Pancreatitis Flashcards

1
Q

What are the 2 components of the pancreatic juice and where are they secreted?

A

↓ vol, viscous, enzyme-rich - Acinar cells

↑ vol, watery, HCO3- rich - Duct & Centroacinar cells

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2
Q

What 3 protective mechanisms are there in the pancreas to prevent autodigestion?

A

Proteases are released as inactive pro-enzymes protects acini & ducts from auto-digestion

Pancreas contains a trypsin inhibitor to prevent trypsin activation

Enzymes only activated in duodenum

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3
Q

What are pancreatic enzymes synthesised and stored in prior to activation?

A

Zymogen granules

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4
Q

Where is enterokinase produced and what is its function?

A

Produced in duodenal mucosa

Converts trypsinogen into trypsin

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5
Q

Trypsin function

A

Conversion of pro-proteases and some pro-lipases into active enzymes

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6
Q

Difference of inflammation between acute and chronic pancreatitis

A
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7
Q

Causes of acute pancreatitis

A

G – gallstones
E – ethanol (alcohol)
T – trauma
S – steroids
M – mumps and other viruses (EBV, CMV)
A – auto-immune (Polyarteritis nodosa, SLE)
S – scorpion/snake bite
H – hypercalcaemia, hypertriglyceridaemia, hypothermia
E – ERCP
D – drugs (SAND: steroids and sulphonamides, azothioprine, NSAIDS,
diuretics [loop/thiazide])

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8
Q

Describe the 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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9
Q

What are the 3 types of acute pancreatitis

A

Oedematous pancreatitis

Haemorrhagic pancreatitis

Necrotic pancreatitis
(+/- superseding infection > infected necrosis)

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10
Q

Give the 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 haemorrhagic pancreatitis)

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11
Q

Give the symptoms of acute pancreatitis

A

Epigastric pain radiating to back
often eased by sitting forward

N&V (vomiting +++)

Fevers

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12
Q

What differential diagnoses are causative 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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13
Q

Outline the investigations into acute pancreatitis and what they’re each used for

A

Blood tests
Amylase/lipase
other causes of ↑ amylase include:
Parotitis
renal failure

X rays
Erect CXR
AXR (sentinal loop, GS)

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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14
Q

What criteria is used to assess the severity of pancreatitis

A

Modified glasgow/ransons criteria
P – PO2 <8KPa
A – age >55yrs
N – WCC >15
C – calcium <2mmol/L
R – renal: urea >16mmol/L
E – enzymes: AST >200iu/L, LDH >600iu/L
A – Albumin <32g/L
S – sugar >10mmol/L

Score of >3 indicates severe pancreatitis

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15
Q

Apart from glasgow/ranson criteria what can you use to predict severity of pancreatitis

A

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

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16
Q

Outline the local complications of acute pancreatitis

A

Pancreatic necrosis +/- infection (infected necrosis)
Pancreatic abscess
Pancreatic pseudocyst
Haemorrhage: due to bleeding from eroded 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

Outline the 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

17
Q

How do you manage acute infected necrotic pancreatitis

A

Antibiotics + Percutaneous Drainage

18
Q

What is a pancreatic pseudocyst

A

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

19
Q

What conditions do you need to drain a pancreatic pseudocyst under?

A

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

20
Q

What 3 methods are there of managing a 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

21
Q

Outline the endocrine and exocrine functions of the pancreas

A

Endocrine - 2%
Islets of Langerhans
Secrete hormones into blood - Insulin & Glucagon (also Somatostatin and Pancreatic Polypeptide)

Exocrine - 98%
Secretes pancreatic juice into duodenum via MPD/sphincter of Oddi/ampulla
Digestive function (Pancreas Lecture)

22
Q

What occurs in chronic pancreatitis?

A

Destroys endocrine & exocrine tissue → fibrosis of pancreas
IDDM & steatorrhea

23
Q

How can you manage chronic pancreatitis?

A

Endoscopically
Surgically - resection/drainage