GI III Flashcards
(47 cards)
Longitudinal layer of the appendix
The appendix forms a wormlike (vermiform) structure as it does not elongate as rapidly as the rest of the colon.
The average length is 10 cm (range from 2-20 cm). The wall of the appendix consists of two layers of muscle, an inner circular and outer longitudinal. The longitudinal layer is a continuation of the taeniae coli.
The appendix is lined by colonic epithelium. Few submucosal lymphoid follicles are noted at birth. These follicles enlarge, peak from 12-20 years, and then decrease. This correlates with the incidence of appendicitis.
Blood supply to the appendix is mainly from the appendicular artery, a branch of the ileocolic artery. This artery courses through the mesoappendix posterior to the terminal ileum.
The base of the appendix is fairly constant and is located at the posteromedial wall of the caecum about 2.5 cm below the ileocaecal valve. This is also where the taeniae converge. The base is at a constant location, whereas the position of the tip of the appendix varies.
In 65% of patients, the tip is located in a retrocaecal position; in 30%, it is located at the brim or in the true pelvis; and, in 5%, it is extraperitoneal, situated behind the caecum, ascending colon, or distal ileum.
The location of the tip of the appendix determines early signs and symptoms.
Perineal body attachments
Deep transverse perinei
External anal sphincter
Levator ani
Pubovaginalis
The tendinous centre of the perineum or perineal body is a small wedge-shaped mass of fibrous tissue located at the centre of the perineum.
Other structures attached include the external anal sphincter, levator prostate which is a part of levator ani, bulbospongiosus and superficial and deep transverse perinei.
Gastric MALT disease
Gastric MALT tumours are associated with H. pylori infection in approximately 98% of cases, and all that is usually required in low grade disease is eradication therapy.
High grade disease is best treated with chemotherapy, and the prognosis for these tumours is excellent.
Paraproteinaemia is commonly found.
Malabsorption and HPylori
Malabsorption may be associated with numerous disorders but typically occurs with:
Pancreatic exocrine deficiency Short bowel syndromes Coeliac disease, and Inflammatory bowel disease (IBD). Helicobacter is associated with peptic ulceration not malabsorption.
Chronic mesenteric ischaemia is typically associated with pain soon after eating but many patients lose weight due to malabsorption.
Dupuytren’s contracture associations
Alcoholic liver cirrhosis
Diabetes mellitus
Epilepsy IncorrectIncorrect answer selected
Peyronie’s disease
Volkmann’s ischaemic contracture is not associated.
Dupuytren’s contracture is a progressive thickening of the palmar fascia causing a flexion contracture of the hand, mainly affecting the ring and little fingers.
It is also associated with diabetes mellitus.
Crohns disease associations
U AIM APE
Crohn’s disease is associated with:
Arthropathy Ankylosing spondylitis Iritis Malabsorption Erythema nodosum Pyoderma gangrenosum. Urinary oxalate stones
Achalasia features
Achalasia is a functional obstruction of the lower oesphageal sphincter with dilatation of the oesphagus above caused by degeneration of the ganglion cells on the muscle of the mid and lower oesophagus.
The diagnosis is made radiologically, and manometry confirms the diagnosis by showing an elevated sphincter pressure - there is a failure of relaxation of the sphincter.
Dysphagia is an early feature, slowly progressive both for solids and liquids.
Interscapular pain may be associated with pain though not characteristic.
Carcinoma is a rare complication. Iron deficiency is characteristically associated with a post-cricoid web (Patterson Brown-Kelly or Plummer Vinson syndrome) and unrelated disorder of the oesophagus.
UC features
UC is associated with
Arthropathy Ankylosis Ascending cholangitis Sclerosing cholangitis Cholangiocarcinoma Cirrhosis Cholelithiasis. The hepatic features are more typical of UC than Crohn's.
It is also associated with a greater risk of malignancy.
Bile
Normal bile is an alkaline hypotonic electrolyte solution composed of bile pigments and salts, with about 500 ml secreted per day.
A small amount of unesterified cholesterol is excreted in bile.
Ninety five percent of bile salts are absorbed from the terminal ileum.
Reflux oesophagitis
Reflux oesophagitis is associated with
Barrett's oesophagus The use of agents such as steroids Obesity Raised intrabdominal pressure. There is no reliable histological appearance, but it is generally a clinical diagnosis.
GI malignancy conditions
Barrett’s oesophagus
Coeliac disease
Peutz-Jeghers syndrome
Menetrier’s disease
Gastric ulceration is associated with cancer. Duodenal ulceration (untreated by surgery) may afford some protection from gastric cancer.
Barrett’s oesophagus is related to oesophageal carcinoma. Reflux is probably aetiological in Barrett’s oesophagus. There may be an association between chronic reflux and cancer.
Coeliac disease is associated with intestinal lymphoma.
Peutz-Jeghers syndrome, once considered to be benign, is also associated with an increased risk of bowel neoplasia.
Menetrier’s disease is a hypersecretory gastropathy which has an increased risk of gastric cancer. (Meniere’s disease is a condition of the middle ear).
differential diagnosis of a young man with bloody diarrhoea.
Infective causes plus inflammatory bowel disease should be considered in the differential diagnosis of a young man with bloody diarrhoea.
Shigellosis is a possible cause. Most cases of Shigella infection are related to foreign travel. Unrelated to foreign travel, there has been an increase in sexually transmitted Shigella infection in men who have sex with men.
Trophozoites seen in acute dysentery. Cysts for E. Histolitica are not 100% sensitive for amoebic dysentery.
Watery diarrhoea would be expected with cholera and giardiasis.
Gastric cancer assoications
Not with chronic gastric ulcer.
Gastric carcinoma should be considered if the symptoms of the duodenal ulcer return many years after partial gastrectomy. The risk increases above the rate in the normal population about 15 years after surgery. The overall risk is between 3% and 10%.
Helicobacter pylori infection increases the risk of gastric carcinoma by 3-6%.
Ménétrier’s disease is giant hyperplasia of the gastric folds. The patients are often hypochlorhydric.
Pernicious anaemia, associated with atrophic gastritis, increases the risk of gastric carcinoma by a factor of 3.
The risk of gastric carcinoma in blood group A is increased by 16%-20%.
UC > Crohns disease signs
Ulcerative colitis begins in the rectum and progresses proximally. Conversely, the rectum is usually spared in Crohn’s disease.
The characteristic finding in ulcerative colitis is continuous, fine mucosal ulceration with loss of the haustral pattern.
In Crohn’s disease there are discrete and fissured ulcers. These often track deep into the bowel wall and may progress to sinus and fistula formation.
Strictures (often multiple) and skip lesions are also features of Crohn’s disease.
Causes of toxic megacolon
PUS PA
Amoebic dysentery Pneumatosis cystoides intestinalis Pseudomembranous colitis Salmonella gastroenteritis Ulcerative colitis
Complications of amoebiasis include
Fulminant colitis Stricture formation Haemorrhage Amoeboma Amoebic liver abscess. Pseudomembranous colitis is caused by Clostridium difficile and associated with antibiotic use. Symptoms vary from mild diarrhoea to fulminating toxic megacolon. Salmonella is also a recognised cause, particularly in children.
Pneumatosis cystoides intestinalis is associated with chronic bronchitis - multiple gas filled cysts in sub-mucosa of colon. It is mainly asymptomatic, but can cause abdominal pain, diarrhoea and rupture to produce pneumoperitoneum.
Salmonella enterocolitis produces colitis, acute appendicitis in young and mesenteric thrombosis in the elderly.
Regarding colon cancer AR/AD
In familial polyposis coli the increased cancer risk is due to inheritance of a mutated suppressor gene
Both familial polyposis coli and Gardner’s syndrome are autosomal dominant.
An allelic deletion of a putative tumour suppressor gene on 5p.
Quantitative and qualitative alterations in gene expression accumulate in colorectal cancer cells. These include alterations of pro-oncogene expression and chromosomal abnormalities (deletions at 17p and 18q are seen in 70% of colorectal carcinomas).
Peutz-Jeghers syndrome is dominantly inherited pigmentation of skin and mucous membranes, and hamartomatous polyps in the stomach and larger intestine. The polyps only rarely undergo malignant change.
The rectum and sigmoid colon are the commonest sites.
Complications more in UC c.f. Crohns
Toxic megacolon can complicate Crohn’s colitis, pseudomembranous colitis and infectious colitis, but is most commonly seen with severe UC.
Aphthous mouth ulcers are more common with Crohn’s disease than UC but may be seen in up to 10% of patients with active UC.
Despite a widely held view to the contrary, there is good evidence that with the same duration and anatomic extent, the risk of colon cancer in Crohn’s disease is at least as great as with UC. Only a small percentage of those with CD however have extensive colitis.
Gallstones are seen in 15-30% of patients with small bowel Crohn’s disease, due to alterations in the bile salt pool secondary to ileal dysfunction +/- surgical resection.
Perianal fissures/fistulae/abscesses eventually occur in about one third of patients with Crohn’s disease.
Coeliac disease associations
Oesophageal carcinoma is associated with coeliac disease, probably due to the malabsorption syndrome that leads to multiple nutritional deficiencies. There is an association with gastrointestinal lymphomas and, less commonly, adenocarcinoma (most often in the jejunum). Gastrointestinal hamartomas are associated with the hereditary Peutz-Jeghers syndrome.
Gluten-sensitive enteropathy is a disorder in which small bowel mucosal damage is the result of a permanent sensitivity to dietary gluten. The disorder does not present until gluten products have been introduced into the diet. Typically, the most common period of presentation is between six months and two years of age. Incidence is 1:10,000 live births.
Three components interact in the pathogenesis
Toxicity of certain cereals
Genetic predisposition
Environmental factors.
The disorder develops only after chronic dietary exposure to the protein gluten, which is found in wheat, rye, oats, and barley. The activity of gluten resides in the gliadin fraction which contains certain repetitious amino acid sequences (motifs) that lead to sensitisation of lamina propria lymphocytes.
The immunologic response to gluten results in villus atrophy, crypt hyperplasia, and damage to the surface epithelium in the small bowel. The injury is greatest in the proximal small bowel and extends distally for a variable distance.
The mode of presentation is variable; the majority present with diarrhoea. Children can have failure to thrive or vomiting as the only manifestation.
Perhaps as many as 10% of children referred to endocrinologists for growth retardation without an endocrine or overt gastrointestinal disorder have gluten sensitivity.
Anorexia is common and may be the major cause of weight loss or lack of weight gain.
Infants with gluten-sensitive enteropathy are often, but not always, clingy, irritable, unhappy children who are difficult to comfort. In contrast to infants with cystic fibrosis, they are not interested in food, although this is not always the case. Pallor and abdominal distension are common. Large, bulky stools suggestive of constipation have been described in some children with this condition. Digital clubbing can occur.
There is an increased prevalence of gluten-sensitive enteropathy in children with selective IgA deficiency or diabetes mellitus compared to unaffected children. Lymphocytic gastritis occurs in a rare child with gluten-sensitive enteropathy.
The most useful screening test for malabsorption is a microscopic examination of stool for fat.
The two antibody screening tests are: tissue transglutamine antibody (tTGA) and endomysial antibody (EMA).
Other initial studies should include a complete blood count, serum albumin, and serum immunoglobulin levels.
Nutrients that may be measured in blood include
Iron, the level of which depends on transferrin concentration as well as on absorption
Folic acid, the red cell concentration being a more accurate reflection of nutritional status than the serum concentration
Calcium and magnesium
Vitamin D and its metabolites
Vitamin A
Vitamin B12.
Causes of flattened small bowel mucosa
Not Crohns
Autoimmune enteropathy
Giardiasis
Milk protein intolerance
Transient gluten enteropathy
The mucosa in Crohn’s disease depends on the severity. Initially there is superficial apthous ulceration. There may be subsequent florid ulceration and pseudopolyps. There is no flattening of the mucosa.
The diffuse lesion of the upper small intestinal mucosa that characterises coeliac disease is seen in a peroral suction biopsy specimen. Short, flat villi, deepened crypts, and irregular vacuolated surface epithelium with lymphocytes in the epithelial layer are seen by light microscopy. Similar abnormalities occur in other conditions but none is likely to be confused with coeliac disease.
Infections such as Rotavirus enteritis, Giardia lamblia, or tropical sprue can cause villus flattening and elongated crypts, but not the marked abnormalities of enterocytes.
A flat mucosa occurs in kwashiorkor but may represent a response to infestation rather than to undernutrition.
Tropical sprue, a poorly understood tropical enteropathy, can cause a lesion that is indistinguishable from that of coeliac disease.
Some cases of cow’s milk protein or soy protein intolerance are associated with lesions similar to those of coeliac disease in children.
In immune deficiency and eosinophilic gastroenteritis, villi can be partially shortened. Infants with familial enteropathy have short villi, but the crypt dimensions are normal.
Autoimmune enteropathy is a poorly characterised syndrome of chronic diarrhoea and malabsorption.
If symptoms initially develop after the first 6 months of life, the disorder is likely to be mistaken for gluten-sensitive enteropathy.
Typically, the lack of response to a gluten-free diet leads to further evaluation. Histology findings in the small bowel include total villus atrophy, crypt hyperplasia, and an increase in chronic inflammatory cells in the lamina propria.
Specific serum anti-enterocyte antibodies may be identified with indirect immunofluorescent staining, using normal small-bowel mucosa and the kidney. The colon can also be involved.
Extra-intestinal autoimmune disorders are usual and include arthritis, membranous glomerulonephritis, thrombocytopenia, and haemolytic anaemia.
Treatment has included prednisone, azathioprine, cyclophosphamide (Cytoxan), and cyclosporine.
Hypertrophic pyloric stenosis
Hypertrophic pyloric stenosis occurs in approximately 3:1,000 live births. Males (especially first born) are affected approximately four times as often as females. Family clustering occurs.
Pyloric stenosis is associated with other congenital defects including tracheo-oesophageal fistula.
The vomiting usually starts after three weeks of age but symptoms may develop as early as the first week of life and as late as the fifth month.
Non-bilious vomiting is the initial symptom which progressively becomes more vigorous. As vomiting continues there is a progressive loss of fluid, hydrogen ion, and chloride, leading to a hypochloraemic metabolic alkalosis.
The diagnosis is established by palpating the pyloric mass. The mass is firm, movable, approximately 2 cm in length, olive shaped, hard, best palpated from the left side, and located above and to the right of the umbilicus in the mid-epigastrium beneath the liver edge.
Imaging procedures (USS or barium meal) are reserved for those infants in whom the diagnosis remains in doubt.
Infants with GORD
Infants with GOR usually present with
Failure to thrive
Vomiting
Recurrent pneumonias.
Older children may present with heartburn.
Severe oesophagitis may require proton pump inhibitors.
Barrett’s ulcers result from chronic GOR causing metaplasia of oesophagus to gastric epithelium.
In children with recurrent croup with no infective symptoms, GOR should be considered.
Symptoms usually improve as the lower oesophageal sphincter tone improves with age.
Worse prognosis signs in pancreatitis
If a patient has an modified Imrie score of 2 or greater they are considered to have severe acute pancreatitis (which carries a mortality rate of 30%).
A CT scan of the abdomen should be performed on the third day after the onset of symptoms; findings which carry a worse prognosis are peri-pancreatic fluid or evidence of haemorrhage or necrosis.
Positive blood cultures are significant as they may represent infected pancreatic necrosis (mortality more than 50%).
There appears to be no difference in outcome depending on the aetiology, however alcoholics appear to have more attacks.
Imrie criteria age more than 55 and hypocalcaemia are both positive parameters.
Predisposing factors in oesophageal cancer
Excess alcohol is mainly associated with squamous cell carcinoma (SCC) of the oesophagus. Other factors in the development of SCC of the oesophagus are:
smoking
human papilloma virus
Plummer-Vinson syndrome, and
tylosis (autosomal dominant with a risk of 70%).
Cancer of the stomach is associated with:
blood group A
pernicious anaemia
partial gastrectomy
atrophic gastritis.
Foramen of Bochdalek and congenital hernias
Congenital diaphragmatic hernias occur in approximately 1 in 4,000 live births.
Ninety percent occur in the posterior portion of the diaphragm through the foramen of Bochdalek and 90% occur on the left.
The commonest clinical presentation is with respiratory distress in the neonatal period and due to pulmonary hypoplasia and compression. The abdomen often has a scaphoid appearance.
About 40% of patients have associated congenital anomalies.
The diagnosis can be confirmed radiologically with bowel loops seen in the chest.
Neonates usually require sedation, ventilation and intestinal decompression prior to surgery between 36 and 72 hours after birth.
