Acute & Chronic Pancreatitis Flashcards

1
Q

What is pancreatitis?

What are the 2 different types?

A

a condition involving inflammation of the pancreas

pancreatitis can be acute or chronic

acute pancreatitis can return to normal after resolution of the episode

chronic pancreatitis involves continuing inflammation, often with irreversible structural changes

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2
Q

What 2 factors account for the vast majority of cases of acute pancreatitis?

A

gallstones and alcohol

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3
Q

How does the severity of acute pancreatitis vary?

What is the mortality in the more severe form and why?

A

severity varies from mild self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage

mortality is 40-50% in the more severe form as damage can result in the release of lytic enzymes into the blood

this contributes to severe shock and digestion of surrounding tissue

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4
Q

What does the acronym GET SMASHED stand for?

A

GET SMASHED are the causes of acute pancreatitis

G - gallstones

E - ethanol (alcohol)

T - trauma

S - steroids

M - mumps

A - autoimmune (e.g. SLE)

S - scorpion bites

H - hypercalcaemia, hypothermia, hyperlipidaemia

E - ERCP

D - drugs - e.g. azathiaprin

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5
Q

What element is suggested to be raised in the final common pathway for pancreatitis?

What does this lead to?

What lifestyle factor can also influence this process?

A

the final common pathway has a marked rise in intracellular calcium

this leads to activation of intracellular proteases

there is evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells

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6
Q

What is the result of activation of intracellular proteases following an increase in intracellular calcium?

A

proteases digest the walls of blood vessels, leading to blood extravasation

amylase is released into the blood

(this is a non-specific diagnostic marker)

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7
Q

As well as amylase, what is released into the blood following blood extravasation?

What “sign” can this lead to?

A

released lipases are a better diagnostic marker than amylase

they cause fat necrosis within the abdomen and subcutaneous tissue

this can lead to discolouration of the skin - Grey Turner’s sign

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8
Q

What is Grey Turner’s sign?

A

this refers to discolouration of the skin / bruising of the flanks

it appears as a blue discolouration

this is a sign of retroperitoneal haemorrhage or bleeding behind the peritoneum

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9
Q

How can levels of calcium and glucose be affected in pancreatitis and why does this happen?

A
  • fatty acids are released into the blood following extravasation and lipase release

these can bind to Ca2+ and lead to hypocalcaemia

  • concomitant destruction of adjacent islets can lead to hyperglycaemia

this can then cause Type II diabetes

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10
Q

What can occur following necrosis and destruction of pancreatic tissue in pancreatitis?

A
  • formation of abscesses or cysts within the pancreas or adjacent tissues can occur
  • infection secondary to pancreatic tissue damage does not always occur, but can
  • not all cases of infection lead to cyst / pseudocyst formation
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11
Q

Why can pulmonary failure occur in acute pancreatitis?

What does this eventually lead to?

A

pulmonary failure in acute pancreatitis is caused by circulating activated digestive enzymes

(e.g. phospholipase A2, trypsin)

this leads to a loss of surfactant, atelectasis and irritation

this eventually leads to ARDS and pleural effusion

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12
Q

What else can occur in acute pancreatitis as a result of circulating activated digestive enzymes?

A
  • cardiac depression
  • breakdown of the blood brain barrier
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13
Q

What is the main clinical feature of acute pancreatitis?

How does this change as inflammation spreads?

A

upper abdominal pain that usually starts in the epigastrium and is accompanied by nausea and vomiting

as inflammation spreads in the peritoneal cavity, the pain becomes more intense

involvement of the retroperitoneum frequently leads to back pain

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14
Q

What clinical features may be present in severe cases of acute pancreatitis?

A
  • tachycardia
  • hypotension
  • oliguria (reduced urine output)
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15
Q

What might be seen on abdominal examination in acute pancreatitis?

A
  • widespread tenderness with guarding
  • reduced / absent bowel sounds
  • periumbilical bruising (Cullen’s sign) and flank bruising (Grey Turner’s sign)
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16
Q

What is Cullen’s sign?

A

haemorrhagic discolouration of the umbilical area due to intraperitoneal haemorrhage of any cause

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17
Q

What does it mean if Cullen’s sign and Grey Turner’s sign are present?

A

if these signs are present they show severe necrotising pancreatitis

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18
Q

What sign, if present, is indicative of poor prognosis in acute pancreatitis?

A

left-sided pleural effusion

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19
Q

What will blood tests show in acute pancreatitis?

A
  • raised serum amylase
  • raised serum lipase

amylase is not prognostic and the level is not related to the degree of tissue damage

lipase levels are more specific and relate to the level of tissue damage, but levels do not rise until up to 8 hours after the onset of symptoms

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20
Q

What does raised amylase suggest?

A

raised amylase, many times above the normal level, is an important indication of pancreatic inflammation

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21
Q

Why might a chest X-ray be performed when diagnosing acute pancreatitis?

A
  • CXR excludes gastroduodenal perforation, which also causes raised serum amylase
  • CXR may show gallstones or pancreatic calcification
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22
Q

Why might an USS be performed in suspected acute pancreatitis?

What might this show?

A

USS is performed to look for gallstones which may cause pancreatitis

It may also show pancreatitic swelling and necrosis

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23
Q

Why might a contrast-enhanced spiral CT be performed in acute pancreatitis?

A
  • to assess the extent of pancreatic necrosis
  • to detect complications such as abscesses, fluid collection and pseudocyst formation
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24
Q

What is the purpose of performing an MRI in acute pancreatitis?

A

MRI (MRCP) assesses the degree of pancreas damage

it can be used to locate gallstones

it can also differentiate between fluid and solid inflammation

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25
Q

What is ERCP?

Why might it be used?

A

endoscopic retrograde cholangiopancreatography

this is used to look at the pancreatic duct for inflammatory fibrosis or tumours

pancreatic juice can be collected and biochemically examined

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26
Q

What is APACHE and what does a score >8 suggest?

A

acute physiology and chronic health evalulation score

it assesses the severity of a wide spectrum of illness

it is adjusted for age + obesity and other health problems

it has a high sensitivity as early as 24 hours after symptom onset

a score >8 indicates severe disease

27
Q

What scoring system is used to assess the severity and prognosis of pancreatitis?

What acronym does this use?

A

the Glasgow scoring system can be used to assess the prognosis and severity of pancreatitis

it can be remebered with the acronym PANCREAS

28
Q

What does PANCREAS stand for in the Glasgow scoring system?

A

P - PO2:

  • oxygen < 60 mmHg or 7.9 kPa

A - Age:

  • age > 55

N - Neutrophilia:

  • white blood cells > 15

C - Calcium:

  • calcium < 2 mmol/L

R - Renal urea:

  • urea > 16 mmol/L

E - Enzymes:

  • lactate dehydrogenase (LDH) > 600 iu/L
  • aspartate transaminase (AST) > 200 iu/L

A - Albumin:

  • albumin < 32 g/L

S - Sugar:

  • glucose > 10 mmol/L
29
Q

What are the initial supportive treatments for acute pancreatitis?

A
  • replace lost fluids (IV) and a urinary catheter might be necessary
  • nasogastric suction to prevent abdominal distension and vomitus, lowering risk of aspiration pneumonia
  • continuous oxygen administration may be necessary depending on sats
30
Q

What types of medication might be prescribed for acute pancreatitis?

A

Prophylactic antibiotics:

  • these should broad spectrum - e.g. cefuroxime or aztreonam
  • reduces risk of infection complications

Analgesia:

  • pethidine and tramadol administered under patient control system
31
Q

What other treatment may be given to a patient in hospital with acute pancreatitis?

A

enteral nutrition via nasojejunal tubes

32
Q

What treatment is given to patients with multiorgan failure?

A

ventilation and renal support

this has a mortality rate > 80%

33
Q

What do mortality and morbidity reflect in the first week of acute pancreatitis and after this?

A
  • within the first week, mortality and morbidity reflect the systemic inflammatory response, which in turn results in multiple organ failure
  • after this, prognosis is related to the extent of pancreatic necrosis
34
Q

What is extensive pancreatic necrosis associated with?

What happens if the necrotic pancreas becomes infected?

A

extensive necrosis (>50%) is associated with higher risk of further complications

these frequently need surgical intervention

infection of the necrotic pancreas can lead to sepsis and resection of infected areas of pancreas may be needed

35
Q

Why might surgical intervention be needed in an infected necrotic pancreas?

A
  • some fluid collections are surrounded by granulation tissue (pseudocysts)
  • larger ones (>6cm) may become infected or lead to intraperitoneal bleeding
  • these need to be drained surgically
36
Q

What is the prognosis like overall for acute pancreatitis?

What happens in people with severe acute pancreatitis?

A
  • vast majority with mild or moderate acute pancreatitis will make a full recovery
  • severe acute pancreatitis patients may become pancreatically insufficient with respect to exocrine (malabsorption) and endocrine function (diabetes)
37
Q

What is the most common cause of chronic pancreatitis?

A

alcohol accounts for the vast majority of cases (60-80%)

this may either be chronic pancreatitis or repeated episodes of acute pancreatitis

38
Q

What are rarer inherited causes of chronic pancreatitis?

A
  • rare autosomal dominant trait associated with aminoaciduria or hyperparathyroidism
  • cystic fibrosis due to CFTR problems, which causes mucus problems
  • benign or malignant obstruction of the pancreatic duct
  • congenital abnormalities, such as pancreas divisum
39
Q

What is thought to be involved in the pathogenesis of chronic pancreatitis that is hereditary?

A
  • due to inappropriate activation of enzymes within the pancreas
  • genetic abnormalities of cationic trypsinogen and its inhibitory proteins lead to unopposed trypsin activity within the pancreas
40
Q

What lifestyle factor can also influence trypsin activity within the pancreas?

Why is trypsin thought to be the main enzyme involved in chronic pancreatitis?

A
  • chronic alcohol intake raises the level of trypsinogen relative to its inhibitor
  • human trypsinogen also has a tendency to auto-activate
  • this leads to more unopposed activity and damage to the pancreas
41
Q

What is the result of intrapancreatic protein activity?

How can this lead to further pancreatic damage?

A
  • intrapancreatic protein activity leads to precipitation of proteins within the pancreatic duct lumen in the form of plugs
  • plugs form a starting point for calcification and lead to ductal hypertension
  • this causes further pancreatic damage
42
Q

What factors can perpetuate the formation of pancreatic plugs?

A

cytokine activation and oxygen stress perpetuate the process via inflammation

43
Q

What is the pain like in chronic pancreatitis?

What can make it worse and what symptom usually accompanies it?

A
  • pain is usually epigastric and radiates through into the back
  • pain may be episodic
  • exacerbations may follow further alcohol excess
  • during periods of abdominal pain, weight loss may be severe
44
Q

What are other clinical features of chronic pancreatitis?

A
  • malabsorption develops due to exocrine insufficiency
  • diabetes develops due to endocrine insufficiency
  • jaundice secondary to common bile duct obstruction is a feature in a small number of patients
45
Q

What will ERCP show in someone with chronic pancreatitis?

A
  • distorted pancreatic ducts due to scar tissue resulting from a chronic inflammatory process
46
Q

What would an X-ray of the upper abdomen show in someone with chronic pancreatitis?

A

flecks of calcification due to previous fat necrosis

47
Q

What tests might be abnormal in chronic pancreatitis?

A
  • serum amylase and lipase levels are elevated
  • faecal elastase levels are abnormal in the majority of patients
48
Q

Why is a faecal elastase test done?

A

elastase is produced by exocrine tissue in the pancreas

the test measures the amount of elastase within the stool to evaluate whether the pancreas is functioning properly

49
Q

What is prescribed for pain relief in chronic pancreatitis?

A
  • a combination of NSAIDs and opiate (tramadol) used for pain relief
  • tricyclic antidepressant (e.g. amitriptyline) used for chronic pain
50
Q

How can pancreatic enzyme supplements improve pain in chronic pancreatitis?

A

pancreatic enzyme supplements reduce pancreatic stimulation by a negative feedback mechanism

this reduces the intensity of the pain

51
Q

How does pain change over time in chronic pancreatitis?

What option is available for patients with debilitating pain?

A

pain improves over time

after 6 to 10 years, 60% of patients are pain free

for patients with debilitating pain, surgical intervention is an option

duct drainage and limited resection can relieve pain in 80% of patients, but has a 5% mortality

52
Q

What is the purpose of endoscopic techniques in treatment of chronic pancreatitis?

A

endoscopic techniques can improve pancreatic drainage

53
Q

What other group of medication is given in chronic pancreatitis and why?

A

an acid suppressor - H2-receptor antagonist or PPI

this compensates for decreased bicarbonate secretion

54
Q

How effective is treatment for chronic pancreatitis?

A

a proportion of patients still continue to malabsorb due to inadequate mixing of pancreatic supplements with the food as well as the low pH in the duodenum

55
Q

What is pancreatin?

A

a pancreatic enzyme supplement consisting of protease, lipase and amylase

56
Q

How must supplements like pancreatin be taken and why?

A

protease, lipase and amylase are inactivated by gastric acid and heat

supplements must be taken with food (but not mixed with very hot food)

and either concurrently with gastric acid suppression therapy or as enteric-coated formulations

57
Q

What drug tends to be used as gastric acid suppression therapy alongside pancreatin?

A

cimetidine

this is a H2 receptor antagonist

a PPI could also be used

58
Q

How is dosage of pancreatin adjusted?

A

dosage is adjusted according to size, frequency and consistency of stools

59
Q

What are the unwanted effects of pancreatin?

A
  • irritation of the mouth and perianal skin
  • nausea and vomiting
  • abdominal discomfort
60
Q

How is the amount of pancreatin given balanced with side effects?

A
  • to reduce side effects, the amount of pancreatin given has to be reduced
  • this means that the amount of total dietary fat consumed also has to be reduced
  • otherwise it could result in steatorrhoea
61
Q

What are the complications of chronic pancreatitis?

A
  • same as acute pancreatitis (e.g. pseudocyst formation)
  • formation of ascites
  • accumulation of serous fluid in the peritoneal cavity
  • occasionally pleural effusions
62
Q

What is steatorrhoea?

A

the passage of fat in large amounts in the faeces (up to 30 mmol per 24 hours)

due to failure to digest and absorb the fat

it is associated with pancreatic insufficiency

63
Q

What usually improves steatorrhoea?

A

pancreatic enzyme supplements (e.g. pancreatin) and a low fat diet