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Pathology > GI > Flashcards

GI Flashcards

1
Q

What are the anatomic and motor disorders of the oesophagus

A
  • 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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2
Q

What are the features of oesophagitis

A
  • 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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3
Q

Describe the features of Barretts oesophagus

A
  • Metaplastic columnar mucosa - red on endoscopy

- Squamous mucosa changes to columnar

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4
Q

Name an infectious type of oesophagitis

A
  • Candida
  • more common in diabetes/ immunocompromised
  • White plaques on endoscopy with hyphae
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5
Q

Discuss herpes oesophagitis and eosinophilic oesophagitis

A

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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6
Q

What are the two main types of oesophageal cancer

A

-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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7
Q

How do doctors deal with Barrets metaplasia

A
  • 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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8
Q

How is oesophageal cancer staged

A

-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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9
Q

What causes acute/ erosive gastritis

A
  • NSAIDS/ ferrous sulphate
  • Alcohol
  • Ingestion of corrosives
  • Cancer chemo
  • Uraemia
  • Severe stress/ shock
  • Ischaemia
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10
Q

What are the causes of chronic gastritis

A

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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11
Q

What are the complications of H. Pylori infection

A

-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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12
Q

Types of Gastric carcinoma and their features

A

-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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13
Q

What causes gastric lymphoma

A
  • 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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14
Q

What are GI stromal tumours

A
  • 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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15
Q

Discuss the features of a small intestine adenocarcinoma

A
  • 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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16
Q

Discuss the features of a small intestine carcinoid tumour

A
  • 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

17
Q

Discuss the features of malignant lymphomas in the small intestine

A
  • Primary or secondary to systemic disease
  • Classified by subtype and staging - CT scan, bone marrow
  • T Cell = worse prognosis than B cell

Various types

  1. MALT- Mucosa associated lymphoid tissue lymphoma - most common, low grade B cell especially in stomach- H. Pylori
  2. Burkitts lymphoma - Children/ young adults/ terminal ileum/ chemoresponsive
  3. Follicular lymphoma- low grade b cell, duodenum or mesenteric nodes
  4. Mantle cell lymphoma - intermediate grade - in large bowel
  5. Enteropathy associated T-cell lymphoma - aggressive high grade - coealiac disease associated. Ileum and jejunum
  6. Post transplant lymphoproliferative disorder - EBV driven, patients on immunosuppression
18
Q

Discuss the features of small bowel metastases

A

Can come from

  • colon
  • lung
  • Ovary
  • Stomach
  • Lobular carcinoma of breast
  • Metastatic melanoma
19
Q

What are the various types of colorectal polyps

A

Hyperplastic - very common, little malignant potential

Adneomatous polyps - common but increased risk of malignancy, a mix of tubular and villous polyps , dysplastic

20
Q

Discuss familial adenomatous polyposis

A
  • Hundreds of adenomatous polyps
  • Autosomal dominant
  • High risk of colorectal adenocarcinoma in 30s/ 40s
21
Q

Discuss the features of colorectal adenocarcinoma

A
  • Usually sporadic
  • More common in west - diets high in saturated animal fats and low in fibre
  • Can be due to
  1. Hereditary non polyposis colon cancer mutation in DNA repair genes
  2. FAP
  3. IBD - esp ulcerative colitis and sclerosis cholangitis
22
Q

What is the adenoma carcinoma sequence

A

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

23
Q

What is the vogelstein model of colon cancer

A

All contribute to development of colon cancer

  1. Instability of chromosomes and CIN gene mutations
  2. MSI pathway causes mismatch repair inactivation so inactivates tumour suppressor genes ]
  3. Activation of oncogenes
24
Q

Discuss the clinical features of colorectal cancer

A
  • Suspect in any bowel change in an older person*
  • Anaemia
  • Abdo mass
  • Abdo pain
  • Change in bowels
  • Bleeding
  • Incontinence
  • Obstruction
  • Tenesmus
  • Rectal mass
25
Q

How is colorectal cancer staged

A

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

26
Q

Why is the anatomy of the rectum hard for tumour treatment

A

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

27
Q

What are the features of tumours of the appendix

A
  • 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
28
Q

Discuss tumours of the anus

A

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
29
Q

Discuss the features of a chronic peptic ulcer and what are the complications

A
  • 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
30
Q

What is the pathogenesis of chronic peptic ulcers

A
  • 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
31
Q

What is the pathogenesis of chronic peptic ulcers

A
  • 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
32
Q

Describe the features of coeliac disease and describe it’s pathogenesis

A
  • 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
33
Q

How to diagnose coeliac

A
  • 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
34
Q

What are the associations and complications of coeliac

A

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
35
Q

Describe the features of gastroenteritis

A
  • 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

Pathology (12 decks)

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