GI Flashcards by Roma Bannon

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

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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

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Describe the features of Barretts oesophagus

Metaplastic columnar mucosa - red on endoscopy

- Squamous mucosa changes to columnar

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Name an infectious type of oesophagitis

Candida
more common in diabetes/ immunocompromised
White plaques on endoscopy with hyphae

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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

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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

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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

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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

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What causes acute/ erosive gastritis

NSAIDS/ ferrous sulphate
Alcohol
Ingestion of corrosives
Cancer chemo
Uraemia
Severe stress/ shock
Ischaemia

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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)

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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

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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

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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

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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

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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

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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

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