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CP3 Medicine > HPB 2 > Flashcards

HPB 2 Flashcards

1
Q

How does bacterial infection of the liver occur?

A

3 main routes:
Ascending spread from cholangitis
Portal spread from a focus of sepsis in the abdomen
Systemic bloodstream spread in septicaemia

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2
Q

How do pyogenic liver abscesses occur?

A

Ascending spread from the abdomen (appendicitis, perforation)

Other causes: biliary sepsis, trauma or bacteraemia

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3
Q

What are the most common organisms causing pyogenic liver abscesses?

A

E.coli, Strep Milleri or anaerobes

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4
Q

What is the presentation of pyogenic liver abscess?

A

?Long history of malaise
Can be: abdominal sepsis and a tender enlarged liver

May be pleural effusions in the right lower chest

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5
Q

What investigations can be done for pyogenic liver abscess?

A

USS/CT

CXR: may show elevation of the right diaphragm +/- pleural effusion

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6
Q

What is the management of pyogenic liver abscess?

A

Aspiration under USS guidance and IV antibiotics, as well as treating the underlying cause

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7
Q

What is an amoebic abscess caused by?

A

Faecal-oral spread of entamoeba histiolytica

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8
Q

What are the acute presentations of amoebic abscesses?

A

Asymptomatic
Mat have profuse/bloody diarrhoea

Swinging high fever, with RUQ pain and tenderness

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9
Q

What are the investigations for amoebic abscess?

A

Stool microscopy - shows offending organism, blood and pss

USS/CT will visualise the abscess

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10
Q

What is the management for an amoebic abscess?

A

Metranidazole for 5 days

USS drainage may be required

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11
Q

What is the cause of a hyatid cyst?

A

Caused by echinococcus granulosus (dog tapeworm), can be multiple
Infects humans coming into contact with infected dogs or food/water contaminated with dog faeces

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12
Q

What are the symptoms of hyatid cyst?

A

May be symptomless, may have dull ache in RUQ

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13
Q

What are the ix for hyatid cyst?

A

Positive hyatid complement fixation test / haemaglutinaiton, eosinophilia

AXR may show calcification of the wall, and USS/CT may also demonstrate the cyst

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14
Q

What is the management of hyatid cyst?

A

Albendazole and FNA under USS guidance and deworming of pet dogs

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15
Q

What is the main cause of liver tumours?

A

Mets - 90%

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16
Q

Where are common primaries that metastasise to the liver?

A

Lung, stomach, colon, breast, uterus

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17
Q

What is the management of liver mets?

A

Investigation to find the primary

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18
Q

What is hepatocellular carcinoma?

A

Malignant tumour of hepatocytes, accounting for 90% primary liver cancers

Common in China/Sub-Saharan Africa but rare in the west

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19
Q

What are the causes of HCC?

A 
Chronic hepatitis 
Cirrhosis
Metabolic liver diseases
Aspergillus alfatoxin
Parasites
Anabolic steroids
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20
Q

What are the symptoms of HCC?

A

Non-specific fever, malaise and weight loss

RUQ pain

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21
Q

What are the signs of HCC?

A

Hepatomegaly (may be smooth or hard/irregular)
Signs of chronic liver disease / decompensation
Abdominal mass / bruit over the liver
Jaundice is late (c.f. cholangiocarcinoma)

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22
Q

What are the investigations for HCC?

A

Bloods: FBC, LFTs, clotting, hepatitis serology, AFP
(raised in 50% of HCC)

USS/CT to identify lesions and guide biopsy
MRI to distinguish benign and malignant lesions
ERCP/biopsy if cholangiocarcinoma suspected

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23
Q

What are the treatments for HCC?

A

Surgery for solitary HCCs <3cm but high risk of recurrence
Transplantation if there are small tumours due to cirrhosis
Resection in cirrhosis can lead to decompensation

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24
Q

What is the prognosis for HCC?

A

Bad - <6 months

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25
Q

What is cholangiocarcinoma?

A

Adenocarcinoma arising from the biliary tree e.g. at the ampulla of Vater
Comprise 10% of hepatic primaries

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26
Q

What are the symptoms of cholangiocarcinoma?

A

Painless jaundice

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27
Q

What are the predispositions for cholangiocarcinoma?

A

Any form of chronic inflammation predisposes e.g. primary sclerosing cholangitis or parasite infestation

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28
Q

How does cholangiocarcinoma spread?

A

Direct invasion of the liver

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29
Q

What are the management for cholangiocaricinoma?

A

If they present early, they can be cured with an extended liver resection

Often present late, in which case palliation can be achieved by ERCP stenting to relieve the jaundice

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30
Q

What are the most common benign liver tumours?

A

Haemangioma - incidental finding on CT / USS

If patient is young woman on OCP, more likely to be a liver cell adenoma

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31
Q

In what circumstances should benign liver tumours be treated?

A

IF symptomatic of >5cm

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32
Q

What is cirrhosis?

A

Irreversible consequence of chronic hepatic injury:

Destruction of liver cells
Associated chronic inflammation, stimulating fibrosis
Regeneration of hepatocytes to form nodules

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33
Q

How does fibrosis of the liver occur?

A

Due to growth factors released from inflammatory cells, Kuppfer cells and hepatocytes

Inflammatory cells may be due to hepatitis or recruited in response to liver cell necrosis (chronic alcoholism)

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34
Q

How do nodules form in fibrosis?

A

Stellate cells are activated to form myofibroblasts and secrete collagen and nodules form due to the natural capacity of hepatocytes to divide and regenerate in response to damage

These nodules lack normal vascular and bile drainage connections

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35
Q

What is micro / macronodular cirrhosis and when does each occur?

A

micronodular cirrhosis: <3mm occurs as a result of alcoholic liver damage or biliary tract disease

macronodular cirrhosis: >3mm occurs due to previous hepatitis

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36
Q

What are the common causes of cirrhosis?

A

Alcoholic liver disease
Cryptogenic liver disease
Non-alcoholic Fatty liver disease
Chronic viral hepatitis

37
Q

What are the less common causes of cirrhosis?

A

autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Budd-Chiari syndrome or cystic fibrosis

38
Q

What are the very rare causes of cirrhosis?

A

Haemochromatosis
Wilson’s disease
alpha-1-antitrypsin deficiency

39
Q

What is primary biliary cirrhosis?

A

Autoimmune destruction of intra-hepatic bile cannaliculi
Occurs mainly in 40-60 year old females

Positive AMA

40
Q

What are the presentations of primary biliary cirrhosis?

A

Jaundice, pruritus and skin xanthomas. Associated with IBD

Raised AMA (anti-mitochondrial antibodies)

41
Q

Describe the prognosis and management of primary biliary cirrhosis?

A

Slowly progressive condition - average survival 6 years from diagnosis

Replacement of fat soluble vitamins is important in management

42
Q

What is primary sclerosing cholangitis?

A

Autoimmune inflammation and fibrosis around the bile ducts in the liver
This leads to secondary cirrhosis due to chronic biliary obstruction

43
Q

What are the outcomes in primary sclerosing cholangitis?

A

Cholangiocarcioma can develop in 10-15% cases

There is no effective treatment except transplantation

44
Q

What are the symptoms of chronic liver disease?

A

Fatigue

weight loss/ anorexia: early satiety with hepatomegaly
May get central weight gain of ascites

Jaundice

Leg swelling: increased intra-abdominal pressure , low oncotic pressure

Bleeding/bruising: decreased synthetic function

Itching: bile salt accumulation

45
Q

What are the signs of chronic liver disease?

A

Nails: leuconychia due to low albumin, clubbing
Hands: palmar erythema, Duyputren’s contracture, liver flap

Skin: pigmentation, spider nave, striae

Feminization: gynaecomastia, testicular atrophy and loss of body hair

Secondary hyperaldosteronism: due to activation of RAAS because hypoalbuminaemia leads to a lower circulating volume

Signs of portal hypertension: caput medusae, hepatosplenomegaly, ascites

Signs of hepatocellular failure: bruising, prolonged clotting

46
Q

What are the signs of portal hypertension?

A

caput medusae
hepatosplenomegaly
Ascites

47
Q

What are the signs of decompensated liver disease?

A

Encephalopathy
Ascites
Jaundice

48
Q

What are the precipitants of chronic liver disease ‘decompensating’?

A

Alcohol binge
variceal bleed
hepatotoxic drugs
portal/hepatic vein thrombosis

49
Q

What is the Child-Pugh score?

A 
Gives 1/2 year mortality scores in chronic liver disease, using certain variables: 
total bilirubin
Serum albumin 
PT/INR
Ascites
Hepatic encephalopathy
50
Q

What are the complications of chronic liver disease?

A

Hepatocellular failure, portal hypertension, malignant change, renal failure (hepatorenal syndrome)

51
Q

How is severity of cirrhosis determined?

A

Liver function: albumin and INR are the best indicators
Liver damage: LFTs
Complications: U&Es, ABG (hepatorenal / hepatopulmonary syndrome)

52
Q

What is the liver screen?

A 
Viral serology
serum autoantibodies/immunoglobulins
AFP
Iron studies (hereditary haemochromatosis), serum copper/caeruloplasmin (Wilson's disease)
alpha-1-antitrypsin level
53
Q

What imagine is done for liver disease?

A 
USS and duplex: 
liver can be shrunken or enlarged
splenomegaly may be present
portal system flow may be reversed 
Can also show focal lesions or portal vein thrombosis

Endoscopy: detection and treatment of suspected carves should be undertaken

Further investigation: Ascitic tap for MCS if infection suspected
Liver biopsy

54
Q

What is Wilson’s disease?

A

Rare autosomal recessive inborn error of copper metabolism, leading to deposition of copper in many organs:
classically, liver, basal ganglia and cornea

Symptoms: neuro, liver, rings

REDUCED Caerulosplasmin and REDUCED serum copper (bound by caeruloplasmin)

55
Q

What investigations are done for Wilson’s disease?

A

Serum caeruloplasmin (reduced)

Urinary copper (increased) and a liver biopsy showing increased copper

Serum copper will be reduced as copper is bound by caeruloplasmin

56
Q

What are the treatments for Wilson’s disease?

A

Chelating agents e.g. D-penicillamine or trientenje

57
Q

What is haemochromatosis?

A

bronze diabetes
Inherited condition AUTOSOMAL RECESSIVE
characterised by excess iron deposition in various organs, leading to fibrosis and organ failure

58
Q

What are the symptoms of haemochromatosis?

A

Triad:
Bronze skin discolouration
Hepatomegaly
Diabetes mellitus

early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)

59
Q

What are the other symptoms of haemochromatosis?

A

Hypogonadism: impotence, testicular atrophy due to pituitary iron deposition

60
Q

What are the investigations for haemochromatosis?

A

Serum iron/ferritin (both raised)
total iron binding capacity (decreased)
genetic testing and liver biopsy
transferrin saturation

61
Q

What is the management for haemochromatosis?

A

Venesection - basically drawing blood out of the body

1 unit per week initially

62
Q

What are the complications of cirrhosis?

A

Ruptured gastro-oesophageal varices

Ascites

Encephalopathy

63
Q

What % of patients with cirrhosis develop gastro-oesophageal varices?

A

90% over 10 years

1/3 of these patients will suffer a bleed

64
Q

What is ascites?

A

Fluid in the peritoneal cavity which can accumulate slowly or rapidly

65
Q

What is the management of ascites?

A

Initial bed rest and fluid restriction plus low salt diet and spironolactone (to counter the deranged RAAS)

Furosemide if the response is poor, with therapeutic paracentesis and albumin infusion for large volume ascites

If spontaneous bacterial peritonitis is suspected (fever, pain, deterioration), give ceftriaxone IV until sensitivities are known
Then long term norfloxacin as recurrence is high

66
Q

What is encephalopathy caused by?

A

Nitrogenous waste building up in the circulation, leading to cerebral oedema when astrocytes attempt to clear it

67
Q

Describe Grades I-IV encephalopathy?

A

Grade I: altered mood/behaviour, sleep disturbances
Grade II: Increasing drowsiness and confusion
Grade III: Stupor, incoherence, restlessness
Grade IV: coma

68
Q

What is the management of encephalopathy?

A

ICU admission with 20 degree head tilt and oral lactulose with regular enemas, to clear the bowel of nitrogen forming organisms

If there is evidence of cerebral oedema, IV mannitol and hyperventilation may be used

69
Q

What is the purpose of the hepatic portal vein?

A

Portal vein collects nutrient blood from the abdominal part of the alimentary tract, and carries it to the liver, where its branches divide and end in expanded capillaries: the venous sinusoids of the liver

70
Q

What are the locations of the porto-systemic anastomoses?

A

Cardia of the stomach: gastric/oesophageal varices

Anus: rectus varices

Retroperitoneal organs: stomal varices

Paraumbilical veins of the anterior abdominal wall: caput medusae

71
Q

What happens when portal blood flow through the liver is obstructed?

A

Blood from the portal territory is Able to use these collateral routes to return to the heart as the portal system has no valves, so blood can flow in a reverse direction

72
Q

What is portal hypertension defined as?

A

Pressure in the portal vein >10mmHg

73
Q

What are the pre-hepatic causes of portal hypertension?

A

Portal vein thrombosis (often due to portal pyaemia / prothrombotic states)

74
Q

What are the hepatic causes of portal hypertension?

A 
Cirrhosis 
Hepatitis e.g. alcoholic
Idiopathic, non-cirrhotic portal hypertension 
Schistosomiasis 
Congenital hepatic fibrosis
75
Q

What are the post-hepatic causes of portal hypertension?

A

Budd-Chiari syndrome (obstruction of the hepatic veins, most commonly due to thrombosis or obstruction due to external mass)

76
Q

What are the manifestations of portal hypertension?

A 
Variceal bleeding
Haemorrhoids / caput medusae
Ascites
Splenomegaly (portal congestion)
Porto systemic encephalopathy (toxins bypass liver)
77
Q

What is the emergency treatment for bleeding oesophageal varices?

A

A-E resuscitaton
Vitamin K + FFP to correct clotting (activate MHP)
IV terlipressin (or somatostatin analogues)
IV antibiotic prophylaxis (decreases mortality - quinolone)

endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy

Sengstaken-Blakemore tube if uncontrolled haemorrhage

Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail
connects the hepatic vein to the portal vein
exacerbation of hepatic encephalopathy is a common complication

78
Q

What is the definitive procedure for bleeding oesophageal varices resistant to banding?

A

Transjugular intrahepatic portosystmic shunting (TIPSS - shunt between portal and hepatic veins)
Carried out by interventional radiology

Surgical porto-caval shunts = alternative option

79
Q

What is the secondary prophylaxis for bleeding oesophageal varices?

A

Following an initial bleed, endoscopy is indicated as soon as haemodynamically stable to identify the site of the bleeding, estimate the risk of rebleeding and administer adrenaline and band Therapy

sclerotherapy = second line

failing this; beta blockers

80
Q

What drugs are given in liver disease and for what purpose?

A

Pruritus: cholestyramine

Ascites: fluid/salt restriction, spironolactone +/- furosemide

Encephalopathy: lactulose titrated

Analgesia: paracetamol preferred, NSAIDs avoided, opioids ideally avoided as constipation

Nausea: domperidone = useful, may improve encephalopathy

Alcohol detox: chlordiazepoxide + pabrinex IV. Oral thiamine is then required for 28 days

81
Q

What are the common causes of splenomegaly?

A

Infection

Inflammation e.g. RA, SLE, Sarcoidosis

Portal hypertension

Haematological disease (haemolytic anaemia, leukaemia, lymphoma, myeloproliferative disorders)

82
Q

When is massive splenomegaly seen?

A

3Ms: myelofibrosis, CML, malaria

Myelofibrosis
Chronic myeloid leukaemia 
lymphoma
malaria 
lieshmaniasis 
Gaucher's disease
83
Q

What is the result of hypersplenism?

A

Pancytopenia, increased plasma volume and haemolysis

84
Q

What are the indications for splenectomy?

A

Splenic trauma
Hypersplenism
Autoimmune haemolysis (ITP, congenital haemolytic anaemia)

85
Q

What are the potential causes of splenic rupture?

A

Blunt trauma - occasionally by penetrating injuries

Pre-existing illness

86
Q

What is the presentation of splenic rupture?

A

Immediate massive bleeding, peritonism from progressive blood loss and eventual shock

87
Q

What is the main issue following splenectomy?

A

Increased risk of infection, mainly by encapsulated organisms e.g. Strep Pneumonia, as the spleen usually contains large numbers of macrophages that phagocytose such bacteria

88
Q

What is the management following splenectomy?

A

Mobilise soon after operation due to transient increase in platelets, so LMWH given whilst in hospital and aspirin in short term

Immunise according to local regimens:
pneumococcal 2 weeks prior to surgery or ASAP following emergency surgery, plus HIB, Men C and annual flu vaccine

Lifelong penicillin V

Advice to carry alert card, seek immediate medical attention if ?infection

If travelling abroad, warn of severe malaria risks

CP3 Medicine (19 decks)

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