Gi - 2-24 - Path Of Gastric Diseases

Front 1

Fundus location and cells

Back 1

Above the GI junction

Parietal cells (acid) and chief cells (pepsin)

ECL cells too?

Front 2

ECL cells secrete...

Back 2

histamine (in fundus and corpus/body I believe)

Front 3

Antrum

Back 3

Part of stomach nearest to duodenum.

Mucous cells and G cells (gastrin)

Front 4

Cardia

Back 4

Closest to GE junction

Mucous cells.

Front 5

4 main layers of the stomach

Back 5

mucosa
submucosa
muscularis propria
serosa

Front 6

entire stomach covered by...

Back 6

foveolar compartment.

glandular compartment is underneath that.

Front 7

parietal cell appearance

Back 7

very pink

Front 8

ECL cell appearance

Back 8

clear halo around them and not prominent unless there is an inflammatory condition.

Front 9

Protective barrier of teh stomach components

Back 9

mucus secretion
bicarb secretion
epithelial barrier
mucosal blood flow
PG synthesis.

Front 10

is chronic gastritis just long standing acute gastritis?

Back 10

no

Front 11

Incisura

Back 11

The notch on the lesser curvature of the stomach.

The portion of the stomach distal to this is the antrum

Front 12

Cardia and pylorus/antrum main role

Back 12

mucus-secreting

Front 13

Fundus/body main role

Back 13

Oxyntic epithelium (acid-producing)

Front 14

Acute gastritis

Back 14

Transient, no signif inflammation in lamina propria.

Erosion to the muscular layer of the mucosa.

Front 15

Acute gastritis can progress to...

Back 15

ulcer - defect extends to the submucosa (second layer)

Front 16

Easily forgettable causes of acute gastritis

Back 16

stress, ethanol, smoking, nsaids, ischemia.

bile salt regurg and chemother agents

Front 17

Congenital lesions of the stomach

Back 17

Heterotopia - non neoplastic epith where it doesn't belong (e.g. pancreas tissue in the stomach)

Hernias

Congenital hypertrophic pyloric stenosis - more often affects males and has early onset projectile vomiting because the pyloris is too thick.

Front 18

Types of acute gastritis

Back 18

Hemorrhagic and erosive

Front 19

Types of chronic gastritis

Back 19

Helicobacter pylori and autoimmune

Front 20

Curling ulcer

Back 20

Acute gastritis ulcer due to a burn.

Front 21

Cushing ulcer

Back 21

Acute gastritis ulcer due to trauma.

Front 22

Two types of helicobacter chronic gastrtitis

Back 22

Both due to bac colonization of surface foveolar epithelium.

Antral - gives rise to duodenal ulcers and has less risk of progressing to gastric CA. In the antrum.

Diffuse pangastritis - higher relationship with CA.

Front 23

Complic of chronic H. pylori gastritis

Back 23

Peptic ulcers, gastric atrophy, intestinal metaplasia, gastric dysplasia, gastric carcinoma, gastric lymphoma (MALT)

Front 24

Autoimmune chronic gastritis

Back 24

Ab mediated destruction of parietal cells.

Associated with pernicious anemia

Causes gastric atrophy and intestinal metaplasia

Front 25

Pathogen of autoimmune chronic gastritis

Back 25

Parietal cells destroyed and G cells sense this so they make more gastrin and stimular ECL cells.

So you get ECL cell hyperplasia and gastric carcinoids.

Front 26

When will you see nodular clusters of ECL cells?

Back 26

autoimmune chronic gastritis BUT NOT H PYLORI!!!

Front 27

When do gastric carcinoids arise?

Back 27

almost exclusively in background of autoimmune gastritis.

Front 28

Menetrier disease

Back 28

AKA hypertrophic gastropathy

marked foveolar hyperplasia

Front 29

Gastric polyps (4)

Back 29

Hyperplastic and gastric fundus gland polyps - both are almost always benign.

Peutz-Jeghers polyp (hamartomatous polyp) - arborizing appearance in the SM layer.

Adenomatous polyp - pre-malignant potential and it is neoplastic.

Front 30

Gastric fundic gland polyp assocated with...

Back 30

long term PPI use and familial adenomatous polyposis.

Front 31

Dx criteria of chronic gastritis

Back 31

Chronic inflamm cells in the lamina propria.

Note that it often goes to duodenal ulcers.

Front 32

Where is H pylori most often found

Back 32

antrum

Front 33

Freq of gastric malignancies

Back 33

Carcinoma - Adenocarcinoma (90%)

Lymphoma (4%)

Carcinoid tumor (3%) - endocrine cell phenotype

Gastrointestinal stromal tumor (2%) - interstitial cell of Cajal phenotype.

Front 34

Gastric carcinoma - two types

Back 34

They are both epithelial

Intestinal - malig cells form glands. Arises from dysplasia and due to progressive genetic changes. Males more often affected and decreasing incidence in the US because of less H pylori infections.

Diffuse type - Malig cells infiltrate individually. Precursor lesion may not be present. May manifest as linitis plastica ("leather bottle"). Males and females eqqually affected. No change in incidence.

Front 35

Staging of gastric carcinoma

Back 35

TNM

Front 36

Gastric lymphoma

Back 36

Most arise in chronic H pylori gastritis.

MALT lymphomas usually - infiltration of neoplastic lymphoid cells into the epithelium to replace the parenchyma.

Front 37

Gastric MALT lymphoma pathogen

Back 37

H pylori stim T cells which activate B cells/

In the intial phase, B cells are T cell dependent and lymphoma can be eradicated by antibody therapy for H pylori.

In later stages though, t11;18 occurs and B cells become T cell independent so you must treat with chemo (no longer responsive to antibiotics).

Front 38

Gastric carcinoids

Back 38

Indolent endocrine cell tumors. Usually from ECL cells.

May also arise from MEN or Z-E

Front 39

Gastrointestinal stromal tumors

Back 39

mesenchymal.

Can't tell if they will be benign or metastatic.

Resemble interstitial cells of Cajal (pacemaker cells in musc propria that set pace of peristalsis).

Positive for c-kit, CD24 and actin. Negative for desmin.

Mutations in c-kit or PDGFR which upreg tyrosine kinase so they are responsive to imatinib/Gleevec.

Usually in stomach-->SI-->colon

Front 40

Diff between solitary or multiple GISTs

Back 40

Multiple associated with NF-1 and has multiple tumors. But better px becasue there is no mutation in c-kit.

Front 41

Location of gastric carcinomas

Back 41

Dis proportionally in the antrum/pylorus or cardia even though body makes up most of the stomach mass.

Diff to distinguish cancer from cardia vs. from Baret's esoph.

Front 42

Px of gastric carcinoma

Back 42

Depth is most important with penetration into muscularis propia being a big step.

LN inv - Virchow's node is the left supraclavicular node.

Mets from gastric CA to other organs - usually liver or lungs. if to ovaries bilaterally, it is caleld Krukenberg tumor (this is imp to know)

Front 43

Mets to the stomach

Back 43

Breast and lung - looks like diffuse

Lymphoma

Melanoma

Front 44

general note abt studying for this class

Back 44

Hi all,

I hope everyone is enjoying learning a bit about GI and not getting too overwhelmed. While the material is not overly complicated there is a lot to cover in a relatively short period of time. In studying the various topics, focus on understanding the physiology, pathology and pathophysiology of each organ system. Learn the presenting features and defining characteristics of the conditions/diseases covered. Treatment is not a big focus on the exam, except for the pharmacology questions or when understanding the treatment really underscores physiologic principles, as in my emphasis on H2 blockers proton pump inhibitors and gastric surgery during the acid secretion talk. I would not, for example, expect you to know which drug to use to treat Crohn's disease, but I will introduce you to the various drugs that we use.

We do spend a fair bit of time discussing the tests used to diagnose various disorders because clinically this is important, but this too is not a big focus on the exam. There won't be questions asking would you order a CT or MRI or ERCP for a specific condition but we will discuss our use of these tests in class.

Some of the material may be re-emphasized in various lectures, for example my "Meal" lecture will review all of the physiology to date. Topics that are emphasized repeatedly in class will be important for you to understand.

Concerning pathology there will be photomicrograph slides from the labs and lectures on the test.

Coming to class, conference and labs I feel is important in really understanding the material.

The lecture notes should complement the PowerPoint presentations. If there are specific details or tables and charts mentioned in the lecture notes that are not covered in class, I would not worry about them.

Lastly I tightened up the pancreas slides a bit and have reposted them on blackboard, use the latest version to study from.

Steve Bensen