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Phase 2a > Liver > Flashcards

Liver Flashcards

1
Q

What are five main functions of the liver?

A

Albumin and clotting factor production, bilirubin metabolism, drug metabolism, detoxification, storage of vitamins/metals.

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2
Q

What two broad categories are measures of liver function?

A

LFTs and hepatic enzymes.

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3
Q

Which three LFTs are markers of liver function?

A

Bilirubin, albumin and prothrombin time (clotting factors).

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4
Q

What are LFTs if there is liver damage and why?

A

Bilirubin is increased, albumin is decreased and prothrombin time is increased.
-Bilirubin isn’t metabolised so remains in the blood.
-Albumin isn’t produced so there are low levels.
-Clotting factors aren’t produced so prothrombin time is increased.

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5
Q

Which enzymes are related to liver damage?

A

-Aminotransferases - ALT and AST.
-ALP.
-GGT.

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6
Q

Why are aminotransferases high in the blood in liver damage?

A

When hepatocytes are damaged, they leak into the blood.

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7
Q

When is ALP (alkaline phosphate) raised?

A

In biliary tree damage.

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8
Q

What is liver failure?

A

Liver loses it’s ability to repair and regenerate leading to compensation.

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9
Q

What are the types of liver failure?

A

Acute and chronic.

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10
Q

What is acute liver failure?

A

The loss of liver function that occurs quickly (days/weeks) in someone with no previous liver disease.

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11
Q

What is chronic liver failure?

A

Progressive decline in liver function over 6 months in someone with existing liver disease.

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12
Q

What are the three main causes of acute liver failure?

A

Viral (hepatitis, CMV and EBV).
Autoimmune hepatitis.
Paracetamol overdose.

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13
Q

What are the four main causes of chronic liver failure?

A

ALD (mc), NAFLD, viral hepatitis, alcohol.

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14
Q

What are three other causes of chronic liver failure?

A

Autoimmune (PBC, PSC)
Metabolic (haemochromatosis, Wilson’s, A1ATD)
Malignancy.

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15
Q

How does acute liver failure present?

A

Jaundice, nausea, anorexia and malaise.

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16
Q

What are the 12 signs/symptoms of chronic liver failure?

A

Jaundice, pruritus, malaise, anorexia.
Oedema, gynecomastia, clubbing, palmar erythema.
Xanthelasma, spider naevi/caput medusae.
Hepatosplenomegaly and easily bruising/bleeding.

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17
Q

Explain the prognosis of acute liver failure.

A

90% of acute liver failure leads to recovery.
10% leads to fulminant liver failure.

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18
Q

Explain the progression of chronic liver failure.

A

A liver disease either leads to fibrosis and then cirrhosis and eventually liver failure.
-Some will resolve.
-Some will progress to liver failure.

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19
Q

What is ESLD and what is it a risk factor for?

A

End stage liver disease which is decompensated cirrhosis.
Big risk factor for HCC.

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20
Q

What investigations are done for liver failure?

A

LFTs - inc. bilirubin, dec. albumin, inc. INR.
Imaging and microbiology (investigate infections).

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21
Q

How is acute liver failure treated?

A

Acutely with ABCDE, fluid and analgesia.
-Treat the underlying cause and any complications.

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22
Q

What are the five main complications of acute liver failure?

A

Increased ICP, HE, ascites, haemorrhage and sepsis.

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23
Q

What is the gold standard diagnosis for chronic liver disease?

A

Liver biopsy (determines disease extent).

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24
Q

What are two other investigations for chronic liver failure?

A

LFTs and imaging (USS).

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25
Q

What is the main treatment for chronic liver failure?

A

Prevent the progression of the disease by lifestyle modifying (no alcohol, decrease BMI, avoid drugs).
-Manage complications.

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26
Q

When would a liver transplant be considered for chronic liver failure?

A

If decompensated - ESLF.

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27
Q

What is liver cirrhosis?

A

Replacement of hepatocytes with scar tissue as a result of chronic inflammation of the liver.

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28
Q

What are the common causes of liver cirrhosis?

A

ALD, NAFLD, hepatitis B/C.

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29
Q

What are the seven other causes of liver cirrhosis?

A

Autoimmune hepatitis, PBC, PSC, drugs.
Metabolic - Haemochromatosis, Wilson’s, A1ATD.

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30
Q

What are the 9 symptoms of liver cirrhosis?

A

-The same as chronic liver failure:
Jaundice, hepatosplenomegaly, spider naevi, palmar erythema, gynecomastia, bruising, ascites, caput medusae.

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31
Q

What are the investigations for liver cirrhosis?

A

The same as chronic liver failure:

-Liver biopsy, bloods (LFTs), USS/CT/MRI - hepatosplenomegaly.

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32
Q

What is the definitive treatment for liver cirrhosis?

A

Liver transplant.

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33
Q

In someone with liver cirrhosis, what is screened for and how often?

A

HCC every 6 months.

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34
Q

How is liver cirrhosis managed?

A

Conservatively with fluids, analgesia, no alcohol and better diet.
-Manage complications.

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35
Q

What are the five main complications of liver cirrhosis?

A

Ascites, portal hypertension and oesophageal varices, HE, HCC, SBP.

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36
Q

What is alcoholic liver disease?

A

The result from the effects of long term excessive consumption of alcohol on the liver.

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37
Q

What is the most common cause of liver failure?

A

Alcoholic liver disease.

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38
Q

How are alcohol units calculated?

A

Strength (ABV) x volume (ml) divided by 1000.

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39
Q

What are the three main risk factors for alcohol liver disease?

A

Chronic alcohol, obesity and smoking.

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40
Q

Explain the pathophysiology of alcoholic liver disease.

A

Steatosis (undamaged fatty liver) - Alcohol hepatitis (Mallory bodies) - Alcohol cirrhosis (micronodular).

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41
Q

What are the early symptoms of alcoholic liver disease?

A

Asymptomatic.

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42
Q

What are the symptoms of late stage alcoholic liver disease?

A

Chronic liver symptoms and alcohol dependence.

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43
Q

What is a quick screen for harmful alcohol consumption?

A

CAGE questions:

-Cut down? (thought)
-Annoyed? (when others comment)
-Guilty?
-Eye opener? (drink in morning to help nerves).

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44
Q

How is alcoholic liver disease diagnosed?

A

History of heavy drinking:

-LFTs with inc. GGT and AST:ALT ratio >2.
-FBC (raised MCV).
-Biopsy to confirm if ALD or hepatitis.
-CT/MRI.

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45
Q

How is ALD managed conservatively?

A

Stop drinking alcohol permanently, healthy diet, lower BMI, vitamins.

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46
Q

When would liver transplant be considered in someone with ALD?

A

With ESLD and abstinence for 3+ months.

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47
Q

What are 7 complications of drinking too much alcohol?

A

Pancreatitis, HE, Wernicke-Korsakoff syndrome, cirrhosis/HCC, Mallory Weiss tear, ALD and alcohol dependence, alcoholic cardiomyopathy.

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48
Q

If someone has alcohol dependence, what happens if they stop drinking?

A

They will develop withdrawal symptoms.

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49
Q

Describe the stages of alcohol withdrawal and their symptoms.

A

6-12h - Tremor, sweating, headache, craving and anxiety.
12-24h - Hallucinations.
24-48h - Seizures.
24-72h - Delirium tremens.

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50
Q

What is delirium tremens?

A

Medical emergency associated with alcohol withdrawal.

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51
Q

What is the mortality rate of delirium tremens?

A

35%.

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52
Q

Describe the pathophysiology of delirium tremens.

A

Alcohol stimulates GABA receptors, relaxing the brain.
Alcohol inhibits glutamate receptors, further relaxing.
Chronic alcohol use results in GABA system being down-regulated and glutamate system being up-regulated to balance the effects of alcohol.
-When alcohol is removed, GABA under-functions and glutamate over-functions causing extreme excitability in the brain (excess adrenergic activity).

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53
Q

How does delirium tremens present?

A

Neuro - confusion, agitation, delusion/hallucination, ataxia, tremor.
-Tachycardia, hyperthermia, arrhythmias, hypertension.

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54
Q

How is alcohol withdrawal managed?

A

With benzodiazepines and high dose IV B, followed by oral thiamine.

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55
Q

What is not-alcoholic fatty liver disease?

A

Chronic liver disease due to fat deposits in the hepatocytes (not due to alcohol).

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56
Q

What are seven risk factors for NAFLD?

A

Obesity, hypertension, T2DM, drugs, FHx, endocrine disorders, hyperlipidaemia.

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57
Q

What are the stages of NAFLD?

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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58
Q

How does NAFLD present?

A

Typically Asx.
-If very severe, signs of chronic liver failure.

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59
Q

How is NAFLD diagnosed?

A

1st line - Imaging (USS).
Bloods and LFTs.

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60
Q

How is NAFLD treated?

A

Weight loss, exercise, stop smoking, control diabetes, BP and cholesterol, avoid alcohol.

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61
Q

What is hepatitis? What are the different types?

A

Inflammation of the liver.
Can be chronic or acute and viral or autoimmune.

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62
Q

What causes acute hepatitis?

A

-Viral (Hep A-E, herpes viruses etc.).
-Other infection (Bacteria, parasites).
-Autoimmune hep, metabolic.
-Drugs, pregnancy.
-NAFLD.

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63
Q

What causes chronic hepatitis?

A

-Viral hepatitis.
-Drugs, autoimmune hep, metabolic.
-NAFLD.

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64
Q

Describe the hepatitis A infection.

A

Acute and mild, self limiting with no chronic disease.
-100% immunity after infection.

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65
Q

Does hepatitis A cause fulminant liver failure?

A

Very rarely.

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66
Q

How is hepatitis A spread?

A

Faeco-oral spread, associated with contaminated food and water

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67
Q

What are the three main risk factors for hepatitis A?

A

Overcrowding, poor saturation, exotic travel (Africa).

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68
Q

How does hepatitis A usually present?

A

Usually symptomatic:
-Malaise, fever, N+V, jaundice.

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69
Q

How is hepatitis A diagnosed?

A

Bloods - leukopenia and increased ESR.
LFTs - Increased bilirubin.
HAV serology (anti-HAV antibodies IgM and IgG).

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70
Q

What is the management for hepatitis A?

A

Supportive treatment:
-Monitor LFTs.
-Travel vaccine (primary prevention).

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71
Q

Describe the genetics of the hepatitis A virus.

A

RNA virus.

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72
Q

Describe the genetics of the hepatitis B virus.

A

DNA virus.

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73
Q

Describe the hepatitis B infection.

A

Acute and chronic virus that is blood borne.

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74
Q

How is hepatitis B spread?

A

Via blood and body fluids:
-Vertical transmission.
-Needles.
-Sexually.
-Contaminated household.

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75
Q

What are the risk factors for hepatitis B infection?

A

IVDU, gay sex, healthcare workers.

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76
Q

Describe the progression of hepatitis B infection.

A

Most people fully recover within two months.
10% becomes chronic hepatitis B carriers which can lead to cirrhosis, liver failure and risk of HCC.

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77
Q

How is hepatitis B prevented?

A

Vaccination.

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78
Q

Which antibodies is tested for in HepB screening?

A

HBcAb (core antibody) for previous infection.
HBsAb (surface antibody) for current infection.

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79
Q

If hepatitis B screening is positive, what is further tested?

A

-HBeAg (antigen) that implies infectiousness/viral replication.
-HBV DNA (DNA) which counts direct viral load.

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80
Q

What is given in a hepatitis B vaccine?

A

HBsAg is given in the vaccine.

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81
Q

What does presence of HbsAb in the blood imply?

A

An immune response against HbsAg so vaccination or previous/current infection.

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82
Q

What marker of Hepatitis B can be helpful in distinguishing the level of infection?

A

HbcAb (core antibodies):

-IgM of it implies current infection.
-IgG of it implies past infection (when HbsAg is negative).

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83
Q

What does positive HBeAg mean in a hepatitis B infection?

A

Implies the patient is in the acute phase of the infection and the virus is replicating.

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84
Q

In hepatitis B, what does negative HBeAg and positive HBeAb signify?

A

The active phase has stopped, the virus has stopped replicating.
-Less infectious.

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85
Q

In Hepatitis B serology, what is the marker for an active infection?

A

HBsAg (surface antigen).

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86
Q

In hepatitis B serology, what implies vaccination or past infection?

A

HBsAb (surface antibody).

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87
Q

In hepatitis B serology, what is a marker of viral replication and a marker for infectivity?

A

HBeAg (E antigen).

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88
Q

In hepatitis B serology, what signifies the active phase is finished?

A

HBeAb (E antibody).

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89
Q

In hepatitis B serology, what signifies past and current infection?

A

HBcAb (core antibodies).
-IgM is active.
-IgG is past.

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90
Q

In hepatitis B serology, what is a markers of direct viral load?

A

HBV DNA.

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91
Q

What are the investigations for hepatitis B?

A

LFTs and serology.

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92
Q

How is hepatitis B managed?

A

Vaccine is available.
Antivirals if needed.
-Improve diet and lifestyle.
-Treat complications.

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93
Q

Describe the hepatitis D infection.

A

Acute and chronic, blood borne RNA virus which can only survive if someone is infected with Hepatitis B.

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94
Q

Why does hepatitis D only survive if a patient is already infected with hepatitis B?

A

It attaches to HBsAg and uses HBV to replicate.

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95
Q

How common is hepatitis D in the UK?

A

Very low rates.

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96
Q

What are the complications of hepatitis D?

A

Will make hepatitis B infection worse and increase the chances of cirrhosis.

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97
Q

How is hepatitis D treated?

A

No specific treatment.

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98
Q

Describe the hepatitis C virus/infection.

A

Acute and chronic blood borne RNA virus.

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99
Q

Is there a vaccine available for hepatitis C?

A

No.

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100
Q

What is the most common hepatitis virus in the UK?

A

Hepatitis C.

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101
Q

How is hepatitis C spread?

A

Blood borne - IVDU, vertical transmission, sex.

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102
Q

Describe the prognosis of hepatitis C.

A

25% make a recovery.
75% progress to liver cirrhosis and can turn into HCC.

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103
Q

How is hepatitis C diagnosed?

A

LFTs and serology:
-HCV antibody.
-HCV RNA.

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104
Q

What is the management for hepatitis C?

A

Treated with directly acting antivirals.
-Improve lifestyle.
-Treat complications.

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105
Q

Is hepatitis E common in the UK?

A

No, very rare.

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106
Q

Describe hepatitis E.

A

RNA virus spread via the faeco-oral route.

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107
Q

How severe is hepatitis E? Does it need treatment?

A

Not severe, only producing a mild illness which can be asymptomatic.
-No treatment required.
-No vaccine.

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108
Q

How often does hepatitis E progress to chronic liver disease?

A

Tends to only be in those who are immunocompromised.

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109
Q

Which hepatitis infections are notifiable diseases?

A

All of them.

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110
Q

Compare all viral hepatitis infections.

A

A - RNA, faeco-oral. 100% immunity,
B - DNA, blood-borne. 10% fulminant liver failure.
C - RNA, blood-borne. 75% fulminant liver failure.
D - RNA, blood-borne. Binds to HBVsAg to survive.
E - RNA, faeco-oral. 100% immunity.

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111
Q

What is autoimmune hepatitis?

A

A T-cell mediated response against hepatocytes which results in chronic hepatitis.

112
Q

What causes autoimmune hepatitis?

A

No clear cause, thought to be genetic predisposition and triggered by viral infection.

113
Q

How rare is autoimmune hepatitis?

A

Very rare cause of chronic hepatitis.

114
Q

What are the four risk factors for autoimmune hepatitis?

A

Females, autoimmune diseases, viral hepatitis, HLADR3/4.

115
Q

What are the types of autoimmune hepatitis?

A

Type 1 - Adult females (40s/50s). Less acute.
Type 2 - Young females (teens/20s). Acute.

116
Q

Which autoantibodies are present in type 1 autoimmune hepatitis?

A
  1. Anti-nuclear autoantibodies (ANA).
  2. Anti-smooth muscle autoantibodies (ASMA).
  3. Anti-soluble liver antigen (ASLA/LP).
117
Q

Which autoantibodies are present in type 2 autoimmune hepatitis?

A
  1. Anti-liver kidney microsomes-1 (ALKM1).
  2. Anti-liver cytosol antigen type 1 (ALC1).
118
Q

How is autoimmune hepatitis diagnosed?

A

Liver biopsy and serology (for autoantibodies).

119
Q

What are the symptoms/signs of autoimmune hepatitis?

A

25% asymptomatic.
-Jaundice, fever, hepatosplenomegaly.

120
Q

How is autoimmune hepatitis treated?

A

High dose steroids (prednisolone).
-Hepatitis vaccinations.
-If ESLD, liver transplant.

121
Q

What is biliary tract disease?

A

Three main conditions that affect the biliary tree:
-Gallstones.
-Cholecystitis.
-Ascending cholangitis.

122
Q

In biliary tract disease, when do you get RUQ pain?

A

All 3 conditions:
-Gallstones
-Cholecystitis
-Ascending cholangitis

123
Q

In biliary tract disease, when do you get fever?

A

With ascending cholangitis and cholecystitis.

124
Q

In biliary tract disease, when do you get jaundice?

A

With ascending cholangitis.

125
Q

What is biliary colic?

A

The temporary blockage of the cystic or common bile duct by gallstones which causes pain.

126
Q

What are the contents of gallstones?

A

Cholesterol (80%), pigment, bilirubin, bile salts.

127
Q

What are the risk factors for biliary colic?

A

5Fs - Fat, forty, female, family history, fertile.
-T2DM, NAFLD.

128
Q

What are the symptoms of gallstones?

A

RUQ pain often after fatty meals.
-Referred shoulder pain and N+V.

129
Q

How are gallstones diagnosed?

A

Abdo USS - thick wall, stones and duct dilation.

130
Q

How are gallstones managed?

A

Elective laparoscopic cholecystectomy if symptomatic.
-Analgesia for pain and decrease fat in diet.

131
Q

What is cholecystitis?

A

Blockage of the cystic duct which causes a buildup of bile and causes inflammation of the gallbladder.

132
Q

How does cholecystitis present?

A

RUQ pain with fever and referred pain to tip of right shoulder.

133
Q

How is cholecystitis diagnosed?

A

FBC, CRP and LFTs show leukocytosis and neutropenia.
-Positive Murphy sign - press on gallbladder and ask patient to inhale - PAIN.
-Abdo USS - thick gallbladder wall.

134
Q

How is cholecystitis managed?

A

Laparoscopic cholecystectomy within a week.
-IV fluid, analgesia, IV antibiotics.

135
Q

What is ascending cholangitis?

A

Prolonged bile duct blockage so instead of being flushed into GI tract by bile, bacteria ascend through the biliary tree which can lead to sepsis.

136
Q

What is the presentation of ascending cholangitis?

A

Charcot’s triad - RUQ pain, fever and jaundice (post - dark piss, pale shite).
If sepsis - Reynold’ pentad (Charcot’s triad, confusion, sepsis).

137
Q

What is the gold standard investigation for ascending cholangitis?

A

MRCP - magnetic resonance cholangio pancreatography.

138
Q

What is the first line investigation for ascending cholangitis?

A

USS abdo.

139
Q

What other investigations are done for ascending cholangitis?

A

Bloods: LFTs, FBC, CRP.
-Blood cultures for sepsis.

140
Q

What is the treatment for ascending cholangitis?

A

ERCP (Endoscopic retrograde cholangiopancreatography) and laparoscopic cholecystectomy.

141
Q

What is jaundice?

A

The yellowing of the skin and eyes due to the accumulation of bilirubin.

142
Q

What are the types of jaundice?

A

Pre-hepatic.
Hepatic.
Post-hepatic.

143
Q

How does pre-hepatic jaundice present?

A

Normal urine and stool colour, no itching and generally normal LFTs.

144
Q

How does hepatic and post-hepatic jaundice present?

A

Dark urine, pale stools, can itch, abnormal LFTs.

145
Q

What causes pre-hepatic jaundice?

A

Increased RBC breakdown - Gilbert’s syndrome and haemolytic anaemias:
-Sickle cell, G6DP deficiency, thalassaemia, malaria.

146
Q

What causes hepatic jaundice?

A

Disease of the liver itself:
-HCC, ALD, NAFLD, hepatitis, drugs.

147
Q

What causes post-hepatic jaundice?

A

Biliary tree obstruction:
-Pancreatic cancer, autoimmune (PBC, PSC), gallstones.

148
Q

Explain the pathophysiology of pre-hepatic jaundice.

A

Increased RBC breakdown overwhelms the liver’s ability to conjugate bilirubin, causing unconjugated bilirubinemia.

149
Q

Explain the pathophysiology of intra-hepatic jaundice.

A

Dysfunction of the hepatocytes and they lose their ability to conjugate bilirubin. Causing both unconjugated and conjugated bilirubinaemia.

150
Q

Explain the pathophysiology of post-hepatic jaundice.

A

Obstruction of biliary tree, so the bilirubin that is excreted has already been to the liver so this causes conjugated bilirubinaemia.

151
Q

What is primary biliary cholangitis?

A

The progressive autoimmune destruction of the small bile ducts within the liver. This obstructs the outflow of bile leading to cholestasis and eventually fibrosis, cirrhosis and liver failure.

152
Q

What are the four risk factors for primary biliary cholangitis?

A

Female, 40-50y, other autoimmune disease, smoking.

153
Q

How does primary biliary cholangitis present?

A

Initially asymptomatic.
-Pruritus, itching, jaundice, hepatosplenomegaly.
-Xanthelasma and xanthoma (lipid deposits on skin).

154
Q

Explain the pathophysiology of the symptoms of primary biliary cholangitis.

A

Bile usually contains bile salts, cholesterol and bilirubin. When the outflow of bile is obstructed, these build up.
-Bile salts cause itching.
-Cholesterol deposits in the skin and causes xanthoma/xanthelasma.
- Bilirubin causes jaundice.

155
Q

How is primary biliary cholangitis diagnosed?

A
  1. LFTs - alkaline phosphatase, bilirubin.
  2. Liver biopsy.
  3. Autoantibodies (AMA, ANA).
156
Q

What is the management for primary biliary cholangitis?

A
  1. Ursodeoxycholic acid (reduces cholestasis).
  2. Cholestyramine (binds to bile to prevent absorption in gut, helps pruritus).
  3. Steroids considered in some.
  4. ESLD - liver transplant.
157
Q

What is primary sclerosing cholangitis?

A

When the intrahepatic and extrahepatic ducts become stiff and fibrotic.
This leads to the obstruction of bile outflow and eventually hepatitis, fibrosis and cirrhosis.

158
Q

Which condition is associated with primary sclerosing cholangitis?

A

Ulcerative colitis (70% of people).

159
Q

What causes primary sclerosing cholangitis?

A

Unclear.
-Thought to be a combination of genetic, autoimmune and environmental.

160
Q

What are the four risk factors for primary sclerosing cholangitis?

A

Male, 30-50, ulcerative colitis and FHx.

161
Q

How does primary sclerosing cholangitis present?

A

Initially asymptomatic:
-Jaundice, fatigue, pruritus, RUQ pain, hepatosplenomegaly.

162
Q

How is PSC diagnosed?

A

GS - MRCP.
LFTs show ‘cholestatic’ - ALP raised first.
Serology - pANCA positive in 95%, ANA in 75%.

163
Q

How is PSC managed?

A
  1. Cholestyramine (binds to bile to prevent it being absorbed).
  2. ERCP - dilation and stenting of ducts.
  3. Manage complications.
  4. If ESLD - liver transplant.
164
Q

What is pancreatitis?

A

Inflammation of the pancreas.

165
Q

What are the types of pancreatitis?

A

Acute and chronic pancreatitis.

166
Q

What is acute pancreatitis?

A

Rapid onset of pancreas inflammation and symptoms. Normal function usually returns after.

167
Q

What is chronic pancreatitis?

A

Long-term inflammation and symptoms with a progressive and permanent decrease in pancreas function.

168
Q

What are the three main causes of acute pancreatitis?

A

Gallstones, alcohol, post-ERCP.

169
Q

How do gallstones cause acute pancreatitis?

A

Gallstones obstruct flow of pancreatic secretions and digestive enzyme accumulate in pancreas. Ca2+ is released, activates trypsinogen and autodigestion.

170
Q

How does alcohol cause pancreatitis?

A

Directly toxic to pancreatic cells, resulting in inflammation.
-Also contracts ampulla of vater.

171
Q

What are the causes of acute pancreatitis? (acronym).

A

IGETSMASHED:

Idiopathic, gallstones, ethanol (alcohol), trauma, steroids, mumps/malignancy, autoimmune, scorpion venom, hyperlipidaemia, ERCP, drugs.

172
Q

How does someone with acute pancreatitis present?

A

Sudden severe epigastric pain which radiates to the back.
-Jaundice, pruritus, N+V, tachycardia.
-Grey turner and Cullen sign - bleeding.

173
Q

How is pancreatitis diagnosed?

A

GS - Bloods (increased serum amylase/lipase, CRP).
-CT/USS to assess cause/complications.

174
Q

How is acute pancreatitis managed?

A

ABCDE - NBM, IV fluids, analgesia, prophylactic Abx.
-Treat cause (gallstones - ERCP).

175
Q

What are three complications to acute pancreatitis?

A

Infection, abscess, chronic pancreatitis.

176
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol.

177
Q

How does chronic pancreatitis present?

A

The same as acute pancreatitis but usually less intense and more longer lasting.

178
Q

What are features of chronic pancreatitis that don’t manifest in acute pancreatitis?

A

Exocrine and endocrine dysfunction, abscess formation and chronic epigastric pain.

179
Q

How is chronic pancreatitis managed?

A
  1. Abstaining from alcohol and smoking.
  2. Analgesia for pain (NSAIDs).
  3. Replace enzymes and hormones that.
  4. Treat complications.
180
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity.

181
Q

What are the four main causes of ascites?

A

Liver cirrhosis, malignancy (GI, ovary, lymphoma), heart failure, nephrotic syndrome.

182
Q

How does ascites present?

A

Abdominal distension, weight gain, respiratory distress, N+V, discomfort.
-Signs of underlying cause.

183
Q

How is ascites diagnosed?

A

Examination:
-Shifting dullness to flanks.
-Ascitic tap and cytology.

184
Q

How is ascites managed?

A

Treat underlying cause.
-Spironolactone, loop diuretics.
-Paracentesis.
-Surgery and liver transplant.

185
Q

What is the main complication of ascites? In how many people does it occur and what is the mortality rate?

A

Spontaneous bacterial peritonitis (SBP):
-Occurs in 20% of patients and mortality rate is 20%.

186
Q

What is Wernicke’s encephalopathy?

A

A degenerative brain disorder caused by the lack of thiamine (vitamin B1) which usually results from alcohol abuse.

187
Q

What usually causes Wernicke’s encephalopathy?

A

Alcohol abuse as vitamin B1 is poorly absorbed in the presence of alcohol and they tend to have poor diets.

188
Q

How does someone with Wernicke’s encephalopathy present and why?

A

With confusion, ataxia, and oculomotor disturbances as B1 deficiency causes damage to the brain.

189
Q

Is Wernicke’s encephalopathy permanent?

A

No, it can be reversed if treated fast.

190
Q

What is Korsakoff syndrome? What usually precedes it?

A

An irreversible disabling memory disorder and form of dementia that results from vitamin B1 deficiency and alcoholism.
-Occurs after Wernicke’s encephalopathy.

191
Q

How does Korsakoff syndrome present?

A

With memory impairment and behavioural changes.

192
Q

Explain the pathophysiology of Korsakoff syndrome.

A

Lack of vitamin B1 damages both the nerve cells and supporting cells in the brain and spinal cord.

193
Q

What is hepatic encephalopathy?

A

Changes in the brain that occur in patients with liver disease due to the build up of toxins (mostly ammonia).

194
Q

How does hepatic encephalopathy usually present?

A

With personality changes, intellectual impairment, impaired memory and coma.

195
Q

What is the most common cause of hepatic encephalopathy?

A

Chronic liver disease.

196
Q

How is hepatic encephalopathy treated?

A

-Laxatives - helps to clear ammonia from the gut before being absorbed.
-Antibiotics - reduces bacteria in gut producing ammonia.

197
Q

What are three common metabolic liver diseases?

A
  1. Haemochromatosis.
  2. Wilson’s disease.
  3. A1ATD.
198
Q

What is haemochromatosis?

A

Iron storage disorder that results in excessive total iron in the body and iron deposits in the tissues.

199
Q

Explain the pathophysiology of haemochromatosis.

A

Autosomal recessive mutation of HFE gene on chromosome 6. HFE gene usually regulates iron storage. When the gene is faulty the storage of iron is impaired.

200
Q

Who is haemochromatosis more common in?

A

Men as women lose iron in menstruation.

201
Q

What are the nine signs/symptoms of haemochromatosis?

A

Fatigue, joint pain, hypogonadism, slate grey/bronze skin, osteoporosis, heart failure, hair loss and memory/mood disturbance.

202
Q

How is haemochromatosis diagnosed?

A

Iron studies:
-High serum ferritin.
-High transferrin saturation.

Genetic testing for HFE gene, liver biopsy with Perl’s stain.
CT/MRI.

203
Q

How is haemochromatosis treated?

A

1.Venesection (to remove iron) and iron chelation.
2. Avoid alcohol.
3. Monitor and treat complications.

204
Q

What are six complications of haemochromatosis?

A

T1DM, liver cirrhosis, cardiomyopathy, HCC, hypothyroidism, pseudogout.

205
Q

What is Wilson’s disease?

A

Excessive accumulation of copper in the body and tissues.

206
Q

Explain the pathophysiology of Wilson’s disease.

A

Autosomal recessive mutation of ATP7B gene on chromosome 13. Defective enzyme and impaired copper secretion.

207
Q

What are the typical patients with Wilson’s disease?

A

Young (20y) with family history.

208
Q

How does Wilson’s disease present?

A

-Neuro problems - parkinsonism, memory issues, dystonia, dysarthria.
-Psychiatric - From depression to psychosis.
-Hepatic - Hepatitis and cirrhosis.
-Ophthalmic - Kayser Fleischer rings.
-Other - Haemolytic anaemia, osteopenia, RTA.

209
Q

How is Wilson’s disease diagnosed?

A

Serum caeruloplasmin is low, low serum copper.
GS - Liver biopsy.
-24h urine copper assay.

210
Q

How is Wilson’s disease treated?

A

Copper chelation with penicillinamine and trientine.

211
Q

What is the last resort treatment for Wilson’s disease?

A

Liver transplant.

212
Q

What is alpha-1 antitrypsin deficiency?

A

A deficiency of alpha-1 antitrypsin enzymes caused by an autosomal recessive mutation of protease inhibitor gene on chromosome 14.

213
Q

Explain the pathophysiology of A1ATD.

A

A1AT usually inhibits neutrophil elastase enzymes which digest connective tissues.
If there is decreased A1AT, there will be increased NE which affects the lungs and the liver.

214
Q

How does A1ATD affect the lungs?

A

Lack of A1AT leads to excess protease enzymes which attack connective tissue in the lung and causes bronchiectasis and emphysema.

215
Q

How does A1ATD affect the liver?

A

A mutant version of A1AT is produced and builds up in the liver and causes damage, eventually cirrhosis and then risk of HCC.

216
Q

How does A1ATD present?

A

A young/middle aged male with little/no smoking history with COPD like symptoms:
-SOB, chronic cough and sputum.
-May have liver Sx (jaundice).

217
Q

How is A1ATD diagnosed?

A

-Serum A1AT is decreased.
-Liver biopsy - cirrhosis and acid-Schiff-positive staining globules.
-CT thorax - emphysema and bronchiectasis.
-Genetic test for gene.

218
Q

How is A1AT disease managed?

A

Stopping smoking, managing symptoms.
-If ESLD consider liver transplant.
-Monitor for complications (HCC).

219
Q

What is portal hypertension?

A

Increased pressure in the pressure in the portal vein.

220
Q

What are the three main groups of causes for portal hypertension?

A

Prehepatic, hepatic and post-hepatic.

221
Q

What is the main cause of pre-hepatic portal hypertension?

A

Portal vein thrombosis.

222
Q

What are the two causes of hepatic portal hypertension? (UK vs worldwide).

A

-Liver cirrhosis (mc in UK).
-Schistomiasis (mc world).

223
Q

What are the two main post-hepatic causes of portal hypertension?

A

Budd Chiari, right sided heart failure.

224
Q

Explain how liver cirrhosis leads to portal hypertension and oesophageal varices.

A

Cirrhosis causes increased resistance to flow so dilation and increased CO to compensate, there is a fluid overload in the portal vein which means blood shunts to the gastroesophageal vein, causing oesophageal varices.

225
Q

How does portal hypertension present?

A

Mostly asymptomatic until oesophageal varices rupture.

226
Q

How often does portal hypertension cause oesophageal varices and how many rupture?

A

90% cause varices,
1/3rd rupture.

227
Q

What are oesophageal varices?

A

Thin dilated veins that develop in the lining of the lower oesophagus.

228
Q

When are oesophageal varices symptomatic?

A

When they rupture.

229
Q

What is the most common complication of oesophageal varices?

A

Rupture and bleeding.

230
Q

How are oesophageal varices diagnosed?

A

Oesophagogastroduodenoscopy (OGD - upper GI).

231
Q

How do patients with ruptured oesophageal varices present?

A

With hematemesis (vomiting blood) and melaena (black turds due to upper GI bleeding).

232
Q

How are bleeding oesophageal varices treated?

A

IV terlipressin, variceal banding, vitamin K.

233
Q

How are stable oesophageal varices treated?

A

Beta-blockers, nitrates and banding.
-TIPS (transjugular intrahepatic portosystemic shunt) - shunt from portal vein to hepatic vein to relieve pressure on portal system.

234
Q

What is perotinitis?

A

Inflammation of the peritoneum.

235
Q

What are the causes of perotinitis?

A

Primary - SBP (mc) and ascites.
Secondary - due to underlying cause.

236
Q

What are the bacterial causes of SBP?

A

Staph aureus, E. coli and klebisella.

237
Q

What are three chemical causes of peritonitis?

A

Ruptured ectopic pregnancy, intestine perforation, bile.

238
Q

How does peritonitis usually present?

A

Sudden onset severe abdo pain.
-Then collapse, septic shock, fever.

239
Q

How is peritonitis diagnosed?

A

Ascitic tap shows neutrophilia, cultures show causative organisms.
-Bloods: Increased ESR and CRP.
-Exclusion of pregnancy and bowel obstruction.

240
Q

How is peritonitis treated?

A

Emergency - ABCDE, IV fluid and IV antibiotics.
-Treat underlying cause.

241
Q

What are two complications of peritonitis?

A

Sepsis and abscesses.

242
Q

Explain the pathophysiology of pancreatic cancer.

A

Adenocarcinoma of exocrine pancreas of ductal origin.

243
Q

In pancreatic cancer, which areas are most commonly affected?

A

60% head, 25% body, 15% tail.

244
Q

Who is pancreatic cancer most common in?

A

Males above 60.

245
Q

What are five risk factors for pancreatic cancer?

A

Smoking, alcohol, diabetes, family history, chronic pancreatitis.

246
Q

What is the average 5y survival for pancreatic cancer?

A

3%.

247
Q

Why is pancreatic cancer dangerous?

A

It metastasises early and quickly.

248
Q

What is the key presenting symptom of pancreatic cancer?

A

Painless obstructive jaundice.
-With jaundice, pale stools, dark urine and itching.

249
Q

What are six other signs/symptoms of pancreatic cancer?

A

N+V, abdo pain, Courvoisier sign (palpable GB and jaundice), change in bowel habit, weight loss, new onset diabetes or worsening of T2DM.

250
Q

What are the investigations for pancreatic cancer? 1st line and GS?

A

Abdo USS (1st),CT scan (GS).
-Pancreatic biopsy.
-CA19-9 tumour marker may be raised.

251
Q

How is pancreatic cancer treated?

A

Surgery considered in small tumours.
-Chemo and palliative care.

252
Q

What is Gilbert’s syndrome?

A

Hereditary jaundice caused by autosomal recessive mutation in UDP1A1 gene which leads to UGT enzyme deficiency.

253
Q

What are the two risk factors for Gilbert’s syndrome?

A

Male, T1DM.

254
Q

Describe the pathophysiology of Gilbert’s syndrome.

A

UGTs are enzymes that catalyse phase II glucuronidation reactions in the liver so they bilirubin isn’t metabolised, leading to unconjugated hyperbilirubinaemia and jaundice.

255
Q

What is the most common cause of hereditary jaundice?

A

Gilbert’s syndrome.

256
Q

What are the symptoms of Gilbert’s syndrome?

A

Presents with painless jaundice at a young age.
30% asymptomatic.

257
Q

What is Criggler Najjar?

A

A more severe and rare hereditary jaundice.

258
Q

How is Gilbert’s syndrome and Criggler Najjar treated?

A

Gilbert’s - no treatment.
CN - phototherapy (breaks down bilirubin).

259
Q

What are the primary liver cancers?

A

Hepatocellular carcinoma (80%) and cholangiocarcinoma (20%).

260
Q

What are the most common primary locations for cancers to metastasise to the liver?

A

GI tract, breast, lung.

261
Q

Is primary or secondary lung cancer more common?

A

Secondary.

262
Q

What are six risk factors for primary liver cancer?

A

Liver cirrhosis, hepatitis (viral/auto), alcohol, ALD, NAFLD, haemochromatosis.

263
Q

What are three main signs of liver cancer?

A

-Decompensated liver failure (jaundice, ascites, HE).
-Signs of cancer (TATT, weight loss, night sweats).
-Hepatosplenomegaly.

264
Q

What are three symptoms of liver cancer?

A

Non-specific symptoms - abdo pain, anorexia, N+V.

265
Q

What are two risk factors for cholangiocarcinoma?

A

Parasites, PSC.

266
Q

What investigations are used for liver cancer? 1st line and GS?

A

GS - ERCP (chol), CT (HCC).
1st - USS.
Tumour markers:
-Alpha-feroprotein (HCC), CA19-9 (chol).

267
Q

How is liver cancer treated?

A

Surgical resection of tumour.
Chemo, radio, stents.

268
Q

What are two benign liver cancers?

A

Haemangioma and hepatic adenoma.

269
Q

What is a hernia?

A

Protrusion of an organ through defect in its containing cavity (usually the bowel).

270
Q

What are the six types of hernia?

A

Inguinal, femoral, hiatal, epigastric, incisional, umbilical.

271
Q

What can hernias be?

A

Reducible - pushed back into place.
Irreducible - obstructed, strangulated, incarceration.

272
Q

What is the curative option of hernias?

A

Surgery.

273
Q

What is a hiatal hernia?

A

When the stomach herniates through the diaphragm aperture.

274
Q

What is the most common type of hernia?

A

Inguinal (direct and indirect).

275
Q

How would you diagnose ALD with LFTs?

A

AST:ALT ratio is 2:1.

276
Q

What is Wernicke’s encephalopathy triad?

A

Ataxia (wide base), encephalopathy (confusion) and ophthalmoplegia (not following finger with eyes).

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