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101 Cards in this Set

  • Front
  • Back
Difficulty in swallowing
dysphagia
retrosternal burning pain, regurgitation of gastric contents
heartburn
blood in stools
melena
vomiting of blood
hematamesis
lower gi bleeds
hematochezia
dilated tortous veins protrude into esophagus
esophageal varices
esophageal varices is result of what?
portal hypertension and chronic alcoholism
injury to the esophageal mucosa with subsequent inflammation.
esophagitis
esophagitis has been correlated strongly with this
esophageal carcinoma
narrow of esophagus
stricture
due to chronic GI reflux, this is the replacement of normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells
barrett esophagus
significant clinical outcome of barrett esophagus
dev. of adenocarcinoma, thus screening recommended
90% of esophageal cancers but in US not so much.
Squamous cell carcinoma
dominant esophageal cancer in US
adenocarcinoma
only recognized precursor to esophageal adenocarcinoma
barret esophagus
1. iron deficiency anemia
2. atrophic glossitis (bald tongue)
3. dysphagia (dif. swallowing)
plummer-vinson syndrome, common in swedish women who also have atrophic gastritis and esophageal webs.
chronic inflammation of stomach
atrophic gastritis
overused term, inflammation of the gastric mucosa
gastritis
chronic mucosal inflammatory changes leading to muscosal atrophy and epi. dysplasia
chronic gastritis
most important etiologic association for chronic gastritis
H. pylori
autoantibodies to the gastric gland parietal cells
autoimmune gastritis
name two types of chronic gastritis
1. H. Pylori
2. autoimmune
h. pylori induced proliferations of lymphoid tissue w/in gastric mucosa can lead to
gastric lymphomas
patients with peptic ulcer often have what?
h. pylori infection
acute mucosal inflammatory process of transient nature
acute gastritis (NOT ASSOCIATED WITH H. PYLORI)!!
major cause of hematameses (throwing up blood), complicated by NSAID use
acute gastritis (NOT ASSOCIATE WITH H. PYLORI)!!
breach in epi. of mucosa only.
erosion
a breach in the mucosa of the GI that extends through the musc. mucosa into the submucosa or deeper.
ulcer
chronic, usually solitary lesions that occur in any portion of the GI exposed to the aggressive action of acid-peptic juices.
peptic ulcers
ratio of peptic ulcers in duodenum to stomach
4:1
remitting, relapsing lesions with no racial or genetic influence
peptic ulcers
name the two key facts regarding peptic ulcers
1. fundamental requisite is mucosal exposure to gastric acid and pepsin
2. strong causal assoc. w/ H. Pylori (70% of cases)
Other major cause of peptic ulcers (besides H. pylori)
NSAIDs, ^ w/ age, dose of NSAID & prolonged usage. Suppression of prostaglandin synthesis is key to nsaid indused peptic ulceration
extremely common condition in peptic ulcer disease patients
chronic gastritis
what do NSAID associated peptic ulcer disease pts + H. pylori results in
Chronic gastritis, without H. Pylori, won't have chron. gastritis
Multiple peptic ulcerations in the stomach, duodenum and even jejunum due to excess gastrin by a tumor (a paraneoplastic syndrome)
Zollinger-Ellison Syndrome
focal, acutely developing gastric mucosal defects due to stresses
Acute Gastric Ulcerations
acute gastric ulcerations due to trauma defined as:
major surgery, sepsis
ulcers due to extensive burns
Curling ulcers
ulcers due to trauma or surgical injury to the CNS or intracerebral hemorrhage
Cushing ulcers
final type of acute gastric ulcerations, do to irritants:
NSAIDs and corticosteroids, typically.
leading gastric cancer, has intestingal and diffuse types
Gastric carcinoma
malignancy that arises from gastric mucous cells having undergone metaplasia due to chronic gastritis. Well differentiated, form neoplastic intestinal glands, declining in US
Intestinal type gastric carcinoma
arrises de novo from native gastric mucous cells, not assoc. w/ chronic gastritis, poorly differentiated, no glands, permeate mucosa and infiltrative growth pattern, 1/2 of GC in the US
Diffuse type gastric carcinoma
metastasis involving supraclavicular lymph node
Virchow's node
metastatic invasion to ovaries
Krukenberg tumor
predisposing factors to adenocarcinoma:
1.chronic gastritis associated w/ H. Pylori
2. diet
distension of colon greater than 6-7 cm, congenital and acquired disorder
Hirschsprung disease, congenital megacolon
cause of hirschsprung/megacolon
caudad migration of neural crest-derived cells along GI arrests before reaching anus
variceal dilations of anal and perianal submucosal venous plexuses
hemorrhoids (straining or chronic constipation or pregnancy)
increased stool mass, frequency or fluidity
diarrheal disease
viral, bacterial, parasitic or protozoal GI infection
enterocolitis
bacterial diarrhea due to toxins
bacterial enterocolitis, an example of a toxin would be C. Botulinum
enteric pathogen that adheres to mucosal epi.
bacterial enterocolitis, incubation of several hours to days before onset
suboptimal absorption of any or all ocmponents of normal diet
malabsorption syndromes
defective intraluminal digestion
pancreatic insufficiency, undigested nutrients ^ osmotic pressure, result in diarrhea
mucosal cell abnormalities
lactose intolerance, a deficiency of disaccharidase
reduced small intestinal surface area
gluten sensitive enteropathy, aka celiac disease
prototypical noninfectious malabsorption due to reduced absorptive surface area
celiac disease
sensitivity to gliadin
celiac disease, leads to total flattening of mucosal villi and loss of absorptive surf. area due to immune response
malabsorption due to intestinal infection
tropical sprue
Crohn disease an dulcerative colitis, collectively known as
idiopathic inflammatory bowel disease
affects any level of GI, mouth to anus, mostly small intestine and colon. a systemic inflammatory diesaes w/ predominant GI involvement.
Regional Enteritis (Crohn Disease)
skip lesions
sharply delimited and typically transmural involvement of the bowel by an inflammatory process with mucosal damage (Crohn Disease)
Granulomas in alimentary tract
presence of non-caseating granuloma in 40-50% of cases of Crohn Disease
fistula formation
the 3rd characteristic of CD
ulceroinflammatory disease affecting the colon but limited to the mucosa and submucosa except in the most sever cases. Begins in rectum and extends proximally in continuous fashion
Ulcerative colitis
well formed granulomas are absent
UC
no skip lesions
UC
mucosal ulcers rarely extend below submucosa and serosal surface typically normal
UC
much greater risk for carcinoma than Crohn Disease
Ulcerative Colitis - think inflammation = predisposition to cancer
blind pouch leading off GI tract
colonic diverticulosis
most common location for diverticula
colon
2 causes of diverticula
1. exaggerated peristaltic contractions with abnormal elevation of intraluminal pressure
2. focal defects peculiar to the normal musculature of colonic wall
weakness or defect in wall of peritoneal cavity, protrusion of pouch like sac of peritoneum
hernial sac
adhesions between bowel segments or abdominal wall, often post surgery
intestinal adhesions
telescoping of proximal segment of bowel into immediately distal segment
intussusception
twisting of a loop of bowel about its base or attachment
volvulus
tumorous mass that protrudes into lumen of gut
polyps
90% of all epi. polyps, no malig. potential
non-neoplastic polyps
most common type of non-neoplastic polyp, small and multiple
hyperplastic polyps
normal tissue, all jumbled around
hamartoma
juvenile or peutz-jeghers
examples of hamartomatous polyps
hamartomatous proliferation occurs most freq in kids
juvenile polyps
a familial polyposis syndrome, hamartomatous polyps. does not develop colonic carcinomas but is assoc. w/ ^ risk of malignancy
Peutz-Jephers Syndrome
500 to 2500 colonic adenomas that carpet mucosa, due to mutation in APC gene. min of 100 polyps for dx. colonic cancer 100% by midlife
familial adenomatous polyposis FAP
APC mutation, has several extraintestinal tumors, hundreds of thousands of adenoma, colon cancer 100% by midlife
Gardener's syndrome
Two polyp syndrome related to mutated APC gene
Familial adenomatous polyposis (FAP) and Gardener's Syndrome
hamartomatous polyps in GI, does not develop colonic carcinomas, but is associated with ^ risk of malignancy
Cowden syndrome
Two syndromes, both w/ hamartomatous polyps, don't becme carcinomas, but are associated w/ ^ risk of malignancy
1. Peutz-Jephers Syndrome
2. Cowden Syndrome
2 pathways for colon cancer development
1. APC/Beta catenin pathway
2. MSI microsatellite instability pathway
loss of APC tumor supressor gene is believed to be the earliest event in the formation of adenomas. Chromosomal instability.
APC/Beta Catenin pathway *most colon cancers*
germline mutations in APC gene giving rise to hundreds of adenomas that progress to form cancers
adenoma-carcinoma sequence, part of APC/b catenin pathway
defective *DNA repair* caused by inactivation of DNA mismatch repair genes
MSI microsatellite instability. *non polyps*
MSI pathway gives rise to this type of cancer
hereditary nonpolyposis colon carcinoma
unique tumor from enterochromaffin cells of gut
Carcinoid tumors, mainly small intestine
problem with GI carcinoids
often have secratory products, ex: zollinger-ellison (excess gastrin) cushing syndrome (ACTH secretion).
GI carcinoids that have metastasized to liver
Carcinoid Syndrome
w/ GI carcinoids, what must be present for development of syndrome?
hepatic dysfunction due to metastases from other sites.
chronic gastritis and H. Pylori predispose to what lymphatic cancer?
gastrointestinal lymphoma
result of fecalith
acute appendicitis.