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Phase 2A Tom > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

What is acute liver failure?

A

Liver failure without an underlying chronic failure

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2
Q

What 3 things characterise ALF?

A
  1. Jaundice
  2. Hepatic encephalopathy
  3. Coagulopathy (derangement in clotting)
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3
Q

What 3 categories can ALF be divided into?

A
  • Hyperacute: HE within 7 days of noticing jaundice. Best prognosis as much better chance of survival and spontaneous recovery.
  • Acute: HE within 8-28 days of noticing jaundice
  • Subacute: HE within 5-12 weeks of noticing jaundice (ALF may be defined up to 28 weeks). Worst prognosis as usually associated with shrunken liver and limited chance of recover
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4
Q

What is the main cause of liver failure in developed countries?

A
  • Drug induced (mainly paracetamol but can also be morphine, NSAID, anti-depressants
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5
Q

What is the main cause of ALF worldwide?

A

Viral hepatitis

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6
Q

What are some other causes of ALF?

A
  • Infections (yellow fever, EBV)
  • Toxin induced
  • Pregnancy related
  • Wilson’s disease
  • Budd-chiari disease
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7
Q

Describe the pathophysiology of ALF?

A
  • Direct insult to the liver causes massive necrosis/apoptosis of liver tissue which prevents the liver from carrying out it’s normal function
  • As the condition progresses it can lead to ahyperdynamic circulatory statewith low systemic vascular resistance due to a profound inflammatory response. Collectively, this causes poor peripheral perfusion and multi-organ failure. Patients also develop significantmetabolic derangements(e.g. hypoglycaemia, electrolyte derangement) and are atincreased risk of infection.

Marked cerebral oedema occurs, which is a major cause of morbidity and mortality in ALF. This is thought to be due to hyperammonaemia (as liver fails to clear ammonia) causing cytotoxic oedema and increased cerebral blood flow that disrupts cerebral autoregulation.

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8
Q

What are the key presentations of ALF?

A
  • Jaundice
  • Hepatic encephalopathy
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9
Q

What are some symptoms of ALF?

A
  • Bruising
  • GI bleeding
  • Hypotension and tachycardia
  • Fetor hepaticus (smell of pear drops suggest liver isn’t clearing toxins)
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10
Q

What symptoms are associated with hepatic encephalopathy?

A
  • Altered mental status
  • Confusion
  • Apraxia - difficulty with motor planning
  • Asterixis: flapping tremor suggestive of HE
  • Raised intracranial pressure: papilloedema, bradycardia, hypertension, low GCS
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11
Q

How would you grade the severity of HE?

A

Using the west haven criteria
- Grade 1: change in behaviour with minimal consciousness change
- Grade II: gross disorientation, drowsiness and inappropriate behaviour
- Grade III: marked confusion, incoherent speech, sleeping, not much response other than to verbal stimuli
- Grade IV: coma that is unresponsive to verbal or painful stimuli. Evidence of decorticate or decerebrate posturing.

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12
Q

How would you treat HE?

A
  • Hepatic encephalopathy - caused by liver’s inability to clear harmful substances produced by bacteria in GI tract. Constipation is the main driver of HE.
    • First line treatments:Involves laxatives (i.e. lactulose 15-20 mls QDS)to maintain bowel motions.
    • Second-line treatments:Involves the long-term use of antibiotics (i.e. rifaximin).
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13
Q

What tests would you perform to asses the severity of ALF?

A
  • Liver function tests
  • Prothrombin time ( elevated INR)
  • FBC
  • ABG
  • Basic metabolic panel
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14
Q

What tests would you run to asses the cause of ALF?

A
  • Paracetamol serum level
  • Alpha-1 antitrypsin levels
  • Autoimmune markers: ANA, autoantibodies, immunoglobulins, ANCA
  • Toxicology screen: serum/urine
  • Viral screen:
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15
Q

How do you treat ALF?

A
  • Treat underlying cause
  • Liver transplant if damage is too bad
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16
Q

What are the complications associated with ALF?

A
  • GI bleeding
  • AKI
  • Sepsis
  • Hypoglycaemia
  • High output cardiac failure
  • Cerebral dysfunction
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17
Q

What is the prognosis of ALF?

A

Survival from ALF is greater than 60% and around 55% of patients will have spontaneous recovery without need for liver transplantation.

The overall one year survival following emergency liver transplantation is around 80%.

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18
Q

What is chronic liver disease?

A

Chronic liver disease is caused by repeated insults to the liver, which can result in inflammation, fibrosis and ultimately cirrhosis.

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19
Q

What is cirrhosis?

A

Cirrhosis is a diffuse pathological process, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules.

It can arise from a variety of causes and is the final stage of any chronic liver disease. In general, it is considered to be irreversible in its advanced stages, although there can be significant recovery if the underlying cause is treated.

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20
Q

What 3 things can cirrhosis of the liver lead to?

A

It can lead to portal hypertension, liver failure, and hepatocellular carcinoma

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21
Q

What are the main causes of CLD?

A
  • Alcohol
  • Viral hepatitis B, C
  • Inherited (alpha 1, Wilsons),
  • Metabolic
  • Autoimmune
  • Medication
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22
Q

What causes cirrhosis?

A

Progressive insults to the liver leads toinflammation (hepatitis), fatty deposits (steatosis) and scarring (fibrosis). The normal liver architecture is replaced by fibrotic tissue and regenerative nodules when this is irreversible it is said to be cirrhosis

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23
Q

What are the symptoms of cirrhosis?

A
  • Coagulopathy
  • Jaundice
  • Encephalopathy
  • Ascites
  • GI bleeding due to portal hypertension
  • Clubbing
  • Ankle swelling oedema
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24
Q

What are the key presentations of CLD?

A
  • Blood in vomit and black stool
  • Hand and nail features (white nails, redness of hands and palms)
  • Spider naevi- dilated blood vessels
  • Splenomegaly
  • Gynaecomastia breast formation due to reduced removal of androgens
  • Caput medusa:distended and engorged superficial epigastric veins around the umbilicus.
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25
Q

What biochemical tests would you run to test CLD?

A
  • LFTs- Raised ASTand ALT
  • FBC (thrombocytopenia)
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26
Q

What would be the diagnostic tests for CLD?

A
  • Ultrasound 65-95% detection
  • MRI highly sensitive
  • Liver biopsy (gold standard but invasive)
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27
Q

How do you treat CLD?

A
  • Treat underlying pathology e.g. alcohol cessation, removal of offending medications or use of anti-viral therapies in chronic hepatitis.
  • Transplantation based on patient’s ‘United Kingdom model for end-stage liver disease’ (UKELD) score
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28
Q

How would you monitor someone with CLD?

A

Six month surveillance with an ultrasound

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29
Q

What are the complications of CLD?

A
  • Hepatic encephalopathy
  • Ascites
  • Gastrointestinal bleeding(i.e. variceal bleed)
  • Bacterial infections(i.e. SBP)
  • Acute kidney injury
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
  • Hepatocellular carcinoma
  • Acute-on-chronic liver failure
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30
Q

What are the 3 stags of alcoholic liver disease?

A
  1. Fatty liver
  2. Alcoholic hepatitis (inflammation and necrosis)
  3. Alcoholic liver cirrhosis
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31
Q

What is the prevalence of alcohol use disorders in men and women?

A

14.8% in men
3.5% in women

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32
Q

What are the risk factors for developing ALD?

A
  • Prolonged and heavy alcohol consumption
  • Hepatitis C
  • Female sex
  • Genetic predisposition
  • Obesity
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33
Q

What two pathways metabolise alcohol in the liver?

A
  • Cytochrome P450
  • Alcohol dehydrogenase
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34
Q

Why does alcohol cause liver cirrhosis?

A
  • The chemical pathways for metabolising alcohol create free radicals
  • However people with chronic alcohol consumption with be deficient in antioxidants such as glutathione and vitamin E
  • Also Chronic alcohol exposure also activates a third site of metabolism: hepatic macrophages, which produce tumour necrosis factor (TNF)-alpha and induce the production of reactive oxygen species in the mitochondria.
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35
Q

What are some symptoms of ALD?

A
  • Jaundice
  • Splenomegaly
  • Hepatomegaly
  • Finger clubbing
  • Venous collaterals - engorged para-umbilical veins (caput medusae), present in advanced alcoholic liver disease.
  • Parotid enlargement
  • Marcocytic anaemia
  • Spider naevi
  • Easy bruising
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36
Q

What are some symptoms of ALD?

A
  • Jaundice
  • Splenomegaly
  • Hepatomegaly
  • Finger clubbing
  • Venous collaterals - engorged para-umbilical veins (caput medusae), present in advanced alcoholic liver disease.
  • Parotid enlargement
  • Macrocytic anaemia
  • Spider naevi
  • Easy bruising
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37
Q

What tow liver enzymes are the most common to be elevated in ALD?

A
  1. Aspartate aminotransferase
    2 Alanine aminotransferase
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38
Q

What ratio of AST to ALT is indicative of ALD?

A

A ratio of 2 is seen in 70% of cases.

A reversal of this ratio can indicate viral hepatitis or non-alcoholic fatty liver disease

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39
Q

What other tests would you perform for ALD?

(basically all the tests)

A
  • Full blood count
  • Urea & electrolytes
  • Liver function tests
  • Bone profile
  • C-reactive protein
  • Magnesium
  • Coagulation(INR)
  • Non-invasive liver screen
  • Liver ultrasound
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40
Q

How would you treat ALD

A
  • Alcohol cessation (disulfiram can be used in chronic alcohol dependence (causes negative effects for patients due to acetaldehyde build-up - aversion therapy)
  • Diazepam (for withdrawal)
  • IV thiamine to prevent wernicke-Korsakoff encephalopathy
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41
Q

What advice would you give for someone with liver cirrhosis?

A
  • Reduce salt intake
  • Avoid aspirin and NSAIDs
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42
Q

What are some complications for ALD?

A
  • Liver cirrhosis
  • CNS
  • Obesity, diarrhoea, peptic ulcers
  • Coagulopathy, anaemia
  • Heart arrhythmias/cardiomyopathy/cardiac arrest
  • Low testosterone and high oestrogen
  • Withdrawal from alcohol
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43
Q

What is the prognosis for ALD?

A
  • Fatty liver is reversible, but may progress to cirrhosis with continued drinking.
  • 80% of people with alcoholic hepatitis progress to cirrhosis. Mild episodes of alcoholic hepatitis do not affect mortality but severe episodes associated with 50% mortality at 30 days. 1 yr after admission for alcoholic hepatitis, 40% mortality.
  • 5 yr survival is 48% with cirrhosis, if drinking continues.
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44
Q

What is Wernicke’s Encephalopathy?

A
  • A disorder that results from an inadequate level of vitamin b1 (thiamine)
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45
Q

What are the symptoms of Wernicke’s Encephalopathy?

A
  • Ataxia
  • Ophthalmoplegia
  • Confusion
  • Short term memory loss
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46
Q

What causes Wernicke’s Encephalopathy?

A
  • Alcohol addiction as it impairs GI absorption and hepatic storage
  • Also eating disorders, prolonged vomiting, GI malignancy, amphetamine addiction or Crohn’s disease
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47
Q

What is the treatment of Wernicke’s Encephalopathy

A
  • High dose IV thiamine and then continue with oral afterwards
  • If patient is hypoglycaemic correct thiamine first as glucose can make symptoms worse
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48
Q

What is Korsakoff’s syndrome?

A

This is a complication of untreated Wernicke’s encephalopathy, although it can occur without prior symptoms of Wernicke’s

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49
Q

What are the symptoms of Korsakoff’s syndrome?

A
  • Amnesia
  • Loss of orientation in time and space
  • Mild euphoria
  • Making up stories
  • Apathy
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50
Q

What is the prognosis for Wernicke’s encephalopathy?

A

Death occurs in 20%
Korsakoff’s syndrome occurs in 85% of patients. When both occur together, it is known as Wernicke-Korsakoff syndrome

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51
Q

What is the prognosis for Korsakoff’s syndrome?

A

In thiamine deficiency, Korsakoff’s is considered irreversible, however:
- 20% of patients will fully recover, but
- 25% of patients will require prolonged institutional care
- Symptoms may improve up to 14 months after onset

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52
Q

What are the differences on an MRI between Wernicke’s encephalopathy and Korsakoff’s?

A

There is brainstem involvement with Korsakoff’s

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53
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A

NALFD refers to a fatty liver that cannot be attributed to alcohol or viral causes

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54
Q

What are the 4 stages of NAFLD?

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
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55
Q

Describe the epidemiology of NAFLD

A
  • Most common liver disorder in the world
  • Affects 3/4 of all obese individuals
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56
Q

What are the risk factors for developing NAFLD?

A
  • Obesity
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
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57
Q

How does fat accumulate in the liver?

A
  • Insulin plays a role. Overtime insulin receptors become less responsive and this increases liver fat storage and reduces oxidation. There is also increased uptake of fatty acids
  • This causes fat droplets to accumulate within hepatocytes and swell up.
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58
Q

Why does fat accumulating in the liver causes problems?

A
  • Overtime the fat is vulnerable to degradation especially to free-radicals which causes fatty acid free radical formation this damages the lipid membrane of cells leading to inflammation
  • This damage attracts neutrophils and long term can lead to cirrhosis
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59
Q

What are the symptoms of NAFLD?

A
  • May be asymptomatic even at advanced stages
  • Lots of vague symptoms, malaise and fatigue
  • More advanced can show classic liver failure symptoms, itching, ascites, pain, bruising, hepatomegaly
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60
Q

What investigations would you perform for someone with suspected NAFLD?

A
  • Serum ALT and AST. Normally ALT would be higher than AST unlike AFLD.
  • FBC could be anaemia and thrombocytopenia
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61
Q

What is used to asses the severity of NAFLD?

A

Enhanced Liver Fibrosis (ELF) blood test

< 7.7 indicates none to mild fibrosis
≥ 7.7 to 9.8 indicates moderate fibrosis
≥ 9.8 indicates severe fibrosis

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62
Q

How would you manage NAFLD?

A
  • Healthy and active lifestyle
  • Avoid alcohol
  • Medication to control blood glucose
  • Vitamin E may improve histology of fibrosis
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63
Q

What are the complications of NAFLD?

A

Progression to steatosis
- Ascites
- Varices and variceal haemorrhage
- Encephalopathy
- Hepatocellular carcinoma
- Hepatorenal syndrome - renal disease secondary to liver failure
- Hepatopulmonary syndrome - shortness of breath and hypoxemia caused by vasodilation in the lungs of patients with liver disease.

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64
Q

What are the complications of NAFLD?

A

Progression to steatosis
- Ascites
- Varices and variceal haemorrhage
- Encephalopathy
- Hepatocellular carcinoma
- Hepatorenal syndrome - renal disease secondary to liver failure
- Hepatopulmonary syndrome - shortness of breath and hypoxemia caused by vasodilation in the lungs of patients with liver disease.

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65
Q

What is hepatitis?

A

Hepatitis describes inflammation in the liver. This can vary from a chronic low level inflammation to acute and severe inflammation that leads to large areas of necrosis and liver failure.

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66
Q

What is the prognosis for NAFLD?

A

The overall prognosis in patients with steatosis (fatty liver without evidence of active inflammation) is considered to be good and a majority of patients will remain stable throughout their lifetime.

The same cannot be said of non-alcoholic steatohepatitis (NASH), which is considered the progressive form of NAFLD.

Patients who have NASH progress to cirrhosis 9% to 20% of the time. Up to one third of these patients will die from complications from liver fa

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67
Q

What are the causes of hepatitis?

A
  • Alcohol
  • Non alcoholic fatty liver disease
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced
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68
Q

What are the general presentations of hepatitis?

A
  • Abdominal pain
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Jaundice
  • Fever
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69
Q

What are the biochemical findings of hepatits?

A

Typical biochemical findings are that liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells.

Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

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70
Q

What are the biochemical findings of hepatitis?

A

Typical biochemical findings are that liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells.

Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

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71
Q

What are the types of viral hepatitis?

A

Hepatitis A,B,C,D,E
Herpes viruses e.g., EBV (Epstein-Barr virus) CMV (Cytomegalovirus), VZV (Varicella Zoster Virus)

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72
Q

Which types of hepatitis result in chronic liver disease?

A

Hepatitis B and Hepatitis C

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73
Q

What is hepatitis A?

A

It is a non-enveloped single stranded RNA virus

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74
Q

How is hepatitis A spread?

A

Via the faeco-oral route (contaminated food and water(. Hand washing and good hand hygiene are key to reducing transmission. It is endemic in certain areas e.g., Africa and south America but is rare in UK

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75
Q

What are the risk factors for catching hepatitis A?

A
  • Travel: those travelling to endemic areas
  • Sexual:**high risk activities (e.g analingus, digital-rectal contact, chemsex), multiple partners
  • Haematological disorders: factor VIII and factor IX concentrates have been implicated in transmission
  • Occupational risks: for example laboratory or sewage workers
  • IV drug users:**known to be at increased risk
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76
Q

What are the 4 clinical phases of Hepatitis A?

A
  1. Incubation: has a long incubation period that may last from 2-6 weeks
  2. Prodromal: Early part of the disease. characterised by fever, joint pain and rash
  3. Icteric: As well as jaundice, there is anorexia, abdominal pain and change in bowel habit
  4. Convalescent: Recovery phase as the body returns to normal. Symptoms such as malaise may last for months
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77
Q

What are the signs of hepatitis A?

A
  • Dark urine and pale stools
  • Hepatomegaly (85%)
  • Jaundice
  • Splenomegaly (15%)
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78
Q

Are symptoms more common in children or adults with hepatitis A?

A

Adults

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79
Q

Is hepatitis A a notifiable disease?

A

YES

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80
Q

What are the investigations for Hep A?

A
  • Look for antibodies against antigen on Hep A.

IgM antibodies indicate recent infection 2-6 weeks, and then IgG indicate previous infection or later in disease progression

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81
Q

What are some potential complications of Hep A?

A
  • Relapsing hepatitis(may occur in 5-15%)
  • Fulminant liver failure
  • Prolonged cholestasis
  • Others(interstitial nephritis, acute pancreatitis, red cell aplasia, Guillian-Barre syndrome)
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82
Q

What type of virus is Hepatitis B?

A

It is an enveloped DNA virus that belongs to the Hepadnaviridae family and can cause acute or chronic hepatitis:

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83
Q

How is Hepatitis B transmitted?

A

Direct contact with blood or bodily fluids
- Sexual intercourse
- Sharing needles
- Sharing contaminated household products e.g., toothbrush
- Direct contact of minor cuts or abrasions
- Mother to child (vertical transmission)

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84
Q

What perecentage of people who catch Hep B will go on to have a chronic infection?

A

10%

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85
Q

How does a chronic Hep B infection occur and what is it defined as?

A

When the virus DNA has integrated into the infected persons so they will continue to make the viral proteins.

Chronic disease is defined as detectable levels of surface antigen (HBsAg) 6 months after infection.

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86
Q

What are the symptoms of an acute Hep B infection?

A
  • Subclinical: no symptoms
  • Anicteric: no specific illness just nausea fever, vomiting, pain in liver and itching
  • Icteric - presents same as anicteric, with jaundice
  • Fulminant hepatitis failure - rare, presents with jaundice, confusion and coagulopathy
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87
Q

What are the symptoms of a chronic Hep B infection?

A
  • Asymptomatic carrier state
  • Chronic hepatitis - wide range of symptoms depending on the severity of hepatitis and underlying liver impairment. May mimic acute hepatitis B symptoms.
  • Cirrhosis - hepatomegaly, splenomegaly, portal hypertension
  • Decompensated cirrhosis - ascites, encephalopathy, jaundice, coagulopathy and GI bleeding.
  • Extra-hepatic manifestations - polyarteritis nodosa (PAN), glomerulonephritis, mixed cryoglobulinaemia, papular acrodermatitis
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88
Q

What are the different viral markers to test for in Hep B?

A
  • Surface antigen (HbsAg): indicates current infection
  • E antigen (HbeAg): implies high infectivity
  • Core antibodies (HbcAb): implies past or current infection
  • Surface antibody(HbsAb): implies vaccination or past or current infection
  • Hepatitis B DNA: indicates viral load
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89
Q

How do you manage a chronic Hep B infection?

A
  • Avoid alcohol
  • Antiviral therapy
  • Nucleos(t)ide analogues
  • Pegylated Interferon
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90
Q

How often should someone with chronic Hep B be screened?

A

Every 6 months

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91
Q

What are the complications of Hep B?

A
  • Cirrhosis
  • Liver failure
  • Hepatocellular carcinoma
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92
Q

What is the prognosis for chronic Hep B?

A

Without treatment, the estimated 5-year incidence of cirrhosis in adults with chronic hepatitis B is up to 20%.

Globally, up to 1 million patients die from hepatitis B each year. Patients who are HBeAg-negative due to seroconversion (i.e. development of Anti-HBe) with low or undetectable HBV DNA levels have better outcomes due to the slower rate of disease progression and less development of cirrhosis and HCC. Five-year survival rates among people with untreated decompensated cirrhosis can be as low as 15%.

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93
Q

What is Hep C?

A

Hepatitis C is an RNA virus. It is spread by blood and body fluids. No vaccine is available. It is now curable with direct acting antiviral medications.

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94
Q

What are risk factors for Hep C progression?

A
  • Male
  • Older
  • High viral load
  • Use of alcohol
  • HIV
  • HBV
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95
Q

How many people will develop chronic Hep C?

A

3 in 4 become chronic

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96
Q

What are the signs of a chronic Hep C infection?

A
  • Most patients are asymptomatic
  • 10% have mild influenza-like illness with jaundice and a rise in serum aminotransferases (ALT and AST)
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97
Q

What are the presentations of chronic Hep C infections?

A
  • Cirrhosis
  • Liver failure
  • Hepatocellular carcinoma
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98
Q

What is the screening test for Hep C?

A
  • Hepatitis C antibody is the screening test
  • Hepatitis C RNA testing is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype
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99
Q

How would you approach the management of Hep C

A
  • Have a low threshold for screening patients that are at risk of hepatitis C
  • Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
  • Refer to gastroenterology, hepatology or infectious diseases for specialist management
  • Notify Public Health (it is a notifiable disease)
  • Stop smoking and alcohol
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100
Q

What is the management for Hep C?

A
  • Triple therapy with direct acting antivirals (DAAs) - treatment is usually a once daily, oral tablet regimen for either 8 or 12 weeks
    • NS5A (initiates viral replication) inhibitor end in ASVIR e.g. ledipasvir, ombitasvir, ritonasvir
    • NS5B (needed for viral replication) inhibitors end in BUVIR e.g. sofosbuvir, dasabuvir
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101
Q

What are some complications of Hep C?

A
  • Thyroiditis
  • Autoimmune hepatitis
  • Polymyositis - inflammatory disease that causes muscle weakness affecting both sides of the body
  • Porphyria cutanea tarda - porphyrin build up in skin
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102
Q

Which types of hepatitis is there a vaccine available for?

A

Hep A and Hep B

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103
Q

What is hepatitis D?

A

Hepatitis D is an RNA virus. It can only survive in patients who also have a hepatitis B infection. It attaches itself to the HBsAg to survive and cannot survive without this protein.

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104
Q

What are the complications of Hep D?

A

It increases the complications and severity of Hepatitis B. There is no treatment for it. It is a notifiable disease.

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105
Q

What is Hep E?

A

Hepatitis E is an RNA virus. It is transmitted by the faecal oral route. It is very rare in the UK

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106
Q

What are the symptoms of Hep E?

A

Normally it produces only a mild illness, the virus is cleared within a month and no treatment is required.

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107
Q

What are some complications of Hep E?

A

Hepatic complications

  • Fulminant hepatitis in pregnancy(20% mortality)
  • Decompensated cirrhosis or ACLF
  • Acute liver failure
  • Rapidly progressive fibrosis(chronic hepatitis E)

Extrahepatic complications

  • Neurological: wide variety of neurological problems associated with hepatitis E (e.g. Guillain-Barré syndrome, brachial neuritis, mononeuritis multiplex, meningoencephalitis).
  • Haematological: thrombocytopaenia, MGUS, cryoglobulinemia
  • Renal: glomerulonephritis
  • Other: pancreatitis, autoimmune thyroiditis, polyarthritis, among others.
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108
Q

Who is most susceptible to serious Hep E infections?

A

Immunocompromised people

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109
Q

What is autoimmune hepatitis?

A

Autoimmune hepatitis (AIH) is a chronic inflammatory disease of the liver of unknown aetiology.

It is characterised by the presence of circulating auto-antibodies with a high serum globulin concentration, inflammatory changes on liver histology, and a favourable response to immunosuppressive treatment

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110
Q

Is autoimmune hepatitis more common in men or women?

A

Women

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111
Q

What is a possible cause of autoimmune hepatitis?

A

Genetic predisposition triggered by environmental factors such as a viral infection that causes a T cell-mediated response against the liver cells.

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112
Q

Who does type 1 autoimmune hepatitis affect?

A

Adults, typically presents around or after menopause in women presents with liver disease on examination

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113
Q

What autoantibodies are associated with type 1 autoimmune hepatitis?

A
  • Anti-nuclear antibodies
  • Anti-smooth muscle antibodies
  • Anti-soluble liver antigen
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114
Q

Who does type 2 autoimmune hepatitis affect?

A

Children/young adults

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115
Q

What are the key presentations of type 2 autoimmune hepatitis?

A

Acute hepatitis with high levels of ALT, AST and IgG antibodies.

116
Q

What are the autoantibodies associated with type 2 autoimmune hepatitis?

A
  • Anti-liver kidney microsomes
  • Anti-liver cytosol antigen
117
Q

What is the treatment for autoimmune hepatitis?

A

Treatment is with high dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine, are introduced

118
Q

What is the prognosis for autoimmune hepatitis?

A

10-20% of patients will require a transplant. Nevertheless, the overall prognosis is good with a 10-year survival in excess of 90%.

119
Q

What 2 main products can Haem be broken into?

A

Biliverdin and Fe2+

120
Q

What enzyme converts biliverdin to unconjugated bilirubin?

A

Biliverdin reductase

121
Q

What protein does unconjugated bilirubin bind to and why?

A

Albumin as it is not soluble it needs to travel to the liver

122
Q

What does conjugated bilirubin form?

A

Urobilinogen

123
Q

What converts conjugated bilirubin to urobilinogen?

A

Intestinal bacteria

124
Q

What can urobilinogen form?

A
  1. It can go back to the liver
  2. It can go to the kidneys and rom urinary urobilin
  3. Can form stercobilin which is secreted in faeces
125
Q

What is pre-hepatic jaundice?

A

When a condition or infection speeds up the breakdown of RBCs. This causes increased bilirubin

126
Q

What can cause pre-hepatic jaundice?

A

Malaria, Thalassaemia and sickle cell

127
Q

What is intra-hepatic jaundice?

A

When there is a problem in the liver that affects it’s ability to process bilirubin.

128
Q

What can cause intra-hepatic jaundice?

A

Hepatitis/B/C, alcoholic liver disease, Gilbert’s syndrome, drug misuse.

129
Q

What is post-hepatic jaundice?

A

When the bile duct system is inflamed or obstructed which means no bile is moved into the digestive system

130
Q

What causes post-hepatic jaundice?

A

Gall stones, pancreatitis, Gall/pancreatic cancer

131
Q

What compound causes dark urine?

A

Conjugated bilirubin

132
Q

A patient with jaundice has pale stools. What compound is absent?

A

Stercobilinogen.

133
Q

What is the affect on conjugated and unconjugated bilirubin levels in someone with pre-hepatic jaundice?

A
  • Unconjugated will be increased with slight increase in conjugated
134
Q

What is the affect on conjugated and unconjugated bilirubin levels in someone with intrahepatic jaundice?

A
  • Increased unconjugated but normal conjugated
135
Q

What is the affect on conjugated and unconjugated bilirubin levels in someone with post-hepatic jaundice?

A
  • Conjugated is elevated but unconjugated is normal. Urobilinogen will be decreased
136
Q

What is the affect on the urine and stools in a patient with pre-hepatic jaundice?

A

Normal

137
Q

What is the affect on the urine and stools in a patient with intra-hepatic jaundice?

A

Dark urine and slightly paler stools

138
Q

What is the affect on the urine and stools in a patient with post-hepatic jaundice

A

Dark urine and pale stools

139
Q

What is Cholelithiasis?

A

Gallstones refers to the development of solid deposit or stone within the gallbladder

140
Q

What is bile?

A
  • It is secreted by hepatocytes in the liver and then stored in the gall bladder. Comprised of bile salts, phospholipid, bilirubin and cholesterol
141
Q

What causes gallstones?

A
  • Cholesterol stones are the most common. Due to crystallisation of cholesterol within bile 70-80%
  • Black pigment stones caused by calcium bilirubinate. Too much bilirubin due to increased haemolysis 10-20%
  • Brown pigment stones occur due to infection
142
Q

What are the risk factors for developing gallstones?

A

he classic risk factors for gallstone disease are described as the ‘4 F’s’:

  • Female: 2-3 times more likely to develop gallstones than men
  • Fat: a BMI > 30 is a key risk factor
  • Forties: the risk increases significantly from approximately 40 years old
  • Fertile: pregnancy is an important risk factor
143
Q

What are the symptoms of gallstones?

A

Biliary colic- This is an acute, severe epigastric that can radiate to the right shoulder due to inflammation of the phrenic nerve in the diaphragm pain that tends to be self-limiting

144
Q

What are the complications of gallstones?

A

-Acute cholecystitis
- Acute cholangitis(most common cause)
- Acute pancreatitis (gallstones most common cause
-Gallbladder cancer

145
Q

What investigations would you perform for gallstones?

A
  • LFT
  • Gallstones
  • Abdominal ultrasound
146
Q

What is the management for gallstones?

A

Remove the stones or gallbladder

It is important to note that if gallstones are found incidentally and the patient has been asymptomatic, surgery is not recommended!

147
Q

What is the prognosis for gallstones?

A

The majority of patients with gallstones will be asymptomatic. 1-4% of patients develop gallstone-related complications, the most common being biliary colic. 10-20% of those who have had an attack of biliary colic will go on to develop a more serious complication, such as acute cholecystitis.

148
Q

What is Cholecystitis?

A

inflammation of the gallbladder most commonly occurring due to impacted gallstones

149
Q

What percentage of patients with gallstones will develop cholecystitis?

A

10%

150
Q

Where does the blockage normally occur in cholecystitis?

A

Cystic duct or neck of the gallbladder

151
Q

How does an impacted gallstone cause cholecystitis?

A

Inflammation and infection occur when a stone becomes impacted in the cystic duct.

An impacted stone leads to impaired drainage of gallbladder contents and the release of inflammatory mediators. This leads to bacterial overgrowth, usually involving gram-negative rods or anaerobes.

152
Q

What is the difference between biliary colic and cholecystitis ?

A

There is an inflammatory response in cholecystitis

153
Q

What are the symptoms of cholecystitis?

A
  • Similar to biliary colic but with more prolonged pain and fever more likely pain to go to the shoulder
  • Murphy’s sign
  • Jaundice
  • Palpable mass
154
Q

What is murphy’s sign?

A

There will be RUQ pain that is worse on inspiration. You put your hand under the patients ribs and ask them to breathe in. As they do so gallbladder will be forced against your hand causing severe pain

Only a sign if not present on left side

155
Q

What investigations would you do for cholecystitis?

A
  • FBC:leukocytosis with neutrophilia
    Serum amylase to rule out pancreatitis
156
Q

What is the gold standard test for cholecystitis?

A

Abdominal ultrasound will detect dilated bile duct, gallbladder wall thickening

157
Q

What is the non-surgical treatment for cholecystitis?

A
  • Nil by mouth
  • Antibiotics (even if not infection): Cefuroxime – 1.5mg/8h IV
    Metronidazole – add if patient is particularly ill
158
Q

What are the surgical options for cholecystitis?

A

Immediate Cholecystectomy – performed laparoscopically. Mortality <1%. Should be performed within 48 hours of presentation if patient is able to tolerate surgery.

Delayed cholecystectomy is available for some but outcomes aren’t as good.

Can also perform cholecystostomy which involves draining fluid from gallbladder

159
Q

What are the complications of cholecystitis?

A
  • Gallbladder empyema: acute inflammation which can lead to gallbladder filling with pus and perforating
  • Gallstone ileus: gallstone causes obstruction in intestine
  • Acute cholangitis: infection of the biliary tree commonly caused by gallstones which move into the common bile duct
160
Q

What is the prognosis for cholecystitis?

A

Gallbladder perforation has a mortality of over 30%, whilst untreated acute acalculous cholecystitis has a mortality of up to 50%

161
Q

What is acute cholangitis?

A

Acute cholangitis refers to infection of the biliary tree characteristically resulting in pain, jaundice and fevers.

162
Q

What are the main causes of acute cholangitis?

A
  • Stones in the bile duct resulting in impaired drainage and overgrowth of bacteria
  • Benign structure/malignant leading to a obstruction
  • Post ERCP operation
163
Q

What is the most common bacteria that causes cholangitis?

A

E.coli

164
Q

What are the key presentations of cholangitis?

A

-Charcot’s triad abdominal pain, jaundice and fever
- Hypotension and change in mental state Reynold’s pentad associated with sepsis

165
Q

What are the symptoms of cholangitis?

A
  • RUQ abdominal pain
  • Jaundice
  • Fever: the most common feature
  • Nausea and vomiting
  • Malaise
  • Pruritis
  • Dark urine and pale stool (cholestasis)
  • Confusion: part of Reynold’s pentad
166
Q

What investigations would you perform for cholangitis?

A

FBC- high white cell
Raised urea and creatine
ABG to check for sepsis
Ultrasound would be best

167
Q

What is the surgical treatment for cholangitis?

A
  • Biliary decompression:
    • ERCP: first-line procedure usually performed within 24-48 hours. Allows for endoscopic exploration of the biliary tract with the removal of gallstones to facilitate drainage. Sphincterotomy may be performed to reduce the risk of future blockage.
168
Q

What is primary biliary cholangitis?

A

An autoimmune condition characterised by granulomatous destruction of the intrahepatic biliary ducts, leading to cholestasis and subsequent leakage of bile into the circulation.

169
Q

What causes PBC?

A

serum anti-mitochondrial antibodies (AMA) are found in almost all patients.

This allows T-cells to target the cells in the intrahepatic ducts and destroy them.

170
Q

What are risk factors for developing PBC?

A
  • Female gender
  • Autoimmune conditions
  • Family history
  • Past pregnancy
  • Smoking
  • Excessive use of nail polish and hair dye
  • Chronic urinary tract infection
171
Q

Describe the pathophysiology of PBC?

A
  • There is destruction of the intralobular ducts within the liver causing obstruction of the outflow of bile. (cholestasis)
  • This leads to the trapping of bile acids in the liver causing progressive fibrosis, cirrhosis and eventually liver failure
172
Q

What are the key presentations of PBC?

A
  • Severe itching as bile acids build up in the blood usually in middle aged women when the disease is most prevalent
  • May also be abnormal LFTs
173
Q

What are the signs of PBC?

A
  • Skin hyperpigmentation
  • Clubbing
  • Mild hepatosplenomegaly
  • Xanthelasma and xanthomata (late sign) - due to leakage of cholesterol
174
Q

What are the symptoms of PBC?

A
  • Pruritis (itchy skin) - leakage of bile salts
  • Fatigue and weight loss
  • Dry eyes and dry mouth - Sjogren’s syndrome
  • Obstructive jaundice (late sign) - due to leakage of bile and conjugated bilirubin
175
Q

What are the investigations to consider for PBC?

A
  • Antimitochondrial antibodies
  • LFTs raised ALT and GGT
  • Transabdominal ultrasound
176
Q

What is the management of PBC?

A
  • Ursodeoxycholic acid dampens the inflammatory response
  • Fat soluble vitamins ADEK
  • Cholestyramine: bile acid sequestrant for symptomatic relief of pruritis
  • Codeine phosphate: for diarrhoea
  • Bisphosphonates: for osteoporosis
177
Q

What are the complications of PBC?

A
    • Malabsorptionof fat-soluble vitamins A, D, E and K due to cholestasis; may result in coagulopathy due to decreased bilirubin in gut lumen
  • Hypercholesterolaemia:cholestasis is associated with hypercholesterolaemia
  • Liver cirrhosis:end-stage disease results in fibrosis and eventual cirrhosis, whilst portal hypertension may cause ascites and variceal bleeding
  • Hepatocellular carcinoma: 20-fold increased risk
  • Metabolic bone disease:osteoporosis and osteomalacia
178
Q

What is the prognosis for PBC?

A

Median survival is approximately 9 years, however, in patients diagnosed at an asymptomatic stage, survival is twice as high compared to those diagnosed at a symptomatic stage.

179
Q

What is primary sclerosing cholangitis (PSC)?

A

Where the intrahepatic or extrahepatic ducts become strictured and fibrotic

180
Q

What are the risk factors for developing PSC?

A
  • Male
  • Usually have a history of IBS. Usually ulcerative colitis
  • Family history
181
Q

What % of people with PSC have also got ulcerative colitis?

A

80%

4% of people with ulcerative colitis will develop PSC

182
Q

What causes PSC?

A
  • There is an element of genetic elements and environmental factors (host gut microbiome)
  • The damage of the bile ducts leads to cholestasis, and bile and toxin build up in the liver
183
Q

What are the Key presentations of PSC?

A
  • Usually asymptomatic at first and will be detected on routine blood tests
  • History of IBS and male sex
184
Q

What are the signs of PSC in later stages of the disease?

A
  • Jaundice
  • Signs of complications e.g., acute cholangitis and chronic liver disease
185
Q

What are the symptoms of PSC?

A
  • Pruritis
  • Fatigue
  • Abdominal pain
  • IBS symptoms
186
Q

What is the gold standard test for diagnosing PSC?

A

MRCP magnetic resonance Cholangiopancreatography. This involves an MRI scan of the liver, bile ducts and pancreas. In primary sclerosis cholangitis it may show bile duct lesions or strictures

Used to be ERCP but this is less invasive

187
Q

What other tests would you perform for PSC?

A
  • LFTs - raised ALP and raised bilirubin, raised GGT, raised ALT and AST if liver damage present, decreased albumin.
  • Viral hepatitis screen:screen for HBsAg and anti-HCV in all patients
188
Q

What are the treatments for PSC?

A
  • Observation and lifestyle
  • Cholestyramine for the relief of itching
  • Fat soluble vitamin supplementation
189
Q

What are the complications associated with PSC/

A
  • Cholangiocarcinoma (20%) will develop cancer of biliary tree most common cause of death
  • Liver problems
    • Hepatocellular carcinoma:liver cancer has a reported prevalence of 2-4%
  • Colorectal carcinoma:an increased risk of colorectal cancer in patients with UC who also have PSC compared to those with UC only
190
Q

What is acute pancreatitis?

A

Acute pancreatitis presents with a rapid onset of inflammation and symptoms. After an episode of acute pancreatitis, normal function usually returns.

191
Q

What are the most common causes of pancreatitis?

A

50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors.

192
Q

Name the different causes of acute pancreatitis?

A

I- Idiopathic
G- Gallstones
E- Ethanol
T- trauma
S- steroid use
M- mumps
A- autoimmune
S- scorpion sting
H- hyperlipidaemia / hypercalcaemia
E- ERCP endoscopic retrogade cholangiopancreatography
D- drugs

** I GET SMASHED**

193
Q

Describe the pathophysiology of pancreatitis?

A
  • It is caused by early activation of trypsinogen and digestive enzymes within the pancreas this leads to inflammation and oedema.
  • Gallstones cause obstruction in the biliary tree which may obstruct the ampulla this causes biliary reflux and raised pressures that result in pancreatitis
194
Q

What are the symptoms of pancreatitis?

A
  • Severe epigastric pain that radiates to the back
  • Associated vomiting
  • Abdominal tenderness
  • Signs of hypovolemia e.g., tachycardic, tachypnoea and low BP
195
Q

What are the signs of pancreatitis?

A

Cullen’s sign – bruising around periumbilical region
Grey Turner’s sign – bruising on flanks

196
Q

What are the diagnostic tests for pancreatitis?

A
  • Serum amylase- levels rises faster than lipase levels also fall faster within 24-48 hours. Less specific as can be raised in other conditions
  • Serum lipase is more specific and levels last longer but rise slower.

Amylase more tested should be 3 times normal range

197
Q

What is the treatment for pancreatitis?

A
  • IV fluids
  • Nil by mouth
  • Analgesia
  • Antibiotics if sign of infection
198
Q

How would you monitor pancreatitis?

A
  • Hourly pulse, BP, urine output.
  • Daily FBC, U&E, Ca2+, glucose, amylase and ABG.
199
Q

What are the complications of pancreatitis?

A
  • Necrosis of the pancreas
  • Infection of the necrotic area
  • Sepsis
  • ARDS
  • Chronic pancreatitis
200
Q

What is the mortality rate of pancreatitis?

A

5%

201
Q

What is chronic pancreatitis?

A

Chronic pancreatitis describes irreversible inflammation and/or fibrosis of the pancreas characterised by epigastric pain and progressive decline in endocrine and exocrine function.

202
Q

What causes chronic pancreatitis?

A

It often occurs secondary to repeated episodes of acute pancreatitis. Alcohol is responsible for up to 80% of cases. Other causes include ductal obstruction (e.g. gallstones), autoimmune pancreatitis, and cystic fibrosis.

This leads to loss of exocrine and endocrine function

203
Q

What are the signs and symptoms of chronic pancreatitis?

A
  • Epigastric tenderness
  • Skin nodules due to fat necrosis by lipase
  • Nausea and vomiting
  • Features of diabetes
  • Steatorrhea and diarrhoea due to lack of enzymes to digest food
204
Q

What is the management for chronic pancreatitis?

A
  • Pancreatic enzyme replacement e.g., Creon
  • Low fat and vitamin supplementation diet
  • Insulin for diabetes
205
Q

What is the surgical management of chronic pancreatitis?

A

ERCP with stenting can be used to treat strictures and obstruction to the biliary system and pancreatic duct.

Surgery may be required by specialist centres to treat:

Severe chronic pain (draining the ducts and removing inflamed pancreatic tissue)
Obstruction of the biliary system and pancreatic duct
Pseudocysts
Abscesses

206
Q

What is ascites?

A

The accumulation of free fluid in the peritoneal cavity

207
Q

What are the two categories of ascites?

A
  • Normal portal pressure
  • Raised portal pressure
208
Q

What are the causes of ascites?

A
  • Malignancy
  • Low albumin
  • Pancreatitis
  • Bowel obstruction
  • Portal hypertension
209
Q

What are the risk factors for developing ascites?

A
  • High sodium diet
  • Hepatocellular carcinoma
210
Q

What test is used to determine the cause of ascites?

A
  • SAAG the serum ascites-albumin gradient
211
Q

What do the different results of SAAG indicate?

A

High SAAG >1.1g/dl or 11 g/l= raised portal pressure and cirrhosis (transudate)
Low SAAG <1.1g/dl or 11g/l= normal portal pressure (exudate)

212
Q

How would you manage ascites?

A
  • A shunt
  • Spironolactone to increase sodium excretion
  • Paracentesis
213
Q

How would you manage ascites?

A
  • A shunt
  • Spironolactone to increase sodium excretion
  • Paracentesis
214
Q

What are the complications of ascites

A
  • Severe hypovolemia
  • Peritonitis
215
Q

What is the prognosis for someone who has ascites?

A

10-20% survival 5 years from onset

216
Q

What is portal hypertension?

A

Elevated pressure in the portal venous system. It is defined as pressure 5 mm Hg greater than the inferior vena cava

(normal pressure 5-10)

217
Q

What are the causes of portal hypertension?

A

Thrombosis
Cirrhosis (80% UK)
Schistosomiasis (commonest worldwide)
Heart failure

218
Q

How does cirrhosis cause portal hypertension?

A
  • There is increased resistance to blood flow causing blood to backflow into the portal vein.
  • This causes splanchnic vasodilation and therefore drop in BP causing a increase in HR to compensate further worsening the problem
219
Q

What are some signs of portal hypertension?

A

Splenomegaly due to portal hypertension
Liver failure
Variceal bleeding

220
Q

What investigations to confirm portal hypertension?

A

Abdominal ultrasound- dilated portal vein
Doppler ultrasound

221
Q

What is the treatment for portal hypertension?

A
  • Treat underlying cause
  • Salt reduction and diuretics
  • Beta-blockers and nitrate to reduce blood pressure
222
Q

What are the complications of portal hypertension?

A
  • Varices and variceal haemorrhage
  • Ascites
  • Hepatopulmonary syndrome
  • Liver failure
  • Hepatic encephalopathy
  • Cirrhotic cardiomyopathy
223
Q

What are oesophageal varices?

A

Oesophageal varices are abnormal, dilated veins that occur at the lower end of the oesophagus; they account for 10-20% of upper GI bleeds

224
Q

What causes oesophageal varices?

A

Portal hypertension

225
Q

How do oesophageal varices form?

A

Veins of the oesophagus drain into the portal vein. Due to hypertension there is backflow from the portal vein causing the veins to enlarge and dilate

226
Q

How do oesophageal varices form?

A

Veins of the oesophagus drain into the portal vein. Due to hypertension there is backflow from the portal vein causing the veins to enlarge and dilate.

227
Q

What are oesophageal varices dangerous?

A

They can cause GI bleeds

228
Q

How do you treat oesophageal varices?

A

Endoscopic variceal band ligationis first line

sclerotherapy with N-butyl-2-cyanoacrylate can also be done. Injection of medicine into vessels causing them to shrink

229
Q

What are some preventions for oesophageal varices?

A
  • Beta-blocker:allto reduce portal pressure. This reduces rebleeding and mortality
  • Endoscopic variceal band ligation(EVL): used asprimary preventionfor people with cirrhosis who have medium to large oesophageal varices. Performed at two-weekly intervals until all varices are eradicated, alongside a proton pump inhibitor to prevent EVL-induced ulceration
230
Q

What is peritonitis?

A

Inflammation of the peritoneum

231
Q

What are the two types of peritonitis?

A
  • Primary peritonitis - inflammation caused by spontaneous bacterial peritonitis. This is the most common type of peritonitis
    • e.g. E.coli, klebsiella, staphylococcus aureus
  • Secondary peritonitis - caused by something else e.g. chemical such as, bile
232
Q

What are the two ways that bacteria spread in peritonitis?

A

Direct spread: through the bacterial wall
Haematogenous spread: bacteria enter ascites via the blood stream

233
Q

What are the symptoms of peritonitis?

A
  • Sudden onset of severe pain in the abdominal area
  • Poorly localised pain
  • Rigid abdomen
  • Pain relieved by resting hands on abdomen - thereby stopping movement of peritoneum and thus pain
  • Lying still - people with peritonitis want to stay still
234
Q

What tests would you perform for peritonitis?

A
  • Ascitic tap - high white cell count
  • Blood cultures
235
Q

What is the management for peritonitis?

A
  • Iv fluids
  • Give broad-spectrum antibiotics e.g., cephalosporins rifaximin
236
Q

What are the complications of peritonitis?

A
  • Sepsis
  • Kidney failure
  • Paralytic ileus
237
Q

What is the prognosis for peritonitis?

A

The one year survival following an episode of SBP is 30-50%.

238
Q

What is hemochromatosis?

A

Is an iron storage disorder that results in excessive total iron and deposition of iron in tissues.

239
Q

What is the most common mutation for hemochromatosis?

A

The human haemochromatosis protein (HFE) gene is located on chromosome 6.

It is an autosomal recessive allele on this gene that causes disease

240
Q

What are risk factors for developing hemochromotosis?

A
  • Family history
  • Alcoholism
  • History of chronic transfusion: only relevant inacquiredhaemochromatosis, for example in patients with thalassaemia
241
Q

Describe the pathophysiology of hemochromatosis

A
  • There is unregulated absorption of iron from the gut causing iron overload
  • This results in iron deposition on multiple tissues most commonly affecting liver, pancreas, and the heart
242
Q

What are the symptoms of hemochromatosis?

A
  • Chronic tiredness
  • Joint pain
  • Bronze pigmentation of skin
  • Hair loss
  • Erectile dysfunction
  • Amenorrhoea
  • Cognitive symptoms
243
Q

How would you initially test for hemochromatosis?

A
  • Serum ferritin will be high but can also be high in other conditions
  • Serum transferrin if this is high as well then likely to be hemochromatosis
244
Q

What are the gold standard tests for hemochromatosis?

A

Now genetic testing is gold standard

Liver biopsy with Perl’s stain can be used to establish the iron concentration in the parenchymal cells used to be the gold standard

245
Q

What is the treatment for hemochromatosis?

A
  • venesection involves draining small amounts of blood around 500ml
  • Iron chelation can be used Deferoxamine
  • Patients should avoid alcohol
246
Q

What are the complications of hemochromatosis?

A
  • Type 1 diabetes
  • Liver cirrhosis
  • Endocrine and sexual problems
  • Cardiomyopathy
  • Hepatocellular carcinoma
  • Hypothyroidism
247
Q

What is wilson’s diseae?

A

An excessive accumulation of copper in the body and tissue.

248
Q

What mutation causes wilson’s disease?

A

“Wilson disease protein” on chromosome 13. It is an autosomal recessive disease

249
Q

How does Wilson’s causes disease?

A
  • There is dysfunction of the transport protein for copper resulting in less copper excretion in the bile.
  • Therefore copper accumulates in hepatocytes and subsequently leaks into the blood and accumulates in the basal ganglia, kidney and cornea
250
Q

What are the 3 main affects of Wilson’s disease?

A

Hepatic problems (40%)
Neurological problems (50%)
Psychiatric problems (10%

251
Q

What are the hepatic problems of Wilson’s disease?

A
  • Hepatosplenomegaly
  • Hepatitis and cirrhosis
  • Jaundice
  • Ascites
252
Q

What are the neurological problems associated with wilson’s disease?

A
  • Dysarthria (speech difficulties)
  • Dystonia
  • Parkinsonism (tremor, rigidity)
  • Motor symptoms often asymmetric
253
Q

What are the psychiatric problems associated with Wilson’s?

A
  • Depression
  • Psychosis
254
Q

What is another sign of Wilson’s disease?

A

Kayser-Fleischer rings in cornea (

255
Q

What are the first line investigations for Wilson’s disease?

A

Reduced ceruloplasmin and increased24 hour urinary copper excretion is highly suggestive of Wilson’s disease.

256
Q

What is the gold standard test for Wilson’s disease?

A

Liver biopsy to see levels of copper

257
Q

What is the treatment for Wilson’s disease?

A
  • Copper chelation
    D-penicillamine or trientine hydrochloride
258
Q

What is alpha 1 antitrypsin deficiency (A1AD)?

A

Alpha-1-antitrypsin deficiency is a condition caused by an abnormality in the gene for a protease inhibitor called alpha-1-antitrypsin.

259
Q

What does A1AT protein do?

A

-Alpha-1 antitrypsin (A1AT) is aprotease inhibitormade in the liver which predominantly acts to protect the lungs from neutrophil elastase.

260
Q

How does A1AD cause disease in the liver?

A
  • In the liver as the protein is misfolded it gets stuck in the hepatocyte. This causes cell death leading to liver damage (Jaundice, hepatitis, cirrhosis and hepatocellular carcinoma)
261
Q

How does A1AD cause disease in the lungs?

A
  • Normally neutrophil elastase (induced by smoking) destroys infection but can also destroy elastin in the alveoli. A1AT usually regulates this.
  • Without this there is destruction of cells leading to emphysema and lung dysfunction
262
Q

What are the symptoms of A1AD?

A
  • Respiratory early onset COPD and SOB
  • Liver symptoms will only occur in certain subtypes but will be the symptoms of liver failure e.g., hepatic encephalopathy , Jaundice, coagulopathy, ascites
263
Q

How would you test for A1AD?

A
  • Serum A1AT levels:reduced with levels < 20 micromol/L
  • Genetic testing
264
Q

How would you manage A1AD?

A
  • Smoking cessation
  • Symptomatic management
  • NICE recommend against the use of replacement alpha-1-antitrypsin, however the research and debate is ongoing regarding the possible benefits
265
Q

How would you manage A1AD?

A
  • Smoking cessation
  • Symptomatic management
  • NICE recommend against the use of replacement alpha-1-antitrypsin, however the research and debate is ongoing regarding the possible benefits
266
Q

hernias: what are they and what are the types?

A

Hernia: the protrusion of a viscus part or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.

Irreducible: contents cannot be pushed back into place
Obstructed: bowel contents cannot pass – features of intestinal obstruction
Strangulated: ischaemia occurs – the patient requires urgent surgery
Incarceration: contents of the hernial sac are stuck inside by adhesions

Clinical manifestations: Usually presents as lump and pain

267
Q

Femoral hernias

A

Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin.

Occur more often in women, middle age and elderly

Irreducible and strangulate

Treatment – surgical repair

268
Q

Incisional hernias

A

Follow breakdown of muscle closure after surgery

If obese, repair is not easy

Mesh repair – less recurrence but more infections compared to sutures

269
Q

Inguinal hernias

A

Indirect hernias pass through the internal inguinal ring and out through the external inguinal ring

Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall

Predisposing conditions:
Male sex
Chronic cough
Urinary obstruction
Past abdominal surgery

Examination:
Is lump visible? Ensure it is not a scrotal lump
Ask patient to cough – should appear above and medial to pubic tubercle
Indirect hernias can strangulate, while direct hernias don’t

Irreducible hernias
Long-standing hernias may become painful and irreducible
Try to reduce them to prevent strangulation and necrosis

Repairs
Lose weight and stop smoking pre-op
Hernias may recur
Mesh techniques – polypropylene mesh reinforces posterior wall

270
Q

What are the symptoms of A1AD?

A
  • Respiratory early onset COPD and SOB
  • Liver symptoms will only occur in certain subtypes but will be the symptoms of liver failure e.g., hepatic encephalopathy , Jaundice, coagulopathy, ascites
271
Q

What is pancreatic cancer?

A
  • Adenocarcinoma of the exocrine pancreas (99% of ductal origin)
  • Typically affects the head of the pancreas
272
Q

Who is typically affected by pancreatic cancer?

A

Males
60+

273
Q

What are the risk factors for developing pancreatic cancer?

A
  • Smoking
  • Alcohol
  • Diabetes mellitus
  • Chronic pancreatits
274
Q

What are the signs and symptoms of pancreatic cancer?

A
  • Weight loss
  • Acute pancreatitis

Body and tail of pancreas:
Epigastric pain that radiates to back
Relieved by sitting forward

Head of pancreas:
Painless jaundice (Courvoisier’s Sign)
Weight loss

275
Q

What is Courvoisier’s Sign?

A

Painless jaundice and a palpable gallbladder
Likely pancreatic cancer or cholangiocarcinoma

276
Q

What are the diagnostic tests for pancreatic cancer?

A

1st line: abdominal ultrasound
Gold standard: Pancreatic CT protocol diagnostic in 97% of cases use a biopsy

277
Q

What is the tumour marker that indicates the progression of of pancreatic cancer?

A

Ca19-9

278
Q

What is Hepatocellular carcinoma (HCC)?

A

arise from liver parenchyma
90% all primary liver cancers

279
Q

What are the risk factors for HCC?

A
  • Chronic hepatitis
  • Cirrhosis of the liver
  • Hemochromatosis
280
Q

What diagnostic investigations are done for HCC?

A

Imaging:
1st line - Abdo ultrasound
GS - CT (confirms diagnosis)

May also biopsy and Histology for diagnosis

Raised serum AFP (alpha fetoprotein)

281
Q

What is a cholangiocarcinoma?

A

adenocarcinoma that arises from the biliary tree

282
Q

How would a patient with cholangiocarcinoma present?

A

Abdo pain
jaundice
weight loss
pruritis
fever
Late constellation Sx of tumour since it is slow growing

283
Q

What are the investigations for cholangiocarcinoma?

A

1st line - Abdo USS + CT
GS ERCP - imagine of biliary tree
Biopsy

284
Q

What is more common, primary or secondary liver tumours?

A

Secondary are more common

285
Q

Where can secondary Liver tumours come from?

A

GI tract
Lungs
Breast

Phase 2A Tom (15 decks)

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