Stomach Flashcards
Pyloric stenosis
Congenital hypertrophy of pyloric smooth muscle
Classic presentation
2 weeks after birth (takes time to develop)
- Projectile nonbilious vomiting (b/c bile enters duodenum and contents haven’t met the duodenum)
- Visible (can see!) peristalsis
- Olive-like/ovoid mass in abdomen (thigh pyloric sphincter)
Acquired pyloric stenosis
Comes from antral gastritis or peptic ulcers near pylorus
Normal body/fundic/corpus mucosa
Very thick
Shallow pits (foveolae)
Highly cellular glands w/prominent pink cytoplasm (from parietal cells which secrete gastric acid) in upper layers and more purplish cytoplasm in lower layers (from chief cells which secrete pepsinogen, gastric lipase, chymosin, purple b/c of lots of rER)
Normal antral mucosa
Still thick
Deep pits (foveolae)
Cellular glands now produce mostly mucus (so stain more pale)
Minimum LP (not very cellular)
Acute gastritis
Acidic damage to stomach mucosa
Pathophys of acute gastritis
Due to imbalance b/w mucosal defenses and acidic environment
Defenses of gastric mucosa (4)
- Mucin layer (produced by foveolar cells) –> elderly produce less so have increased susceptibility
- Bicarbonate secretion by surface epithelium
- Normal blood supply (provides nutrients and picks up leaked acid
- Epithelial regenerative capacity
Risk factors for Acute Gastritis (6)
- Severe burn (Curling ulcer) –> hypovolemia leads to decreased blood supply to mucosa
- NSAIDS (decreased PGE2) –> decreased bicarb
- Heavy alcohol consumption and smoking –> direct cellular injury
- Chemotherapy –> mitotic inhibitors –> decrease epi regeneration
- Increased intracranial pressure (Cushing ulcer) –> increased stimulation of CN10 –> increased ACh –> increased acid production
- Shock –> multiple stress ulcers (ICU pts) –> can also be due to sepsis or severe trauma –> hypoxia and decreased BF b/c of stress-induced splanchnic vasoconstriction
What does PGE2 do as protection of gastric mucosa?
- Increased bicarb secretion
- Decreases acid secretion
- Increases mucin synthesis
- Increases vascular perfusion
How often is gastric mucosa regenerated?
Entire mucosal layer is replaced every 2-6 days
How does acid damage appear morphologically? (3 possibilities)
- Superficial inflammation (normally there are NO inflammatory cells in gastric mucosa)
- Erosion (loss of superficial epi)
- Ulcer (loss of mucosal layer)
Sx of acute gastritis?
ASx or epigastric pain w/ N/V
Morphology of acute gastric ulcer
Shallow, rounded, small
Rugae normal
Base = brown/black b/c acid digestion of extravasated blood
No scarring or thickening of BV seen in chronic gastritis
Marked expansion of lamina propria by mononuclear inflammatory cells
2 causes of chronic gastritis
Helicobacter pylori gastritis (90%) and autoimmune gastritis (10%)
Autoimmune gastritis - Cause
Autoimmune destruction of gastric parietal cells (located in stomach body/corpus and fundus)
Autoimmune gastritis associated w/
Antibodies to parietal cells and/or intrinsic factor (IF) –> useful for Dx, NOT cause of damage, consequence of damage
Pathogenesis of autoimmune gastritis
Type 4 hypersensitivity –> T cell mediated to parietal cells
Clinical features of autoimmune gastritis (6)
- Atrophy of mucosa w/ intestinal metaplasia
- Achlorhydria (due to defective gastric acid secretion) w/ increased gastrin levels (body’s compensation for decreased acid secretion) and antral G-cell hyperplasia
- Megaloblastic (pernicious anemia) due to lack of IF (b/c parietal cells make IF, no parietal cells = no IF –> disables terminal ileal vit B12 absorption. IF binds B12 in intestine)
- Increased risk for gastric adenocarcinoma (intestinal type)
- Decreased serum pepsinogen I from chief cell destruction (b/c gastric gland destroyed during attack on parietal cells)
- Associated w/other autoimmune diseases (e.g. DM and Graves disease)
Tx for autoimmune gastritis
Immunosuppression so that glands are not destroyed and so stem cells can regenerate mucosa
Morphology for autoimmune gastritis
Loss of rugae Atrophic mucosa in body and fundus Intestinal metaplasia (goblet cells + NCCE) Located in body of stomach Increased lymphocytes and macrophages
Chronic H. pylori gastritis - Cause
H. pylori-induced acute and chronic inflammation
Most common type of gastritis
H. pylori gastritis
Pathophys behind H. pylori gastritis
H. pylori ureases (NH4 inhibit gastric bicarb transporters) and proteases + inflammation weaken mucosal defenses
Most common site for H. pylori gastritis
Antrum
Sx of H. pylori gastritis
Epigastric abdominal pain
Increased risk for ulceration (PUD), gastric adenocarcinoma (intestinal type), and MALT lymphoma (gastric)
Tx for H. pylori gastritis
Triple therapy (PPI and antibiotics, PPI to allow ulcer/gastritis to heal and intestinal metaplasia to reverse and antibiotics to kill off H. pylori)
How to confirm eradication of H. pylori?
Negative urea breath test and lack of stool antigen
4 Features of H. pylori
- Flagella allow motility in viscous mucus
- Urease –> NH4 –> increase gastric pH –> inhibit bicarb and increase acid production
- Adhesins –> to stick to foveolar cells
- Toxins –> can lead to ulcer/cancer (uncertain mxn)
Morphology of H. pylori gastritis
Neutrophils in gland epi
Giemsa stain for organisms (locked in mucin layer at surface of epi, have spiral/helical shape)
Reminder –> pernicious anemia (B12 def) –> MOST COMMON CAUSE IS CHRONIC AUTOIMMUNE GASTRITIS
Atrophic glossitis (smooth, beefy red tongue)
Epithelial megaloblastosis
Malabsorptive diarrhea
Peripheral neuropathy (numbness/paresthesias)
Spinal cord lesions (loss of vibration and position sense, sensory ataxia w/ + Romberg sign, limb weakness, spasticity, extensor plantar responses)
Irreversible cerebral dysfunction (mild personality changes to memory loss to psychosis)
PUD - location of ulcer
Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)
Duodenal ulcer - cause
H. pylori (most common, >95%)
Zollinger-Ellison Syndrome (ZES; rare)
Presentation of duodenal ulcer
Epigastric pain that improves w/meals (b/c duodenum prepares itself to receive acidic food bolus from stomach by secreting acid-neutralizing substances)
Endoscopy biopsy of duodenal ulcer
Hypertrophy of Brunner glands (only found in duodenum of small intestine, secrete bicarbonate-rich mucus to protect against acidic chyme from stomach; also secrete urogastrone –> inhibits parietal and chief cells of the stomach from secreting acid and their digestive enzymes)
Complication of duodenal ulcer
Rupture –> bleeding from gastroduodenal artery (posterior ulcer) or acute pancreatitis (posterior ulcer)
Gastric ulcer - cause
H. pylori (75%)
Other causes = NSAIDS and bile reflux
Presentation of gastric ulcer
Epigastric pain that worsens w/meals (b/c meal –> increased gastric acid secretion –> increased mucosal inflammation)
Location of gastric ulcer
Lesser curvature of antrum
Complication of gastric ulcer
Risk of bleeding from L gastric artery (b/c it runs along the lesser curvature of stomach)
DDx of ulcers includes…
Carcinoma
Are duodenal ulcers malignant?
Extremely rarely
Gastric ulcers can be caused by…
Gastric carcinoma (intestinal subtype)
Appearance of benign peptic ulcers
Small, sharply demarcated (“punched out”), surrounded by radiating folds of mucosa
Appearance of malignant peptic ulcers
Large, irregular, heaped up margins
How to tell for sure b/w benign and malignant peptic ulcers?
Biopsy
Ultimate cause of PUD?
Imbalance b/w mucosal defenses and acid production
Microscopic appearance to ulcer
Superficially (luminal side) –> layer of mucus, cellular debris, inflammatory cells (esp. neutrophils)
Next –> layer of granulation tissue (capillaries, fibroblasts, variable inflammation)
Deepest –> fibrous tissue + variable inflammation
In general PUD complications
Perforation, Bleeding, Obstruction (esp. in duodenum b/c of fibrosis deformation and narrowing of lumen)
Gastric Adenocarcinoma
Malignant proliferation of surface epithelial cells
2 types of Gastric Adenocarcinoma
Intestinal and diffuse types
Which subtype is more common?
Intestinal
How does the intestinal type of gastric adenocarcinoma present?
Large, irregular ulcer with heaped up
margins
Tumors typically grow as a single recognizable mass, whether it be exophytic, flat, or ulcerated
Precursor lesion = chronic gastritis
Where is most common location of intestinal subtype of gastric adenocarcinoma?
Lesser curvature of the antrum (similar to gastric ulcer)
Risk factors for intestinal subtype of gastric adenocarcinoma?
Intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis) Nitrosamines in smoked foods (Japan) Blood type A
Morphology of diffuse subtype of gastric adenocarcinoma
Signet ring cells that diffusely infiltrate the gastric
wall
Desmoplasia (reactive stromal response) results in thickening of stomach wall (w/diffuse rugal flattening –> leather bottle appearance = linitis plastica)
Do not form recognizable glands and do not typically produce a discrete mass
No precursor lesion
Does the diffuse subtype of gastric adenocarcinoma have similar risk factors to intestinal subtype?
NO!
NOT associated w/H. pylori, intestinal metaplasia, or nitrosamines
How are signet ring cells formed in diffuse subtype gastric adenocarcinoma?
Tumor cells produce abundant cytoplasmic mucus, which expands the cell and pushes the nucleus to the side, resulting in a signet ring appearance
Presentation of gastric carcinoma
Late with weight loss, abdominal pain, anemia, and early satiety
This last sign is classic for diffuse type b/c thickening of stomach wall prevents full stomach distension so pts get full faster
Rarely presents as acanthosis nigricans (thickening and darkening of axillary region) or Leser-Trelat sign (explosive onset of multiple seborrheic keratoses; aka many pigmented skin lesions)
Spread to lymph nodes in gastric carcinoma involves which LN?
Left supraclavicular node (Virchow node)
What sites are involved in metastatic gastric carcinoma?
Most commonly = liver
Other sites =
1. periumbilical region (Sister Mary Joseph nodule –> seen with intestinal type)
2. Bilateral ovaries (Krukenberg tumor –> seen with diffuse type)
Are peptic ulcers pre-malignant?
NO
“Cancers often ulcerate, but ulcers never cancerate”
2 Types of hypertrophic gastropathy
Menetrier dx and Zollinger-Ellison Syndrome (ZES)
Features of Menetrier Dx (7)
- Diffuse hyperplasia of foveolar epi of body and fundus
- Hypoproteinemia due to protein-losing enteropathy (decreased albumin)
- Wt loss
- Diarrhea
- Peripheral edema
- Rare
- Children (self-limiting, after resp. infxn); adults (increased risk of gastric adenocarcinoma)
Morphology of Menetrier Dx
Irregular enlargement of gastric rugae in body and fundus
Hyperplasia of foveolar mucus cells
Corkscrew glands
Tx for Menetrier Dx
Supportive w/ IV albumin and parenteral nutritional supplementation
Cause of ZES?
Gastrin-secreting tumors (gastrinomas)
Features of ZES?
Slow growing
Malignant
Sporadic (75%)
Found most often in small intestine and pancreas
Morphology of ZES
Thickening of mucosal layer b/c of increased parietal cells
Increased mucin production b/c hyperplasia of mucus neck cells
Tx of ZES
Blockade of acid hypersecretion (PPIs, H2R blockers)
What does prognosis of ZES depend on?
Gastrinoma
Types of Gastric Polyps (3)
- Inflammatory/Hyperplastic (75%)
- Fundic gland (15%)
- Gastric adenoma (10%)
Features of inflammatory/hyperplastic gastric polyp?
50-60 y.o.
Chronic gastritis (reactive hyperplasia)
Risk of dysplasia increases w/size
Multiple, ovoid, smooth
Features of fundic gland gastric polyp?
50 y.o.
»F
Sporadic or FAP (familial adenomatous polyposis)
Increased incidence b/c of PPI tx (due to increased gastrin secretion due to decreased gastric acid –> glandular hyperplasia)
Sx = Asx or N/V w/epigastric pain
Morphology = no inflammation, smooth surface
Features of gastric adenoma (gastric polyp)?
50-60 y.o. >>> M Incidence increases w/age FAP + background of chronic gastritis w/atrophy and intestinal metaplasia Increased risk of adenocarcinoma w/size Located in antrum of stomach
Gastric lymphoma (MALTomas) - Most common cause
Chronic H. pylori infection
Gastric lymphoma (MALTomas) - morphology
Dense lymphocytic infiltrate in LP
Dx lymphoepithelial lesions
Reactive-appearing B-cell follicles
Gastric lymphoma (MALTomas) - Sx
Dyspepsia and epigastric pain
Less common = Hematemesis, melena, and constitutional symptoms such as weight loss
Difficult to distinguish b/w gastric MALTomas and H. pylori gastritis
Carcinoid (carcinoma-like) tumor
Well-differentiated neuroendocrine carcinomas
Carcinoid tumor associated w/
Endocrine cell hyperplasia, chronic atrophic gastritis, and Zollinger-Ellison syndrome
Carcinoid tumor - Morphology
Yellow or tan in color and are very firm due to intense desmoplastic reaction –> kinking of the bowel and obstruction
Salt and pepper appearance –> microscopically
Carcinoid tumor - Clinical features
Peaks in 6th decade
Sx determined by the hormones produced (e.g. Gastrin –> Zollinger-Ellison syndrome; ileal tumors –> carcinoid syndrome = cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right-sided cardiac valvular fibrosis)
Carcinoid tumor - Most important prognostic determination
Location of tumor –> foregut (stomach + duodenum; rarely metastasize, cured by resection); midgut (jejunum and ileum) = multiple and aggressive; hindgut (appendix and colorectum) = incidental; appendix ones = benign; rectal = produce polypeptide hormones and if Sx, then abdominal pain and weight loss
Most common mesenchymal tumor of abdomen?
Gastrointestinal stromal tumor (GIST)
Clinical features of GIST
> in M
Peak age = 60
Sx = mass effects, ulceration –> blood loss and anemia (50%)
Pathogenesis of GIST
Majority caused by oncogenic, gain-of-function mutations of the gene encoding the tyrosine kinase c-KIT (CD117), which is the receptor for stem cell factor
Morphology of GIST
Can be large, solitary, well-circumscribed fleshy mass w/ulcerated mucosa
Metastases = multiple serosal nodules throughout the peritoneal cavity or 1 or > nodules in the liver; spread outside of the abdomen is uncommon
Spindle cell type and/or epithelioid type
Best dx marker = c-KIT
Tx of GIST
Complete surgical resection
Prognosis
Based on tumor size (recurrence = 10 cm common) mitotic index, and location
