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CP3 Medicine > HPB Medicine > Flashcards

HPB Medicine Flashcards

1
Q

What is hepatitis?

A

Inflammatory disease of the liver, which can be acute or chronic

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2
Q

What are the acute causes of hepatitis?

A

Viral infections (hepatitis A-E / non A-E infections)
Autoimmunen
Drug reacitons
Alcohol

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3
Q

What are the chronic causes of hepatitis?

A 
Hepatitis B +/- Hepatitis D 
Hepatitis C 
Autoimmune hepattis 
Alcohol
Hyperlipidaemia (NAFLD) 
Drugs (methyldopa /nitrofurantoin)

Metabolic disorders (Wilson’s disease, alpha-1-antitrypsin deficiency, haemochromatosis)

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4
Q

What are the components of a liver screen?

A

Microbiology: Viral screen
Clinical chemistry: ferritin/transferrin, lipids, caeruloplasmin, AFP, alpha-1-antitrypsin
Immunology: autoantibodies
Abdominal USS

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5
Q

What type of virus is hepatitis A?

A

RNA picorna virus

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6
Q

How is hepatitis A transmitted?

What is the incubation period?

A

feco-orally

Incubation period is 2-6 weeks

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7
Q

What type of disease does Hepatitis A lead to?

A

80% = asymptomatic and naturally cleared
Does not lead to chronic liver disease and thus there are no carriers

Typically affects children / young adults

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8
Q

What is the treatment for hepatitis A?

A

No specific treatment, mortality 0.1%

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9
Q

What type of virus is hepatitis E?

A

RNA calcivirus

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10
Q

How is hepatitis E transmitted?

A

Feco-orally

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11
Q

What type of disease does hepatitis E lead to?

A

Similar to hepatitis A infection Epidemics of acute, self-limiting hepatitis with no progression to chronic disease

Common in indo-china, so consider if recent travel
Can cause severe disease in pregnant women

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12
Q

What kind of virus is hepatitis B?

A

Hepa-DNA virus, transmitted in the blood, semen and saliva via skin breaks or mucous membranes

Vertical transmission

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13
Q

What is the incubation period of hepatitis B?

A

1-6 months

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14
Q

Describe the structure of hepatitis B?

A

Inner core (HBcAg) surrounded by an outer envelope of surface protein (HBsAg)

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15
Q

Does Hepatitis B cause chronic disease?

A

Yes - around 10% of those infected will develop chronic disease and 1% will develop fulminant liver disease

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16
Q

What is the structure of hepatitis D?

A

Incomplete RNA virus, that can only cause infection in the presence of Hep B as it requires the Hep B virus for its own assembly

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17
Q

How is hepatitis D transmitted

A

Also transmitted by bodily fluids and can be both acute or chronic

Can be acquired simultaneously with Hep B or occur later

Patients with hepatitis D superadded to hepatitis B infection are more likely to develop fulminant liver disease

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18
Q

What is the structure of Hepatitis C?

A

RNA flavivirus, clinically similar to Hep B infection

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19
Q

How is hepatitis C transmitted?

A

Via bodily fluids - particularly common in IVDUs

Vertical transmission is rare and sexual transmission is uncommon

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20
Q

What are the long term effects of Hepatitis C?

A

85% become chronically infected

and 30% get cirrhosis in 20 years

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21
Q

For which hepatitis strains are there vaccines for?

A

Vaccines for A and B but not C

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22
Q

What are ‘non A-E infections’?

A

hepatotropic viral infections that cannot be typed

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23
Q

Describe the morphology of acute hepatitis?

A

Hepatocytes undergo degenerative changes (swelling and vacuolation) before necrosis and rapid removal

Necrosis is usually maximal in zone 3, as this is centrilobular and thus receives the least oxygenated blood

Extent can vary from scattered necrosis to multiracial necrosis leading to fulminant hepatic failure

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24
Q

What is chronic hepatitis?

A

Any hepatitis lasting more than 6 months

principal cause of chronic liver disease, cirrhosis and hepatocellular carcinoma

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25
Q

Describe the pathology of chronic hepatitis?

A

Chronic inflammatory cell infiltrates are present in the portal tracts

There may also be a loss of definition of the portal/periportal limiting plate, confluent necrosis and fibrosis

This eventually leads to cirrhosis

The overall severity is judged by the degree of inflammation and the extent of fibrosis / cirrhosis (staging), using various scoring systems such as the Child Pugh score

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26
Q

What is HbsAg?

A

Hepatitis B surface antigen

Marker of viral replication and thus ACTIVE infection

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27
Q

When does HbsAg appear and disappear?

A

Appears within 6 weeks of infection, disappears by 3 months after

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28
Q

What is HbsAb?

A

Anti-hepatitis B surface antibody

Marker of previously cleared infection / vaccination

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29
Q

What is HBeAg?

A

Hepatitis B E antigen

Marker of a high degree of viral replication (infectivity)

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30
Q

What is HBeAb

A

Hepatitis B e antibody

Marker of natural immunity to hepatitis B

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31
Q

What is HBcAb IgG?

A

Anti-hepatitis B core IgG antibody

Non-specific marker of current / previous infection (persists after 6 months)

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32
Q

What is HbcAb IgM?

A

Anti-hepatitis B core IgM antibody

Infection within the last 6 months (acute viral hepatitis)

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33
Q

What is HBV PCR?

A

The best marker of viraemia?

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34
Q

What markers indicate the immune tolerance phase?

A

HBsAg / HbeAg and PCR positive, transaminases negative

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35
Q

What markers indicate acute hepatitis?

A

All markers positive except HbsAb

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36
Q

What markers indicate chronic hepatitis?

A

All markers positive for >6 months
LFTs less deranged
HbeAg will be positive, and HbeAb negative

37
Q

What markers indicate natural immunity?

A

HbsAg negative, HbsAb positive
HBcAb IgG positive, IgM negative
HbeAg negative, HBeAb positive

38
Q

What markers indicate vaccination?

A

HbsAg negative, HbsAb positive

HbcAb NEGATIVE, HbeAb negative

39
Q

What is the presentation of acute viral hepatitis?

A

Pre-icteric phase:
1-2 week prodrome of malaise, arthralgia, headache and anorexia
Classic aversion to cigarette smoke
Vague RUQ pain

Icteric phase: patient becomes icteric with associated pale stools and dark urine, pruritus and skin rash

May be associated lymphadenopathy, plus hepato/splenomegaly

Hepatitis A and C often cause very mild or no symptoms
Extra-hepatic features more common in hepatitis B

40
Q

What is the presentation of acute alcoholic hepatitis?

A

Presents after a binge with jaundice, RUQ pain and systemic upset

There may be signs of chronic liver disease (acute on chronic presentation)

41
Q

What tests predict survival in acute hepatitis?

A

Bilirubin, prothrombin time and hepatic encephalopathy

combined - discriminant function

42
Q

What discriminant function does acute alcoholic hepatitis carry?

A

> 32 (discriminant function is bilirubin, prothrombin time and hepatic encephalopathy)
mortality here is >50% (consider steroids, monitor closely)

43
Q

What does AST:ALT >2.0 suggest?

A

Alcoholic liver disease

AST –> AStella Artois haha

44
Q

What does autoimmune hepatitis most commonly present as?

A

Acute hepatitis
Up to 40% patients manifest as acute hepatitis with jaundice

Non-specific symptoms of tiredness, arthralgia, fevers and weight loss

45
Q

What are the age peaks for autoimmune hepatitis?

A

15-25 or perimenopausal ages

46
Q

What investigations can be done for autoimmune hepatitis?

A

High transaminases and immunoglobulin (IgG) levels

Negative viral serology

High titres of autoantibodies (non-specific, e.g. ANA, ASMA). Final diagnosis is via liver biopsy

47
Q

What are the symptoms of chronic hepatitis?

A

often asymptomatic unless complications such as cirrhosis develop

Can only be diagnosed when serum ALT levels are elevated for over 6 months (e.g. on follow up for acute viral hepatitis diagnoses)

48
Q

What are the treatment options for autoimmune hepatitis?

A

Prednisolone 30mg O.D
Add azathioprine 1mg/kg/day after TMPT assays

If there are falls in transaminases, gradually reduce the prednisolone dose to maintain the fall (to 10mg/day over 4 weeks)

Long term therapy with low-dose prednisolone (5-10mg) and azathioprine is then recommended

Bone protection plus monitoring required

49
Q

What is the management of acute hepatitis B?

A

Supportive therapy and alcohol avoidance (95% will recover and develop immunity)

First line management is with subcutaneous peginterferon-alfa-2a for 48 weeks (NICE)

50
Q

What is the management of Hepatitis C?

A

New drugs on the market

Very specialist

51
Q

How is liver biopsy performed?

A

Needly biopsy, USS/CT, laparoscopic

52
Q

What are the indications for liver biopsy?

A

Chronic hepatitis, cirrhosis, suspected neoplastic disease, storage diseases or unexplained hepatomegaly

53
Q

What are the contraindications for liver biopsy?

A

Prolonged PT
Platelet count <80
Ascites
Extra hepatic cholestasis

54
Q

What are the complications of liver biopsy?

A

abdominal / shoulder pain and minor intraperitoneal bleeding

Rarer complications: haemothorax, pleurisy, haemobilia, biliary peritonitis

55
Q

What are the newer alternatives to liver biopsy?

A

Fibroscan (transient elastography) which allows the liver stiffness to be measured non-invasively

This score can be used to stage fibrosis

Non invasive: MR elastography and serum biomarker tests

56
Q

Which drugs are more likely to cause chronic hepatitis?

A

Methyldopa, nitrofurantoin, minocycline, lisinopril and diclofenac

57
Q

Is paracetamol an intrinsic or extrinsic hepatotoxin?

A

Intrinsic

58
Q

How does paracetamol metabolism happen normally?

A

At therapeutic doses, it is conjugated with glucuronide and sulphate

Small amount it metabolised by mixed function oxidase systems to form N-acetyl-p-benziquinoneminime (NAPQI)

NAPQI immediately conjugated with glutathione due to its toxicity

59
Q

What happens in paracetamol overdose?

A

Normal conjugation pathways become saturated, meaning large amounts of NAPQI are created

This overwhelms the liver glucothione stores to cause cellular damage. Severity is dose related, however, malnourished individuals / those with high alcohol intake appear to be more susceptible

60
Q

What is the presentation of paracetamol overdose?

A 
Most remain asymptomatic for 24h or at most develop anorexia, nausea and vomiting, then symptoms after 24h: 
RUQ pain
Metabolic acidosis 
Hypotension
Hypoglycaemia 
Pancreatitis 
Arrhythmias
61
Q

Describe the pattern of liver damage following overdose with paracetemol

A

Not detectable on blood tests until 18 hours after ingestion

Damage peaks at 72-96 hours post-ingestion (deranged ALT/ALP and INR)

Without treatment, some will develop fulminant liver failure
Renal failure due to acute tubular necrosis can also occur

62
Q

What is the management for paracetamol overdose?

A

A-E assessment
Lavage if >12g (>150mg/kg in children) taken within 1 hour

Activated charcoal if <1 hour insect ingestion

Take bloods 4 hours post ingestion: INR, ABG, LFTs, U&Es, glucose, blood salicylate and paracetamol level

N-acetyl-cysteine if meets treatment threshold
Stop when plasma paracetemol levels return below the treatment line and patient is asymptomatic with normal biochemistry

63
Q

How does N-acetylcysteine work?

A

Replenishes cellular glucothione stores and may repair oxidative damage

Can cause rash, oedema, hypotension and bronchospasm in 5% but these are rarely serious and these can be treated with IV chlorphenamine

64
Q

What is the alternative to N-acetyl-cysteine?

A

Oral methionine
can only be used up to 12 hours post ingestion

Unreliable if vomiting, or activated charcoal has been used

65
Q

What is the lifespan of a RBC?

What happens to RBC at the end of their lifespan?

A

120 days

Destroyed in the reticuloendothelial system of the spleen

66
Q

What happens to haem following destruction?

A

Haem –> biliverdin –> bilirubin (insoluble/indirect bilirubin) which is bound by albumin in the plasma

Bilirubin can be taken up by hepatocytes and conjugated to bilirubin gluconide by glucuronyl transferase

67
Q

What happens to bilirubin gluconide (soluble bilirubin)?

A

Excreted in the bile into the bowel lumen, where it is transformed by bacteria to urobilinogen
Most urobilinogen is excreted in the stools to give it the dark colour (aka stercobilinogen)

68
Q

What happens to urobilinogen?

A

Small amount is reabsorbed from the intestine into the portal venous tributaries and passes back to the liver, where most of it is excreted once more into the gut

Some of this reabsorbed urobilinogen reaches the systemic circulation, and this is excreted by the kidney into the urine

When the urobilinogen in the urine is exposed to air, it is oxidised to urobilin to give urine a dark colour (why urine goes dark when u don’t flush)

69
Q

What is jaundice and when does jaundice arise?

A

Yellowing of the skin

Usually when the bilirubin level reaches 50micromol/L with the upper limit of normal being 25

70
Q

What is the cause of pre-hepatic jaundice?

A

Occurs secondary to increased erythrocyte breakdown e.g. in haemolysis or reabsorption of a large haematoma

Haemolytic anaemia
Gilbert’s syndrome
Criggler-Najjar syndrome

The bilirubin has not yet been processed by the liver, thus is mainly unconjugated in the blood

71
Q

What is the cause of cholestatic jaundice?

A

There is an obstruction to bile outflow from the liver, leading to ‘cholestasis’

72
Q

Is cholestatic jaundice conjugated or unconjugated?

A

Bilirubin has been processed by the liver, so mainly conjugated

73
Q

What is the effect of cholestatic jaundice on urine and stool?

A

Can enter the urine giving dark urine

Cannot enter the GIT and is not excreted in faeces, so you get pale stools

74
Q

What is intrahepatic obstruction?

A

Obstruction of the hepatic bile canniliculi
Can occur due to multiple different causes including:
hepatitis
cirrhosis
neoplasm
Drugs (chlorpromazine, flucloxacillin, isoniazid, OCP)
Pregnancy

75
Q

What is extra hepatic obstruction?

A

Obstruction of the hepatic ducts, or biliary tree
Causes within the lumen: gallstones
Causes within the wall: cholangiocarcinoma, primary sclerosing cholangitis, congenital atresia of the common bile duct

External causes: pancreatitis, tumour of the pancreatic head

76
Q

What is hepatocellular jaundice?

A

There is an issue with the cells of the liver, leading to dysfunction and a partial inability to conjugate bilirubin

This leads to mixed conjugated / unconjugated bilirubin in the blood
If severe, there can be a total inability to conjugate bilirubin and an unconjugated hyperbilirubinaemia?

77
Q

What are the causes of hepatocellular jaundice?

A

Alcoholic liver disease
Viral hepatitis
Iatrogenic, e.g. medication: paracetamol, methyldopa
Hereditary haemochromatosis
Autoimmune hepatitis
Primary biliary cirrhosis or primary sclerosing cholangitis
Hepatocellular carcinoma

78
Q

What is the cause of isolated unconjugated hyperbilirubinaemia, with no evidence of liver damage?

A

Gilbert’s syndrome

79
Q

What is Gilbert’s syndrome?

A

Congenital lack of glycoronyltransferase
affects up to 7% of the population

Of no clinical significance but can lead to transient episodes of jaundice, particularly following an infection such as URTI

Serum unconjugated bilirubin will be raised, but LFTs and reticulocytes normal

80
Q

Describe the appearance of stool in prehepatic jaundice?

A

Large amounts of bilirubin excreted into gut, thus stercobilinogen is raised to give normal / dark stools

Urinary urobilinogen is thus also raised due to greater re-absorption, which can be tested for, but clinically there will not be dark urine as urobilinogen is not dark in colour until oxidised

81
Q

What is the appearance of stool in obstructive / cholestatic jaundice?

A

Very little bile can enter the gut, thus stercobilinogen low, giving pale stools

As such, there is no urinary urobilinogen as there is no enterohepatic recycling

AS bilirubin is conjugated in teh blood, urinary bilirubin is present, giving dark urine

82
Q

What is the appearance of stools and urine in hepatocellular jaundice?

A

Can present with elements of both prehepatic and cholestatic jaundice:

Urinary urobilinogen may also be raised in hepatocellular jaundice, due to the inability of the liver to re-excrete urobilinogen reabsorbed from teh bowel

Bilirubin may be present if conjugated bilirubin levels are high enough, giving dark urine

Stools may be paler than usual, due to a decrease in teh ability to conjugate bilirubin and thus excrete it into the gut

83
Q

What investigations can be done for jaundice?

A

Bloods: FBC, reticulocytes, LFTs, U&Es, clotting, glucose, bilirubin levels

Transaminases most raised in hepatocellular jaundice / intrahepatic obstruction
ALP most raised in extra hepatic cholestasis
Glucose may be low in liver failure, or raised in pancreatic disease

Urinary urobilinogen/bilirubin

84
Q

What further investigations can be done for jaundice?

A

Blood films / Coomb’s test if suspecting prehepatic jaundice

Viral serology / autoantibodies: if suspecting hepatitis

USS: Will show dilated duct system to confirm obstruction / gallstones

MRCP: non-invasive high resolution imaging of the biliary tree

CT/MRI: useful to demonstrate intrahepatic lesions , which may need to be accurately needle biopsied
Can also show pancreatic lesions

Needle biopsy: can give important info with regard to hepatic pathology
Prothrombin time should be corrected first if deranged (with FFP/platelets)

85
Q

What is ERCP?

A

Endoscopic retrograde cholangiopancreatography
If the ductal system is dilated, the ampulla of Vater is cannulated using an endoscope, and contrast is injected to demonstrate lesions

This should only be used therapeutically

86
Q

What should be given prior to ERCP?

A

Ciprofloxacin as antibiotic prophylaxis with sedation and analgesia prior to procedure

87
Q

What are the complications of ERCP?

A

Pancreatitis, perforation or cholangitis (give IV abx before)

Post op bleeding

88
Q

What is PTC?

A

Percutaneous transhepatic cholangiography

Percutaneous cannulation of a dilated bile duct within the liver, generally used for therapeutic intervention if ERCP is not possible

Can be used to stent obstructing bile duct lesions, but does not allow ampulla/pancreatic duct to be visualised

CP3 Medicine (19 decks)

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