Gastroenterology Flashcards
(300 cards)
1
Q
Outline the spectrum of alcohol-related liver disease?
A
- Alcoholic fatty liver disease<div>- Alcoholic hepatitis</div><div>- Cirrhosis</div>
2
Q
How can alcohol-related liver disease progress?
A
- Can be a stepwise progression; fatty liver –> alcoholic hepatitis –> cirrhosis<div>- In reality progression can be highly variable</div><div>- Influenced by genetic predisposition</div>
3
Q
What is alcoholic fatty liver?
A
- Excess ingestion of alcohol and its subsequent metabolism leads to the deposition of excess fat in the liver<div>- May occur with or without concurrent inflammation</div><div>- Reversible in around 2 weeks following cessation of drinking</div>
4
Q
What is alcoholic hepatits?
A
- Acute onset of symptomatic hepatitis due to severe inflammation of the liver<div>- Associated with sustained excess alcohol ingestion or acutely due to binge drinking</div><div>- Mild forms are reversible with permanent abstinence of drinking</div>
5
Q
What is alcohol-related liver cirrhosis?
A
- Irreversible scaring of the liver<div>- Associated with numerous complications</div><div>- Abstinence can prevent further damage</div><div>- Continued drinking has very poor prognosis</div>
6
Q
What is the rough threshold alcohol consumption that is said to significantly increases the risk of developing alcoholic hepatitis?
A
- Consumption <b>>100g per day for 15-20 years</b><div>- Approximately 12.5 units per day</div>
7
Q
What is the relationship between alcohol units and ABV?
A
”- 1L of 5% ABV = 5 units<div>- 1L of 40% ABV = 40 units</div><div><br></br></div><div><br></br></div><div><b>Units = ABV / (1000/Volume )</b></div>”
8
Q
Outline the DoH guidance for alcohol consumption in the UK?
A
- No more that 14 units per week spread evenly over 3 or more days<div>- No more than 5 units in any single day</div><div>- Alcohol should be completely avoided in pregnancy</div>
9
Q
What questions can be used to screen for harmful alcohol use?
A
“<b><u>CAGE Questions;</u></b><div>- <b><u>C</u>utting down</b>; has patient considered cutting down</div><div>- <b><u>A</u>nnoyed</b>; does patient get annoyed about others commenting on their drinking</div><div>- <b><u>G</u>uilt</b>; has patient ever felt guilty about drinking</div><div>- <b><u>E</u>ye opener</b>; does pateint ever drink in the morning to help with hangovers/nerves</div>”
10
Q
What questionnaire can be used to screen patients for harmful alcohol use?
A
<b><u>AUDIT Questionnaire;</u></b><div>- Alcohol use disorders identification test</div><div>- Score > 8 indicates harmful use</div>
11
Q
Outline some of the complications of alcohol?
A
- Alcoholic liver disease<div>- Cirrhosis and the complications of which can include hepatocellular carcinoma</div><div>- Alcohol dependance and withdrawal</div><div>- Wernicke-Korsakoff Syndrome (WKS); vitamin B1(<b>thiamine</b>) deficiency</div><div>- Pancreatitis</div><div>- Alcoholic Cardiomyopathy</div>
12
Q
Which scoring system can be used to assess the severity of alcoholic hepatitis?
A
<b><u>Maddrey Discriminant Function (DF)</u></b><div>- Based on prothrombin time and serum bilirubin</div><div>- DF > 32; severe hepatitis</div><div>- DF < 32; mild-to-moderate hepatitis</div>
13
Q
What scoring system can be used to assess mortality amoung patients with alcoholic hepatitis?
A
<b><u>Glascow Alcoholic Hepatitis Score (GAH);</u></b><div>- Score > 9; severe alcoholic hepatitis, 46% 28-day survival</div>
14
Q
What signs can often be seen upon examination of a patient with alcoholic liver disease?
A
- Jaundice<div>- Hepatomegaly</div><div>- Spider naevi</div><div>- Palmar erythema</div><div>- Dupuytren’s contracture</div><div>- Bruising; due to abnormal clotting</div><div>- Ascites</div><div>- Caput medusae; engorged superficial epigastric veins due to portal hypertension</div><div>- Asterixis; flapping tremor in decompensated liver disease</div>
15
Q
What blood tests should be carried out in a patient with suspected alcoholic liver disease?
A
- FBCs; raised MSV in alcholics, likely elevated neutrophil count<div>- LFTs; derranged</div><div>- Clotting; elevated prothrombin time</div><div>- U&Es; may be derranged in hepatorenal syndrome</div>
16
Q
What imaging can be used to investigate potential alcoholic liver disease?
A
<b>- Liver ultrasound</b> with dopplers can be used to assess the achitecture of the liver, may show fatty changes described as <b>increased echogenicity</b><div><b>- FibroScan</b>; can be used to assess the elasticity of the liver to assess the degree of cirrhosis</div>
17
Q
What is meant by a non-invasive liver screen?
A
”- Series of non-invasive investigations to determine the possible causes of liver disease<div>- Includes screening questions, imaging and blood tests</div><div><img></img><br></br></div>”
18
Q
Outline some of the changes that may be seen in the LFT blood test results for a patient with alcoholic liver disease?
A
- Elevated ALT and AST; <b>AST/ALT ratio > 2 </b>(secondary to pyridoxal-5-phosphate deficiency)<div>- Particularly raised γ-GT</div><div>- ALP can also be raised in late-stage disease</div><div>- Low albumin due to reduced <b>synthetic function </b>of the liver</div><div>- Elevated bilirubin in cirrhosis</div>
19
Q
Why may the INR or prothrombin time be elevated in patients with alcoholic liver disease?
A
<div>- Reduced synthetic function of the liver</div>
- Impaired synthesis of coagulation factors<div>- Hence increased time to coagulate</div>
20
Q
What investigation can be carried out in severe cases of alcoholic liver disease or in patients who are being considered for steroid therapy?
A
- <b>Liver biopsy</b>; assess for underlying cirrhosis, steatosis, neutrophil infiltration, hepatocytes ballooning, <b>Mallory-Denk bodies</b>
21
Q
What are Mallory-Denk bodies?
A
“<span>- <b>Eosinophilic accumulations</b> of proteins within the cytoplasms of hepatocytes that may be seen in liver biopsies</span><div><span>- Whilst they have no pathological role in disease they are a <b>marker </b>of <b>alcohol-induced liver disease</b></span></div><div><img></img><span><b><br></br></b></span></div>”
22
Q
Outline the key management principles for alcoholic liver disease?
A
- <b>Managing alcohol withdrawal</b>; CIWA Scoring, benzodiazepines, alcohol team input<div>- <b>Alcohol cessation</b></div><div>- <b>Hydration</b>; fliud resuscitation, HAS in patients with ascites</div><div>- <b>Nutrition</b>; high dose thiamine (Pabrinex)</div><div>- <b>Treatment of complications</b>; infection, portal hypertension and oesophageal varices</div><div>- <b>Pharmacolgical therapy</b>; corticosteriods (prednisolone, 40mg OD, 28-days)</div>
23
Q
Outline some of the effects of alcohol withdrawal?
A
- 6-12hrs; tremor, sweating, headache, cravings, anxiety<div>- 12-24hrs; hallucinations</div><div>- 24-48hrs; seizures</div><div>- 24-72hrs; <b>delerium tremens</b></div>
24
Q
What is delerium tremens?
A
- Medical emergency associated with alcohol withdrawal<div>- Potential fatal complication if left untreated (35% mortality)<br></br><div>- Signs</div><div> o Acute confusion</div><div> o Severe agitation</div><div> o Delusions and hallucinations</div><div> o Tremor</div><div> o Tachycardia</div><div> o Hypertension</div><div> o Hyperthermia</div><div> o Ataxia</div></div>
25
What causes delerium tremens?
- Alcohol stimulates GABAnergic neurones and inhbits NMDA glutamatergic neurones
- Chronic alcohol used results in an up-regulation of the GABA system and a downregulation of the glutamate system to balance these effects- When alcohol is removed the GABA system underfunctions and the glutamate system overfunctions
- This leads to extreme excitability in the brain leading to excess adrenergic stimulation
26
What scoring system can be used to assess the severity of alcohol withdrawal symptoms and guide treatment?
CIWA-Ar Tool;
- Scores > 9 require medication for withdrawal
27
Outline some of the pharmacological managment options for patients experiencing alcohol withdrawal?
- Chlordiazepoxide (Librium); oral benzodiazepine, reducing regime (10-40mg every 1-4hrs) for 5-7 days
- Thiamine suppliments; intitially IV high dose (Pabrinex) followed by regular dose oral thiamine
28
What is Wernicke-Korsakoff Syndrome (WKS)?
- Combination of Wernicke's encephalopathy and Korsakoff's syndrome
- Caused by thiamine deficiency
29
What is Wernicke's encephalopathy?
- Medical emergency with a high mortality rate
- Confusion
- Oculomotor disturbances
- Ataxia
- Due to vitamin B1 (thiamine) deficiency
30
What is Korsakoff's syndrome?
- Irreversible complication seen in alcoholic liver disease
- Results in patient requiring full-time institutional care
- Memory impairement; both retrograde and anterograde
- Behavioural changes
31
What is liver cirrhosis?
- Result of chronic inflammation and damage to liver cells
- Damaged liver cells are replaced by areas of scar tissue (fibrosis)
- These areas of fibrotic scar tissue form nodules
32
What is the main result of liver fibrosis?
- Scarring of the liver affects the structure and blood flow
- Results in increased resistance in the portal vessels
- Leads to portal hypertension
33
What are the most common causes of liver cirrhosis?
- Alcohol-related liver disease (ArLD)
- Non-Alcoholic Fatty Liver Disease (NAFLD)
- Hepatitis B (HEP-B)
- Hepatitis C (HEP-C)
34
Outline some of the rarer causes of liver cirrhosis?
- Autoimmune hepatitis
- Primary biliary cirrhosis
- Haemachromatosis
- Wilson's disease
- α1 anti-trypsin deficiency
- Cystic fibrosis
- Drugs; amiodarone, methotrexate, sodium valproate
35
Outline some of the clinical signs of liver cirrhosis?
- Jaundice; caused by raised bilirubin
- Hepatomegaly; in early stages, but liver may skrink as it becomes more cirrhotic
- Splenomegaly; due to portal hypertension
- Spider naevi; telangiectasias
- Palmar erythema; hyperdynamic circulation
- Gynaecomastia and testicular atrophy; endocrine dysfunction and raised oestrogens
- Bruising; due to abnormal clotting
- Acites; due to hypoalbuminaemia as a result of decreased synthetic function of liver
- Caput medusae; engorged superficial epigastric veins to due to portal hypertension
- Asterixis; flapping tremor in decompensated liver disease
36
What blood tests can be used to investigate liver cirrhosis?
- LFTs; may be normal but all (AST, ALT, ALP, γGT and bilirubin) can be raised in decompensated disease
- Albumin/Prothrombin time (or INR); marker for synthetic function of liver
- U&Es; hyponatraemia indicates fluid retention which may be seen in severe disease
- Creatinine; may be derranged along with the urea in hepatorenal syndrome
- Viral markers/autoantibodies; other causes of cirrhosis
- α-feroprotein; hepatocellular carcinoma marker
- Enhanced liver fibrosis (ELF) test; first-line in NAFLD only
37
What is the enhanced liver fibrosis (ELF) blood test?
- Blood test for assessing the degree of fibrosis
- First-line in non-alcoholic fatty liver disease (NAFLD) only
- Assesses 3 markers of cirrhosis; hyaluronic acid (HA), procollagen-III aminoterminal peptide (PIIINP) and tissue inhibitor of matrix metalloprotease-1 (TIMP-1)
38
How is the ELF blood test used to indicate the degree of liver cirrhosis in patients with NAFLD?
- < 7.7; none to mild degree of fibrosis
- 7.7 - 9.8; moderate fibrosis
- > 9.8; severe fibrosis
39
What imaging techniques can be used to investigate liver cirrhosis?
- Liver ultrasound; first-line
- FibroScan; check elasticity
- Endoscopy; if oesophageal varices suspected
- CT and MRI; look for HCC
40
What are the indications for FibroScan investigations every 2 years in patients at risk of liver cirrhosis?
- Hepatitis C
- Heavy alcohol drinkers
- Diagnosed alcoholic liver disease
- NAFLD and evidence of fibrosis on ELF blood test
- Chronic hepatitis B
41
What scoring system can be used to estimate the prognosis of patients with liver cirrhosis?
"Child-Pugh Score;
- Patient scores 1-3 depending on 5 features
- Can be used to give 1-year survival rate
- Sum of values used to confer class of cirrhosis from A to C
![]()
"
42
How can the Child-Pugh Score be used to grade the degree of liver cirrhosis?
- Score 5-6; Class A, 100% 1-year survival rate
- Score 7-9; Class B, 80% 1-year survival rate
- Score 10-15; Class C, 45% 1-year survival rate
43
"Which scoring system is recommended by NICE to be used every 6 months in patients with compensated cirrhosis in order to estimate 3-month mortality and guide transplant referral?"
MELD-Na Score;
- Dialysis
- Creatinine
- Bilirubin
- INR
- Na+
44
Outline the general management principles for liver cirrhosis?
- Liver US and α-feroprotein every 6-months
- Endoscopy every 3 years
- High protein, low Na+ diet
- MELD-Na Scoring every 6-months
- Consideration for liver tranplantation
- Management of complications
45
Outline the common complications seen in liver cirrhosis?
- Malnutrition
- Portal hypertension, varices and variceal bleeding
- Ascites and spontaneous bacterial peritonitis (SBP)
- Hepatorenal syndrome
- Hepatic encephalopathy
- Hepatocellular carcinoma
46
How can you advise patients to manage and prevent malnutrition that may occur as a result of liver cirrhosis?
- Regular meals every 2-3hrs
- Low Na+ diet
- High protein and calorie diets
- Avoid alcohol
47
What causes varices to develop as a result of liver cirrhosis?
- Increased resistance to blood flow in the liver
- Leads to portal hypertension
- Back-pressure causes porto-systemic anastamoses to engorge with blood to divert away from the portal system
- The swelling of these systemic vessels causes swollen, tortuous varices to develop
48
Where are varices often found?
- Gastro-oesophageal junction
- Iliocaecal junction
- Rectum
- Anterior abdominal wall via the umbilical vein
49
Outline the treatment options for stable varices?
- Propranolol; reduces the portal hypertension
- Elastic band ligation
- Injection of sclerosant agents; such as sodium tetradecyl sulfate
- Transjugular intra-hepatic portosystemic shunt (TIPS)
50
What is a transjugular intra-hepatic porstosystemic shunt (TIPS) and how can it be used in the treatment of stable varices?
"- Interventional radiologist inserts wire under X-Ray guidance into jugular vein![]()
"
- Wire guided into the liver via the hepatic vein
- Connection is made through the liver tissue between the hepatic vein and the hepatic portal vein
- Stent inserted into this connection
- Blood allowed to bypass the liver directly from the hepatic portal vein into the hepatic vein
- Relieves portal hypertension and the pressure in the varices
51
Outline the initial resuscitation steps involved in treating bleeding oesophageal varices?
- Terlipressin; AVP analogue that causes splanchnic vasoconstriction
- Prophylactic broad-spectrum antibiotics; prevent spontaneous bacterial peritonitis and reduce mortality
- Correct coagulopathy; vitamin K and FFP
- Consider intubation; ITU admission
52
Outline the endoscopic management options in a patient with bleeding oesophageal varices?
- Variceal band ligation (VBL); using elastic bands placed around the varices
- Endoscopic sclerotherapy; used to cause inflammatory obliteration of the vessel
53
What interventions can be considered in patients with bleeding oesophageal varices where pharmacological and/or endoscopic interventions have failed?
- Sengstaken-Blakemore Tube; inflatable tube inserted into the oesophagus to tamponade the bleeding varices, remove within 24hrs to avoid oesophageal necrosis
- Oesophageal Stenting; alternative to Sengstaken-Blakemore tube
- Transjugular Intra-hepatic Portosystemic Shunt (TIPS); in appropriately selected patients
54
What kind of ascites is caused by liver cirrhosis?
- Transudative cirrhosis; low protein content acsites
55
How can liver cirrhosis cause ascites?
Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel into the peritoneal cavity
56
How can ascites secondary to liver cirrhosis be managed?
- Low Na+ diet
- Aldosterone anagonists; spironolactone
- Paracentesis; ascitic tap or drain
- Prophylactic antibiotics; ciprofloxacin or norfloxacin in patients with less than 15g L-1 of protein in ascitic fluid
- Consider TIPS/transplantation referral in refractory ascites
57
What is meant by refractory ascites?
"Ascites that does not recede or that recurs shortly after therapeutic paracentesis, despite sodium restriction and diuretic treatment"
58
How can spontaneous bacterial peritonitis present?
- Can be asymptomatic
- Fever
- Abdominal pain
- Derraged bloods; raised WBC, CRP, creatinine or in metabolic acidosis
- Ileus
- Hypotension
59
What is the relation between spontaneous bacterial peritonitis (SBP) and liver cirrhosis?
- Around 10% of patients with liver cirrhosis will go on to develop SBP
- Infections easily develop in ascitic fluid without any clear cause
60
What are the most common organisms that cause spontaneous bacterial peritonitis?
- Escherichia coli
- Klebsiella pneumoniae
- Gram positive cocci; staphylococcus and enterococcus
61
Outline the management of spontaneous bacterial peritonitis?
- Ascitic culture; prior to antibiotic administration
- Antibiotics; IV cephalosporin such as cefotaxime
62
What is hepatorenal syndrome?
"
- Liver cirrhosis causes portal hypertension
- Increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity.
- Leads to a loss of blood volume in other areas of the circulation, including the kidneys
- This leads hypotension in the kidney and activation of the renin-angiotensin system.
- This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney
- This leads to rapid deteriorating kidney function
- Fatal within a week or so unless liver transplant is performed
"
63
What is hepatic encephalopathy?
- Portosystemic encephalopathy
- Caused by build up of brain toxins as a result of deteriorating liver function
- Ammonia in particular is raised for two reasons; decreased metabolism and direct entry into systemic circulation due to portosystemic anastomoses
64
How may hepatic encephalopathy present?
- Reduced consciousness
- Confusion
- Changes to personality and mood
65
What are the preciptating factors for hepatic encephalopathy?
- Constipation
- Electrolytes disturbances
- Infection
- GI bleeding
- High protein diet
- Medications; sedatives
66
How can hepatic encephalopathy be managed?
- Laxatives (lactulose); promote excretion of ammonia, may require initial enema
- Antibiotics (rifaycin); reduced intestinal bacteria producing ammonia
- Nutritional support; NG tube insertion
67
What is non-alcoholic fatty liver disease (NAFLD)?
- Metabolic syndrome
- Chronic health condition due to defects in processing and storing energy
- Increases risk of heart disease, stroke and diabetes
- Characterised by fatty deposits in the liver
68
Although it doesnt cause problems initially, what is the concern with NAFLD?
- Can progress to hepatitis and cirrhosis
- Upto 30% of adults have NAFLD
69
What are the stages of non-alcoholic fatty liver disease (NAFLD)?
- Stage 1; non-alcoholic fatty liver disease (NAFLD)
- Stage 2; non-alcoholic steatohepatitis (NASH)
- Stage 3; liver fibrosis
- Stage 4; liver cirrhosis
70
What are the risk factors for developing NAFLD?
- Obesity
- Poor diet
- Low activity levels
- T2DM
- Hypercholesterolaemia
- Middle age onwards
- Smoking
- Hypertension
71
How may non-alcoholic fatty liver disease present?
NAFLD is often picked up by chance following derranged liver function blood tests
72
What should be carried out in all patients who are found to have new derranged LFTs?
"Non-Invasive Liver Screen;![]()
"
- US liver
- Hepatitis B and C serology
- Autoantibodies; autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis
- Caeruloplasmin; Wilson's disease
- α1 anti-trypsin levels
- Ferritin and transferrin saturation; hereditory haemachromatosis
73
What is the first-line recommended investigation for assessing fibrosis in NAFLD?
ELF Blood Test;
- Assesses 3 markers of cirrhosis
- Hyaluronic acid (HA), procollagen-III aminoterminal peptide (PIIINP) and tissue inhibitor of matrix metalloprotease-1 (TIMP-1)
74
How is the ELF blood test used to indicate the degree of liver cirrhosis in patients with non-alcoholic fatty liver disease (NAFLD)?
- < 7.7; none to mild degree of fibrosis
- 7.7 - 9.8; moderate fibrosis
- > 9.8; severe fibrosis
75
What is the second line recommended assessment for liver fibrosis?
NAFLD Fibrosis Score;
- Helpful in ruling out fibrosis
- Based on age, BMI, liver enzymes, platelets, albumin and diabetes
- Used where ELF is not available
76
What is the third-line investigation that is performed in NAFLD where the ELF blood test of NAFLD fibrosis score indicates fibrosis?
FibroScan; can be used to assess the elasticity of the liver to assess the degree of cirrhosis
77
Outline the management options for patients with NAFLD?
- Weight loss
- Exercise
- Smoking cessation
- Control co-mobidities; diabetes, HTN and cholesterol
- Avoid alcohol
- Referral to liver specialist; patients with fibrosis (can prescribe vitamin E or pioglitazone)
78
What is hepatitis?
Inflammation of the liver
79
How can hepatitis inflammation vary?
- Low grade, chronic inflammation
- Acute and/or severe inflammation
- Can lead to liver necrosis and liver failure
80
Outline the common causes of hepatitis?
- Alcoholic hepatitis
- Non-alcoholic liver disease
- Viral hepatitis
- Autoimmune hepatitis
- Drug induced hepatitis; paracetamol overdose
81
How can hepatitis present?
- May be asymptomatic
- If symptomatic these symptoms tend to be non-specific
82
What non-specific symptoms may be associated with hepatitis?
- Abdominal pain
- Fatigue
- Pruritis (itching)
- Muscle and joint aches
- Nausea and vomiting
- Jaundice
- Fever (viral causes)
83
What common biochemical changes are seen in the liver function tests of patients with hepatitis?
"Derranged LFTs; the hepatitic picture
- High transaminases; elevated ALT/AST
- Proportionally lower rise in ALP
- Bilirubin may also be raised
"
84
Which virus is the most common cause of viral hepatitis?
Hepatitis A
85
What type of viral genome does hepatitis A virus (HAV) have?
Non-enveloped ssRNA
86
How is hepatitis A virus transmitted?
- Faecal-oral route
- Contaminated food/water
87
How can hepatitis A infections present?
- Nausea/vomiting
- Anorexia
- Jaundice
- Cholestasis
88
What is meant by cholestasis?
Slowing of bile through the biliary tree
89
What are the symtpoms of cholestasis?
- Dark brown urine and pale stools
- Due to excretion of bilirubin in urine
- Moderate hepatomegaly
90
Outline the management of heptatitis A?
- Resolves without treatment in 1-3months
- Management with basic analgesia
91
What public health measures are used to prevent hepatitis A infection?
- Vaccination
- Notifiable disease
92
What type of viral genome does hepatitis B virus (HBV) have?
Enveloped partially dsDNA
93
How is hepatitis B transmitted?
- Direct contract with bodily fluids
- Sexual intercourse
- Needle sharing
- Contaminated household products (toothbrushes etc)
- Minor cuts or abrasions
- Vertical transmission; from mother to child during pregnancy
94
What are the two different prognoses for patients infected with hepatitis B virus?
- Most (90%) fully recover from the infection within 2 months
- Latent infections; some (10%) can go on to become chronic hepatitis B carriers
95
What are the key protein products of the HBV viral genome?
- Hepatitis B Surface Antigen (HBsAg); needed for the construction of the outer HBV envelope
- Hepatitis B Core Antigen (HBcAg); composed within the nucleocapsid core of the virus
- Hepatitis B E Antigen (HBeAg); acts as an immune decoy to promote viral persistence, marker of viral replication and infectivity
- DNA Polymerase; involved in the synthesis of DNA molecules, possesses reverse transcriptase activity
- X protein; transcriptional regulator that promotes cell cycle progression
96
Which hepatitis B protein indicates active infection?
HBsAg
97
Which hepatitis B protein indicates viral replication and high infectivity?
HBeAg
98
Which proteins can be assayed for to indicate past or current HBV infection?
HBcAb
99
Which proteins can be assayed for to indicate vaccination or past or current HBV infection?
HBsAb
100
Which hepatitis B virus components can be used to measure viral load?
Hepatitis B Virus DNA (HBV DNA)
101
When screening for hepatitis B infection, which protein should be assayed for to indicate previous infection?
HBcAb
102
When screening for hepatitis B infection, which protein should be assayed for to indicate active infection?
HBsAg
103
If a patient is found to be positive for HBcAb and/or HBsAg, which tests should be carried out next?
- HBeAg; indicates viral replication and infectivity
- HBV DNA; indicates viral load
104
Which hepatitis B virus antigen is given in the vaccine against HBV, what is the significance of this?
- HBsAg is given in the vaccine
- A patient positive for HBsAb could either have been vaccinated OR be infected
105
Which test can be used to distinguish acute, chronic and past infection of HBV?
HBcAb
106
Which type of immunoglobulins to HBcAg will be elevated in an acute infection and low in a chronic infection with HBV?
IgM variants of HBcAb will be elevated in acute infections with HBV
107
Which type of immunoglobulins to HBcAg will be elevated in a past infection with HBV?
IgG variants of HBcAb will be elevated in past infections
108
What does the presence of the HBeAg protein indicate?
- Patient is an an acute phase of the infection where the virus is actively replicating
- Levels of HBeAg indicate infectivity
109
What does the absence of HBeAg but presence of HBeAb indicate?
- Patient has been through a phase where the virus was replicating but has now stopped
- These patients are less infectious
110
Which HBV antigen are patients tested for following vaccination?
HBsAb
111
Outline the management options for patients with hepatitis B infections?
- Screen for other BBVs and STIs; HAV and HIV
- Refer to gastroenterology/hepatology/infectious diseases
- Notify PHE
- Stop smoking and alcohol
- Educate about reducing transmission
- Test for complications; FibroScan and USS
- Antiviral medication to slow progression
- Liver transplantation in end-stage disease
112
What kind of viral genome does the hepatitis C virus (HCV) have?
Enveloped ssRNA
113
How is hepatitis C virus spread?
Blood and bodily fluids only
114
How can heptitis C virus infections be treated?
- No vaccine
- Direct acting antiviral medications can cure
115
Outline the different prognoses for hepatitis C infections?
- 25% make a full recovery
- 75% develop chronic infection
116
What are the main complications of hepatitis C infection?
- Liver cirrhosis
- Hepatocellular carcinoma (HCC)
117
How can hepatitis C virus infection be tested for?
- Hepatitis C virus antibody is used to screen for potential infections
- Hepatitis C virus RNA testing can be used to confirm diagnosis as well as calculate viral load and genotype
118
How can hepatitis C infections be treated?
Direct acting antivirals (DAAs)
- Cure 90% of patients
- Simeprevir
- Sofosbuvir
119
What is significant about the hepatitis D virus?
- It is a defective virus
- Requires co-infection with hepatitis B
- Attaches to and cannot survive without HBsAg
120
What kind of viral genome does hepatitis D virus have?
Enveloped ssRNA
121
What kind of genome does the hepatitis E virus have?
Non-enveloped ssRNA
122
How is hepatitis E transmitted?
Foecal-oral route
123
How does hepatitis E infections progress?
- Resolves spontaneously within 1 month
- Requires no treatment
124
What is autoimmune hepatitis?
- Rare cause of chronic hepatitis
- Unknown aetiology
- T cells of the immune system recognise liver cells are harmful
125
What are the type types of autoimmune hepatitis?
- Type 1; occurs in adults, typically post-menopausal women, less acute
- Type 2; occurs in children and young adults, more acute
126
Which LFTs will be abnormal in patients with autoimmune hepatitis?
- ALT and AST will be elevated
- Serum IgG may also be elevated
127
Which autoantibodies may be raised in patients with type 1 autoimmune hepatitis?
- Anti-nuclear antibodies (ANAs)
- Anti-smooth muscle antibodies or anti-actin (ASMA/ACA)
- Anti-soluble liver antigen (anti-SLA/LP)
128
Which autoantibodies may be raised in patients with type 2 autoimmune hepatitis?
- Anti-liver kidney microsomes (anti-LKM1)
- Anti-liver cytosol antigen type 1 (anti-LC1)
129
How can a diagnosis of autoimmune hepatitis be confirmed?
Liver biopsy
130
How is autoimmune hepatitis treated?
- High dose steriods tapered over time; prednisolone
- Immunosuppressants; azathioprine
- Liver transplant; in end-stage disease (can recur in transplanted livers)
131
What is haemachromatosis?
Iron storage disorder that results in excessive total body iron and the subsequent deposition of iron into the tissues
132
What causes the majority of haemachromatosis?
Autosomal recessive mutation in the human haemachromatosis protein (HFE) gene located on chromosome 6
133
How does the age at presentation differ in patients with haemachromatosis?
- After 40
- Presents later in females due to menstruation eliminating iron from the body
134
Outline some of the symptoms associated with haemochromatosis?
- Chronic tiredness
- Joint pain
- Pigmentation (bronze/slate-grey discolouration)
- Hair loss
- Erectile dysfunction
- Amenorrhoea
- Cognitive symptoms (memory/mood disturbance)
135
How can haemochromatosis be diagnosed?
- Serum ferritin
- Transferrin saturation
136
What caveat is there to using serum ferritin to diagnose haemochromatosis?
- Ferritin is also an acute phase reactant that is elevated in inflammation
- Transferrin saturations are therefore helpful in distinguishing elevated ferritin due to infection or iron overload
137
How can transferrin saturations be used to distinguish haemochromatosis from excess iron on the background of inflammation?
Transferrin saturations will be elevated in haemochromatosis but normal in cases of inflammation or NAFLD
138
What test is used to confirm a diagnosis of haemochromatosis after serum ferritin and transferrin saturations have been carried out?
HFE genetic testing
139
What other tests can be used to diagnose haemochromatosis?
- Liver biopsy with Perl's stain
- CT abdomen
- MRI
140
Outline the complications associated with haemochromatosis?
- T1DM; iron affected the functioning of the pancreas
- Liver cirrhosis
- Endocrine and sexual dysfunction; iron deposition in pituitary and gonads leading to hypogonadism, impotence, amenorrhoea and infertility
- Cardiomyopathy
- Hepatocellular carcinoma
- Hypothyroidism
- Chrondocalcinosis/pseudogout
141
How can haemochromatosis be managed?
- Weekly venesection; removal of blood to decrase total iron
- Monitoring serum ferritin
- Avoid alcohol
- Genetic counselling
- Monitoring and treating complications
142
What is Wilson's Disease?
An inherited multi-system progressive disorder of copper metabolism that leads to abnormal deposition of copper in the body tissues
143
What is the cause of Wilson's Disease?
Mutation in the Wilson's disease protein (ATP7B copper binding protein) located on chromosome 13
144
What is the inheritence pattern of Wilson's disease?
Autosomal recessive
145
Which organ systems are affected by Wilson's disease?
- Hepatic problems (40%)
- Neurological problems (50%)
- Psychiatric problems (10%)
146
Outline the neurological features that may be seen in Wilson's disease?
- Akinetic-rigid syndrome; slow initiation of movement similar to PD
- Pseudosclerosis; clinical picture dominated by tremor which is coarse and flapping
- Ataxia; both cerebellar ataxia and acroataxia affecting the distal portion of the limbs
- Dystonic syndrome; abnormal muscle tone, slow, repetative, involuntary muscle contractions
147
Outline the hepatic features that may be seen in Wilson's disease?
- May be asymptomatic
- Derranged LFTs
- Acute liver failure
- Chronic hepatitis and cirrhosis
148
Outline the psychological features that may be seen in Wilson's disease?
- Behavioural changes are more common in younger patients
- Lability of mood
- Impulsiveness
- Sexual exhibitionism
- Decline in academic performance
- Psychosis
- Depression
149
Outline the ophthalmic features that may be seen in Wilson's disease?
"- Kayser-Fleischer Rings; copper deposits in Descemet's membrance ![]()
![]()
"
- Sunflower Cataracts; copper deposits affecting the lens
150
Outline some of the haematological and osteological features associated with Wilson's disease?
- Haemolytic anaemia (DCT negative)
- Osteopenia
- Renal tubular damage leading to renal tubular acidosis
151
What is the initial investigation of choice when considering a diagnosis of Wilson's disease?
Serum caerloplasmin;
- Low levels indicate Wilson's disease
- Non-selective; may be falsely normal or elevated
152
What is the gold-standard investigation used to diagnose Wilson's disease?
Liver biopsy; assay for liver copper content
153
What other investigations may be useful in diagnosing Wilson's disease?
"- 24hr urinary copper; tends to be elevated
- Serum copper levels; tends to be decreased although free copper is elevated
- Slit-lamp examination; Kayeser-Fleischer rings, sunflower cataracts
- MRI/CT head; may reveal changes in basal ganglia, panda face sign
- Genetic testing; aids family screening
"
154
What radiological sign is associated with Wilson's disease?
"Panda Face Sign; seen on brain MRI![]()
"
155
What are the main aims of treatment in Wilson's disease?
- Reduce copper levels
- Prevent end-organ damage
156
Outline the general managament involved in Wilson's disease?
- Genetic counselling
- Lifestyle changes; avoid toxic drugs and alcohol
- Follow-up
157
What pharmacological agents can be used to treat Wilson's disease?
- D-Penicillamine; copper chealator that promotes urinary excretion
- Trientine; another copper chealator used in patients that cannot tolerate D-penicillamine
158
Outline the prognosis of Wilson's disease?
- Untreated, it is fatal; due to liver complications
- Progressive
- Early diagnosis and treatment can limit the progression and is associated with better long-term outcomes
159
What is α1-anti-trypsin deficiency?
Autosomal recessive disorder caused by mutations in the protease inhibitor enzyme α1 anti-trypsin that causes pulmonary and liver disease
160
What does the α1 anti-tryspin gene encode?
α1 anti-trypsin (A1AT) is an elastase inhibitor that specifically inhibits the activity of neutrophil elastase enzymes
161
What is the cause of α1 anti-trypsin deficiency?
Mutations in the A1AT gene located on chromosome 14
162
Which two main organ systems are affected by α1 anti-trypsin deficiency?
- Liver; cirrhosis
- Lungs; bronchiectasis and emphysema
163
How do A1AT mutations cause pathology in the liver?
- α1 anti-trypsin is normally produced in the liver and travels to the lungs where it inhibits elastase
- Mutant A1AT remains trapped in the liver and builds up
- This causes damage to the liver tissue resulting in cirrhosis
- It may then progress to hepatocellular carcinoma (HCC)
164
How do A1AT mutations cause pathology in the lungs?
- Loss of function of A1AT results in a loss of inhibition of neutrophil elastase
- Neutrophil elastase activity leads to excessive breakdown of elastin in the alveoli
- This leads to loss of elastacitiy and subsequent emphysematous changes and bronchiectasis
165
How can α1 anti-trypsin deficiency commonly present?
Features of COPD;
- Dry cough
- Dyspnoea (SOB)
- Wheeze
- Ankle swelling; peripheral oedema as a result of cor pulmonale/right sided heart failure
Features of hepatic disease;
- Jaundice
- Bruising; derranged clotting due to loss of synthetic function
- Spider naevi
- Palmar erythema
- Hepatomegaly
- Ascites
- Leukonychia
- Confusion
- Asterixis; flapping tremor due to encephalopathy
- Cachexia
166
When should a diagnosis of α1 anti-trypsin deficiency be investigated?
- All patients with evidence of COPD; particularly early onset (>45 years) or non-smokers
- All patients with evidence of chronic liver disease
- Family history of COPD and/or chronic liver disease
- Adult onset asthma with poor response to bronchodilators
167
How can α1 anti-trypsin deficiency be diagnosed?
- Serum α1 anti-trypsin levels
- Liver biopsy; indicates cirrhosis and acid Schiff positive staining globules
- Genetic testing; for A1AT mutation
- High resolution CT thorax; bronchiectasis and emphysema
168
Outline the management of α1 anti-trypsin deficiency?
- Smoking cessation
- Symptomatic management
- Organ transplant for end-stage disease
- Monitoring
169
What is primary biliary cirrhosis?
Condition where the immune system attacks the small bile ducts within the liver
170
Which ducts are primarily affected first in primary biliary cirrhosis?
Intralobular ducts (Canals of Hering)
171
What occurs as a result of primary biliary cirrhosis?
- Cholestasis; obstruction of the outflow of bile due to autoimmune inflammation of the small bile ducts
- Back pressure of bile may progress to fibrosis, cirrhosis and liver failure
172
Which compounds build up in the blood as a result of primary biliary cirrhosis?
- Bile acids
- Cholesterol
- Bilirubin
173
How do the sypmtoms of primary biliary cirrhosis reflect the compounds that are elevated as a result of the disease process?
- Elevated bilirubin causes jaundice
- Elevated bile acids in the blood causes pruritis (itching)
- Elevated blood cholesterol causes xanthelasma in the eyes and xanthomas in the skin and tendons as well as increasing risk of cardiovascular disease
- Lack of bile acid secretion into the GI tract causes malabsorption and greasy stools
- Lack of bilirubin secretion into the GI tract causes stools to appear pale
174
How can primary biliary cirrhosis present?
- Fatigue
- Pruritis
- GI disturbance; malabsorption and pale, greasy stools that dont flush
- Jaundice
- Xanthoma and xantholasma
- Signs of cirrhosis and liver failure; ascites, splenomegaly, spider naevi
175
Which important conditions are often associated with primary bililary cirrhosis?
- Middle aged females
- Other autoimmune conditions; Grave's disease, coeliac
- Rheumatoid conditions; systemic sclerosis, Sjogren's or RA
176
How can primary biliary sclerosis be diagnosed?
- LFTs
- Autoantibodies
- Other blood tests
- Liver biopsy
177
Which liver ennzyme is the first to become raised in obstructive liver disease?
Alkaline phosophatase (ALP)
178
Which specific LFTs may be abnormal in a patient with primary biliary cirrhosis?
- Raised ALP; first liver enzyme to be raised
- AST/ALT and bilirubin may be raised in later disease
179
Which autoantibodies are important to test for when investigating a potential diagnosis of primary biliary cirrhosis?
- Anti-mitochondrial antibodies (anti-mt)
- Anti-nuclear antibodies (ANA)
180
Other than LFTs and auto-antibodies, what imporant blood tests should be carried out when investigating a patient for primary biliary cirrhosis?
- ESR; raised in patients with PBC
- IgM; raised in patients with PBC
181
Outline the pharmacological treatment for primary bililary cirrhosis (PBC)?
- Ursodeoxycholic acid; reduces the intestinal absorption of cholesterol
- Colestyramine; bile acid sequestrant that prevents GI absorption, particularly useful in treating prurits
- Immunosuppressants; steriods
182
What are the main complications that arise as a result of progression of primary biliary cirrhosis?
- Advanced liver cirrhosis
- Portal hypertension
183
What treatment can be considered in end-stage disease as a result of primary biliary cirrhosis?
Liver transplantation
184
What is primary sclerosing cholangitis?
A condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic causing obstruction of the bile outflow
185
What is the difference between primary biliary cirrhosis and primary sclerosing cholangitis?
"- Primary biliary cirrhosis affects ONLY the intrahepatic ducts (most commonly the intralobular ducts)![]()
"
- Primary sclerosing cholangitis affects BOTH the intrahepatic and extrahepatic ducts
186
What are the downstream effects of chronic bile obstruction in primary sclerosing cholangitis?
Liver inflammation (hepatitis), fibrosis and cirrhosis
187
What causes primary sclerosing cholangitis?
- Exact aetiology unknown
- Genetic, autoimmune, intestinal microbiome and environmental factors
188
What condition has a significant associated with primary sclerosing cholangitis?
Ulcerative colitis; concurrence rate of around 70%
189
Outline the main risk factors for primary sclerosing cholangitis?
- Male
- 30-40 years old
- Ulcerative colitis
- Family history of the disease
190
How do patients with primary sclerosing cholangitis often present?
- Jaundice
- Chronic RUQ pain
- Pruritis
- Fatigue
- Hepatomegaly
191
Which liver function test is likely to be the most abnormal in patients with primary sclerosing cholangitis?
- Alkaline phosphatase (ALP); most often raised first and most severely
- Bilirubin may also be raised
- ALT/AST will become raised later as disease progresses to hepatitis
192
Which autoantibodies are useful to test in patients who are being considered for having primary sclerosing cholangitis?
- ANCA; raised in 94%
- ANA; raised in 77%
- Anti-Cardiolipin (anti-CARD); raised in 63%
193
What is the gold-standard investigation used to diagnose primary sclerosing cholangitis?
Magnetic resonance cholangiopancreatography (MRCP):
- Simimlar to ERCP
- Can show bile duct lesions or strictures
194
Outline some of the complications associated with primary sclerosing cholangitis?
- Acute bacterial cholangitis
- Cholangiocarcinoma (10-20%)
- Colorectal cancer
- Cirrhosis and liver failure
- Biliary strictures
- Fat soluble vitamin deficiency (ADEK)
195
How does the diagnosis of primary biliary cirrhosis and primary sclerosing cholangitis differ?
"Primary Biliary Cirrhosis;
- Raised autoantibodies (AMA, ANA)
- Derranged LFTs; raised ALP
- ESR/IgM
- Liver biopsy
Primary Sclerosing Cholangitis;
- MRCP
- Derranged LFTs; raised ALP
- ANCA/ANA and CARD may also be elevated
"
196
Outline the pharmacological management of primary sclerosing cholangitis?
- Ursodeoxylcholic acid; reduces cholesterol uptake and slows disease progression
- Cholestyramine; bile acid sequestrant that prevents absorption and can treat the pruritis
197
What kind of long-term monitoring are patients with primary sclerosing cholangitis required to undergo?
Screening for complications such as cholangiocarcinoma, colorectal cancer, cirrhosis and oesophageal varices secondary to portal hypertension
198
What interventional procedure can be used to identify and treat any strictures that may be present in patients with primary sclerosing cholangitis?
Endoscopic retrograde pancreatography (ERCP);
- Camera inserted down the oesophagus through to the duodenum
- Go through Sphincter of Oddi into the Ampulla of Vater
- Contrast injected into the biliary tree and imaged under X-rays
- Strictures can be identified and stented to improve symptoms
199
What are the two main types of primary liver cancer?
- Hepatocellular carcinoma (HCC); accounts for 80%
- Cholangiocarcinoma; accounts for 20%
200
What are the two broad classifications of liver cancers?
- Primary liver cancers
- Secondary liver cancers
201
Which cancers metastasise to the liver?
- Almost all cancers can metastasise to the liver
- Particularly breast, melanoma, pancreatic, stomach, colorectal, oesophageal and lung cancers
202
When a tumour in the liver is first identified, what investigation should be carried out?
- Full body CT scan; to look for primary
- Thorough examination particularly of the skin and breasts
203
What is the main risk factors for developing hepatocellular carcinoma (HCC)?
Liver cirrhosis;
- Viral hepatitis; B and C
- Alcoholic hepatisis
- NAFLD
- Chronic liver diseases
204
What is the main risk factor for cholangiocarcinoma?
Primary sclerosing cholangitis
205
At what age does cholangiocarcinoma often present?
Patients over 50 years old (unless related to primary sclerosing cholangitis)
206
How does cholangiocarcinoma often present?
- Painless jaundice
- Very similar to pancreatic cancer (so must be considered as a DDx)
207
What non-specific symptoms can all liver cancers present with?
- Weight loss
- Abdominal pain
- Anorexia
- Nausea and vomiting
- Jaundice
- Pruritis
208
Which tumour marker should be tested for in hepatocellular carcinoma?
α-fetoprotein
209
Which tumour marker should be tested for in cholangiocarcinoma?
CA19-9
210
Which imaging investigation should be used as a first line in the diagnosis of liver cancer?
Liver USS; to identify tumours
211
Which imaging investigation can be used to stage liver tumours or where first-line imaging is inconclusive?
CT and/or MRI
212
What technique can be used in liver cancers to take biopsies as well as diagnose cholangiocarcinoma?
ERCP
213
Outline the management options for hepatocellular carcinoma?
- Surgical resection; in early-stage disease
- Liver transplantation; can be curative if the cancer is isolated
- Kinase inhibitors
- Palliative chemotherapy/radiotherapy
214
What drugs can be used in the management of hepatocellular carcinoma?
Kinase inhibitors; sorafenib, regorafenib and lenvatinib
215
Why is chemotherapy/radiotherapy not usually offered in HCC?
HCC is considered to be resistant to chemotherapy and/or radiotherapy
216
Outline the prognoses of primary liver cancers?
Both HCC and cholangiocarcinoma have very poor outcomes unless diagnoised and treated early
217
Outline the treatment options for cholangiocarcinoma?
- Surgical ressection; if caught early
- ERCP; stent obstructed bile duct
- Palliative chemo/radiotherapy
218
What are the most common benign tumours of the liver?
- Haemangioma
- Focal nodular hyperplasias
219
Which patients have a righer risk of developing focal nodular hyperplasias?
- Women
- Particularly females taking the oral contraceptive pill (OCP)
220
What are the three different types of liver transplant?
- Orthostatic liver transplant; whole live transplanted from newly deceased donor
- Split liver transplant; liver from a newly deceased donor is split and transplanted into two recipients
- Living donor transplant; portion or lobe from a living donor is transplanted into the recipient, both portions regenerate
221
What are the two different indications for liver transplantation?
- Acute liver failure; caused by viral hepatitis and paracetamol overdoses, need immediate transplant
- Chronic liver failure; these patients wait longer (around 5 months) for a liver transplant
222
Which factors are considered to be contraindicative of a liver transplant?
- Significant co-morbidities; severe kidney or CV disease
- Excessive weight loss and/or malnutrition
- Active hepatitis B or C or other infection
- End stage HIV
- Active alcohol use; 6-months of abstinence is required
223
Which centres can carry out liver transplantation?
Specialist transplant centres
224
What two types of incision can be used for liver transplantation?
"
![]()
"
- Rooftop incision
- Mercedes-Benz incision
225
What long-term post-transplantation care is required for patients who have undergone liver transplantation?
- Life-long immunosuppression
- Lifestyle changes; avoid smoking and alcohol
- Monitoring and treatment for complications
226
What medications are used to suppress the immune system in order to prevent transplant rejection?
- Azothioprine
- Steriods
- Tacrolimus
227
What is gastro-oesophageal reflux disease (GORD)?
Where stomach acid refluxes through the lower oesophageal sphincter (LOS) and irritates the lining of the oesophagus
228
What makes the oesophagus susceptible to damage and irritation by stomach acid?
Oesophagus has a squamous epithelial lining making it more sensitive to the acid compared to the columnar epithelium of the stomach which is also protected by mucous
229
What are the most common features associated with a presentation of GORD?
- Dyspepsia; indigestion
- Heartburn
- Acid regurgitation into the mouth
- Retrosternal or epigastric pain
- Bloating
- Nocturnal cough
- Hoarse voice
230
What are the most common risk factors associated with GORD?
- High BMI
- Smoking
- Genetic association
- Pregnancy
- Hiatus hernia; where part of the stomach pushes up through the diaphragm
- NSAIDs, caffeine and alcohol
231
How is GORD commonly diagnosed?
Based solely on the clinical manifestations and characterstic symptoms
232
What red flag symptoms should be looked at for when investigating whether a patient has GORD?
- Dysphagia; difficulty swallowing gets a 2-week wait referral
- Weight loss- Anaemia; low Hb
- New onset dyspepsia in patients aged >55; these need urgent referral
- Symptoms refractory or resistant to treatment
- Upper abdominal pain
- Raised platelet count
- Nausea and vomiting
233
What indications are there for endoscopy in patients with GORD?
- Any red flag symptom
- Evidence of GI bleeding
- Resistence to treatment
234
Which red flag symptoms require an urgent (2-week wait) referral for endoscopy in GORD?
- Dysphagia
- Age >55
- Malaena/coffee-ground vomit
235
Outline some of the differential diagnoses that should be considered in patients who present with symptoms indicating GORD?
- Functional heartburn
- Achalasia; failed relaxation of LOS
- Eosinophilic oesophagitis
- IHD
- Pericarditis
- Peptic ulcer disease (PUD)
- Malignancy
236
What lifestyle advice is important to give to patients who are diagnosed with GORD?
- Reduced tea, coffee and alcohol consumption
- Weight loss
- Smoking cessation
- Smaller, lighter meals
- Avoid heavy meals before bedtime
- Stay upright after meals rather than lying flat
237
What acid neutralising medication can be taken PRN in patients with GORD?
- Gaviscon
- Rennie
238
Outline the medical management options used in the treatment of GORD?
- 2-week trial of proton pump inhibitor (PPI); lasoprazole, omeprazole (20mg)
- H2 receptor antagonists; ranitidine (150mg BD)
239
What procedure can be carried out in patients who develop side effects, complications or who do not want to take medication in the treatment of GORD?
"Laparoscopic Nissen Fundoplication; fundus of the stomach is wrapped around the lower oesophagus to narrow the LOS![]()
"
240
What are the indications for Nissen fundoplication in patients with GORD?
- Patient developing side effects from medications
- Complications; erosion, strictures etc.
- Non-compliance/adherence to medications
241
Outline the complications associated with GORD?
- Erosive oesophagitis; inflammation of the oesophagus leading to ulceration, bleeding and peptic stricture formation
- Strictures; scarring and narrowing of the oesophagus associated with repeated damage that may cause dysphagia
- Barrett's oesophagus; pre-malignant condition due to columnar metaplasia (squamous --> columnar epithelium) that predisposes to oesophageal adenocarcinoma
242
Which bacteria is commonly associated with GORD?
Helicobacter pylori; a gram negative aerobic bacteria that resides in the stomach and can damage the mucosal barrier exposing the underlying epithelium to stomach acid
243
What test should be carried out in all patients presenting with symptoms of dyspepsia prior to commencing PPI?
H. pylori test; most commonly a H. pylori stool antigen test
244
What different tests can be used to determine H. pylori infection in patients presenting with dyspepsia?
- Stool antigen test; most commonly used in primary care
- Rapid urease test; used during endoscopy
- Urea breath test; mainly used to test for eradication
245
Outline how rapid urease tests can be used to diagnose H. pylori infections?
"- Performed during endoscopy ![]()
"
- Biopsy taken of stomach mucosae
- Urea added to the sample
- If H. pylori is present the urea is converted to ammonia by urease enzymes expressed by the bacteria
- Ammonia presence turns the solution alkaline resulting in a colour change
246
What caveat is there to offering a H. pylori stool antigen test in patients with GORD?
Stool sample must be taken following 2 weeks of no PPI use to give an accurate result
247
What is the treatment for H. pylori infections?
Triple Therapy;
- Proton pump inhibitor; omeprazole (20mg BD)
- Two antbiotics; clarithromycin (250mg BD), metronidazole (400mg BD)
248
Which test can be used to test for H. pylori eradication following treatment?
Urease breath test; patients inhale urea containing radiolabelled carbon-13, detection of radiolabelled CO2 on exhalation indicates presence of H. pylori due to conversion of urea to ammonia releasing CO2
249
What change in symptoms is associated with development of Barrett's oesophagus in patients with GORD?
Improvement in symptoms
250
How can Barrett's oesophagus progress?
Metaplasia --> low grade dysplasia --> high grade dysplasia --> oesophageal adenocarcinoma
251
Outline the treatment options for Barrett's oesophagus?
- PPI
- Endoscopic surveillance
- Endoscopic therapy; ablation used in patients with low and high grade dysplasia
252
What is peptic ulcer disease?
Disease characterised by the presence of peptic ulcers in the mucosa of the UGI tract
253
What are the two main types of peptic ulcers?
- Gastric ulcers
- Duodenal ulcers
254
Which type of peptic ulcer is more common?
Duodenal ulcers
255
How may peptic ulcer disease often present?
- Dyspepsia
- Epigastric discomfort or pain
- Nausea and vomiting
- Bleeding causing haematemesis and malaena
- Iron deficiency anaemia
256
What is the difference between peptic ulceration and erosion?
- Peptic erosion; superficial/partial break within the epithelium or mucosal surface
- Peptic ulceration; deep break through the full thickness of the epithelium or mucosal surface that extends through the muscularis mucosae
257
What are the three main aeitologies for developing peptic ulceration?
"- H. pylori infection![]()
"
- Mediations; NSAIDs, corticosteroids, alcohol
- Others; Zollinger-Ellison syndrome (gastrin secreting tumour), acute stress, malignancy, IBD
258
What is the broad pathophysiology of peptic ulcer disease?
- Breakdown in the protective barrier of the stomach and/or duodenum; mucus and bicarbonate
- Damage to the epithelial lining
- Increase in stomach acid production
259
What is the most common cause of peptic ulcer disease?
H. pylori infection
260
How do the incidence of gastric and duodenal ulcers differ?
- Duodenal ulcers; more common in men, peaks around 45-64 years
- Gastric ulcers; incidence increases with age, affects both sexes equally
261
How can the presentation of gastric and duodenal ulcers subtly differ?
- Gastric ulcers; eating worsens the pain associated
- Duodenal ulcers; eating improves the pain associated
262
What factors can increase the production of stomach acid and make PUD worse?
- Stress
- Alcohol
- Caffeine
- Smoking
- Spicy foods
263
What investigations should be carried out in a patient suspected of having PUD?
- H. pylori testing
- ECG; cardiac pathology should always be considered in patients with epigastric pain
- FBCs; looking for iron-deficiency anaemia associated with bleeding due to rupture
- LFTs; rule out biliary pathology differential
- Amylase; rule out pancreatitis
- Endoscopy; if ALARMS or >55 at onset
264
Which symptoms warrant urgent refferal in any patient presenting with symptoms of PUD?
"ALARMS;
- Anaemia
- Loss of weight
- Anorexia
- Rapid onset
- Malaena
- Swallowing difficulties (dysphagia)
"
265
What is the indication for upper GI endoscopy in patients with suspected peptic ulcer disease?
- Any one of the ALARMS symptoms
- New presentation > 55 years
- Significant UGI bleeding
266
How can peptic ulcer disease be managed?
- Avoid triggers
- Lifestyle changes; obesity, smoking etc
- Treat underlying cause; H. pylori infections
- PPI
267
What are the two acute complications associated with peptic ulcer disease that patients may present with?
- Acute UGIB; haematemesis +/- malaena
- Perforation; acute, severe abdominal pain and tenderness +/- guarding
268
What are the three main complications associated with peptic ulcer disease?
- UGIB
- Perforation
- Gastric outlet obstruction
269
How can peptic ulcer perforations be managed?
- Supportive care
- Antibiotics
- Laparoscopic repair
270
What causes gastric outlet obstruction in patients with peptic ulcer disease?
Scarring and strictures in the muscle and mucosae leads to pyloric stenosis
271
What is an upper GI bleed?
A common gastrointestinal emergency caused by bleeding from a source proximal to the ligament of Treitz
272
What features may a patient with an upper GI bleed present with?
- Haematemesis
- Malaena
- Shock
273
What is the most common cause of UGIB?
Peptic ulcer disease
274
What are the three most common causes of UGIB?
- Peptic ulcer disease (50%)
- Gastritis (20%)
- Oesophageal varices (10-20%)
275
How are upper GI bleeds classified?
Depending on anatomical location
276
What are the three main areas that upper GI bleeds can arise from?
- Oesophageal; varices, oesophagitis, malignancy, Mallory-Weiss
- Gastric; ulcers, gastritis, malignancy
- Duodenal; ulcers, duodenitis, diverticulitis, aortoduodenal fistulae
277
Give examples of some of the rarer causes of UGI bleeds?
- Swallowed blood
- Bleeding disorders
- Dieulafoy's lesion; large tortuous arteriole in the gastric submucosa
- Aortoenteric fistulae
- Osler-Weber-Rendu Syndrome; heriditory haemorrhagic telangiectasia
- Gastric antral vascular ectasia; watermelon stomach
278
How can peptic ulcer disease cause upper GI bleeds?
- Peptic ulcers can erode fully through the gastric mucosa and into blood vessels
- Most commonly this affects the gastroduodenal artery
279
How can gastritis cause upper GI bleeding?
Erosive gastritis results in inflammation of the stomach lining that erodes into blood vessels
280
What is an oesophageal varice?
Engorged portosystemic anastamosis that has forms secondary to portal hypertension as a result of chronic liver disease/cirrhosis. This allows venous blood to bypass the hepatic circulation
281
What is a Mallory-Weiss tear?
Linear mucosal lacerations that occur following repeated episodes of retching +/- vomiting
282
List some of the risk factors for developing UGIB?
- NSAID use
- Anticoagulants
- Alcohol abuse; varices due to chronic liver disease/cirrhosis
- Chronic liver disease
- Chronic kidney disease
- Advancing age
- Previous PUD or H. pylori infection
283
How do NSAID confer a greater risk of developing UGIB?
- NSAID inhibit the production of prostaglandins
- Prostaglandins are considered gastroprotective
- Prostaglandinc inhibit enterochromaffin-like cells (ECLs) from secreting histamine
- Histamine stimulates the parietal cells to secrete hydrochloric acid
- Inhibition of prostaglandin synthesis therefore increases gastric acid secretion
284
What are the two characteristic findings in UGIB?
- Haematemesis; coffee-ground vomit
- Malaena; black, tarry, foul smelling stools
285
What is the main diagnostic test used to diagnose UGIB?
Upper GI endoscopy
286
Outline the timeframe for UGI endoscopy in patients presenting with haematemesis and/or malaena?
- Immediate UGI endoscopy in any unstable patient
- Within 24hrs if patient is stable
287
What imaging investigation may be useful in patients with suspected UGI bleeding?
Erect CXR; evaluate for aspiration pneumomediastinum (oesophageal perforation) and free air under the diaphragm (perforation of abdominal viscus)
288
What scoring system can be used to assess the risk of a patient developing an upper GI bleed based on their initial presentation?
"Glascow-Blatchford Score;![]()
"
- Haemaglobin
- Urea
- Systolic BP
- Sex
- Heart rate
- Malaena
- Syncope
- Hepatic disease
- Cardiac failure
289
How is the Glascow-Blatchdford score used to indicate risk of UGI bleeding?
Any score > 0 indicates high risk of UGI bleeding
290
Why does the blood urea rise in upper GI bleeding?
- Bleeding results in blood in the GI tract thatis broken down by the acid and digestive enzymes
- Urea is released from RBCs as they are broken down
- This urea is then absorbed into the blood in the intestines
291
What scoring system can be used to assess the risk of re-bleeding and/or mortality in patients that have had an UGI who have undergone endoscopy?
"Rockall Score (ABCDE)![]()
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- Age
- Blood pressure (and heart rate)
- Comorbidity
- Diagnosis
- Endoscopic findings
292
How is the Rockall Score used to inform risk of re-bleeding and/or mortality post endoscopy in patients with UGIB?
Rockall Score;
- Score 0 - 1; low risk- Score 2 - 4; high risk
- Score 5 +; immediate risk
293
How can the management of UGI bleeding be remembered?
"ABATED;
- ABCDE approach as for the unstable patient
- Bloods; FBC, G&S and CS
- Access; ideally 2 large-bore cannulae for IV transfusion
- Transfusion; if Hb below 70
- Endoscopy; urgent if unstable, within 24hrs if stable
- Drugs; stop anticoagulation and NSAIDs
"
294
Which bloods are important to get in a patient with UGIB?
- FBCs; Hb and platelets particularly important
- Urea; elevated in UGIB
- CS; INR and/or prothrombin time
- LFTs; indication of underlying liver disease
- G&S; two samples taken 15mins apart or by two different people
295
Outline the blood products that should be transfused in massive UGI bleeds?
- Blood
- Clotting factors (FFP)
- Platelets (if platelet count lower than 50)
296
What can be given to patients taking warfarin who are suffering from UGI bleeding?
Prothrombin complex concentrate (Oxtaplex)
297
Outline the two different management strategies for non-variceal UGI bleeds?
- Endoscopic mangement; mechanical or thermal coagulation
- Medical management; PPIs
298
Outline the two different management strategies for variceal UGI bleeds?
- Endoscopic management; variceal band-ligation (VBL), transjugular intrahepatic portosystemic shunt (TIPS)
- Medical management; terlipressin (splanchnic vasoconstrictor), prophylactic antibiotics (reduce SBP)
299
What interventions can be used in variceal UGI bleeds where endoscopic and/or medical therapy has failed?
- Sengstaken-blakemore tube; balloon inflated in the lower oesophagus, risk of oesophageal necrosis
- Oesophageal stenting; alternative to sengstaken-blakemore tube
- Transjugular intrahepatic portosystemic shunt (TIPS); shunt between portal and systemic venous circulation to reduce portal pressure
300
What is the name for the definitive treatment used in upper GI bleeding that allows intervention following idenitification of the source of the bleed?
Oesophagogastroduodenoscopy (OGD)
