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gen surg > Hepatology > Flashcards

Hepatology Flashcards

1
Q

Age group most affected by cholangiocarcinoma

A

Mostly in those aged over 60

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2
Q

Risk factors for cholangiocarcinoma

A

Patients with chronic ulcerative colitis who develop sclerosing cholangitis

Infection with liver flukes

Chemical exposure

Congenital abnormalities

Hep C, HIV, cirrhosis and diabetes

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3
Q

Presentation of cholangiocarcinoma

A

Jaundice(early feature)
Hepatomegaly
Abdo pain(localised to RUQ)
Weight loss
Pale-coloured stools, passage of dark urine
Splenomegaly if prolonged biliary obstruction
Courvoisier’s sign

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4
Q

What is courvoisier’s sign

A

Palpable gallbladder may occur with tumours distal to the cystic duct

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5
Q

IX for cholangiocarcinoma

A

LFTs(Elevated conjugated bilirubin, cholestatic picture)

Prothrombin and INR prolonged

Tumour markers(CA 19-9 and CEA)

Ultrasound and CT

Contrast MRI for diagnosis

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6
Q

Surgical management of cholangiocarcinoma

A

Complete surgical resection

Liver resection for intrahepatic tumours

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7
Q

Non-surgical management of cholangiocarcinoma

A

Stenting of bile duct to relieve symptoms using ERCP

Palliative chemotherapy

Radiotherapy

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8
Q

Complications of cholangiocarcinoma

A

Biliary tract sepsis

Secondary biliary cirrhosis

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9
Q

What is primary sclerosing cholangitis

A

Intrahepatic or extra hepatic ducts become structured and fibrotic causing obstruction to bile flow out of liver and into the intestines

Chronic bile obstruction eventually leads to liver inflammation(hepatitis), fibrosis and cirrhosis

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10
Q

Which condition is associated with primary sclerosing cholangitis

A

Ulcerative colitis

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11
Q

Risk factors for PSC

A

Male
Aged 30-40
Ulcerative colitis
Family history

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12
Q

Presentation of PSC

A 
Jaundice 
Chronic RUQ pain 
Pruritus 
Fatigue 
Hepatomegaly
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13
Q

What do liver function tests show in PSC

A

Cholestatic picture - Elevated ALP

May be a rise in bilirubin as strictures become severe and prevents bilirubin from being excreted through bile duct

Other LFTs can also be deranged as disease progresses to hepatitis

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14
Q

What autoantibodies may indicate an autoimmune element to PSC

A 
Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
Antinuclear antibodies (ANA) in up to 77%
Anticardiolipin antibodies (aCL) in up to 63%
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15
Q

Diagnosis of PSC

A

MRCP - shows bile duct lesions or strictures

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16
Q

Complications of PSC

A 
Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies
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17
Q

Management of PSC

A

Liver transplant
ERCP to dilate and stent strictures
Colestyramine
Monitor for complications

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18
Q

What is colestyramine

A

Bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

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19
Q

Causes of hepatitis

A 
Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis (e.g. paracetamol overdose)
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20
Q

Hepatitis presentation

A 
Abdominal pain
Fatigue
Pruritis (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (viral hepatitis)
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21
Q

Typical LFTs in hepatitis

A

High transaminases(AST/ALT) with proportionally less of a rise in ALP

Bilirubin can also rise as a result of inflammation of the liver cells.

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22
Q

Most common viral hepatitis

A

Hep A

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23
Q

How is Hep A transmitted

A

faecal-oral route usually by contaminated water or food

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24
Q

Presentation of hep A

A

nausea, vomiting, anorexia and jaundice. It can cause cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools and moderate hepatomegaly.

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25
Q

Disease progression of hep A

A

Resolves without treatment in around 1-3 months

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26
Q

Management of Hep A

A

Basic analgesia

Notable disease

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27
Q

What type of virus is Hep B

A

DNA virus

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28
Q

How is hep B transmitted

A

Direct contact with blood or bodily fluids, such as during sexual intercourse or sharing needles (i.e. IV drug users or tattoos).

It can also be passed through sharing contaminated household products such as toothbrushes or contact between minor cuts or abrasions.

It can also be passed from mother to child during pregnancy and delivery (known as “vertical transmission”).

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29
Q

Disease course of hep B

A

Most people fully recover from the infection within 2 months, however 10% go on to become chronic hepatitis B carriers.

In these patients the virus DNA has integrated into their own DNA and so they will continue to produce the viral proteins.

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30
Q

Test for active hepatitis b infection

A

HBsAg

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31
Q

Test for previous hep b infection

A

HBcAb

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32
Q

What should be tested if HBsAg and HBcAb are positive

A

Further testing for HBeAg and viral load

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33
Q

How can Hep B c antibodies be used to distinguish acute, chronic and past infections

A

IgM implies an active infection and will give a high titre with an acute infection and a low titre with a chronic infection.

IgG indicates a past infection where the HBsAg is negative.

34
Q

Importance of Hep B e antigen test

A

Where the HBeAg is present it implies the patient is in an acute phase of the infection where the virus is actively replicating.

The level of HBeAg correlates with their infectivity.

When the HBeAg is negative but the hepatitis B e antibody is positive this implies they have been through a phase where the virus was replicating and but the virus has now stopped replicating

35
Q

What is the Hep B vaccination

A

involves injecting the hepatitis B surface antigen. Vaccinated patients are tested for HBsAb to confirm their response to the vaccine

36
Q

Management of hep B

A 
Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
Refer to gastroenterology
Notify public health 
Smoking and alcohol cessation 
Antiviral meds 
Liver transplantation
37
Q

What type of virus is hep C

A

RNA virus

38
Q

How is hep c transmitted

A

Spread by blood and body fluids

39
Q

Complications of hep B

A

Cirrhosis

HCC

40
Q

Disease course of hep c

A

1 in 4 fights off the virus and makes a full recovery

3 in 4 it becomes chronic

41
Q

Complications of hep c

A

liver cirrhosis

HCC

42
Q

Test for hep c

A

Hepatitis C antibody is the screening test

Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype

43
Q

Management of hep c

A 
Screen for other blood born viruses
Notify Public Health
Smoking and alcohol cessation 
Antiviral treatment with direct acting antivirals 
Liver transplant
44
Q

Features of hep d

A

RNA virus
Can only survive in patients who have hep b
Attaches itself to HBsAg
Increases complications and disease severity of hep B

45
Q

Management of hep D

A

No specific treatment for hep D

Notifiable disease

46
Q

What is Hep E

A

RNA virus

47
Q

How is Hep E transmitted

A

Faecal oral route

48
Q

Disease course of Hep E

A

Produces only a mild illness, the virus is cleared within a month and no treatment is required.

Rarely it can progress to chronic hepatitis and liver failure, more so in patients that are immunocompromised.

49
Q

What is autoimmune hepatitis associated with

A

Can be associated with a genetic predisposition and triggered by environmental factors such as viral infection that causes a T cell-mediated response against liver cells

50
Q

What are the two types of autoimmune hepatitis

A

Type 1: occurs in adults

Type 2: occurs in children

51
Q

Features of type 1 autoimmune hepatitis

A

Typically affects women in their late forties or fifties.

It presents around or after the menopause with fatigue and features of liver disease on examination.

It takes a less acute course than type 2.

52
Q

Features of type 2 autoimmune hepatitis

A

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

53
Q

General IX for type 1 and type 2 autoimmune hepatitis

A

Raised transaminases (ALT and AST), IgG levels and it is associated with many autoantibodies.

54
Q

Specific autoantibodies associated with type 1 autoimmune hepatitis

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

55
Q

Specific autoantibodies associated with type 2 autoimmune hepatitis

A

Anti-liver kidney microsomes-1 (anti-LKM1)

Anti-liver cytosol antigen type 1 (anti-LC1)

56
Q

Diagnosis of autoimmune hepatitis

A

Liver biopsy

57
Q

Treatment for autoimmune hepatitis

A 
High dose steroids(prednisolone) 
Immunosuppressants(azathioprine) 
Liver transplant(autoimmune hepatitis can recur)
58
Q

Aetiology of hepatic encephalopathy

A

Not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.

59
Q

what is hepatic encephalopathy associated with

A

Often associated with acute liver failure it may also be seen with chronic disease

60
Q

Which procedure can precipitate encephalopathy

A

transjugular intrahepatic portosystemic shunting (TIPSS) may precipitate encephalopathy

61
Q

Features of hepatic encephalopathy

A

confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
raised ammonia level (not commonly measured anymore)

62
Q

EEG features - hepatic encephalopathy

A

triphasic slow waves on EEG

63
Q

Grading of hepatic encephalopathy

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

64
Q

precipitating factors in hepatic encephalopathy

A 
infection e.g. spontaneous bacterial peritonitis
GI bleed
TIPPS
constipation
hypokalaemia
renal failure
increased dietary protein (uncommon)
65
Q

Drugs implicated in hepatic encephalopathy

A

Sedative

Diuretics

66
Q

Mx of hepatic encephalopathy

A

treat any underlying precipitating cause
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy

67
Q

How does lactulose work in hepatic encephalopathy

A

lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria

68
Q

How do antibiotics work in hepatic encephalopathy

A

antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production

69
Q

Types of drug-induced liver disease

A

Hepatocellular
Cholestatic
Mixed

70
Q

Causes of hepatocellular drug-induced liver disease

A 
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis meds
statins
alcohol
71
Q

Causes of cholestatic/mixed drug-i induced liver disease

A 
COCP
Abx
anabolic steroids
chlorpromazine, prochlorperazine
sulphonylureas
fibrates
72
Q

Drugs which can cause liver cirrhosis

A

Methotrexate
Methyldopa
Amiodarone

73
Q

Risk factors for HCC

A

Liver cirrhosis due to:

Viral hep(B and C)
Alcohol
NAFLD

74
Q

Tumour marker associated with HCC

A

Alpha-fetoprotein

75
Q

Drugs associated with HCC

A

COCP

Anabolic steroids

76
Q

Features of HCC

A

tends to present late
features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly

possible presentation is decompensation in a patient with chronic liver disease

77
Q

When should screening be considered for HCC

A

Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:

patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol

78
Q

Mx of HCC

A

early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation

79
Q

What might be seen on light microscopy in chronic hep B

A

Ground-glass hepatocytes

80
Q

Definition of chronic hep c

A

persistence of HCV RNA in the blood for 6 months.

81
Q

Eye problem associated with chronic hep c

A

Sjogren’s syndrome

gen surg (24 decks)

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