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Phase 2a > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

What are the 7 functions of the liver?

A
  1. Oestrogen regulation
  2. Detoxification
  3. Metabolism of carbohydrates
  4. Albumin production
  5. Clotting factor production
  6. Bilirubin regulation
  7. Immunity
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2
Q

What is alcoholic liver disease?

A

Liver damage caused by excess alcohol intake

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3
Q

Describe the epidemiology of alcoholic liver disease

A
  • Most common cause of chronic liver disease in the western world
  • Usually presents in men in 40s-50s
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4
Q

What are 2 causes of alcoholic liver disease?

A
  1. Excessive consumption of alcohol (main)
  2. Some genetic predisposition
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5
Q

Describe the order of alcoholic liver disease

A

Fatty liver (steatosis) –> alcoholic hepatitis –> cirrhosis

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6
Q

Describe the pathophysiology of fatty liver (steatosis)

A
  • Metabolism of alcohol produces fat in the liver
  • Cells become swollen with fat with large amounts of alcohol
  • Fat disappears on alcohol abstinence
  • Alcohol directly affects stellate cells (fat-storing cells) which are transformed into collagen-producing myofibroblast cells
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7
Q

Describe the pathophysiology of alcoholic hepatitis

A
  • Fatty change and infiltration by polymorphonuclear leukocytes and hepatocyte necrosis
  • Presence of mallory bodies and giant mitochondria
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8
Q

What are 4 signs of alcoholic liver disease?

A
  1. Hepatomegaly
  2. Ascites
  3. Rapid onset jaundice
  4. Encephalopathy
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9
Q

What are the symptoms of fatty liver (alcoholic liver disease)?

A

Usually asymptomatic

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10
Q

What are 4 symptoms of alcoholic hepatitis (alcoholic liver disease)?

A
  1. Nausea and vomiting
  2. Diarrhoea
  3. Anorexia
  4. RUQ pain
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11
Q

What is a symptom of alcoholic cirrhosis (alcoholic liver disease)?

A

May be asymptomatic
- Spider naevi (clusters of RBCs visible under skin)

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12
Q

What are 8 investigations for patients with alcoholic liver disease?

A
  1. LFTs
  2. FBC
  3. PTT (increased)
  4. Abdominal ultrasound
  5. Fibroscan
  6. Endoscopy
  7. CT/MRI
  8. Liver biopsy
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13
Q

Describe LFT results for patients with alcoholic liver disease

A
  • GGT = very raised
  • AST:ALT = raised ratio (2:1)
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14
Q

Describe FBC results for patients with alcoholic liver disease

A
  • Macrocytic anaemia (elevated MCV)
  • Thrombocytopenia
  • Hypoglycaemia
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15
Q

What is the recommended alcohol consumption?

A
  • No more than 14 units per week for both men and women
  • No more than 5 units in a day
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16
Q

How do you calculate the number of units of alcohol?

A

Strength (ABV) x volume (ml) / 1,000

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17
Q

What is the treatment for alcoholic liver disease?

A
  • Lifelong abstinence from alcohol
  • Corticosteroids (to control inflammation)
  • IV thiamine
  • Diet high in vitamins and proteins
  • Liver transplant
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18
Q

What are 5 complications of alcoholic liver disease?

A
  1. Liver failure
  2. Wernicke-Korsakoff encephalopathy
  3. Acute/chronic pancreatitis
  4. Mallory-Weiss tear
  5. Increased risk of cancers (particularly breast/mouth/throat)
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19
Q

What is non-alcoholic fatty liver disease?

A

Range of conditions caused by a build-up of fat in the liver

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20
Q

Describe the epidemiology of non-alcoholic fatty liver disease

A

25% of population

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21
Q

What are 3 risk factors for non-alcoholic fatty liver disease?

A
  1. Obesity
  2. Diabetes
  3. Hyperlipidaemia
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22
Q

Describe the order of non-alcoholic fatty liver disease

A

Healthy –> steatosis –> steatohepatitis –> fibrosis –> cirrhosis

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23
Q

What are 2 signs of non-alcoholic fatty liver disease?

A
  1. Hepatomegaly
  2. Jaundice
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24
Q

What are 5 symptoms of non-alcoholic fatty liver disease?

A

Asymptomatic
1. Nausea and vomiting
2. Diarrhoea
3. Fatigue
4. Malaise
5. RUQ pain

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25
Q

What are 4 investigations for patients with non-alcoholic fatty liver disease?

A
  1. LFTs (raised ALT and sometimes AST)
  2. CT/MRI
  3. Ultrasound
  4. Liver biopsy
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26
Q

What is the treatment for non-alcoholic fatty liver disease?

A
  • Reduce weight
  • No effective drug treatments
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27
Q

What is autoimmune hepatitis?

A

Liver inflammation due to the immune system attacking hepatocytes

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28
Q

Describe the epidemiology of autoimmune hepatitis

A
  • Type 1 occurs in adults (typically women in 40s-50s around/after menopause)
  • Type 2 occurs in children (typically teenagers/early 20s)
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29
Q

What are 4 signs and symptoms of autoimmune hepatitis?

A
  1. Hepatosplenomegaly
  2. Fatigue
  3. Fever
  4. Jaundice
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30
Q

What are 5 investigations for patients with type 1 autoimmune hepatitis?

A
  1. Biopsy
  2. Raised ALT and AST
  3. Anti-nuclear antibodies (ANA)
  4. Anti-smooth muscle antibodies (acin-acin)
  5. Anti-soluble liver antigen (anti-SLA/LP)
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31
Q

What are 4 investigations for patients with type 2 autoimmune hepatitis?

A
  1. Biopsy
  2. Raised ALT and AST
  3. Anti-liver kidney microsomes-1 (anti-LKM1)
  4. Anti-liver cytosol antigen type 1 (anti-LC1)
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32
Q

What is the treatment for autoimmune hepatitis?

A
  • High dose steroids e.g. prednisolone, azathioprine
  • Usually successful in inducing remission but is required life long
  • Liver transplant (can recur)
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33
Q

What is viral hepatitis?

A

Inflammation of the liver as a result of direct viral infection

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34
Q

Describe the epidemiology of Hepatitis A

A
  • Most common viral hepatitis worldwide
  • Common in Africa and South America
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35
Q

How is Hepatitis A spread?

A
  • Faecal oral route (facilitated by overcrowding and poor sanitation)
  • Arises from ingestion of contaminated food/water e.g. shellfish
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36
Q

What are 3 risk factors for Hepatitis A?

A
  1. Shellfish
  2. Travellers
  3. Food handlers
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37
Q

Describe the pathophysiology of Hepatitis A

A
  • Small, unenveloped RNA virus (picornavirus)
  • Incubation period of 28 days
  • Viral replication occurs in infected hepatocytes
  • Hepatocytes destroyed due to immune response and viral life cycle
  • = acute hepatitis
  • Viral particles excreted in bile then faeces
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38
Q

What are 3 signs of Hepatitis A?

A
  1. Cholestasis
  2. Jaundice (after 2 weeks)
  3. Hepatomegaly (after 2 weeks)
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39
Q

What are 4 symptoms of Hepatitis A?

A
  1. Nausea and vomiting
  2. Anorexia
  3. Abdominal pain
  4. Dark urine and pale stool (after 2 weeks)
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40
Q

What are 2 investigations for patients with Hepatitis A?

A
  1. Raised ALT
  2. Antibody to HAV (IgM)
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41
Q

What is the treatment for Hepatitis A?

A
  • Resolves without treatment in 1-3 months
  • Treat symptoms = analgesia
  • Avoid alcohol
  • Vaccination
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42
Q

What are 2 complications of Hepatitis A?

A
  1. Cholestatic hepatitis
  2. Acute liver failure (rare)
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43
Q

How is Hepatitis B spread?

A

Direct contact with blood/bodily fluids (needles, sexual, IV drugs users, vertical transmission etc.)

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44
Q

What are 6 risk factors for Hepatitis B?

A
  1. Healthcare personnel
  2. Emergency/rescue teams
  3. CKD/dialysis patients
  4. Travellers
  5. Homosexual men
  6. IV drug users
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45
Q

Describe the pathophysiology of Hepatitis B

A
  • Enveloped DNA virus
  • HBsAg produced in excess by infected hepatocytes
  • Virus penetrates into hepatocytes and loses its coat
  • Virus core is transported to nucleus without processing
    = acute and chronic hepatitis
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46
Q

What are 2 signs of Hepatitis B?

A
  1. Jaundice
  2. Hepatomegaly
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47
Q

What are 3 symptoms of Hepatitis B?

A
  1. Flu-like symptoms
  2. Fever
  3. Pruritus (itchy skin)
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48
Q

What are 3 investigations for patients with Hepatitis B?

A
  1. Blood = raised ALT
  2. Antibody tests:
    - HBsAG (Hep B surface antigen)
    - HBsAb (Hep B surface antibody)
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49
Q

What is the treatment for Hepatitis B?

A
  • Most people fully recover from infection within 2 months
  • Vaccination
  • Stop smoking and drinking alcohol
  • 10% go on to become chronic hepatitis B carriers
  • Antiviral medication e.g. pegylated interferon-alpha 2a (48 week long treatment course)
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50
Q

What are chronic hepatitis B carriers?

A

Hepatitis B virus DNA has integrated into the host’s DNA so viral proteins continue to be produced

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51
Q

What are 2 complications of Hepatitis B?

A
  • Cirrhosis and chronic infection –> hepatocellular carcinoma
  • Fulminant hepatic failure (rare)
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52
Q

Describe the epidemiology of Hepatitis C

A

Six numbered genotypes = no.1 affects 50% of cases, no.2 and 3 make up 40%

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53
Q

How is Hepatitis C spread?

A

Via blood/bodily fluids (e.g. poorly sterilised instruments, shared needles etc.)

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54
Q

Describe the pathophysiology of Hepatitis C

A
  • Enveloped RNA virus
  • Incubation period of 6-9 weeks
  • Chronic infection causes a slowly progressive fibrosis over years
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55
Q

What are 3 symptoms of Hepatitis C?

A

Often asymptomatic in acute phase but in chronic:
1. Malaise
2. Weakness
3. Anorexia

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56
Q

What are 2 investigations for patients with Hepatitis C?

A
  1. Hepatitis C antibody screening test
  2. Hepatitis C RNA testing
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57
Q

What is the treatment for Hepatitis C?

A
  • 1/4 fight off and make full recovery
  • 3/4 become chronic
  • No vaccine available
  • Stop smoking and drinking alcohol
  • Curable with direct acting antiviral medications e.g. pegylated interferon-alpha 2a (8-12 week course)
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58
Q

What are 2 complications of Hepatitis C?

A
  1. Liver cirrhosis
  2. Hepatocellular carcinoma
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59
Q

How is Hepatitis D spread?

A

Blood-borne transmission (sexually, IVDU)

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60
Q

Describe the pathophysiology of Hepatitis D

A
  • RNA virus
  • Only occurs in people who are also infected with Hepatitis B
  • Attaches to HBsAg to survive
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61
Q

What are 2 signs of Hepatitis D?

A

Signs of acute HBV infection:
1. Jaundice
2. Hepatomegaly

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62
Q

What are 3 symptoms of Hepatitis D?

A

Symptoms of acute HBV infection:
1. Flu-like symptoms
2. Fever
3. Pruritus

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63
Q

What is the treatment of Hepatitis D?

A

Same treatment as HBV:
- Stop smoking and drinking alcohol
- Antiviral medication e.g. pegylated interferon-alpha 2a (48 week long treatment course)

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64
Q

What is the complication of Hepatitis D?

A

Increases complications/disease severity of hepatitis B

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65
Q

Describe the epidemiology of Hepatitis E

A

Most common cause of acute hepatitis in the UK

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66
Q

How is Hepatitis E spread?

A

Faecal-oral transmission (raw/undercooked pork meat)

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67
Q

Describe the pathophysiology of Hepatitis E

A
  • RNA virus
  • Usually results in self-limiting acute hepatitis
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68
Q

What are the symptoms for Hepatitis E?

A

95% of cases are asymptomatic (usually self-limiting)

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69
Q

What is the investigation for patients with Hepatitis E?

A

Serology

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70
Q

What is the treatment for Hepatitis E?

A
  • Often not required
  • Treat symptoms
  • No vaccine available
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71
Q

What is a complication of Hepatitis E?

A

Can progress to cirrhosis in immunocompromised (rare)

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72
Q

What is liver cirrhosis?

A

Scarring of the liver (fibrosis) caused by continuous, long-term liver damage - chronic inflammation and damage to hepatocytes

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73
Q

What are the 4 main causes of liver cirrhosis?

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease
  3. Hepatitis B
  4. Hepatitis C
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74
Q

What are 2 rarer causes of liver cirrhosis?

A
  1. Hereditary haemochromatosis (HH)
  2. Wilson’s disease (WD)
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75
Q

Describe the pathophysiology of liver cirrhosis

A
  • Damaged hepatocytes are replaced with scar tissue (fibrosis)
  • Fibrosis affects the structure and blood flow through the liver
  • This increases resistance in the vessels leading into the liver (portal hypertension)
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76
Q

What are 4 signs of liver cirrhosis?

A
  1. Jaundice
  2. Hepatosplenomegaly
  3. Ascites
  4. Asterixis (inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements)
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77
Q

What are 5 symptoms of liver cirrhosis?

A
  1. Spider naevi/caput medusae
  2. Palmar erythema
  3. Gynaecomastia
  4. Testicular atrophy
  5. Bruising
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78
Q

What are the 7 investigations for patients with liver cirrhosis?

A
  1. Bloods
  2. Imaging (CT/MRI/ultrasound/fibroscan)
  3. Endoscopy
  4. Liver biopsy
  5. Enhanced liver fibrosis blood test
  6. Child-Pugh score
  7. MELD score
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79
Q

What are the results of bloods in patients with liver cirrhosis?

A
  • High AST:ALT ratio
  • High bilirubin
  • Decreased albumin
  • Increased PTT/NR
  • Thrombocytopenia
  • Hyponatraemia
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80
Q

What is the enhanced liver fibrosis blood test?

A

< 7.7 = none to mild fibrosis
7.7-9.8 = moderate fibrosis
>9.8 = severe fibrosis

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81
Q

What does the child-pugh score calculate?

A

Indicates severity of cirrhosis

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82
Q

What does the MELD score calculate?

A

Gives a percentage estimated 3 month mortality

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83
Q

What is the treatment for liver cirrhosis?

A
  • High protein, low sodium diet
  • Fluids
  • Analgesia
  • Alcohol abstinence
  • Liver transplant
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84
Q

What are 6 complications of liver cirrhosis?

A
  1. Malnutrition
  2. Portal hypertension, varices, variceal bleeding
  3. Ascites and spontaneous bacterial peritonitis
  4. Hepato-renal syndrome
  5. Hepatic encephalopathy
  6. Hepatocellular carcinoma
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85
Q

What is jaundice?

A

Yellow discolouration of sclera and skin due to hyperbilirubinaemia

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86
Q

What is the jaundice threshold?

A

Occurs at bilirubin levels roughly greater than 50 umol/L

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87
Q

What are 3 causes of pre-hepatic jaundice?

A
  1. Haemolytic anaemia (e.g. sickle cell, malaria)
  2. Gilbert’s syndrome
  3. Criggler-Najjar syndrome
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88
Q

What are 6 causes of intrahepatic jaundice?

A
  1. Alcoholic liver disease
  2. Viral/autoimmune hepatitis
  3. Iatrogenic
  4. Hereditary haemochromatosis
  5. Primary biliary cirrhosis/primary biliary cholangitis
  6. Hepatocellular carcinoma
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89
Q

What are 3 causes of posthepatic jaundice?

A
  1. Intra-luminal causes e.g. gallstones
  2. Mural causes e.g. cholangiocarcinoma, stricture, drug-induced cholestasis
  3. Extra-mural cases e.g. pancreatic cancer, abdominal masses (e.g. lymphoma)
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90
Q

What is bilirubin?

A

Breakdown product from catabolism of haem (formed from destruction of RBCs)

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91
Q

What usually happens to bilirubin?

A
  • Conjugates with liver (becomes water soluble)
  • Excreted via bile into GI tract
  • Excreted in faeces as urobilinogen/stercobilin
  • 10% of urobilinogen is reabsorbed into bloodstream and excreted via kidneys
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92
Q

Describe the pathophysiology of pre-hepatic jaundice

A
  • Excessive breakdown of RBCs
  • Liver overwhelmed to conjugate bilirubin
  • = unconjugated hyperbilirubinaemia
  • = unconjugated bilirubin in bloodstream
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93
Q

Describe the pathophysiology of intrahepatic jaundice

A
  • Dysfunction of hepatic cells
  • Liver loses ability to conjugate bilirubin
  • Cirrhotic liver can cause obstruction
  • = unconjugated and conjugated bilirubin in bloodstream
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94
Q

Describe the pathophysiology of post-hepatic jaundice

A
  • Obstruction of biliary drainage
  • Bilirubin is conjugated but cannot be excreted
  • = conjugated bilirubin in bloodstream
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95
Q

Describe the clinical presentation/investigations of pre-hepatic jaundice

A
  • Yellow sclera and skin
  • Normal urine and stool
  • No itching
  • Normal LFTs
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96
Q

Describe the clinical presentation of intrahepatic jaundice

A
  • Yellow sclera and skin
  • Dark urine and pale stool
  • Itching
  • Abnormal LFTs
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97
Q

Describe the clinical presentation of post-hepatic jaundice

A
  • Yellow sclera and skin
  • Dark urine and pale stool
  • Itching
  • Abnormal LFTs
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98
Q

What are the 2 causes of Wernicke’s encephalopathy and Korsakoff syndrome?

A
  1. Alcohol excess
  2. Thiamine (vitamin B1) deficiency
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99
Q

Describe the pathophysiology of Wernicke’s encephalopathy and Korsakoff syndrome

A
  • Thiamine is poorly absorbed in the presence of alcohol
  • Thiamine deficiency causes damage to the hypothalamus and thalamus
  • Further deficiency leads to damaged nerve cells and supporting cells in the CNS
  • Wernicke’s = acute phase
  • Korsakoff = chronic phase
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100
Q

What are 3 symptoms of Wernicke’s encephalopathy?

A
  1. Confusion
  2. Ataxia (difficulty with coordinated movements)
  3. Oculomotor disturbances
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101
Q

What are 3 symptoms of Wernicke’s encephalopathy?

A
  1. Confusion
  2. Ataxia (difficulty with coordinated movements)
  3. Oculomotor disturbances
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102
Q

What are 2 symptoms of Korsakoff’s syndrome?

A
  1. Memory impairment
  2. Behavioural changes
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103
Q

What is the treatment for Wernicke’s encephalopathy?

A
  • Thiamine supplementation
  • Abstaining from alcohol
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104
Q

What are complications of Wernicke’s encephalopathy and Korsakoff’s syndrome?

A
  • Death if left untreated
  • Korsakoff’s syndrome is irreversible and usually results in patients requiring full time institutional care
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105
Q

What is hepatic encephalopathy?

A

Changes in the brain that occur due to build up of toxins in the blood, particularly ammonia

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106
Q

What are 6 causes of hepatic encephalopathy?

A
  1. Constipation
  2. Electrolyte disturbance
  3. Infection
  4. GI bleed
  5. High protein diet
  6. Medications (particularly sedatives)
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107
Q

Describe the pathophysiology of hepatic encephalopathy

A
  • Liver cirrhosis causes functional impairment of hepatocytes
  • Hepatocytes cannot metabolise ammonia into harmless waste products
  • Collateral circulation occurs in chronic liver disease (consequence of portal hypertension)
  • Collateral vessels are made between portal and systemic circulation so ammonia can bypass liver
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108
Q

What are 2 symptoms of acute hepatic encephalopathy?

A
  1. Confusion
  2. Reduced consciousness
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109
Q

What are 3 symptoms of chronic hepatic encephalopathy?

A
  1. Personality changes
  2. Memory changes
  3. Mood changes
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110
Q

What is the treatment for hepatic encephalopathy?

A
  • Laxatives (to clear ammonia from gut)
  • Antibiotics (to reduce no. of bacteria in gut that produce ammonia)
  • Nutritional support
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111
Q

Describe the epidemiology of pancreatic cancer

A
  • 99% in exocrine component of pancreas
  • More common in males >60
  • Majority are adenocarcinomas
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112
Q

What are 7 risk factors for pancreatic cancer?

A
  1. Smoking
  2. Excessive alcohol/coffee intake
  3. Excessive use of aspirin
  4. Diabetes
  5. Chronic pancreatitis
  6. Family history
  7. Genetic mutations (presence of PRSS-1 mutation)
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113
Q

Describe the pathophysiology of pancreatic cancer

A
  • Originates in ductal epithelium and evolves from pre-malignant lesions to full-invasive cancer
  • 60% arise in pancreatic head
  • 25% arise in body
  • 15% arise in tail
  • Tumour in head can grow large enough to compress the bile ducts and cause obstructive jaundice
  • Tend to spread and metastasise early, particularly to liver, peritoneum, lungs and bones
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114
Q

What are 2 signs of pancreatic cancer?

A
  1. Acute pancreatitis
  2. Courvoisier’s law = palpable gallbladder and jaundice is usually caused by cholangiocarcinoma or pancreatic cancer
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115
Q

What are 3 symptoms of pancreatic cancer?

A
  1. Anorexia
  2. Weight loss
  3. Jaundice
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116
Q

What is a symptom of pancreatic cancer (body and tail)?

A

Epigastric pain that radiates to the back that is relieved by sitting forward

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117
Q

What are 3 symptoms of pancreatic cancer (head)?

A

Painless obstructive jaundice:
1. Yellow skin and sclera
2. Dark urine and pale stools
3. Generalised itching

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118
Q

What are 3 investigations for pancreatic cancer?

A
  1. Abdominal ultrasound/CT
  2. Biopsy
  3. Carbohydrate antigen 19-9 tumour marker = raised
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119
Q

What is the treatment for pancreatic cancer?

A
  • Surgery
  • Palliative therapy (often diagnosed late and has a very poor prognosis - 5% 3 year survival)
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120
Q

What are 4 surgeries for pancreatic cancer?

A
  1. Total pancreatectomy
  2. Distal pancreatectomy
  3. Radical pancreaticoduodenectomy (Whipple procedure)
  4. Pylorus-preserving pancreaticoduodenectomy (PPPD - modified Whipple procedure)
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121
Q

What are 5 palliative therapies for pancreatic cancer?

A
  1. Stents (to relieve biliary obstruction)
  2. Surgery to improve symptoms (e.g. bypassing biliary obstruction)
  3. Palliative chemotherapy
  4. Palliative radiotherapy
  5. End of life care
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122
Q

Describe the epidemiology of hepatocellular carcinoma

A

80% of primary liver cancers

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123
Q

What are 4 risk factors for hepatocellular carcinoma?

A

Liver cirrhosis due to:
1. Viral hepatitis B and C
2. Alcohol
3. Non alcoholic fatty liver disease
4. Other chronic liver disease

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124
Q

What are 2 signs of hepatocellular carcinoma?

A
  1. Hepatomegaly
  2. Ascites
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125
Q

What are 9 symptoms of hepatocellular carcinoma?

A

Often remains asymptomatic for a long time
1. Fever
2. Malaise
3. Weight loss
4. Abdominal pain
5. Anorexia
6. Nausea/vomiting
7. Jaundice
8. Pruritus
9. RUQ pain

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126
Q

What are 4 investigations for patients with hepatocellular carcinoma?

A
  1. CT/MRI liver
  2. Biopsy
  3. Alpha-fetoprotein (ATP) = raised
  4. Bloods = clotting abnormalities/deranged LFTs
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127
Q

What is the treatment for hepatocellular carcinoma?

A
  • Poor prognosis
  • Surgical resection
  • Radiofrequency ablation
  • Chemo/radiotherapy (palliative)
  • TACE (transarterial chemoembolism - blocks blood supply to tumour)
  • Kinase inhibitors (inhibits proliferation of cancer cells)
  • Liver transplant
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128
Q

Describe the epidemiology of cholangiocarcinoma

A
  • 20% of primary liver cancers
  • Usually >50
  • 90% = ductal adenocarcinomas
  • 10% = squamous cell carcinomas
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129
Q

What are 2 risk factors for cholangiocarcinoma?

A
  1. Associated with primary sclerosing cholangitis (10%)
  2. Viral hepatitis B and C
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130
Q

What are 2 signs of cholangiocarcinoma?

A
  1. Hepatomegaly
  2. Ascites
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131
Q

What are 4 symptoms of cholangiocarcinoma?

A
  1. Painless jaundice
  2. Fever
  3. Malaise
  4. RUQ pain
132
Q

What are 4 investigations for patients with cholangiocarcinoma?

A
  1. CT/MRI liver
  2. Biopsy (ERCP - endoscopic retrograde cholangiopancreatography)
  3. CA19-9 tumour marker = raised
  4. Bloods = clotting abnormalities/deranged LFTs
133
Q

What is the treatment for cholangiocarcinoma?

A
  • Poor prognosis
  • Surgical resection
  • ERCP - stent placed in bile duct
  • Chemo/radiotherapy (palliative)
134
Q

What is Gilbert’s syndrome?

A

Higher than normal levels of bilirubin in the blood

135
Q

Describe the epidemiology of Gilbert’s syndrome

A
  • Most common cause of hereditary jaundice
  • More common in males
136
Q

What is the cause of Gilbert’s syndrome?

A

Genetic - autosomal recessive mutation in UDP1A1 gene (UGT enzyme deficiency)

137
Q

What are 2 risk factors for Gilbert’s syndrome?

A
  1. Type 1 diabetes
  2. Being male
138
Q

Describe the pathophysiology of Gilbert’s syndrome

A
  • Deficient/abnormal UGT
  • Causes unconjugated hyperbilirubinaemia
139
Q

What are 4 symptoms of Gilbert’s syndrome?

A

30% asymptomatic
1. Painless jaundice = yellow skin and sclera
2. Criggler Najjar = jaundice
3. Criggler Najjar = nausea/vomiting
4. Criggler Najjar = lethargy

140
Q

What is the treatment for Gilbert’s syndrome/Criggler Najjar?

A
  • Gilbert’s = fine without treatment
  • Criggler Najjar = phototherapy (breaks down unconjugated bilirubin)
141
Q

What is an inguinal hernia?

A

Protrusion of abdominal cavity contents through the inguinal canal

142
Q

Describe the epidemiology of inguinal hernias

A
  • Commonest type of hernia
  • More common in males >40
  • Direct (20%) and indirect (80%)
  • Accounts for ~70% of all abdominal hernias
143
Q

What are 5 risk factors for inguinal hernias?

A
  1. Male
  2. Chronic cough
  3. Constipation
  4. Heavy weight lifting
  5. Ascites
144
Q

Describe the pathophysiology of an indirect inguinal hernia

A
  • High abdominal pressure causes the internal organs to push through a weakened section of the abdominal wall
  • Protrudes through the deep inguinal ring
  • Lateral to inferior epigastric vessels
  • Can strangulate
145
Q

Describe the pathophysiology of a direct inguinal hernia

A
  • High abdominal pressure causes the internal organs to push through a weakened section of the abdominal wall
  • Protrudes directly into inguinal canal
  • Medial to inferior epigastric vessels
  • Rarely strangulates
146
Q

Describe the clinical presentation of inguinal hernias

A
  • Swelling of groin associated with coughing/straining (due to bowel movements/heavy lifting)
  • Points to groin
  • Appearance of lump
  • Usually asymptomatic
  • Pain indicates strangulation (indirect)
147
Q

What are 2 investigations for patients with inguinal hernias?

A
  1. Look for lump
  2. Ultrasound
148
Q

What is the treatment for inguinal hernias?

A
  • Truss (belt to keep hernia contained and prevent further progression)
  • Surgical repair
149
Q

What are 2 complications of all hernias?

A
  1. Incarceration (part of intestine/abdominal tissue becomes trapped in hernia sac)
  2. Strangulation (cuts off blood flow)
150
Q

What is a femoral hernia?

A

Protrusion of abdominal cavity contents through femoral canal

151
Q

Describe the epidemiology of femoral hernias

A
  • More common in females - middle age and elderly
  • Idiopathic
152
Q

Describe the pathophysiology of femoral hernias

A
  • High abdominal pressure causes the internal organs to push through a weakened section of abdominal wall
  • Bowel enters femoral canal
153
Q

Describe the clinical presentation of femoral hernias

A
  • Mass in upper medial thigh or above inguinal ligament (lateral and inferior to pubic tubercle)
  • Points down leg
  • Increase in swelling on cough
154
Q

What are 2 investigations for patients with femoral hernias?

A
  1. Look for lump
  2. Ultrasound
155
Q

What is the treatment for femoral hernias?

A
  • Surgical repair
  • Herniotomy (ligation and excision of sac)
156
Q

What is an umbilical hernia?

A

Protrusion of abdominal cavity contents at umbilicus

157
Q

Describe the epidemiology of umbilical hernias

A

10-30% of all hernias

158
Q

What are 3 causes of umbilical hernias?

A
  1. Occur congenitally as a result of developmental error
  2. 90% in adults acquired through multiple and difficult pregnancies
  3. Also occur in adults with ascites and obesity
159
Q

Describe the pathophysiology of umbilical hernias

A

Organs develop outside of abdominal cavity and enter through an opening in the umbilicus

160
Q

Describe the clinical presentation of umbilical hernias

A
  • Mass at site of umbilicus
  • Can be asymptomatic
  • Pain if abdominal wall contracts (worsened on straining)
161
Q

What are 2 investigations for patients with umbilical hernias?

A
  1. Look for lump
  2. Ultrasound
162
Q

What is the treatment for umbilical hernias?

A

<1cm = usually close spontaneously by 5 years
1-5cm = usually requires repair with preservation of umbilicus

163
Q

What is an incisional hernia?

A

Protrusion of abdominal cavity contents at site of an incision from previous surgery

164
Q

Describe the epidemiology of incisional hernias

A

15% of abdominal operations result in incisional hernias

165
Q

What is the cause of incisional hernias?

A

Failure of wound to heal following an abdominal operation

166
Q

Describe the pathophysiology of incisional hernias

A

Internal organs push through improperly healed sections of abdominal wall

167
Q

Describe the clinical presentation of incisional hernias

A
  • Mass
  • Location depends on location of incision
168
Q

What is the investigation for patients with incisional hernias?

A

Look for lump (observation)

169
Q

What is the treatment for incisional hernias?

A

Urgent repair with reinforcing mesh

170
Q

What is an additional complication of incisional hernias?

A

Recurrence in 50% of large hernias

171
Q

What is an epigastric hernia?

A

Protrusion of abdominal cavity contents in the epigastric area

172
Q

Describe the epidemiology of epigastric hernias

A

Most common in men between 20-50

173
Q

What is the main risk factor for epigastric hernias?

A

Obesity

174
Q

Describe the pathophysiology of epigastric hernias

A

Internal organs push through a weakened section of abdominal muscle

175
Q

Describe the clinical presentation of epigastric hernias

A
  • Mass above umbilicus in the linea alba
  • Usually asymptomatic
  • Can be made to bulge by asking the patient to strain
  • Possible bloating, nausea and vomiting (often after meals)
176
Q

What are 3 investigations for patients with epigastric hernias?

A
  1. Look for lump
  2. Ultrasound
  3. CT
177
Q

What is the treatment for epigastric hernias?

A

Surgical correction

178
Q

What is a hiatus hernia?

A

Protrusion of part of the stomach through the oesophageal hiatus of the diaphragm

179
Q

Describe the epidemiology of hiatus hernias

A
  • 30% of patients >50
  • Sliding and rolling/para-oesophageal (uncommon)
180
Q

What is the main risk factor for hiatus hernias?

A

Obesity

181
Q

Describe the pathophysiology of sliding hiatus hernias

A

Oesophageal-gastric junction slides through the hiatus and lies above the diaphragm

182
Q

Describe the pathophysiology of rolling/para-oesophageal hiatus hernias

A
  • Gastric fundus rolls up through hiatus alongside oesophagus
  • Gastro-oesophageal junction remains below level of the diaphragm
183
Q

Describe the clinical presentation of hiatus hernias

A

Asymptomatic except for symptomatic GORD

184
Q

What are 2 investigations for patients with hiatus hernias?

A
  1. Barium swallow
  2. Upper GI endoscopy
185
Q

What is the treatment for hiatus hernias?

A
  • Lose weight
  • Treat reflux symptoms
  • Surgery
186
Q

What is biliary colic?

A

Obstruction of the cystic or common bile duct by a stone migrating from the gallbladder

187
Q

Describe the epidemiology of gallstones

A
  • 10-20% of the population
  • More common in females
  • Prevalence increases with age
  • Cholesterol gallstones = 80% of the western world’s gallstones
188
Q

What are 3 causes of cholesterol gallstones?

A

Multifactorial
1. Cholesterol super saturation
2. Nucleation factors
3. Reduced gallbladder motility

189
Q

What are 3 causes of pigment gallstones?

A
  1. Chronic haemolysis (increased bilirubin production)
  2. Cirrhosis
  3. Complication of a cholecystectomy/with duct strictures
190
Q

What are the 5 risk factors for gallstones?

A

5Fs
1. Fat
2. Fertile (pregnant)
3. Forty (or over)
4. Female
5. Family history

191
Q

Describe the pathophysiology of cholesterol gallstones

A
  • Cholesterol held in solution by detergent action of bile salts and phospholipids
  • Forms micelles and vesicles
  • Excess of cholesterol (lithogenic bile) = lack of bile salts and phospholipids
  • Cholesterol crystals and gallstones form
192
Q

Describe the pathophysiology of pigment gallstones

A
  • Bilirubin polymers and calcium bilirubinate
  • Caused by excess of bilirubin
193
Q

What are the 2 symptoms of gallstones?

A

70% are asymptomatic
1. Biliary colic
2. Acute cholecystitis

194
Q

What are 2 symptoms of biliary colic?

A
  1. ‘Colicky’ RUQ pain that is worse after eating large/fatty meals and may radiate to epigastrium/back
  2. Nausea and vomiting
195
Q

What is a symptom of acute cholecystitis?

A

Distension of gallbladder leading to necrosis and ischaemia

196
Q

What is the diagnostic test for gallstones/biliary colic?

A

Ultrasound:
- Stones
- Gallbladder wall inflammation
- Duct dilation suggests distal blockage

197
Q

What are 3 other investigations for gallstones/biliary colic?

A
  1. FBC and CRP = signs of inflammatory response
  2. LFTs = raised ALP but normal bilirubin/ALT
  3. Amylase = check for pancreatitis
198
Q

What is the treatment for gallstones?

A
  • NSAIDs/analgesia
  • IV antibiotics
  • Optional laparoscopic cholecystectomy
199
Q

What are 6 complications of gallstones?

A
  1. Obstructive jaundice
  2. Acute cholecystitis
  3. Acute cholangitis
  4. Pancreatitis
  5. Gallstone ileus (occludes intestinal lumen)
  6. Empyema (obstructed gallbladder fills with pus)
200
Q

What is cholecystitis?

A

Cystic duct impaction - inflammation of the gallbladder due to obstruction of bile ducts and build-up of bile

201
Q

Describe the pathophysiology of cholecystitis

A
  • Stone blocks bile ducts
  • Bile builds up and distends gallbladder
  • Vascular supply may be reduced as a result of distension
  • Retained bile leads to inflammation of gallbladder
202
Q

What are 3 symptoms of cholecystitis?

A
  1. Generalised epigastric pain migrating to severe RUQ pain
  2. Signs of inflammation e.g. fever/fatigue
  3. Pain associated with tenderness and guarding from inflamed gallbladder and local peritonitis
203
Q

What are 3 investigations for patients with cholecystitis?

A
  1. Positive Murphy’s sign (severe pain on deep inhalation with hand pressed into RUQ)
  2. FBC and CRP = inflammatory markers
  3. Ultrasound = thick gallstone walls (inflammation)
204
Q

What is the treatment for cholecystitis?

A
  • IV antibiotics
  • Heavy analgesia
  • IV fluids
  • Cholecystectomy
205
Q

What is acute cholangitis?

A

Bacterial infection of biliary system due to prolonged bile duct blockage

206
Q

Describe the epidemiology of acute cholangitis

A

5-10% mortality

207
Q

Describe the pathophysiology of acute cholangitis

A
  • The bile duct is blocked and so prevents bile from being able to ‘flush’ out into GI tract
  • Bacteria can climb up from the GI tract and cause biliary tree infection and consolidation
  • Infection can affect pancreas as it shares ducts with the gallbladder
208
Q

What are 3 signs of acute cholangitis?

A
  1. Sepsis
  2. Pancreatitis
  3. Reynolds pentad
209
Q

What is Reynolds pentad (acute cholangitis)?

A
  1. Charcot’s triad
  2. Confusion
  3. Septic shock
210
Q

What are 3 symptoms of acute cholangitis?

A

Charcot’s triad:
1. Jaundice
2. Severe RUQ pain
3. Fever (rigors)

211
Q

What are 3 investigations for patients with acute cholangitis?

A
  1. FBCs, LFTs and CRP = leukocytosis, raised ALP/bilirubin/CRP
  2. Blood cultures/MC&S = work out what pathogen it is
  3. Ultrasound +/- ERCP
212
Q

What is the treatment for acute cholangitis?

A
  • Treat sepsis (IV antibiotics)
  • ERCP and stenting (to mechanically clear blockage)
  • Surgery - cholecystectomy
213
Q

What is primary biliary cholangitis also known as?

A

Primary biliary cirrhosis

214
Q

Describe the epidemiology of primary biliary cholangitis

A
  • 90% of patients = women aged 40-50
  • More common in females (9:1)
  • Typical presentation at 50
215
Q

What are 5 risk factors of primary biliary cholangitis?

A
  1. Family history
  2. Many UTIs
  3. Smoking
  4. Past pregnancy
  5. Autoimmune disease
216
Q

Describe the pathophysiology of primary biliary cholangitis

A
  • Interlobar bile ducts are damaged by chronic autoimmune granulomas
  • This results in inflammation and leakage of bile into the blood and hepatocytes
  • = inflammation and bile stasis
217
Q

What are 5 clinical presentations of primary biliary cholangitis?

A
  1. Hepatomegaly
  2. Variceal bleeding
  3. Asymptomatic
  4. Lethargy and fatigue
  5. Joint pain and arthropathy
218
Q

What are 2 clinical presentations of primary biliary cholangitis due to leakage of bile?

A
  1. Pruritus (itchy skin)
  2. Jaundice
219
Q

What are 3 clinical presentations of primary biliary cholangitis due to leakage of cholesterol?

A
  1. Pigmented xanthelasma (yellow fat deposited under skin around eyelids)
  2. Xeropthalmia (dryness of conjunctiva and cornea)
  3. Corneal arcus (white/grey ring around cornea)
220
Q

What are 4 investigations for patients with primary biliary cholangitis?

A
  1. Antibody tests = presence of anti-mitochondria antibodies (AMA) and raised serum IgM
  2. LFTs = raised ALP/GTT/cholesterol
  3. Ultrasound
  4. Liver biopsy
221
Q

What is the treatment for primary biliary cholangitis?

A
  • Ursodeoxycholic acid (reduces cholesterol absorption and improves bilirubin and aminotransferase levels)
  • Cholestyramine (reduces cholesterol absorption)
  • Bisphosphonates (for osteoporosis)
  • Vitamin ADEK supplementation
  • Liver transplant
222
Q

What is primary sclerosing cholangitis?

A

Progressive sclerosis of the biliary tree leading to chronic cholestasis and end-stage liver disease

223
Q

Describe the epidemiology of primary sclerosing cholangitis

A
  • Associated with IBD, mainly UC
  • More common in males
  • Median age = 35
224
Q

Describe the pathophysiology of primary sclerosing cholangitis

A
  • Chronic inflammation and fibrosis of bile ducts
  • Progressive obliterative fibrosis in the intra- and extra-hepatic ducts can cause strictures of the ducts
225
Q

What are 4 symptoms of primary sclerosing cholangitis?

A

50% asymptomatic until advanced disease
1. Non-specific pruritus
Charcot’s triad:
2. Fever (with chills)
3. RUQ pain
4. Jaundice

226
Q

What are 3 investigations for patients with primary sclerosing cholangitis?

A
  1. Ultrasound (can show bile duct dilatation)
  2. ERCP (endoscopic retrograde cholangio pancreatography)
  3. LFT (elevated ALP/GGP and serum albumin levels drop with progression)
227
Q

What is the treatment for primary sclerosing cholangitis?

A
  • Manage symptoms of liver failure
  • ERCP (can dilate extra-hepatic strictures to slow progression)
  • High dose ursodeoxycholic acid (can slow progression)
  • Liver transplant
228
Q

What are 4 complications of primary sclerosing cholangitis?

A
  1. Liver failure
  2. Hepatocellular carcinoma
  3. Cholangiocarcinoma
  4. Colorectal cancer
229
Q

What is acute pancreatitis?

A

Sudden inflammation of the pancreas leading to autodigestion of the gland

230
Q

What are the 11 causes of acute pancreatitis?

A

I GET SMASHED
1. Idiopathic (20%)
2. Gallstones (40%)
3. Ethanol (alcohol - 30%)
4. Trauma
5. Steroids
6. Mumps/malignancy
7. Autoimmune
8. Scorpion stings
9. Hypertriglyceridemia/hypercalcaemia
10. (post) ERCP
11. Drugs (tobacco/thiazides)

231
Q

Describe the pathophysiology of alcohol induced acute pancreatitis

A
  • Pancreas releases exocrine enzymes (zymogen and trypsinogen) that cause autodigestion of the organ
  • Increased intracellular calcium leads to activation of intra-cellular proteases and release of pancreatic enzymes
  • Can result in acinar cell injury and necrosis
232
Q

Describe the pathophysiology of gallbladder induced acute pancreatitis

A
  • Gallstones block the bile duct (sphincter of Oddi)
  • This causes back pressure in the pancreatic duct
233
Q

What are 5 signs of acute pancreatitis?

A
  1. Cullen’s sign (bruising around periumbilical region)
  2. Grey Turner’s sign (bruising on flanks)
  3. Tachycardia
  4. Distension
  5. Abdominal guarding and tenderness
234
Q

What are 3 symptoms of acute pancreatitis?

A
  1. Epigastric/upper abdominal pain radiating through to the back
  2. Nausea and vomiting
  3. Fever with chills
235
Q

What are 3 investigations for patients with acute pancreatitis?

A
  1. CT abdomen (evidence of inflammation, necrosis and pseudocyst)
  2. Abdominal Xray (shows no psoas shadow due to raised retroperitoneal fluid)
  3. LFTs (serum amylase 3x greater, raised lipase/ALT/AST)
236
Q

What is the treatment for mild acute pancreatitis?

A
  • Pain relief
  • IV fluids
237
Q

What is the treatment for severe acute pancreatitis?

A
  • IV antibiotics if necrotising
  • Nasogastric tube
238
Q

What are 7 complications of acute pancreatitis?

A
  1. Pancreatic necrosis
  2. Pancreatic ascites
  3. Pancreatic pseudocysts (25%)
  4. Insulin dependent DM
  5. ARDS
  6. DIC
  7. Sepsis
239
Q

What is chronic pancreatitis?

A

Long standing inflammation of the pancreas from irreversible damage

240
Q

What are 4 causes of chronic pancreatitis?

A
  1. Excess alcohol consumption (main)
  2. Hereditary
  3. Autoimmune
  4. Complication of cystic fibrosis
241
Q

Describe the pathophysiology of chronic pancreatitis

A
  • Pancreas releases exocrine enzymes (zymogen and trypsinogen) that cause autodigestion of the organ
  • Leads to precipitation of protein plugs within duct lumen, forming a nidus for calcification
  • This leads to ductal hypertension and pancreatic damage
  • Small and large duct pancreatitis (large associated with calcification)
242
Q

What are 2 signs of chronic pancreatitis?

A
  1. Diabetes
  2. Steatorrhoea (increase in fat excretion in blood)
243
Q

What are 4 symptoms of chronic pancreatitis?

A
  1. Severe epigastric abdominal pain radiating through to the back
  2. Severe weight loss (due to malabsorption)
  3. Jaundice
  4. Nausea and vomiting
244
Q

What are 2 investigations for patients with chronic pancreatitis?

A
  1. Xray/CT (display calcification)
  2. Secretin stimulation test (detects if pancreas exocrine function is damaged)
245
Q

What is the treatment for chronic pancreatitis?

A
  • Pain relief
  • Cessate alcohol
  • Replace pancreatic enzymes
  • Surgery - local resection to alleviate duct dilatation
246
Q

What are 2 complications of chronic pancreatitis?

A
  1. Insulin dependent DM
  2. Pancreatic carcinoma
247
Q

What is ascites?

A

Fluid in the peritoneal cavity

248
Q

Describe the pathophysiology of ascites

A

Increased pressure in portal system causes fluid to leak out of the capillaries in the liver and bowel and into the peritoneal cavity

249
Q

How is the cause of ascites determined?

A

SAAG - serum-ascites albumin gradient

250
Q

Describe what it means if there is a high SAAG value (>1.1)

A
  • Not much albumin
  • Fluid = hepatic lymph
  • Fluid produced by a sinusoid with increased hydrostatic pressure and decreased oncotic pressure
    CAUSE = PORTAL HYPERTENSION
251
Q

Describe what it means if there is a low SAAG value (<1.1)

A
  • Lots of albumin
  • Fluid = plasma
    CAUSE = EXTRAHEPATIC SOURCE:
  • Malignancy
  • Infection (TB)
  • Trauma
  • Pancreatitis
252
Q

What are 2 investigations for patients with ascites?

A
  1. Fluid sample
  2. Ultrasound/MRI/CT
253
Q

What is portal hypertension?

A

Elevated pressure in the portal venous system

254
Q

What is a pre-hepatic cause of portal hypertension

A

Portal vein thrombosis

255
Q

What are 4 intra-hepatic causes of portal hypertension?

A
  1. Cirrhosis
  2. Schistosomiasis
  3. Budd Chiari syndrome
  4. Sarcoidosis
256
Q

What are 3 post-hepatic causes of portal hypertension?

A
  1. RH failure
  2. IVC obstruction
  3. Constrictive pericarditis
257
Q

Describe the pathophysiology of portal hypertension

A
  • Following liver injury and fibrogenesis, activated myofibroblasts contract (mediated by endothelin, NO and prostaglandins)
  • This increases resistance to blood flow
  • = portal hypertension
  • Splanchnic vasodilation causes a drop in BP
  • CO increases to compensate for low BP
  • Salt and water are retained to increase blood volume
  • = hyperdynamic circulation
  • Causes formation of collaterals between portal and systemic systems
258
Q

What is the difference between compensated and decompensated portal hypertension?

A

Compensated - liver can still function effectively
Decompensated - when the liver is damaged to the point that it cannot function adequately

259
Q

What are 9 presentations of portal hypertension?

A
  1. Ascites/oedema
  2. Hepatic encephalopathy
  3. Splenomegaly
  4. Oesophago-gastric varices (and GI bleeding)
  5. Xanthelasma (yellow fat deposits under skin of eyelids)
  6. Spider naevi
  7. Palmar erythema
  8. Finger clubbing
  9. Leukonychia (white discolouration on nails)
260
Q

What is a symptom of portal hypertension?

A

Bruising

261
Q

What are 3 symptoms of compensated portal hypertension?

A

Usually asymptomatic
1. Weight loss
2. Weakness
3. Fatigue

262
Q

What are 3 symptoms of decompensated portal hypertension?

A
  1. Jaundice
  2. Pruritus
  3. Abdominal pain (due to ascites)
263
Q

What are 3 investigations for patients with portal hypertension?

A
  1. Liver biopsy
  2. LFTs (raised bilirubin/AST/ALT)
  3. Ultrasound/MRI/CT
264
Q

What is the treatment for portal hypertension?

A
  • Treat underlying cause
  • Liver transplant
  • Good nutrition
265
Q

What are 5 complications of portal hypertension?

A
  1. Coagulopathy (fall in clotting factors II, VII, IX and X)
  2. Encephalopathy
  3. Thrombocytopenia
  4. Hepatocellular carcinoma
  5. Hypoalbuminemia
266
Q

What are oesophageal varices?

A

Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage

267
Q

Describe the epidemiology of oesophageal varices

A
  • 90% of patients with cirrhosis develop this over 10 years (but only a third bleed)
  • 10-20% of all upper GI bleeding
268
Q

What are 2 causes of oesophageal varices?

A
  1. Chronic liver disease
  2. Portal hypertension
269
Q

Describe the pathophysiology of oesophageal varices

A
  • High pressure in portal vein
  • Vessels are thin and not meant to transport higher pressure blood
  • This causes damage and can lead to bleeding from the varices into the oesophagus
  • Rupture –> haematemesis –> blood digested –> melaena
270
Q

Describe the clinical presentation of oesophageal varices

A
  • Liver disease
  • Shock (low BP, high HR)
  • Haematemesis (vomiting blood)
  • Pallor
271
Q

What is the investigation for oesophageal varices?

A

Upper GI endoscopy

272
Q

What is the medicinal treatment for oesophageal varices?

A
  • Resuscitation/maintain airway
  • Beta blocker (to reduce CO and portal pressure)
  • Nitrate (to reduce portal pressure)
273
Q

What is the surgical treatment for oesophageal varices?

A
  • Band ligation
  • Trans jugular intrahepatic portosystemic shunt (TIPSS)
274
Q

What are 2 complications of oesophageal varices?

A
  1. 70% chance of rebleeding
  2. Significant risk of death
275
Q

What is spontaneous bacterial peritonitis?

A

Infection of ascitic fluid and peritoneal lining without any clear cause

276
Q

Describe the epidemiology of spontaneous bacterial peritonitis

A
  • Occurs in 10% of patients with ascites secondary to cirrhosis
  • Mortality of 10-20%
277
Q

What are the 3 most common causes of spontaneous bacterial peritonitis?

A
  1. E. coli
  2. Klebsiella pneumoniae
  3. Gram positive cocci e.g. staphylococcus and enterococcus
278
Q

What are 2 signs of spontaneous bacterial peritonitis?

A
  1. Ileus (temporary lack of normal muscle contractions of intestines)
  2. Hypotension
279
Q

What are 2 symptoms of spontaneous bacterial peritonitis?

A

Can be asymptomatic
1. Fever
2. Abdominal pain

280
Q

What are the investigations for patients with spontaneous bacterial peritonitis?

A

Bloods:
- Raised WBC/CRP/creatinine
- Metabolic acidosis

281
Q

What is the treatment for spontaneous bacterial peritonitis

A

IV cephalosporin e.g. cefotaxime

282
Q

What is haemochromatosis?

A

Multi system disorder of dysregulated dietary iron absorption and increased iron release from macrophages

283
Q

Describe the epidemiology of haemochromatosis

A

Usually presents between 40-60

284
Q

What are 2 causes of haemochromatosis?

A
  1. HFE gene mutations (C282Y and H63D - autosomal recessive)
  2. Secondary iron overload due to multiple transfusions
285
Q

Describe the pathophysiology of haemochromatosis

A
  • Deficiency of hepcidin (iron regulatory hormone)
  • Increased intestinal iron absorption
  • Iron accumulates in liver, joints, pancreas, heart, skin and gonads
286
Q

What are 4 signs of haemochromatosis?

A
  1. Arrhythmia
  2. Hepatomegaly
  3. Heart failure
  4. Chronic liver disease
287
Q

What are 5 symptoms of haemochromatosis?

A

Often asymptomatic until later stages
1. Slate grey (brown/bronze) skin
2. Fatigue
3. Weakness
4. Hypogonadism e.g. erectile dysfunction
5. Arthralgia

288
Q

What are 4 investigations for haemochromatosis?

A
  1. Blood (iron study)
  2. Genetic testing
  3. Liver biopsy (gold standard)
  4. MRI
289
Q

What is the treatment for haemochromatosis?

A
  • 1st line = venesection
  • 2nd line = iron chelation
  • Liver transplant
290
Q

What are 4 complications of haemochromatosis?

A
  1. Cirrhosis
  2. Hepatocellular carcinoma
  3. Diabetes
  4. Heart disease
291
Q

What is Wilson’s disease?

A

Disorder of copper metabolism resulting in a build-up of copper in the liver and CNS

292
Q

Describe the epidemiology of Wilson’s disease

A

Onset usually in 20s-30s

293
Q

What is the cause of Wilson’s disease?

A

Mutation in the gene defecting the enzyme involving in biliary excretion of excess copper (autosomal recessive)

294
Q

Describe the pathophysiology of Wilson’s disease

A

Copper accumulates in liver, basal ganglia and cornea

295
Q

What are 3 signs of Wilson’s disease?

A
  1. Cirrhosis
  2. Hepatitis
  3. Psychiatric/neurological presentation = Parkinsonian
296
Q

What are 7 symptoms of Wilson’s disease?

A
  1. Psychiatric/neurological presentation = depression
  2. Kayser-Fleischer rings (green/brown ring around cornea)
  3. Tremor
  4. Reduced memory
  5. Involuntary movements
  6. Dysphagia (swallowing difficulties)
  7. Dysarthria (difficult/unclear articulation of speech)
297
Q

What are 3 investigations for patients with Wilson’s disease?

A
  1. 1st line = 24 hour urine copper and blood ceruloplasmin = high copper, low ceruloplasmin
  2. Liver biopsy
  3. Slit lamp analysis
298
Q

What is ceruloplasmin?

A

Protein that stores and carries copper from the liver to other parts in the blood

299
Q

What is the treatment for Wilson’s disease?

A
  • Avoid high copper foods (e.g. liver, chocolate, nuts, mushroom, shellfish)
  • Avoid alcohol
  • Penicillamine (copper chelation)
  • Liver transplant
300
Q

What are 3 complications of Wilson’s disease?

A
  1. Liver failure
  2. Neurological problems
  3. Death if left untreated
301
Q

What is alpha-1 antitrypsin deficiency?

A

Deficiency of serine protease inhibitor alpha-1 antitrypsin

302
Q

Describe the epidemiology of alpha-1 antitrypsin deficiency

A
  • Presents between 30s-50s (earlier in smokers)
  • More common in white people
303
Q

What is the cause of alpha-1 antitrypsin deficiency?

A

Mutation in SERPINA1 gene (autosomal recessive)

304
Q

Describe the pathophysiology of alpha-1 antitrypsin deficiency

A
  • A1AT inhibits the action of neutrophil elastase
  • This is a proteolytic enzyme produced by neutrophils in the presence of inflammation/infection/smoking
  • When this is deficient, elastase can break down elastin without inhibition
  • Alveolar walls and liver are destroyed
305
Q

What are 4 signs of alpha-1 antitrypsin deficiency?

A
  1. Early onset emphysema
  2. Neonates may present with hepatitis
  3. Cirrhosis
  4. Liver failure
306
Q

What are 2 symptoms of alpha-1 antitrypsin deficiency?

A
  1. COPD like symptoms e.g. SOB
  2. Neonates may present with jaundice
307
Q

What are 2 investigations for patients with alpha-1 antitrypsin deficiency?

A
  1. Serum levels of A1AT
  2. Liver biopsy
308
Q

What is the treatment for alpha-1 antitrypsin deficiency?

A
  • Smoking cessation
  • Corticosteroids
  • Bronchodilators
  • Treat infection
  • Drinking cessation
  • Possible liver transplant
309
Q

Describe the normal physiology of paracetamol metabolism

A
  • 95% is converted into non-toxic metabolites via phase II metabolites which conjugates with sulfate and glucuronide
  • The other 5% is converted to a highly reactive intermediate NAPQI by cytochromes P450 2E1 and 3A4
  • NAPQI is detoxified by conjugation with glutathione to form cysteine and mercapturic acid conjugates
310
Q

Describe the pathophysiology of paracetamol overdose

A
  • Phase II metabolic pathways become saturated
  • More paracetamol is shunted to the cytochrome P450 system to produce NAPQI
  • Hepatocellular supplies of glutathione become depleted due to the higher demand
  • Lack of glutathione results in NAPQI remaining in the liver (toxic form)
  • NAPQI reacts with cellular membrane molecules to result in widespread hepatocyte damage and death
311
Q

What are 2 signs of paracetamol overdose?

A
  1. Fulminant liver failure
  2. Hepatic encephalopathy
312
Q

What are 3 symptoms of paracetamol overdose?

A

Asymptomatic
1. Vomiting
2. RUQ pain
3. Jaundice

313
Q

What is the treatment for paracetamol overdose?

A
  • Activated charcoal
  • IV N-acetylcysteine
  • Liver transplant
314
Q

What is the difference between acute and chronic liver failure?

A

Acute - rapid onset (no evidence of prior liver disease)
Chronic - progressive (evidence of prior liver disease)

315
Q

What are 4 causes of acute liver failure?

A
  1. Paracetamol DILI
  2. Alcohol
  3. Viral hepatitis
  4. Drugs
316
Q

What is the difference between hyperacute, acute and subacute liver failure?

A

Hyperacute = onset of encephalopathy less than 7 days after the development of jaundice
Acute = onset of encephalopathy 8-28 days after the development of jaundice
Subacute = onset of encephalopathy 28-72 days after the development of jaundice

317
Q

What are 2 signs of acute liver failure?

A
  1. Hypoglycaemia (rarer)
  2. Asterixis (inability to maintain sustained posture with subsequent brief, shock-like involuntary movements - rarer)
318
Q

What are 4 common symptoms of acute and chronic liver failure?

A
  1. Malaise
  2. Anorexia
  3. Jaundice
  4. Pruritus
319
Q

What are 4 other symptoms of acute liver failure?

A
  1. Nausea
  2. Confusion (rarer)
  3. Bleeding (rarer)
  4. RUQ pain (rarer)
320
Q

What are 2 investigations for liver failure?

A
  1. LFTs (high bilirubin, low albumin, high PTT)
  2. Liver hepatic enzymes (raised AST/ALT/ALP)
321
Q

What is the treatment for liver failure?

A
  • Fluids
  • Analgesia
  • Liver transplant
322
Q

What is the treatment for complications of liver failure?

A
  • Ascites = diuretics
  • Cerebral oedema = mannitol
  • Bleeding = vitamin K
  • Encephalopathy = lactulose
  • Sepsis = antibiotics
  • Hypoglycaemia = dextrose
323
Q

What are 7 causes of chronic liver failure?

A
  1. Alcohol
  2. Viral hepatitis
  3. Autoimmune (PBC/PSC)
  4. Metabolic (HH, WD, A1AT def)
  5. Neoplastic
  6. NAFLD
  7. AFLD
324
Q

Describe the progression of chronic liver failure

A

Chronic liver condition –> liver damage –> liver symptoms –> liver cirrhosis (if prolonged) –> liver failure

325
Q

What are 2 signs of chronic liver failure?

A
  1. Ascites/oedema
  2. Hepatosplenomegaly
326
Q

What are 8 symptoms of chronic liver failure?

A
  1. Gynaecomastia
  2. Dupuytren’s contracture (one/more fingers bent towards palm)
  3. Clubbing/leukonychia (white nails)
  4. Palmar erythema
  5. Xanthelasma (yellow growths on/near eyelids)
  6. Spider naevi/caput medusae
  7. Haematemesis
  8. Easy bruising
327
Q

What is a complication of chronic liver failure?

A

Higher risk of hepatocellular carcinoma

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