Pancreatitis Flashcards

1
Q

How does the pancreas protect itself from autodigestion : acute pancreatitis

A

Proteases released as inactive pro-enzymes

Pancreas contains trypsin inhibitor to prevent activation of trypsin

Enzymes only activated in duodenum

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2
Q

What is the brush border enzyme that converts trypsinogen?

A

Enterokinase

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3
Q

What is acute pancreatitis?

A

Rapid onset inflammation of the pancreas vs chronic long standing inflammation

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4
Q

Acute pancreatitis Aetiology?

A

GET SMASHED

Gall stones

Ethanol

trauma

steroids

mumps / virus

auto-immune ( polyarteritis nodosa )

scorpian/snake bite

hypercalcaemia, hypertriglyceridaemia, hypothermia

ERCP

Drugs ( steroids, sulphonamides, azothioprine, NSAIDS, diuretics )

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5
Q

Pathogenesis of acute pancreatitis?

A

↑ permeability of pancreatic duct epithelium (Alcohol, acetylsalicylic acid, histamine)
Acinar cell enzymes diffuse into periductal interstitial tissue

Alcohol ppts proteins in ducts → ↑ upstream pressure

Pancreatic enzymes activated intracellularly
proenzymes & lysosomal proteases incorporated into same vesicles → trypsin activated

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6
Q

5 mechanisms of pancreatitis?

A

Pressure increase

Bile reflux

Reflux of activated enzymes from duodenum

Enzyme diffusion

Premature activation

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7
Q

What can trypsin activation cause?

A

hypocalcemia

Hyperglycemia

Pancreatic gangrene

Pain

shock

hypoxia

anuria

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8
Q

What types of acute pancreatitis are there?

A

Oedematous

haemorrhagic

Necrotic / infected necrosis

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9
Q

Clinical symptoms of acute pancreatitis?

A

Epigastric pain radiating to back
often eased by sitting forward

N&V (vomiting +++)

Fevers

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10
Q

Clinical signs of acute pancreatitis?

A

Haemodynamic instability (tachycardic, hypotensive)

Peritonism in upper abdomen/generalised

Grey-Turner’s sign (bruising in flanks)

Cullen’s sign (bruising around umbilicus)

(Grey Turner’s & Cullen’s signs seen in heamorrhagic pancreatitis

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11
Q

Differential diagnosis of acute pancreatitis?

A

Gallstone disease & associated complications (e.g. biliary colic & acute cholecystitis)

Peptic ulcer disease/perforation

Leaking/ruptured AAA

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12
Q

Investigations for acute pancreatitis?

A
Blood tests
Amylase/lipase 
other causes of ↑ amylase include:
Parotitis
renal failure
Macroamylasaemia
bowel perforation
lung/ovary/pancreas/colonic malignancies can produce ectopic amylase) 

X rays
Erect CXR
AXR (sentinal loop, GS)

Investigations

USS
look for GSs as cause for pancreatitis

CT abdomen
patients not settling with conservative management & only 48-72 hrs after symptom onset

MRCP
If GS pancreatitis suspected with abnormal LFTs (CBD stone)

ERCP
To remove CBD GS

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13
Q

Assess severity of Acute P with Glasgow criteria?

A

PO2 <8KPa

age >55yrs

WCC >15

calcium <2mmol/L

renal: urea >16mmol/L
enzymes: AST >200iu/L, LDH >600iu/L

Albumin <32g/L

sugar >10mmol/L

Score of 3 or > within 48hrs of onset - suggests severe pancreatitis

CRP is an independent predictor of severity
>200 suggests severe pancreatitis

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14
Q

Management of acute pancreatitis?

A

Fluid resuscitation (IV fluids, urinary catheter, strict fluid balance monitoring)
Analgesia
Pancreatic rest (+/- nutritional support if prolonged recovery [NJ feeding or TPN])
Determining underlying cause

95% settle with conservative treatment

If severe pancreatitis on scoring –> HDU

Antibiotics controversial –> commence if necrotic pancreatitis/infected necrosis, but not routinely

Surgery only very rarely required

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15
Q

Systemic complications of acute pancreatitis?

A

Hypocalcaemia
lipase → FFAs → chelate Ca2+ salts → ↓ serum levels (saponification)

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

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16
Q

Local complications of acute pancreatitis?

A
  • Pancreatic necrosis +/- infection (infected necrosis)
  • Pancreatic abscess
  • Pancreatic pseudocyst
  • Haemorrhage: due to bleeding from erroded vessels
    Small vessels –> haemorrhagic pancreatitis (Cullen’s/Grey Turner’s sign)
    Large vessels (e.g. Splenic artery)
    –> life threatening bleed (unless forms pseudoaneurysm)

Thrombosis of splenic vein, SMV, portal vein (in order of frequency)

 - > ascites
 - > small bowel venous congestion/ischaemia

Chronic pancreatitis/pancreatic insufficiency (if recurrent attacks)

17
Q

How to manage infected necrosis AP?

A

Antibiotics + Percutaneous Drainage (?Surgery)
Infected pancreatic necrosis only indication for surgical intervention in the context of acute pancreatitis
high mortality if dead infected tissue is not debrided

Surgery involves necrosectomy (excision of necrotic tissue)

18
Q

What is a Pancreatic pseudocyst?

A

peri-pancreatic fluid collection
↑ [pancreatic enzymes] within a fibrous capsule
presents >6 weeks after pancreatitis

95% spontaneously resolve over 6 months
require no intervention unless:

  • Pseudocyst symptomatic (pain)
  • Pseudocyst causing compression of surrounding structures e.g. CBD (obstructive jaundice), duodenum (high SBO)
  • Pseudocyst infected (abscess)

These 3x situations pseudocyst → drained

19
Q

How to manage pancreatic pseudocyst?

A

Percutaneously under radiological guidance (CT)
Endoscopically - EUS puncturing posterior wall of stomach & inserting stent
Surgically via laparoscopic/open:
pseudocystgastrostomy (cyst opened into stomach)
pseudocystjejunostomy

20
Q

Describe the chronic pancreatitis inflammatory process?

A

Destroys endocrine & exocrine tissue → fibrosis of pancreas

Insulin-dependent diabetes mellitus & steatorrhea

21
Q

Chronic pancreatitis management?

A

Surgical resection
Surgical drainage
Endoscopic

22
Q

chronic pancreatitis effects?

A

Tissue atrophy
Ductal stenosis
Periductal fibrosis

Pain
Malabsorption
Weight loss

Diabetes mellitus
Pancreatic ascites
Thrombosis of portal and splenic vein

Obstructive jaundice
Diarrhea
Pseudocysts