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FinalMB Part I - Medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Outline the spectrum of alcohol-related liver disease?

A
  • Alcoholic fatty liver disease<div>- Alcoholic hepatitis</div><div>- Cirrhosis</div>
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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>
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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>
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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>
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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>
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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>
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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>”

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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>
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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>”

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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>

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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>
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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>

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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>

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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>
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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>
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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>

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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>”

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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>
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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>
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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>
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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>”

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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>
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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>
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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>
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25
Q

What causes delerium tremens?

A

<div>- Alcohol <b>stimulates GABA</b>nergic neurones and <b>inhbits</b><b>NMDA glutamate</b>rgic neurones</div>

  • Chronic alcohol used results in an <b>up-regulation</b> of the <b>GABA</b> system and a <b>downregulation</b> of the <b>glutamate</b> system to balance these effects<div>- When alcohol is removed the <b>GABA system underfunctions</b> and the <b>glutamate system overfunctions</b></div><div>- This leads to <b>extreme excitability</b> in the brain leading to <b>excess adrenergic</b> stimulation</div>
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26
Q

What scoring system can be used to assess the severity of alcohol withdrawal symptoms and guide treatment?

A

<b><u>CIWA-Ar Tool;</u></b><div>- Scores > 9 require medication for withdrawal</div>

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27
Q

Outline some of the pharmacological managment options for patients experiencing alcohol withdrawal?

A
  • <b>Chlordiazepoxide</b> (Librium); oral benzodiazepine, reducing regime (10-40mg every 1-4hrs) for 5-7 days<div>- <b>Thiamine suppliments</b>; intitially IV high dose (Pabrinex) followed by regular dose oral thiamine</div>
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28
Q

What is Wernicke-Korsakoff Syndrome (WKS)?

A
  • Combination of Wernicke’s encephalopathy and Korsakoff’s syndrome<div>- Caused by thiamine deficiency</div>
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29
Q

What is Wernicke’s encephalopathy?

A
  • Medical emergency with a high mortality rate<div>- Confusion</div><div>- Oculomotor disturbances</div><div>- Ataxia</div><div>- Due to vitamin B1 (thiamine) deficiency</div>
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30
Q

What is Korsakoff’s syndrome?

A
  • Irreversible complication seen in alcoholic liver disease<div>- Results in patient requiring full-time institutional care<br></br><div>- Memory impairement; both retrograde and anterograde</div></div><div>- Behavioural changes</div>
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31
Q

What is liver cirrhosis?

A
  • Result of <b>chronic inflammation</b> and damage to liver cells<div>- Damaged liver cells are replaced by areas of <b>scar tissue</b> (fibrosis)</div><div>- These areas of fibrotic scar tissue form <b>nodules</b></div>
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32
Q

What is the main result of liver fibrosis?

A
  • Scarring of the liver affects the structure and blood flow<div>- Results in <b>increased resistance </b>in the portal vessels</div><div>- Leads to <b>portal hypertension</b></div>
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33
Q

What are the most common causes of liver cirrhosis?

A
  • Alcohol-related liver disease (ArLD)<div>- Non-Alcoholic Fatty Liver Disease (NAFLD)</div><div>- Hepatitis B (HEP-B)</div><div>- Hepatitis C (HEP-C)</div>
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34
Q

Outline some of the rarer causes of liver cirrhosis?

A
  • Autoimmune hepatitis<div>- Primary biliary cirrhosis</div><div>- Haemachromatosis</div><div>- Wilson’s disease</div><div>- α1anti-trypsin deficiency</div><div>- Cystic fibrosis</div><div>- Drugs; amiodarone, methotrexate, sodium valproate</div>
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35
Q

Outline some of the clinical signs of liver cirrhosis?

A
  • <b>Jaundice</b>; caused by raised bilirubin<div>- <b>Hepatomegaly</b>; in early stages, but liver may skrink as it becomes more cirrhotic</div><div>- <b>Splenomegaly</b>; due to portal hypertension</div><div>- <b>Spider naevi</b>; telangiectasias</div><div>- <b>Palmar erythema;</b>hyperdynamic circulation</div><div>- <b>Gynaecomastia and testicular atrophy</b>; endocrine dysfunction and raised oestrogens</div><div>- <b>Bruising</b>; due to abnormal clotting</div><div>- <b>Acites</b>; due to hypoalbuminaemia as a result of decreased synthetic function of liver</div><div>- <b>Caput medusae</b>; engorged superficial epigastric veins to due to portal hypertension</div><div>- <b>Asterixis</b>; flapping tremor in decompensated liver disease</div>
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36
Q

What blood tests can be used to investigate liver cirrhosis?

A
  • <b>LFTs</b>; may be normal but all (AST, ALT, ALP, γGT and bilirubin) can be raised in decompensated disease<div>- <b>Albumin/Prothrombin time</b> (or INR); marker for synthetic function of liver</div><div>- <b>U&Es</b>; hyponatraemia indicates fluid retention which may be seen in severe disease</div><div>- <b>Creatinine</b>; may be derranged along with the urea in hepatorenal syndrome</div><div>- <b>Viral markers/autoantibodies</b>; other causes of cirrhosis</div><div>- <b>α-feroprotein</b>; hepatocellular carcinoma marker</div><div>- <b>Enhanced liver fibrosis</b> (ELF) test; first-line in NAFLD only</div>
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37
Q

What is the enhanced liver fibrosis (ELF) blood test?

A
  • Blood test for assessing the degree of fibrosis<div>- First-line in non-alcoholic fatty liver disease (<b>NAFLD</b>)<b> only</b></div><div>- Assesses 3 markers of cirrhosis; hyaluronic acid (HA), procollagen-III aminoterminal peptide (PIIINP) and tissue inhibitor of matrix metalloprotease-1 (TIMP-1)</div>
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38
Q

How is the ELF blood test used to indicate the degree of liver cirrhosis in patients with NAFLD?

A
  • < 7.7; none to mild degree of fibrosis<div>- 7.7 - 9.8; moderate fibrosis</div><div>- > 9.8; severe fibrosis</div>
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39
Q

What imaging techniques can be used to investigate liver cirrhosis?

A
  • <b>Liver ultrasound;</b> first-line<div>- <b>FibroScan</b>; check elasticity</div><div>- Endoscopy; if oesophageal varices suspected</div><div>- CT and MRI; look for HCC</div>
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40
Q

What are the indications for FibroScan investigations every 2 years in patients at risk of liver cirrhosis?

A
  • Hepatitis C<div>- Heavy alcohol drinkers</div><div>- Diagnosed alcoholic liver disease</div><div>- NAFLD and evidence of fibrosis on ELF blood test</div><div>- Chronic hepatitis B</div>
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41
Q

What scoring system can be used to estimate the prognosis of patients with liver cirrhosis?

A

“<b><u>Child-Pugh Score;</u></b><div>- Patient scores 1-3 depending on 5 features</div><div>- Can be used to give 1-year survival rate</div><div>- Sum of values used to confer class of cirrhosis from A to C<br></br><div><img></img><br></br></div></div>”

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42
Q

How can the Child-Pugh Score be used to grade the degree of liver cirrhosis?

A
  • Score <b>5-6; Class A, 100%</b> 1-year survival rate<div>- Score <b>7-9; Class B, 80%</b> 1-year survival rate</div><div>- Score <b>10-15; Class C, 45%</b> 1-year survival rate</div>
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43
Q

“Which<span>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?</span>”

A

<b><u>MELD-Na Score;</u></b><div>- Dialysis</div><div>- Creatinine</div><div>- Bilirubin</div><div>- INR</div><div>- Na+</div>

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44
Q

Outline the general management principles for liver cirrhosis?

A
  • Liver US and α-feroprotein every 6-months<div>- Endoscopy every 3 years</div><div>- High protein, low Na+diet</div><div>- MELD-Na Scoring every 6-months</div><div>- Consideration for liver tranplantation</div><div>- Management of complications</div>
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45
Q

Outline the common complications seen in liver cirrhosis?

A
  • Malnutrition<div>- Portal hypertension, varices and variceal bleeding</div><div>- Ascites and spontaneous bacterial peritonitis (SBP)</div><div>- Hepatorenal syndrome</div><div>- Hepatic encephalopathy</div><div>- Hepatocellular carcinoma</div>
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46
Q

How can you advise patients to manage and prevent malnutrition that may occur as a result of liver cirrhosis?

A
  • Regular meals every 2-3hrs<div>- Low Na+diet</div><div>- High protein and calorie diets</div><div>- Avoid alcohol</div>
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47
Q

What causes varices to develop as a result of liver cirrhosis?

A
  • Increased resistance to blood flow in the liver<div>- Leads to portal hypertension</div><div>- Back-pressure causes porto-systemic anastamoses to engorge with blood to divert away from the portal system</div><div>- The swelling of these systemic vessels causes swollen, tortuous varices to develop</div>
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48
Q

Where are varices often found?

A
  • Gastro-oesophageal junction<div>- Iliocaecal junction</div><div>- Rectum</div><div>- Anterior abdominal wall via the umbilical vein</div>
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49
Q

Outline the treatment options for stable varices?

A
  • Propranolol; reduces the portal hypertension<div>- Elastic band ligation</div><div>- Injection of sclerosant agents; such as sodium tetradecyl sulfate</div><div>- Transjugular intra-hepatic portosystemic shunt (TIPS)</div>
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50
Q

What is a transjugular intra-hepatic porstosystemic shunt (TIPS) and how can it be used in the treatment of stable varices?

A

”- Interventional radiologist inserts wire under X-Ray guidance into jugular vein<div>- Wire guided into the liver via the hepatic vein</div><div>- Connection is made through the liver tissue between the hepatic vein and the hepatic portal vein<br></br></div><div>- Stent inserted into this connection</div><div>- Blood allowed to bypass the liver directly from the hepatic portal vein into the hepatic vein</div><div>- Relieves portal hypertension and the pressure in the varices</div><div><img></img><br></br></div>”

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51
Q

Outline the initial resuscitation steps involved in treating bleeding oesophageal varices?

A
  • <b>Terlipressin</b>; AVP analogue that causes splanchnic vasoconstriction<div>- Prophylactic broad-spectrum <b>antibiotics</b>; prevent spontaneous bacterial peritonitis and reduce mortality</div><div>- Correct coagulopathy; vitamin K and FFP</div><div>- Consider intubation; ITU admission</div>
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52
Q

Outline the endoscopic management options in a patient with bleeding oesophageal varices?

A
  • <b>Variceal band ligation</b> (VBL); using elastic bands placed around the varices<div>- <b>Endoscopic sclerotherapy</b>; used to cause inflammatory obliteration of the vessel</div>
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53
Q

What interventions can be considered in patients with bleeding oesophageal varices where pharmacological and/or endoscopic interventions have failed?

A
  • <b>Sengstaken-Blakemore Tube</b>; inflatable tube inserted into the oesophagus to tamponade the bleeding varices, remove within 24hrs to avoid oesophageal necrosis<div>- <b>Oesophageal Stenting</b>; alternative to Sengstaken-Blakemore tube</div><div>- Transjugular Intra-hepatic Portosystemic Shunt (<b>TIPS</b>); in appropriately selected patients</div>
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54
Q

What kind of ascites is caused by liver cirrhosis?

A
  • T<b>ransudative cirrhosis</b>; low protein content acsites
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55
Q

How can liver cirrhosis cause ascites?

A

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

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56
Q

How can ascites secondary to liver cirrhosis be managed?

A
  • Low Na+diet<div>- Aldosterone anagonists; spironolactone</div><div>- <b>Paracentesis</b>; ascitic tap or drain</div><div>- Prophylactic antibiotics; ciprofloxacin or norfloxacin in patients with less than 15g L-1 of protein in ascitic fluid</div><div>- Consider TIPS/transplantation referral in refractory ascites</div>
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57
Q

What is meant by refractory ascites?

A

“<span>Ascites that does not recede or that recurs shortly after therapeutic paracentesis, despite sodium restriction and diuretic treatment</span>”

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58
Q

How can spontaneous bacterial peritonitis present?

A
  • Can be asymptomatic<div>- Fever</div><div>- Abdominal pain</div><div>- Derraged bloods; raised WBC, CRP, creatinine or in metabolic acidosis</div><div>- Ileus</div><div>- Hypotension</div>
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59
Q

What is the relation between spontaneous bacterial peritonitis (SBP) and liver cirrhosis?

A
  • Around 10% of patients with liver cirrhosis will go on to develop SBP<div>- Infections easily develop in ascitic fluid without any clear cause</div>
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60
Q

What are the most common organisms that cause spontaneous bacterial peritonitis?

A
  • <i>Escherichia coli</i><div>- <i>Klebsiella pneumoniae</i></div><div>- Gram positive cocci; <i>staphylococcus</i> and <i>enterococcus</i></div>
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61
Q

Outline the management of spontaneous bacterial peritonitis?

A
  • <b>Ascitic culture</b>; prior to antibiotic administration<div>- Antibiotics; <b>IV cephalosporin</b> such as cefotaxime</div>
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62
Q

What is hepatorenal syndrome?

A

“<div>- Liver cirrhosis causes <b>portal hypertension</b></div><div>- I<span>ncreased pressure in the portal system causes <b>fluid to leak out</b> of the capillaries in the liver and bowel and in to the peritoneal cavity.</span></div><div>- Leads to a loss of blood volume in other areas of the circulation, including the kidneys</div><div>- This leads <b>hypotension in the kidney </b>and activation of the renin-angiotensin system.</div><div>- This causes <b>renal vasoconstriction</b>, which combined with low circulation volume leads to <b>starvation</b> of blood to the kidney</div><div>- This leads to rapid <b>deteriorating kidney function</b></div><div>- Fatal within a week or so unless liver transplant is performed</div>”

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63
Q

What is hepatic encephalopathy?

A
  • Portosystemic encephalopathy<div>- Caused by build up of brain toxins as a result of deteriorating liver function</div><div>- Ammonia in particular is raised for two reasons; decreased metabolism and direct entry into systemic circulation due to portosystemic anastomoses</div>
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64
Q

How may hepatic encephalopathy present?

A
  • Reduced consciousness<div>- Confusion</div><div>- Changes to personality and mood</div>
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65
Q

What are the preciptating factors for hepatic encephalopathy?

A
  • Constipation<div>- Electrolytes disturbances</div><div>- Infection</div><div>- GI bleeding</div><div>- High protein diet</div><div>- Medications; sedatives</div>
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66
Q

How can hepatic encephalopathy be managed?

A
  • Laxatives (lactulose); promote excretion of ammonia, may require initial enema<div>- Antibiotics (rifaycin); reduced intestinal bacteria producing ammonia</div><div>- Nutritional support; NG tube insertion</div>
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67
Q

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

A
  • Metabolic syndrome<div>- Chronic health condition due to defects in processing and storing energy</div><div>- Increases risk of heart disease, stroke and diabetes</div><div>- Characterised by fatty deposits in the liver</div>
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68
Q

Although it doesnt cause problems initially, what is the concern with NAFLD?

A
  • Can progress to hepatitis and cirrhosis<div>- Upto 30% of adults have NAFLD</div>
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69
Q

What are the stages of non-alcoholic fatty liver disease (NAFLD)?

A
  • Stage 1; non-alcoholic fatty liver disease (NAFLD)<div>- Stage 2; non-alcoholic steatohepatitis (NASH)</div><div>- Stage 3; liver fibrosis</div><div>- Stage 4; liver cirrhosis</div>
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70
Q

What are the risk factors for developing NAFLD?

A
  • Obesity<div>- Poor diet</div><div>- Low activity levels</div><div>- T2DM</div><div>- Hypercholesterolaemia</div><div>- Middle age onwards</div><div>- Smoking</div><div>- Hypertension</div>
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71
Q

How may non-alcoholic fatty liver disease present?

A

NAFLD is often picked up by chance following <b>derranged liver function blood tests</b>

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72
Q

What should be carried out in all patients who are found to have new derranged LFTs?

A

“<b><u>Non-Invasive Liver Screen;</u></b><div>- US liver</div><div>- Hepatitis B and C serology</div><div>- Autoantibodies; autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis</div><div>- Caeruloplasmin; Wilson’s disease</div><div>- α1anti-trypsin levels</div><div>- Ferritin and transferrin saturation; hereditory haemachromatosis</div><div><img></img><br></br></div>”

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73
Q

What is the first-line recommended investigation for assessing fibrosis in NAFLD?

A

<b><u>ELF Blood Test;</u></b><div>- Assesses 3 markers of cirrhosis</div><div>- Hyaluronic acid (HA), procollagen-III aminoterminal peptide (PIIINP) and tissue inhibitor of matrix metalloprotease-1 (TIMP-1)</div>

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74
Q

How is the ELF blood test used to indicate the degree of liver cirrhosis in patients with non-alcoholic fatty liver disease (NAFLD)?

A
  • < 7.7; none to mild degree of fibrosis<div>- 7.7 - 9.8; moderate fibrosis</div><div>- > 9.8; severe fibrosis</div>
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75
Q

What is the second line recommended assessment for liver fibrosis?

A

<b><u>NAFLD Fibrosis Score;</u></b><div>- Helpful in ruling out fibrosis</div><div>- Based on age, BMI, liver enzymes, platelets, albumin and diabetes</div><div>- Used where ELF is not available</div>

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76
Q

What is the third-line investigation that is performed in NAFLD where the ELF blood test of NAFLD fibrosis score indicates fibrosis?

A

FibroScan; can be used to assess the elasticity of the liver to assess the degree of cirrhosis

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77
Q

Outline the management options for patients with NAFLD?

A
  • Weight loss<div>- Exercise</div><div>- Smoking cessation</div><div>- Control co-mobidities; diabetes, HTN and cholesterol</div><div>- Avoid alcohol</div><div>- Referral to liver specialist; patients with fibrosis (can prescribe vitamin E or pioglitazone)</div>
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78
Q

What is hepatitis?

A

Inflammation of the liver

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79
Q

How can hepatitis inflammation vary?

A
  • Low grade, chronic inflammation<div>- Acute and/or severe inflammation</div><div>- Can lead to liver necrosis and liver failure</div>
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80
Q

Outline the common causes of hepatitis?

A
  • Alcoholic hepatitis<div>- Non-alcoholic liver disease</div><div>- Viral hepatitis</div><div>- Autoimmune hepatitis</div><div>- Drug induced hepatitis; paracetamol overdose</div>
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81
Q

How can hepatitis present?

A
  • May be asymptomatic<div>- If symptomatic these symptoms tend to be non-specific</div>
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82
Q

What non-specific symptoms may be associated with hepatitis?

A
  • Abdominal pain<div>- Fatigue</div><div>- Pruritis (itching)</div><div>- Muscle and joint aches</div><div>- Nausea and vomiting</div><div>- Jaundice</div><div>- Fever (viral causes)</div>
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83
Q

What common biochemical changes are seen in the liver function tests of patients with hepatitis?

A

“<b><u>Derranged LFTs; the hepatitic picture</u></b><div>- High transaminases; <b>elevated ALT/AST</b></div><div>- Proportionally <b>lower rise in ALP</b></div><div>- Bilirubin may also be raised</div>”

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84
Q

Which virus is the most common cause of viral hepatitis?

A

Hepatitis A

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85
Q

What type of viral genome does hepatitis A virus (HAV) have?

A

Non-enveloped ssRNA

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86
Q

How is hepatitis A virus transmitted?

A
  • Faecal-oral route<div>- Contaminated food/water</div>
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87
Q

How can hepatitis A infections present?

A
  • Nausea/vomiting<div>- Anorexia</div><div>- Jaundice</div><div>- Cholestasis</div>
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88
Q

What is meant by cholestasis?

A

Slowing of bile through the biliary tree

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89
Q

What are the symtpoms of cholestasis?

A
  • Dark brown urine and pale stools<div>- Due to excretion of bilirubin in urine</div><div>- Moderate hepatomegaly</div>
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90
Q

Outline the management of heptatitis A?

A
  • Resolves without treatment in 1-3months<div>- Management with basic analgesia</div>
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91
Q

What public health measures are used to prevent hepatitis A infection?

A
  • Vaccination<div>- Notifiable disease</div>
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92
Q

What type of viral genome does hepatitis B virus (HBV) have?

A

Enveloped partially dsDNA

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93
Q

How is hepatitis B transmitted?

A
  • Direct contract with bodily fluids<div>- Sexual intercourse</div><div>- Needle sharing</div><div>- Contaminated household products (toothbrushes etc)</div><div>- Minor cuts or abrasions</div><div>- Vertical transmission; from mother to child during pregnancy</div>
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94
Q

What are the two different prognoses for patients infected with hepatitis B virus?

A
  • Most (90%) fully recover from the infection within 2 months<div>- Latent infections; some (10%) can go on to become <b>chronic hepatitis B carriers</b></div>
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95
Q

What are the key protein products of the HBV viral genome?

A
  • Hepatitis B Surface Antigen (<b>HBsAg</b>); needed for the construction of the outer HBV envelope<div>- Hepatitis B Core Antigen (<b>HBcAg</b>); composed within the nucleocapsid core of the virus</div><div>- Hepatitis B E Antigen (<b>HBeAg</b>); acts as an immune decoy to promote viral persistence, marker of viral replication and infectivity</div><div>- <b>DNA Polymerase</b>; involved in the synthesis of DNA molecules, possesses reverse transcriptase activity</div><div>- <b>X protein</b>; transcriptional regulator that promotes cell cycle progression</div>
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96
Q

Which hepatitis B protein indicates active infection?

A

HBsAg

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97
Q

Which hepatitis B protein indicates viral replication and high infectivity?

A

HBeAg

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98
Q

Which proteins can be assayed for to indicate past or current HBV infection?

A

HBcAb

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99
Q

Which proteins can be assayed for to indicate vaccination or past or current HBV infection?

A

HBsAb

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100
Q

Which hepatitis B virus components can be used to measure viral load?

A

Hepatitis B Virus DNA (HBV DNA)

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101
Q

When screening for hepatitis B infection, which protein should be assayed for to indicate previous infection?

A

HBcAb

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102
Q

When screening for hepatitis B infection, which protein should be assayed for to indicate active infection?

A

HBsAg

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103
Q

If a patient is found to be positive for HBcAb and/or HBsAg, which tests should be carried out next?

A
  • HBeAg; indicates viral replication and infectivity<div>- HBV DNA; indicates viral load</div>
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104
Q

Which hepatitis B virus antigen is given in the vaccine against HBV, what is the significance of this?

A
  • HBsAg is given in the vaccine<div>- A patient positive for HBsAb could either have been vaccinated OR be infected</div>
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105
Q

Which test can be used to distinguish acute, chronic and past infection of HBV?

A

HBcAb

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106
Q

Which type of immunoglobulins to HBcAg will be elevated in an acute infection and low in a chronic infection with HBV?

A

IgM variants of HBcAb will be elevated in acute infections with HBV

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107
Q

Which type of immunoglobulins to HBcAg will be elevated in a past infection with HBV?

A

IgG variants of HBcAb will be elevated in past infections

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108
Q

What does the presence of the HBeAg protein indicate?

A
  • Patient is an an acute phase of the infection where the virus is actively replicating<div>- Levels of HBeAg indicate infectivity</div>
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109
Q

What does the absence of HBeAg but presence of HBeAb indicate?

A
  • Patient has been through a phase where the virus was replicating but has now stopped<div>- These patients are less infectious</div>
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110
Q

Which HBV antigen are patients tested for following vaccination?

A

HBsAb

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111
Q

Outline the management options for patients with hepatitis B infections?

A
  • Screen for other BBVs and STIs; HAV and HIV<div>- Refer to gastroenterology/hepatology/infectious diseases</div><div>- Notify PHE</div><div>- Stop smoking and alcohol</div><div>- Educate about reducing transmission</div><div>- Test for complications; FibroScan and USS</div><div>- Antiviral medication to slow progression</div><div>- Liver transplantation in end-stage disease</div>
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112
Q

What kind of viral genome does the hepatitis C virus (HCV) have?

A

Enveloped ssRNA

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113
Q

How is hepatitis C virus spread?

A

Blood and bodily fluids only

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114
Q

How can heptitis C virus infections be treated?

A
  • No vaccine<div>- Direct acting antiviral medications can cure</div>
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115
Q

Outline the different prognoses for hepatitis C infections?

A
  • 25% make a full recovery<div>- 75% develop chronic infection</div>
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116
Q

What are the main complications of hepatitis C infection?

A
  • Liver cirrhosis<div>- Hepatocellular carcinoma (HCC)</div>
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117
Q

How can hepatitis C virus infection be tested for?

A
  • Hepatitis C virus antibody is used to screen for potential infections<div>- Hepatitis C virus RNA testing can be used to confirm diagnosis as well as calculate viral load and genotype</div>
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118
Q

How can hepatitis C infections be treated?

A

<b><u>Direct acting antivirals (DAAs)</u></b><div>- Cure 90% of patients</div><div>- Simeprevir</div><div>- Sofosbuvir</div>

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119
Q

What is significant about the hepatitis D virus?

A
  • It is a defective virus<div>- Requires co-infection with hepatitis B</div><div>- Attaches to and cannot survive without HBsAg</div>
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120
Q

What kind of viral genome does hepatitis D virus have?

A

Enveloped ssRNA

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121
Q

What kind of genome does the hepatitis E virus have?

A

Non-enveloped ssRNA

122
Q

How is hepatitis E transmitted?

A

Foecal-oral route

123
Q

How does hepatitis E infections progress?

A
  • Resolves spontaneously within 1 month<div>- Requires no treatment</div>
124
Q

What is autoimmune hepatitis?

A
  • Rare cause of chronic hepatitis<div>- Unknown aetiology</div><div>- T cells of the immune system recognise liver cells are harmful</div>
125
Q

What are the type types of autoimmune hepatitis?

A
  • <b>Type 1</b>; occurs in adults, typically post-menopausal women, less acute<div>- <b>Type 2</b>; occurs in children and young adults, more acute</div>
126
Q

Which LFTs will be abnormal in patients with autoimmune hepatitis?

A
  • ALT and AST will be elevated<div>- Serum IgG may also be elevated</div>
127
Q

Which autoantibodies may be raised in patients with type 1 autoimmune hepatitis?

A
  • Anti-nuclear antibodies (ANAs)<div>- Anti-smooth muscle antibodies or anti-actin (ASMA/ACA)</div><div>- Anti-soluble liver antigen (anti-SLA/LP)</div>
128
Q

Which autoantibodies may be raised in patients with type 2 autoimmune hepatitis?

A
  • Anti-liver kidney microsomes (anti-LKM1)<div>- Anti-liver cytosol antigen type 1 (anti-LC1)</div>
129
Q

How can a diagnosis of autoimmune hepatitis be confirmed?

A

Liver biopsy

130
Q

How is autoimmune hepatitis treated?

A
  • High dose steriods tapered over time; prednisolone<div>- Immunosuppressants; azathioprine</div><div>- Liver transplant; in end-stage disease (can recur in transplanted livers)</div>
131
Q

What is haemachromatosis?

A

Iron storage disorder that results in excessive total body iron and the subsequent deposition of iron into the tissues

132
Q

What causes the majority of haemachromatosis?

A

Autosomal recessive mutation in the human haemachromatosis protein (HFE) gene located on chromosome 6

133
Q

How does the age at presentation differ in patients with haemachromatosis?

A
  • After 40<div>- Presents later in females due to menstruation eliminating iron from the body</div>
134
Q

Outline some of the symptoms associated with haemochromatosis?

A
  • Chronic tiredness<div>- Joint pain</div><div>- Pigmentation (bronze/slate-grey discolouration)</div><div>- Hair loss</div><div>- Erectile dysfunction</div><div>- Amenorrhoea</div><div>- Cognitive symptoms (memory/mood disturbance)</div>
135
Q

How can haemochromatosis be diagnosed?

A
  • Serum ferritin<div>- Transferrin saturation</div>
136
Q

What caveat is there to using serum ferritin to diagnose haemochromatosis?

A
  • Ferritin is also an acute phase reactant that is elevated in inflammation<div>- Transferrin saturations are therefore helpful in distinguishing elevated ferritin due to infection or iron overload</div>
137
Q

How can transferrin saturations be used to distinguish haemochromatosis from excess iron on the background of inflammation?

A

Transferrin saturations will be elevated in haemochromatosis but normal in cases of inflammation or NAFLD

138
Q

What test is used to confirm a diagnosis of haemochromatosis after serum ferritin and transferrin saturations have been carried out?

A

HFE genetic testing

139
Q

What other tests can be used to diagnose haemochromatosis?

A
  • Liver biopsy with Perl’s stain<div>- CT abdomen</div><div>- MRI</div>
140
Q

Outline the complications associated with haemochromatosis?

A
  • T1DM; iron affected the functioning of the pancreas<div>- Liver cirrhosis</div><div>- Endocrine and sexual dysfunction; iron deposition in pituitary and gonads leading to hypogonadism, impotence, amenorrhoea and infertility</div><div>- Cardiomyopathy</div><div>- Hepatocellular carcinoma</div><div>- Hypothyroidism</div><div>- Chrondocalcinosis/pseudogout</div>
141
Q

How can haemochromatosis be managed?

A
  • Weekly venesection; removal of blood to decrase total iron<div>- Monitoring serum ferritin</div><div>- Avoid alcohol</div><div>- Genetic counselling</div><div>- Monitoring and treating complications</div>
142
Q

What is Wilson’s Disease?

A

An inherited multi-system progressive disorder of copper metabolism that leads to abnormal deposition of copper in the body tissues

143
Q

What is the cause of Wilson’s Disease?

A

Mutation in the Wilson’s disease protein (ATP7B copper binding protein) located on chromosome 13

144
Q

What is the inheritence pattern of Wilson’s disease?

A

Autosomal recessive

145
Q

Which organ systems are affected by Wilson’s disease?

A
  • Hepatic problems (40%)<div>- Neurological problems (50%)</div><div>- Psychiatric problems (10%)</div>
146
Q

Outline the neurological features that may be seen in Wilson’s disease?

A
  • <b>Akinetic-rigid syndrome</b>; slow initiation of movement similar to PD<div>- <b>Pseudosclerosis</b>; clinical picture dominated by tremor which is coarse and flapping</div><div>- <b>Ataxia</b>; both cerebellar ataxia and acroataxia affecting the distal portion of the limbs</div><div>- <b>Dystonic syndrome</b>; abnormal muscle tone, slow, repetative, involuntary muscle contractions</div>
147
Q

Outline the hepatic features that may be seen in Wilson’s disease?

A
  • May be asymptomatic<div>- Derranged LFTs</div><div>- Acute liver failure</div><div>- Chronic hepatitis and cirrhosis</div>
148
Q

Outline the psychological features that may be seen in Wilson’s disease?

A
  • Behavioural changes are more common in younger patients<div>- Lability of mood</div><div>- Impulsiveness</div><div>- Sexual exhibitionism</div><div>- Decline in academic performance</div><div>- Psychosis</div><div>- Depression</div>
149
Q

Outline the ophthalmic features that may be seen in Wilson’s disease?

A

”- <b>Kayser-Fleischer Rings</b>; copper deposits in Descemet’s membrance<div>- <b>Sunflower Cataracts</b>; copper deposits affecting the lens</div><div><img></img><br></br></div><div><img></img><br></br></div>”

150
Q

Outline some of the haematological and osteological features associated with Wilson’s disease?

A
  • Haemolytic anaemia (DCT negative)<div>- Osteopenia</div><div>- Renal tubular damage leading to renal tubular acidosis</div>
151
Q

What is the initial investigation of choice when considering a diagnosis of Wilson’s disease?

A

<b>Serum caerloplasmin;</b><div>- Low levels indicate Wilson’s disease</div><div>- Non-selective; may be falsely normal or elevated</div>

152
Q

What is the gold-standard investigation used to diagnose Wilson’s disease?

A

Liver biopsy; assay for liver copper content

153
Q

What other investigations may be useful in diagnosing Wilson’s disease?

A

”- <b>24hr urinary copper</b>; tends to be elevated<div>- <b>Serum copper levels</b>; tends to be decreased although free copper is elevated</div><div>- <b>Slit-lamp examination</b>; Kayeser-Fleischer rings, sunflower cataracts</div><div>- <b>MRI/CT head</b>; may reveal changes in basal ganglia, panda face sign</div><div>- <b>Genetic testing</b>; aids family screening<br></br></div>”

154
Q

What radiological sign is associated with Wilson’s disease?

A

“<b>Panda Face Sign</b>; seen on brain MRI<div><img></img><br></br></div>”

155
Q

What are the main aims of treatment in Wilson’s disease?

A
  • Reduce copper levels<div>- Prevent end-organ damage</div>
156
Q

Outline the general managament involved in Wilson’s disease?

A
  • Genetic counselling<div>- Lifestyle changes; avoid toxic drugs and alcohol</div><div>- Follow-up</div>
157
Q

What pharmacological agents can be used to treat Wilson’s disease?

A
  • <b>D-Penicillamine</b>; copper chealator that promotes urinary excretion<div>- <b>Trientine; </b>another copper chealator used in patients that cannot tolerate D-penicillamine</div>
158
Q

Outline the prognosis of Wilson’s disease?

A
  • Untreated, it is fatal; due to liver complications<div>- Progressive</div><div>- Early diagnosis and treatment can limit the progression and is associated with better long-term outcomes</div>
159
Q

What is α1-anti-trypsin deficiency?

A

Autosomal recessive disorder caused by mutations in the protease inhibitor enzyme α1anti-trypsin that causes pulmonary and liver disease

160
Q

What does the α1anti-tryspin gene encode?

A

α1anti-trypsin (A1AT) is an elastase inhibitor that specifically inhibits the activity of neutrophil elastase enzymes

161
Q

What is the cause of α1anti-trypsin deficiency?

A

Mutations in the A1AT gene located on chromosome 14

162
Q

Which two main organ systems are affected by α1anti-trypsin deficiency?

A
  • Liver; cirrhosis<div>- Lungs; bronchiectasis and emphysema</div>
163
Q

How do A1AT mutations cause pathology in the liver?

A
  • α1anti-trypsin is normally produced in the liver and travels to the lungs where it inhibits elastase<div>- Mutant A1AT remains trapped in the liver and builds up</div><div>- This causes damage to the liver tissue resulting in cirrhosis</div><div>- It may then progress to hepatocellular carcinoma (HCC)</div>
164
Q

How do A1AT mutations cause pathology in the lungs?

A
  • Loss of function of A1AT results in a loss of inhibition of neutrophil elastase<div>- Neutrophil elastase activity leads to excessive breakdown of elastin in the alveoli</div><div>- This leads to loss of elastacitiy and subsequent emphysematous changes and bronchiectasis</div>
165
Q

How can α1anti-trypsin deficiency commonly present?

A

<b><u>Features of COPD;</u></b><div>- Dry cough</div><div>- Dyspnoea (SOB)</div><div>- Wheeze</div><div>- Ankle swelling; peripheral oedema as a result of cor pulmonale/right sided heart failure</div><div><br></br></div><div><b><u>Features of hepatic disease;</u></b></div><div>- Jaundice</div><div>- Bruising; derranged clotting due to loss of synthetic function</div><div>- Spider naevi</div><div>- Palmar erythema</div><div>- Hepatomegaly</div><div>- Ascites</div><div>- Leukonychia</div><div>- Confusion</div><div>- Asterixis; flapping tremor due to encephalopathy</div><div>- Cachexia</div>

166
Q

When should a diagnosis of α1anti-trypsin deficiency be investigated?

A
  • All patients with evidence of COPD; particularly early onset (>45 years) or non-smokers<div>- All patients with evidence of chronic liver disease</div><div>- Family history of COPD and/or chronic liver disease</div><div>- Adult onset asthma with poor response to bronchodilators</div>
167
Q

How can α1anti-trypsin deficiency be diagnosed?

A

<b>- Serum α1anti-trypsin levels</b><div>- Liver biopsy; indicates cirrhosis and acid Schiff positive staining globules</div><div>- Genetic testing; for A1AT mutation</div><div>- High resolution CT thorax; bronchiectasis and emphysema</div>

168
Q

Outline the management of α1anti-trypsin deficiency?

A
  • Smoking cessation<div>- Symptomatic management</div><div>- Organ transplant for end-stage disease</div><div>- Monitoring</div>
169
Q

What is primary biliary cirrhosis?

A

Condition where the immune system attacks the <b>small bile ducts </b>within the liver

170
Q

Which ducts are primarily affected first in primary biliary cirrhosis?

A

Intralobular ducts (Canals of Hering)

171
Q

What occurs as a result of primary biliary cirrhosis?

A
  • Cholestasis; obstruction of the outflow of bile due to autoimmune inflammation of the small bile ducts<div>- Back pressure of bile may progress to fibrosis, cirrhosis and liver failure</div>
172
Q

Which compounds build up in the blood as a result of primary biliary cirrhosis?

A
  • Bile acids<div>- Cholesterol</div><div>- Bilirubin</div>
173
Q

How do the sypmtoms of primary biliary cirrhosis reflect the compounds that are elevated as a result of the disease process?

A
  • Elevated bilirubin causes jaundice<div>- Elevated bile acids in the blood causes pruritis (itching)</div><div>- Elevated blood cholesterol causes xanthelasma in the eyes and xanthomas in the skin and tendons as well as increasing risk of cardiovascular disease</div><div>- Lack of bile acid secretion into the GI tract causes malabsorption and greasy stools</div><div>- Lack of bilirubin secretion into the GI tract causes stools to appear pale</div>
174
Q

How can primary biliary cirrhosis present?

A
  • Fatigue<div>- Pruritis</div><div>- GI disturbance; malabsorption and pale, greasy stools that dont flush</div><div>- Jaundice</div><div>- Xanthoma and xantholasma</div><div>- Signs of cirrhosis and liver failure; ascites, splenomegaly, spider naevi</div>
175
Q

Which important conditions are often associated with primary bililary cirrhosis?

A
  • Middle aged females<div>- Other autoimmune conditions; Grave’s disease, coeliac</div><div>- Rheumatoid conditions; systemic sclerosis, Sjogren’s or RA</div>
176
Q

How can primary biliary sclerosis be diagnosed?

A
  • LFTs<div>- Autoantibodies</div><div>- Other blood tests</div><div>- Liver biopsy</div>
177
Q

Which liver ennzyme is the first to become raised in obstructive liver disease?

A

Alkaline phosophatase (ALP)

178
Q

Which specific LFTs may be abnormal in a patient with primary biliary cirrhosis?

A

<div>- Raised ALP; first liver enzyme to be raised</div>

<div>- AST/ALT and bilirubin may be raised in later disease</div>

179
Q

Which autoantibodies are important to test for when investigating a potential diagnosis of primary biliary cirrhosis?

A
  • Anti-mitochondrial antibodies (anti-mt)<div>- Anti-nuclear antibodies (ANA)</div>
180
Q

Other than LFTs and auto-antibodies, what imporant blood tests should be carried out when investigating a patient for primary biliary cirrhosis?

A
  • ESR; raised in patients with PBC<div>- IgM; raised in patients with PBC</div>
181
Q

Outline the pharmacological treatment for primary bililary cirrhosis (PBC)?

A
  • <b>Ursodeoxycholic acid</b>; reduces the intestinal absorption of cholesterol<div>- <b>Colestyramine</b>; bile acid sequestrant that prevents GI absorption, particularly useful in treating prurits</div><div>- Immunosuppressants; steriods</div>
182
Q

What are the main complications that arise as a result of progression of primary biliary cirrhosis?

A
  • Advanced liver cirrhosis<div>- Portal hypertension</div>
183
Q

What treatment can be considered in end-stage disease as a result of primary biliary cirrhosis?

A

Liver transplantation

184
Q

What is primary sclerosing cholangitis?

A

A condition where the intrahepatic or extrahepatic ducts become strictured and fibrotic causing obstruction of the bile outflow

185
Q

What is the difference between primary biliary cirrhosis and primary sclerosing cholangitis?

A

”- Primary biliary cirrhosis affects ONLY the intrahepatic ducts (most commonly the intralobular ducts)<div>- Primary sclerosing cholangitis affects BOTH the intrahepatic and extrahepatic ducts</div><div><img></img><br></br></div>”

186
Q

What are the downstream effects of chronic bile obstruction in primary sclerosing cholangitis?

A

Liver inflammation (hepatitis), fibrosis and cirrhosis

187
Q

What causes primary sclerosing cholangitis?

A
  • Exact aetiology unknown<div>- Genetic, autoimmune, intestinal microbiome and environmental factors</div>
188
Q

What condition has a significant associated with primary sclerosing cholangitis?

A

Ulcerative colitis; concurrence rate of around 70%

189
Q

Outline the main risk factors for primary sclerosing cholangitis?

A
  • Male<div>- 30-40 years old</div><div>- Ulcerative colitis</div><div>- Family history of the disease</div>
190
Q

How do patients with primary sclerosing cholangitis often present?

A
  • Jaundice<div>- Chronic RUQ pain</div><div>- Pruritis</div><div>- Fatigue</div><div>- Hepatomegaly</div>
191
Q

Which liver function test is likely to be the most abnormal in patients with primary sclerosing cholangitis?

A
  • Alkaline phosphatase (ALP); most often raised first and most severely<div>- Bilirubin may also be raised</div><div>- ALT/AST will become raised later as disease progresses to hepatitis</div>
192
Q

Which autoantibodies are useful to test in patients who are being considered for having primary sclerosing cholangitis?

A
  • ANCA; raised in 94%<div>- ANA; raised in 77%</div><div>- Anti-Cardiolipin (anti-CARD); raised in 63%</div>
193
Q

What is the gold-standard investigation used to diagnose primary sclerosing cholangitis?

A

<b><u>Magnetic resonance cholangiopancreatography (MRCP):</u></b><div>- Simimlar to ERCP<br></br><div>- Can show bile duct lesions or strictures</div></div>

194
Q

Outline some of the complications associated with primary sclerosing cholangitis?

A
  • Acute bacterial cholangitis<div>- Cholangiocarcinoma (10-20%)</div><div>- Colorectal cancer</div><div>- Cirrhosis and liver failure</div><div>- Biliary strictures</div><div>- Fat soluble vitamin deficiency (ADEK)</div>
195
Q

How does the diagnosis of primary biliary cirrhosis and primary sclerosing cholangitis differ?

A

“<b><u>Primary Biliary Cirrhosis;</u></b><div>- Raised autoantibodies (AMA, ANA)</div><div>- Derranged LFTs; raised ALP</div><div>- ESR/IgM</div><div>- Liver biopsy</div><div><br></br></div><div><b><u>Primary Sclerosing Cholangitis;</u></b></div><div>- MRCP</div><div>- Derranged LFTs; raised ALP</div><div>- ANCA/ANA and CARD may also be elevated</div>”

196
Q

Outline the pharmacological management of primary sclerosing cholangitis?

A
  • <b>Ursodeoxylcholic acid</b>; reduces cholesterol uptake and slows disease progression<div>- <b>Cholestyramine</b>; bile acid sequestrant that prevents absorption and can treat the pruritis</div>
197
Q

What kind of long-term monitoring are patients with primary sclerosing cholangitis required to undergo?

A

Screening for complications such as cholangiocarcinoma, colorectal cancer, cirrhosis and oesophageal varices secondary to portal hypertension

198
Q

What interventional procedure can be used to identify and treat any strictures that may be present in patients with primary sclerosing cholangitis?

A

<b><u>Endoscopic retrograde pancreatography (ERCP);</u></b><div>- Camera inserted down the oesophagus through to the duodenum</div><div>- Go through Sphincter of Oddi into the Ampulla of Vater</div><div>- Contrast injected into the biliary tree and imaged under X-rays</div><div>- Strictures can be identified and stented to improve symptoms</div>

199
Q

What are the two main types of primary liver cancer?

A
  • <b>Hepatocellular carcinoma</b> (HCC); accounts for 80%<div>- <b>Cholangiocarcinoma</b>; accounts for 20%</div>
200
Q

What are the two broad classifications of liver cancers?

A
  • Primary liver cancers<div>- Secondary liver cancers</div>
201
Q

Which cancers metastasise to the liver?

A
  • Almost all cancers can metastasise to the liver<div>- Particularly breast, melanoma, pancreatic, stomach, colorectal, oesophageal and lung cancers</div>
202
Q

When a tumour in the liver is first identified, what investigation should be carried out?

A
  • Full body CT scan; to look for primary<div>- Thorough examination particularly of the skin and breasts</div>
203
Q

What is the main risk factors for developing hepatocellular carcinoma (HCC)?

A

<b><u>Liver cirrhosis;</u></b><div>- Viral hepatitis; B and C</div><div>- Alcoholic hepatisis</div><div>- NAFLD</div><div>- Chronic liver diseases</div>

204
Q

What is the main risk factor for cholangiocarcinoma?

A

Primary sclerosing cholangitis

205
Q

At what age does cholangiocarcinoma often present?

A

Patients over 50 years old (unless related to primary sclerosing cholangitis)

206
Q

How does cholangiocarcinoma often present?

A
  • Painless jaundice<div>- Very similar to pancreatic cancer (so must be considered as a DDx)</div>
207
Q

What non-specific symptoms can all liver cancers present with?

A
  • Weight loss<div>- Abdominal pain</div><div>- Anorexia</div><div>- Nausea and vomiting</div><div>- Jaundice</div><div>- Pruritis</div>
208
Q

Which tumour marker should be tested for in hepatocellular carcinoma?

A

α-fetoprotein

209
Q

Which tumour marker should be tested for in cholangiocarcinoma?

A

CA19-9

210
Q

Which imaging investigation should be used as a first line in the diagnosis of liver cancer?

A

Liver USS; to identify tumours

211
Q

Which imaging investigation can be used to stage liver tumours or where first-line imaging is inconclusive?

A

CT and/or MRI

212
Q

What technique can be used in liver cancers to take biopsies as well as diagnose cholangiocarcinoma?

A

ERCP

213
Q

Outline the management options for hepatocellular carcinoma?

A
  • Surgical resection; in early-stage disease<div>- Liver transplantation; can be curative if the cancer is isolated</div><div>- Kinase inhibitors</div><div>- Palliative chemotherapy/radiotherapy</div>
214
Q

What drugs can be used in the management of hepatocellular carcinoma?

A

Kinase inhibitors; sorafenib, regorafenib and lenvatinib

215
Q

Why is chemotherapy/radiotherapy not usually offered in HCC?

A

HCC is considered to be resistant to chemotherapy and/or radiotherapy

216
Q

Outline the prognoses of primary liver cancers?

A

Both HCC and cholangiocarcinoma have very poor outcomes unless diagnoised and treated early

217
Q

Outline the treatment options for cholangiocarcinoma?

A
  • Surgical ressection; if caught early<div>- ERCP; stent obstructed bile duct</div><div>- Palliative chemo/radiotherapy</div>
218
Q

What are the most common benign tumours of the liver?

A
  • Haemangioma<div>- Focal nodular hyperplasias</div>
219
Q

Which patients have a righer risk of developing focal nodular hyperplasias?

A
  • Women<div>- Particularly females taking the oral contraceptive pill (OCP)</div>
220
Q

What are the three different types of liver transplant?

A
  • <b>Orthostatic liver transplant</b>; whole live transplanted from newly deceased donor<div>- <b>Split liver transplant</b>; liver from a newly deceased donor is split and transplanted into two recipients</div><div>- <b>Living donor transplant</b>; portion or lobe from a living donor is transplanted into the recipient, both portions regenerate</div>
221
Q

What are the two different indications for liver transplantation?

A
  • <b>Acute liver failure;</b> caused by viral hepatitis and paracetamol overdoses, need immediate transplant<div>- <b>Chronic liver failure;</b> these patients wait longer (around 5 months) for a liver transplant</div>
222
Q

Which factors are considered to be contraindicative of a liver transplant?

A
  • Significant <b>co-morbidities</b>; severe kidney or CV disease<div>- Excessive <b>weight loss</b> and/or <b>malnutrition</b></div><div>- <b>Active</b> hepatitis B or C or other <b>infection</b></div><div>- End stage <b>HIV</b></div><div>- Active <b>alcohol use</b>; 6-months of abstinence is required</div>
223
Q

Which centres can carry out liver transplantation?

A

Specialist transplant centres

224
Q

What two types of incision can be used for liver transplantation?

A

“<div>- Rooftop incision<br></br></div><div>- Mercedes-Benz incision</div><div><br></br></div><div><img></img><br></br></div><div><br></br></div>”

225
Q

What long-term post-transplantation care is required for patients who have undergone liver transplantation?

A
  • Life-long immunosuppression<div>- Lifestyle changes; avoid smoking and alcohol</div><div>- Monitoring and treatment for complications</div>
226
Q

What medications are used to suppress the immune system in order to prevent transplant rejection?

A
  • Azothioprine<div>- Steriods</div><div>- Tacrolimus</div>
227
Q

What is gastro-oesophageal reflux disease (GORD)?

A

Where stomach acid refluxes through the lower oesophageal sphincter (LOS) and irritates the lining of the oesophagus

228
Q

What makes the oesophagus susceptible to damage and irritation by stomach acid?

A

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
Q

What are the most common features associated with a presentation of GORD?

A
  • Dyspepsia; indigestion<div>- Heartburn</div><div>- Acid regurgitation into the mouth</div><div>- Retrosternal or epigastric pain</div><div>- Bloating</div><div>- Nocturnal cough</div><div>- Hoarse voice</div>
230
Q

What are the most common risk factors associated with GORD?

A
  • High BMI<div>- Smoking</div><div>- Genetic association</div><div>- Pregnancy</div><div>- Hiatus hernia; where part of the stomach pushes up through the diaphragm</div><div>- NSAIDs, caffeine and alcohol</div>
231
Q

How is GORD commonly diagnosed?

A

Based solely on the clinical manifestations and characterstic symptoms

232
Q

What red flag symptoms should be looked at for when investigating whether a patient has GORD?

A

<div>-<b>Dysphagia</b>; difficulty swallowing gets a 2-week wait referral<br></br></div>

  • Weight loss<div>- Anaemia; low Hb</div><div>- New onset dyspepsia in patients aged >55; these need urgent referral</div><div>- Symptoms refractory or resistant to treatment</div><div>- Upper abdominal pain</div><div>- Raised platelet count</div><div>- Nausea and vomiting</div>
233
Q

What indications are there for endoscopy in patients with GORD?

A
  • Any red flag symptom<div>- Evidence of GI bleeding</div><div>- Resistence to treatment</div>
234
Q

Which red flag symptoms require an urgent (2-week wait) referral for endoscopy in GORD?

A
  • Dysphagia<div>- Age >55</div><div>- Malaena/coffee-ground vomit</div>
235
Q

Outline some of the differential diagnoses that should be considered in patients who present with symptoms indicating GORD?

A
  • Functional heartburn<div>- Achalasia; failed relaxation of LOS</div><div>- Eosinophilic oesophagitis</div><div>- IHD</div><div>- Pericarditis</div><div>- Peptic ulcer disease (PUD)</div><div>- Malignancy</div>
236
Q

What lifestyle advice is important to give to patients who are diagnosed with GORD?

A
  • Reduced tea, coffee and alcohol consumption<div>- Weight loss</div><div>- Smoking cessation</div><div>- Smaller, lighter meals</div><div>- Avoid heavy meals before bedtime</div><div>- Stay upright after meals rather than lying flat</div>
237
Q

What acid neutralising medication can be taken PRN in patients with GORD?

A
  • Gaviscon<div>- Rennie</div>
238
Q

Outline the medical management options used in the treatment of GORD?

A
  • 2-week trial of proton pump inhibitor (PPI); lasoprazole, omeprazole (20mg)<div>- H2receptor antagonists; ranitidine (150mg BD)</div>
239
Q

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?

A

“<b>Laparoscopic Nissen Fundoplication</b>; fundus of the stomach is wrapped around the lower oesophagus to narrow the LOS<div><img></img><br></br></div>”

240
Q

What are the indications for Nissen fundoplication in patients with GORD?

A
  • Patient developing side effects from medications<div>- Complications; erosion, strictures etc.</div><div>- Non-compliance/adherence to medications</div>
241
Q

Outline the complications associated with GORD?

A
  • <b>Erosive oesophagitis</b>; inflammation of the oesophagus leading to ulceration, bleeding and peptic stricture formation<div>- <b>Strictures</b>; scarring and narrowing of the oesophagus associated with repeated damage that may cause dysphagia</div><div>- <b>Barrett’s oesophagus</b>; pre-malignant condition due to columnar metaplasia (squamous –> columnar epithelium) that predisposes to oesophageal adenocarcinoma</div>
242
Q

Which bacteria is commonly associated with GORD?

A

<i><b>Helicobacter pylori</b>; </i>a gram negative aerobic bacteria that resides in the stomach and can damage the mucosal barrier exposing the underlying epithelium to stomach acid

243
Q

What test should be carried out in all patients presenting with symptoms of dyspepsia prior to commencing PPI?

A

<i>H. pylori </i>test; most commonly a <i>H. pylori</i> stool antigen test

244
Q

What different tests can be used to determine H. pylori infection in patients presenting with dyspepsia?

A
  • <b>Stool antigen test</b>; most commonly used in primary care<div>- <b>Rapid urease test</b>; used during endoscopy</div><div>- <b>Urea breath test</b>; mainly used to test for eradication</div>
245
Q

Outline how rapid urease tests can be used to diagnose H. pylori infections?

A

”- Performed during endoscopy<div>- Biopsy taken of stomach mucosae</div><div>- Urea added to the sample</div><div>- If H. pylori is present the urea is converted to ammonia by urease enzymes expressed by the bacteria</div><div>- Ammonia presence turns the solution alkaline resulting in a colour change</div><div><img></img><br></br></div>”

246
Q

What caveat is there to offering a H. pylori stool antigen test in patients with GORD?

A

Stool sample must be taken following 2 weeks of no PPI use to give an accurate result

247
Q

What is the treatment for <i>H. pylori </i>infections?

A

<b><u>Triple Therapy;</u></b><div>- Proton pump inhibitor; omeprazole (20mg BD)</div><div>- Two antbiotics; clarithromycin (250mg BD), metronidazole (400mg BD)</div>

248
Q

Which test can be used to test for H. pylori eradication following treatment?

A

<b>Urease breath test</b>; patients inhale urea containing radiolabelled carbon-13, detection of radiolabelled CO2on exhalation indicates presence of H. pylori due to conversion of urea to ammonia releasing CO2

249
Q

What change in symptoms is associated with development of Barrett’s oesophagus in patients with GORD?

A

Improvement in symptoms

250
Q

How can Barrett’s oesophagus progress?

A

Metaplasia –> low grade dysplasia –> high grade dysplasia –> oesophageal adenocarcinoma

251
Q

Outline the treatment options for Barrett’s oesophagus?

A
  • PPI<div>- Endoscopic surveillance</div><div>- Endoscopic therapy; ablation used in patients with low and high grade dysplasia</div>
252
Q

What is peptic ulcer disease?

A

Disease characterised by the presence of peptic ulcers in the mucosa of the UGI tract

253
Q

What are the two main types of peptic ulcers?

A
  • Gastric ulcers<div>- Duodenal ulcers</div>
254
Q

Which type of peptic ulcer is more common?

A

Duodenal ulcers

255
Q

How may peptic ulcer disease often present?

A
  • Dyspepsia<div>- Epigastric discomfort or pain</div><div>- Nausea and vomiting</div><div>- Bleeding causing haematemesis and malaena</div><div>- Iron deficiency anaemia</div>
256
Q

What is the difference between peptic ulceration and erosion?

A
  • <b>Peptic erosion</b>; superficial/partial break within the epithelium or mucosal surface<div>- <b>Peptic ulceration</b>; deep break through the full thickness of the epithelium or mucosal surface that extends through the muscularis mucosae</div>
257
Q

What are the three main aeitologies for developing peptic ulceration?

A

”- <i><b>H. pylori</b></i> infection<div>- <b>Mediations</b>; NSAIDs, corticosteroids, alcohol</div><div>- <b>Others</b>; Zollinger-Ellison syndrome (gastrin secreting tumour), acute stress, malignancy, IBD</div><div><img></img><br></br></div>”

258
Q

What is the broad pathophysiology of peptic ulcer disease?

A
  • Breakdown in the protective barrier of the stomach and/or duodenum; mucus and bicarbonate<div>- Damage to the epithelial lining</div><div>- Increase in stomach acid production</div>
259
Q

What is the most common cause of peptic ulcer disease?

A

H. pylori infection

260
Q

How do the incidence of gastric and duodenal ulcers differ?

A

<div>- <b>Duodenal ulcers</b>; more common in <b>men</b>, peaks around 45-64 years</div>

<div>- <b>Gastric ulcers</b>; incidence <b>increases with age</b>, affects both sexes equally<br></br></div>

261
Q

How can the presentation of gastric and duodenal ulcers subtly differ?

A
  • <b>Gastric ulcers</b>; eating worsens the pain associated<div>- <b>Duodenal ulcers</b>; eating improves the pain associated</div>
262
Q

What factors can increase the production of stomach acid and make PUD worse?

A
  • Stress<div>- Alcohol</div><div>- Caffeine</div><div>- Smoking</div><div>- Spicy foods</div>
263
Q

What investigations should be carried out in a patient suspected of having PUD?

A
  • H. pylori testing<div>- ECG; cardiac pathology should always be considered in patients with epigastric pain</div><div>- FBCs; looking for iron-deficiency anaemia associated with bleeding due to rupture</div><div>- LFTs; rule out biliary pathology differential</div><div>- Amylase; rule out pancreatitis</div><div>- Endoscopy; if ALARMS or >55 at onset</div>
264
Q

Which symptoms warrant urgent refferal in any patient presenting with symptoms of PUD?

A

“<b><u>ALARMS;</u></b><div><b>- <u>A</u>naemia</b></div><div><b>- <u>L</u>oss of weight</b></div><div><b>- <u>A</u>norexia</b></div><div><b>- <u>R</u>apid onset</b></div><div><b>- <u>M</u>alaena</b></div><div><b>- <u>S</u>wallowing </b>difficulties (dysphagia)</div>”

265
Q

What is the indication for upper GI endoscopy in patients with suspected peptic ulcer disease?

A
  • Any one of the ALARMS symptoms<div>- New presentation > 55 years</div><div>- Significant UGI bleeding</div>
266
Q

How can peptic ulcer disease be managed?

A
  • Avoid triggers<div>- Lifestyle changes; obesity, smoking etc</div><div>- Treat underlying cause; H. pylori infections</div><div>- PPI</div>
267
Q

What are the two acute complications associated with peptic ulcer disease that patients may present with?

A
  • <b>Acute UGIB</b>; haematemesis +/- malaena<div>- <b>Perforation</b>; acute, severe abdominal pain and tenderness +/- guarding</div>
268
Q

What are the three main complications associated with peptic ulcer disease?

A
  • UGIB<div>- Perforation</div><div>- Gastric outlet obstruction</div>
269
Q

How can peptic ulcer perforations be managed?

A
  • Supportive care<div>- Antibiotics</div><div>- Laparoscopic repair</div>
270
Q

What causes gastric outlet obstruction in patients with peptic ulcer disease?

A

Scarring and strictures in the muscle and mucosae leads to pyloric stenosis

271
Q

What is an upper GI bleed?

A

A common gastrointestinal emergency caused by bleeding from a source proximal to the ligament of Treitz

272
Q

What features may a patient with an upper GI bleed present with?

A
  • Haematemesis<div>- Malaena</div><div>- Shock</div>
273
Q

What is the most common cause of UGIB?

A

Peptic ulcer disease

274
Q

What are the three most common causes of UGIB?

A
  • Peptic ulcer disease (50%)<div>- Gastritis (20%)</div><div>- Oesophageal varices (10-20%)</div>
275
Q

How are upper GI bleeds classified?

A

Depending on anatomical location

276
Q

What are the three main areas that upper GI bleeds can arise from?

A
  • <b>Oesophageal</b>; varices, oesophagitis, malignancy, Mallory-Weiss<div>- <b>Gastric</b>; ulcers, gastritis, malignancy</div><div>- <b>Duodenal</b>; ulcers, duodenitis, diverticulitis, aortoduodenal fistulae</div>
277
Q

Give examples of some of the rarer causes of UGI bleeds?

A
  • Swallowed blood<div>- Bleeding disorders</div><div>- Dieulafoy’s lesion; large tortuous arteriole in the gastric submucosa</div><div>- Aortoenteric fistulae</div><div>- Osler-Weber-Rendu Syndrome; heriditory haemorrhagic telangiectasia</div><div>- Gastric antral vascular ectasia; watermelon stomach</div>
278
Q

How can peptic ulcer disease cause upper GI bleeds?

A
  • Peptic ulcers can erode fully through the gastric mucosa and into blood vessels<div>- Most commonly this affects the <b>gastroduodenal artery</b></div>
279
Q

How can gastritis cause upper GI bleeding?

A

Erosive gastritis results in inflammation of the stomach lining that erodes into blood vessels

280
Q

What is an oesophageal varice?

A

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
Q

What is a Mallory-Weiss tear?

A

Linear mucosal lacerations that occur following repeated episodes of retching +/- vomiting

282
Q

List some of the risk factors for developing UGIB?

A
  • NSAID use<div>- Anticoagulants</div><div>- Alcohol abuse; varices due to chronic liver disease/cirrhosis</div><div>- Chronic liver disease</div><div>- Chronic kidney disease</div><div>- Advancing age</div><div>- Previous PUD or <i>H. pylori </i>infection</div>
283
Q

How do NSAID confer a greater risk of developing UGIB?

A
  • NSAID inhibit the production of prostaglandins<div>- Prostaglandins are considered gastroprotective</div><div>- Prostaglandinc inhibit enterochromaffin-like cells (ECLs) from secreting histamine</div><div>- Histamine stimulates the parietal cells to secrete hydrochloric acid</div><div>- Inhibition of prostaglandin synthesis therefore increases gastric acid secretion</div>
284
Q

What are the two characteristic findings in UGIB?

A
  • Haematemesis; coffee-ground vomit<div>- Malaena; black, tarry, foul smelling stools</div>
285
Q

What is the main diagnostic test used to diagnose UGIB?

A

Upper GI endoscopy

286
Q

Outline the timeframe for UGI endoscopy in patients presenting with haematemesis and/or malaena?

A
  • Immediate UGI endoscopy in any unstable patient<div>- Within 24hrs if patient is stable</div>
287
Q

What imaging investigation may be useful in patients with suspected UGI bleeding?

A

Erect CXR; evaluate for aspiration pneumomediastinum (oesophageal perforation) and free air under the diaphragm (perforation of abdominal viscus)

288
Q

What scoring system can be used to assess the risk of a patient developing an upper GI bleed based on their initial presentation?

A

“<b><u>Glascow-Blatchford Score;</u></b><div>- Haemaglobin</div><div>- Urea</div><div>- Systolic BP</div><div>- Sex</div><div>- Heart rate</div><div>- Malaena</div><div>- Syncope</div><div>- Hepatic disease</div><div>- Cardiac failure</div><div><img></img><br></br></div>”

289
Q

How is the Glascow-Blatchdford score used to indicate risk of UGI bleeding?

A

Any score > 0 indicates high risk of UGI bleeding

290
Q

Why does the blood urea rise in upper GI bleeding?

A
  • Bleeding results in blood in the GI tract thatis broken down by the acid and digestive enzymes<div>- Urea is released from RBCs as they are broken down</div><div>- This urea is then absorbed into the blood in the intestines</div>
291
Q

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?

A

“<b><u>Rockall Score (ABCDE)</u></b><div>- Age</div><div>- Blood pressure (and heart rate)</div><div>- Comorbidity</div><div>- Diagnosis</div><div>- Endoscopic findings</div><div><img></img><br></br></div>”

292
Q

How is the Rockall Score used to inform risk of re-bleeding and/or mortality post endoscopy in patients with UGIB?

A

<div><b><u>Rockall Score;</u></b></div>

  • Score 0 - 1; low risk<div>- Score 2 - 4; high risk</div><div>- Score 5 +; immediate risk</div>
293
Q

How can the management of UGI bleeding be remembered?

A

“<b><u>ABATED;</u></b><div>- <b><u>A</u>BCDE</b> approach as for the unstable patient</div><div>- <b><u>B</u>loods</b>; FBC, G&S and CS</div><div>- <b><u>A</u>ccess</b>; ideally 2 large-bore cannulae for IV transfusion</div><div>- <b><u>T</u>ransfusion</b>; if Hb below 70</div><div>- <b><u>E</u>ndoscopy</b>; urgent if unstable, within 24hrs if stable</div><div>- <b><u>D</u>rugs</b>; stop anticoagulation and NSAIDs</div>”

294
Q

Which bloods are important to get in a patient with UGIB?

A
  • <b>FBCs;</b> Hb and platelets particularly important<div>- <b>Urea</b>; elevated in UGIB</div><div>- <b>CS</b>; INR and/or prothrombin time</div><div>- <b>LFTs</b>; indication of underlying liver disease</div><div>- <b>G&S</b>; two samples taken 15mins apart or by two different people</div>
295
Q

Outline the blood products that should be transfused in massive UGI bleeds?

A
  • Blood<div>- Clotting factors (FFP)</div><div>- Platelets (if platelet count lower than 50)</div>
296
Q

What can be given to patients taking warfarin who are suffering from UGI bleeding?

A

Prothrombin complex concentrate (Oxtaplex)

297
Q

Outline the two different management strategies for non-variceal UGI bleeds?

A
  • <b>Endoscopic mangement</b>; mechanical or thermal coagulation<div>- <b>Medical management</b>; PPIs</div>
298
Q

Outline the two different management strategies for variceal UGI bleeds?

A
  • <b>Endoscopic management</b>; variceal band-ligation (VBL), transjugular intrahepatic portosystemic shunt (TIPS)<div>- <b>Medical management;</b> terlipressin (splanchnic vasoconstrictor), prophylactic antibiotics (reduce SBP)</div>
299
Q

What interventions can be used in variceal UGI bleeds where endoscopic and/or medical therapy has failed?

A
  • <b>Sengstaken-blakemore tube</b>; balloon inflated in the lower oesophagus, risk of oesophageal necrosis<div>- <b>Oesophageal stenting</b>; alternative to sengstaken-blakemore tube</div><div>- <b>Transjugular intrahepatic portosystemic shunt </b>(TIPS); shunt between portal and systemic venous circulation to reduce portal pressure</div>
300
Q

What is the name for the definitive treatment used in upper GI bleeding that allows intervention following idenitification of the source of the bleed?

A

Oesophagogastroduodenoscopy(OGD)

FinalMB Part I - Medicine (12 decks)

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