GI Flashcards
What are the anatomic and motor disorders of the oesophagus
- Stenosis- congenital or acquires- progressive dysphasia due to stricture
- Atresia (oesophagus not developed properly) /fistula - newborn with aspiration, pneumonia/ rest distress
- Perforation- acquired, traumatic- results in mediastinitis
- Achalasia - dysmotility of lower 1/3 and proximal dilation - stasis of food causes inflammation - predisposed to SCC of oesophagus
- Varicies- increased portal venous HTN- Dilated submucosal veins at portosystemic anastamosis
What are the features of oesophagitis
- Commonest is reflux oesophagitis
- Caused by regurgitation of gastric content into lower oesophagus -GORD
- Incompetent lower oesophageal sphincter, increased intrabdominal pressure
- Heart burn, dysphagia
Complications:
Ulceration - inflam and necrosis of squamous epithelium
Stricture and stenosis- chronic inflam and fibrosis
Barrett’s metaplasia- replacement of stratified squamous epithelium with columnar mucosa
Describe the features of Barretts oesophagus
- Metaplastic columnar mucosa - red on endoscopy
- Squamous mucosa changes to columnar
Name an infectious type of oesophagitis
- Candida
- more common in diabetes/ immunocompromised
- White plaques on endoscopy with hyphae
Discuss herpes oesophagitis and eosinophilic oesophagitis
Herpes- Associated with odynophagia- pain drinking hot and cold liquids
- Usually in immunocompromised - leukaemia, lymphoma
- Punched out ulcers
Eosinophilic- Eosinophilia in blood, concentric ring in trachea
-Common in young men
What are the two main types of oesophageal cancer
-Squamous carcinoma (middle 1/3) and Adenocarcinoma (distal 1/3)
SCC- most common type
Risk factors -alcohol and tobacco, Dietary fungi, achalasia, genetics
3 patterns
1. Necrotising malignant ulcer
2. Polypoid luminal mass
3. 3 Diffuse neoplasms causing stricture
Adenocarcinoma- on the rise in west - obese middle aged white men
Risk factors - GORD, obesity , barretts oesophagus, alcohol tobacco
Affects distal 1/3 with similar patterns to SCC
How do doctors deal with Barrets metaplasia
- Endoscopic surveillance to detect dysplastic change
- If dysplastic change- radio frequency ablation of barretts mucosa
-Many patients only present when disease is very advanced
How is oesophageal cancer staged
-By depth and invasion of primary tumour through wall
T3 = invasion of muscular propria
pT3 N1 is most common stage that patients present at- invasion through oesophageal wall and into lymph nodes and perioesophageal tissues - may also have mets - present with dysphasia and weight loss
Advanced pt3 Ni - chemo then surgery or chemo and radio / stenting
What causes acute/ erosive gastritis
- NSAIDS/ ferrous sulphate
- Alcohol
- Ingestion of corrosives
- Cancer chemo
- Uraemia
- Severe stress/ shock
- Ischaemia
What are the causes of chronic gastritis
Type A - auto-immune lymphocytic, pernicious anaemia
Type B- chronic active gastritis due to H.pylori (gram neg rod colonises gastric muscosa, secretes urease and brings on inflam reaction - ammonia breath test)
Type C - mucosal injury and regenerative change- reflux of bile or drug exposure (NSAIDS and alcohol)
What are the complications of H. Pylori infection
-Gastritis
-Peptic ulcers , duodenal and gastic ulcers (if infection is in antrum of stomach)
-Atrophy, intestinal metaplasia- body of stomach infection
-Gastric carcinoma
-Gastric lymphoma
-Bleeding - haematemasis or melaena
-Perforation
Scarring/ stenosis of pylorus
Types of Gastric carcinoma and their features
-Intestinal type carcinoma - lymphovascular spread and vascular, hepatic mets more likely to form one tumour compared to other type
-Diffuse type gastric carcinoma- involvement of stomach wall causing linitis plastic (when stomach wall becomes rigid)
Associated with peritoneal spread and mets - ovarian tumours
- Weight loss, anorexia , epigastric mass
- Mets of Virchows node
- Spread to ovaries- Krunkenberg tumours contraindicaton for surgery
What causes gastric lymphoma
- Longstanding H. pylori infection leading to accumulation of lymphoid follicles
- MALT - mucosa associated lymphoid tissue - can progress to low grade malignant lymphoma
- Eradication of H.pylori at this stage can cause lymphoma regression , some can’t
What are GI stromal tumours
- mesenchymal spindle tumours
- Stomach and bowel particularly affected
- Big ones= malignant- Dumbell shaped
- Can cause liver mets
- CD117 tyrosine kinase defect
- Imatininb inhibits tyrosine kinase ans is used to treat
Discuss the features of a small intestine adenocarcinoma
- Less common than colonic adenocarcinoma
- Usually sporadic
- Common sites are duodenal (associated with FAP) and jejunum (napkin ring stricture)
- Many associated with Crohn’s or coeliac
- Often present late - poor prognosis
Discuss the features of a small intestine carcinoid tumour
- A neuroendocrine tumour- low/ intermediate grade malignancy
- Appendix (best site to get) then stomach, ileojejunal= worst place to get
- If greater than 2cm its 80% likely to met
- Synthesises peptids and can cause carcinoid syndrome
To diagnose carcinoid syndrome
-Urinary 5HIAA (breakdown of serotonin)
Facial flushing, sweating, wheezing , diarrhoea , right sided hf - endocardial fibrosis
Discuss the features of malignant lymphomas in the small intestine
- Primary or secondary to systemic disease
- Classified by subtype and staging - CT scan, bone marrow
- T Cell = worse prognosis than B cell
Various types
- MALT- Mucosa associated lymphoid tissue lymphoma - most common, low grade B cell especially in stomach- H. Pylori
- Burkitts lymphoma - Children/ young adults/ terminal ileum/ chemoresponsive
- Follicular lymphoma- low grade b cell, duodenum or mesenteric nodes
- Mantle cell lymphoma - intermediate grade - in large bowel
- Enteropathy associated T-cell lymphoma - aggressive high grade - coealiac disease associated. Ileum and jejunum
- Post transplant lymphoproliferative disorder - EBV driven, patients on immunosuppression
Discuss the features of small bowel metastases
Can come from
- colon
- lung
- Ovary
- Stomach
- Lobular carcinoma of breast
- Metastatic melanoma
What are the various types of colorectal polyps
Hyperplastic - very common, little malignant potential
Adneomatous polyps - common but increased risk of malignancy, a mix of tubular and villous polyps , dysplastic
Discuss familial adenomatous polyposis
- Hundreds of adenomatous polyps
- Autosomal dominant
- High risk of colorectal adenocarcinoma in 30s/ 40s
Discuss the features of colorectal adenocarcinoma
- Usually sporadic
- More common in west - diets high in saturated animal fats and low in fibre
- Can be due to
- Hereditary non polyposis colon cancer mutation in DNA repair genes
- FAP
- IBD - esp ulcerative colitis and sclerosis cholangitis
What is the adenoma carcinoma sequence
Sequence of changes associated with tumour progression
Associated with the acquisition of increased numbers of molecular abnormalities - somatic mutations in oncogenes, tumour surpressor genes act
Number of genes changing= important in sequence
What is the vogelstein model of colon cancer
All contribute to development of colon cancer
- Instability of chromosomes and CIN gene mutations
- MSI pathway causes mismatch repair inactivation so inactivates tumour suppressor genes ]
- Activation of oncogenes
Discuss the clinical features of colorectal cancer
- Suspect in any bowel change in an older person*
- Anaemia
- Abdo mass
- Abdo pain
- Change in bowels
- Bleeding
- Incontinence
- Obstruction
- Tenesmus
- Rectal mass
How is colorectal cancer staged
TNM or Dukes system
Spread is most powerful prognostic factor
Important!!!!! TNM staging pT1- submucosa pT2 - muscle coat pT3 - subserosa/ mesentery pt4 - serosa/ perforation/ adjacent organs
pN1 1-3 lymph nodes
pN2 over 3 lymph nodes
M1 - Mets
Why is the anatomy of the rectum hard for tumour treatment
Upper 1/3 rectum completely covered by peritoneum except posteriorly
Middle and vital third are extra-peritoneal with soft tissue margin
In rectal surgery- total mesolectal excision - complete removal of fatty connective tissue around the rectum - crucial to prevent recurrence
What are the features of tumours of the appendix
- Mucocoele- dilated mucus filled mass- obstructed or non obstructed
- Can be due to cystadenoma or cysadrenocarcinoma - low grade
- Associated with mutinous ovarian tumours or occult colorectal neoplasia - mets spread into peritoneal cavity if mucoseal ruptures
Carcinoid tumours of appendix (endocrine cell tumours)
- Most common usually at tip
- All age groups but more females
- Small
- Goblet cell differentiation= most aggressive
Discuss tumours of the anus
Upper half
-Columnar mucosa
Lower half
-Squamous muscosa (SCC)
Anus and oesophagus are two primary sights for malignant melanoma
- Warts HPV 6/11
- Anal intraepithelial neoplasia HPV 16/18
Anal canal squamous cell carcinoma = HPV related/ immunosuppression
- Low rectal tumour
- 2 types basaxoid or keratinising squamous cell carcinoma
- Treat via chemoradiotherapy
Discuss the features of a chronic peptic ulcer and what are the complications
- May affect stomach or duodenum
- Some ulcers are malignant- ulcerating adenocarcinoma but peptic ulcers in duodenum usually benign
- Acid and helicobacter pylori related
- Foodstuffs , alcohol , smoking ,stress related , NSAIDs, crohns, corticosteroids, zollinger- ellison syndrome
Complications
- Haematemasis , malena , chronic anaemia
- Gastric outlet obstruction - exclude cancer first especially when ulcer is in pylorus
- Perforation, peritonitis, penetration of pancreas - acute abdomen
- Malignancy - rare in duodenum, common in stomach
What is the pathogenesis of chronic peptic ulcers
- Distal gastritis causes loss of acid regulatory feedback and hypergastrinaemia this causes hyperchlorhydria and duodenitis.
- 1st past of the duodenum undergoes gastric metaplasia with HP colonisation leading to duodenal ulceration
What is the pathogenesis of chronic peptic ulcers
- Distal gastritis causes loss of acid regulatory feedback and hypergastrinaemia this causes hyperchlorhydria and duodenitis.
- 1st past of the duodenum undergoes gastric metaplasia with HP colonisation leading to duodenal ulceration
Describe the features of coeliac disease and describe it’s pathogenesis
- Immunologically mediated chronic inflam condition
- Intolerance to gliadin (component of gluten)
- Affects any age
- Genetic susceptibility- HLA haplotypes
- Unexplained anaemia, weight loss, chronic diarrhoea, IBS, malabsorption
Pathogenesis
- Increased intraepithelial lymphocytes will damage villi
- Villous damage leads to shortened and club shaped villi with partial or total villous atrophy
- Plasmacytosis in the lamina propria = an antibody immune response
How to diagnose coeliac
- Serology- Anti- TGA primary screening tool
- Antiendomysial antibody
- Biopsy -OGD showing increased IELs and villous atrophy with crypt hyperplasia
- Clinical-Gluten withdrawal will improve symptoms and histology
What are the associations and complications of coeliac
Associations
- Autoimmune conditions with HLA haplotypes - T1D and hypothyroid
- Dermatitis herpetiformis
Complications
- Malabsorption, osteoporosis, vitamin deficiency, anaemia
- Predisposition to small bowel lymphoma: enteropathy associated with T cell NHL
- Increased risk of small bowel adenocarcinoma and some other GI cancers
Describe the features of gastroenteritis
- Minor or major illness
- More serious in old and immunosuppressed
- Transmission faeco-oral, water , food
- Diagnosis: stool analysis
- Culture/ microscopy/ PCR
Can be viral - SRSVs , rotaviruses (infants, children), adenovirus , enterovirus (polio/ coxsackie) , HIV
Can be bacterial- E.coli, shigella, salmonella, campylobacter, C Diff.
Other GI tract infections
- Mycobacteria - TB
- Protozoa infection- guardia, cryptospoidiosis
- Helminth infection- worm
