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Year 1 - BRS > 11.12 - Pancreatitis > Flashcards

11.12 - Pancreatitis Flashcards

1
Q

What are pancreatic acinar cells arranged around?

A

Intercellular canaliculus

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2
Q

What are the two components of pancreatic juice?

A
  • exocrine component - low volume, viscous, enzyme-rich, from acinar cells
  • high volume, watery, HCO3- rich, from duct and centroacinar cells
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3
Q

What are the acinar enzymes?

A
  • lipases (fat)
  • proteases (protein)
  • amylase (carbohydrates)
  • synthesised and stored in zymogen granules
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4
Q

What is the problem for an organ making a cocktail of digestive enzymes?

A

Autodigestion –> acute pancreatitis

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5
Q

What are the protective mechanisms for the enzymes?

A
  • proteases are released as inactive pro-enzymes - protects acini and ducts from autodigestion
  • pancreas contains a trypsin inhibitor to prevent trypsin activation
  • enzymes are only activated in the duodenum
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6
Q

How are enzymes only activated in the duodenum?

A
  • duodenal mucosa secretes enterokinase (enteropeptidase)
  • converts trypsinogen into trypsin
  • trypsin then converts all other proteolytic and some lipolytic pro-enzymes into enzymes
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7
Q

What is acute pancreatitis?

A
  • rapid onset inflammation of the pancreas
  • the pancreas is the grey mass in the middle - very oedematous = peripancreatic inflammation
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8
Q

What is the abbreviation for the aetiology (causes) for acute pancreatitis?

A

GETSMASHED

  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps and other viruses (EBV, CMV)
  • Autoimmune (polyarteritis nodosa, SLE)
  • Scorpion/snake bite
  • Hypercalcaemia, hypertriglyceridaemia, hypothermia
  • ERCP (endoscopic retrograde cholangiopancreatography) - cannulating common bile duct blindly, can accidentally enter main duct and trigger pancreatitis
  • Drugs (SAND - steroids and sulphonamides, azothioprine, NSAIDs, diuretics [loop/thiazide])
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9
Q

What is the pathogenesis of acute pancreatitis?

A
  • gall stones cause build up of pancreatic juice and therefore pressure in pancreatic duct
  • gall stones block ampulla = bile juice from bile duct reflux into pancreatic duct
  • weak ampulla = reflux of duodenal contents (activated enzymes) into pancreatic duct –> pancreas
  • increased permeability of pancreatic duct epithelium by alcohol, acetylsalicyclic acid (aspirin), histamine = acinar cell enzymes diffuse into periductal interstitial tissue
  • alcohol can precipitate proteins in ducts = plugs duct and increases upstream pressure
  • pancreatic enzymes activated intracellularly - proenzymes and lyosomal proteases get incorporated into same vesicles by accident which activates trypsin
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10
Q

What can activation of trypsin intracellularly/extracellularly in pancreas activate?

A
  • phospholipase A2
  • elastase
  • complement
  • prothrombin
  • kallikrein
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11
Q

What does phospholipase A2 do?

A
  • causes fat necrosis which leads to Ca2+ sequestration –> saponification (soap formation) –> hypocalcaemia
  • also causes hyperalbuminemia –> hypocalcaemia
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12
Q

What does elastase do?

A
  • causes arrosion with bleeding - causes haemorrhagic pancreatitis
  • causes islet necrosis which decreases insulin levels –> hyperglycaemia
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13
Q

What does complement do?

A
  • leads to cell toxicity –> vessel arrosion –> bleeding –> pancreatic gangrene
  • cell toxicity –> islet necrosis –> decreases insulin –> hyperglycaemia
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14
Q

What does prothrombin do?

A

Prothrombin –> thrombin –> thrombosis –> ischaemia –> pancreatic gangrene

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15
Q

What does kallikrein do?

A

Kallikrein –> bradykinin, kallidin –> vasodilation and plasma exudation –> pain and shock

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16
Q

What systemic damage can occur due to trypsin activation?

A
  • phospholipase A2 and free fatty acids from fat necrosis can destroy the surfactants of the alveolar epithelium –> hypoxia
  • kallikrein can lead to anuria
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17
Q

What are the three types of acute pancreatitis?

A
  • oedematous pancreatitis - fluid build up
  • haemorrhagic pancreatitis - bleeding pancreatitis
  • necrotic pancreatitis - superseding infection, infected necrotic tissue
18
Q

What are the symptoms of acute pancreatitis?

A
  • epigastric pain radiating to back - often eased by sitting forward
  • nausea and vomiting
  • fevers - does not mean sepsis (infection) but because inflammatory reaction causes high temperatures
19
Q

What are the signs of acute pancreatitis?

A
  • haemodynamic instability (tachycardic, hypotensive) as you lose a lot of fluid
  • peritonism in upper abdomen/generalised
  • Grey-Turner’s sign - bruising in flanks (associated with haemorrhagic pancreatitis)
  • Cullen’s sign - bruising around umbilicus (associated with haemorrhagic pancreatitis)
20
Q

What are some of the differential diagnoses if not acute pancreatitis?

A
  • gallstone disease and associated complications e.g. biliary colic and acute cholecystitis
  • peptic ulcer disease/perforation
  • leaking/ruptured AAA
21
Q

What is a blood test for when investigating acute pancreatitis?

A
  • elevated amylase/lipase
  • other causes of elevated amylase include:
  • parotitis
  • renal failure
  • macroamylasaemia
  • bowel perforation
  • lung/ovary/pancreas/colonic malignancies can produce ectopic amylase
22
Q

What X-rays can be done when investigating acute pancreatitis?

A
  • erect chest X-ray to exclude a perforated viscus
  • abdominal X-ray (AXR) where you may see gallstones
23
Q

What is an ultrasound for when investigating acute pancreatitis?

A

Look for gallstones as a cause for pancreatitis

24
Q

When do we do a CT abdomen when investigating acute pancreatitis?

A

Patients not settling with conservative management & only 48-72 hours after symptom onset

25
Q

When is MRCP done when investigating acute pancreatitis?

A

When gallstone pancreatitis is suspected with abnormal liver function tests (looking for common bile duct stone)

26
Q

When is ERCP done when investigating acute pancreatitis?

A
  • to remove common bile duct stones
  • this is a therapy rather than an investigation
27
Q

What are the criteria for assessing severity of acute pancreatitis?

A

Modified Glasgow criteria - PANCREAS

  • P - PO2 < 8kPa
  • A - age >55 years
  • N - WCC > 15
  • C - calcium <2mmol/L
  • R - renal - urea >16mmol/L
  • E - enzymes - AST >200 iu/L, LDH >600 iu/L
  • A - albumin <32g/L
  • S - sugar >10mmol/L
  • score of 3+ within 48 hours of onset suggests severe pancreatitis
28
Q

What is an independent predictor of severity of acute pancreatitis?

A
  • CRP is an independent predictor of severity
  • > 200 suggests severe pancreatitis
29
Q

How is acute pancreatitis managed?

A
  • ABC - airway, breathing, circulation
  • 4 principles of management
  • 95% settle with conservative treatment
  • if severe pancreatitis on scoring - send to HDU (high dependency unit)
  • antibiotics controversial - commence if necrotic pancreatitis/infected necrosis, but not routinely
  • surgery only very rarely required
30
Q

What are the four principles of management? (Acute pancreatitis)

A
  • fluid resuscitation - IV fluids, urinary catheter to see if kidneys working properly, strict fluid balance monitoring
  • analgesia
  • pancreatic rest (+/- nutritional support if prolonged recovery - nasojejunal feeding or total parental nutrition)
  • determining underlying cause
31
Q

What are the systemic complications that can occur with acute pancreatitis?

A
  • hypocalcaemia: lipase –> FFAs –> chelate Ca2+ salts –> less serum levels
  • hyperglycaemia (diabetes if significant beta cell damage)
  • SIRS (systemic inflammatory response syndrome)
  • ARF (acute renal failure)
  • ARDS (adult respiratory distress syndrome)
  • DIC (disseminated intravascular coagulation)
  • MOF (multi organ failure) + death
32
Q

What are the local complications that can occur with acute pancreatitis?

A
  • pancreatic necrosis +/- infection (infected necrosis)
  • pancreatic abscess
  • pancreatic pseudocyst
  • haemorrhage - due to bleeding from eroded vessels - in small vessels we get haemorrhagic pancreatitis (Cullen’s/Grey Turner’s sign), in large vessels like splenic artery we can get life threatening bleed unless it forms a pseudoaneurysm (weakness in arterial wall secondary to arrosion)
  • thrombosis of splenic vein, SMV, portal vein - interrupted flow back to liver can cause ascites (fluid in abdomen) + small bowel venous congestion/ischaemia
  • chronic pancreatitis/pancreatic insufficiency (if recurrent attacks)
33
Q

What is pancreatic pseudocyst?

A
  • peripancreatic fluid collection (with pancreatic enzymes) within a fibrous capsule
  • presents >6 weeks after pancreatitis
  • 95% spontaneously resolve over 6 months
34
Q

A pancreatic pseudocyst normally requires no intervention unless what?

A
  • pseudocyst symptomatic (pain)
  • pseudocyst causing compression of surrounding structures e.g. CBD (obstructive jaundice), duodenum (high SBO)
  • pseudocyst infected (abscess)
  • requires drainage of pseudocyst
35
Q

How does pseudocyst drainage work?

A
  • percutaneously under radiological guidance (CT)
  • endoscopically - EUS puncturing posterior wall of stomach and inserting stent so the fluid drains from pancreas into stomach
  • surgically via laparoscopic/open-pseudocystgastrostomy (cyst opened into stomach), pseudocystjejunostomy
36
Q

What is the management for infected necrosis acute pancreatitis?

A
  • antibiotics and percutaneous drainage
  • infected pancreatic necrosis is only an indication for surgery in context of acute pancreatitis - high mortality if dead infected tissue is not debrided
  • surgery involves necrosectomy (excision of necrotic tissue)
37
Q

What is chronic pancreatitis?

A
  • long-standing inflammation of the pancreas
  • commonly pancreatic stones of calcium (white circles just above middle of image) that occur in main ducts but also within pancreas called intraparenchymal stones
38
Q

What does chronic pancreatitis lead to?

A
  • destroys endocrine and exocrine tissue and leads to fibrosis of pancreas
  • insulin-dependent diabetes mellitus and steatorrhea
39
Q

How is chronic pancreatitis caused?

A
  • alcohol abuse –> decreased secretion of HCO3- and fluid in pancreatic juice which increases proenzyme concentration
  • leads to protein plug and calcium deposition –> epithelial lesions and enzyme activation
  • alcohol abuse also decreases citrate and lithostatin concentrations which promotes Ca2+ salt precipitation –> calcium deposition
40
Q

What does an increase in pressure from calcium stones lead to?

A
  • pain
  • malabsorption - weight loss
  • tissue atrophy
  • ductal stenosis
  • periductal fibrosis
  • diabetes mellitus
  • pancreatic ascites - pancreatic fluid leaking into abdomen
  • thrombosis of portal and splenic veins
  • obstructive jaundice
  • diarrhoea
  • pseudocysts
41
Q

How is chronic pancreatitis managed?

A
  • only intervene if there is pain
  • can see big white stone in scan
  • endoscopic with ERCP can pull stone out, or lithotripsy if not
  • can put stent in so pancreatic juice can get to where it needs to go
  • can do surgery by opening pancreas and removing stones - can also join part of small bowel onto pancreas = pancreatic juice not obstructed
  • can take away parts of pancreas - total/distal/proximal pancreatectomy

Year 1 - BRS (73 decks)

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