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Phase 2a > LIVER and fwends 2 > Flashcards

LIVER and fwends 2 Flashcards

1
Q

What are the 7 functions of the liver?

A
  1. Oestrogen regulation2. Detoxification3. Metabolism of carbohydrates4. Albumin production5. Clotting factor production6. Bilirubin regulation7. 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. Hepatomegaly2. Ascites3. 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 vomiting2. Diarrhoea3. Anorexia4. 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. LFTs2. FBC3. PTT (increased)4. Abdominal ultrasound5. Fibroscan6. Endoscopy7. CT/MRI8. 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 failure2. Wernicke-Korsakoff encephalopathy3. Acute/chronic pancreatitis4. Mallory-Weiss tear5. 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. Obesity2. Diabetes3. 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. Hepatomegaly2. Jaundice
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24
Q

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

A

Asymptomatic1. Nausea and vomiting2. Diarrhoea3. Fatigue4. Malaise5. 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/MRI3. Ultrasound4. 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. Hepatosplenomegaly2. Fatigue3. Fever4. Jaundice
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30
Q

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

A
  1. Biopsy2. Raised ALT and AST3. 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. Biopsy2. Raised ALT and AST3. 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. Shellfish2. Travellers3. 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. Cholestasis2. 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 vomiting2. Anorexia3. Abdominal pain4. 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 ALT2. 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 hepatitis2. 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 personnel2. Emergency/rescue teams3. CKD/dialysis patients4. Travellers5. Homosexual men6. 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 symptoms2. Fever3. Pruritus (itchy skin)
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48
Q

What are 3 investigations for patients with Hepatitis B?

A
  1. Blood = raised ALT2. 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. Malaise2. Weakness3. Anorexia

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56
Q

What are 2 investigations for patients with Hepatitis C?

A
  1. Hepatitis C antibody screening test2. 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 cirrhosis2. 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. Jaundice2. Hepatomegaly

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62
Q

What are 3 symptoms of Hepatitis D?

A

Symptoms of acute HBV infection:1. Flu-like symptoms2. Fever3. 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 disease2. Non-alcoholic fatty liver disease3. Hepatitis B4. 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. Jaundice2. Hepatosplenomegaly3. Ascites4. 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 medusae2. Palmar erythema3. Gynaecomastia4. Testicular atrophy5. Bruising
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78
Q

What are the 7 investigations for patients with liver cirrhosis?

A
  1. Bloods2. Imaging (CT/MRI/ultrasound/fibroscan)3. Endoscopy4. Liver biopsy5. Enhanced liver fibrosis blood test6. Child-Pugh score7. 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 fibrosis7.7-9.8 = 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. Malnutrition2. Portal hypertension, varices, variceal bleeding3. Ascites and spontaneous bacterial peritonitis4. Hepato-renal syndrome5. Hepatic encephalopathy6. 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 syndrome3. Criggler-Najjar syndrome
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88
Q

What are 6 causes of intrahepatic jaundice?

A
  1. Alcoholic liver disease2. Viral/autoimmune hepatitis3. Iatrogenic4. Hereditary haemochromatosis5. Primary biliary cirrhosis/primary biliary cholangitis6. Hepatocellular carcinoma
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89
Q

What are 3 causes of posthepatic jaundice?

A
  1. Intra-luminal causes e.g. gallstones2. Mural causes e.g. cholangiocarcinoma, stricture, drug-induced cholestasis3. 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 excess2. 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. Confusion2. Ataxia (difficulty with coordinated movements)3. Oculomotor disturbances
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101
Q

What are 3 symptoms of Wernicke’s encephalopathy?

A
  1. Confusion2. 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 impairment2. 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. Constipation2. Electrolyte disturbance3. Infection4. GI bleed5. High protein diet6. 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. Confusion2. Reduced consciousness
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109
Q

What are 3 symptoms of chronic hepatic encephalopathy?

A
  1. Personality changes2. Memory changes3. 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. Smoking2. Excessive alcohol/coffee intake3. Excessive use of aspirin4. Diabetes5. Chronic pancreatitis6. Family history7. 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 pancreatitis2. 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. Anorexia2. Weight loss3. 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 sclera2. Dark urine and pale stools3. Generalised itching

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118
Q

What are 3 investigations for pancreatic cancer?

A
  1. Abdominal ultrasound/CT2. Biopsy3. 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 pancreatectomy2. Distal pancreatectomy3. 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 chemotherapy4. Palliative radiotherapy5. 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 C2. Alcohol3. Non alcoholic fatty liver disease4. Other chronic liver disease

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124
Q

What are 2 signs of hepatocellular carcinoma?

A
  1. Hepatomegaly2. Ascites
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125
Q

What are 9 symptoms of hepatocellular carcinoma?

A

Often remains asymptomatic for a long time1. Fever2. Malaise3. Weight loss4. Abdominal pain5. Anorexia6. Nausea/vomiting7. Jaundice8. Pruritus9. RUQ pain

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126
Q

What are 4 investigations for patients with hepatocellular carcinoma?

A
  1. CT/MRI liver2. Biopsy3. Alpha-fetoprotein (ATP) = raised4. 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. Hepatomegaly2. Ascites
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131
Q

What are 4 symptoms of cholangiocarcinoma?

A
  1. Painless jaundice2. Fever3. Malaise4. RUQ pain
132
Q

What are 4 investigations for patients with cholangiocarcinoma?

A
  1. CT/MRI liver2. Biopsy (ERCP - endoscopic retrograde cholangiopancreatography)3. CA19-9 tumour marker = raised4. 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 diabetes2. 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% asymptomatic1. Painless jaundice = yellow skin and sclera2. Criggler Najjar = jaundice3. Criggler Najjar = nausea/vomiting4. 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. Male2. Chronic cough3. Constipation4. Heavy weight lifting5. 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 lump2. 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 lump2. 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 error2. 90% in adults acquired through multiple and difficult pregnancies3. 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 lump2. Ultrasound
162
Q

What is the treatment for umbilical hernias?

A

<1cm = usually close spontaneously by 5 years1-5cm = 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?

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 lump2. Ultrasound3. 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?

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 swallow2. 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

Multifactorial1. Cholesterol super saturation2. Nucleation factors3. Reduced gallbladder motility

189
Q

What are 3 causes of pigment gallstones?

A
  1. Chronic haemolysis (increased bilirubin production)2. Cirrhosis3. Complication of a cholecystectomy/with duct strictures
190
Q

What are the 5 risk factors for gallstones?

A

5Fs1. Fat2. Fertile (pregnant)3. Forty (or over)4. Female5. 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 asymptomatic1. Biliary colic2. 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/back2. 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 response2. LFTs = raised ALP but normal bilirubin/ALT3. 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 jaundice2. Acute cholecystitis3. Acute cholangitis4. Pancreatitis5. 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 pain2. Signs of inflammation e.g. fever/fatigue3. 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 markers3. 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. Sepsis2. Pancreatitis3. Reynolds pentad
209
Q

What is Reynolds pentad (acute cholangitis)?

A
  1. Charcot’s triad2. Confusion3. Septic shock
210
Q

What are 3 symptoms of acute cholangitis?

A

Charcot’s triad:1. Jaundice2. Severe RUQ pain3. Fever (rigors)

211
Q

What are 3 investigations for patients with acute cholangitis?

A
  1. FBCs, LFTs and CRP = leukocytosis, raised ALP/bilirubin/CRP2. Blood cultures/MC&S = work out what pathogen it is3. 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 history2. Many UTIs3. Smoking4. Past pregnancy5. 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. Hepatomegaly2. Variceal bleeding3. Asymptomatic4. Lethargy and fatigue5. 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 IgM2. LFTs = raised ALP/GTT/cholesterol3. Ultrasound4. 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 disease1. Non-specific pruritusCharcot’s triad:2. Fever (with chills)3. RUQ pain4. 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 failure2. Hepatocellular carcinoma3. Cholangiocarcinoma4. 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 SMASHED1. Idiopathic (20%)2. Gallstones (40%)3. Ethanol (alcohol - 30%)4. Trauma5. Steroids6. Mumps/malignancy7. Autoimmune8. Scorpion stings9. Hypertriglyceridemia/hypercalcaemia10. (post) ERCP11. 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. Tachycardia4. Distension5. Abdominal guarding and tenderness
234
Q

What are 3 symptoms of acute pancreatitis?

A
  1. Epigastric/upper abdominal pain radiating through to the back2. Nausea and vomiting3. 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 necrosis2. Pancreatic ascites3. Pancreatic pseudocysts (25%)4. Insulin dependent DM5. ARDS6. DIC7. 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. Hereditary3. Autoimmune4. 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. Diabetes2. 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 back2. Severe weight loss (due to malabsorption)3. Jaundice4. 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 DM2. 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 pressureCAUSE = PORTAL HYPERTENSION
251
Q

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

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

What are 2 investigations for patients with ascites?

A
  1. Fluid sample2. 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. Cirrhosis2. Schistosomiasis3. Budd Chiari syndrome4. Sarcoidosis
256
Q

What are 3 post-hepatic causes of portal hypertension?

A
  1. RH failure2. IVC obstruction3. 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 effectivelyDecompensated - 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/oedema2. Hepatic encephalopathy3. Splenomegaly4. Oesophago-gastric varices (and GI bleeding)5. Xanthelasma (yellow fat deposits under skin of eyelids)6. Spider naevi7. Palmar erythema8. Finger clubbing9. Leukonychia (white discolouration on nails)
260
Q

What is a symptom of portal hypertension?

261
Q

What are 3 symptoms of compensated portal hypertension?

A

Usually asymptomatic1. Weight loss2. Weakness3. Fatigue

262
Q

What are 3 symptoms of decompensated portal hypertension?

A
  1. Jaundice2. Pruritus3. Abdominal pain (due to ascites)
263
Q

What are 3 investigations for patients with portal hypertension?

A
  1. Liver biopsy2. 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. Encephalopathy3. Thrombocytopenia4. Hepatocellular carcinoma5. 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 disease2. 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 rebleeding2. 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. coli2. Klebsiella pneumoniae3. 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 asymptomatic1. Fever2. 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. Arrhythmia2. Hepatomegaly3. Heart failure4. Chronic liver disease
287
Q

What are 5 symptoms of haemochromatosis?

A

Often asymptomatic until later stages1. Slate grey (brown/bronze) skin2. Fatigue3. Weakness4. Hypogonadism e.g. erectile dysfunction5. 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. Cirrhosis2. Hepatocellular carcinoma3. Diabetes4. 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. Cirrhosis2. Hepatitis3. Psychiatric/neurological presentation = Parkinsonian
296
Q

What are 7 symptoms of Wilson’s disease?

A
  1. Psychiatric/neurological presentation = depression2. Kayser-Fleischer rings (green/brown ring around cornea)3. Tremor4. Reduced memory5. Involuntary movements6. 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 ceruloplasmin2. Liver biopsy3. 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 failure2. Neurological problems3. 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 emphysema2. Neonates may present with hepatitis3. Cirrhosis4. Liver failure
306
Q

What are 2 symptoms of alpha-1 antitrypsin deficiency?

A
  1. COPD like symptoms e.g. SOB2. Neonates may present with jaundice
307
Q

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

A
  1. Serum levels of A1AT2. 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 failure2. Hepatic encephalopathy
312
Q

What are 3 symptoms of paracetamol overdose?

A

Asymptomatic 1. Vomiting2. RUQ pain3. 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 DILI2. Alcohol3. Viral hepatitis4. 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 jaundiceAcute = onset of encephalopathy 8-28 days after the development of jaundiceSubacute = 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. Malaise2. Anorexia3. Jaundice4. Pruritus
319
Q

What are 4 other symptoms of acute liver failure?

A
  1. Nausea2. 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. Alcohol2. Viral hepatitis3. Autoimmune (PBC/PSC)4. Metabolic (HH, WD, A1AT def)5. Neoplastic6. NAFLD7. 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/oedema2. Hepatosplenomegaly
326
Q

What are 8 symptoms of chronic liver failure?

A
  1. Gynaecomastia2. 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 medusae7. Haematemesis8. Easy bruising
327
Q

What is a complication of chronic liver failure?

A

Higher risk of hepatocellular carcinoma

Phase 2a (29 decks)

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