Gastrointestinal Flashcards
What is a tracheoesophageal fistula? How does it present? What is the most common variant?
A congenital defect resulting in an abnormal connection between the esophagus and trachea
Presents with vomiting, polyhydramnios, abdominal distention and aspiration
The most common variant consists of proximal esophageal atresia with the distal esophagus arising from the trachea
What is an esophageal web? How does it present?
Thin protrusion of esophageal mucosa most often in the upper esophagus
Presents with dysphagia for poorly chewed food
What protrudes in an esophageal web? What is there an increased risk for?
The esophageal mucosa
Increased risk for esophageal squamous cell carcinoma
What is Plummer-Vinson syndrome?
Characterized by severe iron deficiency anemia, esophageal web, and beefy-red tongue due to atrophic glossitis (atrophy of the mucosa and exposed blood vessels)
Also has an increased risk for esophageal squamous cell carcinoma
What is a Zenker diverticulum? How does it present?
An outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum - only protruded one part of the wall)
Presents with dysphagia, obstruction and halitosis (food gets trapped and rots)
Mallory-Weiss syndrome: what is it, what causes it, how does it present
Longitudinal laceration of mucosa at the gastroesophageal junction (GE)
Caused by severe vomiting, usually due to alcoholism or bulimia
Presents with painful hematemesis
Where do the following occur:
Mallory-Weiss syndrome
Plummer-Vinson syndrome
Zenker diverticulum
Mallory-Weiss syndrome: gastroesophageal junction (GE) (laceration of the mucosa)
Plummer-Vinson syndrome: esophagus (esophageal web)
Zenker diverticulum: pharynx (outpouching of pharyngeal mucosa)
Boerhaave syndrome
Rupture of the esophagus leading to air in the mediastinum and *subcutaneous emphysema (can push on skin on the neck and feel air bubbles). Seen with sever Mallory-Weiss syndrome.
Esophageal varices: what are they? what causes them? risk?
Dilated submucosal veins in the lower esophagus
Arise secondary to portal hypertension: distal esophageal vein normally drains into portal vein via the left gastric vein. In portal HTN, the left gastric vein backs up into the esophageal vein resulting in dilation (varices).
Asymptomatic but risk of rupture: presents w/ *painless hematemesis, most common cause of death in cirrhosis
What is the most common cause of death in cirrhosis? How does it present?
Rupture of esophageal varices
Presents with *painless hematemesis
Where does the esophageal vein normally drain? What is the significance of this?
The left gastric vein which drains to the portal vein
In portal HTN this gets backed up leading to esophageal varices
What is achalasia? What is it due to? Clinical features?
Meaning “without relaxation” it is disordered esophageal motility with inability to relax the lower esophageal sphincter (LES)
Due to damaged ganglion cells in the myenteric plexus: can be idiopathic or secondary to a known insult (Trypanosoma cruzi infection in Chagas diease)
Clinical features: dysphagia for s/l, putrid breath (rotting food), *high LES pressure on esophageal manometry, ‘bird-beak’ sign on barium swallow study, increased risk for esophageal squamous cell carcinoma
Where are the ganglion cells of the myenteric plexus located? What is there function? What disorder are they associated with?
Between the inner circular and outer longitudinal layers of the muscular is propria
Important for regulating bowel motility and relaxing the LES
Damaged in Achalasia
‘Bird-beak’ sign on barium swallow study?
Achalasia
Gastroesophageal reflux disease (GERD): clinical features
Reflux of acid from the stomach due to reduced LES tone
Clinical features: heartburn, asthma (adult-onset) and cough, damage to enamel of teeth, ulceration with stricture and Barrett esophagus
Risk factors for GERD
OH, tobacco, obesity, fat-rich diet, caffeine, and *hiatal hernia
What is the most common type of hiatal hernia? What is another type?
Sliding (stomach into esophagus) - most common
Paraesophageal (stomach is next to esophagus)
What is Barrett esophagus?
Metaplasia of lower esophageal mucosa from stratified squamous epithelium to *nonciliated columnar epithelium with goblet cells. Seen in 10% of patients w/ GERD - response of the lower esophagus stem cells to acidic stress
Is Barrett esophagus harmless?
No - is may progress to dysplasia and adenocarcinoma
What are the two types of esophageal carcinoma?
Adenocarcinoma
Squamous cell carcinoma
Adenocarcinoma of the esophagus:
What is it?
Where is it most common?
How does it arise?
Malignant proliferation of glands
Most common type of esophageal carcinoma in the West
Arises from preexisting Barrett esophagus; usually involves the lower one-third* of the esophagus
Squamous cell carcinoma of the esophagus: What is it? Where is it most common? Where does it arise? What are the major risk factors?
Malignant proliferation of squamous cells
Most common esophageal cancer worldwide
Usually arises in the upper or middle third of the esophagus
Major risk factors: OH, tobacco, very hot tea (Iran/China), achalasia (rotting food), esophageal web (Plummer-Vinson) esophageal injury (ex/ lye ingestion - hair straightening chemical)
Lymph node spread in esophageal cancer
Upper 1/3: cervical nodes
Middle 1/3: mediastinal or tracheobronchial nodes
Lower 1/3: celiac and gastric nodes
Presentation of squamous cell carcinoma of the esophagus
Progressive dysphagia, WL, pain and hematemesis
As well as, hoarse voice (recurrent laryngeal nerve involvement) and cough (tracheal involvement)
What is gastroschisis?
Meaning “to split”
Congenital malformation of the anterior abdominal wall leading to exposure of abdominal contents
Omphalocele
Persistent herniation of bowel into the umbilical cord. Due to failure of herniated intestines to return to the body cavity during development. *Contents are covered by peritoneum and amnion of the umbilical cord
What is Pyloric stenosis? How does it present? Treatment?
Congenital hypertrophy of pyloric smooth muscle; more common in males
Classically presents two weeks after birth: projective nonbilious vomiting, visible peristalsis, olive-like mass in the abdomen
Treatment is myotomy (muscle is cut out)
Acute gastritis:
Cause
Acidic damage to stomach mucosa. Due to imbalance between mucosal defenses and acidic environment. Defenses include mucin layer production by foveal cells, bicarbonate secretion by surface epithelium, and normal blood supply (provides nutrients and picks up leaked acid)
Acute gastritis risk factors
Severe burn (Curling ulcer) - hypovolemia leads to decreased blood supply
NSAIDs (decreased PGE2 - normally decreases acid and increases mucus, bicarb and blood flow)
Heavy alcohol consumption (toxin directly damages mucosa)
Chemotherapy (knocks out turnover cells)
Increased intracranial pressure (Cushing ulcer) - increased stimulation of vagus nerve leads to increased acid production (ACh - parietal cells)
Shock - multiple (stress) ulcers may be seen in ICU patients
Acid damage in acute gastritis can result in inflammation, erosion or ulcer. What is the difference between erosion and ulcer?
Erosion - loss of superficial epithelium
Ulcer - loss of mucosal layer
What are the two types of chronic gastritis? Which is more common?
Chronic autoimmune gastritis
Chronic H. pylori gastritis (more common, 90%)
Chronic autoimmune gastritis is due to autoimmune destruction of what cells? Where are they located?
Due to autoimmune destruction of gastric parietal cells which are located in the stomach body and fundus
What antibodies are associated with autoimmune chronic gastritis? What is the pathogenesis?
Antibodies against parietal cells and/or intrinsic factor (side effect, not a cause); useful for diagnosis but pathogenesis is mediated by T cells (type IV hypersensitivity)
Clinical features of autoimmune chronic gastritis
Atrophy of mucosa with intestinal metaplasia
Achlorhydria with increased gastrin levels (loss of feedback) and antral G-cell (make gastrin) hyperplasia
Megaloblastic (pernicious) anemia due to lack of intrinsic factor (parietal cells make intrinsic factor that binds B12)
*Increased risk for gastric adenocarcinoma (intestinal type)
Chronic H. pylori gastritis: Mechanism Most common site How does it present Treatment/Testing
Due to H. pylori-induced acute and chronic inflammation; H. pylori ureases and proteases along with inflammation weaken mucosal defenses
Antrum is the most common site
Presents with epigastric abdominal pain
Treatment involves triple therapy: resolves gastritis/ulcer and reverses intestinal metaplasia
Negative urea breath test and lack of stool antigen confirm eradication of H. pylori
H. pylori gastritis has increased risk for…
Ulceration (peptic ulcer disease)
Gastric adenoma (intestinal type)
MALT lymphoma
Peptic ulcer disease:
Locations - where is most common
Solitary mucosal ulcer involving either the proximal duodenum (90%) or distal stomach (10%)
Causes of duodenal ulcer
Almost always H pylori (95%), rarely may be due to ZE (gastinoma, excess gastrin causes parietal cells to produce excess H+)
How does a duodenal ulcer present? How do you diagnose it? Where does it usually arises and what are the possible complications?
Epigastric pain that improves with meals (duodenum increase defense/neutralizing substances w/ a meal)
Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner glands (produce mucus)
Usually arises in anterior duodenum; when present in the posterior duodenum rupture may lead to bleeding from the gastoduodenal artery or acute pancreatitis
Causes of gastric ulcer
How does it present?
Where is it usually located?
Rupture leads to risk of bleeding from which artery?
H pylori (75%), NSAIDs, bile reflux
Presents w/ epigastric pain that worsens with meals
Usually located on the lesser curvature of the antrum
Rupture carries risk of bleeding from left gastric artery
Peptic ulcer disease and risk of carcinoma
Duodenal ulcers are almost never malignant (duodenal carcinoma is extremely rare)
Gastric ulcers can be caused by gastric carcinoma (intestinal subtype)
How to differentiate gastric ulcers (benign vs. malignant)
Gastric ulcers can be caused by gastric carcinoma (intestinal subtype)
Benign peptic ulcers are usually small (), and surround by flat mucosa (not folded up)
Malignant ulcers are large and irregular with heaped up margins (piling up mucosa)
Biopsy is required for definitive diagnosis
Gastric carcinoma
Malignant proliferation of surface epithelial cells (adenocarcinoma)
Sub-classified into intestinal (more common) and diffuse types
Intestinal type (gastric carcinoma):
How does it present?
Most common site
Risk factors
Presents as a large, irregular ulcer with heaped up margins, most commonly involves the lesser curvature of the antrum (similar to gastric ulcer)
Risk factors: intestinal metaplasia (H pylori, autoimmune gastritis), nitrosamines in smoked foods (Japan), and blood type A
Diffuse type (gastric carcinoma):
Characterized by?
Not associated with?
Characterized by signet ring cells that diffusely infiltrate the gastric wall; desmoplasia (growth of fibrous or CT) results in thickening of the stomach wall (linitis plastica)
Not associated with H pylori, intestinal metaphase or nitrosamines
What lymph nodes does gastric cancer spread to?
left supraclavicular node (Virchow node)
How does gastric carcinoma present?
Presents late with WL, abdominal pain, anemia and early satiety
Rarely presents as acanthosis nigricans or Leser-Trelat sign (patient gets dozens of seborrheic keratosis)
Where does gastric carcinoma metastasize to?
Most commonly the liver Periumbilical region (Sister Mary Joseph nodule) - seen with intestinal type Bilateral ovaries (Krukenberg tumor) - seen with diffuse type