GI Flashcards
What is an anal fissure?
Painful tear in sensitive skin-lined lower anal canal, distal to dentate line resulting in pain on defecation
Which type of anal fissure is most common?
90% posterior
Anterior tend to be in childbirth
Women most affected
Isolated primary problem in young middle aged adults or can occur when associated with Crohn’s or ulcerative colitis
What are the main causes of anal fissures?
Hard faeces
Spasm constricting inferior rectal artery resulting in ischaemia making healing difficult and perpetuating problem
Rare causes - syphilis, herpes, trauma, Crohn’s, anal cancer
How do anal fissures present?
Extreme pain on defecation
Bleeding
How are anal fissures diagnosed?
Can usually be made on history
Confirmed on perianal inspection
Rectal examination often not possible due to pain and sphincter spasm
How are anal fissures treated?
Increased dietary fibre and fluids to make stools softer
Lidocaine ointment and GTN ointment or topical diltiazem
Botulinum toxin injection
Surgery if medication fails
What is an anal fistula?
An abnormal connection between epithelised surface of anal canal and skin - track communicates between skin and anal canal/rectum
Blockage of deep intramuscular gland ducts thought to predispose to formation of abscesses with discharge to form fistula
What are the main causes of anal fistulas?
Perianal sepsis Abscesses Crohn's TB Diverticular disease Rectal carcinoma
How do anal fistulas present?
Pain
Discharge - bloody/mucus
Pruritus ani (itchy bottom)
Systemic abscess if becomes infected
How are anal fistulas diagnosed?
MRI to exclude sepsis and detect associated conditions
Endoanal ultrasound - determines track location and underlying causes
How are anal fistulas treated?
Surgery - fistulotomy and excision
Drain abscess with antibiotics if infected
How common is appendicitis?
Most common surgical emergency
More common in men
Can occur at any age but highest incidence in 10-20 yrs
Rare before aged 2 as appendix cone shaped with larger lumen
What can cause appendicitis?
Faecolith (stone made of faeces)
Lymphoid hyperplasia
Filarial worms
What is the pathology of appendicitis?
Occurs when lumen of appendix becomes obstructed by one of the causes resulting in invasion of gut organisms into appendix wall
Leads to oedema, ischaemia, necrosis, and perforation as well as inflammation
If appendix ruptures then infected and faecal matter will enter peritoneum leading to life threatening peritonitis
How does appendicitis present?
Pain in umbilical region that migrates to RIF, specifically McBurney's point after a few hours Colicky pain Anorexia Nausea, vomiting, occasionally diarrhoea Constipation Examination of abdomen = tenderness in RIF with guarding due to localised peritonitis Tender mass in RIF Pyrexic
Name 5 differential diagnoses for appendicitis
Acute terminal ileitis due to Crohn's Ectopic pregnancy UTI Diverticulitis Perforated ulcer Food poisoning
How is appendicitis diagnosed?
Bloods - raised WCC with neutrophil leucocytosis, elevated CRP with ESR USS - detects inflamed appendix CT - high sensitive and specific Pregnancy test to exclude Urinalysis to exclude UTI
How is appendicitis treated?
Surgery - appendicectomy laproscopically
IV antibiotics pre-op to reduce wound infections
If appendix mass present - IV fluids and antibiotics until mass disappears over a few weeks
What are the main complications of appendicitis?
Perforation - commoner with faecolith
Appendix mass - when inflamed appendix becomes covered in omentum foriming a mass - USS/CT, treat with antibiotics then surgery to remove appendix later to prevent further events
Appendix abscess - result if appendix mass fails to resolve but instead enlarged and patient gets more unwell, treat by draining appendix, antibiotics
What is ischaemic colitis?
AKA chronic colonic ischaemia
Low flow to IMA territory, ranging from mild ischaemia to gangrenous colitis
What does AF with abdominal pain suggest?
Mesenteric ischaemia
Which areas of the bowel are most at risk of ischaemia?
Watershed areas in splenic flexure and caecum are most susceptible to ischaemia
How common is acute mesenteric ischaemia?
Usually in those over 50
Almost always involves small bowel
How common is ischaemic colitis?
Usually older age group
Related to underlying atherosclerosis and vessel occlusion
In young - associated with contraceptive pill use - thrombophilia and vasculitis
What are the main types of bowel ischaemia?
Acute mesenteric ischaemia
Chronic mesenteric ischaemia
Ischaemic colitis
What are the causes of acute mesenteric ischaemia?
Superior mesenteric artery thrombosis
Superior mesenteric embolism due to AF
Mesenteric vein thrombosis
Non-occlusive disease - low flow states, poor CO
What are the causes of ischaemic colitis?
Thrombosis Emboli Decreased CO and arrhythmias Drugs - oestrogen, antihypertensives, vasopressin Surgery - cardiac bypass, aortic dissection and repair, aortoiliac reconstruction Vasculitis Coagulation disorders Idiopathic
What can increase your risk of getting ischaemic colitis?
Contraceptive pill
Niorandil drug
Thrombophilia
Vasculitis
What occurs in ischaemic colitis?
Occlusion of branch of SMA or IMA often in older age
How does acute mesenteric ischaemia present?
Acute severe abdominal pain - constant, central or around RIF
No abdominal signs
Rapid hypovolaemia resulting in shock - pale skin, weak rapid pulse, reduced urine output, confusion
How does ischaemic colitis present?
Sudden onset lower left side abdominal pain
Passage of bright red blood with/without diarrhoea
Signs of shock and evidence of underlying CVS disease
What could be a differential diagnosis of ischaemic colitis?
Other causes of acute colitis eg IBD
How is acute mesenteric ischaemia diagnosed?
Bloods - raised Hb due to plasma loss, raised WCC, persistent metabolic acidosis
Abdo x-ray - rule out other pathology, gasless abdomen
Laparotomy - to make diagnosis, may see necrotic bowel if not treated quickly
CT/MRI
How is ischaemic colitis diagnosed?
Urgent CT to exclude perforation
Flexible sigmoidoscopy - biopsy shows epithelial cell apoptosis
Colonoscopy and biopsy
Barium enema
How is acute mesenteric ischaemia treated?
Fluid resuscitation
Antibiotics
IV heparin to reduce clotting
Surgery to remove death bowel
How is ischaemic colitis treated?
Fluid replacement
Antibiotics
Most recover but strictures common
What are the potential complications of acute mesenteric ischaemia?
Septic peritonitis
Systemic inflammatory response syndrome progressive to multi-organ dysfunction syndrome, mediated by bacterial translocation across dying gut wall
What are the potential complications of ischaemic colitis?
Gangrenous ischaemic colitis - presents with peritonitis and hypovolaemic shock
Requires prompt resucitation followed by surgical resection of affected bowel and stoma formation
High mortality
What is coeliac disease?
Condition where there is inflammation of mucosa of upper small bowel that improves when gluten is withdrawn from diet and relapses when gluten is reintroduced
T cell mediated autoimmune disease of small bowel in which prolamin intolerance causes villous atrophy and malabsorption
What are prolamins?
Gliandin in wheat, hordeins in barley and secalins in rye
Component of gluten protein
How common is coeliac disease?
1% of population affected
Occurs at any age but peaks in infancy and 50-60 years
Affects males and females equally
10% risk in 1st degree relatives with 30% risk in siblings
What factors can increase your risk of getting coeliac disease?
Other autoimmune diseases - T1DM, thyroid disease, Sjorgrens IgA deficiency Breast feeding Age of introduction to gluten in diet Rotavirus infection in infancy Viral infections Dysbiosis
What is the pathology of coeliac disease?
Prolamin a-gliandin is toxic and resistant to digestion by pepsin and chymotrypsin due to high glutamine and proline content and remain in intestinal lumen triggering immune response Gliandin peptides pass through epithelium and deaminated by tissue transglutaminase increased immunogenicity Gliandin peptides bind to APCs which interact with CD4+ T cells in lamina propria via HLA class II molecultes DQ2/DQ8 HLA class II molecules activate gluten sensitive T cells = pro-inflammatory cytokines initiating inflammatory cascade Cascade releases metaloproteinkinases and other mediators which contribute to villous atrophy, crypt hyperplasia and intraepithelial lymphocytes typical of disease that result in malabsorption
What can mucosal damage lead to?
Malabsorption
Mucosa of proximal small bowel predominantly affected meaning that B12, folate and iron cannot be absorbed resulting in anaemia
Mucosal damage increases in severity towards ileum as gluten digested into small non-toxic fragments
How does coeliac disease present?
1/3 asymptomatic and only detected on routine bloods Stinking stools/fatty stools Diarrhoea Abdominal pain Bloating Nausea and vomiting Angular stomatitis Weight loss Fatigue Anaemia Osteomalacia - lack of phosphate, calcium and Vit D Dermatitis hepetiformis
How is coeliac disease diagnosed?
Maintain gluten for at least 6 weeks before testing to get true results
FBC - low Hb, low B12, low ferritin
Duodenal biopsy - see villous atrophy, crypt hyperplasia and increased intraepithelial WCC
Serum antibody testing - IgA inceased (endomysial and tissue transglutaminanse antibodies)
How is coeliac disease treated?
Lifelong gluten free diet
Correction of vitamin and mineral deficiencies
DEXA scan to monitor osteoporotic risk
What are the complications of coeliac disease?
Non-responsive coeliac disease (do not improve on strict diet)
Anaemia
Secondary lactose intolerance
T cell lymphoma
Increased risk of malignancy (gastric, oesophageal, bladder, breast and brain) due to increased cell turnover
Osteoporosis
What is a colonic polyp?
Abnormal growth of tissue projecting from colonic muscosa
Range from a few millimetres to severe centimeters and are single or multiple
Adenomas - type of polyp, precursor lesions in most cases of colon cancer - benign, dysplastic tumour of columnar cells or glandular tissue
Most polyps asymptomatic and found by chance
How common are polyps?
Adenoma presence increases with age and rare before 30
Polyps removed at colonoscopy to reduce development into cancer risk
Polyps in rectum or sigmoid colon present with bleeding
How common is colorectal carcinoma?
3rd most common cancer worldwide Usually adenocarcinoma Majority occur in distal colon Majority of presentations over 60 More common in men More common in Western countries
What are the two types of inherited polyps?
Familial adenomatous polyps - autosomal dominant condtion arising from mutation in APC gene, characterised by presence of hundreds to thousands of colorectal and duodenal adenomas, develop adenomas at 16 and cancer at 39
Lynch syndrome - polyps form in colon and may rapidly progress to colon cancer, autosomal dominant condition caused by mutation in one of DNA mismatch repair genes, genes responsible for maintaining stability of DNA during replication, increased risk of DNA damage in replication and thus colorectal carcinoma development
What can increase your risk of developing colorectal carcinoma?
Increasing age Low fibre diet Saturated animal fat and red meat consumption Sugar consumption Alcohol and smoking Colorectal polyps Obestiy Adenomas UC FHx Genetic predisposition - FAP, lynch syndrome
What can reduce your risk of developing colorectal carcinoma?
Vegetables Garlic Milk Exercise Low-dose aspirin
What is the pathology of colorectal carcinoma?
Normal epithelium - adenocarcinoma - colorectal adenocarcinoma
Polypoid mass with ulceration
Spread by direct infiltration through bowel wall then spread to lymphatic and blood vessels and metastasis to liver and lung
How does right sided colorectal carcinoma present?
Usually asymptomatic until present with iron deficiency anaemia due to bleeding Mass Weight loss Low Hb Abdominal pain
How does left sided colorectal carcinoma present?
Change of bowel habit with blood and mucus in stools Diarrhoea Alternation constipation and diarrhoea Thin/altered stools Blood in stools
How does rectal carcinoma present?
Rectal bleeding and mucus
When cancer grows - thinner stools and tenesmus
What is the emergency presentation of colorectal carcinoma?
Obstruction - absolute constipation, colicky abdominal pain, abdominal distension, vomiting
What could be a differential diagnosis for colorectal adenocarcinoma?
Anorectal pathology - haemorrhoids, anal fissure, anal prolapse
Colonic pathology - diverticular disease, IBD, ischaemic colitis
Small intestine and stomach pathology - massive upper GI bleed, Meckle’s diverticulum
How is colorectal adenocarcinoma diagnosed?
Faecal occult blood Tumour markers Colonscopy - biopsy and removal of polyps Double contract barium enema CT colonoscopy MRI to determine spread
How is colorectal carcinoma classified?
Dukes classification
A - limited to muscularis muscosa
B - extension through muscularis muscosa
C - involvement of regional lymph nodes
D - distant metastases
TMN system
T - primary tumour, sufficed by number denoting tumour size
N - lymph node status, number denotes number of lymph nodes/groups of lymph nodes containing metastases
M - anatomical extent of distant metastases
How is colorectal adenocarcinoma treated?
Surgery - only chance of cure, only indicated if no metastasis
Laproscopic
Endoscopic stenting - malignant obstruction, reduces need for colostomy
Radio/chemotherapy
Treated differentially - polyp cancers/rectal cancers
What is Crohn’s disease?
Chronic inflammatory bowel disease characterised by transmural (deep in mucosa) granulomatous inflammation affecting any part of gut from mouth to anus
Can be unaffected bowel between areas of active disease called skip lesions
How common is Crohn’s disease?
Highest incidence and prevalence in Northern Europe, UK, and North America Lower incidence than UC per year Prevalence less if Asian Affects women more than men Unknown cause Smoking increases risk by 3-4x 1 in 5 patients have first-degree relative with disease Presentation mostly at 20-40 years
What can increase your risk of Crohn’s?
Genetic associations stronger than UC - mutations on NOD2 gene on chromosome 16 increases risk
Smoking NSAIDs may exacerbate disease
FHx
Chronic stress and depression triggers flares
Good hygiene - those in poor hygiene families have lower risk of developing CD
Appendicectomy may increase risk of CD development
What does Crohn’s disease look like marcroscopically?
Transmural granulomatous inflammation affecting any part of gut from mouth to anus
Not continuous - skip lesions
Involved bowel usually thickened and often narrowed
Cobblestone appearance due to ulcers and fissures in muscosa
Affects any part of GI tract
What does Crohn’s look like microscopically?
Inflammation extends through all layers (transmural) of bowel
Increase in chronic inflammatory cells and there s lymphoid hyperpalsia
Granulomas present - non-caseating epithelioid cell aggregates with Langerhan’s giant cells
Goblet cells present
Less crypt abscesses’ than in UC
How does Crohn’s disease present?
Diarrhoea with urgency (need to go 5-6 times in 45 mins) Bleeding Pain due to deification Abdominal pain Weight loss Malaise Lethargy Anorexia Abdominal tenderness/mass Perianal abscess Anal strictures Extraintestinal signs - aphthous ulcerations, clubbing, skin, joint, eye problems
What could be a differential diagnosis for Crohn’s?
Alternative causes of diarrhoea
Chronic diarrhoea
How is Crohn’s diagnosed?
Examination - tenderness of RIF, anal exam
Bloods - anaemia due to malabsorption (iron and folate deficiency), B12 anaemia unusual, raised ESR, CRP, WCC and platelets, hypoalbuminaemia in severe disease, liver biochemistry may be abnormal, negative pANCA
Stool sample to exclude infectious causes
Faecal calprotectin - indicated IBD
Colonscopy - biopsy sses skip lesions and granulomatous transmural inflammation
Upper GI endoscopy - exclude oesophageal and gastroduodenal disease
How is Crohn’s treated?
Smoking cessation
Anaemia treated with replacement
Mild attacks - controlled release corticosteroids
Moderate to severe - glucocorticoids
Severe - IV hydrocortisone, treat rectal disease (hydrocotisone per rectum), antibiotics (IV metronidazole for perianal disease and abscesses), if improvement transfer to oral prednisolone
If not improvement switch to anti-TNF antibodies
Maintain remission - azathioprine, methotrexate, anti-TNF antibodies
Surgery - avoided and only minimal resection, indicated in medial therapy failure, failure to thrive and perianal sepsis, temporary ileostomy
What are the potential complications of Crohn’s disease?
Perforation and bleeding Fistula formation Anal - skin tags, fissure, fistula Malabsorption Small bowel obstruction as grossly dilated Toxic dilatation of colon Colorectal cancer Venous thrombosis Amyloidosis
What is diarrhoea?
Abnormal passage of loose of liquid stool more than 3 times daily
What are the main differences between acute and chronic diarrhoea?
Acute - lasts less than 2 weeks, usually due to infection eg Travellers diarrhoea
Chronic - lasts more than 2 weeks, organic causes, anatomical changes, must be differentiated from functional causes - no physical cause for symptoms
What three things can cause decreased stool consistency?
Water
Fat
Inflammtory discharge
What are the different types of water caused diarrhoea?
Osmotic - large quantities of non-absorbed hypertonic substances in bowel draw fluid into intestine, stops when patient stops eating or malabsorptive state discontinued - causes ingestion of non-absorbable substances, generalised malabsorption, specific malabsorptive defect
Secretory - mircoscopic colitis, active intestingla secretion of fluids and electrolytes as well as decreased absorption, continues even when patient fasts - causes enterotoxins (E coli), bile salts in colon following ileal disease, resection or idiopathic bile malabsorption, fatty acids in colon following ileal resection
What does steatorrhoea look like?
Increased gas, offensive smell, floating hard to flush stools
Causes - giardiasis and coeliac disease
Why does inflammatory discharge produce decreased stool consistency?
Damage to intestinal mucosal cells lead to fluid loss and blood and defective absorption of fluid and electrolytes
Causes - infective (shigella or salmonella) or inflammatory eg UC or Crohn’s
How does diarrhoea present?
Sudden onset of bowel frequency associated with crampy abdominal pains and a fever will point to infective cause
Bowel frequency with loose, blood stained stools will point to an inflammatory cause
Passage of pale, offensive stools that float often accompanied by a loss of appetite and weight to steatorrhoea
How is acute diarrhoea diagnosed?
Flexible sigmoidoscopy with colonic biopsy performed if symptoms persist and no diagnosis made
How is chronic diarrhoea diagnosed?
Faecal markers of intestinal inflammation used to differentiate functional disorders from organic disease
How is acute diarrhoea treated?
Treatment symptomatic to maintain hydration with anti-diarrhoeal agents (loperamide hydrochloride) for short term relief and antibiotics for specific indications
What is diverticulitis?
Outpouching of gut wall, usually at sites of entry of perforating arteries
Diverticulosis - presence of diverticula
Diverticular disease - diverticula symptomatic
Diverticulitis - inflammation of diverticulum
How common is diverticulitis?
Frequently found in colon
50% patients over age 50
Most frequent in sigmoid colon, can present throughout whole colon
Diverticulum can be acquired or congenital and may occur elswehere but most important are acquired colonic diverticula
Rare in young
95% asymptomatic
What can cause diverticulitis?
Low fibre diet - commonly eaten in developing countries, rare in rural Africa
Obesity
Smoking
NSAIDs
What can increase your risk of getting diverticulitis?
Low fibre diet
Over the age of 50
How do diverticula form?
Form at gap in wall of gut where blood vessels penetrate
In low fibre diet, colon must push harder to move things along (fibre helps gut motility) so pressure increases
Pressure increase results in pouches of mucosa being extruded through muscular wall through weakened areas near blood vessels leading to diverticula formation
Thickening of muscle layer
When does acute diverticulitis occur?
Occurs when faeces obstruct the neck of diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation
Can lead to bowel perforation, abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death
How does diverticular disease present?
In 95% of cases, asymptomatic and detected incidentally on colonoscopy or barium enema examination
Intermittent LIF pain
Erratic bowel habit
Severe pain and constipation due to luminal narrowing
How does acute diverticulitis present?
Most commonly affects diverticula in sigmoid colon
Severe pain in LIF
Fever and constipation
Symptoms and signs similar to appendicitis but located on L side
On examination
- Febrile, tachycardia, abdominal examination (tenderness, guarding, rigidity on left side of abdomen, palpable tender mass sometimes felt in LIF)
How is diverticular disease diagnosed?
Colonscopy
How is acute diverticulitis diagnosed?
Bloods - polymorphonuclear leucocytosis (increased), ESR and CRP raised
CT colongraphy - will show colonic wall thickening and diverticucla, pericolic collections and abscesses, diagnostic
Abdominal x-ray - identify obstruction or free air
Barium enema
NO SIGMOIDOSCOPY OR COLONOSCOPY DURING ACUTE ATTACK
How is diverticular disease treated?
Well balanced high fibre diet with smooth muscle relaxants
How is acute diverticulitis treated?
Mild attacks - oral antibiotics
Those with signs of systemic upset and significant abdominal pain required bowel reset, IV fluids and IV antibiotics
Surgical resection occasionally
What are the complications of diverticultitis?
Perforation - paracolic or pelvic abscess or generalised peritonitis
Fistula formation into bladder resulting in dysuria or pneumaturia, vagina resulting in discharge
Bleeding
Mucosal inflammation - occurs in areas of diverticula, giving appearance of Crohn’s on endoscopy
What is Meckle’s diverticulum?
Most common congenital abnormalitiy of GI tract
Diverticulum projects from wall of ileum
How common is Meckle’s diverticulum?
Affects 2-3% population
What occurs in Meckle’s diverticulum?
In 50% cases, distal ileum contains gastric mucosa that secretes HCl meaning peptic ulcers can occur which may bleed or perforated
Usually asymptomatic
Acute inflammation occurs and is indistinguishable clinically from acute appendicitis
How is Meckle’s diverticulum treated?
Surgical removal of diverticula, often laparoscopically
What is the most common type of gastric cancer?
Adenocarcinoma
How common are gastric tumours?
4th most common cancer worldwide
More common in men
Incidence increases with age - peak at 50-70
Rare under 30
Highest incidence in Eastern Asia, Eastern Europe and South America
What are the two types of gastric tumours?
Intestinal (type 1) - well formed, differentiated glandular structures, tumours polypoid or ulceration lesions with heaped up, rolled edges, intestinal metaplasia seen in surrounding mucosa, often with H pylori, more likely to involve distal stomach and occur in patients with atrophic gastritis, strong environmental association
Diffuse (type 2) - poorly cohesive undifferentiated cells, tend to infitrate gastric wall, can involve any part of stomach, especially cardia, worse prognosis than intestinal
What can cause gastric cancer?
Smoking
H pylori infection - chronic gastritis - atrophic gastritis and pre-malignant intestinal metaplasia
Dietary factors - high salt and nitrates increase risk, non-starchy vegetables, fruit, garlic and low salt decrease risk
Loss of p53 (tumour supressor gene) and APC genes
First degree relative with gastric tumour - CDH1 gene
Pernicious anaemia - increases risk due to accompanying atrophic gastritis
What can increase your risk of getting gastric tumours?
First degree relative with gastric cancer
Smoking
High salt and nitrates
How does H pylori cause gastric cancer?
Acute gastritis Chronic active gastritis Atrophic gastritis Intestinal metaplasia Dysplasia Advanced gastric cancer
How does gastric cancer present?
Most present with advanced disease
Epigastric pain indistinguishable from peptic ulcer disease, pain constant and severe
Nausea, anorexia
Weight loss
Vomiting frequent and can be severe if tumour encroaches on pylorus
Dysphagia is in fundus
Anaemia from occult blood loss
Liver metastasis resulting in jaundice
Metastases in bone, brain and lung
Palpable lymph node in supraclavicular fossa
How is gastric cancer diagnosed?
Gastroscopy and biopsy to histologyically confirm adenocarcinoma
Endoscopic ultrasound to evaluate depth of invasion
CT/MRI for staging
PET scan to identify metastases
