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Z YEAR 1 BRS Gastroentology > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

What are the two components of pancreatic juice?

A
  • ↓ vol, viscous, enzyme-rich - Acinar cells

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

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2
Q

What are zymogens?

A

Pro enzymes

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3
Q

What are the enzymes synthesised and stored in zymogen granules?

A

Enzymes for digestion of:
• fat (lipases)
• protein (proteases)
•carbohydrates (amylase)

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4
Q

what is the problem for an organ making a cocktail of digestive enzyme?

A
  • Autodigestion

- Acute pancreatitis

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5
Q

What are the protective mechanisms in place?

A
  1. Proteases are released as inactive pro-enzymes
    - protects acini & ducts from auto-digestion
  2. Pancreas also contains a trypsin inhibitor to prevent trypsin activation
  3. Enzymes only activated in duodenum
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6
Q

What enzyme does duodenal mucosa secrete? What does it do?

A

-Enterokinase (enteropeptidase)

•converts trypsinogen → trypsin.

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7
Q

What does trypsin do?

A

Trypsin then converts all other proteolytic & some lipolytic enzymes

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8
Q

What is acute pancreatitis?

A

•Rapid onset inflammation of the pancreas

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9
Q

What is chronic pancreatitis?

A

•Long-standing inflammation of the pancreas

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10
Q

What is the aetiology 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 – hypercalceamia, hypertriglyceridaemia, hypothermia
E – ERCP
D – drugs (SAND: steroids and sulphonamides, azothioprine, NSAIDS,
diuretics [loop/thiazide])

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11
Q

What is some 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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12
Q

What happens in cases of acute pancreatitis?

A
  • usually conservative support sand management

1. Trypsin activated

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13
Q

What happens if trypsin is activated in acute pancreatitis?

A
  • Activates:
    1. Phospholipase A2
    2. Elastase
    3. Complement
    4. prothrombin
    5. Kallikrein
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14
Q

What happens when elastase is activated?

A
  1. Start eat (vessel arrosion) and blending (haemoragic pancreatitis)
  2. Islet necrosis, so decreased insulin so HYPER-GLYCAEMIA
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15
Q

What happens when prothrombin is activated?

A
  1. Activates thrombin
  2. Thrombosis
  3. Causes ischameia (pain) (and pancreatic gangrene)
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16
Q

What happens when phospholipase A2 is activated?

A
  1. Fat necrosis (saponification), casques Ca2+ sequestration
  2. Hypalbuminaemia
    - Both cause hypokalaemia
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17
Q

What happens with kalikrein?

A
  • Bradykinin, Kallidin
  • Vasodilation and plasma
  • Cause shock
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18
Q

What happens if there is systemic damage?

A
  • Hypoxia (from fat necrosis fatty acid and phopshlipae A2 interfere with surfactants off lung)
  • Anuria
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19
Q

What is oedematous pancreatitis?

A

-Changes consistent with pancreatitis

20
Q

What is haemorrhage pancreatitis?

A

-Arroding of blood vessels

21
Q

What is necrotic pancreatitis?

A

-(+/- superseding infection goes to infected necrosis)

22
Q

What are the symptoms of acute pancreatitis?

A
  • Epigastric pain radiating to back
  • often eased by sitting forward
  • N&V (vomiting +++)
  • Fevers
23
Q

What are 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 heamorrhagic pancreatitis

24
Q

What are some differential diagnses of acute pancreatitis?

A
  • Gallstone disease & associated complications (e.g. biliary colic & acute cholecystitis)
  • Peptic ulcer disease/perforation
  • Leaking/ruptured AAA
25
Q

What blood tests are taken?

A

•Amylase/lipase

26
Q

What x-rays would you do?

A
  • Erect CXR (check no perforation)

* AXR (sentinal loop, GS)

27
Q

What are other causes of increase amylase?

A
  • Parotitis
  • renal failure
  • Macroamylasaemia
  • bowel perforation
  • lung/ovary/pancreas/colonic malignancies can produce ectopic amylase)
28
Q

What would you look for in USS?

A

•look for GSs as cause for pancreatitis

29
Q

When would you look for in CT abdomen?

A

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

30
Q

When would you have MRCP?

A

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

31
Q

When would you do a ERCP?

A

•To remove CBD GS

32
Q

How do you assess severity in acute pancreatitis?

A 
Modified Glasgow criteria (alternative is Ranson’s 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 or > within 48hrs of onset - suggests severe pancreatitis
-CRP is an independent predictor of severity
•>200 suggests severe pancreatitis
33
Q

What is the management of acute pancreatitis?

A

•ABC

  • 4 Priniciples of management include:
    1. Fluid resuscitation (IV fluids, urinary catheter, strict fluid balance monitoring)
    2. Analgesia
    3. Pancreatic rest (+/- nutritional support if prolonged recovery [NJ feeding or TPN])
    4. Determining underlying cause
34
Q

How is acute pancreatitis managed?

A
  • 95% settle with conservative treatment
  • If severe pancreatitis on scoring à HDU
  • Antibiotics controversial -> commence if necrotic pancreatitis/infected necrosis, but not routinely
  • Surgery only very rarely required
35
Q

What are systemic complications of acute pancreatitis?

A
  1. Hypocalcaemia
    - lipase → FFAs → chelate Ca2+ salts → ↓ serum levels (saponification)
  2. Hyperglycaemia (diabetes if significant beta cell damage)
  3. SIRS (Systemic Inflammatory Response Syndrome)
  4. ARF (Acute Renal Failure)
  5. ARDS (Adult Respiratory Distress Syndrome)
  6. DIC (Disseminated Intravascular Coagulation)
  7. MOF (Multi Organ Failure) & death
36
Q

What are the local complication of acute pancreatitis?

A
  1. Pancreatic necrosis +/- infection (infected necrosis)
  2. Pancreatic abscess
  3. Pancreatic pseudocyst
  4. Haemorrhage: due to bleeding from arroded vessels
    •Small vessels -> haemorrhagic pancreatitis (Cullen’s/Grey Turner’s sign)
    •Large vessels (e.g. Splenic artery)
    -> life threatening bleed (unless forms pseudoaneurysm)
  5. Thrombosis of splenic vein, SMV, portal vein (in order of frequency)
    -> ascites
    -> small bowel venous congestion/ischaemia
  6. Chronic pancreatitis/pancreatic insufficiency (if recurrent attacks)
37
Q

What is the management of infected necrosis?

A

-Management: Antibiotics + 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)

38
Q

What is a pancreatic abscess?

A

•Complication of infected pancreatic necrosis
•Pancreatic abscess
→ collection of pus from pancreatic tissue necrosis &infection
→ becomes lined by granulation tissue
→ presents 2-4 weeks after attack of pancreatitis

39
Q

What is the management of a pancreatic abscess?

A

Management: Antibiotics + drainage:
•percutaneous (under CT guidance)
•Surgical drainage

40
Q

What is a pancreatic pseudocyst?

A
  • peri-pancreatic fluid collection
  • ↑ [pancreatic enzymes] within a fibrous capsule
  • presents >6 weeks after pancreatitis
41
Q

When do you need to intervene in pancreatic pseudocyst?

A
  • 95% spontaneously resolve over 6 months
  • require no intervention unless:
    1. Pseudocyst symptomatic (pain)
    2. Pseudocyst causing compression of surrounding structures e.g. CBD (obstructive jaundice), duodenum (high SBO)
    3. Pseudocyst infected (abscess)
  • These 3x situations pseudocyst → drained
42
Q

What is the management of pancreatic pseudocyst?

A
  1. Percutaneously under radiological guidance (CT)
  2. Endoscopically - EUS puncturing posterior wall of stomach & inserting stent
  3. Surgically via laparoscopic/open:
    - pseudocystgastrostomy (cyst opened into stomach)
    - pseudocystjejunostomy
43
Q

What is endocrine excretion of pancreas?

A

Endocrine - 2% of gland
•Islets of Langerhans
•Secrete hormones into blood - Insulin & Glucagon (also Somatostatin and Pancreatic Polypeptide)
Regulation of blood glucose, metabolism & growth effects - (Endocrine course)

44
Q

What is exocrine excretion of pancreases?

A 
Exocrine - 98% of gland
•Secretes pancreatic juice into duodenum via MPD/sphincter of Oddi/ampulla
Digestive function (Pancreas Lecture
45
Q

What happens in chronic pancreatitis?

A

Chronic pancreatitis - inflammatory process
Destroys endocrine & exocrine tissue → fibrosis of pancreas
IDDM & steatorrhea

Z YEAR 1 BRS Gastroentology (11 decks)

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