Abdominal Conditions Flashcards
What is GORD
Gastro-oesophageal reflux disease
Symptoms or complications resulting from the reflux of gastric contents into the oral cavity or lung
How does GORD present
Heartburn (burning sensation in chest) usually after eating, which may be worse at night Chest pain (retrosternal or epigastric) Difficulty swallowing (dysphasia) Regurgitation of food or sour liquid (acid) Sensation of lump in throat Chronic nocturnal cough Laryngitis Hoarse voice New or worsening asthma Disrupted sleep
What is ERD
Erosive reflux disease, where erosions are present on endoscopic examination of a patient present with GORD
What is NERD
Nonerosive reflux disease, where no erosions are present on endoscopic examination of a patient present with GORD
What is the epidemiology of GORD
Common condition that affects between 10% and 30% of people in developed countries
There is a global variation, with less than 10% prevalence in East Asia
All age groups affected and no evidence for clear predictive factors
What is the aetiology of GORD
The lower oesophageal sphincter regulates food passage from the oesophagus to the stomach and contains both intrinsic smooth muscle and skeletal muscle.
Episodes of transient lower oesophageal sphincter relaxation are normal but occur more frequently in GORD, causing reflux of gastric contents into the oesophagus.
This relaxation is more common after meals and is stimulated by fat in the duodenum
More likely to occur if there is a hiatal sac containing acid
Those with severe reflux often have a hiatus hernia and decreased resting lower oesophageal sphincter pressure but pressure can be high in mild to moderate reflux
What are the risk factors for GORD
Obesity Hiatal hernia Pregnancy Connective tissue disorders (eg scleroderma) Delayed stomach emptying Older age Family history of heart burn or GORD Smoking Eating large meals or late at night Eating certain trigger foods (eg fatty or fried food) Drinking certain beverages (eg alcohol or coffee) Taking NSAIDs Psychological stress
What is a hiatal hernia
Bulging of the top of the stomach into the diaphragm
What is the difference between the lining of the oesophagus and that of the stomach
Oesophagus has squamous epithelial lining which is more sensitive to the effects of stomach acid than the stomach is due to its columnar epithelial lining which is more protective against stomach acid
What other conditions present similarly to GORD
Acute coronary syndrome Stable angina Functional oesophageal disorder/ functional heartburn Achalasia Functional (non-ulcer) dyspepsia Peptic ulcer disease Eosinophilic oesophagitis Proton pump inhibitor responsive oesophageal eosinophilia Malignancy Laryngipharyngeal reflux
What investigations would be performed for suspected GORD
PPI trial OesophagoGastroDuodenoscopy (OGD) Ambulatory pH monitoring Oesophageal manometry Combined impedance pH testing Barium swallow Oesophageal capsule endoscopy
What does endoscopy assess for
Peptic ulcers
Oesophageal malignancy
Gastric malignancy
Who would be admitted urgently for endoscopy
Patients with evidence of a GI bleed (melaena or coffee ground vomitining)
What are the key red flag features for referral for endoscopy
Dysphagia at any age gets a 2 week wait referral Aged over 55 (generally the cut off for urgent vs routine referrals) Weight loss Upper abdominal pain and reflux Treatment resistant dyspepsia Nausea and/or vomiting Low haemoglobin Raised platelet count
What is the management plan for GORD
Lifestyle advice:
- Reduce tea, coffee and alcohol
- Weight loss
- Smoking cessation
- Smaller, lighter meals
- Avoid heavy meals before bedtime
- Stay upright after meals rather than lying flat
Acid neutralising medication when required:
- Gaviscon
- Rennie
Proton pump inhibitors (reduce acid secretion in the stomach) (most effective acid suppressants):
- Omeprazole
- Lansoprazole
Ranitidine as an alternative to PPIs or can be used in bedtime adjunction with PPI in those with nocturnal symptoms, it is an H2 receptor antagonist (antihistamine) which reduces stomach acid
Surgery
What is the surgery for GORD
A laparoscopic fundoplication
It involves tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter
What is the prognosis for a patient with GORD
Most patients respond to treatment with PPIs
Maintenance PPI therapy recommended for those who’s symptoms relapse when the PPI is discontinued as well as for those with erosive oesophagitis or Barrett’s oesophagus
Barretts oesophagus may result after prolonged GORD
Oesophageal adenocarcinoma may be a serious though rare complication of GORD
What is Helicobacter Pylori
H.pylori is a gram negative aerobic bacteria which lives in the stomach
It causes damage to the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer.
It avoids the acidic stomach environment by breaking into the gastric mucosa, thereby eclipsing the epithelial cells underneath the mucosa to the stomach acid.
H.pylori also produces ammonia, to neutralise the stomach acid, which directly damages the epithelial cells along with other chemicals the bacteria produce
Who is offered an H.pylori test
Anyone with dyspepsia who has had 2 weeks without use of a PPI in order to achieve an accurate result.
What are the 3 tests for H.pylori
Urea breath test (using radiolabelled carbon 13)
Stool antigen test
Rapid ureas test
What is a Rapid Urease test
AKA the CLO test (Campylobacter-like organism test)
It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is then added to the sample. If H.pylori are present they will produce urease enzymes which converts the urea to ammonia, which makes the solution more alkali, resulting in a positive result when pH tested.
What is eradication regime for treatment of H.pylori
Triple therapy with a PPI plus 2 antibiotics for 7 days
(eg. omeprazole, amoxicillin and clarithromycin)
The urea breath test then can be used as a test of eradication after treatment period but not routinely necessary.
What is Barretts Oesophagus
Constant reflux of acid results in the lower oesophageal epithelium changing through metaplasia from squamous to columnar, with this change being called Barretts oesophagus. Typically once this change happens, a patient’s symptoms will improve
It is considered to be premalignant and is a risk factor for the development of adenocarcinoma of the oesophagus
How is Barretts oesophagus managed
Regular endoscopy to monitor for adenocarcinoma
Treatment with PPIs and new evidence for regular aspirin use result in reduced risk of adenocarcinoma development
Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy is used to destroy the columnar epithelium so it is replaced with normal cells. However this is not recommended in patients with no dysplasia but has a role in those with low and high dysplasia in preventing progression to cancer.
What is a peptic ulcer
A break in the mucosal lining of the stomach or duodenum more than 5mm in diameter with depth to the submucosa.
Ulcers smaller than this without obvious depth are called erosions
What is the epidemiology of peptic ulcers
Varied worldwide prevalence of ~0.12% to 1.5%
Incidence increases with age with gastric ulcers peaking from 50-69y/o and duodenal ulcers peaking 10 to 20 years earlier
Both sexes similarly affected
What is the aetiology of peptic ulcers
Two major causes:
- H.pylori infection
- Use of aspirin or NSAIDs
Rarer causes include:
- Gastric ischaemia (stress ulcers)
- Zollinger-Ellison syndrome
- Infections
- Crohn’s disease
- Idiopathic
What is the pathophysiology of peptic ulcers
The stomach mucosa is prone to ulceration from:
-the breakdown of the protective layer of the stomach and duodenum
-the increase in stomach acid
There is a protective layer in the stomach comprised of mucus and bicarbonate secreted by the stomach mucosa, which can be broken down by medications (eg steroids or NSAIDs), or H.pylori
Increased acid can result from:
-stress
-alcohol
-caffeine
-smoking
-spicy foods
What are the risk factors for peptic ulcers
H.pylori infection NSAID use Smoking Increasing age Personal or family history of peptic ulcer disease Patient in intensive care
How do peptic ulcers present
Epigastric discomfort or pain or tenderness
Pointing sign (show site of pain with one finger)
Nausea and vomiting
Early satiety
Weight loss
Diarrhoea
Anaemia (iron deficiency type)
GI bleed (coffee ground vomiting and melaena)
Hypotension
Septic shock
Succussion splash
Dyspepsia
Eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers
What other conditions present similarly to peptic ulcers
Oesophageal cancer Stomach cancer GORD Gastroparesis Billiary colic Acute pancreatitis Non-ulcer dyspepsia (functional dyspepsia) Coeliac disease IBS Pleuritic pain Pericarditis
How would a patient with suspected peptic ulcer be investigated
Upper GO endoscopy with rapid urease test (CLO test) to check for H.pylori
Biopsy should be considered to exclude malignancy
FBC
Fasting serum gastrin level
Urine NSAID screen
What should be discussed with a patient in peptic ulcer cases
Advise to avoid NSAID use Continue to use aspirin if indicated for secondary prevention of cardiac events Discuss risk and benefits of other anticoagulants If H.pylori present, complete course of therapy, even if symptoms resolve Seek medical attention if develop: -blood in stools -black tarry stools -vomiting -abdominal pain Advise for long term management: -smoking cessation -annual review of condition -Self-treatment with antacid
What is the treatment plan for patient with a peptic ulcer
Stop NSAID used where possible
Start high dose proton pump inhibitors for 4-8 weeks
Referral to specialist if unexplained or treatment resistant Gastro-oesophageal symptoms, or if H.pylori has not responded to second line eradication therapy
Endoscopy can be used to monitor the ulcer to ensure it heals and to assess for further ulcers
What are the potential complications of a peptic ulcer
Bleeding- common but potentially life threatening
Perforation- resulting in an ‘acute abdomen’ and peritonitis, requiring urgent surgical repair, usually laparoscopic
Scarring and strictures of the muscle and mucosa can lead to a narrowing of the pylorus (exit od the stomach) causing difficulty in emptying the stomach contents which is known as pyloric stenosis
How does pyloric stenosis present
Upper abdominal pain Distension Nausea Vomiting Particularly worse after eating
What is the prognosis for those with a peptic ulcer
With PPI therapy, duodenal ulcers usually heal within 4 weeks and gastric ulcers usually heal within 8 weeks
For those with peptic ulcers caused by H.pylori, prognosis after eradication is good with recurrence risk of duodenal ulcer being ~20% and that of gastric ulcer being ~30%
For those associated with NSAID use, discontinuation of NSAIDs will lead to low rate of ulcer recurrence
What is an upper GI bleed
A medical emergency involving some form of bleeding from the oesophagus, stomach or duodenum
What causes an upper GI bleed
Oesophageal varices
Mallory-Weiss tear (tear of the oesophageal mucous membrane)
Ulcers of the stomach or duodenum
Cancers of the stomach or duodenum
How does an upper GI bleed present
Haematemesis (vomiting blood)
Coffee ground vomit (vomiting digested blood which looks like coffee grounds)
Melaena (tar like, black, greasy and offensive stools caused by digested blood
Haemodynamic instability (occurs in large blood loss, causing low blood pressure, tachycardia and other songs of shock)
May have symptoms of underlying pathology such as:
-epigastric pain and dyspepsia in peptic ulcers
-jaundice for ascites in liver disease with oesophageal varices
What is the Glasgow-Blatchford score
Used as a scoring system in suspected upper GI bleeds on initial presentation to establish the patients risk of having an upper GI bleed to help form a management plan.
A score > 0 indicated high risk (use an online calculator to calculate the score)
Takes into account various features indicateing an upper GI bleed:
-Drop in Hb
-Rise in urea
-Blood pressure
-Heart rate
-Melaena
-Syncopy
Why does urea rise in an upper GI bleed
Blood in the GI tract gets broken down by the acid and digestive enzymes. One of the breakdown products is urea and this urea is then absorbed in the intestines
What is the Rockall Score
Used for patient that have had an endoscopy yo provide a percentage risk of rebreeding and mortality.
Use an online calculator to calculate the score
Takes in to account the risk factors from clinical presentation and endoscopy findings:
-Age
-Features of shock (tachycardia, hypotension etc)
-Co-morbidities
-Cause of bleeding (Mallory-Weiss, malignancy etc)
-Endoscopic stigmata of recent haemorrage such as clots or visible bleeding vessels
What is the management plan for those with an upper GI bleed
ABATED
A-ABCDE approach to immediate resuscitation
B-Bloods (FBC (Hb and platelets for coagulation), UandEs (urea), INR, LFTs (liver disease), Crossmatch for 2 units of blood)
A-Access (2 large-bore cannula)
T-Transfuse
E-Endoscopy
D-Drugs (stop anticoagulants and NSAIDs)
If oesophageal varices are suspected give:
- Terlipressin
- Prophylactic broad spectrum antibiotics
Definitive treatment is OGD to provide interventions that stop the bleeding (eg. variceal banding or cauterisation of the bleeding vessel)
NICE recommend against using a PPI prior to endoscopy but some senior doctors may still do this
What are the risk factors for an upper GI bleed
Chronic vomiting
Alcoholism
Medications such as NSAIDs and anticoagulants
GI surgery
What is the epidemiology of those with upper GI bleed
Most common GI emergency in UK
Incidence in the UK ranges from 50-150 per 100,000 per year
Men more commonly affected than women
Those in lower socioeconomic groups more commonly affected than those in higher groups
Incidence rises sharply with age
Accounts for ~5000 deaths per year in the UK
What are the differentials for those presenting with symptoms of an upper GI bleed
Peptic ulcer disease Oesophageal varices Oesophagitis Mallory-Weiss tear Boerhaave syndrome (spontaneous oesophageal perforation) Gastric varices Arteriovenous malformation Dieulafoy's lesions Upper GI tumours Aortoenteric fistulae (AEF) Coagulopathy
What is the prognosis after an upper GI bleed
Mortality of 2-10%
What should be transfused in those with an upper GI bleed
Transfusion is based on the individual presentation:
- Transfuse blood, platelets and clotting factors (fresh frozen plasma) in those with massive haemorrhage
- Transfusing more blood than necessary can be harmful
- Platelets should be given in active bleeding and thrombocytopenia
- Prothrombin Complex Concentrate can be given to those taking warfarin that are actively bleeding
What is indicative of thrombocytopenia
Platelets < 50
What are the two types of inflammatory bowel disease
Crohn’s disease and Ulcerative colitis
What is Crohn’s disease
A disorder of unknown aetiology characterised by a transmural inflammation of the GI tract. It may involve any or all parts of the entire GI tract from mouth to perianal area, although it is usually seen in the terminal ilium and perianal locations
Characterised by skip lesions, where normal bowel mucosa is found between diseased areas.
The inflammation often leads to fibrosis causing intestinal obstruction and can also result in sinus tracts that burrow through and penetrate the serosa, thereby leading to perforations and fistulae
What is inflammatory bowel disease
An umbrella term of the diseases which cause inflammation of the walls of the GI tract and have periods of remission and exacerbation
What is Ulcerative colitis
A type of IBD which characteristically involves the rectum and extends proximally to affect a variable length of the colon.
It is recognised as a multifactorial polygenic disease with unknown exact aetiology.
What are the Crohn’s disease features which distinguish it from Ulcerative colitis
(think crows NESTS)
N- No blood or mucus
E- Entire GI tract
S- Skip lesions on endoscopy
T- Terminal ileum most affected and Transmural (full thickness) inflammation
S- Smoking is a risk factor (don’t set the NEST on fire)
Crohn’s is also associated with weight loss, strictures and fistulae
What are the Ulcerative colitis features which distinguish it from Crohn’s disease
(remember 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 sclerosis cholangitis
What is the epidemiology of IBD
~0.3% prevalence in North America
~3 million adults in USA
Equally prevalent among men and women
More common in white people and Ashkenazi Jews
What are the risk factors for Crohn’s disease
White ancestry Age 15-40 or 60-80 Family history of CD Cigarette smoker High refined sugar diet Oral contraceptive pill Not breastfed NSAID use
What are the risk factors for Ulcerative Colitis
Family history of IBD HLA-B27 positive Infection NSAID use Non-smoker or former smoker
How does Crohn’s disease present
Abdominal pain Prolonged diarrhoea Perianal lesions Bowel obstruction Blood in stools Fever Fatigue Abdominal tenderness Weight loss Oral lesions Abdominal maa Extra-intestinal manifestations (eg erythema nodosum or pyoderma gangrenosum)
How does Ulcerative colitis present
Rectal bleeding Diarrhoea Blood in stools Abdominal pain Arthritis and spondylitis Malnutrition Abdominal tenderness Fever Weight loss Constipation Skin rash Uveitis and episcleritis Pallor
What are the differentials for IBD
Both types (CD and UC) are differentials for each other Infectious colitis Indeterminate colitis Pseudomembranous colitis Ischaemic colitis Radiation colitis Yersinia enterocolitica Internal tuberculosis Amoebiasis Cytomegalovirus colitis Colorectal cancer Diverticular disease Acute appendicitis Ectopic pregnancy Pelvic inflammatory disease Endometriosis Irritable bowel syndrome Vasculitis
How would IBD be investigated
Routine bloods for anaemia, infection, thyroid, kidney and liver function
CRP indicated inflammation and active disease
Faecal calprotectin is released by the intestines when inflamed so useful as a screening test and is more than 90% sensitive and specific to IBD in adults
Endoscopy (OGD and colonoscopy) with biopsy is diagnostic
Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulae, abscesses and strictures
What is the management plan for those with Crohn’s disease
Inducing remission:
- First line is steroid (eg oral prednisolone or IV hydrocortisone)
- If steroids alone don’t work, consider adding immunosuppressant under specialist guidance (eg methotrexate, azathioprine or infliximab)
Mainting remission:
Treatment is tailored to patient based on risks, side effects, nature of disease and wishes. It is reasonable to not take medications whilst well.
-First line are azathioprine or mercaptopurine
-Alternatives are methotrexate, infliximab, adalimumab
Surgery:
If the disease is only affecting with distal ileum, it is possible to surgically resect this area and prevent further flares.
Surgery can also be used to treat strictures and fistulae secondary to Crohn’s disease
What is the management plan for those with Ulcerative Colitis
Inducing remission:
Mild to moderate disease:
-First line - Aminosalicylate (eg mesalazine oral or rectal)
-Second line - Corticosteroids (eg prednisolone)
Severe disease:
-First line - IV corticosteroids (hydrocortisone)
-Second line - IV cyclosporin
Maintaining remission:
- Aminosalicylate
- Azathioprine
- Mercaptopurine
Surgery:
Panproctocolectomy to remove the colon and rectum will remove the disease as these are the sites typically affected.
The patient is then left with either a permanent ileostomy or and ileo-anal anastomosis (J-pouch), where the ileum is folded back on itself and fashioned into a larger pouch which functions as a rectum. This J-pouch is then attached to the anus and collects stools prior to the patient passing the motion.
What are the important discussions to have with a patient with IBD
Smoking cessation in CD
Maintain healthy balanced diet to prevent malnutrition
Avoid dairy products
Low fat diet after terminal ileum resection with medium triglyceride supplementation
Preoperative nutrition is of high importance to reduce post surgical complications
Regular exercise
Avoid NSAIDs
Avoid oral contraceptives
Advise on preventative vaccines if immunosuppressive treatments used
Seek medical advice if have any of the following symptoms:
-fever or chills
-bloody stools
-severe abdominal pain
-abdominal bloating and inability to pass stool or gas
-dizziness
-dehydration
-pus draining from anal area or abdominal wall
-intractable vomiting
-worsening of usual symptoms
-weight loss
Provide contacts for local support groups and educational sources (eg Crohn’s and Colitis UK)
What is IBS
Irritable bowel syndrome is a chronic condition characterised by abdominal pain associated with bowel dysfunction. It is a diagnosis of exclusion meaning that a diagnosis is only made when other pathology is excluded. It is a functional bowel disorder meaning there is no identifiable disease underlying the symptoms and is the result of the abnormal functioning of an otherwise normal bowel
What is the epidemiology of IBS
Occurs in up to 20% of the population
Affects women more than men and is more common in younger adults
What is the aetiology of IBS
Probably multifactorial and evidence suggests motility, inflammatory, genetic, immunological, psychological and dietary components
What are the risk factors for IBS
Physical and sexual abuse PTSD Age <50y/o Female Previous enteric infection Stress
How does IBS present
Abdominal discomfort Diarrhoea Constipation Fluctuating bowel habits Change in bowel habits associated with pain Abdominal bloating or distension Normal examination of the abdomen Passage of mucus with stool Urgency of defecation Symptoms worsen after eating Symptoms improved by opening bowels
What are the criteria for diagnosis of IBS
Other pathology to be excluded:
- Normal FBC, ESR and CRP blood tests
- Faecal calprotectin negative to exclude IBD
- Negative coeliac disease serology (anti-TTG antibodies)
- Cancer is not suspect or is excluded if suspected
Symptoms should suggest IBS: Abdominal pain and/or discomfort: - relived on opening bowels or -associated with a change in bowel habit And 2 of: - abnormal stool passage - bloating - worse symptoms after eating - mucus with stools
What is the management of IBS
Provide reassurance that there is no serious underlying pathology
General healthy diet and exercise advice:
- Adequate fluid intake
- Regular small meals
- Reduce process foods
- Limit caffeine and alcohol
- Low FODMAP diet guided by a dietician
- Trial of probiotic supplements for 4 weeks
First line medication:
- Loperamide for diarrhoea
- Laxatives for constipation (avoid lactulose as it can cause bloating, Linaclotide is a specialist laxative for those who don’t respond to first line laxatives)
- Antispasmodics for cramps (eg. buscopan)
Second line medication:
-Tricyclic antidepressants (ie amitriptyline 5-10mg at night)
Third line medication:
-SSRI antidepressants
CBT offered to help patients psychologically manage the condition and reduce distress associated with symptoms
What is acute gastritis
Inflammation of the stomach which presents with nausea and vomiting
What is enteritis
Inflammation the intestines which presents with diarrhoea
What is gastroenteritis
Inflammation all the way from the stomach to the intestines which presents with nausea, vomiting and diarrhoea
What is the most common type of gastroenteritis
Viral
What is the prognosis for gastroenteritis
It is very infectious so people with the diagnosis should isolate until 48 hours symptom free.
Most people recover well but it can be potentially fatal, especially in very young or very old people or those with comorbidities
