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MSRA > Liver, Biliary and Pancreas > Flashcards

Liver, Biliary and Pancreas Flashcards

1
Q

What are the main types of gallstones?

A
  1. Cholesterol containing (80%) - large, solitary

2. Pigment stones (calcium) - small, irregular, from haemolysis

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2
Q

What is cholestasis?

A

Biochemical abnormality (raised ALP) resulting from an abnormality in bile flow

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3
Q

What are the RF for cholesterol gallstones?

A

Increased cholesterol secretion - old age, female, pregnancy, obesity, rapid weight loss

Impaired gallbladder emptying - pregnancy, stasis, fasting, PEG tube, spinal cord injury

Decreased bile salt secretion - pregnancy

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4
Q

What causes pigment gallstones?

A
  • Bacterial/parasitic biliary infection

- Haemolysis

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5
Q

What is biliary collic?

A

Gallstones are syptomatic with cystic dust obstruction or CBD obstruction.

Causes pain in epigastrium/RUQ, radiating to back/scapula that occurs suddenly and lasts 2 hours, may cause jaundice

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6
Q

How is biliary collic managed?

A
  1. Analgesia - paracetamol, NSAIDS or IM diclofenac if severe
  2. Rehydration
  3. Elective laparoscopic cholecystectomy
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7
Q

How does acute cholecystitis occur?

A

Obstruction of gallbladder neck or cystic duct by a glalstone. Leads to gallbladder mucosal damage (usuallly not infective!)

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8
Q

What are the clinical features of acute cholecystitis?

A
  • RUQ pain/epigastric pain (lasting over 6 hours)
  • Right shoulder pain
  • Fever
  • Murphys sign (rigidity worse on inspiration)
  • Palpable mass
  • Vomiting
  • Peritonism

RARELY JAUNDICE

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9
Q

What is Mirizzis syndrome?

A

Common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Causes JAUNDICE.

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10
Q

What investigations should be done in acute cholecystitis?

A

BEDSIDE: urine dip (exclude UTI?), obs
BLOODS: FBC, U&E (dehydration), amylase (exclude pancreatitis), LFTs (raised ALP), CRP
IMAGING: AXR (not that useful), US (gallstones/gallbladder thickening - key diagnosis), CT (sepsis, empyema,perforation), MRCP

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11
Q

How is acute cholecystitis managed?

A

Emergency admission, NBM, pain relief, IV access fluids

MEDICAL - analgeisa, ?antibiotics (cefuorzime)
SURGICAL - lap cholecystectomy, may need open surgery if perforation (ops should be within 4 days of symptom onset)

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12
Q

What are the clinical features of chronic cholecystitis?

A

Recurrent attacks of upper abdo pain, often at NIGHT or after a big MEAL.

Similiar to acute cholecystitis but milder.

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13
Q

How is chronic cholecystitis managed?

A

CONSERVATIVE - may recover spontaneously, diet, fluids
MEDICAL - analgesia (NSAIDS, paracetamol)
SURGICAL - electrive laparoscophic cholecystectomy

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14
Q

What is the difference between MRCP and ERCP?

A

MRCP consists of creating a magnetic resonance field generated by an MRI machine around the patient that then takes images which aid the diagnostic process.

ERCP involves the use of a contrast dye to be inserted while images are being taken - more invasive, uses endoscopy, can diagnose and treat

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15
Q

How does acute cholangitis occur?

A

Bacterial infection of the bile ducts, most commonly due to choledocholithiasis or strictures, or after ERCP

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16
Q

What are the clinical features of acute cholangitis?

A

CHARCOTs triad:

  1. Fever
  2. Jaundice
  3. RUQ pain

May also have pale stools, hypotension, rigors, sepsi, itch

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17
Q

How is acute cholangitis investigated?

A

BEDSIDE: urine dip, obs
BLOODS: FBC, U&E, CRP, LFT, amylase, ABG, blood cultures
IMAGING: US (shows dilated ducts), EUS, CT, ERCP (gold standard)/MRCP

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18
Q

How is acute cholangitis managed?

A

CONSERVATIVE: IV fluids, oxygen
MEDICAL: analgesia, broad spectrum abx (cefuroxime, metronidazole)
NON-SURGICAL: ERCP and placement of drainage stent, percutaneous transheptaic drainage, endoscopic lithiotripsy (these are all forms of biliary decompression)
SURGICAL: last resort!!! laparoscopic cholecystectomy/choledochotomy

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19
Q

What are the complications of acute cholangitis?

A

Repeated cholangitis
Pancreatitis
Bleeding
Perforation

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20
Q

What are the features of gallbladder cancer?

A
  • Adenocarcinoma
  • Gallstones usually present
  • Calcified PORCELAIN GALLBLADDER - high risk of malingnant change
  • May have had chronic infection with salmonella especially if endemic typhoid in the area
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21
Q

What are the features of cholangiocarcinoma?

A
  • Associated with gallstones, PSC, PBC
  • Presents with obstructive jaundice, upper abdo pain, weight loss
  • Elevated CA199
  • Manage by excision of extrahepatic biliary tree, stent insertion across malignant biliary stricture and chemo
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22
Q

What is Sphincter of Oddi dysfunction?

A
  • Increase in contractility of the sphincter located at the junfction of the bile duct and pancreatic duct in the duodenum
  • Usually occurs after gallbladder removal
  • Produces non-calculous obstruction
  • Deranged LFTs, pain, recurrent pancreatitis
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23
Q

How is SOD diagnosed and managed?

A

Diagnosis - ERCP and manometry (measures the pressure!)

Management - depends on severity, nifedipine/amitriptylline/botox or endoscopic sphincterotomy

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24
Q

What causes pancreatitis?

A

Gallstones
Ethanol
Trauma

Steroids
Mumps
Autoimmune
Scorpion
Hyperlipidaemia, hypothermia, hypercalcaemia
ERCP
Drugs

Pregnancy and neoplasia also!!

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25
Q

What are the clinical features of pancreatitis?

A
  • Gradual/acute epigastric.central abdo pain that radiates to the back
  • Vomiting
  • Tachycardia/fever/shock/ileus/rigidity/tenderness
  • Cullens (umbilical bruising)/Grey Turners sign (flank bruising))
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26
Q

What invesitgations should be done in suspected pancreatitis?

A

BEDSIDE; obs, urine dip, pregnancy test if female
BLOODS: FBC, amylase (>3x upper limit), lipase, ABC, U&E, LFT, CRP
IMAGING: AXR, erect CXR (exclude perforation), CT/MRI (gold standard), US (if gallstone and raised AST), ERCP

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27
Q

How is acute pancreatitis managed?

A

CONSERVATIVE: NBM (may need NG), fluids, oxygen
MEDICAL: analgesia (pethidine/morphine), antiemetics, calcium/magnesium replcaememnt therapy, IV abx SOMETIMES
NON-SURGICAL: ERCP and gallstone removal
SURGICAL: none!

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28
Q

How is severity of pancreatitis measured?

A

GLASGOW CRITERIA
3 or more within 48h of onset indicate severe pancreatitis and the need for ITU/HDU:

Pa02 <8
Age >55
Neutrophilia WBC>15
Calcium <2
Renal function Urea>16
Enzymes LDH/AST high 
Albumin <32
Sugar BM >10
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29
Q

How is chronic pancreatitis managed?

A

Investigations:
AXR/CT - pancreatic calcification
Faecal elastase - to assess exocrine function

Management:
Pancreatic enzyme supplements
Analgesia

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30
Q

What are the features of pancreatic cancer?

A
  • 80% adenocarcinoma at head of pancreas
  • Painless jaundice
  • Abdominal mass (most common is hepatomegaly from mets)
  • Loss of endocrine/exocrine function
  • Migratory thrombophleitis (Trousseau sign)
  • May have MEN/BRCA2/KRAS

Diagnose on HRCT - shows double duct sign (simultaneous dilatation of common bile and pancreatic duct)

Courvoisier’s law states that in the presence of a palpable gall bladder, painless jaundice is unlikely to be caused by gallstones

31
Q

How is pancreatic cancer managed?

A
  • Whipples (pancreaticoduodenectomy) + adjuvant chemotherapy
  • ERCP + stent to palliate

SE of surgery: dumping syndrome, PUD

32
Q

What are the features and management of NAFLD?

A

Features:
- Usually asymptomatic
- Hepatomegaly
- ALT >AST
- Increased echogenicity on USS
- Insulin resistance

Management:
- Weight loss
- Enhanced liver fibrosis blood test to check for advanced fibrosis > refer to liver specialist for biopsy
- There may be a role for gastric banding and metformin

33
Q

What are the features and management of NASH?

A

Features:
- Subtype of NAFLD with fat with inflammation
- Similar to changes seen in alcohol hepatitis in the absence of alcohol

34
Q

What are the features of autoimmune hepatitis? How is it managed?

A

Three types:
1 - ANA, SMA, adults and children
2 - LKM1, only children
3 - soluble liver kidney, middle aged adults

  • Associated with HLA B8, DR3
  • Presents as chronic disease or acute hepatitis.
  • Amenorrhoea is common
  • Liver biopsy shows piecemeal necrosis
  • Manage with steroids, immunosuppresants and liver transplant
35
Q

What are the features of hepatitis A?

A
  • Acute fever, abdo pain, malaise and jaundice
  • Markedly elevated AST/ALT
  • IgM hep A positive
  • RNA virus
  • Treatment is supporitve
  • Not associated with chronic liver disease
36
Q

What are the features of hepatitis B?

A
  • Associated with IVDU and sexual transmission
  • May be asymptomatic
  • Some present with cirrhosis/HCC/liver failure
  • DNA virus
  • Supportive care, can treat with tenofovir/entecavir if chronic infection
  • Risk of chronic liver disease
37
Q

What do the following mean:
a) HbsAg?
b) anti-HBs?
c) anti-Hbc?
d) IgM anti-Hbc?
e) IgG anti-Hbc?
f) HbeAg?

A

a) infection with hep B (acute or chronic if >6 months)
b) Immunity (from exposure or immunisation, negative in chronic disease)
c) Previous or current infection
d) Acute or recent infection
e) Infection over 6 months ago
f) marker of infectivity

38
Q

What are the features of hepatitis C?

A
  • RNA flavavirus
  • Transmission via vertical transmission, IVDU or blood transfusion
  • No vaccine available
  • Usually asymptomatic
  • Can lead to chronic liver disease, cirrhossis and HCC
  • Treat with antiviral tables for 8-12 weeks; will clear infection in most people (sobosfuvir, daclatasvir)
  • Treat chronic infection with protease inhibitors + ribavirin (teratogenic)
39
Q

What are the features of hepatitis D?

A
  • Single stranded RNA, requires hep B surface antigen to replicate
  • Coinfection or superinfection
  • Treat with interferon
40
Q

What are the features of hepatitis E?

A
  • RNA hepevirus
  • Faecal oral transmission
  • PORK SAUSAGES!
  • Self-limiting and does not require specific treatment
  • Significant mortality in pregnancy
41
Q

What are the features of primary biliary cholangitis/cirrhosis?

A

-Typically in middle aged females with AI associations
- Sjogrens syndrome assoc!
- Presents as cholestatic jaundice, hyperpigmentation, clubbing, hepatosplenomegaly
- Chronic inflammation damages interlobular bile ducts causing progressive cholestasis and cirrhosis

42
Q

How is PBC diagnosed?

A
  • Anti mitochondrial antibodies (AMA) M2 subtype
  • Raised serum IgM
  • USS or MRCP to exclude obstruction

‘Rule of M’s’

43
Q

How is PBC managed?

A

1st line - ursodeoxycholic acid (improves symptoms and slows disease progression

Cholestyramine for itch
Fat soluble vitamin supplementation
Liver transplant if bilirubin >100

44
Q

What are the features of primary sclerosing cholangitis?

A
  • Associated with UC (75% of those with PSC will have UC) and HIV
  • Presents as cholestasis, RUQ and fatigue
  • Complications include cholangiocarcinoma and colorectal cancer
45
Q

What is the pathophysiology of PSC?

A

Inflammation and fibrosis of intra and extra-hepatic bile ducts

46
Q

How is PSC diagnosed?

A
  • ERCP/MRCP shows beaded biliary strictures
  • Positive p-ANCA
  • Onion skin liver biopsy
47
Q

How is PSC managed?

A

Liver transplant
No medicine slows progression

48
Q

What is ascites and how is it classified?

A

Accumulation of fluid in the abdomen
Classified by serum-ascites albumin gradient

SAAG>11 indicates portal htn:
- Liver disorders
- Heart failure
- Budd-Chiari syndrome
- Portal vein thrombosis
- Myxoedema

SAAG<11:
- Hypoalbuminaemia
- Malignancy
- Tubeculous peritonitis
- Pancreatitis
- Bowel obstruction
- Biliary ascites
- Serositis assoc with CTD

49
Q

How is ascites managed?

A
  • Reduce dietary sodium
  • Fluid restrict if low sodium
  • Aldosterone antagonists
  • Drainage if TENSE(cover with albumin if large volume)
  • Prophylactic antibiotics (-floxacin) if protein <15 or cirrhotic
  • TIPS
50
Q

What is spontaneous bacterial peritonitis?

A
  • Form of peritonitis in pts with ascites and liver disease
  • Presents as fever, abdominal pain and ascites
  • Paracentesis shows high neutrophils (>250), often E.coli related
51
Q

How should SBP be managed?

A

Acute - IV cefotaxime
Prophylactic - PO ciprofloxacin

52
Q

What are the biochemical markers of liver failure?

A
  • Low clotting factors (except VIII which is synethesied elsewhere)
  • Reduced protein C/protein S

PATIENTS ARE AT RISK OF BOTH BLEEDING AND THROMBOSIS

53
Q

What is cirrhosis and how is it diagnosed?

A
  • Cirrhosis is scarring of the liver due to long term liver damage
  • Diagnose with Fibroscan AKA transient elastography (screen if RF)
  • Liver biopsy 2nd line
  • Retest every 2 years if risk factors
54
Q

What are the risk factors for cirrhosis?

A
  • Chronic Hep B/C
  • Alcohol misuse
  • Obesity
  • T2DM
55
Q

How is cirrhosis managed?

A

There is NO CURE. Management focuses on dietary change, diuretics, antihypertensives and managing complications

Offer USS every 6 months to screen for HCC in those with cirrhosis

56
Q

What are the features of hepatic encephalopathy?

A
  • Caused by body’s inability to remove ammonia from the blood stream
  • Presents as consuion, tremor, coma
  • Lactulose used in acute and prophylactic management
  • Rifaximin sometimes given for prevention
57
Q

What are the main risk factors for HCC?

A
  • Cirrhosis
  • Alcohol misuse
  • Haemochromatosis
  • Chronic HBC/HCV infection
  • Primary biliary cirrhosis
58
Q

How does HCC usually present?

A
  • Usually presents late with liver cirrhosis/failure or RUQ pain/jaundice/oedema/early satiety/weight loss
  • Raised AFP (by 75% or >400)
  • Focal liver lesion in a patient with cirrhosis is likely to be HCC
59
Q

How is HCC managed?

A

Early: surgical resection
Late: liver transplant

Also radiofrequency ablation, transarterial chemoembolisation and sorafenib

60
Q

What are the features of haemochromatosis?

A
  • Autosomal recessive disorder of iron absorption/metabolism
  • Mutation in HFE gene on chromosome 6
  • ## Presents as fatigue, ED, arthralgia, bronze skin, diabetes, cardiac failure, hypogonadism, liver stigmata
61
Q

Which features of haemochromatosis are reversible/irreversible?

A

Reversible:
- Cardiomyopathy
- Skin pigmentation

Irreversible:
- Liver cirrhosis
- Diabetes
- Hypogonadotrophic hypogonadism
- Arthropathy

62
Q

What do investigations show in haemochromatosis?

A
  • High transferrin saturation (screening tool)
  • Raised ferritin
  • Low TIBC
  • C282Y/H63D mutations may be present
  • MRI to quantify liver/cardiac iron
63
Q

How is haemochromatosis managed?

A

1st line - venesection (aim transferrin saturation <50% and ferritin <50)

2nd line - desferrioxamine

64
Q

What are the features of Wilson’s disease?

A
  • Autosomal recessive disorder causing copper deposition in tissues
  • Defect in ATP7B gene on chromosome 13
  • Onset of symptoms 10-25y as liver disease or neurological disease (young adults)
  • Liver, neurological features and Kayser-Fleischer rings in the iris, renal tubular acidosis, haemolysis, blue nails
65
Q

What do investigations shows in Wilson’s disease?

A
  • Low caeruloplasmin and low serum copper
  • High free serum copper
  • ATP7B gene confirms diagnosis
  • Slit lamp exam for Kayser-Fleischer rings
66
Q

How is Wilson’s disease managed?

A

1st line - penicillamine to chelate copper
2nd line - trientine hydrochoride

67
Q

Which drugs can cause liver cirrhosis?

A

Methotrexate
Amiodarone
Methyldopa

MAM

68
Q

What are carcinoid tumours?

A

Slow-growing tumours of the neuroendocrine system that grow in the bowel or appendix

69
Q

What is carcinoid syndrome?

A
  • Flushing, diarrhoea, bronchospasm and hypotension due to metastases in the liver which release serotonin into systemic circualtion
  • May also secrete ACTH and gnRH
  • Diagnosed by urinary 5-HIAA
70
Q

What is a sister joseph nodule?

A

Umbilical metastatic nodule from an abdominal or pelvic malignancy

71
Q

What is Blumberg sign?

A

Rebound tenderness indicative of peritonitis

72
Q

What is Riedel’s lobe?

A
  • Downward projection of the anterior edge of the right liver lobe to the right of the gallbladder
  • Normal variant
73
Q

How is alcoholic hepatitis diagnosed and managed?

A

Investigations:
- High GGT
- AST:ALT ratio >2

Management:
- Predinsolone for acute attacks
- Pentoxyphylline can be used if steroids not appropriate

MSRA (24 decks)

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