intensive care unit& multidisciplinary hepatobiliary specialists.

5. Acute pancreatitis:Pathophysiology
 AP occurs from premature intracellular trypsinogen activation, releasing
proteases that digest the pancreas& surrounding tissue.
 Triggers :alcohol, gallstone &PD obstruction .
 There is simultaneous activation of nuclear factor kappaB (NFκB), leading
to mitochondrial dysfunction, autophagy& vigorous inflamma response.
 The normal pancreas has only a poorly developed capsule& adjacent
structures, including the common bile duct, duodenum, splenic vein&
transverse colon, are commonly involved in the inflammatory process.
 The severity is dependent on the balance between the released proteolytic
enzymes& antiproteolytic factors; intracellular panc trypsin inhibitor
protein& circulating β2-macroglobulin, α1-antitrypsin& C1-esterase inhib.
 AP is often self-limiting, in some with severe disease, local complications;
necrosis, pseudocyst or abscess&systemic complications lead to MOF.

7. Acute pancreatitis : Clinical features
 The typical presentation is with severe, constant upper abd pain, of
increasing intensity over 15–60 minutes, which radiates to the back.
 Nausea/vomiting are common.
 There is marked epigastric tenderness, but in the early stages ( in contrast
to a perforated peptic ulcer), guarding/ rebound tenderness are absent
because the inflammation is principally retroperitoneal.
 Bowel sounds become quiet or absent as paralytic ileus develops.
 In severe cases, hypoxia, hypovolaemic shock develop with oliguria.
 Discoloration of the flanks(Grey Turner’s sign) or the periumbilical region
(Cullen’s sign) is a feature of severe pancreatitis with haemorrhage.
 DD:perforated viscus,acute cholecystitis&myocardial infarction.

9. Acute pancreatitis : Clinical features
 Various complications may occur.
 A collection of fluid& debris develop in the lesser sac, following inflamma
rupture of the pancreatic duct; initially contained within a poorly defined,
fragile wall of granulation tissue, which matures over a 6-week period to
form a fibrous capsule (pseudocysts) common, usually asymptomatic,
resolving as the pancreatitis recovers.
 Pseudocysts> 6 cm in diameter seldom disappear spontaneously, can cause
constant abd pain&compress or erode surrounding structures, including
blood vessels, to form pseudoaneurysms.
 Large pseudocysts can be detected clinically as a palpable abdominal mass.
 Pancreatic ascites occurs when fluid leaks from a disrupted pancreatic
duct into the peritoneal cavity.
 Leakage into the thoracic cavity can result in a pleural effusion or a
pleuro-pancreatic fistula.

11. Acute pancreatitis : Lab
 Diagnostic traid: 2 of the 3: pain/enzyme elevation,imaging.
 Diagnosis:raised serum amylase or lipas& U/S or CT evidence of
pancreatic swelling.
 Plain X-rays should be taken to exclude other diagnoses, as perforation or
obstruction& identify pulmonary complications.
 Amylase is efficiently excreted by the kidneys&concentrations may have
returned to normal if measured 24–48 hours after the onset of pancreatitis.
 A persistently elevated serum amylase concentration suggests pseudocyst.
 Peritoneal amylase are massively elevated in pancreatic ascites.
 Serum amylase concentrations are also elevated (but less so) in intestinal
ischaemia, perforated peptic ulcer&ruptured ovarian cyst, while the
salivary isoenzyme of amylase is elevated in parotitis.

12. Acute pancreatitis : Lab
 If available, s lipase preferable to amylase, have greater diagn accuracy.
 Certain invs stratify the severity of AP&have important prognostic value
at the time of presentation,as serial assessment of CRP.
 A peak CRP of > 210 mg/L in the first 4 days predicts severe AP with 80%
accuracy.
 amylase concentration has no prognostic value.

13. Acute pancreatitis : imagings
 U/S can confirm the diagnosis, although in the earlier stages the gland may
not be grossly swollen,also useful because it may show gallstones, biliary
obstruction or pseudocyst formation.
 CE CT, 6–10 days after admission useful in assessing viability, if persisting
organ failure, sepsis or clinical deterioration; features of pan necrosis.
 Necrotising pancreatitis is associated with decreased pancreatic
enhancement on CT, following IV contrast inj.
 The presence of gas within necrotic material suggests infection&impending
abscess formation, in which case percutaneous aspiration of material for
bacterial culture, for appropriate antibiotics.
 Involvement of the colon, blood vessels&other adjacent structures by the
inflammatory process is best seen by CT.

14. Acute pancreatitis : Management
 Establishing the diagnosis& disease severity
 Early resuscitation, according to whether the disease is mild or severe
 Detection& treatment of complications
 Treatment of the underlying cause.
 Opiate analgesics should be given to treat pain&hypovolaemia should be
corrected using normal saline or other crystalloids.
 All severe cases should be managed in a high-dependency ward or ICU.
 A CV line&urinary cath should be inserted to monitor patients with shock.
 Oxygen should be given to hypoxic patients&those who develop systemic
inflammatory response syndrome (SIRS) may require ventilatory support.
 Hyperglycaemia corrected using insulin& hypocalcaemia by IV calcium.
 NG aspiration is required only if paralytic ileus is present.
 Enteral feeding, if tolerated, should be started early in severe AP because
they are in a severely catabolic state& need nutritional support.

15. Acute pancreatitis : Management
 Enteral feeding decreases endotoxaemia&reduce systemic complications.
 Nasogastric feeding is just as effective as nasojejunal route.
 Prophylaxis of thromboembolism with SC LMWH is also advisable.
 Use of prophylactic, broad-spectrum IV antibiotics to prevent inf of panc
necrosis is not indicated, but infected necrosis treated with antibiotics
penetrating necrotic tissue;carbapenems or quinolones, &metronidazole.
 Patients who present with cholangitis or jaundice in association with severe
AP should undergo urgent ERCP to diagnose&treat choledocholithiasis.
 In less severe cases of gallstone pancreatitis, biliary imaging (using MRCP
or EUS) can be carried out after the acute phase has resolved.
 If the liver function tests return to normal&U/S has not demonstrated a
dilated biliary tree, lapchole with an on-table cholangiogram is
appropriate because any CBD stones have probably passed.

16. Acute pancreatitis : Management
 When the operative cholangiogram detects residual CBD stones, should be
removed by laparoscopic exploration or by post-operative ERCP.
 Cholecystectomy should be undertaken within 2 weeks of resolution of
pancreatitis – preferably during the same admission – to prevent further
potentially fatal attacks of pancreatitis.
 Patients with infected pancreatic necrosis or pancreatic abscess require
urgent endoscopic drainage or minimally invasive retroperitoneal
pancreatic (MIRP) necrosectomy to debride all necrotic material.
 Pancreatic pseudocysts can be treated by drainage into the stomach or
duodenum,usually performed after an interval of at least 6 weeks,once a
pseudocapsule has matured, by surgical or endoscopic cystogastrostomy.

18. Chronic pancreatitis :
 A chronic inflammatory disease characterized by fibrosis& destruction of
exocrine pancreatic tissue.
 Diabetes mellitus occurs in advanced cases because islets of Langerhans
are involved.

19. Chronic pancreatitis:causes
 Around 80% result from alcohol misuse.
 In poor countries, severe chronic calcific pancreatitis occurs in non-
alcoholics, possibly as a result of malnutrition, deficiency of trace elements
/ micronutrients& cassava consumption.

22. Chronic pancreatitis: clinical features
 Predominantly affects middle-aged alcoholic men.
 Almost all present with abdominal pain.
 In 50%, this occurs as episodes of ‘acute pancreatitis’, although each
attack results in a degree of permanent pancreatic damage.
 Relentless slowly progressive chronic pain without acute exacerbations
affects 35%, while the remainder have no pain but present with diarrhoea.
 Pain is due to a combination of increased pressure within the pancreatic
ducts&direct involvement of peripancreatic nerves by the inflam process.
 Pain may be relieved by leaning forwards or by drinking alcohol.
 Approximately one-fifth of patients chronically consume opiate analgesics.
 Weight loss is common results from a combination of anorexia, avoidance
of food because of post-prandial pain, malabsorption&/or diabetes.
 Steatorrhoea occurs when> 90% of the exocrine tissue has been destroyed;
protein malabsorption develops only in the most advanced cases.

23. Chronic pancreatitis: clinical features
 Overall, 30% have (secondary) diabetes but rises to 70% in those with
chronic calcific pancreatitis.
 Physical examination reveals a thin, malnourished patient with epigastric
tenderness. Skin pigmentation over the abdomen& back is common results
from chronic use of a hot water bottle (erythema ab igne).
 Many patients have features of other alcohol&smoking-related diseases.

25. Chronic pancreatitis: Investigations
 Aims:
 Make a diagnosis of chronic pancreatitis
 Define pancreatic function
 Demonstrate anatomical abnormalities prior to surgical intervention.

27. Chronic pancreatitis: Management
 1.Alcohol misuse:
 Alcohol avoidance is crucial in halting progression of the disease&reducing
pain.

28. Chronic pancreatitis: Management
 2.Pain relief:
 Analgesic drugs,sp NSAIDs, are valuable but the severe/ unremitting
nature of the pain often leads to opiate use with the risk of addiction.
 Analgesics, as pregabalin/TADs at a low dose, may be effective.
 Oral pancreatic enzyme supplements suppress pancreatic secretion& their
regular use reduces analgesic consumption in some patients.

29. Chronic pancreatitis: Management
 2.Pain relief:
 Patients who are abstinent from alcohol&who have severe chronic pain
resistant to conservative measures should be considered for surgical or
endoscopic pancreatic therapy.
 Coeliac plexus neurolysis sometimes produces long-lasting pain relief,
although relapse occurs in the majority of cases.
 In some, MRCP does not show a surgically or endoscopically correctable
abn, in these individuals, the only approach is total pancreatectomy.
 Even after this operation, some continue to experience pain&the procedure
causes DM,difficult to control, with high risk of hypoglycaemia (since both
insulin& glucagon are absent)&significant morbidity&mortality.

30. Chronic pancreatitis: Management
 3.Malabsorption
 Treated by dietary fat restriction (with supplementary medium-chain
triglyceride therapy in malnourished patients)&oral pancreatic enzyme
supplements.
 A PPI is added to optimize duodenal pH for pancreatic enzyme activity.

31. Chronic pancreatitis: Management
 4.Complications management:
 Surgical or endoscopic therapy may be necessary for the management of
pseudocysts, pancreatic ascites, common bile duct or duodenal stricture&
the consequences of portal hypertension.
 Many patients with chronic pancreatitis also require treatment for other
alcohol/ smoking-related diseases& for the consequences of self-neglect
&malnutrition.

34. Autoimmune pancreatitis:
 A form of chronic pancreatitis that can mimic cancer but responds to
glucocorticoids.
 It is characterised by abd pain, weight loss or obstructive jaundice, without
acute attacks of pancreatitis.
 Blood tests reveal increased serum IgG or IgG4& the presence of other
autoantibodies.
 Imaging shows a diffusely enlarged pancreas, narrowing of the pancreatic
duct&stricturing of the lower bile duct.
 AIP may occur alone or with other autoimmune disorders, such as
Sjögren’s syndrome, primary sclerosing cholangitis or IBD.
 The response to glucocorticoids is usually excellent but some patients
require azathioprine.

35. Pancreatic cancer:
 90% are adenocarcinomas that arise from the pancreatic ducts.
 It involve local structures& metastasise to regional lLNs at an early stage.
 Most patients have advanced disease at the time of presentation.
 Neuro-endocrine tumours also arise in the pancreas but tend to grow more
slowly& have a better prognosis.
 Pancreatic adenocarcinoma affects 10–15/100 000-100/100 000 >70.
 Men are affected twice often as women.
 It is associated with increasing age,smoking&chronic pancreatitis.
 5- 10% have a genetic predisposition: hereditary pancreatitis,HNPCC&
familial atypical mole multiple melanoma syndrome (FAMMM).
 Overall survival is only 3–5%, with a median survival of 6–10 months for
those with locally advanced disease&3–5 months if metastases are present.

36. Pancreatic cancer: Clin features
 Many patients are asymptomatic until an advanced stage, when they
present with central abdominal pain, weight loss&obstructive jaundice.
 The pain results from invasion of the coeliac plexus, characteristically
incessant&gnawing,often radiates from the upper abdomen through to the
back&may be eased a little by bending forwards.
 Almost all patients lose weight& many are cachectic.
 60% arise from the head &involvement of CBD results in the development
of obstructive jaundice, often with severe pruritus.
 A few patients present with diarrhoea, vomiting from duodenal
obstruction, DM, recurrent venous thrombosis, AP or depression.
 Physical exam: evidence of wt loss,abd mass due to the tumour itself, a
palpable gallbladder or hepatic metastasis is commonly found.
 A palpable GB in a jaundiced patient is usually the consequence of distal
biliary obstruction by a pancreatic cancer (Courvoisier’s sign).

37. Pancreatic cancer: Investigations
 The diagnosis is usually made by ultrasound and contrast-enhanced CT
 Diagnosis in non-jaundiced patients is often delayed because presenting
symptoms are relatively non-specific.
 Fit patients with small, localised tumours should undergo staging to define
operability.
 EUS or laparoscopy with laparoscopic ultrasound will define tumour size,
involvement of blood vessels& metastatic spread.
 In patients unsuitable for surgery because of advanced disease, frailty or
comorbidity, EUS- or CT-guided cytology or biopsy can be used to confirm
the diagnosis.
 MRCP& ERCP are sensitive methods of diagnosing pancreatic cancer&
valuable when the diagnosis is in doubt, although differentiation between
cancer& localised chronic/AI pancreatitis can be difficult.
 The main role of ERCP is to insert a stent into the common bile duct to
relieve obstructive jaundice in inoperable patients.

38. Pancreatic cancer: Management
 Surgical resection is the only method of effecting cure& 5-year survival in
patients undergoing a complete resection is around 12%.
 Improved survival (21–29%) with adj chemotherapy using gemcitabine.
 Unfortunately, only 10–15% of tumours are resectable for cure, since most
are locally advanced at the time of diagnosis.

39. Pancreatic cancer: Management
 For the great majority of patients, treatment is palliative.
 Chemotherapy with FOLFIRINOX (5-fluorouracil, leucovorin, irinotecan ,
oxaliplatin) improves median survival to 11 months.
 Pain relief can be achieved using analgesics but, in some patients, coeliac
plexus neurolysis may be required.
 Jaundice relieved by choledochojejunostomy in fit patients& percutaneous
or endoscopic stenting is preferable in the elderly &very advanced disease.
 Ampullary or periampullary ACs are rare,often polypoid, may ulcerate;
frequently infiltrate the duodenum but behave less aggressively than
pancreatic AC&25%undergoing resection survive 5 Ys.