Gastroenterology

Disease Etiology/Pathogenesis Clinical Features Diagnosis Complications Management

Gerd/Reflux LES abnormalities; reduced lower Esophageal -PPI trial Oesophagitis
Esophagitis oesophageal sphincter tone, or basal Heart burn, regurgitation, -Endoscopy (done Barrett’s esophagus (pre-
sphincter tone is normal but reflux occurs dysphagia, water brash (reflex if PPI trial fails or if malignant condition, in which
due to inappropriate sphincter relaxation salivary gland stimulation) alarm symptoms the normal squamous lining of
Defective oesophageal peristalsis in Extraesophageal are present i.e., the lower oesophagus is
patients who have oesophagitis atypical chest pain, >55yrs, dysphagia, replaced by columnar mucosa)
Delayed gastric emptying hoarseness (‘acid laryngitis’), anemia, weight Anaemia
Increased intra-abdominal pressure in recurrent chest infections, loss, positive fecal Benign oesophageal fibrous
pregnancy and obesity chronic cough and asthma occult blood test) stricture
Dietary and environmental factor
Coeliac Immunological Diarrhoea, malabsorption and failure to thrive. In Duodenal biopsy -increased risk of malignancy, Correct existing
Disease Responses To Gluten older children, it may present with non-specific Antibody tests- particularly of deficiencies of
Genetic features, such as delayed growth and pubertal Tissue enteropathyassociated T-cell micronutrients, such as
Association With delay. Mild abdominal distension may be present. transglutaminase lymphoma, small bowel iron, folate, calcium
Human Leukocyte In adults, the presentation is highly variable, (tTG) is now carcinoma and squamous and/or vitamin D, and
antigen depending on the severity and extent of small recognised as the carcinoma of the oesophagus achieve mucosal healing
(HLA)-DQ2/DQ8 bowel involvement. Some have florid autoantigen Ulcerative jejuno-ileitis through a life-long
Dysbiosis of the malabsorption, while others develop non-specific A full blood count Osteoporosis and osteomalacia gluten-free diet(wheat,
intestinal microbiota symptoms, such as tiredness, weight loss, folate may show rye, barley and initially
deficiency or iron deficiency anaemia. Other microcytic or oats)
presentations include oral ulceration, dyspepsia macrocytic anaemia
and bloating.
Peptic Ulcer H. pylori Recurrent abdominal pain that has Endoscopy Perforation; the contents of the H. Pylori eradication; treatment is based on a PPI taken
Disease NSAIDs three notable characteristics: may stomach escape into the simultaneously with two antibiotics (from amoxicillin,
Smoking localisation to the epigastrium, occasionally be peritoneal cavity, leading to clarithromycin and metronidazole) or a quadruple therapy
relationship to food and episodic malignant and peritonitis. sudden, severe regimen, consisting of omeprazole (PPI), bismuth su
occurrence. therefore must pain. The pain initially bcitrate, metronidazole and tetracycline
Occasional vomiting always be develops in the upper Cigarette smoking, aspirin and NSAIDs should be avoided
Vague sense of epigastric unease biopsied and abdomen and rapidly becomes Surgical treatment- for a chronic non-healing gastric ulcer
Anorexia and nausea followed up generalised; shoulder tip pain is partial gastrectomyor Billroth I, and for giant duodenal
Early satiety after meals tested for H. is caused by irritation of the ulcers, partial gastrectomy using a ‘poly’ or Billroth II
Anaemia from chronic undetected pylori infection diaphragm. shallow reconstruction
blood loss, as abrupt haematemesis respiration, and by shock. The Complications of gastric resection/vagotomy
or as acute perforation abdomen is held immobile and Dumping; Rapid gastric emptying with abdominal
there is generalised ‘board- discomfort and diarrhoea
like’ rigidity Duodenogastric bile reflux leading to chronic
Gastric outlet obstruction gastropathy
Bleeding Anaemia; after subtotal gastrectomy iron deficiency is
the most common & folic acid and B12 deficiency are
much less frequent
 Osteoporosis and osteomalacia can occur as a
consequence of calcium and vitamin D malabsorption
Increased risk of gastric cancer
Zollinger– The tumour Triad of severe peptic ulceration, gastric acid Gastric Small and single tumours can be localised and resected
Ellison secretes gastrin, hypersecretion and a neuro-endocrine tumour of the aspiration. In metastatic disease and, in these circumstances, surgery
Syndrome which stimulates pancreas or duodenum Serum gastrin is inappropriate & continuous therapy with omeprazole or
acid secretion to its Severe and often multiple peptic ulcers in unusual sites, levels are other PPIs can be successful in healing ulcers and
maximal capacity such as the post-bulbar duodenum, jejunum or grossly elevated alleviating diarrhoea, although double the normal dose is
oesophagus (10-1000 times) required.
Bleeding, perforations, and diarrhoea
Indications for surgery in peptic ulcer Test for H. Pylori
Emergency Urea Breath Test and Fecal Antigen Test: positive only in
• Perforation • Haemorrhage active infection
Elective Serology
• Gastric outflow obstruction • Persistent ulceration despite adequate Rapid urease test
medical therapy • Recurrent ulcer following gastric surgery Microbial culture
IBD/IBS
Inflammatory Pathophysiology Clinical features Investigations Complications Management
bowel Presence of Ulcerativ Rectal bleeding with passage of mucus and Full blood count may show Haemorrhage Active proctitis:
disease pathogenic factors e colitis bloody diarrhoea anaemia resulting from toxic megacolon (can (inflammation of
such as abnormal Frequent recurrances and rekapse (emotional bleeding or malabsorption occur in both the lining of the
gut microbiota (a stress, intercurrent infection, gastroenteritis, of iron, folic acid or ulcerative colitis and rectum); stool
reduced diversity, antibiotics or nsaid therapy) vitamin B12. Platelet count Crohn’s colitis) and softener
primarily of Tenesmus; frequent and urgent feeling that can also be high as a bacterial toxins pass Active left-sided
Firmicutes and in you need to pass stool, even if your bowels marker of chronic freely across the or extensive
particular, are already empty inflammation diseased mucosa into ulcerative colitis:
Faecalibacterium Abdominal cramps, anorexia, malaise, weight Bacteriology- to exclude the portal and then
prausnitzii), loss and abdominal pain occur and the patient superimposed enteric systemic circulation
immune response is toxic, with fever, tachycardia and signs of infection
dysregulation, peritoneal inflammation Radiology-Barium enema
environmental Ankylosing spondylitis, thromboembolic Endoscopy/
changes, and gene events, migratory polyarthritis Ileocolonoscopy
variants Crohn’s Sites most commonly involved are, in order Ulcerative Colitis: loss of Haemorrhage Acute: ABs
disease of frequency, the terminal ileum and right vascular pattern, Enteroenteric fistulae- (Metronidazole)
side of colon, colon alone, terminal ileum granularity, friability and diarrhoea and Mild/moderate and
alone. The entire wall of the bowl is contact bleeding, with or malabsorption due to severe:
oedematous and thickened, and there are without ulceration blind loop syndrome. Corticosteroids or
deep ulcers that often appear as linear Crohn’s Disease: patchy Enterovesical infliximab and
fissures; thus, the mucosa between them is inflammation, with fistulation causes cyclosporin A
described as ‘cobblestone’. discrete, deep ulcers, recurrent urinary Surgery: Incase of
Abdominal pain, diarrhoea and weight loss strictures and perianal infections and failure of therpy,
disease (fissures, fistulae
 Subacute or even acute intestinal obstruction and skin tags) pneumaturia. An complications
Some patients present with features of fat, enterovaginal fistula (obstruction or
protein or vitamin deficiencies causes a faeculent perforation), &
Anaemia with glossitis and angular stomatitis vaginal discharge failure to grow
Irritable Behavioural and Recurrent abdominal pain (colicky or cramping in nature) in the Done clinically Patient reassureance
bowel psychosocial lower abdomen or discomfort on at least 3 days per month in the Colonoscopy should be Dietary management (wheat-free
syndrome factors; anxiety, last 3 months, associated with two or more of the following: undertaken in older patients diet, some may respond to
(IBS) depression, • Improvement with defecation (over 40 years of age) to lactose, and excess intake of
somatisation, • Onset associated with a change in frequency of stool exclude colorectal cancer. caffeine or artificial sweeteners,
neurosis and panic • Onset associated with a change in form (appearance) of stool Endoscopic examination is such as sorbitol exclusion)
attacks Those with constipation tend to pass infrequent pellety stools, also required in patients who Tricyclic antidepressant
usually in association with abdominal pain or proctalgia. Those with report rectal bleeding to Anti-inflammatory agents, such
diarrhoea have frequent defecation but produce low-volume stools exclude colon cancer and as ketotifen or mesalazine, and
rectal bleeding does not occur IBD the antibiotic rifaximin

Hepatology
Miscellaneous Investigations Management
Hepatitis A RNA Enterovirus Anti-HAV is important in diagnosis, as Prevention by improving social conditions, especially overcrowding and poor
Spread by the faecal–oral route HAV is present in the blood only sanitation
Acute infection transiently during the incubation Immunisation should be considered for individuals with chronic hepatitis b or c
Acute liver failure is rare period infections or close contacts of HAV-infected patients
Immediate protection can be provided by immune serum globulin if this is given
soon after exposure to the virus
Hepatitis B DNA hepadnavirus Serology; polymerase chain reaction Acute Chronic
Acute liver failure (PCR) techniques to measure viral DNA Monitoring for acute liver failure Direct-acting
Spread via blood, saliva, sexual contact levels 5–10% develop a chronic hepatitis b nucleoside/nucleotide
Acute and chronic infection Hepatitis b surface antigen (HBsAg) is an infection that usually continues for antiviral agents; lamivudine,
Most common causes of chronic liver indicator of active infection life, although later recovery and entecavir and tenofovir
disease and hepatocellular carcinoma The persistence of HBsAg for longer than occasionally occurs. Interferon-alfa
Vertical transmission from mother to child 6 months indicates chronic infection Verticalinfection passing from Liver transplantation; post-
in the perinatal period Antibody to HBsAg (anti-HBS) usually mother to child at birth leads to liver transplant prophylaxis
The virus is not directly cytotoxic to cells; appears after about 3–6 months. Anti-HBS chronic infection in the child in with direct-acting antiviral
rather, it is an immune response to viral implies either a previous infection, in 90% of cases and recovery is rare. agents and hepatitis b
antigens displayed on infected hepatocytes which case anti-HBC is usually also Chronic infection is also common in immunoglobulins has
that initiates liver injury present, or previous vaccination, in which immunodeficient individuals, such reduced the reinfection rate
Most patients with chronic hepatitis b are case anti-HBC is not present as those with down’s syndrome or
asymptomatic and develop complications, Chronic HBV infection (see below) is HIV
such as cirrhosis and hepatocellular marked by the presence of HBsAg and Active: Vaccine
carcinoma, only after many years anti-HBC (IgG) in the blood. Usually,
HBeAg or anti-HBE is also present; Passive: Hyperimmune serum globulin
HbeAg indicates continued active
replication of the virus in the liver
Hepatitis C RNA flavivirus Serology and virology; Dual therapy with pegylated
Spread via blood and saliva Anti-HCV antibodies interferon-alfa, given as a weekly
most people remain asymptomatic until progression to cirrhosis occurs, fatigue Active infection is confirmed by the subcutaneous injection, together
can complicate chronic infection and is unrelated to the degree of liver damage. presence of serum hepatitis C RNA in with oral ribavirin, a synthetic
Hepatitis C is the most common cause of what used to be known as ‘non-A, non- anyone who is antibody-positive nucleotide analogue.
B hepatitis’ LFTs may be normal or show direct-acting antiviral agents
Risk factors for progression (from chronic hepatitis to cirrhosis) include male fluctuating serum transaminases (DAAs)
gender, immunosuppression (such as co-infection with HIV), prothrombotic Liver transplantation should be
states and heavy alcohol misuse. considered when complications of
Cirrhosis can progress to ascites and hepatocellular carcinoma cirrhosis occur, such as diuretic-
Jaundice is rare and only usually appears in end-stage cirrhosis resistant ascites
No vaccination
Hepatitis D It requires HBV for replication and has the same sources and modes of spread. It A single antigen to which infected Prevented by hepatitis B
can infect individuals simultaneously with HBV or can superinfect those who are individuals make an antibody (anti- vaccination
already chronic carriers of HBV HDV)
Simultaneous infections give rise to acute hepatitis, which is often severe but is Super-infection of patients with
limited by recovery from the HBV infection. Infections in individuals who are chronic HBV infection leads to the
chronic carriers of HBV can cause acute hepatitis with spontaneous recovery. production of high titres of anti-HDV,
Chronic infection with HBV and HDV frequently causes rapidly progressive initially IgM and later IgG.
chronic hepatitis and eventually cirrhosis
Hepatitis E Clinical presentation and management of hepatitis E are similar to those of In acute infection, IgM antibodies to No vaccination
hepatitis A. Disease is spread via the faecal–oral route or through contaminated hepatitis E virus (HEV) are positive
food; the virus is commonly present in uncooked game and pig-liver sausage
Fulminant hepatitis in pregnant women