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Liver COPY Flashcards

1
Q

Give some functions of the liver. Name what diseases can occur if these go wrong.

A
  • Detoxification (clears ammonia, for example) - hepatic encephalopathy
  • Albumin production - hypoalbuminaemia = oedema = ascites, leukonychia
  • Clotting factor production (except 8) - easy bruising and easy bleeding
  • Immunity (Kupffer cells in reticuloendothelial system) - spontanoeus peritonitis can occur
  • Metabolises carbohydrates - hypoglycaemia
  • Bilirubin regulation - jaundice (stool and urine changes), pruritis
  • Oestrogen regulation - gynecomastia (men), spider naevi (normal but pathological if > 5, caused by vasodilation), palmar erythema
  • Unknown - Dupuytren’s contracture, clubbing
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2
Q

Give 2 possible outcomes of acute liver disease.

A

2 possible outcomes: recovery or liver failure

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3
Q

Give 5 causes of acute liver disease.

A
  1. Viral hepatitis
  2. Drug induced hepatitis
  3. Paracetamol DILI
  4. Vascular
  5. Obstruction
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4
Q

What are the signs and symptoms of acute liver disease/injury?

A
  • Malaise
  • Nausea
  • Anorexia
  • Jaundice
  • Rare:
  • Confusion
  • Bleeding
  • Pain
  • Hypoglycaemia
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5
Q

Give 2 possible outcomes of chronic liver disease.

A
  1. Recovery
  2. Cirrhosis - then liver failure
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6
Q

What are the signs and symptoms of chronic liver disease/injury?

A
  • Ascites
  • Oedema
  • Dupuytren’s contracture
  • Malaise
  • Anorexia
  • Pruritus
  • Clubbing
  • Palmar erythema
  • Xanthelasma
  • Spider naevi
  • Hepatomegaly
  • Bleeding
  • Haematemesis
  • Easy bruising
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7
Q

Give 6 causes of chronic liver disease.

A
  1. Alcohol
  2. NAFLD
  3. Viral hepatitis (B, C, E)
  4. Autoimmune diseases
  5. Metabolic, e.g. haemochromatosis
  6. Vascular, e.g. Budd-Chiari
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8
Q

Describe the progression from a chronic liver condition to chronic liver failure.

A

Chronic liver condition, e.g. NAFLD, Hep B - Liver damage - Liver symptoms - Liver cirrhosis if prolonged - Liver failure ultimately and high risk of hepatocellular carcinoma

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9
Q

In terms of LFTs, which ones give you an idea of how the liver was working?

A
  • Serum bilirubin
  • Serum albumin
  • Prothrombin time - INR
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10
Q

What do the liver hepatic enzymes indicate? What do the levels of some enzymes tell us?

A
  • They DO NOT tell us how well the liver is working but indicate liver damage
  • AST and ALT (aminotransferases) = raised in hepatocyte damage. ALT is more specific in hepatocellular disease
  • ALP (alkaline phosphate) = raised in intra/extrahepatic disease of any cause, e.g. gallstones, primary biliary cirrhosis. Marker for damage to the biliary tree. NOTE: also raised in bone resorption
  • GGT (gamma-glutamyl transferase) = raised in alcoholic liver disease
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11
Q

What is the definition of liver failure? What are the causes of liver failure?

A
  • Liver failure = liver loses its ability to repair and regenerate leading to decompensation (characterised by: abnormal bleeding, ascites, hepatic encephalopathy, jaundice). Acute (< 26 weeks) or chronic

  • Infection – viral hepatitis
  • Metabolic – Wilson’s/Alpha 1 antitrypsin
  • Autoimmune:
  • PBC – interlobular ducts
  • PSC – intra and extra hepatic
  • Neoplastic:
  • HCC
  • Metastatic disease
  • Vascular:
  • Budd Chiari – occlusion of hepatic veins
  • Ischaemia
  • Toxins:
  • Paracetamol
  • Alcohol
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12
Q

What are the symptoms of liver failure?

A
  • Same as acute presentation:
  • Malaise
  • Nausea
  • Anorexia
  • Jaundice
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13
Q

What are the signs of liver failure?

A
  • Coagulopathy (increased prothrombin time/INR)
  • Hepatic encephalopathy:
  • Altered mood/dyspraxia
  • Liver flap/asterixis
  • Fetor hepaticus:
  • Sweet and musty breath / urine
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14
Q

What are the investigations for liver failure?

A
  • Clinical examination = jaundice, liver flap, confused, change in personality (for example, from family member)
  • Bloods:
  • Increased PT
  • Increased AST / ALT
  • Toxicology screen - to look for alchol etc.
  • FBC (as alcohol can cause macrocytic anaemia), U&E
  • If ascites present:
  • Peritoneal tap with microscopy and culture
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15
Q

How do we treat liver failure?

A
  • Conservative:
  • Fluids
  • Analgesia
  • Medical = treat complications:
  • Ascites - diuretics
  • Cerebral oedema - Mannitol = decreases intercranial pressure
  • Bleeding - Vitamin K but if actively bleeding, e.g. haematemesis, give FFP
  • Encephalopathy - lactulose (increases ammonia absorption in bowels = excretion)
  • Sepsis - sepsis 6 (BUFALO = blood cultures, urine output, fluids, antibiotic, lactate, oxygen), antibiotics
  • Hypoglycaemia - dextrose
  • Surgical:
  • Transplant
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16
Q

What happens to alcohol in the liver (excessive)?

A
  • Acted upon by one of 3 enzymes: cytochrome P450 2E1, alcohol dehydrogenase, or catalase
  • All 3 pathways lead to the conversion of alcohol to acetaldehyde
  • Once alcohol dehydrogenase converts alcohol, NAD+ is needed which is converted into NADH. Higher NADH levels = more fatty acids, low NAD+ levels = less fatty acid oxidation. Combined = more fat production in the liver
  • ROS also produced and react with components of hepatocytes, e.g. proteins = serious damage
  • Acetaldehyde can bind to macromolecules + inhibit them - recognised as foreign and destroyed by the immune system - leads to inflammation and eventual cirrhosis
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17
Q

What are the 3 stages of alcoholic liver disease?

A
  • Fatty liver (steatosis)
  • Alcohol hepatitis (presence of Mallory bodies)
  • Alcohol cirrhosis - destruction of liver architecture and fibrosis
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18
Q

What are the signs and symptoms of alcoholic liver disease?

A
  • Fatty liver = vague abdominal signs, e.g. nausea, diarrhoea
  • Alcoholic hepatitis = jaundice, ascites, clubbing, hepatosplenomegaly
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19
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes

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20
Q

What are the investigations for alcoholic liver disease?

A
  • GGT very raised; AST and ALT mildly raised. This is because of leakage due to damage to hepatocytes
  • FBC - Macrocytic anaemia
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21
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT (gamma-glutamyl transferase) will be elevated

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22
Q

What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?

A

Mallory bodies

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23
Q

What are the complications of alcoholic liver disease?

A
  • Wernicke-Korsakoff encephalopathy:
  • Presents with ataxia, confusion, nystagmus, memory impairment
  • Treat with IV thiamine
  • Acute/chronic pancreatitis
  • Mallory-Weiss tear
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24
Q

What is the treatment for alcoholic liver disease?

A
  • Alcohol abstinence
  • Treat malnutrition with good diet and thiamine
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25
Q

What is non-alcoholic liver disease? What are the stages?

A
  • Non-alcoholic liver disease = a spectrum of liver diseases. It results from fat deposition
  • Least severe: steatosis

Steatohepatitis (NASH)

Fibrosis (scarring)

Most severe: cirrhosis

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26
Q

Give 3 causes of non-alcoholic liver disease.

A
  1. Obesity
  2. T2DM
  3. Hypertension
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27
Q

Although the pathophysiology of non-alcoholic liver disease is not fully understood, what role does insulin play?

A
  • Insulin receptors become less responsive to insulin
  • This INCREASES fat storage and DECREASES fatty acid oxidation
  • There is also increased synthesis and uptake of free fatty acids from the blood (STEATOSIS)
  • Steatosis causes fat droplets to form and grow in hepatocytes
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28
Q

How does non-alcoholic steatohepatitis occur?

A
  • Unsaturated fatty acids are vulnerable and react with ROS, e.g. hydroxyl radical to form fatty acid radicals
  • Fatty acid radicals eventually react with another radical = damages lipid membranes = eventual cell death = inflammation
  • Steatosis and inflammation = steatohepatitis (non-alcoholic or NASH)
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29
Q

What is the clinical presentation of non-alcoholic liver disease?

A
  • Asymptomatic even at advanced stages
  • If there is significant damage, there may be:
  • hepatomegaly
  • pain in right upper quadrant
  • jaundice
  • ascites
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30
Q

What are the investigations for non-alcoholic liver disease?

A
  • Biopsy (diagnostic)
  • Imaging, e.g. ultrasound, CT, MRI
  • AST and ALT - raised
  • Enhanced liver fibrosis test - for liver fibrosis
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31
Q

Describe the treatment for non-alcoholic fatty liver disease.

A

Lose weight - this is to prevent it becoming cirrhosis, which is irreversible

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32
Q

What is liver cirrhosis?

A

Loss of normal hepatic architecture, with regenerative nodules surrounded by fibrosis, affecting the liver’s synthetic, metabolic and excretory actions

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33
Q

What are the common and less common causes of liver cirrhosis?

A
  • Common: chronic alcohol abuse (most common in developing countries), Hepatitis B and C, non-alcoholic fatty liver disease from obesity or T2DM
  • Less common: haemochromatosis, Wilson’s disease, alpha-antitrypsin deficiency
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34
Q

What are the two types of liver cirrhosis?

A
  • Compensated - when the liver can still function effectively and there are no, or few, noticeable clinical symptoms
  • Decompensated - when the liver is damaged to the point that it cannot function adequately and overt clinical complications (such as jaundice, ascites, variceal haemorrhage, and hepatic encephalopathy) are present. Can be caused events such as infection, portal venous thrombosis, and infection
  • DECOMPENSATED LIVER CIRRHOSIS = LIVER FAILURE
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35
Q

What are the signs and symptoms of compensated and decompensated liver cirrhosis?

A
  • Compensated (some fibrosis) = asymptomatic or non-specific, e.g. weight loss, weakness, nausea
  • Decompensated (extensive fibrosis) = jaundice, pruritis, ascites, clubbing, hepatic encephalopathy, spider naevi
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36
Q

What are the investigations for liver cirrhosis?

A
  • Definitive diagnostic test - liver biopsy (for histology)
  • Blood tests:
  • platelets low, INR/PT high
  • LFTs
  • FBC - thrombocytopenia
  • serum electrolytes
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37
Q

What feature seen on liver biopsy is diagnostic of cirrhosis?

A

Nodular regeneration

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38
Q

How do we monitor liver cirrhosis?

A
  • Screen for HCC with ultrasonography scan +/- alpha-fetoprotein (raised) every 6 months
  • MELD score
  • Offer upper GI endoscopy for possible oesophageal varices
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39
Q

Describe the treatment for liver cirrhosis.

A
  • Definitive treatment is LIVER TRANSPLANT
  • Conservative - fluids, analgesia, alcohol abstinence, good nutrition
  • Medical - treat complications of liver failure:
  • Ascites – diuretics (spironolactone) and restrict sodium. Prophylactic oral ciprofloxacin if ascites present because you can get spontaneous bacterial perotinitis BUT if you do get it, treat with IV cefotaximine
  • Cerebral oedema - mannitol, decreases ICP
  • Bleeding - Vitamin K (more factors made) or give FFP if active bleeding
  • Encephalopathy - lactulose (decreases ammonia), antibiotics and enemas - stops the flora making NH3
  • Hypoglycaemia (glycogenolysis is not happening) - dextrose
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40
Q

What are the complications of liver cirrhosis?

A
  • HIGH YIELD:
  • ASCITES
  • PORTAL HYPERTENSION
  • VARICES
  • Others:
  • Jaundice
  • Coagulopathy
  • Hypoalbuminaemia (causing oedema)
  • Portosystemic encephalopathy
  • Hepatorenal syndrome and hepatopulmonary syndrome
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41
Q

Why do we get ascites in liver cirrhosis?

A

Ascites is fluid in the peritoneal cavity:

  • Hypoalbuminaemia - reduced plasma oncotic pressure
  • Portal hypertension - increased hydrostatic pressure
  • Renal water retention (peripheral arterial vasodilation mediated by NO etc.)
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42
Q

What are the constituents of bile?

A
  • Cholesterol
  • Lecithin (a phospholipid)
  • HCO3-
  • Bile acids
  • Bile pigment, e.g. bilirubin
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43
Q

Give the pathway of bile from the hepatocytes to expulsion from the gallbladder.

A
  • After bile is produced by hepatocytes, it travels to the gallbladder via the common hepatic duct
  • Once in the gallbladder, it is stored and concentrated
  • Once CCK is released by duodenal I cells, it causes the gallbladder to contract
  • This causes bile to be expelled into the cystic duct + then into the common bile duct
  • Bile is then used to aid the emulsification of lipids
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44
Q

How is bilirubin metabolised?

A
  • RBCs that are old/damaged are ingested by macrophages
  • Their haemoglobin is broken down into haem + globin. Globin is used to generate new RBCs in bone marrow, haem is broken down into biliverdin + iron via haem oxygenase -
  • Iron recycled, biliverdin by biliverdin reductase to form unconjugated bilirubin. This is toxic + lipid-soluble so must be metabolised + excreted
  • Unconjugated bilirubin is then transported to the liver by binding to albumin
  • Once in the liver, unconjugated bilirubin undergoes glucurodination by glucuronyl transferase. This forms conjugated bilirubin, which is soluble so dissolves into bile + enters biliary system
  • Bile enters the duodenum via the sphincter of Oddi and eventually reaches terminal ileum. It aids the absorption of lipids + fat-soluble vitamins through its course
  • Bile reduced by bacteria into urobilinogen (lipid-soluble so can be reabsorbed)
  • About 80% of urobilinogen is further oxidised to stercobilin which is excreted in faeces (partly responsible for the colour of faeces)
  • Around 20% of urobilinogen is reabsorbed into the bloodstream and goes to the liver where some is recycled for bile production, while a small percentage reaches the kidneys = oxidised further into urobilin + excreted into the urine
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45
Q

What is jaundice? What are the three types?

A
  • Discolouration of skin due to high serum bilirubin. 3 types:
  • Pre-hepatic = increased haemolysis = increased unconjugated bilirubin
  • Hepatic jaundice = caused by liver impairment, causes decreased ability of the liver to conjugate bilirubin
  • Post-hepatic jaundice = caused by blockage of bile ducts = backflow of conjugated bilirubin into blood
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46
Q

What are some causes of pre-hepatic jaundice?

A
  • Haemolytic anaemia
  • Gilbert’s syndrome
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47
Q

Describe the urine and stools in someone with pre-hepatic jaundice. How about intra-hepatic and post-hepatic?

A
  • Urine and stools are normal. There is no itching and the LFT’s are normal
  • Dark urine and pale stools. There may be itching and LFT’s are abnormal
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48
Q

What are some useful questions when talking to a jaundiced patient?

A
  1. Dark urine, pale stools, itching?
  2. Symptoms: biliary pain, rigors, abdomen swelling, weight loss?
  3. Past history: biliary disease/intervention, malignancy, heart failure, blood products, autoimmune disease
  4. Drug history
  5. Social history: alcohol, potential hepatitis contact
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49
Q

What are some causes of hepatocellular jaundice?

A
  • Alcoholic liver disease
  • Viral or autoimmune hepatitis
  • Iatrogenic, e.g. medication
  • Hereditary haemochromatosis
  • Primary biliary cirrhosis or primary sclerosing cholangitis
  • Hepatocellular carcinoma
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50
Q

What are some causes of post-hepatic jaundice?

A
  • Intra-luminal causes, e.g. gallstones
  • Mural causes, e.g cholangiocarcinoma
  • Extra-mural causes, e.g. pancreatic cancer
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51
Q

What tests should be performed on a jaundiced patient?

A
  • Liver enzymes: very high AST/ALT suggests liver disease
  • Biliary obstruction - 90% have dilated intrahepatic bile ducts on ultrasound
  • Need further imaging: CT, Magnetic resonance cholangioram MRCP, Endoscopic retrograde cholangiogram ERCP
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52
Q

How is paracetamol metabolised normally?

A
  • Paracetamol is mostly converted to non-toxic metabolites via Phase II metabolism. Here, it conjugated with sulfate and glucuronide, with a small portion being oxidised via the Cytochrome P450 enzyme
  • Phase I: Cytochromes P450 2E1 and 3A4 convert approximately 5% of paracetamol to a highly reactive intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Under normal conditions, NAPQI is detoxified by conjugation with glutathione to form cytsteine and mercapturic acid conjugates
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53
Q

What happens to paracetamol metabolism in the case of a paracetamol overdose?

A
  • Phase II metabolic pathways become saturated + more paracetamol is shunted to the Cytochrome P450 system to produce NAPQI. As a result, hepatocellular supplies of glutathione become depleted, as the demand for glutathione is higher than its regeneration
  • NAPQI remains in its toxic form in the liver and reacts with cellular membrane molecules, resulting in widespread hepatocytes damage and death, leading to acute liver necrosis
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54
Q

What is the presentation of a paracetamol overdose?

A
  • Nausea
  • Vomiting
  • Anorexia
  • RUQ pain
  • Patient may say that they have taken a paracetamol overdose
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55
Q

How do we treat a paracetamol overdose?

A
  • Activated charcoal - within 1 hour of ingestion EXCEPT if already have liver disease, e.g. alcoholic liver disease = give them n-acetylcysteine
  • IV N-ACETYLCYSTEINE to replenish glutathione stores
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56
Q

What is Gilbert’s syndrome? What is its pathophysiology?

A
  • It is an inherited liver disorder that affects the body’s ability to process bilirubin
  • It causes unconjugated hyperbilirubinaemia. This presents as JAUNDICE
  • Autosomal recessive. 70% of cases are caused by a mutation in the UGT gene = decreased UDP glucuronyltransferase
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57
Q

What are the symptoms of Gilbert’s syndrome? What do we have to rule out when diagnosing? What is the treatment?

A
  • 30% are asymptomatic
  • JAUNDICE (intermittent/recurrent), triggers for these episodes = sickness, fasting, dehydration, stress
  • We have to rule out other causes of unconjugated hyperbilirubinaemia (pre-hepatic jaundice), e.g. haemolytic anaemia, Crigler-Najjar syndrome
  • NO treatment required
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58
Q

What are the two venous systems that drain abdominal structures?

A
  • Systemic venous system = returns deoxygenated blood to the right atrium of the heart via the IVC
  • Portal venous system = transports venous blood (rich in nutrients that have been extracted from food) to the liver for processing. Portal vein, S+I meseneteric veins, splenic vein
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59
Q

Where are the 3 connections between the portal venous system and the systemic venous system?

A
  • Inferior portion of the eosophagus
  • Superior portion of the anal canal
  • Round ligament of the liver (umbilical vein in foetal life)
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60
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%

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61
Q

What is portal hypertension? What is its most common cause (explain this)?

A
  • Portal hypertension = increased blood pressure (>12mmHg) in the portal venous system
  • CIRRHOSIS is its most common cause. Endothelin-1 production is increased in cirrhosis -> more vasoconstriction. NO production reduces in cirrhosis -> less vasodilation. Reduced radius -> increased resistance -> higher pressure in portal system
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62
Q

What are the pre-hepatic, intra-hepatic, and post-hepatic causes of portal hypertension?

A
  • Pre-hepatic = portal vein thrombosis
  • Intra-hepatic = schistosomiasis (pre-sinusoidal), cirrhosis (sinusoidal), Budd-Chiari syndrome (post-sinusoidal, clot or tumour obstructs blood flow towards IVC)
  • Post-hepatic = right heart failure, IVC obstruction
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63
Q

Portal hypertension can also cause portosystemic shunts. Explain what these are, where these could occur and the resulting symptoms.

A
  • Portosystemic shunt = blood is diverted away from the portal venous system to the systemic venous system
  • Can happen at the 3 connections: inferior portion of eosophagus, superior portion of the anal canal, and round ligament of liver
  • If happens at eosphagus = eosphageal varices
  • If happens at round ligament = caput medusae
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64
Q

Explain how ascites can form as a result of portal hypertension.

A

Endothelial cells release NO = vasodilation = reduced BP = aldosterone released = kidneys retain sodium and water = fluid gets pushed across tissues - peritoneal cavity = ascites

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65
Q

What are the features of portal hypertension?

A
  • ABCDE:
  • Ascites
  • Bleeding (oesophageal varices)
  • Caput medusae
  • Diminuished liver function
  • Enlarged spleen (splenomegaly)
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66
Q

What are the investigations for portal hypertension?

A
  • Hepatic venous pressure gradient measurement (pressure difference between portal vein and IVC)
  • Liver ultrasound
  • CT scan or MRI
  • FBC, liver enzymes
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67
Q

How do we treat portal hypertension?

A
  • Propanolol - decreases portal venous pressure
  • Treat symptoms:
  • Spironolactone for ascites
  • Ocreotide for bleeding oesophageal varices
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68
Q

Portal hypertension can lead to varices. Explain why.

A

Obstruction to portal blood flow, e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals, e.g. the gastro-oesophageal junction and so causes varices

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69
Q

What are oesophageal varices? What are their potential complications?

A
  • Enlarged veins in the oesophagus
  • As these vessels are thin and not meant to transport higher pressure blood, they can easily RUPTURE = haematemesis OR rupture = blood digested = malaena
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70
Q

What are the investigations for oesophageal varices?

A

1ST LINE/GOLD STANDARD - upper GI endoscopy

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71
Q

What are the symptoms of oesophageal varices?

A
  • Melaena
  • Haematemesis (coffee ground vomit)
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72
Q

How do we treat oesophageal varices?

A
  • GOLD STANDARD - ENDOSCOPIC THERAPY: BAND LIGATION OR SCLEROTHERAPY
  • Active bleed:
  • Urgent gastroscopy/endoscopy
  • Fluid resuscitation, remember can be massive
  • Terlipressin (ADH analogue) or Octreotide
  • Balloon tamponade
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73
Q

How do we prevent recurrence of oesophageal varices?

A

60-80% of recurrence within 2yrs, so we give secondary prophylaxis:

  • Propranolol / Isosorbide
  • Repeat variceal banding
  • TIPSS
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74
Q

What is ascites? What is its 4 main mechanisms? What are its causes?

A
  • Ascites (symptom) = excessive build up of fluid in the peritoneal cavity
  • Pathophysiology:
  • Peritonitis - more leaky
  • RAISED CAPILLARY HYDROSTATIC PRESSURE
  • REDUCED COLLOID ONCOTIC PRESSURE
  • Peritoneal lymphatic draining
  • Cirrhosis is the main cause (50% develop ascites in 10 years), however later stage cancers, CHF, nephrotic syndromes, pancreatitis etc. can cause it
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75
Q

What are the transudative and exudative causes of ascites?

A
  • TRANSUDATE (protein <25g/L) - portal HTN (due to cirrhosis), Budd Chiari, low plasma protein, heart failure
  • EXUDATE (protein >25g/L) - peritonitis, peritoneal malignancy
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76
Q

What are the signs of ascites?

A
  • SHIFTING DULLNESS = classic sign. Percuss abdomen and observe dullness over fluid versus resonance over air. Ask the patient to roll on one side, wait a good few seconds for fluid to settle at a new level and then repercuss on the side and observe the dullness has shifted
  • Large distended abdomen
  • Weight gain
  • Respiratory distress (pleural effusion)
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77
Q

What are the investigations for ascites?

A

Ascitic tap (paracentesis) = culture, gram stain, cytology, protein

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78
Q

What is the treatment for ascites?

A
  • 1st line = salt restriction - low sodium diet of <2000mg/day
  • Diuretics - combination of spironolactone and furosemide to drain fluid
  • Identify cause and treat accordingly
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79
Q

What are the complications of ascites?

A

Spontaneous bacterial peritonitis - an infection of ascitic fluid. Most common causes are E.coli and K.pneumoniae

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80
Q

What is peritonitis? What are the two types and what causes them? Which bacteria is infection commonly caused by?

A
  • Peritonitis = inflammation from infection or irritation to the peritoneum
  • This can be primary (spontaneous bacterial infection, ascites) or secondary (perforation of bowels or appendix or following infection from tubes breaking the skin)
  • Infection is most commonly S.aureus, Klebsiella and E.coli
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81
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis.

It can also affect immunocompromised people and those undergoing peritoneal dialysis

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82
Q

Why does perforation cause irritation?

A

Through the leaked chemicals, e.g. bile, acids and old clotted blood

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83
Q

What is spontaneous bacterial peritonitis usually a complication of?

A

Ascites with cirrhosis

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84
Q

What are the causes of peritonitis?

A

AEIOU PD:

  • Appendicitis
  • Ectopic pregnancy
  • Infection
  • Obstruction
  • Ulcer
  • Peritoneal dialysis
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85
Q

What is the presentation of peritonitis?

A
  • Perforations = sudden onset abdominal pain with generalised shock and collapse
  • Secondary peritonitis = gradual onset, generalised abdominal pain to localised severe abdominal pain (as inflammation moves from visceral to parietal layers)
  • Patient will lie still, rigid abdomen, pain relieved by lying hands on abdomen
  • Pyrexia, tachycardia, confusion, N+V
  • Guarding, rebound tenderness (Blumberg’s sign), rigidity, silent abdomen
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86
Q

What are the investigations for peritonitis?

A
  • Bloods: FBC and CRP, amylase (check pancreatitis), hCG (screen for ruptured ectopic pregnancy as this can cause peritonitis)
  • Erect CXR for air below the diaphragm, AXR to exclude bowel obstruction, CT for abdominal ischaemia
  • Ascitic taps and blood cultures - look for the pathogen
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87
Q

What is the treatment for peritonitis?

A
  • ABCDE
  • Find and treat the underlying cause - might be surgery for perforated bowels etc.
  • IV fluids
  • IV antibiotics - first broad spectrum and then by trust guidelines for after ascitic tap performed and pathogen detected
  • Peritoneal lavage (clean the peritoneum of infection)
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88
Q

Name a drug that can cause drug induced liver injury.

A

Flucloxacillin

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89
Q

Name 3 drugs that are not known to cause drug induced liver injury.

A
  1. Low dose aspirin
  2. NSAIDS
  3. Beta blockers
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90
Q

What are the three most common metabolic liver diseases?

A
  • Haemochromatosis
  • Wilson’s disease
  • Alpha-1-antitrypsin deficiency
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91
Q

Give 3 causes of iron overload.

A
  1. Genetic disorders, e.g. haemochromatosis
  2. Multiple blood transfusions
  3. Haemolysis
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92
Q

What is haemochromatosis? What is its pathophysiology?

A
  • Haemochromatosis is caused by EXCESS IRON everywhere
  • Pathophysiology: autosomal recessive mutation in HFE gene (chromosome 6), which causes increased intestinal iron absorption. This results in iron accumulating in the liver, joints, pancreas, heart, skin, gonads etc. This causes organ damage, e.g. liver, which leads to cirrhosis, HCC etc.
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93
Q

What protein is responsible for controlling iron absorption? What are these levels like in haemochromatosis?

A

Hepcidin. Levels of this protein are decreased in haemochromatosis

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94
Q

What is the presentation of haemochromatosis?

A
  • Early on = fatigue, arthralgia, weakness
  • Hypogonadism, e.g. erectile dysfunction
  • SLATE-GREY SKIN (brownish/bronze)
  • Chronic liver disease, heart failure, arrhythmias
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95
Q

What are the investigations for haemochromatosis?

A
  • Bloods - iron study, LFTs
  • Genetic testing to detect mutation
  • Liver biopsy - GOLD STANDARD
  • MRI - detects iron overload
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96
Q

What histological stain can be used for haemochromatosis?

A

Perl’s stain

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97
Q

What is the management for haemochromatosis?

A
  • 1st line = VENESECTION - every 1-2 weeks take out 400-500ml of blood BUT IF CONTRAINDICATED give desferrioxamine to remove excess iron from the blood
  • 2nd line = reduce iron from diet (IRON CHELATION)
  • Definitive = LIVER TRANSPLANT
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98
Q

What is Wilson’s disease? What is its pathophysiology?

A
  • Wilson’s disease = excess copper in the liver and CNS
  • Pathophysiology: autosomal recessive mutation (A7P7B in chromosome 13) which causes an error in copper metabolism = copper deposition in organs, including liver (liver symptoms), basal ganglia (Parkinson’s symptoms), cornea (Kayser-Fleischer rings)
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99
Q

What is the presentation of Wilson’s disease?

A
  • Psychiatric - depression, neurotic behavioural patterns
  • CNS problems - tremor, dysarthia, involuntary movements, dysphagia, reduced memory, eventual dementia
  • Liver - hepatitis, cirrhosis
  • KAYSER-FLEISCHER RING - copper in cornea, green/brown pigment at outer edge
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100
Q

What are the investigations for Wilson’s disease?

A
  • 1st line = 24hr urinary copper excretion high and ceruloplasmin reduced (but can be normal)
  • GOLD STANDARD = liver biopsy
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101
Q

What is the management for Wilson’s disease?

A
  • Chelating agent - PENICILLAMINE
  • Liver transplant
  • Avoid high copper foods - liver, nuts, chocolate, mushroom, shellfish
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102
Q

What is alpha-1-antitrypsin deficiency? What is alpha-1-antitrypsin? What is its pathophysiology?

A
  • Alpha-1-antitrypsin deficiency = autosomal recessive disorder, may result in liver/lung disease
  • Alpha-1-antitrypsin = SERPINA1 in chromosome 14, produced in liver. Inhibits neutrophil elastase - proteolytic enzyme produced by neutrophils with inflammation, infection, smoking
  • Pathophysiology: with A1T1 deficiency, elastase breaks down elastin unchecked. This affects the lung (alveolar wall destruction) and liver
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103
Q

What is the presentation of alpha-1-antitrypsin deficiency?

A
  • Lung = COPD, SOB, emphysema
  • Liver = cirrhosis, hepatitis, neonatal jaundice
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104
Q

What are the investigations for alpha-1-antitrypsin deficiency?

A
  • Bloods = serum A1T1 levels low
  • CXR, PFTs, LFTs, liver biopsy
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105
Q

What is the management for alpha-1-antitrypsin deficiency?

A
  • Treat complications of the liver and lung
  • Stop smoking
  • Liver transplant
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106
Q

What are the three main biliary tract diseases? How can you distinguish between these?

A
  • Gallstones (cholelithiasis) - biliary colic
  • Cholecystitis
  • Cholangitis (ascending, primary biliary, primary sclerosing)
  • Learn these three conditions together. They follow on from each other as gallstones get worse. You can distinguish between them using CHARCOT’S TRIAD:
  • Biliary colic = RUQ pain
  • Cholecystitis = RUQ pain + fever/increased WCC
  • Cholangitis = RUQ pain, fever/increased WCC + jaundice
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107
Q

Give 3 risk factors for gallstone development.

A
  1. Female
  2. Obese (fat)
  3. Fertile
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108
Q

What is biliary colic? What is the pathophysiology and what is bile made out of? What are the risk factors?

A
  • Biliary colic = gallbladder attack. Dull pain in the middle to upper right area of the abdomen. It occurs when a gallstone blocks the bile duct.
  • Pathophysiology = gallstone is blocking the cystic or common bile duct without signs of cystic inflammation. Gallbladder contracts = moves from bile duct to cystic duct. Gallbladder contracts against stone. Bile is made of cholesterol, pigments, phospholipids, bile acids and HCO3-. Stones form from the supersaturation of bile meaning they are either made of:
  • Cholesterol - excess production: obesity and fatty acids
  • Pigment - seen in haemolytic anaemia
  • Mixed - made of both of the above
  • Risk factors = THE 5 F’s: Fat, Fertile, Forty, Female, FHx
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109
Q

What is the presentation of biliary colic?

A
  • ‘COLICKY’ RUQ PAIN that is WORSE after eating large or FATTY meals (triggers gallbladder to contract against the blockage)
  • May also radiate to epigastrium and back
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110
Q

What are the investigations for gallstones? What is the diagnsotic test?

A
  • FBC and CRP = looking for signs of an inflammatory response - suggestive of cholecystitis
  • LFTs = raised ALP - ALP is associated with biliary pathology. Bilirubin and ALT usually normal
  • Amylase = check for pancreatitis as it can also give RUQ pain, albeit less classically
  • These tests are more to RULE OUT cholecystitis and cholangitis than to confirm gallstones. ULTRASOUND is the diagnostic test
  • ULTRASOUND:
  1. STONES
  2. GALLBLADDER WALL THICKNESS (inflammed)
  3. DUCT DILATION (suggest ductal blockage)
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111
Q

What are the differential diagnoses for gallstones?

A

Think of other causes of RUQ pain: cholecystitis and cholangitis (often progressions from untreated gallstones anyway), IBD, pancreatitis, GORD, peptic ulcers

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112
Q

What is the treatment for gallstones?

A
  • NSAIDs/analgesia
  • Optional cholecystectomy as gallstones often reoccur
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113
Q

What is acute cholecystitis?

A

Acute cholecystitis = blockade of the cystic duct leading to the buildup of bile causing transmural inflammation of the gallbladder

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114
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component

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115
Q

What is the presentation of acute cholecystitis?

A
  • Generalised epigastric pain migrating to severe RUQ pain
  • FEVER or FATIGUE - signs of inflammation
  • Pain associated with tenderness and guarding from inflamed bladder and local peritonitis
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116
Q

What are the investigations for cholecystitis?

A
  • POSITIVE MURPHY’S SIGN = severe pain on deep exhalation with examiners hand pressed into the RUQ
  • FBCs, CRPs - inflammatory markers
  • Ultrasound - thick gallstone walls from inflammation
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117
Q

What is the treatment for acute cholecystitis?

A
  • Early lap cholecystectomy (within 7 days) otherwise wait 6 weeks
  • Heavy analgesia, IV fluids
  • NO Abx (well sometimes)
118
Q

What are the different types of cholangitis?

A
  • Ascending (or acute) cholangitis
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
119
Q

What is ascending cholangitis? Which bacteria are usually involved?

A
  • Ascending cholangitis = medical emergency characterised by bacteria ascending through the biliary tree leading to septicaemia
  • Common bacteria = E.coli, Klebsiella, Enterobacter, Enterococcus
120
Q

What is the presentation of ascending cholangitis?

A
  • Charcot’s triad: severe RUQ pain with fever (rigors) and jaundice
  • Reynold’s pentad: Charcot’s triad + confusion + shock
  • Patient may present as septic and/or have developed some level of pancreatitis
121
Q

What are the investigations for ascending cholangitis?

A
  • FBCs, LFTs and CRP - leukocytosis, raised ALP and bilirubin, raised CRP
  • Blood cultures/MC&S - work out what the pathogen is so you can use the trust’s advised antibiotics
  • Ultrasound (biliary dilation, bile duct wall thickening) +/- ERCP (Endoscopic Retrograde Cholangiopancreatography) (basically a biliary tree contrast x-ray)
122
Q

What is the treatment for ascending cholangitis?

A
  • Treat sepsis: ABCDE, broad-spectrum ABs until pathogen identified (then follow trust guidelines)
  • ERCP and stenting to mechanically clear the blockage
  • Surgery/cholecystectomy when better
123
Q

What is primary sclerosing cholangitis? What is its pathophysiology? What is it associated with?

A
  • Primary sclerosing cholangitis = progressive sclerosis of the biliary tree leading to chronic cholestasis and ESLD
  • Pathophysiology: inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure
  • 80% of cases associated with IBD, most commonly UC
  • p-ANCA and HLA-A1, B8, DR3 association
124
Q

What is the presentation of primary sclerosing cholangitis? What are patients predisposed to developing?

A
  • 50% asymptomatic until advanced disease
  • Non-specific pruritus and fatigue - like PBC
  • Predisposed to developing HCC, cholangiocarcinoma, CRC
125
Q

What are some potential complications of primary sclerosing cholangitis?

A
  • Portal hypertension: fibrosis builds around bile ducts - constricts portal veins = increased pressure
  • Cirrhosis: recurrent cycle of inflammation, healing - tissue scarring - fibrosis
126
Q

What are the investigations for primary sclerosing cholangitis?

A
  • MRCP/ERCP shows intra/extrahepatic bile duct dilation and/or stictures
  • LFTs - elevated conjugated bilirubin, ALP, GGT
  • Liver biopsy - ‘ONION-SKIN FIBROSIS’ on histology
127
Q

What is the diagnostic criteria for primary sclerosing cholangitis?

A
  • ALP > 1.5x normal for more than 6 months
  • Cholangiography showing biliary strictures consistent with PSC (beaded appearance)
  • Liver biopsy consistent with PSC
128
Q

What is the treatment for primary sclerosing cholangitis?

A

Liver transplant, no known medical management

129
Q

What does primary sclerosing cholangitis have a correlation with?

A

ULCERATIVE COLITIS

130
Q

What is primary biliary cholangitis/cirrhosis? What is it associated with? What is its epidemiology?

A
  • Progressive autoimmune destruction of the liver + biliary tree leading to fibrosis and eventually cirrhosis
  • AMA +ve against PDC-E2
  • Associated with autoimmune disease
  • Females > males, familial = 10 fold risk increase
131
Q

What is primary biliary cholangitis associated with?

A

Other autoimmune disorders, e.g Coeliac disease, RA

132
Q

What are the complications of primary biliary cholangitis?

A

Osteoporosis, hyperlipidaemia

133
Q

What is the clinical presentation of primary biliary cholangitis?

A
  • Very non-specific:
  • Fatigue
  • Pruritis
  • RUQ pain
  • Loss of bone density
  • Hypercholesterolaemia
134
Q

What are the investigations for primary biliary cholangitis?

A
  • Abdominal ultrasound/MRCP/CT scan - rule out bile duct obstruction
  • ELEVATED IgM, total cholesterol, HDL, GGT, ALP (released from damaged bile ducts), bilirubin = advanced disease
  • Liver biopsy = interlobular bile duct destruction
135
Q

What is the treatment for primary biliary cholangitis?

A

URSODEOXYCHOLIC ACID - reduces intestinal absorption of cholesterol = reduces cholestasis, improves liver function tests

136
Q

What is acute pancreatitis? Is it reversible?

A
  • Acute pancreatitis = self-perpetuating inflammation of the pancreas causing leakage of enzymes and autodigestion. Reversible but bad
137
Q

What are the 3 different types of acute pancreatitis?

A
  1. 70% are oedematous; acute fluid collection
  2. 25% are necrotising
  3. 5% are hemorrhagic
138
Q

What are the causes of acute pancreatitis? How can we remember this?

A
  • Remember: I GET SMASHED:
  • Idiopathic
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune - prevalent in Japan
  • Scorpion venom
  • Hyperlipidaemia
  • ERCP
  • Drugs - NSAIDs, corticosteroids, ACEi
139
Q

What are the two main causes of acute pancreatitis? Why?

A
  • Gallstones: blockage of bile duct = backup of pancreatic juices = causes Ca2+ release inside pancreatic cells and causes them to activate trypsinogen, which digests the pancreas
  • Alcohol: contracts the Ampulla of Vater, obstructing bile clearance and also messes with Ca2+
140
Q

What is the clinical presentation of acute pancreatitis? What are the two important signs? How does the first one come about?

A
  • SEVERE EPIGASTRIC pain radiating to the BACK
  • N+V, fever, anorexia, jaundice
  • GREY-TURNER’S sign = abdominal flank skin discolouration from retroperitoneal bleeding caused by autodigestion of nearby structures
  • CULLEN’S SIGN = periumbilical region bruising
141
Q

What are the investigations for acute pancreatitis?

A
  • Serum amylase = raised
  • Serum lipase = raised and more specific than amylase
  • Urinalysis = raised urinary amylase
  • CRP and routine bloods = raised CRP
  • Erect CXR (exclude gastroduodenal rupture), abdominal ultrasounds, CT, MRI
142
Q

What are the two scoring systems for acute pancreatitis?

A
  • APACHE2
  • Glasgow & Ranson
143
Q

What 8 points make up the Glasgow + Ranson scoring system?

A

PANCREAS (3+ = ITU):

  • PaO2 < 8kPa
  • Age > 55 years
  • Neutrophils > 15x10^9
  • Calcium < 2mmol/L
  • Raised urea > 15mmol/L
  • Elevated enzymes
  • Albumin < 32g/L
  • Sugar - serum glucose > 15mmol/L
144
Q

What is the treatment for acute pancreatitis?

A
  • Nil by Mouth - drop pancreatic stimulation
  • IV FLUIDS
  • ANALGESIA - usually morphine
  • ANTIBIOTICS
  • Treat underlying cause, e.g. gallstones
145
Q

Give 3 complications of acute pancreatitis.

A
  • ACUTE RENAL FAILURE (high likelihood)
  • Acute pancreatic pseudocyst (25% of cases)
  • Sepsis
146
Q

What is chronic pancreatitis? What is its pathophysiology?

A
  • Persistent, chronic inflammation of the pancreas due to autodigestion
  • Pathophysiology: obstruction of bicarbonate secretion in the pancreatic lumen causes early activation of trypsinogen and autodigestion which is replaced by fibrosis
147
Q

What are the causes of chronic pancreatitis? What is the mnemonic?

A
  • Remember TIGAR-O:
  • Toxins (chronic alcoholism usually causes it)
  • Idiopathic
  • Genetic, e.g. CYSTIC FIBROSIS
  • Autoimmune
  • Recurrent acute pancreatitis
  • Obstruction; gallstones, pancreatic head tumour
148
Q

What is the presentation of chronic pancreatitis?

A
  • Epigastric pain ‘boring’ through the back. Worse after alcohol and better on leaning forward
  • Steatorrhoea
  • N+V, DM, decreased appetite, malabsorption - painless weight loss
  • Patient is typically a 50-ish year old man with an appropriate SHx, e.g. drinks loads of alcohol
149
Q

What are the investigations for chronic pancreatitis?

A
  • Secretin stimulation test
  • Serum amylase and lipase - may be raised if enough cells to make them
  • Abdominal ultrasound, CT, MRI
150
Q

What is the treatment for chronic pancreatitis?

A
  • Stop drinking
  • Creon and PPI to help digestion
  • Insulin to help DM
  • Duct drainage
151
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

152
Q

What is infective diarrhoea? What are the causes?

A
  • Increased stool frequency and volume, decreased consistency
  • Causes:
  • Viral = rotavirus (children), NOROVIRUS (adults), adenovirus
  • Bacterial, e.g. E.COLI, SALMONELLA, C.DIFFICILE, CAMPYLOBACTER JEJUNI
  • Parasites, e.g. GIARDIA LAMBLIA, entamoeba histolytica
  • Antibiotics - rule of Cs, e.g. ciprofloxacin, clindamycin, co-amoxiclav, cephalosporins
  • Other - anxiety, food allergy
  • Chronic - IBS, IBD, Coeliac’s, bowel cancer
153
Q

What are the risk factors for infective diarrhoea?

A
  • Foreign travel
  • Crowded area
  • Poor hygeine
154
Q

What is the diagnostic criteria for traveller’s diarrhoea?

A

>3 unformed stools per day and at least one of:

  • Abdominal pain
  • Cramps
  • Nausea
  • Vomiting

It occurs within 3 days of arrival in a new country

155
Q

Give 3 causes of traveller’s diarrhoea.

A
  1. Enterotoxigenic E.coli (ETEC)
  2. Campylobacter
  3. Norovirus
156
Q

Describe the pathophysiology of traveller’s diarrhoea.

A

Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea

157
Q

Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic e.coli (EHEC) a.k.a e.coli 0157

158
Q

Name a helminth responsible for causing diarrhoeal infection.

A

Schistosomiasis

159
Q

What does EIEC stand for?

A

Enteroinvasive E. coli

160
Q

Which type of e.coli is responsible for causing large volumes of watery diarrhoea?

A

Enteropathogenic E.coli (EPEC)

161
Q

What does EAEC stand for? What does DAEC stand for?

A
  • Enteroaggregative E.coli
  • Diffusely adherent E.coli
162
Q

What is the clinical presentation of infective diarrhoea? What are the red flags?

A
  • Infective diarrhoea
  • N+V, abdominal pain, weight loss
  • Viral: fever, fatigue, headache, myalgia
  • Red flags: blood in the stools, any recent hospital or antibiotic treatment, persistent = worry about dehydration
163
Q

What are the investigations for infective diarrhoea?

A
  • Take a history
  • On examination: dry mucous membrane, increased capillary refill time
164
Q

What is the management for infective diarrhoea?

A
  • Treat the underlying causes, e.g. bacterial diarrhoea is usually treated with Metronidazole
  • ORAL REHYDRATION THERAPY. IV fluids given if very severe
  • Loperamide and codeine = stops the passing of stalls
  • Anti-emetics, e.g. metoclopramide
  • Anti-sickness
165
Q

What is associated with bloody diarrhoea?

A
  • E.coli
  • Salmonella
  • Shigella
166
Q

What is encephalopathy? What is hepatic encephalopathy? What is its pathophysiology?

A
  • Encephalopathy = any disease or injury that affects the brain structure or function
  • Hepatic encephalopathy = brain dysfunction caused by liver insufficiency and/or portosystemic shunts
  • Pathophysiology = liver dysfunction/portosystemic shunt = accumulation of nitrogenous substances in blood = ammonia can cross BBB. Ammonia is detoxified in the astrocytes, which causes glutamine accumulation = increases osmotic pressure = swelling
167
Q

What are the signs and symptoms of hepatic encephalopathy?

A
  • Changed mental status: confusion, poor concentration, stupor, seizures, coma
  • Neuromuscular: ASTERIXIS (jerking movement of limbs), rigidity, hyperreflexia
168
Q

How do we grade hepatic encephalopathy? What are the different grades?

A
  • WEST HAVEN criteria:
  • Grade 1: mild; short attention span; mood, sleep problems
  • Grade 2: moderate; decreased energy, slurred speech, tremors
  • Grade 3: severe; confusion, stupor, anxiety
  • Grade 4: coma
169
Q

What are the investigations for hepatic encephalopathy?

A
  • Bloods - raised ammonia
  • LFTs - abnormal
  • Blood cultures can identify causes, e.g. spontaneous bacterial peritonitis
  • Head CT scan to identify cerebral oedema
170
Q

What is the treatment for hepatic encephalopathy?

A
  • Treat underlying cause
  • Lactulose
  • Rifaximin - stops growth of bacteria that produces toxins
171
Q

What is Wernicke’s encephalopathy? Which patients tend to get this?

A
  • Wernicke’s encephalopathy = an acute and reversible encephalopathy due to a deficiency in thiamine (vitamin B1)
  • Occurs in patients with poor nutritional absorption, intake, or loss:
  • Chronic alcoholism
  • Anorexia nervosa
  • Hyperemesis
  • Prolonged fasting or starving
  • GI surgery
  • Systemic malignancy
172
Q

What are the triad of symptoms for Wernicke’s encephalopathy? What is the sign for Wernicke’s encephalopathy?

A
  • Classic triad = CAN:
  • Confusion
  • Ataxia
  • Nystagmus/opthalmoplegia
  • Sign:
  • ASTERIXIS (‘liver flap’) = general sign of metabolic encephalopathy
173
Q

What are the investigations for Wernicke’s encephalopathy?

A
  • Diagnosis is clinical
  • Low blood thiamine
174
Q

What is the treatment for Wernicke’s encephalopathy? What should we not give first?

A
  • PABRINEX (IV B vitamins including thiamine)
  • DO NOT give glucose before thiamine
175
Q

If Wernicke’s encephalopathy is not managed appropriately, what can happen?

A
  • If not managed appropriately:
  • Fatal in 20%
  • Can progress to KORSAKOFF’S SYNDROME
176
Q

What is Korsakoff’s syndrome? What are its symptoms?

A
  • Irreversible, long-term brain damage (due to B1 deficiency)
  • Symptoms:
  • Decreased ability to acquire new memories
  • Retrograde amnesia
  • Confabulation (invented memories)
177
Q

Are most liver cancers primary or secondary?

A

Secondary - they have metastasised to the liver from the GI tract, breast and bronchus

178
Q

Where have most secondary liver cancers arisen from?

A
  1. The GI tract
  2. Breast
  3. Bronchus
179
Q

What is hepatocellular carcinoma? Is it a primary or secondary liver tumour? What are the risk factors?

A
  • Hepatocellular carcinoma = hepatic malignancy commonly diagnosed in the presence of chronic liver disease
  • It is the most common primary liver tumour (80% of cases)
  • Risk factors:
  • Hepatitis B/C, coinfection with hepatitis D
  • Aflatoxin
  • Smoking and frequent alcohol consumption
180
Q

What are the signs and symptoms of hepatocellular carcinoma?

A
  • Often no symptoms aside from those of chronic liver disease
  • Epigastric pain; appetite; weight loss
  • Palpable abdominal mass; manifestations of decompensated cirrhosis, e.g. splenomegaly, ascites, jaundice
181
Q

What are the investigations for hepatocellular carcinoma?

A
  • CT/MRI
  • RAISED ALPHA-FETO PROTEIN = classic marker
  • Bloods: clotting abnormalities, deranged LFTs
  • Liver biopsy
182
Q

What is the treatment for hepatocellular carcinoma? What is the prognosis of hepatocellular carcinoma?

A
  • Surgical resection - partial hepatectomy or transplant
  • Chemotherapy (TACE)
  • Radiofrequency ablation
  • Prognosis: 3-6 months if unresectable - 90%
183
Q

What is pancreatic cancer? What is the most common type? What are the risk factors?

A
  • Pancreatic cancer = high lethal malignancy of exocrine pancreas
  • Pancreatic adenocarcinoma is the most common type (90%)
  • Risk factors:
  • Chronic pancreatitis
  • Genetic mutations (BRCA-1, BRCA-2 etc.)
  • Smoking; obesity; sedentary lifestyle; Fhx
184
Q

What are the signs and symptoms of pancreatic cancer?

A
  • Pain: epigastric, abdominal, may radiate to the back, may worsen after eating/when lying down
  • Physical weakness; anorexia, nausea; weight loss; jaundice, dark urine
  • Hepatomegaly
  • RUQ mass
  • Courvoisier’s sign (nontender, palpable gallbladder at right costal margin)
  • Trousseau’s sign
185
Q

What are the investigations for pancreatic cancer?

A
  • Bloods: LFTs and CARBOHYDRATE ANTIGEN 9-19 (tumour marker)
  • Biopsy with histological confirmation
  • Abdominal CT +- endoscopic USG
186
Q

What is the treatment for pancreatic cancer? What is its prognosis?

A
  • Surgery = pancreaticoduodenectomy or WHIPPLE’S PROCEDURE (only curative treatment)
  • Chemotherapy with/without chemoradiotherapy
  • 6% overall 5 year survival
187
Q

What is a hernia? What are the different classes and types?

A
  • Hernia = protrusion of an organ through a defect in the wall of its containing cavity
  • Classes:
  • Reducible
  • Irreducible
  • Obstructed = intestinal flow stopped
  • Strangulated = blood supply cut off = ischaemia +/- gangrene
  • Types:
  • Inguinal
  • Femoral
  • Umbilical
  • Incisional
  • Epigastric
  • Hiatal
188
Q

What is an inguinal hernia? What are the two types?

A
  • Inguinal hernia = protrusion of abdominal contents through the inguinal canal
  • Presents superior and medial to the pubic tubercle
  • Two types:
  • Direct = 20%, medial to inferior epigastric artery, enters inguinal canal through a weakness in its posterior wall
  • Indirect = 80%, lateral to the inferior epigastric artery, enters the inguinal canal through the deep inguinal ring
189
Q

What are the risk factors for an inguinal hernia?

A
  • Male
  • Chronic cough
  • Heavy lifting
  • Past abdominal surgery
190
Q

What is the presentation of an inguinal hernia?

A
  • Swelling in the groin/scrotum
  • May be painful
  • Impulse (expansion after cough)
  • May be reducible
191
Q

What are the investigations for an inguinal hernia?

A
  • Clinical Dx
  • Ultrasound, CT scan, MRI
192
Q

What is the treatment for an inguinal hernia?

A
  • Surgery:
  • Open/laparoscopic
  • Urgent if symptomatic
193
Q

What is a femoral hernia? What class is it likely to be and why?

A
  • Femoral hernia = bowel comes through the femoral canal
  • Likely to be irreducible and strangulate due to the rigidity of the canal’s borders
194
Q

What is the presentation of a femoral hernia?

A
  • Mass in upper medial thigh
  • Neck of hernia is inferior and lateral to the pubic tubercle
  • May be a cough impulse
195
Q

What are the investigations and treatment for a femoral hernia?

A
  • Investigations = clinical diagnosis, USS, CT, MRI
  • Treatment = surgery
196
Q

What is a hiatus hernia? What are the two types?

A
  • Hiatus hernia = herniation of the stomach through oesophageal aperture of the diaphragm
  • Two types:
  • Rolling = 20%, GOH remains in abdomen, part of fundus rolls up through hiatus
  • Sliding = 80%, GOJ and part of stomach slides up into chest, LOS less competent
197
Q

What are the risk factors for a hiatus hernia?

A
  • Obesity
  • Female
  • Pregnant
  • Ascites
  • Advanced age
  • Skeletal deformities
198
Q

What is the presentation of a hiatus hernia?

A
  • Heartburn/GORD
  • Dysphagia
199
Q

What are the investigations for a hiatus hernia? What is the management?

A
  • Investigations:
  • CXR
  • Barium swallow
  • Endoscopy
  • Oesophageal manometry
  • Management:
  • Lose weight
  • PPIs for acid reflux
200
Q

What is:

a) an incisional hernia
b) an epigastric hernia
c) an umbilical hernia
d) treatment for all 3?

A

a) incisional hernia = through surgical scar
b) epigastric hernia = through linea alba above umbilicus
c) umbilical hernia = at umbilicus
d) surgery

201
Q

What is hepatitis? What are the two types? What are their definitions?

A
  • Hepatitis = inflammation of the liver
  • Two types:
  • Acute hepatitis = <6 months
  • Chronic hepatitis = >6 months
202
Q

What are the infective and non-infective causes of acute hepatitis?

A
  • Infective:
  • Viral - hepatitis A, B+/D, C, E, EBV
  • Non-viral - spirochaetes, e.g. syphilis mycobacteria, e.g. M.tuberculosis
  • Non-infective:
  • Autoimmune
  • Alcohol
  • Non-alcoholic fatty liver disease
203
Q

What are the symptoms and signs of acute hepatitis? What are the transaminase levels like?

A
  • Symptoms:

– None or non-specific, e.g. malaise, lethargy, myalgia

– Gastrointestinal upset, abdominal pain

– Jaundice + pale stools / dark urine

  • Signs:

– Tender hepatomegaly ± jaundice

– ± signs of fulminant hepatitis (acute liver failure), e.g. bleeding, ascites, encephalopathy

  • Transaminases raised (ALT/AST >> GGT/ALP) + raised bilirubin
204
Q

What are the infective and non-infective causes of chronic hepatitis?

A
  • Infective:
  • Viral - hepatitis B +/ D, C, E
  • Non-infective:
  • Drugs
  • Alcohol
  • Autoimmune hepatitis
205
Q

What are the symptoms and signs of chronic hepatitis? What are the transaminase levels like?

A
  • Can be asymptomatic or have non-specific symptoms only
  • May have signs of chronic liver disease: clubbing, palmar erythema, Dupuytren’s contracture, spider naevi etc.
  • Transaminases (ALT/AST) can be normal
206
Q

What are the potential complications of chronic hepatitis?

A

Uncontrolled inflammation -> fibrosis -> cirrhosis -> HCC

207
Q

What is the pathophysiology of viral hepatitis?

A
  • Virus invades the hepatocytes, causing MHC I to present abnormal proteins
  • Abnormal proteins are recognised by CD8+ T-cells
  • This results in cytotoxic killing and apoptosis of hepatocytes
208
Q

Is hepatitis A a DNA or RNA virus? What is its mode of transmission? Acute or chronic?

A
  • RNA virus
  • Faeco-oral route
  • Acute - 100% immunity after infection
209
Q

What is the most important test when viral hepatitis is suspected?

A

Serology - detecting antibodies or antigens

210
Q

What are the investigations for HAV? What would they show?

A
  • Viral serology = initially IgM (active infection) and then IgG (recovery)
  • Blood = raised AST/ALT, raised bilirubin
211
Q

What is the management of HAV? What is the primary prevention?

A
  • Treatment often not required, generally supportive
  • Primary prevention = vaccines
212
Q

Is hepatitis E a DNA or RNA virus? What is its route of transmission? Acute or chronic?

A
  • Small RNA virus
  • Faeco-oral (UNDERCOOKED MEAT)
  • Usually acute but can there is a risk of chronic disease in immunocompromised people
213
Q

What are the investigations for HEV? What would they show?

A

Viral serology - IgM raised initially, IgG later

214
Q

What is the management for HEV?

A

Supportive treatment

215
Q

Is HBV a DNA or RNA virus? How is it transmitted? Acute or chronic?

A
  • DNA - replicates in hepatocytes
  • Blood-borne (IVDU), SEXUALLY
  • Both
216
Q

Describe the pathophysiology of HBV infection.

A
  • Acute infection infects hepatocyte. Cellular response usually clears it
  • Chronic HBV (5%) if HBsAg >6 months. Depends on age/immunocompetence. Inflammation can last 10 yrs -> cirrhosis
217
Q

What HBV protein triggers the initial immune response?

A

The core protein

218
Q

What are the investigations for HBV?

A

Viral serology: HBV surface antigen can be detected from 6w - 3m or anti-HBV core IgM after 3 months

219
Q

What is the management for HBV? What is the prevention?

A
  • PEGYLATED INTERFERON ALPHA 2A
  • Tenofivir - inhibits viral replication
  • Prevention: vaccine available
220
Q

How would you know if someone had acute or chronic HBV infection?

A

You would do a follow up appointment at 6 months to see if HBV surface Ag had cleared. If it was still present then the person would have chronic hepatitis

221
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis
  2. HCC
222
Q

How can HBV infection be prevented?

A

Vaccination - injecting a small amount of Hbs-Ag

223
Q

HBV treatment: give 3 side effects of alpha interferon treatment.

A
  1. Myalgia
  2. Malaise
  3. Lethargy
224
Q

Is HDV a DNA or RNA virus? Infection of what is needed for HDV to survive? How is HDV transmitted?

A
  • It is a defective RNA virus - it requires HBs-Ag to protect it
  • HDV can’t exits without HBV
  • Blood-borne, usually IVDU
225
Q

What would viral serology find in HDV infection?

A
  • HDV-RNA
  • Anti-HDV
226
Q

What is the management for HDV?

227
Q

Is HCV a DNA or RNA virus? How is it transmitted? Acute or chronic?

A
  • HCV is an RNA virus
  • Blood-borne - IVDU more than sexually
  • Both
228
Q

Give 4 risk factors for developing HBV/HCV infection.

A
  1. IVDU
  2. People who have required blood products, e.g. blood transfusion
  3. Maternal-foetal transmission
  4. Unprotected sexual intercourse
229
Q

How might you diagnose someone with current HCV infection? You want to find out if someone has previously been infected with HCV. How could you do this?

A
  • Viral serology - HCV RNA tells you if the infection is still present
  • Viral serology - anti-HCV IgM/IgG indicates that someone has either a current infection or a previous infection
230
Q

Describe the treatment for HCV.

A
  • Direct acting antivirals (DAA) are currently in use, e.g. NS5A and NS5B
  • Ribavirin
  • Sofosbuvir
231
Q

How can HCV infection be prevented?

A
  1. Screen blood products
  2. Lifestyle modification
  3. Needle exchange
    There is currently no vaccination and previous infection does not confer immunity
232
Q

What percentage of people with acute HCV infection will progress onto chronic infection?

A

Approximately 70%

233
Q

What percentage of people with acute HBV infection will progress onto chronic infection?

A

Approximately 5%

234
Q

What is the female:male ratio of autoimmune hepatitis?

235
Q

What do people with autoimmune hepatitis often have?

A

HLA-DR3 or HLA-DR4 (MHC II surface receptors)

236
Q

What are the signs and symptoms of autoimmune hepatitis?

A
  • Ranges from asymptomatic to cirrhosis and fulminant hepatitis (acute liver failure)
  • May have fever, jaundice, hepatosplenomegaly
237
Q

What are the investigations for autoimmune hepatitis? What would be shown?

A
  • ALT and AST - ALT > AST but both raised
  • Bilirubin and GGT raised
238
Q

What is the management of autoimmune hepatitis?

A
  • Observation and monitoring if inactive or minimally active
  • PREDNISOLONE if active
239
Q

Give 5 symptoms of helminth infection.

A
  1. Fever
  2. Eosinophilia
  3. Diarrhoea
  4. Cough
  5. Wheeze
240
Q

Briefly describe the reproductive cycle of schistosomiasis.

A
  1. Fluke matures in blood vessels and reproduces sexually in human host
  2. Eggs expelled in faeces and enter water source
  3. Asexual reproduction in an intermediate host
  4. Larvae expelled and penetrate back into human host
241
Q

Why is C.diff highly infectious?

A

It is a spore forming bacteria (Gram positive)

242
Q

Give 5 risk factors for c.diff infection.

A
  1. Increasing age
  2. Co-morbidities
  3. Antibiotic use
  4. PPI
  5. Long hospital stays
243
Q

Describe the treatment for c.diff infection.

A

ORAL FIDOXAMICIN OR VANCOMYCIN (metronidazole may be used in some locations)

244
Q

Name 5 antibiotics prone to causing c.diff infection.

A

Rule of C’s:

  1. Ciprofloxacin
  2. Co-amoxiclav
  3. Clindamycin
  4. Cephalosporins
  5. Carbapenems
245
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer

246
Q

Name a protozoa that can cause amoebic liver abscess?

A

Entemoeba histolytica

247
Q

What are the symptoms of e.histolytica?

A
  • RUQ pain
  • Bloody diarrhoea
  • Fever and malaise
    Often the patient has a history of foreign/rural travel
248
Q

What is the treatment for entemoeba histolytica?

A

Metronidazole

249
Q

Name the 2 main pathophysiological factors that contribute to the formation of ascites.

A
  1. High portal venous pressure
  2. Low serum albumin
250
Q

A man has his ascites drained and is advised to restrict his diet. Which non-hormonal substance will promote re-accumulation of the ascites?

251
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis

252
Q

What two enzymes, if raised, suggest pancreatitis?

A

LDH and AST

253
Q

List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.

A
  1. Blood or mucus in the stools?
  2. Family history of bowel problems?
  3. Abdominal pain?
  4. Recent foreign travel history?
  5. Bloating?
254
Q

List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea. List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.

A
  • FBC and ESR/CRP
  • Stool culture and faecal calprotectin
255
Q

What are the two most common causes of liver failure in the UK?

A
  • Alcohol
  • Paracetamol overdose
256
Q

Which biomarker would be raised if a patient presented with hepatocellular carcinoma?

A

Alpha-fetoprotein

257
Q

Calculate the number of units: a patient drinks 3 glasses of wine a week (each glass is 175ml, 13% strength)

A

175 x 13/1000 = 2.275

2.275 x 3 = 6.825 units

258
Q

You are reviewing a 48-year-old man who was admitted with sudden severe abdominal pain, confusion and pyrexia. He has a background of alcoholic cirrhosis and known ascites which is normally asymptomatic. An ascitic tap was done overnight which showed a raised neutrophil count and was sent for urgent microscopy & culture.

What organism is most likely to grow from the ascitic tap?

a) E. coli
b) Staph aureus
c) Klebsiella
d) Streptococcus

A

a) E. coli - most commonly causes spontaneous bacterial peritonitis (although all of these do)

259
Q

A patient presents with history of drinking with dark sticky faeces and blood in her vomit.

Which drug would you use to treat her?

a) Spironolactone
b) Ciprofloxacin
c) Propranolol
d) Amlodipine

A

C) Propanolol

260
Q

A 56-year-old male presents with a 2 week history of diarrhoea after an episode of ‘food poisoning’. Which is the most appropriate investigation?

a) FBC
b) U+E
c) Stool sample for MC&S
d) AXR
e) LFTs

A

C) Stool sample for MC&S

261
Q

Which liver disease does this sign indicate?

a) Hepatitis
b) Haemochromatosis
c) Cirrhosis
d) Wilson’s
e) Fulminant liver failure

A

d) Wilson’s

262
Q

56M, diagnosed with emphysema, presents with a 1 month history of jaundice and ascites. The registrar suspects that this patient may have liver disease secondary to A1T1 deficiency. Select the most likely mode of inheritance from the list below:

a) Autosomal dominant
b) X-linked dominant
c) Autosomal recessive
d) Polygenic
e) None of the above

A

C) Autosomal recessive

263
Q

25F presents with a 24hr history of watery diarrhoea. Opened bowels 11 times since onset of symptoms. Feels nauseous, abdominal cramps, pain. Had a barbeque meal the day previously. HR 69, BP 124/75, temp 37.1. Abdomen is soft, tender in epigastric region, bowel sounds are hyperactive. Patient is normally fit and well with no PMH. What is the most likely diagnosis?

a) IBS
b) Gastroenteritis
c) UC
d) Laxative abuse
e) Crohn’s

A

b) Gastroenteritis

264
Q

What is the most appropriate management for gastroenteritis?

a) Oral rehydration advice, anti-emetics, discharge home
b) Oral antibiotic therapy, discharge home
c) Admission for IV fluid rehydration
d) Admission for IV antibiotic therapy
e) No treatment required

A

a) Oral rehydration advice, anti-emetics, discharge home

265
Q

A 56 year old man presents with abdominal distension and shortness of breath. Examination revealed fever of 38C, a tense distended abdomen with shifting dullness. He also has dullness to percussion in the right lung base. Several spider naevi are seen on his chest. Which is the most important test in the management of this patient?

A. CXR

B. Ultrasound abdomen

C. Echocardiogram

D. Ascitic tap

E. Urine dip

A

D. Ascitic tap

266
Q

A 52 year old lady presents with fatigue and itching. She noticed pale stool and dark urine. She suffers from hypercholesterolaemia and rheumatoid arthritis. She takes simvastatin and cocodamol. Examination revealed jaundice, xanthelasma spider naevi and hepatomegaly. Her bloods showed Bili 150, ALP 988, ALT 80, positive AMA and a raised IgM. What is the most likely diagnosis?

A. Simvastatin induced liver injury

B. Primary biliary cirrhosis

C. Gall stones

D. Autoimmune hepatitis

E. Primary sclerosing cholangitis

A

B. Primary biliary cirrhosis

267
Q

A 16 year old girl is admitted with vomiting and abdominal pain. She reports taking 20 paracetemol tablets after her boyfriend split up with her. Which one of the following test results would you NOT expect to see?

A. Metabolic acidosis

B. A prolonged prothrombin time

C. A raised creatinine

D. Hyperglycaemia

E. ALT 1000

A

D. Hyperglycaemia

268
Q

A 68 year old unkempt and malnourished homeless man was brought to the hospital with haematemesis. Endoscopy found bleeding varices. Subsequent USS showed a coarse shrunken liver. On day 2 admission he was found to be ataxic, confused with nystagmus. What is the most likely cause of his neurological presentation?

A. Alcohol toxicity

B. Alcohol withdrawal

C. Delirium tremens

D. Wernicke’s encephalopathy

E. Korsakoff syndrome

A

D. Wernicke’s encephalopathy

269
Q

Which of the following gives the best indication of liver function?

A. Amylase

B. ALP

C. Prothrombin time

D. AST/ALT ratio

E. Gamma-glutamyl transferase (GGT)

A

C. Prothrombin time

270
Q

Which of the following is not a sign of peritonitis?

  1. Rebound tenderness / positive release sign
  2. Shoulder tip pain
  3. Localised guarding
  4. Rigidity
  5. Pain worse when lying
A
  1. Pain worse when lying
271
Q

Simon, a 63yr old male has presented to A&E with a 1 day history of fevers, rigors and vomiting. He has a history of chronic Hepatitis C infection and on examination has a distended abdomen, shifting dullness and spider naevi on his chest.

What acute condition is this patient suffering from?

  1. Fulminant liver failure
  2. Spontaneous bacterial peritonitis
  3. Bleeding oesophageal varices
  4. Ascending cholangitis
  5. Liver cirrhosis
A
  1. Spontaneous bacterial peritonitis
272
Q

Which is the most common form of inheritance of hereditary haemochromatosis?

  1. Autosomal dominant
  2. Autosomal recessive
  3. X-linked recessive
  4. X-linked dominant
  5. Codominance
A
  1. Autosomal recessive
273
Q

Which is the most common form of inheritance of Wilson’s disease?

  1. Autosomal dominant
  2. Autosomal recessive
  3. X-linked recessive
  4. X-linked dominant
  5. Codominance
A
  1. Autosomal recessive
274
Q

You are on a ward round in the elective general surgical ward, when you see a patient who has recently undergone a Whipple’s procedure for a known adenocarcinoma. The consultant talks you through this patient’s case and notes that the presenting symptoms are weight loss, painless jaundice and steatorrhea.

Which of the following genetic mutations is likely to be present?

  1. CA 19-9
  2. FAP
  3. KRAS
  4. BRCA1
  5. ELMO1
A
  1. KRAS (85-90% of pancreatic cancer cases)
275
Q

A 45-year-old female with a history of sickle cell disease presents to the emergency department with severe epigastric pain that radiates to her back. The patient appears clinically jaundiced. She reports drinking one small glass of red wine a week but no other alcohol consumption. A diagnosis of acute pancreatitis is made.

What is the most likely cause of acute pancreatitis in this patient?

  1. EtOH
  2. Steroids
  3. Splenic atrophy
  4. Gallstones
  5. Autoimmune
A
  1. Gallstones
276
Q

A 56-year-old man presents with epigastric discomfort and episodes of migratory thrombophlebitis. On examination he is mildly jaundiced and has a palpable mass in the RUQ. A CT scan shows peri hilar lymphadenopathy, multiple small masses in the liver and one large mass in the pancreatic head.

Which one of the following is the most likely underlying diagnosis?

  1. Cholangiocarcinoma
  2. Hepatocellular carcinoma
  3. Pancreatic adenocarcinoma
  4. Gallbladder cancer
  5. Squamous cell carcinoma of the pancreas
A
  1. Pancreatic adenocarcinoma
277
Q

A known diabetic presents to his GP for annual review. The doctor notices his abdomen is quite large with lots of fluid buildup. The patient tells you that he is unsure why this could be the case. He mentions that he does not drink or smoke, and feels relatively fit and well.

The doctor is worried about his health due to his high BMI and presenting factors. Which investigation should the doctor order to confirm suspected diagnosis?

a. LFTs
b. FBC
c. Enhanced Liver Fibrosis Test
d. Liver US

A

d. Liver US

278
Q

Tom is a 55 y.o gentleman presenting to the A&E after several episodes of vomiting blood following period of forceful retching and vomiting. He has been binge drinking alcohol for the last few days. He later complains dark colouring of his stools. He has a past medical history of liver disease and hypertension.

O/E: Confused, hepatomegaly and jaundice

Based on the above, what is the most likely diagnosis?

A. Obstructive jaundice

B. Rupture of esophageal varices

C. Mallory-Weiss tear

D. Peptic ulcer disease

E. Anal fissure

A

C. Mallory-Weiss tear

279
Q

A 30 year old female presents with constant RUQ pain with associated fever, nausea and vomiting. On examination the doctor applies pressure to the RUQ and asks the patient to breathe in. Suddenly the patient shouts in pain.

What is the general cause of this patient’s symptoms?

a. Biliary Colic
b. Ascending Cholangitis
c. Acute cholecystitis
d. Pancreatic Cancer

A

c. Acute cholecystitis

280
Q

Mary is a 50 y.o lady who presents to her GP with generalized itching across her body over 2-weeks. Over this time, she has feeling increasingly tired and has no energy to do the things she used to do. She denies any changes to her bowel habits, weight loss or blood coming out from anywhere. However, she said that her husband has been commenting that she looks yellower recently. What antibody is likely to be found in this patient?

a. Anti-mitochondrial Ab
b. Anti-smooth muscle Ab
c. IgA endomysial Ab
d. ANA
e. Anti-tTG

A

a. Anti-mitochondrial Ab

281
Q

A 34 year old man presents to the GP with yellowing of the skin which his wife has mentioned began 2 weeks ago.

a) What are the 3 main types of jaundice and give 2 causes of each? (6)
b) What are other associated signs + symptoms of these types of jaundice?

A

a) Pre-hepatic - unconjugated hyperbilirubinemia caused by haemoglobin breakdown - haemolytic anaemia, Gilbert’s syndrome

Intrahepatic - unconjugated + conjugated hyperbilirubinemia - alcoholic liver disease, PSC

Post-hepatic - conjugated hyperbilirubinemia caused by extrahepatic cholestasis from biliary obstruction - gallstones, pancreatic cancer

b) Pre-hepatic: pallor, fatigue, exertional dyspnoea

Intrahepatic: anorexia, fatigue, nausea, abdominal pain

Post-hepatic: pale stools, dark urine, pruritus, steatorrhoea, RUQ pain, hepatomegaly

282
Q

George is a 56 y.o gentleman complaining of tiredness. This has been going on for a week and during this time he noticed that he appears more tanned even without leaving his house. His glucose levels are raised.

Genetic testing shows the presence of C282Y mutations. Both his levels for transferrin and ferritin is raised.

Based on the most likely diagnosis, how would you manage this patient?

a. Phlebotomy
b. Desferrioxamine
c. Deferasirox
d. Ursodeoxycholic acid
e. Chlordiazepoxide

A

a. Phlebotomy

283
Q

A 20 year old gentleman has shown up to his GP due to a recurrence of jaundice. He has mentioned he’s become more itchy lately and has developed a pain in his upper right abdomen. He is quite into his fitness and has mentioned he has noticed some muscle atrophy and weight loss. After further investigations, alternating strictures and dilated portions of the hepatic ducts are seen on ERCP.

Which condition is NOT associated with the condition described above?

a. Hepatocellular Carcinoma
b. Crohn’s Disease
c. Ischemic Colitis
d. Ulcerative Colitis

A

c. Ischaemic colitis

284
Q

John is a 22 y.o medical student. He noticed that for the past week, he had been having difficulties with picking up his pen and buttoning up his shirt. He has also been shaking involuntarily and thinks it gets worse when he is stressed. He has also noticed that his limbs are pretty stiff and that his movements are slow. His friends have said that he eyes seem to have taken on a different colour. What is the most likely diagnosis?

a. Wilson’s disease
b. Juvenile parkinsonism
c. Alzheimer’s disease
d. Multiple sclerosis
e. Haemochromatosis

A

a. Wilson’s disease

285
Q

A 56 year old woman comes to A+E complaining of increased abdominal pain which seems to be worse 20 minutes after a meal. She mentioned that her stools have become more smellier than usual and tend to float. She tells you that this has happened before and that she is worried that this could be due to her alcohol habit. Under further investigations you notice her blood sugars are substantially elevated.

Given the history, which vitamins would this patient be least likely deficient in?

a. A
b. B12
c. D
d. E
e. K

A

b. B12. Chronic pancreatitis puts the patient at a higher risk of developing a deficiency in fat-soluble vitamins -> A, K, E, D

286
Q

75 y.o gentleman has hepatocellular carcinoma. He drinks a crazy amount of alcohol and has a family of history liver cancer.

a) What cancer marker might be present?
b) Which other cancer could you the rise in the cancer marker in your answer above?
c) Name some risk factors for developing HCC. (Besides the ones mentioned above)

A

a) Alpha-fetoprotein
b) Testicular cancer
c) Chronic hepatitis B infection, chronic hepatitis C cirrhosis, chronic heavy alcohol use, diabetes mellitus, obesity, and family history of liver cancer

287
Q

A current IVDU presents to A&E with worsening abdominal pain which he mentions has been going on for a couple months now. He does not drink or smoke, nor have family history of any liver pathology.

O/E: Temp: 38C, HR: 99bpm, BP 117/78.

He is seen to have a large abdomen with yellow discoloration to his skin.

Blood samples were taken which show:

Hepatitis A IgM: negative

Hep B anti-HBs antibody: positive

Hepatitis C Abs test: positive.

Which of the following best describes the genome of the most likely pathogen responsible?

a) Double stranded DNA virus
b) Double stranded RNA virus
c) Positive sense single-stranded RNA virus
d) Negative sense single-stranded RNA virus

A

c) Positive sense single-stranded RNA virus

288
Q

Mason is a 30 y.o banker who recently developed a productive cough. The cough just came on and he is unsure of any triggers. He gets breathless on exertion. He smokes 1 pack every day. He overhears the doctors saying that his condition might be due to a deficiency of an enzyme in his blood.

O/E: Hepatomegaly and hyperinflated chest. Both parents had emphysema before the age of 50.

What is the inheritance pattern of this disease?

a) Autosomal dominant
b) Autosomal recessive
c) Mitochondrial
d) X-linked recessive
e) X-linked dominant

A

b) Autosomal recessive

289
Q

A 40 year old caucasian female is presenting to the GP complaining of intermittent RUQ pain. She says the pain comes on after eating but it goes away after 2 hours. She is currently overweight.

Given the likely diagnosis, what type of stone would be the most likely cause?

a) Cholesterol stone
b) Black Pigmented stone
c) Brown Pigmented Stone
d) Pink Pigmented Stone

A

a) Cholesterol stone

290
Q

A 50-year-old man presents to the emergency department with a history of black, tarry stools but denies haematemesis or abdominal pain. His family has noticed progressive confusion. You are unable to get a history from him and his family say he is an alcoholic and has a history of liver failure. Which vitamin should be given to this patient?

a) Vitamin B1
b) Vitamin B12
c) Vitamin A
d) Vitamin D
e) Vitamin K

A

a) Vitamin B1

291
Q

A 56 year old man presents to A&E due to severe abdominal pain and signs of jaundice. Whilst palpating you can feel a bulge 4cm below the right costal margin after asking the patient to breathe in.

You decide to take some bloods which show:

ALP - 134 U/L (30-100 U/L)

GGT - 153 U/L (8-60 U/L)

ALT - 317U/L (3-40 U/L)

AST - 634 U/L (3-30 U/L)

What is the most likely diagnosis?

a) Autoimmune Hepatitis
b) Alcoholic Liver Disease
c) Non Alcoholic Fatty Liver disease
d) Cirrhosis

A

c) Non-alcoholic fatty liver disease

292
Q

George is a known alcoholic with a dull-to-percuss belly.

a) Name 3 aetiological causes for his ascites.
b) Name 1 complication that could happen.
c) Following qn 2, how should the patient be managed?

A

a) Inflammation, low protein and malignancy
b) Spontaneous bacterial peritonitis
c) Empirical antibiotics. If sepsis, then sepsis 6

Phase 2a (25 decks)

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