Gastroenterology 2

Question 1

Crohn’s disease

Answer 1

• Crohn’s disease (CD) is a chronic inflammatory bowel disease characterized by transmural inflammation that can affect any part of the gastrointestinal (GI) tract from the mouth to the anus.
• More likely to present with RIF pain mimic of appendicitis, diarrhoea
• Patchy granulomatous, skip lesions
• Strictures, abscess and fistulas may develop due to transmural involvement

Question 2

Crohns disease management
inducing remission, initial phases of treatment

Answer 2

• Smoking cessation - one of the causea and increases disease severity
• Steroids induce remission
• Enteral feeding with elemental diet
• Second line- 5-ASA mesalazine

Question 3

How do you differentiate CD from UC with investigations

Answer 3

serological markers: Anti-Saccharomyces cerevisiae antibodies (ASCA) and perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) may aid in differentiating CD from ulcerative colitis, but they are not diagnostic.

Question 4

Crohns disease

1. When would you use infliximab in Crohn’s disease?
2. What is used for isolated peri-anal disease

Answer 4

1. When would you use infliximab in Crohn’s disease?
   infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
2. What is used for isolated peri-anal disease
   metronidazole is often used for isolated peri-anal disease

Question 5

Crohns disease management
Maintain remission
MOA
What needs to be checked before starting

Answer 5

• azathioprine or mercaptopurine is used first-line to maintain remission
• MOA effects as an antagonist of purine metabolism, resulting in the inhibition of deoxyribonucleic acid (DNA), ribonucleic acid (RNA), and protein synthesis.
• Thiopurine methyltransferase (TPMT) is the main enzyme responsible for inactivating toxic products of azathioprine (AZA) metabolism.

Question 6

What percentage of CD patients will have surgery?
Stricturing terminal ileal disease - what surgery is indicated?

Answer 6

around 80% of patients with Crohn’s disease will eventually have surgery
stricturing terminal ileal disease → ileocaecal resection

Question 7

Ulcerative colitis

Answer 7

Inflammation always starts at rectum (hence it is the most common site for UC), never spreads beyond ileocaecal valve and is continuous.
Will usually present with bloody diarrhoea, urgency and tenesmus with abdo pain in LLQ

Question 8

Describe endoscopy findings in UC

Answer 8

red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

Question 9

Which IBD is referred to when drain pipe appearance is seen in barium enema

Answer 9

long standing disease UC: colon is narrow and short -‘drainpipe colon’
loss of haustrations with superficial ulceration creating pseudopolyps

Question 10

Which disease are gallstones and oxalate renal stones more common in?

Answer 10

UC

Question 11

Describe Kantors string sign

Answer 11

severe narrowing during small bowel barium meal > Crohn’s stricture

Question 12

Describe lead pipe appearance of colon and what this indicates

Answer 12

The lead pipe appearance of colon is the classical barium enema finding in chronic ulcerative colitis, and is also seen with other modalities such as CT, MRI or a plain radiograph. There is a complete loss of the haustral markings in the diseased segment of the colon, appearing smooth-walled and cylindrical.

Question 13

UC management
mild to moderate disease
what is used to manage acute flares

Answer 13

• mild to moderate - aminosalicylates 5ASA
• Corticosteroids: Prednisone, hydrocortisone, and budesonide are used to manage moderate-to-severe UC or acute flares. They should be tapered and discontinued once remission is achieved due to their long-term side effects.

Question 14

UC disease management

What is used second line?
What is used third line?

Answer 14

• Azathioprine, 6-mercaptopurine, methotrexate
• Biologics - anti TNF infliximab
• Anti-interleukin 12/23 agents ustekinumab
• JAK inhibitors tofacitinib

Question 15

What is the main difference in approach to management US vs CD

Answer 15

Surgical Management in UC
Surgery may be indicated for patients with UC who have complications, such as toxic megacolon, perforation, or severe bleeding, or who fail to respond to medical therapy. The standard surgical procedure for UC is proctocolectomy with ileal pouch-anal anastomosis (IPAA), which involves the removal of the entire colon and rectum, with the creation of a pouch from the small intestine to restore bowel continuity.

methotrexate is not recommended for the management of UC (in contrast to Crohn’s disease)
Crohns disease is surgically managed by colectomy

Question 16

What guides management?

Describe how UC can be classified in severity

Answer 16

The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

Question 17

Gastrointestinal hormones

What is the source of Gastrin?

Answer 17

G cells in the antrum of the stomach.

Question 18

What stimuli lead to the release of Gastrin?

Answer 18

Distension of the stomach, vagus nerves (mediated by gastrin-releasing peptide), and luminal peptides/amino acids.

Question 19

What inhibits the release of Gastrin?

Answer 19

Low antral pH and somatostatin.

Question 20

What actions does Gastrin have on the digestive system?

Answer 20

Increases acid secretion by gastric parietal cells, pepsinogen and intrinsic factor (IF) secretion, increases gastric motility, and stimulates parietal cell maturation.

Question 21

What is the source of Cholecystokinin (CCK)?
What stimuli lead to the release of Cholecystokinin (CCK)?

Answer 21

I cells in the upper small intestine.
Partially digested proteins and triglycerides.

Question 22

What actions does Cholecystokinin (CCK) have on the digestive system?

Answer 22

Increases secretion of enzyme-rich fluid from the pancreas, contraction of the gallbladder, relaxation of the sphincter of Oddi, decreases gastric emptying, has a trophic effect on pancreatic acinar cells, and induces satiety.

Question 23

What is the source of Secretin?
What stimuli lead to the release of Secretin?

Answer 23

S cells in the upper small intestine.
Acidic chyme and fatty acids.

Question 24

What actions does Secretin have on the digestive system?

Answer 24

Increases secretion of bicarbonate-rich fluid from the pancreas and hepatic duct cells, decreases gastric acid secretion, and has a trophic effect on pancreatic acinar cells.

Question 25

What is the source of Vasoactive Intestinal Peptide (VIP)?
What stimulates the release of Vasoactive Intestinal Peptide (VIP)?

Answer 25

Question: What is the source of Vasoactive Intestinal Peptide (VIP)?
Answer: Small intestine and pancreas.

Question: What stimulates the release of Vasoactive Intestinal Peptide (VIP)?
Answer: Neural stimulation.

Question 26

What actions does Vasoactive Intestinal Peptide (VIP) have on the digestive system?

Answer 26

Stimulates secretion by the pancreas and intestines, and inhibits acid secretion.

Question 27

What is the source of Somatostatin?
What stimuli lead to the release of Somatostatin?

Answer 27

SOMATOSTATIN
D cells in the pancreas and stomach.
Fat, bile salts, and glucose in the intestinal lumen.

Question 28

What actions does Somatostatin have on the digestive system?

Answer 28

Decreases acid and pepsin secretion, decreases gastrin secretion, decreases pancreatic enzyme secretion, decreases insulin and glucagon secretion, inhibits trophic effects of gastrin, and stimulates gastric mucous production.

Question 29

Alcoholic liver disease

What are the three manifestations of ALD?

Answer 29

alcoholic fatty liver disease
alcoholic hepatitis 30%
cirrhosis

Isolated GGT
But ratio of AST:ALT is normall more than 2 - suggesting alcoholic hepatitis

Question 30

Describe an early onset of alcoholic fatty liver

Answer 30

Fatigue
Malaise
Abdominal pain
Anorexia
Weakness
Nausea and/or vomiting

Question 31

How is acute alcoholic hepatitis managed?
What scoring system is used to identify patients with severe acute alcoholic hepatitis

Answer 31

• glucocorticoids are used to improve short term survival
• The NICE guidelines suggest the use of Maddrey’s discriminant function (DF) to identify patients with severe acute alcoholic hepatitis
  DF of >32 predicts a high mortality within 90 days, and means a liver biopsy should be considered, with corticosteroid treatment initiation

Question 32

Classify the manifestations of chronic liver disease

1. Liver related manifestations (Describe these)
2. Estrogenic effects (levels rise with progressive liver damage as liver metabolises estrogen)
3. Portal hypertension manifestations

Answer 32

1. Liver related manifestations (Describe these)

• Jaundice (common)
• Right upper quadrant pain (common)
• Hepatomegaly (common, present in 70% of patients with ALD)
• Generally an enlarged and smooth edge, but rarely tender to palpation
• Palmar erythema
• Peripheral oedema
• Clubbing
• Dupuytren’s contracture (present in 30% of patients with alcoholic liver disease)
• Pruritis
• If there is cholestasis leading to bile salt deposition in skin
• Xanthomas
• Spider angiomas

Question 33

Classify the manifestations of chronic liver disease

Describe the estrogenic effects of chronic liver disease

Answer 33

Gynaecomastia and testicular atrophy (in males)
Loss of body hair
Amenorrhoea (in females)
Loss of libido

Question 34

Classify the manifestations of chronic liver disease

As inflammation and scarring occurs, alcoholic cirrhosis progresses and can lead to portal hypertension resulting in its own variety of features including:

Answer 34

Ascites (within 10 years of the diagnosis of cirrhosis, >50% of patients will develop this)
Dilated veins (e.g. caput medusae)
Variceal bleeding and haemorrhage
Splenomegaly

Question 35

Hepatic encephalopathy

Answer 35

• mild cognitive impairment
• confusion, altered GCS (see below)
  asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
  constructional apraxia: inability to draw a 5-pointed star
  triphasic slow waves on EEG
  raised ammonia level (not commonly measured anymore)

Question 36

Grading scale of hepatic encephalopathy

Answer 36

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

Question 37

Precipitants of hepatic encephalopathy

Answer 37

infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)

Question 38

Management of precipitating factors

Answer 38

Management
treat any underlying precipitating cause
lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
other options include embolisation of portosystemic shunts and liver transplantation in selected patients

Question 39

Child pugh classification

Answer 39

Question 40

Alcoholic ketoacidosis

Answer 40

Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation. Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones. Hence the patient develops a ketoacidosis.

It typically presents with a pattern of:
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

Question 41

Alcoholic ketoacidosis management

Answer 41

The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis

Question 42

Acute upper GI bleed differentials
1. Oesophageal causes
2. Gastric causes
3. Duodenal causes

Answer 42

Oesophageal causes
* Oesophageal varices
* Oesophagitis
* Cancer
* Mallory Weiss tear

Gastric causes
* Gastric ulcer
* Gastric cancer
* Dieulafoy lesion
* Diffuse erosive gastritis

Duodenal causes
* Ulcer
* Aorto-enteric fistula

Question 43

Presentation of acute upper GI bleed

Answer 43

Clinical features
* haematemesis
* the most common presenting feature
* often bright red but may sometimes be described as ‘coffee gound’
* melena
* the passage of altered blood per rectum
* typically black and ‘tarry’
* a raised urea may be seen due to the ‘protein meal’ of the blood
* features associated with a particular diagnosis e,g,
* oesophageal varices: stigmata of chronic liver disease
* peptic ulcer disease: abdominal pain

Question 44

Differentiate between Blatchford and Rockall score

Answer 44

Risk assessment
* the Glasgow-Blatchford score at first assessment
* helps clinicians decide whether patient patients can be managed as outpatients or not
* Patients with a Blatchford score of 0 may be considered for early discharge.

the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
* includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
*

Question 45

Management of acute upper GI bleed - severe bleed

Answer 45

Resuscitation
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
should be offered immediately after resuscitation in patients with a severe bleed
all patients should have endoscopy within 24 hours

Question 46

Acute upper GI bleed

Management of non-variceal bleeding

Answer 46

Management of non-variceal bleeding
* NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
* if further bleeding then options include repeat endoscopy, interventional radiology and surgery

Question 47

Management of variceal bleeding

Answer 47

Management of variceal bleeding
* 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

Question 48

Acute pancreatitis causes

Answer 48

Popular mnemonic is GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)

Question 49

Causes of raised serum amylase
other than pancreatitis

Answer 49

pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis

Question 50

Acute pancreatitis investigation

Answer 50

however, early ultrasound imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction
other options include contrast-enhanced CT

Question 51

Complications of acute pancreatits

Answer 51

• Peripancreatic fluid collections
• Pseudocysts
• Pancreaetic necrosis
• Pancreratic abscess
• Haemorrhage
• ARDS

Question 52

Pseudocysts

• Timing
• Investigations
• Location
• Management

Answer 52

In acute pancreatitis result from organisation of peripancreatic fluid collection. They may or may not communicate with the ductal system.
The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more after an attack of acute pancreatitis
Most are retrogastric
Investigation is with CT, ERCP and MRI or endoscopic USS
Symptomatic cases may be observed for 12 weeks as up to 50% resolve
Treatment is either with endoscopic or surgical cystogastrostomy or aspiration

Question 53

Chronic pancreatitis

What is it normally caused by?
Other causes
Features

Answer 53

Around 80% of cases are due to alcohol excess with up to 20% of cases being unexplained.

Other than alcohol, causes include:
genetic: cystic fibrosis, haemochromatosis
ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas

Features
pain is typically worse 15 to 30 minutes following a meal
steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin

Question 54

Management of chronic pancreatitis

Answer 54

functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
Management
pancreatic enzyme supplements
analgesia
antioxidants: limited evidence base - one study suggests benefit in early disease

Question 55

COELIAC DISEASE

Presentation

Answer 55

Signs and symptoms
* Chronic or intermittent diarrhoea
* Persistent or unexplained GI symptoms including nausea vomiting
* Prolonged fatigue TATT
* Recurrent abdo pain, cramps, distension
* Sudden or unexpected weight loss
* Unexplained IDA

Associated conditions
* Autoimmune thyroid disease
* Dermatitis herpetiformis
* Irritable bowel syndrome
* Type 1 diabetes
* First-degree relatives (parents, siblings or children) with coeliac disease

Question 56

How does coeliac disease cause malabsorption?
How is diagnosis usually made?

Answer 56

• Coeliac disease is caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.
• Diagnosis is made by a combination of serology and endoscopic intestinal biopsy.

Question 57

HYATID CYSTS

what is the cause? what hypersensitivity reaction is involved?

Answer 57

Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm parasite Echinococcus granulosus. An outer fibrous capsule is formed containing multiple small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.

Question 58

Biliary rupture of hyatid cysts

What is the triad?

Answer 58

biliary colic, jaundice, and urticaria

Question 59

Management of hyatid cysts

Answer 59

Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the contents sterilised first).

Question 60

Whipples disease

Answer 60

• Caused by tropheryma whippelii infection
• Malabsorption - diarrhoea, weight loss
• Large joint arthralgia
• Lymphadenopathy
• Pleurisy, pericarditis
• Neurological symptoms are rare

Question 61

Whipples disease

Investigation
Management

Answer 61

Investigation
jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules

Management
guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin