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Gastroenterology > Pancreatitis,PSC,PBC > Flashcards

Pancreatitis,PSC,PBC Flashcards

1
Q

What scoring system is used to assess the severity of pancreatitis?

A

The glasgow score

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2
Q

What value is considered mild pancreatitis, moderate pancreatitis and severe pancreatitis and what scoring system do you use?

A

The GLASGOW SCORE

Mild = 0 or 1
Moderate = 2
Severe = 3 or more

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3
Q

What is the pathophysiology of ACUTE pancreatitis?

A

Autodigestion of pancreatic tissue by pancreatic enzymes, leading to necrosis (usually due to gallstones or alcohol. Gallstones will block ampulla of vater causing pancreatic juices to backflow into the pancreas destroying it leading to it’s inflammation)

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4
Q

How would a patient pressent if they have acute pancreatitis?What clinical signs on the abdomen is seen when examining (if they have had pancreatitis unnoticed for a long time)?

A

Severe epigastric pain
Radiating through to the back
Associated vomiting
Abdominal tenderness
Systemically unwell (e.g., low-grade fever and tachycardia)

Clincal sign: Cullen’s sign and Grey-Turner’s sign

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5
Q

What is the criteria for the glasgow score? For each point, that is 1 point. (HINT: PANCREAS mnemonic)

A

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

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6
Q

What investigations do you order if you suspect pancreatitis?

A

FBC (for WCC)
U&E (for urea)
LFT (for transaminases and albumin)
Calcium
ABG (for PaO2 and blood glucose)

Ultrasound (to look for gallstones if you suspect gallstone pancreatitis)

CT abdomen (to look for complications of pancreatitis like necrosis)

CRP to monitor inflammation

Look for AMYLASE AND LIPASE (these are raised in acute pancreatitis).

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7
Q

What happens to the amylase levels when a patient has acute pancreatitis? How is it different in chronic?

A

It is raised more than 3 TIMES the upper limit of normal.
In chronic pancreatitis, the pancreas has reduced function so amylase may not rise.

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8
Q

What are the 3 most common causes of pancreatitis?

A

Gallstones
Alcohol
Post-ERCP

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9
Q

Pancreatitis can be caused by many things. Use the I GET SMASHED mnemonic to list the different causes?

A

I – Idiopathic
G – Gallstones
E – Ethanol (alcohol consumption)
T – Trauma
S – Steroids
M – Mumps
A – Autoimmune
S – Scorpion sting (the one everyone remembers)
H – Hyperlipidaemia
E – ERCP
D – Drugs (furosemide, thiazide diuretics and azathioprine)

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10
Q

What happens in gallstone pancreatitis?

A

Gallstone pancreatitis is caused by gallstones getting trapped at the end of the biliary system (ampulla of Vater), blocking the flow of bile and pancreatic juice into the duodenum. The reflux of bile into the pancreatic duct, and the prevention of pancreatic juice containing enzymes from being secreted, results in inflammation in the pancreas. Gallstone pancreatitis is more common in women and older patients.

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11
Q

What happens in alcohol induced pancreatitis?

A

Alcohol is directly toxic to pancreatic cells, resulting in inflammation. Alcohol-induced pancreatitis is more common in men and younger patients.

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12
Q

What is the management for acute pancreatitis?

A

Initial resuscitation (ABCDE approach)
IV fluids
Nil by mouth
Analgesia
Careful monitoring
Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
Antibiotics if there is evidence of a specific infection (e.g., abscess or infected necrotic area)
Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

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13
Q

What are the complications of acute pancreatitis?

A

Necrosis of the pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collections
Pseudocysts (collections of pancreatic juice) can develop 4 weeks after acute pancreatitis
Chronic pancreatitis

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14
Q

What are the key complications that may arise due to having chronic pancreatitis?

A

Chronic epigastric pain
Loss of exocrine function (particularly lipase which is supposed to be secreted into the GI)
Loss of endocrine function (lack of insulin can lead to diabetes)
Damage and strictures to the duct system (obstruction in pancreatic juice and bile excretion)
Formations of pseudocysts and abscesses

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15
Q

How do you manage chronic pancreatitis?

A

ABSTINENCE FROM ALCOHOL AND SMOKING
Analgesia (for pain)
Replacing pancreatic enzymes with Creon
S/C insulin (for diabetes)
ERCP with stenting to treat strictures and obstruction in biliary system

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16
Q

When may surgery be needed if a patient has chronic pancreatitis?

A

In severe chronic pain, obstruction to the biliary system and pancreatic duct, if the pt has pseudocysts and abcesses

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17
Q

What is primary sclerosing cholangitis?

A

a condition where the intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct the flow of bile OUT of the liver and into the intestines.

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18
Q

What can chronic bile obstruction lead to?

A

Hepatitis
Fibrosis
Cirrhosis

19
Q

What are the risk factors for primary sclerosing cholangitis?

A

Male
Aged 30-40
Ulcerative colitis
Family history

20
Q

What condition is usually associated with primary sclerosing cholangitis?

A

Ulcerative colitis

21
Q

What may patients present with if they have primary sclerosing cholangitis?

A

Abdominal pain in the right upper quadrant
Pruritus (itching)
Fatigue
Jaundice
Hepatomegaly
Splenomegaly

22
Q

What are the investigations for primary sclerosing cholangitis? Which liver marker rises first and is the most important marker? What is the gold standard investigation?

A

ALP rises first
Then bilirubin
Other liver enzymes are raised later in the disease

Gold standard investigation is MRCP (MRI scan of liver, bile ducts and pancreas)

Colonoscopy (to assess UC)
Liver biopsy (if diagnosis is unclear)

23
Q

What is the gold standard investigation to for primary sclerosing cholangitis?

A

MRCP (MRI scan of liver, bile ducts and pancreas)

24
Q

How can you manage primary sclerosing cholangitis (surgically)?

A

Liver transplant (see notes for this)
ERCP (strictures are dilated with stents)

25
Q

How can you manage primary sclerosing cholangitis (medically)?

A

Ursodeoxycholic acid (to slow it’s progression)
Colestyramine ( a bile acid sequestrate)
Replace the fat-soluble vitamins

26
Q

What are some of the complications of primary sclerosing cholangitis?

A
  • Biliary strictures
  • Acute bacterial cholangitis
  • Cholangiocarcinoma develops in 10-20% of cases
  • Cirrhosis and the related complications (e.g., portal hypertension and oesophageal varices)
  • Fat-soluble vitamin deficiency (A, D, E and K)
  • Osteoporosis
  • Colorectal cancer in patients with ulcerative colitis
27
Q

What is IgG4-related sclerosing cholangitis?

A

Is similar to primary sclerosing cholangitis.

But there are elevated IgG4 levelsin the blood

Unlikely primary sclerosing cholangitis, IgG4-related sclerosing cholangitis responds well to treatment withsteroids. It is associated withautoimmune pancreatitis.

28
Q

In primary biliary cholangitis, what would you see in the bloods? (HINT: 3 raised substances which are supposed to be excreted through the bile ducts to the intestines, but cannot due to the obstructed bile ducts)

A

1.Bile acids
2.Bilirubin
3. Cholesterol

29
Q

What does raised bilirubin, raised bile acids and raised cholesterol have on the blood?

A

Raised bile acids: Itching/pruritis

Raised bilirubin: Jaundice

Raised cholesterol: Xanthelasma and xanthomata

30
Q

What is cholestasis?

A

Reduced flow of bile

31
Q

What happens to the ducts in primary biliary cholangitis?

A

This disease affects the small bile ducts in the liver (the intrahepatic ducts).

It causes inflammation and damage to the epithelial cells of the bile ducts (the cholangiocytes).This (overtime) causes obstruction of bile flow through the ducts.

The back of bile then affects the liver and can cause liver cirrhosis, fibrosis and failure.

32
Q

What cells are affected in primary biliary cholangitis?

A

The epithelial cells of the bile ducts (the cholangiocytes)

33
Q

How does obstructed bile ducts affect stool and urine?

A

If the bile ducts are obstructed (like in the case of primary biliary cholangitis), then the

34
Q

What is primary biliary cholangitis and what ducts does it affect?

A

It is an AUTOIMMUNE CONDITION that affects the ducts IN the liver (intrahepatic ducts) causing obstructive jaundice and liver disease. The immune system attacks the small bile ducts in the liver.

35
Q

What cells become damaged and inflammed in primary biliary cholangitis?

A

Cholangiocytes

36
Q

What happens to the stool, urine and skin when the bile ducts are obstructed in primary biliary cholangitis?

A

Bile contains bile acids, bilirubin and cholesterol (which are normally excreted). But if the bile ducts are blocked, it leads to these substances building up in the blood.
Build of bile acids in blood (but less going to the intestines) causes pruritus and reduction of fat digestion leading to malabsroption of fat—> causes greasy stool
Pruritus (build up of bile acids in the blood) and fattty stool (fats not absorbed in the gut)

Bilirubin causes —-> pale stools (due to lack of it). Leads to bilirubin build up in blood instead and be excreted by kidneys (causing dark urine)
Bilirubin also causes jaundice

Cholesterol build up in blood leads to —-> xanthomata and xanthelasma (upon examination)

37
Q

What liver marker is raised first in primary biliary cholangitis?

A

ALP (there is a larger increase in this). All other liver markers increase after

38
Q

What auto-antibodies are SPECIFIC for primary biliry cholangitis?

A

Anti-mitochondrial antibodies (AMA)

39
Q

Why would you do an ultrasound and liver biopsy if a pt has primary biliary cholangitis?

A

Ultrasound —> to exclude other pathology
Liver biopsy —> for diagnosing and staging the disease

40
Q

What is the treatment for primary biliary cholangitis?

A

UDCA (Ursodeoxycholic acid).
It is a non-toxic and hydrophilic bile acid that protects the cholangiocytes from damage and inflammation

41
Q

Other than UDCA, what other treatments can be used for primary biliary cholangitis?

A
  • Obeticholic acidWhen UCDA is not tolerated or is inadequate. But this drug can have SIGNIFICANT SIDE EFFECTS
  • ColestyramineIs a bile acid sequestrant . it reduces the intestinal absorption of bile acids
  • Replacement of fat-soluble vitaminsDue to fat loss in stool
  • Immunosuppression (with steroids)Is considered in some patients
  • Liver transplantIn end-stage liver disease
42
Q

What are some complications of primary biliary cholangitis?

A

LIVER CIRRHOSIS (portal hypertension and hepatocellular carcinoma)

  • Fat-soluble vitamin deficiency (A, D, E and K)
  • Osteoporosis
  • Hyperlipidaemia (raised cholesterol)
  • Sjögren’s syndrome (dry eyes, dry mouth and vaginal dryness)
  • Connective tissue diseases (e.g., systemic sclerosis)
  • Thyroid disease
43
Q
A

Gastroenterology (10 decks)

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