Histo Path - upper GI

Question 1

Epithelial composition of oesophagus

Answer 1

Proximal 2/3 - squamous
Distal 1/3 - columnar

joined together by the z line - squamocolumnar junction

Question 2

increased neutrophils in the submucosa as well as neutrophils infiltrating into the squamous mucosa

Answer 2

Acute oesophagitis

Red, swollen, hot, tender

Question 3

Loss of overlying squamous epithelium with only necrotic debris remaining.

In the upper GI endoscope, there are rounded, erythematous ulcerations of the lower esophagus. Biopsies of these lesions reveals intranuclear inclusions in squamous epithelial cells

Answer 3

Ulceration caused by herpetic oesophagitis

Question 4

epithelial metaplasia to gastric-type mucosa above the gastroesophageal junction.

intestinal metaplasia as well (note the goblet cells in the columnar mucosa)

Answer 4

Barrett’s Oesophagus

Intestinal metaplasia suggests more severe
Due to GORD
Z line migrates up
If migration <2cm, its called ‘short segment’

Question 5

Tan-yellow plaques are seen in the lower esophagus, along with mucosal hyperemia. The same lesions are also seen at the upper right in the stomach.

Answer 5

Candida oesophagitis

Question 6

Most common oesophagial cancer in UK

Answer 6

Adenocarcinoma

Associated with Barrett’s oesophagus so usually seen in distal 1/3
Other risk factors incl: smoking, obesity, prior radiation therapy
Most common in Caucasians, M»F

Question 7

Progressive dysphagia (solids then fluids), odynophagia (pain),
anorexia, severe weight loss

Mass in neck

Answer 7

Squamous Cell Carcinoma

Associated with ETOH and smoking
Other risk factors incl: achalasia of cardia, Plummer-Vinson syndrome, nutritional
deficiencies, nitrosamines, HPV (in high prevalence areas)
6x more common in Afro-Carribeans, M>F
Usually found in middle 1/3 (50%). Upper 1/3 – 20%, Lower 1/3 – 30%

Most die in 1 year, LN spread very aggressive.

Question 8

Engorged veins

Answer 8

Varices

Portal HTN

Emergency endoscopy for banding

Question 9

This gastric mucosa shows infiltration by neutrophils.

Answer 9

Acute gastritis

insult e.g. aspirin, NSAIDs, corrosives (bleach), acute H. pylori,
severe stress (burns)

Question 10

Ulcers

Answer 10

Important to biopsy to rule out malignancy

Ulcers will penetrate over time if they do not heal. Penetration leads to pain. If the ulcer penetrates through the muscularis and through adventitia, then the ulcer is said to “perforate” and leads to an acute abdomen. An abdominal radiograph may demonstrate free air with a perforation.

Question 11

The rod-shaped bacteria are seen here with a methylene blue stain.

Answer 11

Helicobacter Pylori causing peptic ulcer disease

Question 12

What is mechanism for an ulcer to turn cancerous?

Answer 12

Ulcer

Gastritis

Metaplasia - we see goblet cells from intestinal mucosa 

Dysplasia 

Cancer

Question 13

Gastric Cancer

Answer 13

> 95% of malignancies in stomach are adenocarcinomas. Most arise from ulcers.

    Can easily metastasise to Liver

Question 14

Gastric cancer

cells are discohesive and secrete mucus, which is delivered in the interstitium, producing large pools of mucus/colloid

Answer 14

Diffuse

    Poorly differentiated (linitis plastica) 

    Includes singlet ring cell carcinoma

Question 15

Causes of chronic gastric inflammation

Answer 15

Infectious: H. Pylori

Chemical: NSAIDS, bile reflux to the antrum 

Autoimmune: antiparietal antibodies

Question 16

Infiltration of lymphocytes +/- neutrophils in chronic gastritis

Answer 16

MALToma (eventually)
    B cell (marginal zone) lymphoma 

Enough time to mobilise plasma cells and T cells (i.e. lymphocytes) 

Induction of lymphoid follicles:  
Mucosal Associated Lymphoid Tissue (MALT) 

Mainly talking about H. pylori infection when we talk about MALT induction

Question 17

H. Pylori treatment

Answer 17

Cag-A-Positive H pylori has a needle that injects toxins into intracellular junction, so bacteria can attach more easily.

    Associated with more chronic inflammation, and cancer, for this reason 

Treat with antibiotic triple therapy: amoxicillin + clarithromycin + PPI 

    Can even make a lymphoma go away!!

Question 18

What is the pathophysiology of duodenitis

Answer 18

Increased acid and pepsin production in stomach which spills into duodenum

Leads to chronic inflammation, then gastric metaplasia, followed by H pylori infection 

    H pylori enjoy gastric mucosa, so metaplasia towards gastric mucosa benefits them.

Question 19

Duodenal ulcer

Answer 19

Duodenitis can lead to ulcer formation - similar to how gastric ulcers are formed.

4 times more common than GU
Epigastric pain, worse at night
Relieved by food and milk
Occurs in younger adults
RFs: H. pylori, drugs, aspirin, NSAIDs, steroids, smoking, ↑ drugs, acid secretion
Complications: anaemia (IDA) and perforation (erect CXR)

Question 20

What other pathogens may be found on duodenum?

Answer 20

Usually in the immunosuppressed, we can see:

CMV 

Cryptosporidiosis  

Giardia lamblia 

    Greatest risk in Eastern Europe (St. Petersburg!) 

Whipple's Disease

Question 21

Histological findings of malabsorption

Answer 21

Malabsorption: partial villous atrophy

Histological features include: 

    Villous atrophy (smaller) 

    Crypt hyperplasia (bigger) 

        Ratio becomes more like 1:2, not 2:1. 

    Increased lymphocyte infiltration (intraepithelial)

Question 22

Coeliac related MALTomas

Answer 22

MALTomas in Coeliac are:

    Duodenal 

    T-cell (Enteropathy-associated T-cell lymphoma: EATL) 

C.f. to MALTomas due to H. Pylori: 

    Stomach 

    Marginal zone B-cell lymphocytes

Question 23

Absence of ganglion cells in myenteric plexus

hypertrophied nerve fibres w/out ganglia.

Answer 23

Hirschprung

Presents with symptoms and signs of obstruction in young babies, mostly males
o Associated with Down’s syndrome (2%)
o Genetics – RET proto-oncogene Cr10+
o Biopsy – hypertrophied nerve fibres, no ganglia
o Treatment – resection of affected (constricted) segment