GI pathology

Question 1

What is a tracheoesophageal fistula? How does it present?

Answer 1

TE fistula is a congenital defect resulting in the proximal esophagus ending in a blind pouch (atretic) and the distal esophagus arising from the trachea. Presents with vomiting, polyhydramnios (excess amniotic fluid), abdominal distension (some of the air breathed will go into the GI tract) and aspiration (some of the food that is vomited goes through the trachea and into the lungs)

Question 2

What is a esophageal web? How does it present? What syndrome is it a key element in?

Answer 2

When the mucosa layer of the esophageal wall protrudes into the lumen and causes obstruction.
Presents with dysphagia for poorly chewed food
A characteristic of Plummer-Vinson syndrome: severe iron deficiency anemia, esophageal web and beefy-red tongue tue to atrophic glossitis

Question 3

What is Zenker diverticulum?

Answer 3

When the esophageal mucosa protrudes backwards through the muscular wall of the esophagus (as opposed to forward into the lumen). Presents with dysphagia, obstruction and halitosis (food can get stuck in the out pouching and rot)

Question 4

What causes Mallory-Weiss syndrome? How does Mallory-Weiss syndrome present?

Answer 4

Severe vomiting (due to alcoholism or bulimia) causes linear/longitudinal lacerations of the mucous at the gastroesophageal junction. Presents with painFUL hematemesis (vomiting of blood).

Question 5

What is the cause of esophageal varices? How do they present?

Answer 5

Portal hypertension causes the left gastric vein to back up into the veins in the lower esophagus, resulting in dilation. Asymptomatic but can rupture, leading to painLESS hematemesis and death. Most common cause of death in people with cirrhosis

Question 6

What is achalasia? What is the cause of achalasia? What are the clinical findings?

Answer 6

The inability to relax the lower esophageal sphincter. Caused by damage to ganglion cells in the myenteric plexus (between circular and longitudinal muscles) from a idiopathic insult or Chagas disease (infection with trypanosome cruzi).
Clinical findings:
bird beak sign on barium swallow (food gets trapped in esophagus and dilates it)
dysphagia for both solids and liquids
halitosis
high LES on esophageal manometry

Question 7

What is an ulcer? How does it heal?

Answer 7

An ulcer is when some insult (e.g. acid) destroys the epithelium, mucosa and part of the submucosa. Because the stem cells are in the mucosa, wiping out the mucosa means the ulcer can’t heal by regeneration; it has to heal by fibrosis. The scar that forms causes the tissue to narrow and tighten

Question 8

What is GERD? What are its risk factors?

Answer 8

GERD is reflex of acid from the stomach due to reduced lower esophageal tone.
Risk factors - hiatial hernia (cardia of the stomach herniates into the esophagus),alcohol, tobacco, obesity, caffeine

Question 9

What are the clinical features of GERD?

Answer 9

heartburn
adult onset asthma and cough
damage to enamel of teeth (from acid in mouth)
ulceration and stricture of esophagus
Barrett esophagus

Question 10

What is Barrett esophagus?

Answer 10

Metaplasia of the lower esophagus mucosa from non-keratinizing stratified squamous epithelium to non-ciliated columnar epithelium with goblet cells (the mucous produced by the goblet cells protects the esophagus from acid)

Question 11

What are the two types of esophageal carcinoma? What are their different risk factors? Which part of the esophagus do they mainly arise in? How does esophageal carcinoma present?

Answer 11

Adenocarcinoma and squamous cell carcinoma.
Adenocarcinoma arises from Barrett esophagus; distal 1/3 of esophagus
Squamous cell carcinoma arises from irritation: alcohol, tobacco, very hot tea, rotting food (achalasia and esophageal web) and esophageal injury (ingesting harsh chemicals like lye)
Present like with progressive dysphagia, weight loss, pain, hematemesis and hoarse voice (if recurrent laryngeal nerve is involved in tumor) or cough (if trachea is involved in tumor)

Question 12

What is the difference between a gastroschisis and an omphalocele?

Answer 12

A gastroschisis is a congenital malformation where the sides of the abdomen don’t grow together and fuse at the midline, resulting in no anterior abdominal wall and exposure of abdominal contents.
An omphalocele arises when the herniated intestines fail to return to the body cavity. Unlike the gastroschisis, the intestines are covered by peritoneum and amnion of the umbilical cord

Question 13

What is the pathogenesis of pyloric stenosis? How does it present?

Answer 13

Congenital hypertrophy of pyloric smooth muscle, preventing gastric contents from going into the duodenum.
Presents two weeks after birth with projectile non bilious vomiting, visible peristalsis and an olive-like mass in the abdomen

Question 14

What is the difference in pathogenesis of acute gastritis and chronic gastritis?

Answer 14

Acute gastritis is due to acidic damage to the stomach mucosa.
Chronic gastritis is due to chronic inflammation of the stomach mucosa

Question 15

How does the stomach protect itself from the acidic environment?

Answer 15

1) Mucin layer produced by foveolar cells
2) bicarbonate secretion by surface epithelium
3) normal blood supply picks up and carries away any leaked acid

Question 16

What are the risk factors for acute gastritis?

Answer 16

severe burns cause Curling ulcer (hypovolemia leads to decreased blood supply defense)
NSAIDs (prostaglandins stimulate all the stomach’s defenses)
heavy alcohol consumption
Chemotherapy
Increased intracranial pressure causes Cushing ulcer (increased stimulation of vagus nerve leads to increased acid production)
Shock (stress ulcers)

Question 17

What is the difference between erosion and ulceration?

Answer 17

Erosion is loss of superficial epithelium

Ulceration is loss of mucosal layer

Question 18

What are the two etiologies of chronic gastritis?

Answer 18

Chronic autoimmune gastritis and chronic H Pylori gastritis

Question 19

What is the pathogenesis of chronic autoimmune gastritis? What are its clinical findings?

Answer 19

T cell mediated autoimmune destruction of parietal cells.
Clinical findings: atrophy of mucosa with intestinal metaplasia, achlorhydria with increased gastrin levels and astral G-cell hyperplasia, pernicious anemia due to lack of intrinsic factor, increased risk for gastric adenocarcinoma

Question 20

What three chemical can induce the production of acid in parietal cells?

Answer 20

acetylcholine (from Vagus nerve), histamine and gastrin

Question 21

How does H pylori cause gastritis? Where in the stomach does H pylori usually infect? Besides gastritis, what are H pylori infections at increased risk for? How do you confirm eradication of H pylori?

Answer 21

It stimulates an inflammatory response and secretes ureases and proteases both of which weaken mucosal defenses. Antrum in the most common site and the bacteria lay on the surface of the epithelium (do not burrow into the crypts).
Increased risk of ulceration (peptic ulcer disease), gastric adenocarcinoma and MALT lymphoma
Eradication is confirmed by a negative urea breath test and a lack of stool antigen

Question 22

What are the causes of a duodenal ulcer?

Answer 22

95% due to H pylori
rarely due to Zollinger-Ellison syndrome (a small tumor in the pancreas or small bowel secretes high levels of gastrin into the blood, causing the stomach to secrete more acid)
almost never due to duodenal carcinoma

Question 23

What are the causes of gastric ulcers?

Answer 23

75% due to H pylori
NSAIDs
bile reflux
gastric carcinoma (intestinal type)

Question 24

How does the presentation of a duodenal ulcer differ from the presentation of a gastric ulcer?

Answer 24

Both present with epigastric pain but for a duodenal ulcer, the pain improves with meals. For a gastric ulcer, the pain worsens with meals.

Question 25

Where are gastric ulcers usually located? What would happen if the wall of the stomach ruptured?

Answer 25

Lesser curvature of the antrum, thus rupture carries the risk of bleeding from the left gastric artery

Question 26

What are the two types of gastric carcinomas?

Answer 26

Intestinal type (more common) and diffuse type

Question 27

What are the morphological characteristics of an intestinal type gastric carcinoma? Diffuse type?

Answer 27

Intestinal type - Large, irregular ulcer with heaped up margins
Diffuse type - signet ring cells (contain a large amount of mucin that pushes the nucleus to the periphery of the cell) that diffusely infiltrate the gastric wall. Linitis plastica (thickening of the stomach wall from growth of fibrous or connective tissue)

Question 28

What are the risk factors for intestinal type gastric carcinoma? Diffuse type?

Answer 28

Intestinal type - intestinal metaplasia due to H pylori and autoimmune gastritis, nnitrosamines in smoked foods (explains Japan’s high rate of gastric carcinoma) and blood type A
Diffuse type - None

Question 29

What is duodenal atresia? What are the presenting signs and symptoms?

Answer 29

A congenital failure of the duodenum to canalize, causing the duodenum to end in a blind pocket.
Presents with polyhydramnios, distension of the stomach and duodenum (double bubble sign on x-ray), bilious vomiting

Question 30

What is meckel diverticulum? What is the ‘rule of 2s’?

Answer 30

An out pouching of all three layers of the bowel wall due to failure of the vitelline duct (umbilical cord) to involute.
Rule of 2s - seen in 2% of population (most common congenital anomaly of GI tract), 2 inches long, within 2 feet of the ileocecal valve, presents within first 2 years of life (most cases are asymptomatic)

Question 31

How can you distinguish between tropical sprue and celiac disease?

Answer 31

They both are characterized by damage to the small bowel villi, but:
tropical sprue occurs in tropical regions whereas celiac occurs everywhere
tropical sprue arises after infectious diarrhea and responds to antibiotics whereas celiac does not respond to antibiotics
tropical sprue causes damage in the jejunum and ileum whereas celiac causes damage to the duodenum

Question 32

What is Whipple’s disease? How does it present?

Answer 32

Tissue damage (most often small bowel lamina propria) characterized by macrophages loaded with Tropheryma whippelii organisms that cannot be destroyed in macrophage lysosomes.
Presents as fat malabsorption and steatorrhea because the macrophages in the lamina propria of the small bowel compress the lacteals so fat cannot be transferred from the enterocytes to the lymphatics.

Question 33

What gets damaged in celiac disease? What is the pathogenesis?

Answer 33

Celiac disease is immune-mediated damage of the small bowel villi (most prominent in duodenum). Gliadin, a component of gluten, is absorbed and deamidated by tissue transglutaminase (tTG) and then presented by APCs via MHC class II to helper T cells which then mediate the tissue damage.

Question 34

How does celiac disease present in children? Adults? what dermatological finding is associated with celiac disease?

Answer 34

Children - abdominal dissension, diarrhea and failure to thrive
Adults - chronic diarrhea and bloating
Associated with dermatitis herpetiformis which are small, herpes-like vesicles that form from IgA depositing at the tips of dermal papillae and causing the epidermis to separate from the dermis.

Question 35

What are the histological characteristics of celiac disease?

Answer 35

Flattening of villi, hyperplasia of crypts and increased intraepithelial lymphocytes