GERD: Upper Lower GI pathology
Upper and lower GI - Mahmoud
Terms in this set (88)
causes of esophageal obstruction
etiology and morphology of dismotility
diffuse esophageal spasm, narrow lumen.
Etiology and morphology of Stenosis
Idiopathic or secondary to inflammation and scarring
Fibrous thickening of sub mucosa and atrophy of muscle layer
esophageal web. Etiology,morphology?
women over 40//associated with Plummer Vinson syndrome
M: ledge like protrusions of the mucosa, the web is fibrovascular CT submucosa.
ESophageal ring. Etiology, Morphology?
M: similar to web but circumferential.
Triad of Achalasia
1. Failure of LES to relax in resp to swallowing
2. Absence of peristalsis in the body of esophagus
3. Increased LES tone.
General cause of achalasia
any condition which leads to destruction of the myenteric plexus.
Secondary causes of achalasia
Diabetes: Autonomic neuropathy
Causes of Esophagitis
-Mallory weiss tears; lacerations
-chemical and infectious
-reflux esophagtitis GERD
- Barrett's esophagus
Esophagitis via laceration. Etio/Morph?
E: Mallory weiss tears
M: Linear lacerations, may cross the GE junction
Esophagitis chemicals. E/M?
E: pill induced, chemotherapy, radiation
M: Ranges from mild inflammation to strictures, perforations and hemorrhage
Esophagitis via infection. E/M?
E- herpes simplex, CMV, Candida
M- Punched out ulcers (HSV), shallow ulcers (CMV), Grey pseudomembrane (Candida)
Reflux esophagitis. E/M?
M- Hyperemia, eosinophils and basal zone hyperplasia
Mallory weiss tear
a tear in the mucosal layer at the junction of the esophagus and stomach
Barrett's esophagus morphology
Gross- velvety mucosa
Micro- abnormal mucosa above the GE junction
Histo- intestinal METAPLASIA defined by goblet cells and DYSPLASIA defined by atypical mitosis and failure of ep cells to mature
Barrets esophagus asw/increased risk of?
herniation of stomach through an enlarged esophageal hiatus in diaphragm
Pathogenesis Hiatal hernia
widening space btwn the diaphragm and esophagus--> incompetence of lower esophageal sphincter
transient, mucosal, acidic damage to stomach mucosa
etiology of acute gastritis
due to imbalance between mucosal defense and acidic environment
Acute gastritis, 3 different cases
superficial inflammation= mild acute gastritis,
erosion (loss of superficial epithelium)= acute erosive hemorrhagic gastritis, or
Ulceration (loss of mucosal layer)
chronic inflammation of stomach mucosa
chronic gastritis etiology
due to H. Pylori or autoimmune destruction
morphology in chronic gastritis
atrophy, metaplasia and carcinoma (autoimmune)
peptic ulcer, adenocarcinoma
mechanism of acute gastritis
1. deficient mucin protective layer: NSAID
2. inhibition of gastric bicarbonate: uremia
3. Direct cell injury: alcohol
specific causes of acute gatritis
Nsaids (decreased PGE2), excessive alcohol, heavy smoking, chemo, uremia, systemic infections (salmonella), severe stress, ischemia and shock, suicide attempts with acids/alkali, mechanical trauma (NG tube)
Morphology of Mild acute gastritis
edema, congestion, surface epithelium is intact. PMNs (active inflammation)
acute erosive hemorrhagic gastritis morphology
inflammation, hemorrhage, and erosion of surface epithelium.
acute gastric ulcer morpholoyg
loss mucosal layer (surface epithelium and lamina propria)
acute gastritis picture
acute erosive hemorrhagic gastritis picture
acute gastric ulcer picture
Chronic H pylori gastritis mechanism
H pylori urease and protease weaken mucosal defenses
Chronic autoimmune gastritis
Autoimmune destruction by CD4 T cells hypersensitivity reaction against parietal cells
associated conditions with chronic H pylori vs autoimmune gastritis
H pylori- low socioeconomic status/poverty
autoimmune- autoimmune dz, diabetes.
sequelae of H pylori vs autoimmune gastritis
H pylori- Peptic ulcer, adenocarcinoma
Autoimmune- Atrophy, pernicious anemia, adenocarcinoma and carcinoid syndrome
Most likely location of chronic H pylor gastritis
ML location of chronic autoimmune gastritis
body and fundus
Histo: Chronic H pylori gastritis
Acid, oxyntic cells, inflammatory cells, gastrin
Acid increased or slightly decreased
Oxyntic cells are not colonized
Subepithelial plasma cells
Normal gastric or decreased
Histo: chronic autoimmune gastritis
acid, oxyntic cells, inflammatory cells, gastrin
loss of parietal cells and acid producing oxyntic cells, achlorohydria
Lymphocytes macrophages deep in central glands
Antral G cells hyperplasia with INCREASED Gastrin level
Chronic gastritis H pylori picture
Autoimmune chronic gastritis picture
Peptic ulcer disease
Chronic solitary ulcer (The presence of chronic gastritis distinguish PUD from acute gastric ulcer since the mucosa adjacent to the ulcer is NORMAL IN acute gastric ulcers)
PUD commonly asw/
sites of PUD
First portion of duodenum (90%),Gastric antrum (10%), esophagus, meckel's diverticulum.
likely cause of duodenal PUD vs Gastric PUD
duodenal- almost always due to H pylori.
G- due to H pylori, NSAID, bile reflux.
Pain timing PUD duodenal vs gastric
d- pain improves with meals
g- worsen with meals
ruptures in PUD duodenal vs gastric
d- rupture leads to bleeding from Gastroduodenal artery
g- rupture leads to bleeding from left gastric artery
which PUD is more frequent in pts with chronic renal failure, COPD, alcoholic cirrhosis and hyperparathyroidism
sharply punched out, margins are not elevated unlike cancerous ulcers. + slide 41
Zollinger Ellison syndrome
hyper gastrinemia stimulating extreme Gastric secretion --> peptic ulcers
- gastrinoma (gastrin secreting tumor)
- Pancrease, stomach or duodenom
- intractable ulcer
MC (congenital?) anomaly
- derived from persistence of proximal portion of omphalomesenteric duct
- true diverticulum
congenital defect of periumbilical abdominal MUSCULATURE
-creates a membranous sac, into which intestines HERNIATE.
Hirschprung disease/ Congenital Megacolon
1. neural crest gives rise to Neurons and glia of ANS
2. In the embryo, the migration of neural crest-derived cells along the alimentary tract arrests at some point before reaching the anus-->aganglionic segment formed that lacks both the Meissner submucosal and Auerbach myenteric plexuses--> functional obstruction and progressive distention of the colon proximal to the affected segment.
3. Ganglia are absent from the muscle wall and submucosa of the constricted segment but may be present in the dilated portion.
clinical presentation of Hirschprung disease/congenital megacolon
1.delay occurs in the initial passage of meconium,
2. which is followed by vomiting in 48 to 72 hours
complication of Hirschprung dz/congenital megacolon
superimposed enterocolitis with fluid and electrolyte disturbances
Ischemic bowel disease
End arteries occlusion--> small focal lesions or
Major mesenteri vessel--> segmental infarction
predisposing causes of ischemic bowel disease
1. Arterial thrombosis
2. Arterial embolism
3. Venous thrombosis
Tumors which invade blood vessels (HCC)
severity of injury in ischemic bowel disease
1. Transmural infarction: in ACUTE ischemia
2. Mural infarction: in ACUTE/CHRONIC ischemia
3. Mucosal infarction: in Acute/Chronic ischemia
serosa is spared in which form of bowel ischemia
Mucosal and Mural
causes of Ischemic bowel disease
Acute arterial occlusion or Hypoperfusion
Acute arterial occlusion occurs in
Hypoperfusion occurs in
pathogenesis of ischemic bowel disease- two phases of injury
1. initial hypoxic injury- mild
2. reperfusion injury- severe due to ROS
which watershed zones are most vulnerable in ischemic BD
which epithelium is more vulnerable in ischemic BD
Surface epithelium is more vulnerable that crypt (glands) epithelium. Surface epithelial atrophy with hyperproliferation of crypts is pathogonomic of ischemic intestinal disease
transmural infarction morphology in ischemic BD
1. w/in 18-24 hours Reaches serosa.
Micrscopically: Pseudomembrane resembling Clostridium pseudomembrane colitis
2. With arterial occlusion the demarcation from adjacent normal bowel is fairly sharply defined.
3. Within 24 hours
Wet gangrene and perforation
isch BD picture
Tortuous dilations of submucosal and mucosal veins, venules (cecum or right colon).
after SIXTH decade of life.
Prone to rupture and bleed into the lumen.
Such lesions account for 20% of significant lower intestinal bleeding.
The hemorrhage may be chronic and intermittent and only cause severe anemia, but rarely it is acute and massive.
variceal dilations of the anal and perianal submucosal venous plexuses
Malabsorption presents as
Chronic diarrhea (STEATORRHEA is hallmark)
Mechanism of Malabsorption
Defects in one or more of the following
malabsorption in Celiac disease, tropical sprue and IBD is due to defects in
terminal digestion, transepithelial transport
malabsorption in Cystic Fibrosis b/c defect in
malabsorption in Chronic pancreatitis b/c defect in
same as CF: intralumial digestion
malabsorption in Whipple disease b/c defect in
malabsorption in Viral, parasitic and bacterial GE is b/c defect in
Terminal digestion and transepithelial transport
Malabsorption in Celiac disease is due to
Due to a hypersensitivity response of the intestinal mucosa to gliadin, a component of gluten, which is the major protein in wheat, rye, barley and oats
- generalized malabsorption
tx malabsorption in celiac disease
Prompt clinical and histopathological response to withdrawal of gluten containing food from diet
Celiac disease morphology
- increased numbers of intraepithelial lymphocytes (IELs),
-epithelial proliferation with crypt elongation .
immune mechanism in celiac disease
both innate and adaptive
-gliadin peptides induce epithelial cells to express IL-15,
Epithelial cells triggers activation and proliferation of CD8+ intraepithelial lymphocytes
CD 8+ T lymphocytes are induced to express NKG2D, a natural killer cell marker.
These lymphocytes become cytotoxic and kill enterocytes
These NKG2D+ CD8+ T cells do not recognize gliadin. (???)
Malabsorption in celiac disease is associated with sequelae:
dermatitis herpetiformis (pic slide 70)
Inflammatory bowel disease
discussed in lab:
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