Gastroenterology 2 Flashcards
IBD, alcoholic liver disease, CLD, acute upper GI bleed
Crohn’s disease
- 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
Crohns disease management
inducing remission, initial phases of treatment
- Smoking cessation - one of the causea and increases disease severity
- Steroids induce remission
- Enteral feeding with elemental diet
- Second line- 5-ASA mesalazine
How do you differentiate CD from UC with investigations
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.
Crohns disease
- When would you use infliximab in Crohn’s disease?
- What is used for isolated peri-anal disease
- 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 - What is used for isolated peri-anal disease
metronidazole is often used for isolated peri-anal disease
Crohns disease management
Maintain remission
MOA
What needs to be checked before starting
- 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.
What percentage of CD patients will have surgery?
Stricturing terminal ileal disease - what surgery is indicated?
around 80% of patients with Crohn’s disease will eventually have surgery
stricturing terminal ileal disease → ileocaecal resection
Ulcerative colitis
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
Describe endoscopy findings in UC
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
Which IBD is referred to when drain pipe appearance is seen in barium enema
long standing disease UC: colon is narrow and short -‘drainpipe colon’
loss of haustrations with superficial ulceration creating pseudopolyps
Which disease are gallstones and oxalate renal stones more common in?
UC
Describe Kantors string sign
severe narrowing during small bowel barium meal > Crohn’s stricture
Describe lead pipe appearance of colon and what this indicates
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.
UC management
mild to moderate disease
what is used to manage acute flares
- 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.
UC disease management
What is used second line?
What is used third line?
- Azathioprine, 6-mercaptopurine, methotrexate
- Biologics - anti TNF infliximab
- Anti-interleukin 12/23 agents ustekinumab
- JAK inhibitors tofacitinib
What is the main difference in approach to management US vs CD
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
What guides management?
Describe how UC can be classified in severity
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)
Gastrointestinal hormones
What is the source of Gastrin?
G cells in the antrum of the stomach.
What stimuli lead to the release of Gastrin?
Distension of the stomach, vagus nerves (mediated by gastrin-releasing peptide), and luminal peptides/amino acids.
What inhibits the release of Gastrin?
Low antral pH and somatostatin.
What actions does Gastrin have on the digestive system?
Increases acid secretion by gastric parietal cells, pepsinogen and intrinsic factor (IF) secretion, increases gastric motility, and stimulates parietal cell maturation.
What is the source of Cholecystokinin (CCK)?
What stimuli lead to the release of Cholecystokinin (CCK)?
I cells in the upper small intestine.
Partially digested proteins and triglycerides.
What actions does Cholecystokinin (CCK) have on the digestive system?
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.
What is the source of Secretin?
What stimuli lead to the release of Secretin?
S cells in the upper small intestine.
Acidic chyme and fatty acids.
What actions does Secretin have on the digestive system?
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.
What is the source of Vasoactive Intestinal Peptide (VIP)?
What stimulates the release of Vasoactive Intestinal Peptide (VIP)?
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.
What actions does Vasoactive Intestinal Peptide (VIP) have on the digestive system?
Stimulates secretion by the pancreas and intestines, and inhibits acid secretion.
What is the source of Somatostatin?
What stimuli lead to the release of Somatostatin?
SOMATOSTATIN
D cells in the pancreas and stomach.
Fat, bile salts, and glucose in the intestinal lumen.
What actions does Somatostatin have on the digestive system?
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.
Alcoholic liver disease
What are the three manifestations of ALD?
alcoholic fatty liver disease
alcoholic hepatitis 30%
cirrhosis
Isolated GGT
But ratio of AST:ALT is normall more than 2 - suggesting alcoholic hepatitis
Describe an early onset of alcoholic fatty liver
Fatigue
Malaise
Abdominal pain
Anorexia
Weakness
Nausea and/or vomiting
How is acute alcoholic hepatitis managed?
What scoring system is used to identify patients with severe acute alcoholic hepatitis
- 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
Classify the manifestations of chronic liver disease
- Liver related manifestations (Describe these)
- Estrogenic effects (levels rise with progressive liver damage as liver metabolises estrogen)
- Portal hypertension manifestations
- 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
Classify the manifestations of chronic liver disease
Describe the estrogenic effects of chronic liver disease
Gynaecomastia and testicular atrophy (in males)
Loss of body hair
Amenorrhoea (in females)
Loss of libido
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:
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
Hepatic encephalopathy
- 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)
Grading scale of hepatic encephalopathy
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
Precipitants of hepatic encephalopathy
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
Management of precipitating factors
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
Child pugh classification
Alcoholic ketoacidosis
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
Alcoholic ketoacidosis management
The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis
Acute upper GI bleed differentials
1. Oesophageal causes
2. Gastric causes
3. Duodenal causes
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
Presentation of acute upper GI bleed
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
Differentiate between Blatchford and Rockall score
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
*
Management of acute upper GI bleed - severe bleed
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
Acute upper GI bleed
Management of non-variceal bleeding
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
Management of variceal bleeding
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
Acute pancreatitis causes
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)
Causes of raised serum amylase
other than pancreatitis
pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis
Acute pancreatitis investigation
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
Complications of acute pancreatits
- Peripancreatic fluid collections
- Pseudocysts
- Pancreaetic necrosis
- Pancreratic abscess
- Haemorrhage
- ARDS
Pseudocysts
- Timing
- Investigations
- Location
- Management
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
Chronic pancreatitis
What is it normally caused by?
Other causes
Features
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
Management of chronic pancreatitis
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
COELIAC DISEASE
Presentation
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
How does coeliac disease cause malabsorption?
How is diagnosis usually made?
- 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.
HYATID CYSTS
what is the cause? what hypersensitivity reaction is involved?
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.
Biliary rupture of hyatid cysts
What is the triad?
biliary colic, jaundice, and urticaria
Management of hyatid cysts
Surgery is the mainstay of treatment (the cyst walls must not be ruptured during removal and the contents sterilised first).
Whipples disease
- Caused by tropheryma whippelii infection
- Malabsorption - diarrhoea, weight loss
- Large joint arthralgia
- Lymphadenopathy
- Pleurisy, pericarditis
- Neurological symptoms are rare
Whipples disease
Investigation
Management
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
