Module 2: GI: Gastric Cancer, Gastric Tumors, Meckel's and Malabsorption Syndromes Flashcards Preview

Pathology Post Midterm > Module 2: GI: Gastric Cancer, Gastric Tumors, Meckel's and Malabsorption Syndromes > Flashcards

Flashcards in Module 2: GI: Gastric Cancer, Gastric Tumors, Meckel's and Malabsorption Syndromes Deck (39):

The next topic to discuss is gastric adenocarcinoma. First off what are the two types?

1. Intestinal
2. Diffuse


What are features of intestinal gastric adenocarcinoma?

1. Much more common than diffuse
2. Caused by H. pylori (most common)
--in the antrum and pylorus
3. Autoimmune
--located in the body and fundus
4. Common in the older men
5. Malignant gastric ulcers usually arise de nova (malignant from the get go): following chronic gastritis.
6. Pre-disposing factor: dietary -- Japanese culture with nitrosamines and nitrites from smoked food


What are features of diffuse gastric adenocarcinoma?

1. Much more common in younger females
2. Mutation in E cadherin
3. Leather bottle stomach on gross: linitis plastic, highly desmoplastic (extensive fibrosis), signet ring cells on biopsy (intracellular metaplasia and PAS stain)
4. Complications: Bilateral ovarian metastases called Krukenburg tumors; through seeding of the peritoneal cavity you get direct spread (lymph nodes first)
5. Glands: dysplastic or malignant glands invading all layers


What is the presentation for gastric adenocarcinoma?

Early Satiety
Acanthosis nigricans (non specific black neck)
Epigastric Pain
Enlarged Virchow's Node
Para Umbilical Subcutaneous Metastasis (called Sister Mary Joseph Nodule)


The best investigation is an Upper GI scope with a biopsy, what would a biopsy show for intestinal?

Malignant glands invading submucosa and muscularis propria
--secrete mucin if well differentiated in function
--dysplasia is precursor lesion


On gross image of intestinal, what is the defined factor that it is in fact cancer?

heaped up margins on gross
--arent seen in benign gastric ulcers
---due to invasion


What are the complications for intestinal adenocaricnoma?

Metastasis to regional lymph nodes
Bleeding -- melena --- iron deficiency anemia
Obstruction --- pyloric -- pyloric vomiting
Perforate --- peritonitis --- sepsis --DIC


What tumor marker is used for both intestinal and diffuse gastric adenocarcinoma?

P CLUBS (Gallbladder cancer)


The next topic to touch on briefly is gastrointestinal stromal tumor (GIST). What are some features?

#1 mesenchymal tumor of GI tract
--60% occur in the stomach
Derived from interstitial cells of Cajal (pacemaker cells)
---express CD117 (c-kit) and majority have c-kit mutations in exon 11


What is seen on histology for GIST?

Spindle-shaped tumor cells


What is the treatment for GIST?

Same treatment as chronic myeloid leukemia


Moving onto the Small intestine. The only congenital anomaly to speak about is Meckel's Diverticulum. What is the pathogenesis?

Due to incomplete involution of the vitelline duct
---congenital true diverticulum (all layers of the bowel) on the anti-mesenteric boarder of the terminal ileum


What is the presentation for Meckel's Diverticulum?

--incidental finding (upon surgery for something else)


What is the rule of 2 in regards to Meckel's Diverticulum?

2% of the population
2x as common in males
More commonly seen in the first 2 years of life
2 inches long
2 feet from the ileocecal valve
2 tissues (gastric and pancreatic considered choristomas)


What are the complications for Meckel's Diverticulum?

Acutely inflammed --- fecal obstruction and mimics appendicitis (fever, RLQ pain and elevated WBC due to neutrophilia)
Fistula formation (communication b/t two hollow organs)
Perforation --peritonitis ---gastric tissue ulceration
Bleeding -- iron deficiency anemia


Now moving onto the three malabsorption diseases to be discussed in this course. A big thing, is how to identify differences between the three. The first disease is Celiac Disease (gluten sensitive enteropathy). What is the etiology for this disease?

Autoimmune destruction of the mucosa of the small bowel in response to gluten
--oats, rye, barley and wheat (steatorrhea)
--common in Europeans


What is the pathogenesis for Celiac Sprue?

--affects small bowel (Duodenum -- terminal ileum) however changes are more marked in proximal part of intestine
CD4 and CD8 T cells damage the mucosa of the small bowel
---due to HLA DQ2 and HLA DQ8


On biopsy slide 8, explain the histology on the right and left

Right: flattening of the villi and therefore this reduces absorption, hyperplasia and elongation of crypts, increased CD4 T cells in lamina propria, CD8 T cells in epithelial lining in crypts
--loss of vili so the vili to crypts ratio is basically 1:1 and that is not normal (hyperplasia of crypts)


What is the presentation for Celiac Sprue?`

Steatorrhea (foul smelling, pale bulky stols)
Flatulence (lots of gas)
Weight loss (losing nutrients)
Malabsorption of Vit ADEK
---A: night blindness
--D: osteoporosis, osteomalacia, tetany and cardaic symptoms
---K: petechiae, purpura, ecchymosis
--E: increased risk for cancer
Malabsorption of iron, folate and B12
--remember B12 has neurologic symptoms
--folate develops first due to no long stores


What are the extraintestinal manifestations for celiac sprue?

Dermatitis Herpeteformis
--vesicles that look like herpes
--due to IgA damage to the skin
IgA neuropathy damages the glomerular membrane
---hematuria, oliguria, azotemia, mild proteinuria, and hypertension


What is the best investigation for celiac sprue?

Serological Tests:
--Anti-TTG (tissue trans glutaminase) antibodies: mostly IgA, if IgA deficiency then the TTG would be IgG (So dont use in patients with IgA deficiency)
--Antigliadin antibodies
---Antiendomysial antibodies


What are complications for celiac sprue?

Extraintestinal complications (renal failure due to IgA neuropathy/Berger's disease )
Intestinal T cell lymphoma (aggregates of CD4 T cells in the lamina propria) (only time you get T cell lymphoma in the GI tract)
Heart failure (Due to iron deficiency)
Osteomalacia/osteoporosis (malabsorption of vit D)


What is the treatment for Celiac Disease?

Gluten free diet
--they can recover because mucosa can regenerate


Just a quick review, were are iron, folate and B12 absorbed in the body?

Iron: absorbed in the duodenum
Folate: absorbed in Jejunum and ileum
B12: absorbed in terminal ileum along with bile acids


The next malabsorption to be discussed is Tropical Sprue or Post infectious Sprue. What kind of ppl is this seen in?

Seen in adults living in or visiting the tropics who contract diarrheal illness
--so the stem will say something about recent travel


What is the pathogenesis for Tropical Sprue?

Damage to the brush border --- failure of reabsorption of micelles
--pathogenesis related to bacterial infection superimposed on pre-existing small intestinal injury
--all parts of small intestine equally involved
--small intestinal bacterial overgrowth


Tropical Sprue presents like celiac disease, so what is the diagnostic test that is the difference?

Serology is negative
--because this is due to a bacteria so patient will respond to abx
--patient may present with symptoms months or even years after visit
--can cause folate, b12 and iron deficiency due to affecting the whole SI


The last malabsorption disease to be discussed in Whipple's Disease. What is the etiology and who is affected?

Etiology: gram positive bacteria T. whipii
--older white men (old white male farmer)


What is the pathogenesis for Whipple's Disease?

Gram positive bacteria causes malabsorption (of the entire small intestine)
--macrophages engulf the bacteria, however, can not fully kill the bacteria so macrophages become distended and obstruct the lymphatic channels ---- causes dilatation of the channels ---- which stretch out and flatten the vili -- leading to malabsorption


Therefore what do you see on Upper GI scope and biopsy for Whipples? slide 9

In lamina propria of mucosa within the macrophages is the bacteria, that back up into the vili
--PAS positive (red on stain)
--Gram Positive
--H and E stain unable to see the bacteria just see the macrophages in the lamina propria


Intestinal TB looks the same on histology as Whipples, what is the difference then on histology?

Whipple's: PAS positive
TB: Ziehl Neelsen Stain


What is presentation for Whipple's?

Weight Loss
Malabsorption of fat soluble vitamins, b12, folate and iron


Now what makes Whipple's different from the other malabsorption diseases is the extraintestinal manifestations. What are they?

Due to organism travel: these are gonna help you in the stem
-Brain (dementia and seizure)(most common)
-Heart (mitral and aortic regurg)
-Eyes (uveitis)
--Joints (migratory polyarthritis)
--Skin (hyperpigmentation)


What is the treatment for Whipple's?

--same as tropical sprue


Finally a quick note of peptic duodenitis, what is the pathogenesis for this?

Hyperacidity of gastric contents
--proximal duodenal inflammation


What is seen on histology for peptic duodenitis?

Acute and chronic inflammation
--gastric foveolar metaplasia due to H. pylori
--may be a precursor to peptic duodenal ulcer


Finally just a note of Giardia how is it acquired?

Protozoan gut pathogen with flagellum
--acquired from drinking water contaminated with cysts due to poor sanitation and crowded living conditions


What is seen on histology for Giardia?

Organism is on top of the epithelium, not intracellular
--immunosuppression increases risk of infection


A note on Cryptosporidium, what are some features?

Self limiting in healthy individuals
--chronic diarrhea in AIDS patients
Histology: intracellular but at top of the cell

Decks in Pathology Post Midterm Class (50):