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

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

1
Q

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

A
  1. Intestinal

2. Diffuse

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2
Q

What are features of intestinal gastric adenocarcinoma?

A
  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
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3
Q

What are features of diffuse gastric adenocarcinoma?

A
  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
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4
Q

What is the presentation for gastric adenocarcinoma?

A

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

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5
Q

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

A

Malignant glands invading submucosa and muscularis propria

  • -secrete mucin if well differentiated in function
  • -dysplasia is precursor lesion
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6
Q

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

A

Intestinal:
heaped up margins on gross
–arent seen in benign gastric ulcers
—due to invasion

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7
Q

What are the complications for intestinal adenocaricnoma?

A

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

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8
Q

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

A 
CEA 
P CLUBS (Gallbladder cancer)
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9
Q

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

A

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

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10
Q

What is seen on histology for GIST?

A

Spindle-shaped tumor cells

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11
Q

What is the treatment for GIST?

A

Same treatment as chronic myeloid leukemia

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12
Q

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

A

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

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13
Q

What is the presentation for Meckel’s Diverticulum?

A

Asymptomatic

–incidental finding (upon surgery for something else)

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14
Q

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

A

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)

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15
Q

What are the complications for Meckel’s Diverticulum?

A 
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
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16
Q

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?

A

Autoimmune destruction of the mucosa of the small bowel in response to gluten

  • -oats, rye, barley and wheat (steatorrhea)
  • -common in Europeans
17
Q

What is the pathogenesis for Celiac Sprue?

A

Type IV HSR
–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

18
Q

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

A

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)

19
Q

What is the presentation for Celiac Sprue?`

A

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

20
Q

What are the extraintestinal manifestations for celiac sprue?

A

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

21
Q

What is the best investigation for celiac sprue?

A

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
22
Q

What are complications for celiac sprue?

A

Malabsorption
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)

23
Q

What is the treatment for Celiac Disease?

A

Gluten free diet

–they can recover because mucosa can regenerate

24
Q

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

A

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

25
Q

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

A

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

26
Q

What is the pathogenesis for Tropical Sprue?

A

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
27
Q

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

A

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
28
Q

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

A

Etiology: gram positive bacteria T. whipii

–older white men (old white male farmer)

29
Q

What is the pathogenesis for Whipple’s Disease?

A

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

30
Q

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

A

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
31
Q

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

A

Whipple’s: PAS positive

TB: Ziehl Neelsen Stain

32
Q

What is presentation for Whipple’s?

A

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

33
Q

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

A

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)
34
Q

What is the treatment for Whipple’s?

A

ABX

–same as tropical sprue

35
Q

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

A

Hyperacidity of gastric contents

–proximal duodenal inflammation

36
Q

What is seen on histology for peptic duodenitis?

A

Acute and chronic inflammation

  • -gastric foveolar metaplasia due to H. pylori
  • -may be a precursor to peptic duodenal ulcer
37
Q

Finally just a note of Giardia how is it acquired?

A

Protozoan gut pathogen with flagellum

–acquired from drinking water contaminated with cysts due to poor sanitation and crowded living conditions

38
Q

What is seen on histology for Giardia?

A

Organism is on top of the epithelium, not intracellular

–immunosuppression increases risk of infection

39
Q

A note on Cryptosporidium, what are some features?

A

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

Pathology Post Midterm (50 decks)

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