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Year 3 Gastrointestinal > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

What is acute pancreatitis?

A

An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.

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2
Q

What characterises mild and severe pancreatitis? Name of classification?

A

MILD: associated with minimal organ dysfunction and uneventful recovery; SEVERE: associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst. 1992 ATLANTA CLASSIFICATION.

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3
Q

What is the aetiology of acute pancreatitis?

A

Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation.

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4
Q

What are the causes of acute pancreatitis?

A

GET SMASHED: Gallstones, ethanol, trauma, steroids, mumps/malignancy, autoimmune, scorpion sting, hyperlipidaemia/hyperparathyroidism, ERCP, drugs (azathioprine, thiazides, valproate).

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5
Q

What is the epidemiology of acute pancreatitis: Incidence? Age? Cause for each gender?

A

Common. Annual UK incidence – 1/1000. Peak age is 60. Males – most common cause is alcohol-induced; females – most common cause is gallstones.

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6
Q

What are the symptoms of acute pancreatitis? (x3)

A

o PAIN: severe, epigastric (upper or RUQ because affects head) or abdominal. Radiating to BACK (because pancreas partly retroperitoneal). Relieved by sitting forward. Aggravated by movement.

o Anorexia

o Nausea and vomiting, worse when eating

o Dehydration (from fluid shifts and oedema leading to hypovolaemia)

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7
Q

What are the signs of acute pancreatitis? (x5)

A

o Epigastric tenderness

o Fever

o Shock: tachycardia and tachypnoea.

o Reduced bowel sounds (due to ileus)

o If severe and haemorrhagic: Turner’s sign or Cullen’s sign.

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8
Q

What is the aetiology of Turner’s and Cullen’s sign?

A

Bruising due to blood vessel auto-digestion and retroperitoneal haemorrhage.

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9
Q

What are the investigations for acute pancreatitis? (x5)

A

o BLOODS: raised amylase (usually at least 3 times normal), raised lipase (especially alcoholic pancreatitis), FBC (increased WCC), U&Es, increased glucose, hypocalcaemia, LFTs may be deranged if gallstone pancreatitis or alcohol pancreatitis), ABG (for hypoxia and metabolic acidosis).

o USS: for gallstones or biliary dilatation

o ERECT CXR: there may be pleural effusion. Mainly for excluding other causes.

o AXR: to exclude other causes of acute abdomen. Psoas shadow may be lost (muscle; if no shadow, can be an indication of increased retroperitoneal fluid). ‘Sentinel loop’ of proximal jejunum from ileus (solitary air-filled dilatation).

o CT SCAN: if diagnostic uncertainty or if persisting organ failure, signs of sepsis or deterioration.

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10
Q

What is diagnostic of acute pancreatitis?

A

Bloods (high amylase) and symptoms alone are diagnostic. The point of other investigations is to EXCLUDE other differentials which you may suspect.

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11
Q

How may amylase levels be obscured in a patient without pancreatitis? (x2)

A

Renal failure results in reduced amylase clearance, so amylase is high though pancreatitis not present. AND amylase is non-specific; you may see elevated levels in cholecystitis, mesenteric infarction and GI perforation.

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12
Q

What is the cause of hypovolaemic shock in acute pancreatitis? Precipitated?

A

Oedema and fluid shifts e.g. ascites, extracellular fluid trapped in the gut, peritoneum and retroperitoneum. NB that hypovolaemia is worsened by vomiting – obviously.

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13
Q

Note about severity of acute pancreatitis and amylase?

A

Does not correlate with severity.

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14
Q

How can LFTs distinguish between alcoholic and gallstone pancreatitis?

A

ALCOHOLIC: increased ALT as this indicates hepatic injury. GALLSTONE: increased ALP and GGT

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15
Q

How can ALT and AST ratio determine pancreatitis cause?

A

Higher ALT than AST indicates chronic; higher AST than ALT indicates acute alcoholic or liver cirrhosis.

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16
Q

How is acute pancreatitis severity assessed? (x3)

A

o Modified Glasgow combined with CRP

o APACHE-II score

o Ranson’s criteria

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17
Q

Specificity of Modified Glasgow criteria vs APACHE-II score?

A

Glasgow is specific to pancreatitis; APACHE-II is non-specific and used in ITU settings.

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18
Q

What is the Modified Glasgow criteria for predicting pancreatitis severity?

A

PANCREAS: PaO2 low, Age over 55years, Neutrophilia high WCC, Calcium low, Renal function high urea, Enzymes high LDH and AST, Albumin low, Sugar high.

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19
Q

How is the Modified Glasgow criteria interpreted?

A

If you have at least three of the criterions, your pancreatitis is severe.

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20
Q

What is the APACHE-II score?

A

More physiological: PaO2, temp, MAP, pH, HR, RR, Na+, K+, creatinine, Hct, WCC, GCS.

21
Q

What are the local complications of pancreatitis? (x10)

A

o Pancreatic necrosis from autodigestion by pancreatic enzymes

o Pseudocyst (peripancreatic fluid collection 4 weeks from onset; associated with fever, abdominal mass and persistent increased amylase/LFTs)

o Abscess: peripancreatic fluid from pancreatic necrosis, occurring more than 4 weeks after pancreatitis

o Ascites (fluid leakage from pancreas)

o Pseudoaneurysm (collection of blood between tunica media and adventitia – different from dissection which is between tunica intima and media)

o Venous thrombosis (of splenic vein)

o Bleeding from elastase eroding major vessels e.g. splenic artery.

o Pleural effusion

o Chronic pancreatitis

o Gastric varices

22
Q

What makes a pancreatic pseudocyst ‘pseudo’?

A

It is a collection of fluid in the LESSER SAC i.e. not lined by epi or endothelium.

23
Q

What is the difference in management of pancreatic pseudocyst and abscess?

A

Abscess NEEDS drainage; pseudocyst may need draining/may resolve.

24
Q

How is recurrent oedematous pancreatitis managed?

A

Near-total pancreatectomy.

25
Q

What are the systemic complications of pancreatitis? Aetiology of each? (x7)

A

o Multiorgan dysfunction from shock

o Sepsis

o Renal failure (from hypoxaemia, high amylase, decrease in renal perfusion pressure from shock and ascites)

o ARDS (acute respiratory distress syndrome; from pancreatic enzymes causing inflammation in the lungs)

o DIC (theorised that this is from early intravascular consumption of coagulation factors secondary to circulating pancreatic enzymes)

o Hypocalcaemia (unknown mechanism but the pancreas contains a lot of calcium)

o Diabetes

26
Q

How do we reduce risk of renal failure in pancreatitis?

A

Give lots of fluid!

27
Q

How is acute pancreatitis medically managed? (x7)

A

o Fluid and electrolyte resuscitation

o Urinary catheter

o NG tube if vomiting

o Nil by mouth, consider NJ feeding as it will result in decreased pancreatic stimulation. Enteral preferred to parenteral feeding is shown to reduce infective complications and mortality

o Analgesia

o Blood sugar control

o Prophylactic antibiotics for infective pancreatitis

28
Q

How is acute pancreatitis managed non-conservatively for gallstone pancreatitis?

A

ERCP and sphincterotomy

29
Q

How is acute pancreatitis managed when pancreatic necrosis or sepsis?

A

Undergo image-guided fine needle aspiration for culture

30
Q

How is acute pancreatitis managed surgically?

A

Necrotising pancreatitis should be managed with minimal abscess or open necresectomy (drainage and debridement of necrotic tissue).

31
Q

What is the prognosis of acute pancreatitis?

A

20% follow severe course with high mortality (infected pancreatic necrosis associated with 70% mortality). 80% run milder course, but mortality is still 5%.

32
Q

What is chronic pancreatitis? What characterises it? (x3)

A

Chronic inflammatory disease of the pancreas characterised by irreversible atrophy, fibrosis leading to impaired endocrine and exocrine function, and recurrent abdominal pain.

33
Q

What is the aetiology of chronic pancreatitis? Contribution of each cause? (x10)

A

o Alcohol (70%)

o Idiopathic (20%) – unknown, spontaneous

o Recurrent acute pancreatitis

o Ductal obstruction

o Pancreas divisum – congenital abnormality a single pancreatic duct is not formed, but rather remains as two distinct dorsal and ventral ducts

o Hereditary pancreatitis

o Tropical pancreatitis

o Autoimmune pancreatitis

o Hyperparathyroidism

o Hypertriglyceridemia

o NOT gallbladder as this would be acute

34
Q

What is the epidemiology of chronic pancreatitis: Incidence? Prevalence? Age?

A

1/100 000 incidence; 3/100 000 prevalence. Mean age 40-50 years.

35
Q

What are the symptoms of chronic pancreatitis? (x5)

A

o Recurrent severe epigastric pain, radiating to back, relieved by sitting forward or hot water bottles, can be exacerbated by eating or drinking alcohol

o Weight loss over many years

o Bloating

o Pale offensive stool (steatorrhea) – some lipases are secreted in the pancreas

o Erythema ab igne (mottled, scaly, hyperpigmented skin from chronic application of hot water bottles)

36
Q

What are the signs of chronic pancreatitis? (x3)

A

Epigastric tenderness, weight loss, malnutrition.

37
Q

What is the pathogenesis of chronic pancreatitis? (x3)

A

Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilatation, cyst and stone formation. Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming ECM, cytokines and growth factors in response to injury. Pain is associated with raised intraductal pressures and inflammation.

38
Q

What are the investigations for chronic pancreatitis? (x6)

A

o BLOOD: glucose (increase may indicate endocrine dysfunction), glucose intolerance test, amylase and lipase (usually NORMAL), increased immunoglobulins especially IgG4 in autoimmune pancreatitis.

o USS: percutaneous or endoscopic showing hyperechoic foci (bright-coloured) with post-acoustic shadowing – sign of inflammation

o ERCP or MRCP: early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternative dilatation (‘chain of lakes’ appearance – see photo)

o AXR: pancreatic calcification may be visible

o CT SCAN: pancreatic cysts, calcification. Calcifications are DIAGNOSTIC

o TESTS OF PANCREATIC EXOCRINE FUNCTION: faecal elastase

39
Q

What are the local complications of chronic pancreatitis? (x8)

A

Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma, splenic vein thrombosis, local arterial aneurysm, gastric varices

40
Q

What are gastric varices? Relationship with pancreatitis?

A

Dilated gastric submucosal veins associated with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow.

41
Q

What are the systemic complications of chronic pancreatitis? (x4)

A

Diabetes, steatorrhea, chronic pain syndromes, dependence on strong analgesics.

42
Q

What is the nature of diabetes in pancreatitis?

A

It is BRITTLE, meaning hard to control.

43
Q

What is the prognosis of chronic pancreatitis: Surgery? Life expectancy reduction?

A

Difficult to predict. Surgery improves symptoms in 60-70% but results are often sustained. Life expectancy can be reduced by 10-20 years.

44
Q

How is chronic pancreatitis managed conservatively? (x5)

A

TREATMENT IS MAINLY SYMPTOMATIC AND SUPPORTIVE e.g. dietary advice (especially low fats as lipase function of pancreas is compromised), abstinence (self-enforced restraint from indulging in bodily activities that are widely experienced as giving pleasure) from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements, analgesia for pain exacerbations.

45
Q

What is oral pancreatic enzyme replacement?

A

Creon – lipase.

46
Q

What specialist pain relief can be offered to patients with chronic pancreatitis? (x2)

A

The sensory nerves to the pancreas transverse the coeliac ganglia and splanchnic nerve: therefore, COELIAC PLEXUS BLOCK (CT or EUS-guided neurolysis) and TRANSTHORACIC SPLANCHIOCECTOMY (surgical excision of one or more segments of the splanchnic nerves) can offer variable degrees of pain relief.

47
Q

How is chronic pancreatitis managed endoscopically? (x5)

A

Sphincterotomy, stone extraction, dilatation, or stenting of strictures. Extracorporeal shock-wave lithotripsy (shock waves used to physically destroy/fragment stones; done from outside the body) is sometimes used for fragmentation of larger pancreatic stones prior to endoscopic removal.

48
Q

When is surgical management of chronic pancreatitis indicated?

A

When medical management has failed.

49
Q

How is chronic pancreatitis surgically managed? (x2 (x1 and x3))

A

o DRAINAGE PROCEDURES: lateral pancreaticojejunal drainage (modified Puestow procedure)

o RESECTIONAL PROCEDURES: pancreaticoduodenectomy (or Whipple’s), limited resection of the pancreatic head (Beger procedure), combined opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure).

Year 3 Gastrointestinal (29 decks)

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