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Pathologies ADULTS > GI > Flashcards

GI Flashcards

1
Q

What causes acute pancreatitis?

A

Alcohol or gallstones.

Steroid can also cause acute pancreatitis

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2
Q

What is gastro-oesophageal reflux disease (GORD)?

A

Where acid from the stomach refluxes through lower oesophageal sphincter and irritates the lining of the oesophagus.

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3
Q

What are the symptoms of GORD?

A

Heartburn

Acid regurg

Retrosternal or epigastric pain

Bloating

nocturnal cough

Hoarse voice

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4
Q

What are the red flags of GORD that indicate referral for endoscopy?

A
  • Dysphagia (difficulty swallowing) at any age gets a two week wait referral
  • Aged over 55 (this is generally the cut off for urgent versus routine referrals)
  • Weight loss
  • Upper abdominal pain / reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count
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5
Q

Management of GORD: Acid neutralising medication

A

Gaviscon and Rennie

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6
Q

Management of GORD: proton pump inhibitor (reduce acid secretion on the stomach)

A

Omeprazole

Lansoprazole

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7
Q

Management of GORD: Ranitidine - what is this?

What is the surgical option for GORD?

A

This is an alternative to PPIs

H2 receptor antagonist (antihistamines)

Reduces stomach acid

Surgical option is laparoscopic fundoplication

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8
Q

What sort of bacteria is H. pylori? and what does it do in the stomach?

A

It is a gram negative aerobic bacteria that can cause damage to the epithelial lining of the stomach resulting in gastritis, ulcers, and increase the risk of stomach cancer.

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9
Q

What chemical is produces by H. pylori, which will then damage the epithelial cells?

A

Ammonia

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10
Q

What tests are used to detect H. pylori?

A

1) Urea breath test (using radiolabelled carbon 13(
2) Stool antigen test
3) Rapid urease test (can be performed during endoscopy)

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11
Q

What does a rapid urease test (also known as CLO test (campylobacter-like organism test) entail?

A

it is performed during endoscopy and involves taking biopsy of stomach mucosa.

Urea added to the sample: if H.pylori present, they produce urease enzyme that converts urea to ammonia. - Ammonia makes solution alkali giving positive result when PH tested.

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12
Q

How can you eradicate H. pylori?

A

It is a regime involving triple therapy with PPI plus 2 antibiotics (e,g, amoxicillin and clarithromycine) for 7 days.

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13
Q

How does Barretts Oesophagus manifest? and what is it?

A

Constant acid reflux results in lower oesophageal epithelium changes by a process called metaplasia from squamous to a columnar epithelium.

Barretts oesophagus is a premalignant condition and is a risk factor for the development of adenocarcinoma - so patient are regularly monitored by endoscopy.

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14
Q

What is the progression stages of barretts oesophagus to adenocarcinoma?

A

Barretts oesophagus with no dysplasia to low grade dysplasia to high grade dysplasia to adenocarcinoma.

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15
Q

What is the treatment of barretts oesophagus

A

Proton pump inhibitors e.g. Omeprazole..

With people that has low or high grade dysplasia, they are given ablation therapy during endoscopy using photodynamic therapy, laser therapy or cyrotherapy

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16
Q

What is peptic ulcer? which one is more common? What is the pathophysiology? What can cause the breakdown of the protective layer in the stomach?

A

ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer). Duodenal ones are more common.

stomach mucosa prone to ulceration from breakdown of protective layer ( comprised of mucus and bicarbonate secreted by the stomach mucosa) or by increase in stomach acid.

Protective layer breakdown due to medication (e.g. steroids or NSAIDs) and H. pylori.

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17
Q

What factors increase stomach acids?

A
  • Stress
  • alcohol
  • caffeine
  • smoking
  • spicy food
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18
Q

What are the symptoms of peptic ulcers?

A
  • epigastric discomfort or pain
  • Nausea and vomiting
  • Dyspepsia
  • Bleeding causes haematemesis, “coffee ground” vomiting and melaena.
  • Iron deficiency anaemia (due to constant bleed)
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19
Q

How to distinguish gastric ulcers and duodenal ulcers from symptoms?

A

Eating worsens the pain in gastric ulcers and improves the pain in duodenal ulcers.

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20
Q

How to make diagnosis for peptic ulcer? Medication for peptic ulcers?

A

Endoscopy - rapid urease testing (CLO test), also biopsy is used to exclude malignancy.

Medication: Same as GORD but usually with high dose proton pump inhibitors (PPI)

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21
Q

What are the 3 complications that can arise from peptic ulcers?

A

1) Bleeding
2) Perforation resulting in acute abdomen and peritonitis
3) Scarring and strictures of muscle and mucosa - lead to pyloric stenosis

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22
Q

What are the features of acute pancreatitis?

A
  • severe epigastric pain that may radiate through the back
  • vomiting
  • epigastric tenderness, ileus and low grade fever
  • periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign)
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23
Q

What is the triad used to diagnose ascending cholangitis?

A

Charcots triad - right upper quadrant pain, fever and jaundice

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24
Q

What specific investigation can be conducted to diagnose acute pancreatitis?

A
  • Serum amylase: raised (also raised in pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis)
  • serum lipase
  • Imaging: ultrasound (however, diagnosis can be made without imagining), can also do contrast-enhance CT.
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25
Q

What scoring system is used to identify cases of severe pancreatitis?

What are some of the common factors that indicate severe pancreatitis?

A
  • Ranson Score
  • Glasgow-imrie score
  • APACHE 2

Factors include:

  • age above 55
  • hypocalcaemia
  • hyperglycaemia
  • hypoxia
  • neutrophila
  • elevated LDH and AST.
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26
Q

What commonly causes acute upper GI bleed?

A

Oesophageal varices or peptic ulcers.

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27
Q

What scoring tool is used for acute upper GI bleed? When do you do tehse?

A
  • Glasgow-Blatchford score at first assessment (helps to know if patients can be managed outpatient or not).
  • Rockall score after endoscopy
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28
Q

what is the resus for acute upper GI bleed?

When should endoscopy be offered?

A
  • ABC, wide-bore intravenous access * 2
  • platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
  • fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
  • prothrombin complex concentrate to patients who are taking warfarin and actively bleeding

Endoscopy offered immediately after resus

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29
Q

What is management of non-variceal bleeding?

A

proton pump inhibitors (PPIs) - HOWEVER, NICE recommends to NOT use PPI before endoscopy.

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30
Q

What is the management of variceal bleed?

A
  • terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
  • band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
    transjugular intrahepatic
  • portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
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31
Q

What does diverticular disease consists of?

A

herniation of colonic mucosa through muscular wall of the colon - usual site is between taenia coli.

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32
Q

What are the symptoms of diverticular disease?

A
  • Altered bowel
  • rectal bleeding
  • abdominal pain
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33
Q

What are the treatment for diverticular disease?

A
  • increase fibre intake
  • mild attacks of diverticulitis managed with antibiotics
  • peri-colonic absesses drained surgically or radiologically.
  • recurrent episodes of acute diverticulitis will need segment resection.
  • Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma.
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34
Q

What are the 3 types of colon cancer?

A
  • Sporadic (95%)
  • hereditary non-polyposis colorectal carcinoma (HNPCC, 5%).
  • Familial adenomatous polyposis (FAP, less than 1%)
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35
Q

What mutation cause familial adenomatous polyposis (FAP)?

A

tumour suppressor gene called adenomatous polyposis coli (APC) gene.

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36
Q

The mutation of what gene cause hereditary non-polyposis colorectal cancer (HNPCC)?

A
  • MSH2 (60% of cases)

- MLH1 (30%)

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37
Q

What gene mutation cause Gilbert’s syndrome?

A

UGT1A1

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38
Q

What is gilbert’s syndrome?

A

it is a hereditary condition that affects the liver’s ability to conjugate bilirubin and that can lead to raised serum levels of unconjugated bilirubin.

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39
Q

What criteria is used to diagnose colorectal cancer?

A

The Amsterdam criteria
sometimes used to aid diagnosis:
- at least 3 family members with colon cancer
- the cases span at least 2 generations
- at least one case diagnosed before the age of 50 years

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40
Q

What does crohn’s disease cause in young patients?

A

Fistula

Crohn’s disease cause inflammation throughout the GI tract, accounting oral ulcers and inflammation of the ileum.

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41
Q

What are the features of Crohn’s disease?

A 
Crohn's (Crows NESTS)
N- No blood or mucus 
E- Entire GI tract
S - 'Skip lesion' on endoscopy
T- Terminal ileum most affected and Transmural (full thickness) inflammation.
S - Smoking is a risk factor

Crohn’s is also associated with weight loss, strictures and fistulas

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42
Q

What are the features of ulcerative colitis?

A

Ulcerative colitis (U-C-CLOSEUP)

C- Continuous inflammation
L- Limited to colon and rectum 
O- Only superficial mucosa affected 
S - Smoking is protective 
E - Excrete blood and mucus 
U - Use aminosalicylates
P - Primary Sclerosing Cholangitis
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43
Q

What testing is used for inflammatory bowel disease? (Crohn’s and diverticulitis)

A
  • Routine blood
  • CRP
  • Faecal calprotectin (released by intestines when inflamed)
  • Endoscopy with biopsy
  • Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures.
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44
Q

What is the first time treatment for Crohn’s to induce remission? What would you give this alone doesn’t work?

A

Steroids e.g prednisolone or IV hydrocortisone

Steroid doesn’t work, add immunosuppressant medication under specialist guidance:

  • Azathioprine
  • Mercaptopurine
  • Methotrexate
  • Infliximab
  • Adalimumab
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45
Q

Whats the first-line treatment for maintaining remission for Crohn’s disease?

A
  • Azathioprine
  • Mercatopurine

Alternatives (based on risk, side effects, nature of the disease and patient’s wishes)

  • Methotrexate
  • Infliximab
  • Adalimumab
46
Q

When can surgery be used in Crohns?

A
  • if the disease only affects the distal ileum

- to treat strictures and fistulas secondary to Crohns

47
Q

What is the management for inducing remission for ulcerative colitis?

  • Mid to moderate disease (first and second line)
  • Severe disease (first and second line)
A

Mild to moderate

  • First line: aminosalicylate (e.g. mesalazine oral or rectal)
  • second line: corticosteroids (e.g. prednisolone)

Severe disease

  • first line: IV corticosteroids (e.g. hydrocortisone)
  • second line: IV ciclosporin
48
Q

What medication is used to maintain remission in ulcerative colitis?

A
  • Aminosalicylate (e.g. mesalazine oral or rectal)
  • Azathioprine
  • Mercaptopurine
49
Q

What surgery can be conducted for ulcerative colitis?

A
  • removal of colon and rectum (panproctocolectomy): since disease typically affect these area this can remove the disease.
  • then the patient undergoes permanent ileostomy (leaves a J-pouch) which is when the ileum is folded back in itself and fashioned into a larger pouch that functions a bit like a rectum. This “J-pouch” which is then attached to the anus and collects stools prior to the person passing the motion.
50
Q

What artery is at risk with duodenal ulcers on the posterior wall?

A

Gastroduodenal artery

51
Q

When is transient jaundice seen in individuals with Gilbert’s syndrome?

A

after physiological stress such as illness, exercise and fasting

52
Q

What is Gilbert’s syndrome? How would you investigate it?

A

Autosomal recessive condition of defective conjugation due to a deficiency of UDP glucuronosyltransferase.

Individuals are seen with unconjugated hyperbilirubinaemia and transient jaundice.

Investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid

53
Q

What are the boundaries of the deep inguinal ring? (Hesselbach’s triangle)

A
  • Superolaterally: transversalis fascia

- Inferomedially: inferior epigastric artery

54
Q

What muscle layer is found on the wall of the large intestines?

A
  • Circular muscles
55
Q

What is diverticulosis?

A

the presence of diverticula, without inflammation or infection.

56
Q

What are the two types of oesphageal carcinomas?

A
  • Squamous cell carcinoma (most common- occurs at any level of the oesophagus)
  • Adenocarcinoma - occurs in inferior third of the oesophagus and associated with Barrett’s oesophagus.
57
Q

What is oesophageal varices?

A

Abnormally dilated sub-mucosal veins, usually produced when patients have portal hypertension.

Portal hypertension occurs secondary to chronic liver disease such as cirrhosis or obstruction of portal vein.

patients present with haematemesis. Alcoholic are at high risk of developing oesophageal varices.

58
Q

What is a hiatus hernia?

A

when part of the stomach protrudes into the chest through the oesophageal hiatus

59
Q

What are the two main types of hiatus hernia?

A
  • Sliding hiatus hernia: the lower oesophageal sphincter slides superiorly, reflux is common.
  • Rolling hiatus hernia: lower oesophageal sphincter remains in place, but a part of the stomach herniates into the chest next to it, requires surgical correction to prevent strangulation of herniated pouch.
60
Q

What are the signs and symptoms of apendicitis?

A
  • pain starting in central and moves down to right iliac fossa within 24 hours.
  • tenderness in McBurney’s point (1/3 from anterior superior iliac spine (ASIS) to the umbilicus.
  • anorexia
  • Rovsing’s sign (palpation of left iliac fossa cause pain in RIF)
  • guarding
  • rebound tenderness in RIF
  • percussion tenderness

NOTE!
Rebound tenderness and percussion tenderness suggest peritonitis, potentially indicating ruptured appendix.

61
Q

What can be used for the diagnosis of appendicitis

A
  • clinical presentation
  • raised inflammatory markers
  • CT scan
  • Ultra sound used in females to rule out gynae issues (and also in children due to radiation)
62
Q

Management of appendicitis

A

appendicectomy - laparoscopic is safe then open surgery

63
Q

What is Meckel’s Diverticulum?

A

a malformation of the distal ileum - usually asymptomatic and no treatment required. However, it can bleed, become inflamed, rupture or cause a volvulus or intussusception

64
Q

What are the 3 causes of pancreatitis? and some others - I GET SMASHED?

A
  • Gallstones
  • Alcohol
  • Post-ERCP
I – Idiopathic
G – Gallstones
E – Ethanol (alcohol consumption)
T – Trauma
S – Steroids
M – Mumps
A – Autoimmune
S – Scorpion sting (the one everyone remembers)
H – Hyperlipidaemia
E – ERCP
D – Drugs (furosemide, thiazide diuretics and azathioprine)
65
Q

How does acute pancreatitis present?

A

Acute onset of:

  • sever epigastric pain
  • radiating through the back
  • associated vomiting
  • Abdo tenderness
  • systemically unwell (fever, tachycardia etc.)

NOTE: raised amylase levels (3 times the upper limit of normal in acute), in chronic, it may not rise because pancreas has reduced function.

66
Q

What investigations are done for acute abdo and acute pancreatitis?

A
  • FBC (for white cell count)
  • U&E (for urea)
  • LFT (for transaminases and albumin)
  • Calcium
  • ABG (for PaO2 and blood glucose)-
  • Amylase
  • CRP
  • Ultrasound for gallstones
  • CT abdo fro complication (necrosis, abscesses etc.)
67
Q

What scoring determines the severity of pancreatitis? and what does each score mean?

A

Glasgow score

0 or 1 – mild pancreatitis
2 – moderate pancreatitis
3 or more – severe pancreatitis

68
Q

What are the criteria for the Glasgow Score? (Pancreas mnemonic)

A 
P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

1 point each one

69
Q

Management of acute pancreatitis?

A

Management involves:

  • Initial resuscitation (ABCDE approach)
  • IV fluids
  • Nil by mouth
  • Analgesia
  • Careful monitoring
  • Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
  • Antibiotics if there is evidence of a specific infection (e.g., abscess or infected necrotic area)
  • Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

Most patients will improve within 3-7 days.

70
Q

What are the complications of acute pancreatitis?

A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocysts (collections of pancreatic juice) can develop 4 weeks after acute pancreatitis
  • Chronic pancreatitis
71
Q

What is the common cause of chronic pancreatitis?

A

alcohol

72
Q

What are the key complications of chronic pancreatitis?

A
  • Chronic epigastric pain
  • Loss of exocrine function (lack pancreatic enzymes e.g lipase secreted into GI tract)
  • Damage and strictures in the duct system, resulting in obstruction in the excretion of pancreatic juice and bile.
  • Formation of pseudocysts or abscesses
73
Q

What are the management for chronic pancreatitis?

A
  • Abstinence from alcohol and smoking
  • Analgesia
  • Replacement of pancreatic enzymes
  • Subcutaneous insulin regimes to maybe treat diabetes
  • ERCP to treat strictures and obstruction to biliary system and pancreatic duct.

Also surgery may be required to treat:

  • Severe chronic pain (draining the ducts and removing inflamed pancreatic tissue)
  • Obstruction of the biliary system and pancreatic duct
  • Pseudocysts
  • Abscesses
74
Q

What are the 4 risk factor of developing gall stones?

A

4 Fs

FAT
FORTY
FEMALE
FAIR

75
Q

What does obstruction in the bilary system show on LFTs?

A
  • Bilirubin: raised levels with pale stool and dark urine
  • Alkaline Phosphatase (ALP) raised
  • Aminotransferases (Alanine amiotransferase (ALT) and aspartate aminotransferase (AST)): raised
76
Q

LFT results: how do you distinguish a obstructive picture to a hepatitic picture?

A

ALT and AST will be higher compared to ALP in a hepatic picture.

SO…

ALP will be higher than ALT and AST in an obstructive picture.

77
Q

What other pathologies can a raised alkaline phosphate level suggest?

A
  • liver or bone malignancy
  • primary biliary cirrhosis
  • Paget’s disease of the bone
    etc.
78
Q

How is acute cholecystitis seen in an ultrasound?

A

thickened gallbladder wall, stones or sludge in gallbladder and fluid around the gallbladder

79
Q

What is a magnetic resonance cholangio-pancreatography (MRCP)?

A

MRI scan that is specific to screening the biliary system.

With gallstones, this is done as further investigation if ultrasound doesn’t show stones but bile duct is dilated or raised bilirubin levels

80
Q

What ultrasound findings may be seen with gallstones?

A
  • Gallstones in the gallbladder
  • Gallstones in the ducts
  • Bile duct dilatation (normally less than 6mm diameter)
  • Acute cholecystitis
  • The pancreas and pancreatic duct
81
Q

What is an endoscopic retrograde cholangio-pancreatography (ERCP)?

A

endoscope into the CBD and used to:

  • (mainly) to clear stones in the bile ducts.
  • Inject contrast and take x-ray to visualise the biliary system and diagnose pathology (e.g. stones and strictures)
  • insert stents to improve bile duct drainage
  • Take biopsies of tumours
82
Q

What are the key complications of endoscopic retrograde cholangio-pancreatography (ERCP)?

A
  • Excessive bleeding
  • Cholangitis (infection in bile duct)
  • Pancreatitis
83
Q

Why may a CT be used for gallstones?

A

look for differential diagnosis and complications such as perforation and abscesses.

84
Q

Key definitions: Cholestasis?

A

blockage of the flow of bile

85
Q

Key definitions: Cholelithiasis

A

gallstones are present

86
Q

Key definitions: Choledocholithiasis

A

gallstones in the bile duct

87
Q

Key definitions: biliary colic

A

intermittent right upper quadrant pain caused by gallstones irritating bile ducts

88
Q

Key definitions: Cholecystitis

A

Inflammation of the gallbladder

89
Q

Key definitions: Cholangitis

A

Inflammation of the bile duct

90
Q

Key definitions: gallbladder empyema

A

pus in the gallbladder

91
Q

Key definitions: Cholecystostomy

A

inserting a drain into the gallbladder

92
Q

What is post-cholecystectomy syndrome? and what symptoms does it consists of?

A 
It involves a group of non-specific symptoms that can occur after a cholecystectomy.
Symptoms include:
- Diarrhoea 
- Indigestion
- RUQ/epigastric pain 
- Nausea
- Intolerance to fatty food
- Flatulence
93
Q

What is the presentation of acute cholecystitis?

A

RUQ pain which may radiate to the right shoulder.

Other features include:

Fever
Nausea
Vomiting
Tachycardia (fast heart rate) and tachypnoea (raised respiratory rate)
Right upper quadrant tenderness
Murphy’s sign
Raised inflammatory markers and white blood cells

94
Q

What sign is indicative of acute cholecystitis? And how is it done?

A

Murphys’s sign

  • Place a hand in RUQ and apply pressure.
  • Ask the patient to take a deep breath in.
  • The gallbladder will move downwards during inspiration and come in contact with your hand.
  • Stimulation of the inflamed gallbladder results in acute pain and sudden stopping of inspiration.
95
Q

What ultrasound finding is seen in acute cholecystitis?

A
  • Thickened gallbladder wall
  • Stones or sludge in gallbladder
  • Fluid around the gallbladder

NOTE can also do MRCP

96
Q

Patients with suspected acute cholecystitis need emergency admission for investigations and management. What does the management consist of?

A

Conservative management involves:

  • Nil by mouth
  • IV fluids
  • Antibiotics (as per local guidelines)
  • NG tube if required for vomiting

ERCP

Cholecystectomy - performed within 72 hours of symptoms in acute admissions. BUT in some cases, it may be delayed for 6-8 weeks after the acute episode to allow the inflammation to settle.

97
Q

What are the complications of acute cholecystitis?

A

Sepsis
Gallbladder empyema
Gangrenous gallbladder
Perforation

98
Q

What is the management of gallbladder empyema?

A

IV antibiotics
Cholecystectomy
Cholecystostomy - to drain infected content.

99
Q

What is liver cirrhosis?

A

It is the result of chronic inflammation and damage to liver cells. When the cells are damaged, they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver.

100
Q

What can fibrosis of liver lead to?

A

It affects the structure and blood flow through the liver, which causes increased resistance in the vessels leading to liver: PORTAL HYPERTENSION

101
Q

What are the 4 most common causes of liver cirrhosis?

A
  • Alchoholic liver disease
  • Non alcoholic fatty liver disease
  • Hepatitis B and Hepatitis C
102
Q

What are some of the rare causes of liver cirrhosis?

A
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Haemochromatosis
  • Wilsons Disease
  • Alpha-1 antitrypsin deficiency
  • Cystic fibrosis
  • Drugs (e.g. amiodarone, methotrexate, sodium valproate)
103
Q

What are the signs of liver cirrhosis?

A
  • Jaundice – caused by raised bilirubin
  • Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
  • Splenomegaly – due to portal hypertension
  • Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
  • Palmar Erythema – caused by hyperdynamic cirulation
  • Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – distended paraumbilical veins due to portal hypertension
  • Asterixis – “flapping tremor” in decompensated liver disease
104
Q

What sort of blood test is done for liver cirrhosis? and what results indicates a positive result?

A
  • LFT is often normal, unless if it decompensated cirrhosis (all markers becomes deranged).
  • Albumin and prothrombin time: useful markers of the ‘synthetic function” of liver. Albumin level drops and prothrombin time increases.
  • Hyponatraemia
  • Abnormal urea and creatinine
  • Alpha-fetoprotein
  • Enhanced Liver fibrosis (ELF) blood test.
105
Q

What is alpha-fetoprotein a tumour marker for?

A

Hepatocellular carcinoma

BUT
also checked every 6 months in patients with liver cirrhosis alongside ultrasound.

106
Q

What is the first line recommended investigation for non-alcoholic fatty liver disease?

A

Enhanced Liver fibrosis (ELF) blood test

107
Q

What 3 markers is measured in an Enhanced liver Fibrosis (ELF) blood test and what does the results indicate?

A

3 markers: HA, PIIINP, TIMP-1

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

108
Q

What does a cirrhosis ultrasound show?

A
  • Nodularity on the surface of the liver.
  • A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow.
  • Enlarged portal vein with reduced flow.
  • Ascites
  • Splenomegaly
109
Q

What is FibroScan? How is it conducted?

A

It is used to check the elasticity of the liver by sending high frequency sound waves into the liver.
Helps to assess the degree of cirrhosis.

NICE recommend retesting every 2 years in patients at risk of cirrhosis.

110
Q

What is the scoring systems are used for Cirrhosis?

A

Child-Pugh score - scores the features that is seen in Cirrhosis (Bilirubin, albumin, INR etc.)- scored 1 to 3.

MELD score - used every 6 months in patients with compensated cirrhosis. takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant

Pathologies ADULTS (9 decks)

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