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BRS GASTROENTEROLOGY > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

Describe the protective mechanisms of the pancreas to ensure than auto-digestion does not occur?

A
  1. Proteases released as inactive zymogens and are only activated once in the duodenum
  2. Also, stored with the enzymes are protease inhibitors to prevent trypsin activation
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2
Q

What is the definition of acute pancreatitis?

A

Rapid onset of inflammation of the pancreas

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3
Q

What is the definition of chronic pancreatitis?

A

Long-standing inflammation of the pancreas

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4
Q

What are the causes of acute pancreatitis?

A 
Gall stones
Ethanol - Alcohol
Trauma
Steroid
Mumps and other viruses
Auto-immune conditions
Scorpion/snake bite
Hypothermia/hypercalcaemia, typertriglyceridemia
ERCP
Drugs
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5
Q

What are the drugs which can cause acute pancreatitis?

A

Steroids and sulphonamides
Azothioprine
NSAIDs
D - Diuretics

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6
Q

What is azothioprine?

A

An immunosuppressant

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7
Q

Which autoimmune conditions can cause acute pancreatitis?

A

Polyarteritis nodosa, SLE

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8
Q

Which viruses can cause AP?

A

Mumps, EBV - Epstein-Barr Virus, CMV - Cytomegalovirus

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9
Q

What three factors can cause an increase in the permeability of the pancreatic duct?

A

Alcohol, acetylsalicylic acid, histamine

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10
Q

What happens to the acinar cell enzymes when the permeability of pancreatic duct epithelium is increased?

A

Acinar cell enzymes diffuse into periductal interstitial tissue

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11
Q

What are the two most common causes of acute pancreatitis

A

Alcohol and Gall Stones

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12
Q

What three things can happen as a result of gall stones in the ampulla which result in acute pancreatitis?

A
  1. Stuck in ampulla = blocks pancreatic juice secretion which increases pressure on acini
  2. Stuck in ampulla = reflux of bile into the pancreas
  3. Gall stone that was previously stuck become loosened, howeer sphincter of Oddi loses its competence which means that some activated duodenal enzymes might reflux into the pancreatic duct
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13
Q

How does alcohol contribute to acute pancreatitis?

A
  1. Causes the precipitate of proteins in the pancreatic duct which increase the pressure inside the duct
  2. Alcohol also increases the permeability of the pancreatic duct epithelium

The increased back pressure encourages pancreatic enzyme to leak out the duct further

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14
Q

What affect does trypsin activation have on the islet cells of the pancreas?

A

Causes islet necrosis which decrease insulin secretion and therefore increases glucose = hyperglycaemia

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15
Q

How does trypsin activation cause bleeding?

A

Activates elastase which degrade blood vessel walls, leading to bleeding

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16
Q

How does trypsin activation cause ischaemia?

A

Activates thrombin which leads to ischaemia in some parts of the vessel

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17
Q

What is meant by oedematous pancreatitis?

A

Swelling of the pancreas

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18
Q

What is meant by haemorrhagic pancreatitis?

A

The pancreas is bleeding

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19
Q

What is meant by necrotic pancreatitis?

A

The pancreatic tissue is dying - can be identifies on a scan with a porridge consistency of a pancreas

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20
Q

What are the three main symptoms of AP?

A

Epigastric pain
N and V - Alot of V
Fever

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21
Q

What eases the epigastric pain that patients with acute pancreatitis experience?

A

Sitting forward

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22
Q

What type of pain do patients with AP experience?

A

Epigastric pain radiating to back

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23
Q

Why do patients with AP experience fevers?

A

Due to infection

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24
Q

What is Grey-Turner’s sign?

A

Bruising in flanks

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25
Q

What is Cullen’s sign?

A

Bruising around the umbilicus

26
Q

Which two signs are seen in haemorrhagic pancreatitis?

A

Grey-Turner’s Sign

Cullen’s Sign

27
Q

What are two signs of haemodynamic instability that are commonly seen in patients with AP?

A

tachycardia and hypotensiveness

28
Q

What is peritonism?

A

Inflammation of the peritonium

29
Q

What are the four main clinical signs of AP?

A
  1. Haemodynamic instability
  2. Peritonism
  3. Grey-Turner’s Sign
  4. Cullen’s sign
30
Q

What are three differential diagnoses of AP?

A

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

Peptic ulcer disease/perforation

Leaking/ruptured AAA

31
Q

What is a cardinal sign of AP which can be determined from a blood test?

A

Raised Amylase

32
Q

What else other than AP could increase amylase?

A 
Parotitis
renal failure
Macroamylasaemia
bowel perforation
lung/ovary/pancreas/colonic malignancies can produce ectopic amylase)
33
Q

In what instance would an MRCP be done?

A

If GS pancreatitis suspected with abnormal LFTs (CBD stone)

34
Q

In what instance would a CT of the abdomen be done?

A

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

35
Q

IN what instance would a ultrasound be done?

A

To look for gall stones as a cause of pancreatitis

36
Q

In what instance would an endoscopic retrograde cholangiopancreatography (ERCP) be done?

A

To remove common bile duct gall stones as a cause of a patients acute pancreatitis

37
Q

Which X Rays can be done as part of an AP investigation?

A

Erect Chest X Ray

AXR of Sentinal loop to check for gall stones

38
Q

What is used to assess the severity of Acute Pancreatitis?

A

Glasgow Criteria

39
Q

What is the Glasgow criteria? PANCREAS

A 
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
40
Q

What does a score of 3 or more on the Glasgow Scale within 48 hours suggest?

A

Severe Pancreatitis

41
Q

What can be considered an independant indicator of severity of AP, aside from the Glasgow Scale?

A

CRP

42
Q

What score of CRP indicates severe pancreatitis?

A

> 200

43
Q

What do the four principles of management include for AP?

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

44
Q

Where are patients placed if they have severe pancreatitis on scoring?

A

High Dependency Unit

45
Q

Is surgery an option for AP?

A

Only rarely required

46
Q

What are the systemic complications of Acute Pancreatitis?

A

Hypocalcaemia

Hyperglycaemia

SIRS (Systemic Inflammatory Response Syndrome)
ARF (Acute Renal Failure)
ARDS (Adult Respiratory Distress Syndrome)
DIC (Disseminated Intravascular Coagulation)
MOF (Multi Organ Failure) & death

47
Q

How does Acute pancreatitis lead to hypocalcaemia?

A

Increased lipase = lipase Free fatty Acids = Increased chelate Ca2+ salts which lower serum levels of Ca2+

48
Q

what are 6 local complications associated with AP?

A 
Pancreatic necrosis
Pancreatic Abscess
Pancreatic pseudocyst
Haemorrhage
Thrombosis
Chronic Pancreatitis
49
Q

How does AP lead to haemorrhage?

A

erosion of blood vessels

50
Q

What does haemorrhage of small blood vessels lead to?

A

Haemorrhagic pancreatitis - can be seen using cullen’s and Grey Turners Sign

51
Q

Which veins are most likely to get thrombosis?

A

Splenic artery
Superior Mesenteric Artery
Portal Vein

52
Q

How is pancreatic necrosis treated?

A

Surgery - high mortality rate if dead infected tissue is not debrided

53
Q

How is Acute Pancreatitis Managed?

A

Antibiotics and Percutaneous Drainage

54
Q

What is a Pancreatic Pseudocyst?

A

Peri-pancreatic fluid collection with increased pancreatic enzymes within a fibrous capsule

55
Q

When can Pancreatic Pseudocyst be seen following AP?

A

> 6 weeks after pancreatitis

56
Q

In what three situations would it be considered essential to get a pseudocyst drained?

A
  1. Pseudocyst symptomatic (pain)
  2. Pseudocyst causing compression of surrounding structures e.g. CBD (obstructive jaundice), duodenum (high SBO)
  3. Pseudocyst infected (abscess)
57
Q

What are the three routes of management for 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

58
Q

What is Chronic Pancreatitis?

A

Long-standing inflammation of the pancreas which destroys exocrine and endocrine tissue leading to fibrosis of the pancreas, Insulin-dependant Diabetes Mellitus and Steathorrea

59
Q

What is meant by chronic inflammation?

A

Long-standing inflammation of the pancrea

60
Q

How is steathorrea from chronic pancreatitis cured?

A

Creon medication

61
Q

Unless chronic pancreatitis is symptomatic, patients are left untouched. What treatments might be undergone if the patient experiences pain?

A
  1. Surgical drainage

2. Endoscopic management

BRS GASTROENTEROLOGY (25 decks)

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