Gastroenterology Flashcards
What is gastro-oesophageal reflux disease (GORD)?
Retrograde flow of gastric contents into oesophagus. Rarely life threatening but frequently chronic and affects QOL, heart pain and can induce premalignant change in esophagus.
What is the anti-reflux barrier?
Lower oesophageal sphincter (LOS) has transient changes in pressure - GORD have lower LOS pressures on average
Diaphragm acts as external sphincter
What is in the refluxed material?
Acid and pepsin
What are the oesophageal defence mechanisms?
- Oesophageal clearance = gravity and peristalsis (?peristaltic dysfunction or hiatus hernia if oesophageal clearance impaired)
- Saliva contains bicarbonate to neutralise acid
- Oesophageal mucosa = mucous, bicarbonate and prostaglandins are protective
What are the risk factors for GORD?
- Pregnancy (pressure against diaphragm)
- Hiatus hernia
- Genetic
- Smokers
- Obesity
- Large meals late at night
- High fat content
- Excess alcohol or caffeine
- Drugs e.g. TCAs, anticholinergics, nitrates, Ca blockers
What are the symptoms of GORD?
- Heartburn related to meals, lying down, relieved by antacids
- Retrosternal discomfort
- Acid brash - regurgitation acid or bile
- Water brash - excessive salivation
- Odynophagia - pain on swallowing due to sever oesophagitis or stricture
What are the atypical symptoms of GORD?
Non-cardiac chest pains
Dental erosions
Respiratory symptoms: asthmatic symptoms ie wheeze, laryngitis, chronic cough, chronic hoarseness
Episodic or chronic aspiration can cause pneumonia, lung abscess and interstitial pulmonary fibrosis
In GORD, what symptoms are alarm symptoms and should be referred immediately?
- Acute GI bleed
- Dyspepsia (indigestion) with:
a) chronic GI bleed
b) Progressive unintentional weight loss
c) Progressive difficulty swallowing
d) Persistent vomiting
e) Iron deficiency anaemia
f) Epigastric mass
What is the management of GORD?
- Drug tx with PPI omeprazole
- Lose weight
What are the causes of upper GI bleeding?
- Peptic ulcer disease
- Duodenitis
- Gastritis
- Varix rupture (varicose veins rupture lower oesophagus)
- Oesophagitis
What are the signs and symptoms of upper GI bleeding?
- General abdominal discomfort
- Haematemesis (vomiting of blood)
- Malaena (blood rectally)
- Shock (from loss of blood)
- Changes in orthostatic vital signs
What are the causes of oesphageal varices (where varicose veins at lower end of oesophagus get larger and burst)?
Portal hypertension:
- Chronic alcohol abuse and liver cirrhosis
- Ingestion of caustic substances
What is the pathophysiology of peptic ulcers?
Erosions caused by gastric acid. Defect in the gastric or duodenal wall that extends through the muscularis mucosae into deeper layers of wall (submucosa or muscularis). Can erode through major blood vessels causing haemorrhage
What are the causes of peptic ulcers?
Drugs - NSAIDs, corticosteroid use Alcohol/tobacco use H.pylori Stress Changes in gastric mucin consistency (may be genetically determined
What are the signs and symptoms of peptic ulcers?
Abdominal pain
Haematemesis and melaena if haemorrhagic rupture
What is the treatment of peptic ulcers?
Surgery only if haemorrhage or perforation.
Must reduce acid secretion, neutralise the acid secretion and protect mucosa
Consider histamine blockers (H2 receptor antagonists), prostaglandin analogues, antacids, PPIs, chelates, antibiotics
What are the signs and symptoms of Crohns disease?
Diarrhoea GI bleeding Nausea/vomiting Abdominal pain/cramping - intestinal obstruction and acute inflammation (appendicitis like) Fever Weight loss
What are the oral signs and symptoms of Chrohns disease?
Cobblestone mucosa
Granulomatous lesions (swollen lower lip, angular cheilitis)
Generalised inflammation
Recurrent aphthous stomatitis
Where do apthous ulcers most commonly present?
Inside of lips, cheeks, on tongue, on base of gums
Does ulcerative colitis have any oral manifestations
No - but secondary to iron deficiency anaemia
What conditions can cause apthous-like ulcers?
- Immune system disorders
- Blood diseases e.g. HIV
- Vitamin deficiencies
- Hormonal e.g. menstrual
- Allergies
- Stress
- Trauma
- GIT problems e.g. Crohns, coeliac disease
What is the treatment for oesophageal varices?
Propanalol to lower BP
What diseases make up inflammatory bowel disease?
Ulcerative colitis = muscosal ulceration in colon
Crohns disease = transmural inflammation in anypart of GI tract
Why is IBS different to IBD?
It is a diagnosis of exclusion
What is the age and sex incidence of inflammatory bowel disease?
Tends to affect younger people Familial pattern (10-25% concordance) but genetic and environmental factors still unresolved
What are the drug groups used in inflammatory bowel disease?
- Symptomatic agents e.g. antispasmodics
- 5-ASA compounds (based on aspirin to reduce inflammation) e.g. sulfasalazine
- Corticoids
- Immunosuppressive
- Antibiotics e.g. metronidazole (against anaerobic)
What is a fistula?
Pathological tract between 2 surfaces and lined with epithelium
What does a barium contrast study show?
Obstructions - black areas = strictures which can lead to infarction of the bowel
What can transmural inflammation develop?
Fistulae
What are the types of fistulae that can be present in the GI tract?
- Mesenteric
- Entero-enteric
- Entero-vesical (bowel and bladder)
- Retroperitoneal
- Entero-cutaneous (bowel and skin e.g. through surgical scar or umbilicus)
- Perianal
What are the systemic complications of IBD?
- Aphthous stomatitis
- Episcleritis (red eye) and uveitis (uneven pupil)
- Arthritis - peripheral large joints, monoarticular - central ankylosing spondylitis and sacroiliitis (base of spine)
- Vascular complications
- E.nodosum causing painful skin rash
- P.gangrenosum on outside of ankle
- Gallstones
- Malabsorption
- Renal stones, fistulae, hydronephrosis, amyloidosis (deposits beta pleated sheets)
- Bleeding with bowel movements - can lead to iron deficiency anaemia (hypochromic, microcytic)
- Malignancy ie colorectal cancer in ulcerative colitis
What two diseases is granulomas seen in and is tested with serum angiotensin converting enzyme to differentiate?
Crohns
Sarcoidosis
What is proctocolitis and which patients is it seen in?
Inflammation of the colon
- Ulcerative colitis
- Crohns
- Radiation pts
- Ischaemia
- Infections with C.diff
- From antibiotics
What is a complication of non-universal ulcerative colitis?
Toxic dilatation/megacolon - can perforate leading to air in abdominal cavity, sepsis and multiorgan failure
What are the indications for surgery in non-universal ulcerative colitis?
- Exsanguinating haemorrhage (pt will bleed to death)
- Growth retardation
- Systemic complications
- Toxicity and/or perforation
- Suspected cancer
- Significant dysplasia (pre-cancerous)
- Intractability
What is the management of non-universal ulcerative colitis?
Medical
Colonectomy will cure condition
What are the features of a peptic duodenal ulcer?
- Intermittent epigastric pain usually post-prandial (1-3hrs post food)
- Posterior ulcer may radiate pain to back
- Haemorrhage - more rapid bleeding = melena (blleding rectal), slower = anaemia.
- H.Pylori in 90%
What are the features of benign peptic gastric ulcer?
- Intermittent epigastric pain
- Chronic
- Can perforate
- H.Pylori in 60%
If a benign peptic gastric ulcer has perforated, what is seen on a chest xray?
Gas under right hemidiaphragm - surgical emergency as free gas in abdominal cavity. (left air normal as this is gastric bubble)
What 3 things are ulcer producing?
What 3 things are protective against ulcers?
Gastric acid, pepsin, H.pylori infection
Prostaglandins, mucus, HCO3-
How do H2 receptor antagonists work in the management of peptic ulcers? Give examples of drugs
Block histamine receptors to reduce gastric acid output
Cimetidine (most popular), Famotidine, Nizatidine, Ranitidine (can be used in hospital)
How do prostaglandin analogues work in the management of peptic ulcers? What drug is most used?
Inhibit gastric acid secretion. PGE2 and PGI2 stimulate mucus and bicarbonate
Inhibit adenylcyclase to reduce cAMP production
Misoprostol (PGE2 analogue)
How do proton pump inhibitors (PPIs) work in the management of peptic ulcers? Give examples of drugs EXAM Q!!
Final step in acid production is action of H+/K+ ATPase (proton pump). PPIs act to inhibit this enzyme. THey are pro-drugs and are activated in an acidic environment
Omeprazole Lansoprazole Esomeprazole Pantoprazole Rabeprazole
How do antacids work in the management of peptic ulcers? What drug is most used?
Weak bases that interact with gastric acid to produce salts. Raise the gastric pH which inactivates pepsin. Magnesium hydroxide, aluminium hydroxide
What are the side effects of magnesium salts? Aluminium salts?
Diarrhoea
Constipation
How do chelates and complexes work in the management of peptic ulcers? Give drug examples
Protect the gastric and duodenal mucosa by coating mucosa. Stimulate bicarbonate and mucous secretion. Inhibit action of pepsin.
Bismuth chelate
Sucralfate (aluminium hydroxide and sulphated sucrose)