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Yr 5 - GI > GI Revision > Flashcards

GI Revision Flashcards

1
Q

Cells lining oesophagus vs stomach?

A

Oesophagus - squamous (more sensitive to the effects of stomach acid)

Stomach - columnar (more protected against stomach acid)

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2
Q

If endoscopy is negative, what is next step in GORD?

A

24hr oesophageal pH monitoring

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3
Q

Gold standard test for diagnosis of GORD?

A

24hr oesophageal pH monitoring

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4
Q

Mechanism of PPIs?

A

Irreversible blockade of H+/K+ ATPase of gastric parietal cell –> block gastric acid secretion.

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5
Q

Adverse effects of long-term PPI use? (4)

A

1) Osteoporosis
2) Hypomagnesaemia, hyponatraemia
3) Increased risk of C. diff
4) Microscopic colitis

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6
Q

If a patient with endoscopically proven oesophagitis has no response after full PPI for 1-2 months, what is next step?

A

Double PPI dose for 1 month

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7
Q

If a patient with endoscopically proven oesophagitis does have a response after full PPI for 1-2 months, what is next step?

A

if response then low dose treatment as required

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8
Q

What is surgical option for GORD?

A

Laparoscopic fundoplication

This involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter.

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9
Q

Usual medical strategy when someone presents with GORD for the first time?

A

1) Exclude red flags

2) Address potential triggers

3) +/- endoscopy

4) Offer a 1 month trial of a proton pump inhibitor

5) Consider H. pylori testing.

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10
Q

What is Barrett’s oesophagus?

A

When the lower oesophageal epithelium changes from squamous to columnar epithelium (metaplasia).

This is a PRE-MALIGNANT condition.

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11
Q

How may Barrett’s oesophagus affect symptoms?

A

Patients may notice improved reflux symptoms after they develop Barrett’s oesophagus.

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12
Q

What is multiple endocrine neoplasia type 1 (MEN1)?

A

An autosomal dominant genetic condition:

1) gastrin secreting gastrinomas
2) tumours of parathyroid gland
3) pituitary gland tumours

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13
Q

Where is the usual site of diverticular disease?

A

Between the taenia coli where vessels pierce the muscle to supply the mucosa.

Hence rectum often spared as lacks taenia coli.

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14
Q

What is the most commonly affected section of bowel in diverticulosis?

A

Sigmoid colon

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15
Q

What type of laxatives can be offered in diverticulosis if patients have constipation?

A

Bulk forming (e.g. isaphula husk)

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16
Q

What type of laxatives should be AVOIDED in diverticulosis?

A

Stimulants e.g. senna

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17
Q

Is a colonoscopy indicated in diverticulitis?

A

No - should be avoided initially due to the increased risk of perforation in diverticulitis

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18
Q

What is Meckel’s diverticulum?

A

A congenital diverticulum of the small intestine –> it is a remnant of the omphalomesenteric duct

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19
Q

Presentation of Meckel’s diverticulum?

A
  • Usually asymptomatic
  • abdominal pain mimicking appendicitis
  • rectal bleeding
  • intestinal obstruction
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20
Q

What is the most common cause of painless massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years?

A

Meckel’s diverticulum

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21
Q

What investigation is recommended for assessing liver fibrosis in chronic hepatitis C?

A

Transient elastography

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22
Q

What is transient elastography?

A

A non-invasive test that measures liver stiffness, which correlates with the degree of fibrosis or scarring within the liver.

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23
Q

Are crypt abscesses more commonly seen in UC or Crohn’s?

A

UC

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24
Q

What medication is used in mx of severe alcoholic hepatitis?

A

Steroids

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25
Q

How to calculate units of alcohol?

A

Volume (ml) x % / 1000

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26
Q

What autoantibody is seen in primary sclerosing cholangitis?

A

p-ANCA

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27
Q

What is the investigation of choice for Meckel’s diverticulum in stable children?

A

Technetium scan

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28
Q

What is the most common cause of pseudomembranous colitis?

A

C. diff infection (typically following abx)

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29
Q

Which cancer is acanthosis nigricans associated with?

A

Gastric adenocarcinoma

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30
Q

Patients with diverticulitis flares can be managed with oral antibiotics at home. If they do not improve within 72 hours, what is next step?

A

Admission to hospital for IV ceftriaxone & metronidazole

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31
Q

What are the 4 most common causes of liver cirrhosis?

A

1) Alcoholic fatty liver disease

2) NAFLD

3) Hep B

4) Hep C

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32
Q

What 2 strains of hepatitis can cause cirrhosis?

A

Hep B & C

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33
Q

Give 3 drugs that can cause cirrhosis

A

1) sodium valproate
2) methotrexate
3) amiodarone

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34
Q

What causes palmar erythema in liver cirrhosis?

A

Increased oestrogen

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35
Q

What is leukonychia associated with?

A

Hypoalbuminaemia

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36
Q

What test is used to assess for Wilson’s disease?

A

Caeruloplasmin

This is a copper transport protein.

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37
Q

Caeruloplasmin levels in liver disease?

A

Low

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38
Q

Caeruloplasmin levels in Wilson’s?

A

Caeruloplasmin will be LOW (due to liver disease).

Urinary copper will be HIGH.

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39
Q

How does liver disease affect albumin?

A

Low albumin due to reduced synthetic function of the liver.

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40
Q

How does liver disease affect platelets?

A

Thrombocytopenia (low platelets) is a common finding and indicates more advanced disease

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41
Q

How does liver disease affect sodium?

A

Hyponatraemia (low sodium) occurs with fluid retention in severe liver disease

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42
Q

What is a tumour marker for HCC?

A

AFP

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43
Q

1st line investigation for assessing fibrosis in NAFLD?

A

Enhanced liver fibrosis (ELF) test

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44
Q

What liver disease is the ELF test used in?

A

ONLY NAFLD

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45
Q

What does the ELF test measure?

A

It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates whether they have advanced fibrosis of the liver.

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46
Q

What ELF test result indicates advanced fibrosis?

A

≥10.51

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47
Q

What is used to diagnose non-alcoholic fatty liver disease (once other causes are excluded)?

A

US

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48
Q

What is used as a screening tool for HCC?

A

US & AFP

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49
Q

What investigation can help determine liver fibrosis?

A

Transient elastography (Fibroscan).

50
Q

Who is a transient elastography used in?

A

It is used in patients at risk of cirrhosis:

1) Alcohol-related liver disease
2) Heavy alcohol drinkers (men drinking more than 50 units or women drinking more than 35 units per week)
3) Non-alcoholic fatty liver disease and advanced liver fibrosis (score 10.51 or more on the ELF blood test)
4) Hepatitis C
5) Chronic hepatitis B

51
Q

What test is used to CONFIRM the diagnosis of cirrhosis?

A

Liver biopsy

52
Q

What score gives an estimated 3-month mortality as a percentage for patients with compensated cirrhosis?

A

MELD (Model for End-Stage Liver Disease) score

53
Q

How often should MELD score be used?

A

Every 6 months in patients with compensated cirrhosis.

54
Q

What is the Child-Pugh score used for?

A

Measure severity of cirrhosis & prognosis.

55
Q

What is involved in the Child-Pugh score?

A

ABCDE:

A – Albumin
B – Bilirubin
C – Clotting (INR)
D – Dilation (ascites)
E – Encephalopathy

56
Q

How are complications monitored for in cirrhosis?

A

1) MELD score every 6m

2) US & AFP for HCC every 6m

3) Endoscopy every 3 years for oesophageal varices

57
Q

What are the 4 key features of decompensated liver failure?

A

AHOY:

A - Ascites
H - Hepatic encephalopathy
O - Oesophageal varices bleeding
Y - Yellow (jaundice)

58
Q

How does cirrhosis lead to splenomegaly?

A

Portal HTN

59
Q

If beta blockers are contraindicated, what is the next option for prophylaxis of bleeding in stable oesophageal varices?

A

Variceal band ligation

60
Q

What does variceal band ligation involve?

A

A rubber band wrapped around the base of the varices, cutting off the blood flow through the vessels.

61
Q

What are 2 other options to control the bleeding in bleeding oesophageal varices?

A

1) Sengstaken-Blakemore tube

2) Transjugular intrahepatic portosystemic shunt (TIPS)

62
Q

What is a Sengstaken-Blakemore tube?

A

an inflatable tube inserted into the oesophagus (through the nose) to tamponade the bleeding varices

63
Q

What is a TIPS?

A

1) An interventional radiologist inserts a wire under x-ray guidance into the jugular vein, down the vena cava and into the liver via the hepatic vein.

2) A connection is made through the liver between the hepatic vein and portal vein, and a stent is inserted.

3) This allows blood to flow directly from the portal vein to the hepatic vein, relieving the pressure in the portal system.

64
Q

What 2 veins are connected in a TIPS?

A

Portal vein & hepatic vein

65
Q

What are the 2 main indications for TIPS?

A

1) Bleeding oesophageal varices
2) Refractory ascites

66
Q

How does cirrhosis lead to fluid and sodium retention?

A

1) Loss of fluid to peritoneal cavity (ascites)

2) The drop in circulating volume caused by fluid loss into the peritoneal cavity causes reduced blood pressure in the kidneys.

3) Kidneys release renin in response

4) This causes increased aldosterone secretion via the renin-angiotensin-aldosterone system.

5) Increased aldosterone causes the reabsorption of fluid and sodium in the kidneys

67
Q

Management options for ascites in cirrhosis?

A

1) Low sodium diet

2) Aldosterone antagonists e.g. spironolactone

3) Paracentesis (ascitic tap or drain)

4) Prophylactic antibiotics e.g. ciprofloxacin or norfloxacin

5) TIPS is considered in refractory ascites

6) Liver transplantation is considered in refractory ascites

68
Q

What procedure is considered in refractory ascites?

A

TIPS

69
Q

What type of diuretics are indicated in ascites?

A

Aldosterone antagonists e.g. spironolactone

70
Q

When are prophylactic abx indicated in ascites?

A

When there is <15 g/l of protein in ascitic fluid

71
Q

What are the 2 most common organisms causing SBP?

A

1) E. coli
2) Klebsiella pneumoniae

72
Q

Mx of SBP?

A

1) Taking a sample of ascitic fluid for culture before giving antibiotics

2) IV broad-spectrum antibiotics according to local policies (e.g., piperacillin with tazobactam)

73
Q

What is most important toxin that can build up in cirrhosis?

A

Ammonia

74
Q

Mx of hepatic encephalopathy?

A

1) Lactulose –> aiming for 2-3 soft stools daily

2) Abx e.g. rifaximin –> reduce the number of intestinal bacteria producing ammonia

3) Nutritional support (NG feeding may be required)

75
Q

What laxative is used in hepatic encephalopathy?

A

Lactulose

76
Q

What is Abx of choice in hepatic encephalopathy?

A

Rifaximin –> it is poorly absorbed and stays in the GI tract

77
Q

What are the 3 stages of alcohol related liver disease?

A

1) Alcoholic fatty liver

2) Alcoholic hepatitis

3) Cirrhosis

78
Q

Define binge drinking

A

6 or more units for women or 8 or more units for men in 1 sitting

79
Q

What LFT results indicates alcoholic related liver disease?

A

1) Raised ALT
2) Raised AST
3) Raised ALP (later on)
4) Raised gamma GT
5) AST:ALT ratio >1.5
6) Low albumin
7) Raised bilirubin (cirrhosis)

80
Q

Mx of alcoholic hepatitis?

A

Steroids

81
Q

What score can be used to screen people for harmful alcohol use?

A

Alcohol Use Disorders Identification Test (AUDIT)

Score of ≥8 indicates harmful drinking

82
Q

When is the peak incidence of delirium tremens in alcohol withdrawal?

A

48-72h

83
Q

Stages of NAFLD?

A

1) NAFLD

2) Non-alcoholic steatohepatitis (NASH)

3) Fibrosis

4) Cirrhosis

84
Q

What is metabolic syndrome?

A

Combination of obesity, diabetes and HTN.

85
Q

What is often first indication in LFTs that a patient has NAFLD?

A

Raised ALT

86
Q

1st line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

The enhanced liver fibrosis (ELF) blood test

87
Q

What is the normal AST:ALT ratio?

A

<1

88
Q

ALT vs AST in NAFLD?

A

ALT is typically greater than AST

(compared in NAFLD)

89
Q

What are the 2 types of autoimmune hepatitis? Who do they affect?

A

Type 1 –> typically women in forties/fifties

Type 2 –> typiaclly children/young people (often girls)

90
Q

Which type of autoimmune hepatitis typically presents more acutely?

A

Type 2

91
Q

Describe typical LFT findings in autoimmune hepatitis

A

1) High transaminases (ALT and AST)

2) Minimal change in ALP levels (a “hepatitic” picture).

3) Raised immunoglobulin G (IgG) levels

92
Q

What autoantibodies are seen in type 1 autoimmune hepatitis? (3)

A

1) Anti-nuclear antibodies (ANA)
2) Anti-smooth muscle antibodies (anti-actin)
3) Anti-soluble liver antigen (anti-SLA/LP)

93
Q

What autoantibodies are seen in type 2 autoimmune hepatitis?

A

1) Anti-liver kidney microsomes-1 (anti-LKM1)
2) Anti-liver cytosol antigen type 1 (anti-LC1)

94
Q

Inheritance of haemochromatosis?

A

Autosomal recessive

95
Q

What gene mutation is involved in haemochromatosis?

A

C282Y mutation in human haemochromatosis protein (HFE) gene on chromosome 6

96
Q

Features of haemochromatosis?

A

1) Chronic tiredness

2) Joint pain

3) Sexual dysfunction

4) Pigmentation (bronze skin)

5) Testicular atrophy

6) Amenorrhoea (absence of periods in women)

7) Hepatomegaly

8) Cognitive symptoms (memory and mood disturbance)

97
Q

At what age does haemochromatosis typically present?

A

Haemochromatosis usually presents after age 40 when the iron overload becomes symptomatic.

Typically presents later in women due to menstruation acting to eliminate iron from the body regularly.

98
Q

Initial investigation in haemochromatosis?

A

Serum ferritin

99
Q

What are some causes of a raised ferritin?

A

1) Haemochromatosis
2) Infections (it is an acute phase reactant)
3) Chronic alcohol consumption
4) Non-alcoholic fatty liver disease
5) Hepatitis C
6) Cancer

100
Q

What test can help distinguish between high ferritin caused by iron overload and other causes?

A

Transferrin saturation

Transferrin is an iron transport protein.

101
Q

What is ferritin?

A

Iron storage protein

102
Q

Stepwise investigation of haemochromatosis?

A

1) Serum ferritin
2) Transferrin saturation
3) Genetic testing for HFE gene mutation

103
Q

What can be used to establish the iron concentration in the liver?

A

Liver biopsy with Perl’s stain

Or MRI

104
Q

Complications of haemochromatosis?

A

1) 2ary diabetes (iron affects the functioning of the pancreas)

2) Liver cirrhosis

3) Endocrine and sexual problems (hypogonadism, erectile dysfunction, amenorrhea and reduced fertility)

4) Cardiomyopathy (iron deposits in the heart)

5) HCC

6) Hypothyroidism (iron deposits in the thyroid)

7) Chondrocalcinosis (calcium pyrophosphate deposits in joints) causes arthritis

105
Q

Inheritance of Wilson’s?

A

Autosomal recessive

106
Q

How is copper excreted?

A

In the bile

107
Q

How does Wilson’s typically present?

A

Liver problems usually arise first

Copper deposition in the liver leads to chronic hepatitis, eventually leading to cirrhosis.

108
Q

Features of Wilson’s?

A

Typically mix of liver & neurological

  • Liver: chronic hepatitis, cirrhosis
  • Neurological e.g. tremor, dysarthria, dystonia, Parkinsonism (tremor, bradykinesia and rigidity)
  • Psychiatric e.g. abnormal behaviour, depression, cognitive impairment and psychosis.
  • Kayser-Fleischer rings
  • Haemolytic anaemia
109
Q

Investigations in Wilson’s?

A

1) Serum caeruloplasmin

2) A 24-hour urine copper assay

3) Liver biopsy

4) Scoring systems

110
Q

Mx of Wilson’s?

A

Copper chelation with either:

1) Penicillamine
2) Trientine

111
Q

How is a-1 antitrypsin deficiency inherited?

A

autosomal co-dominant pattern

112
Q

What is A1AT?

A

A protease INHIBITOR

113
Q

What is a critical protease enzyme that is inhibited by alpha-1 antitrypsin?

A

Neutrophil elastase.

This enzyme is secreted by neutrophils and digests elastin (elastolysis). Elastin is a protein in connective tissue that helps keep the tissues flexible.

Alpha-1 antitrypsin (AAT) offers protection by inhibiting the action of neutrophil elastase.

114
Q

Where is alpha-1 antitrypsin produced?

A

Liver

115
Q

What can a liver biopsy show in alpha-1 antitrypsin deficiency?

A

Liver biopsy shows periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment. These represent a buildup of the mutant proteins.

116
Q

What is the only test recommended for H. pylori post-eradication therapy?

A

Urea breath test

117
Q

What is the 1st line treatment for patients with advanced (including metastatic) HCC?

A

Sorafenib

118
Q

What is the treatment of choice of early stage (T1N0M0) oesophageal cancer?

A

Surgical resection

119
Q

Mx of perianal fistula in Crohn’s?

A

Oral metronidazole

120
Q
A

Yr 5 - GI (5 decks)

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