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Gastroenterology > Liver > Flashcards

Liver Flashcards

1
Q

What are the functions of the liver and the consequences of this with liver failure?

A

1) Stores carbohydrate and glucose homeostasis - therefore hypoglycaemia
2) Albumin production - hypoalbuminemia - oedema, ascites and leukonuchia
3) Ferritin production - macrocytic anaemia
4) Drug metabolism via cp450 system - therefore altered drug metabolism
5) Bilirubin metabolism and secretion - jaundice and pruritus

6) Oestrogen breakdown
- gynaecomastia, loss of male pattern hair, palmar erythema, dupretrons contracture, spider naevi, testicular atrophy and ED

7) completement cascade
- infections

8) clotting factors
- bruising and bleeding easily

9) ammonia excretion
- encephalopathy, asterixis and hepatic foetor

10) portal hypertension - splenomegaly, oesophageal varices, caput medusae

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2
Q

Causes of hypoglycaemia

A

EXPLAIN
Exogenous drugs - insulin/hypoglycaemics, quinolones, quinines, alcohol, pentamidine

P - pituitary insufficiency - no GH or cortisol

L - liver failure

A - adrenal insufficiency - no cortisol

I - insulinomas - immune hypoglycaemia

N - non-pancreatic neoplasms

Malaria

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3
Q

Symptoms of acute liver disease?

A

Symptomatic is often viral
Generalised symptoms of malaise, anorexia and fever
Jaundice may appear as illness progresses

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4
Q

Symptoms of chronic liver disease?

A

Right hypochondrial pain due to liver distension
Ascites
Ankle swelling
GI haemorrhage - haematemesis or melaena
Pruritus
Signs of hyper-oestrogen
Encephalopathy signs

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5
Q

Signs of liver disease?

A

Jaundice, xanthelasmas, spider naevi, loss of body hair, gynaecomastia, liver (small or large), splenomegaly, caput medusae, ascites
Palms - erythema, clubbing, duputrens and xanthomas
Scratch marks from pruritus. Bruising
Oedema
Testicular atrophy
Liver flap, confusion - encephalopathy
Hepatic foetar

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6
Q

What serum bilirubin is needed for jaundice to be detectable clinically?

A

> 50umol/L

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7
Q

3 types of jaundice

A

Pre-hepatic - usually haemolytic
Hepatic - hepatitis (alcohol, drugs, viruses, ischaemic, cirrhosis)
Post-hepatic - obstructive - cholestatic

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8
Q

Causes of obstructive jaundice x5

A 
Gall stones
Sclerosing cholangitis (PSC)
Biliary stricture 
Carcinoma of bile duct, pancreas head, ampulla of vater
Pancreatitic pseudocyst
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9
Q

Presentation of intra and post-hepatic jaundice

A

Pale stools and dark urine - conjugated

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10
Q

Questions to ask if Hep B jaundice suspected?

A 
Country of origin 
Generally a shorter history of presentation
IVDU, tattoos, injections 
Male-male sex 
Female sex workers
Blood transfusion
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11
Q

Questions to be asked if Hep C jaundice suspected?

A

IVDU, injections, tattoos, blood transfusion

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12
Q

Question to ask if Hep A jaundice suspected?

A

Recent consumption of shellfish, recent outbreak of jaundice in the community
Recent travel as regions have high risk Hep A

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13
Q

Other questions to ask jaundice for non-hepatitis causes?

A 
Recent anaesthetic - halothane 
Family history 
Recent biliary tract/carcinoma surgery 
Environment 
Fevers or rigours - cholangitis/liver abscess 
Alcohol history
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14
Q

Different types of hepatomegaly

A

Smooth tender liver - hepatitis with extrahepatic obstruction
Knobbly irregular - metastases

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15
Q

USS when is it useful

A

In jaundice
Shows bile ducts and sizes
Level of obstruction
Cause of obstruction in virtually all tumour patients and 75% of gallstones

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16
Q

Way to approach jaundice in an older patient with no risk factors for hepatitis + weight loss

A

USS (also do liver biochem and viral markers)
If USS is normal - do viral markers. If positive then treat hepatitis.
If USS and viral markers are negative - re-check drug history, autoantibodies test and possible biopsy

If USS shows infiltration, tumour or mets - do liver biopsy

If USS shows CBD dilatation - treat gallstones if found or if other biliary obstruction then do MRCP

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17
Q

Way to approach jaundice in a young patient with risk factors for hepatitis

A 
Viral markers (liver biochem) 
If negative then do USS - treat same as in elderly with CBD dilatation or nothing on USS - autoantibodies and recheck drug history

If viral markers positive then treat hepatitis

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18
Q

Liver biochemistry high in obstructive liver disease

A

ALP and ggt

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19
Q

Liver biochemistry high in hepatitis

A

AST and ALT

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20
Q

Definition of hepatitis

A

Inflammation (swelling) of the liver

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21
Q

Why do you get dark urine in jaundice?

A

Pumps in small bile ducts are defective in the liver disease which cause jaundice
Conjugation is easily done - therefore this continues even in damaged liver
For bilirubin to appear in urine it must be conjugated because unconjugated bilirubin is bound to albumin which is not secreted in the urine
When small bile duct pumps are damaged, bilirubin passes into the bloodstream and then gets cleared by the kidneys in the urine - this can also happen if obstructive

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22
Q

Which viruses can cause viral hepatitis?

A

CMV, EMV, Hep A-E

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23
Q

Which virus is CMV?

A

Herpes virus 5 - DNA virus

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24
Q

How many people infected by CMV in UK?

A

90% by age of 16 - lifelong infection

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25
Q

Presentation of CMV infection?

A

Often asymptomatic in immunocompetent
Can get glandular fever type symptoms with mild hepatitis (deranged LFTs)

More dangerous in infants or immunosuppressed

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26
Q

What do IgG and IgM mean on serology?

A

IgG - infection has occured

IgM - recent infection or reactivation

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27
Q

Which virus is EBV?

A

Herpes virus 4 - DNA virus lifelong infection

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28
Q

Proportion of EBV infection?

A

50% of 5 year olds and 90% of adults

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29
Q

Presentation of EBV infection?

A

Immunocompetent - glandular fever illness - on first infection

Immunosuppressed
- PUO - post transplant lymphoproliferative

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30
Q

What cancers are EBV associated with?

A

Burkitt’s lymphoma, Hodgkin’s lymphoma, nasopharyngeal carcinoma, oral hairy leukoplakia in HIV

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31
Q

Hep A transmission and incubation period

A

Faecal oral or shellfish, 15-50 days

Once showing symptoms - no longer infective

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32
Q

Presentation of Hep A infection

A

Usually children get it, asymptomatic, build up immunity and not come back

In adult, very bad presentation of fever, malaise, anorexia, nausea - followed by jaundice, hepatosplenomegaly and adenopathy

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33
Q

Tests in Hep A infection

A

AST and ALT rise 22-40 days after exposure and ALT very high >100

Will return to normal over 5-20 weeks

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34
Q

Mortality with Hep A

A

Low

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35
Q

Treatment of Hep A

A

Supportive, avoid alcohol

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36
Q

Vaccination Post exposure prevention in Hep A

A

HAV vaccine (Havrix monodose) given if travelling to endemic areas and for people with chronic liver disease, haemophilia or those who work in contact with people with hep a

Vaccinate someone if within 2 weeks of exposure

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37
Q

Hep B number of deaths per year

A

1 million

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38
Q

Where is Hep B endemic?

A

Far east, africa and mediterranean

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39
Q

Incubation period for Hep B

A

1-6months

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40
Q

Transmission of Hep B

A

IVDU, tattoos, sex, blood exposure (transfusions)

Mother to child and child to child transmission is most common cause of it in endemic areas

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41
Q

Acute hep B presentation

A

Similar to hep a - nausea, anorexia, fever, malaise
- Most people get unwell, ALT rise, jaundice and body fights within 6 weeks

Will remain okay unless immunosuppressed

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42
Q

Chronic Hep B pathology and presentation

A

Have infection (can be mild or symptomatic initial infection) but body doesn’t clear it

As you get older body will recognise virus and try and fight it
Get infection and fibrosis and vicious circle

Therefore it is not cytopathic but immune response causes damage

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43
Q

Consequences of Hep B

A

Directly oncogenic - HCC - 80% of all HCC in Asian Americans

Also causes cirrhosis and liver disease

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44
Q

How infectious is Hep B?

A

50-100x more infectious than HIV

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45
Q

Hep B markers

A

HbsAg - Hep B surface antigen - diagnostic test - present 1-6months after exposure and >6 months is carrier status

E antigen - AbeAG - virus makes it, does nothing to human host but implies they are very infective

Hep B DNA and viral load - another indication of infectivity

Surface antibodies - show that person has been shown antibody and built up immunity

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46
Q

Chance of reactivation of Hep B

A

If chemotherapy - will reactive
Also with steroids
Risk continues 6 months post-treatment

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47
Q

Treatment of Chronic Hep B - if liver damage

A

Interferon for a year - increase immune control

Tenofovir/entecavir - viral control - may be needed life long

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48
Q

Places Hep C most prevelant

A

North Africa, Central Asia and Middle East

Egypt and Pakistan have epidemics because of poor vaccination programs

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49
Q

Transmission of Hep C

A

Blood bourne therefore percutaneous exposure

IVDU, unsafe vaccination, tattoos

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50
Q

Presentation of Hep C virus

A

Most do not get symptoms (similar to HAV and HBV)- if they do it means clearing it

85% develop chronic hepatitis

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51
Q

Risk with Hep C

A

25% get cirrhosis and 4% get HCC

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52
Q

Tests in Hep C

A

LFT changes with cirrhosis - exclusion of other viruses

Anti-HCV antibodies confirms exposure - usually positive 8 weeks from infection

HCV RNA can be detected 1-8 weeks after infection on HCV-RNA PCR

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53
Q

Treatment of Hep C virus

A

Stop alcohol
Interferon
Sofosbuvir - RNA polymerase inhibitor
Lots of new drugs coming out

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54
Q

Features of Hep A and E infection

A

faecal-oral transmission

don’t really get chronic phase - unless immunocompromised and then you can

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55
Q

Hep D virus features

A

Small RNA virus - requires Hep B to replicate

Co-infection - two at the same time, clinically indistinguishable from acute HBV infection

Superinfection if you get the two at the same time - acute flare up of Hep B

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56
Q

Hep D transmission

A

Blood bourne therefore mostly IVDU in Uk but can affect any at risk of Hep B

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57
Q

Chronicity of Hep D

A

Relatively infrequent but spontaneous resolution is rare - most develop cirrhosis more rapidly than with Hep B alone

in 15% rapidly progressive to cirrhosis

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58
Q

Treatment for Hep B patients with active liver disease

A

Detected from raised ALT or inflammation on biopsy

Given interferon and adefovir

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59
Q

Hep E virus features

A

RNA virus causing hepatitis clinically very similar to hep A

Enterally transmitted usually by infected water

Endemics in many developing countries and some developed countries where patients had contact with farm animals

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60
Q

Other viral hepatitis with liver failure but more with liver abnormalities

A

Malaria, dengue, yellow fever

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61
Q

Infections with deranged LFTs

A

Avian flu
Q fever, legionella, mycoplasma

Leptospirosis
Rickettsial illness

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62
Q

Female to male ratio of autoimmune hepatitis

A

F:M = 4:1

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63
Q

Presentation age of autoimmune hepatitis

A

Bimodal - 10-30 years and post-menopausal

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64
Q

Presentation of autoimmune hepatitis in young population - teens and early 20s

A

Acute hepatitis with jaundice and very high ALT and AST

  • Clinical features of cirrhosis with hepatosplenomegaly, acne, hirsutes, bruises and sometimes ascites

Can also have features of autoimmune disease

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65
Q

Presentation in peri/post-menopausal group

A

Asymptomatic and found over liver biochemistry
Or because of fatigue
Or because of signs of chronic liver disease on routine examination

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66
Q

Biochemical findings on autoimmune hep

A

ALT and AST raised - lesser elevations in ALP and bilirubin

IgG high

Normochromic, normocytic anaemia with thrombocytopenia and leucopenia

Even before portal hypertension and splenomegaly

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67
Q

Two types of autoimmune hepatitis

A 
AH1 = Type 1 with antibodies - 80% 
- Anti-nuclear antibody (ANA)
- Anti-smooth muscle (ASMA)
- Soluble liver antigen (SLA)
- More common in women and adults
Good response to immunosuppression

AH2 - more common in children - europe >usa
LKM-1 +ve (anti-liver kidney microsomal type 1 antibodies)
ANA and ASMA -ve
More commonly progresses to cirrhosis and less treatable

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68
Q

Management of autoimmune hep

A

Immunosuppression treatment

Budesonide fewer side effects than prednisolone and now favoured

OR

Prednisolone - 30mg/day for 1 month
then slowly decrease it to a maintenance dose of 5-10
Can be stopped after 2 years but relapse common

Azothioprine - steroid sparing

Liver transplantation if really bad

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69
Q

Most common cause of cirrhosis in the west and worldwide?

A 
West = alcohol 
Worldwide = viral infection
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70
Q

What are the characteristic pathological features of cirrhosis?

A

Regenerating nodules of inflammation, necrosis and fibrosis.
Nodules separated by fibrous septa and loss of normal lobular architecture within the nodules

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71
Q

What are the two types of cirrhosis which have been described?

A

Micronodular cirrhosis - regenerating nodules usually

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72
Q

What level of albumin is considered to be associated with poor outcome?

A
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73
Q

Liver biochem in compensated not very severe cirrhosis and in decompensated cirrhosis

A

If not very severe can be normal but usually at least a slight elevation in serum ALP and ALT, AST

In decompensated cirrhosis - all biochemistry is deranged

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74
Q

What serum creatinine is associated with worse prognosis?

A

> 130umol/L

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75
Q

What is scoring system in cirrhosis?

A

Child-Pugh classification

Grade A 10

Risk of variceal bleeding much higher if >8

Bilirubin
50 = 3 points

Albumin
- >35 = 1 point
- 28-35 = 2 points
-

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76
Q

When is endoscopy indicated in cirrhosis?

A

Detection and treatment of varices and portal hypertension gastropathy

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77
Q

Monitoring in patients with decompensated cirrhosis

A

6 monthly ultrasound to detect early development of HCC

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78
Q

Management of a patient with compensated cirrhosis

A 
Restrict salt intake 
Avoid aspirin and NSAIDs 
Avoid alcohol (although if not due to alcohol or viral hep then can be had in small amounts)
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79
Q

Indications for liver transplant general

A

Patients with fulminant hepatic failure
Chronic liver disease - cirrhosis no longer responsive to therapy
All with Child grade C should be referred to transplant clinic

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80
Q

Indications for liver transplant - PBC

A

Serum bilirubin persistently >100umol/l

Or intolerable symptoms eg. itching

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81
Q

Indications for liver transplant Chronic Hep B

A

If HBV DNA negative or levels falling under therapy

Prevent recurrence with hep B immunoglobulin and nucleoside analogues

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82
Q

Indications for liver transplant Chronic Hep C

A

Most common indication for transplant

Reinfection and cirrhosis occurs in 10-20% at 5 years - can give antivirals to delay progression

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83
Q

Indications for liver transplant autoimmune hepatitis

A

Failed to respond to medical therapy or major side-effects of corticosteroid therapy
Can reoccur

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84
Q

Indications for liver transplant - alcoholic liver disease

A

Well-motivated patients who have stopped drinking

85
Q

Contraindications for liver transplant

A 
Patients with active sepsis outside hepatobiliary tree 
Malignancy outside liver 
Liver mets 
Not psychologically committed 
Age >70 not usually transplanted 
HCC recurrence rate is high unless
86
Q

Rejection in liver transplantation

A

Acute/cellular rejection - usually seen 5-10 days post transplant . Can be asymptomatic or can be a fever. Responds to immunosuppresive therapy

Chronic ductopenic rejection - seen 6 weeks-9 months post-transplant, disappearing bile ducts (vanishing bile duct syndrome) and an arteriopathy with narrowing and occlusion of arteries. Early may be reversed with immunosuppression but often requires retransplantation

87
Q

Prognosis with liver transplantation

A

Require lifelong immunosuppression

90% 1 year survival
70-85% 5 year

Most disease recurrence in HCV cirrhosis, PSC and HCC

88
Q

Main sites of collaterals following portal hypertension? (and cause)

A

Venous system dilates following increase in portal pressure - collaterals occur within the systemic venous system

Gastro-oesophageal junction - most likely to give symptoms
Rectum
Left renal vein
Diaphragm
Retroperitoneum
Anterior abdominal wall via umbilical vein - caput medusae

89
Q

Cause of prehepatic portal hypertension?

A

Portal vein thrombosis - cause often unidentified but some due to congenital/inherited defects - eg. prothrombotic conditions

90
Q

Intrahepatic causes of portal hypertension?

A

Usually cirrhosis
Schistosomiasis
Other rarer causes exist

91
Q

Post-hepatic causes of portal hypertension

A

Budd-Chiari syndrome

Prolonged severe heart failure

92
Q

Clinical presentation of portal hypertension

A

Features of chronic liver disease
Splenomegaly
Often asymptomatic
Variceal haemorrhage

93
Q

Occurrence of variceal haemorrhage

A

90% of cirrhosis patients get gastro-oesophageal varices over 10 years - but only 1/3 will bleed from them

94
Q

Management of acute active bleeding episode in variceal bleeding

A

Resus - IV line for bloods, restore blood volume with plasma expander or blood transfusion
Only target HB of 80g/l

Ascitic tap

Monitor alcohol withdrawal - thiamine

Start prophylactic ab’s - cephalosporins eg. cefotaxime - treat and prevent infection and early rebleeding - reduce mortality

Send for urgent endoscopy to confirm diagnosis - banding or injection sclerotherapy

Give vasoconstrictor therapy - restrict portal inflow by splanchnic arterial constriction Terlipressin or somatostatin if first is contraindicated

95
Q

Two options for stopping bleeding with endoscopy

A

Variceal banding - Band on tip of endoscope - suck varix in and then put band on

Scleropathy - inject varices with sclerosing agent

96
Q

Two other therapies to control bleeding if banding/sclerosing is ineffective

A

Balloon tamponade or stenting

97
Q

What to do if variceal bleeding can’t be stopped or early rebleeding occurs within 5 days

A

Transjugular intrahepatic portocaval shunt (TIPS)

Guidewire passed from portal vein to hepatic vein - total shunt past the liver - therefore reduces pressure

98
Q

Long-term management of variceal bleeding

A

Beta-blockade - non-selective - propanolol

Should also be given to patients who have not bled but have cirrhosis and varices - do not prevent development of varices but prevents bleeding

Repeated courses of banding at 2 week intervals -obliterates varices (30-40% return per year therefore follow-up needed)

99
Q

3 factors involved in ascites pathogenesis

A

1) Sodium and water retention - peripheral vasodilatation by nitric oxide, ANP and prostaglandins = activates sympathetic nervous system and renin-angiotensin system therefore sodium and water retention promoted
2) Portal hypertension - exerts local hydrostatic pressure - increased hepatic and splanchnic production of lymph and transudation of fluid into peritoneal cavity
3) Low serum albumin - reduction in plasma oncotic pressure - draws water out into abdomen

100
Q

3 things as a result of accumulating fluid

A

1) Shifting dullness
2) Peripheral oedema
3) Pleural effusion - passage of ascitic fluid through congenital diaphragmatic defects

101
Q

What would be found on ascites fluid aspirate if spontaneous bacterial peritonitus?

A

Neutrophil count >250 cells/mm3

102
Q

Target of management in ascites?

A

Reduce sodium intake and increase renal excretion of sodium
This should produce net reabsorption of fluid from ascites into circulating volume

Maximum mobilisation of ascites is 500-700ml in 24hour

103
Q

Management of ascites?

A

Monitor fluid chart
Restrict dietary sodium to 40mmol in 24hour - maintain protein intake

Stop drugs which contain sodium (antacids, antibiotics, effervescent tablets)

Avoid sodium retaining drugs - NSAIDs and corticosteroids

Diuretic - spironolactone - 100mg daily

If response poor - can increase spironolactone up to 400mg daily
Can also add furosemide

104
Q

Non-medical management of ascites? x2

A

1) Paracentesis - no more than >5l removal because can cause hypovolaemia and renal dysfunction

Can overcome hypovolaemia but infusing albumin - 8g/l of ascitic fluid removed

2) Shunts - TIPD for resistant ascites - if no encephalopathy and minimal disturbance of renal function

105
Q

Features of spontaenous bacterial peritonitis in ascites? Presentation and treatment

A

Complication of ascites with cirrhosis
Occurs in approx 8%
Pain and pyrexia frequently absent but suspect in ascites patient who clinically deteriorates

Treat with cephalosporin, eg. cefotaxime, ceftazidime

106
Q

What is the chronic neuropsychiatric syndrome secondary to cirrhosis and why does it occur?

A

Portosystemic encephalopathy
Occurs due to shunting - either due to collaterals from portal hypertension or in patients with TIPS
This increases circulating levels of toxic metabolites such as ammonia, FFAs, amino acids, false neurotransmitters

Alters brain neurotransmitter balance

107
Q

Presentation of PSE - acutely

A

Acute onset often has precipitating factor (high dietary protein, GI haemorrhage, constipation, infection, TIPS, drugs, development of HCC ) patient becomes increasingly drowsy and comatose

108
Q

Presentation of PSE - chronically

A

Disorder of mood, personality and intellect
N+v, weakness

Signs: - fetor, flap, apraxia, decreased mental function

109
Q

Diagnosis of PSE

A

Clinical

110
Q

Management of PSE

A

Remove precipitating cause
Lactulose and enemas to empty bowel of nitrogenous substances
Maintain nutrition - do not restrict protein for >48hour
Antibiotics - rifaximin (metronidazole in acute setting)
Stop/reduce diuretic therapy
Increase protein in diet to the limit of tolerance as encephalopathy improves

111
Q

When do you get hepatorenal syndrome? What sort of renal failure is it?

A

In patients with advanced cirrhosis, portal hypertension with jaundice and ascites

Functional renal failure - decreased renal output and low sodium concentration

112
Q

Mechanism of hepatorenal syndrome

A

Similar to that of ascites
Peripheral vasodilatation activates homestatic mechanisms (symp NS and renin-angiotensin)
Cause sodium and water retention

There is also a decreased CO inappropriate to degree of vasodilatation

113
Q

2 Pulmonary manifestations in cirrhosis

A

1) Hepatopulmonary syndrome - hypoxaemia occuring in patients with advanced liver disease - due to intrapulmonary dilatation
Normally no resp symptoms but cyanosis - low saturation of arterial blood - can become breathless on standing

2) Porto-pulmonary hypertension - pulmonary hypertension secondary to portal hypertension - occurs in 1-2% of patients

114
Q

What happens in Primary Biliary Cirrhosis?

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation
This causes cholestasis
Can also lead to fibrosis, cirrhosis and portal hypertension

115
Q

Prevalence of PBC

A

F:M = 9:1
Age range usually 40-50 years at presentation
7/100,000

116
Q

What causes PBC?

A

Genetic predisposition but also unknown environmental triggers

Antimitochondrial antibodies (AMA) - M2 is specific to PBC

117
Q

Clinical features of PBC?

A

Often asymptomatic and discovered on routine examination or screening

Pruritus and fatigue often precede jaundice by a few years

Hepatomegaly will be present by the time jaundice appears

Signs of high cholesterol can also be seen

118
Q

Tests in PBC

A

Mitochondrial antibodies seen in 95% -M2 specific

ALP raised may be only liver biochem abnormality originally

High serum immunoglobulins - IgM and cholesterol

Low albumin and high bilirubin

Ultrasound

Liver biopsy not needed but would show histological features of a portal tract infiltrate

119
Q

DDX of PBC

A

Autoimmune hepatitis

Extrahepatic biliary obstruction

Schistosomiasis

120
Q

Treatment of PBC

A

Ursodeoxycholic acid/Ursodiol - improves bilirubin and ALT + AST values but no symptomatic improvement

Vitamin supplementation of fat soluble vitamins - A, D, E, K

Cholestyramine for pruritus
Naltrexone and rifampicin may help pruritus

Liver transplant

121
Q

What is Primary sclerosing cholangitis? PSC

A

Chronic cholestatic liver disease characterised by fibrosing inflammatory destruction of both the intra- and extrahepatic bile ducts

122
Q

What is PSC associated with?

A

IBD - usually UC - in 75% of patients

PSC can predate onset of UC

123
Q

PSC more common in women or men?

A

Men

124
Q

PSC age of onset

A

40 years

125
Q

Presentation of PSC

A

Increasing frequency of being found incidentally in screening of UC patients

Pruritus, fatigue, jaundice
Can also get cholangitis

126
Q

Diagnosis of PSC

A

Can be made with MRCP

127
Q

Tests in PSC

A

ALP raised, then bilirubin raised
AMA -ve
But may be ANA, SMA, ANCA +ve

128
Q

Treatment of PSC

A

Only proven treatment is liver transplant

Colestryramine might help pruritus

Treat cholangitis with antibiotics

129
Q

When does secondary biliary cirrhosis occur?

A

Cirrhosis can occur after prolonged duct obstruction - bile duct strictures, gall stones and sclerosing cholangitis

130
Q

Increased risks associated with PSC?

A

Bile duct, gall bladder, liver and colon cancers are all more common
Therefore yearly screening needed

Cholangiocarcinoma - occurs in 15%

131
Q

What is hereditary haemochromatosis?

A

Inherited disorder of iron metabolism which results in excess deposition of iron in liver and pancreas

Also in joints, heart, pituitary, adrenals and skin

132
Q

What causes hereditary haemochromatosis?- pathologically

A

HFE gene - interacts with receptor in intestine - transferrin receptor 1 - which mediates iron absorption

Also alters hepcidin protein - synthesised in the liver which controls iron absorption from gut. Increased in iron deficient states and vice versa.

Altered expression of this gene results in iron overload

Iron in liver causes fibrosis

133
Q

Difference between men and women in HH?

A

Men present earlier with more overt disease - likely women protected by menstrual loss of iron

134
Q

Prevalence of HH

A

Carrier rate of 1 in 10

Homozygosity = 1 in 200-400

135
Q

Early presentation of HH

A

Nil or tiredness + arthralgia

136
Q

Triad of severe HH presentation

A

Bronze skin pigmentation (melanin deposition), hepatomegaly and DM

137
Q

Other HH symptoms

A

Pit dysfunction - hypogonadism
Heart - arrhythmia’s and HF
Arthropathy

138
Q

Complications of HH

A

30% develop HCC

139
Q

Tests in HH

A

LFTs often normal even with severe disease

Serum iron raised
Serum ferritin raised
Transferrin saturation >45%

High glucose (DM)

Imaging - joint deposition & MRI - iron overload

Liver biopsy

140
Q

Management of HH

A

Venesection (removal of blood) needed for life every 2-3months

If can’t have venesection (anaemia, severe cardiac disease) can give deferoxamine - iron chelator

Low iron diet
Tea, coffee or red wine with meals helps decrease iron absorption (fruit juice or white wine - increase absorption)

141
Q

What is Wilson’s disease?

A

Very rare inborn error of copper metabolism resulting in copper deposition in various organs (liver, basal ganglia)

Normally copper incorporated into apocaeruloplasmin forming caeruloplasmin - this then secreted into blood, rest excreted in faeces and bile

This incorporation doesn’t happen leading to decreased serum caeruloplasmin

But precise cause of copper deposition unclear

142
Q

Presentation of Wilson’s disease

A

Children - hepatic problems
Young adults - more neurological problems - of basal ganglia - tremor, involuntary movements

Kayser-Fleischer rings - copper deposition in corneal membrane

143
Q

Tests in Wilson’s disease

A

Serum copper and caeruloplasmin usually reduced but can be normal

Urinary copper increased usually

Liver biopsy - high copper levels

144
Q

Treatment of Wilson’s disease

A

Lifetime treatment with penicillamine - chelating copper
1-1.5g daily

Monitor urine copper

145
Q

What are the three pathological causes of the changes seen in alcoholic liver disease?

A

1) Acetaldehyde (breakdown product of alcohol) cannot be broken down due to ALDH saturation - powerful chemical agent - leads to production of neo-antigens on hepatocyte cell surface - immune-mediated hepatocyte killing
2) Increased NADH/NAD ratio - increased fatty acid synthesis & decreased fatty acid oxidation therefore hepatic accumulation of fatty acids
3) Impaired oxidation-reduction also impair carb and protein metabolism - cause necrosis of hepatocytes - tumour necrosis factor release leads to release of reactive oxygen species - tissue injury and fibrosis

146
Q

4 stages of liver damage in alcoholic liver disease

A

1) Big liver - cell hypertrophy due to increase demand on liver

2) Fatty liver - Cells can become swollen with fat = steatosis
No liver cell damage yet, fat disappears if stop alcohol

3) Alcoholic hepatitis - leukocyte infiltration and hepatocyte necrosis. Can see Mallory Bodies sometimes
4) Alcoholic cirrhosis - classically micronodular regeneration - continued necrosis

147
Q

Clinical features of fatty liver

A

Often no symptoms or signs

Can have hepatomegaly and some other features of chronic liver disease

148
Q

Clinical features of alcoholic hepatitis

A

Mild-moderate symptoms of ill-health
Occasionally mild jaundice
Chronic liver disease signs
Liver biochem deranged

Can get jaundice and ascites if patient gets ill - abdominal pain and fever also

149
Q

Clinical features of alcoholic cirrhosis

A

Final stage of liver disease but can be quite well

Usually signs of chronic liver disease and other alcoholic systemic features

150
Q

Diagnosis of alcoholic hepatitis and cirrhosis

A

Biopsy

151
Q

Investigations in fatty liver

A

MCV elevated often indicates heavy drinking
Liver biochem mild abnormalities
Gamma gt good for recent alcohol
Ultrasound or CT will show fatty infiltration

152
Q

Investigations in alcoholic hepatitis

A

Leucocytosis - markedly deranged LFTs

Raised bilirubin, AST, ALT, ALP, PT

Low serum albumin may be found

153
Q

Management of alcoholic liver disease

A

Stop alcohol
Treat delirium tremens with diazepam
IV thiamine to prevent Wernickes

Bed rest with high protein diet and vitamin supplements (may need to limit dietary protein if encephalopathy)

Steroid therapy might help alcoholic hepatitis

Treat encephalopathy and ascites

154
Q

What is Budd-Chiari syndrome?

A

Obstruction of venous outflow of the liver - occlusion of the hepatic vein

155
Q

Cause of BC syndrome

A

1/3 causes unknown
Can be hypercoagulablity states, thrombophilia, OCP, leukaemia

Compression from tumours (post abdo wall sarcoma, renal or adrenal tumour, HCC)

Hepatic infection

156
Q

Presentation of acute BC syndrome

A

Abdominal pain
Nausea & vomiting
Tender hepatomegaly
Ascites

157
Q

Chronic presentation of BC syndrome

A 
Enlargement of the liver
Mild jaundice
Ascites
Negative hepatojugular reflex
Splenomegaly
158
Q

Investigations in BC syndrome

A

High protein count ascitic fluid

Histology - congestion, haemorrhage, fibrosis and cirrhosis

Ultrasound, CT or MRI will show occlusion and abnormal parenchyma but caudate lobe spared because of independent blood supply and venous drainage

Doppler sonography

159
Q

Treatment of BC syndrome

A

Acute - thrombolytic therapy

Treat ascites

TIPS

Chronic - liver transplant

160
Q

Two types of liver abscess

A

Pyogenic abscess - bacteria

Amoebic abscess - amoeba

161
Q

Previous most common cause of pyogenic liver abscess?

A

Portal pyaemia from intra-abdominal sepsis eg. appendicitis or gut perforations

Now many cases aetiology not known

162
Q

Common cause of pyogenic abscess in elderly?

A

Biliary sepsis

163
Q

Common organism for pyogenic abscess?

A

E.coli
Streptococcus milleri
Bacteroides

Can also be enterococcus faecalis, proteus vulgaris and staph aureus

164
Q

Presentation of pyogenic abscess

A

Some can have malaise lasting months
or

Fever, rigours, anorexia, vomiting, weight loss, and abdominal pain

Patient can be jaundiced and have tender hepatomegaly

165
Q

Investigations in pyogenic abscess

A

Often investigated as PUO
- will have raised ALP as only sign it is liver origin

Bilirubin may be raised

Raised ALP, ESR and CRP

Serum B12 is very high as vitamin B12 is stored in and subsequently released from the liver

Ultrasound and CT useful for diagnosis

166
Q

Management of pyogenic abscess

A

Aspiration and antibiotics

167
Q

Prognosis of pyogenic abscess

A

Depends on nature of pathology
Unilocular abscess better prognosis
Multiple scattered - very high mortality, 1 in 5 survive

168
Q

When should you consider amoebic abscess?

A

Patient travelling from abroad

169
Q

How do amoebic abscess occur?

A

Carried from bowel to liver via portal venous system

170
Q

Presentation of amoebic abscess

A

Fever, anorexia, weight loss and malaise

Often no hx of dysentery

Tender hepatomegaly

171
Q

Investigations for amoebic abscess

A

Same as pyogenic - bloods (ALP, CRP and ESR raised) serum B12 raised, ultrasound and CT

Serological tests for amoeba - always positive

172
Q

Treatment of amoebic abscess

A

Metronidazole 800mg 3x day for 10 days

Aspiration in patients who fail to respond and large abscess

173
Q

Complications of amoebic abscess

A

Rupture, secondary infection and septicaemia

174
Q

What is the most common liver tumour?

A

Secondary metastatic tumour

175
Q

Where to metastatic liver tumours usually come from?

A

GIT, breast, bronchus

176
Q

Clinical presentation of liver mets

A

Weight loss & malaise
Upper abdominal pain
Hepatomegaly
+/- jaundice

177
Q

Diagnosis of liver mets

A

Ultrasound
CT or MRI (look for primary)
ALP usually always raised

178
Q

Treatment of liver mets

A

Depends on site and burden of liver mets

Chemotherapy or radiofrequency ablation of tumours

179
Q

Are primary liver tumours usually benign or malignant?

A

Malignant

180
Q

Prevalence of HCC

A

5th most common cancer worldwide

M>F

181
Q

Risk of HCC

A

Cirrhosis in 95% of cases of HCC

HBV, HCV (risk higher with HCV than HBV - even higher with both)

Cirrhosis of other cause - alcohol, non-alcoholic fatty liver disease, haemochromatosis

182
Q

Pathology of HCC

A

Can be single or multiple nodules throughout liver

183
Q

Where does HCC metastasise to?

A

Lymph nodes, bones and lungs

184
Q

Clinical features of HCC

A 
Weight loss
Anorexia 
Fever 
RUQ pain 
Ascites

Enlarged irregular tender liver may be felt

185
Q

Investigations in HCC

A

Serum alpha-fetoprotein may be raised (normal in 1/3)
Ultrasound
CT and MRI

Tumour biopsy

186
Q

Treatment of HCC

A

Resection of isolated lesions

187
Q

What is a cholangiocarcinoma?

A

Cancer of mutated epithelial cells of bile ducts

Can be intra or extrahepatic

188
Q

Associations of cholangiocarcinoma

A

Not associated with cirrhosis or Hep B

189
Q

Presentation of cholangiocarcinoma

A

Similar to HCC - malaise, weight loss, RUQ pain, ascites

But also jaundice and cholangitis is more frequent

190
Q

Prognosis of cholangiocarcinoma

A

Resection is rarely possible

Patients usually die within 6 months

191
Q

Most common benign liver tumour

A

Haemangioma - of endothelial cells which line blood vessels

Usually small and single but can be large and multiple

Usually discovered incidentally on ultrasound, CT or MRI

Require no treatment

192
Q

What causes increased risk of hepatic adenoma? Features and management

A

OCP

Present with abdominal pain or intraperitoneal bleeding

Resection for symptomatic patients, tumours >5cm or when stopping OCP doesn’t make it shrink

193
Q

Prevalence of gallstones

A

Can be present at any age, unusual before 30’s
Increase prevalence with age
60-70s = 25-30%
90% remain asymptomatic

F>M

194
Q

3 different types of gallstones

A

1) Cholesterol - 80% of those in western world
- Risk factor is age and obesity
- Usually large and solitary

2) Pigment stones

195
Q

What is biliary colic?

A

Pain from temporary obstruction of cystic or CBD by a stone

Despite term “colic” - is severe but constant - crescendo characteristic

196
Q

Symptoms of biliary colic?

A

Most common mid-evening lasting until early hours of morning

Usually epigastrium pain originally, may be RUQ
Radiation may go over right shoulder or to right sub-scapular region

N+V frequent with severe attacks

Cessation after several hours or with opiate analgesia

197
Q

What causes acute cholecystitis?

A

Obstruction to gall bladder emptying, increased gall bladder glandular secretion and progressive distension

Inflammatory response to retained bile within the gall bladder

198
Q

Presentation of acute cholecystitis?

A

Initially similar to biliary colic

Progresses to severe localised RUQ pain, tenderness and muscle guarding/rigidity

199
Q

Complications of cholecystitis

A

Gall bladder can become distended with pus = empyema

Rarely an acute gangrenous cholecystitis develops - can perforate causing generalised peritonitis

200
Q

Investigations in acute cholecystitis

A

Moderate leucocytosis and raised inflammatory markers

ALP and bilirubin raised

Abdominal USS - most useful investigation (can see gallstones and thickening of gall bladder wall)

201
Q

DDX of biliary colic

A 
IBS with hepatic flexure spasm 
Carcinoma of right side of colon 
Peptic ulcer disease - atypical 
Renal Colic 
Pancreatitis
202
Q

DDX of acute cholecystitis

A

Pancreatitis
Perforated peptic ulceration
Intrahepatic ulcer
MI

203
Q

Management of gall bladder stones

A

Cholecystectomy - lap chole

If acute cholecystitis - NBM, IV fluids, opiate analgesia and IV antibiotics - wait for inflammation to settle

If symptoms eg. due to empyema not improving can do radiologically placed gall bladder drain

204
Q

If cholecystectomy is contraindicated

A

Can try stone dissolution - increase bile salt content of bile

Chenodeoxyocholic acid and ursodeoxycholic acid

Will require long-term therapy

205
Q

Features of CBD stones

A

Biliary colic, fever and jaundice - triad only present in a number of patients (with cholangitis)

Usually just pain - sometimes jaundice

206
Q

Investigations in CBD stones

A

Cholangitis - raised neutrophil count and raised ESR, CRP

Complete CBD obstruction - bilirubin >200, raised ALP and gamma gt

AST and ALT mildly raised, may be more if complete obstruction

Amylase high if stone related pancreatitis

207
Q

Imaging for CBD stones

A

Ultrasound, CT, Endoscopic ultrasound scanning

208
Q

Management of acute cholangitis

A

High mortality and morbidity especially for elderly

IV antibiotics and urgent bile drainage

Sphincterotomy + ERCP

Lap chole with exploration of CBD to remove stones

Gastroenterology (5 decks)

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