Pancreatic disease Flashcards

1
Q

What is acute pancreatitis?

A
  • Acute inflammation of the pancreas
  • Upper abdominal pain
  • Elevation of serum amylase (> 4 x upper limit of normal)
  • May be associated with multi-organ failure in severe cases
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2
Q

What is the aetiology of acute pancreatitis?

A
○ Alcohol Abuse (60-75%)
○ Gallstones (25-40%)
○ Trauma	
- Blunt
- Postoperative
- Post-ERCP
○ Misc.	
- Drugs (steroids, azathioprine, diuretics)
- Viruses (mumps, coxsackie B4, HIV, CMV)
- Pancreatic carcinoma
- Metabolic (raised calcium, raised triglycerides, raised temp)
- Autoimmune
○ Idiopathic  ~10%
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3
Q

What is the pathology of acute pancreatitis?

A
  • Primary insult
  • Release of activated pancreatic enzymes
  • Autodigestion
  • Proinflammatory cytokines and reactive oxygen species
  • Oedema, fat necrosis and hemorrhage
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4
Q

What are the clinical features of acute pancreatitis?

A

○ Abdominal pain (may radiate to back)
○ Vomiting
○ Pyrexia
○ Tachycardia, hypovolemic shock
○ Oliguria, acute renal failure
○ Jaundice
○ Paralytic ileus
○ Retroperitoneal haemorrhage (Grey Turner’s & Cullen’s signs) (pic)
○ Hypoxia (respiratory failure in severe cases)
○ Hypocalcemia (tetany rare)
○ Hyperglycaemia (occasionally diabetic coma)
○ Effusions (ascites & pleural; high amylase)

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5
Q

What investigations are done for acute pancreatitis?

A

○ Blood tests: amylase/lipase, FBC, U&Es, LFTs, Ca2+, glucose, arterial blood gases, lipids, coagulation screen
○ AXR (ileus) & CXR (pleural effusion)
○ Abdominal ultrasound (pancreatic oedema, gallstones, pseudocyst)
○ CT scan (contrast enhanced)

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6
Q

How is the severity of acute pancreatitis assessed?

A
  • White cell count >15 x 109/l
  • Blood glucose >10 mmol/l
  • Blood urea >16 mmol/l
  • AST >200 iu/l
  • LDH >600 iu/l
  • Serum albumin <32 g/l
  • Serum calcium <2.0 mmol/l
  • Arterial PO2 <7.5 kPa
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7
Q

What is the general management of acute pancreatitis?

A
  • Analgesia (pethidine, indomethacin)
  • Intravenous fluids
  • Blood transfusion (Hb <10 g/dl)
  • Monitor urine output (catheter)
  • Nasogastric tube
  • Oxygen
  • May need insulin
  • Rarely require calcium supplements
  • Nutrition (enteral or parenteral) in severe cases
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8
Q

What is the specific management of acute pancreatitis?

A
  • Pancreatic necrosis: CT guided aspiration → antibiotics ± surgery
  • Gallstones
    → EUS/MRCP/ERCP
    → Cholecystectomy
  • No benefit: antiproteases, antibiotics, inhibitors of pancreatic secretion (glucagon, somatostatin), peritoneal lavage
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9
Q

What are the complications of acute pancreatitis?

A
  • Abscess → antibiotics + drainage
  • Pseudocyst
    □ fluid collection without an epithelial lining
    □ Persistent hyperglycemia and/or pain
    □ Dx by ultrasound or CT scan
    □ Complications: jaundice, infection, haemorrhage, rupture
    □ <6 cm diameter = resolve spontaneously
    □ Endoscopic drainage or surgery if persistent pain or complications
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10
Q

What is the outcome of acute pancreatitis?

A

○ Mild AP (75-80% of cases) - mortality <2%
○ Severe AP - mortality 15%
○ Subsequent course dependent on removal of aetiological factor(s)

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11
Q

What is the epidemiology of chronic pancreatitis?

A

○ Prevalence: 0.01% in Japan→5.4% in South India
○ Incidence: 3.5/100 000 pop./year
○ Males>Females
○ Age 35-50 years

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12
Q

What is the aetiology of chronic pancreatitis?

A

○ Alcohol (80%)
○ Cystic Fibrosis (CP in 2%)
○ high frequency of CFTR gene mutations in CP
○ Congenital anatomical abnormalities
○ Annular pancreas
○ Pancreas divisum (failed fusion of dorsal & ventral buds)
○ Hereditary pancreatitis: rare, auto. dom.
○ Hypercalcaemia
○ Diet: antioxidants in tropical pancreatitis?

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13
Q

What is the pathogenesis of chronic pancreatitis?

A
○ Duct obstruction
- calculi
- inflammation
- protein plugs
○ Abnormal sphincter of Oddi function?
- Spasm: raises intrapancreatic pressure
- relaxation: reflux of duodenal contents
○ Genetic polymorphisms?
- Abnormal trypsin activation
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14
Q

What is the pathology of chronic pancreatitis?

A

○ Glandular atrophy & replacement by fibrous tissue
○ Ducts become dilated, tortuous & strictured
○ Inspissated secretions may calcify
○ ‘Exposed’ nerves due to loss of perineural cells
○ Splenic, superior mesenteric & portal veins may thrombose which results in portal hypertension

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15
Q

What are the clinical features of chronic pancreatitis?

A

○ Early disease is asymptomatic
○ Abdominal pain (85-95%)
- exacerbated by food & alcohol; severity decreases with time
○ Weight loss (pain, anorexia, malabsorption)
○ Exocrine insufficiency
- fat malabsorption which results in steatorrhea
□ Decreased fat soluble vitamins (A,D,E,K), decreased Ca2+/Mg2+
- protein malabsorption which results in weight loss, decreased vitamin B12
○ Endocrine insufficiency which results in Diabetes in 30%
○ Misc.: jaundice, portal hypertension, GI haemorrhage, pseudocysts, pancreatic carcinoma?

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16
Q

What are the investigations for chronic pancreatitis?

A

○ Plain AXR (30% have calcification of pancreas)
○ Ultrasound: pancreatic size, cysts, duct diameter, tumours
○ EUS
○ CT scan
○ Blood tests:
- Serum amylase: raised in acute exacerbations
- Lowered albumin, Ca2+/Mg2+, vitamin B12
- Raised LFTs, Prothrombin time (vitamin K), glucose
- Pancreatic function tests (Lundh, pancreolauryl)

17
Q

What is done for pain control in chronic pancreatitis?

A
  • avoid alcohol
  • pancreatic enzyme supplements
  • opiate analgesia (dihydrocodeine, pethidine)
  • Coeliac plexus block
  • referral to pain clinic/psychologist
  • Endoscopic treatment of pancreatic duct stones and strictures
  • Surgery in selected cases
18
Q

What is the management of the endocrine and exocrine functions in chronic pancreatitis?

A
  • Low-fat diet (30-40 g/day)
  • Pancreatic enzyme supplements (e.g. Creon, Pancrex); may need acid suppression to prevent hydrolysis in stomach
  • Vitamin supplements usually not required
  • Insulin for diabetes mellitus (oral hypoglycemics usually ineffective)
19
Q

What is the prognosis of chronic pancreatitis?

A

○ Death from complications of acute-on chronic attacks, cardiovascular complications of diabetes, associated cirrhosis, drug dependence, suicide
○ Continued alcohol intake results in 50% 10 year survival
○ Abstinence results in 80% 10 year survival

20
Q

What are the clinical features of carcinoma of the pancreas?

A
○ 75% are duct cell mucinous adenocarcinoma (head 60%, body 13%, tail 5%, multiple sites 22%)
○ Other pathological types:
- carcinosarcoma
- cystadenocarcinoma (better prognosis)
- Acinar cell
21
Q

What are the clinical features of carcinoma of the pancreas?

A

○ Upper abdominal pain (75%) - Ca body & tail
○ Painless obstructive jaundice (25%) - Ca head
○ Weight loss (90%)
○ Anorexia, fatigue, diarrhoea/steatorrhoea, nausea, vomiting
○ Tender subcutaneous fat nodules (like erythema nodosum) due to metastatic fat necrosis
○ Thrombophlebitis migrans
○ Ascites, portal hypertension

22
Q

What are the physical signs of carcinoma of the pancreas?

A
○ Hepatomegaly
○ Jaundice
○ Abdominal mass
○ Abdominal tenderness
○ Ascites, splenomegaly
○ Supraclavicular lymphadenopathy
- PRESENCE OF ABOVE SIGNS USUALLY INDICATES AN UNRESECTABLE TUMOUR
○ Palpable gallbladder (with ampullary carcinoma)
23
Q

What is the management of carcinoma of the pancreas?

A

○ Majority of patients have advanced disease at presentation and <10% are operable
○ Radical surgery - pancreatoduodenectomy
(Whipple’s procedure)
- Patient is fit, Tumour <3 cm diameter, No metastases
- Operative mortality ~5%
○ Palliation of jaundice
- stent, palliative surgery - cholechoduodenostomy
○ Pain control (opiates, coeliac plexus block, radiotherapy)
○ Chemotherapy only in controlled trials

24
Q

What is the prognosis of carcinoma of the pancreas?

A
○ Inoperable cases: 
- mean survival <6 months
- 1% 5yr survival
○ Operable cases:
- 15% 5 year survival
- Ampullary tumours 30-50% 5 year survival