W5. Disease of oesophagus, stomach and duodenum

Question 1

esophagus + layers

Answer 1

msucular tube from pharynx–>stomach

layers:
mucosa, submucosa, muscularis propria, adevntitia/Serosa

Question 2

congenital anomalies/disorders

Answer 2

• not common
  types:
  1.congenital astresia and stenoses
  2. rings and webs
  3. esophageal diverticula

Question 3

what is atresia and stenosis

Answer 3

ATRESIA:
-congenital disoder which orifice/passage is closed/absent
-anywehere in GIT
-etiology is unkown

STENOSIS
-abnormlal narrowing of tube/orifice
-usulaly aquired and distal esophaegus

Question 4

what is atresia in 85% of cases associated with

Answer 4

Tracheoesopgeal fistula(TF) ->leads to aspiration pneumonai.

in adulthood-presentined w repeated pulmonary infections

Question 5

diagnosn of congenital atresia and stenosis

Answer 5

polyhydramnios(^amniotic fluid in uterus), esopgaheal puch, small/absent stomach bubble, fluid filled loops of bowel on ultrasoudn suggest prenatal diagnosis

Question 6

types of rings and webs

Answer 6

1. esopahgel webs
2. plummer vinson syndrome
3. Schatzki ring

Question 7

Esophageal rings

Answer 7

• thin, mucosal membrane project into esopgaehal lumen
  -anywhere in eso
  -structrye: fibrovascular tissue+mucoa/submucosa around

who: middle aged women
clinical: difficulty swallowing=dysphagia

Question 8

plummer vinson syndrome

Answer 8

-rare
-charactertized by
a. CERVICAL esopgaheal web
b. mucoal lesions of mouth and pharync
c. iron deficiency anemia

clinical: dysphagia

Question 9

schatzki ring

Answer 9

-LOWER esophageal narrowing: gastro-esophageal juntion
- asymptompatic
-intermittent dysphagia

Question 10

esophageal diverticula

Answer 10

True diverticulum:
- outpouching of the wall that contains all layers of the wall
-comgenital
-Meckels diverticulum

False diverticulum/pseudodiverticulum:
- sac has no muscular layer
-aquired
-Zenker diverticulum/esopageal

so true include muscle mens pseudo går gjennom msucle

Question 10

zenkers diverticulum

Answer 10

-when the muscle between the throat and esophagus, known as the cricopharyngeus muscle, over-tightens, causing the throat above it to pouch out
- can acc a large amount of food
- most commen diverticula
-false
-proximal in eso

symp: regurgation of food, w/o dysphagia, recurrent aspirqtion pneumonia can happen
who: men >60y

Question 11

midesohageal (traction) diverticual

Answer 11

-They happen when an external force applies traction to your esophageal wall.
-happen in middle esopgaheus(chest)
-reflect disturbance in esopgaheal mototr function or maybe adhesions
-asymptomatic

Question 12

epiphrenic diverticula

Answer 12

-false
-distal esopgaheal-right above diaphragm
-esophageal motor disturbances like: false diverticula caused by pressure — for example, from your esophagus trying to push food into your stomach through a narrowed passageway.

Question 13

what are esopgaheal motor disorders and say types

Answer 13

• autonomic coordination of muscles when swallowing in motor function
  -dyspgahia is hallmark: awarness that food is nto going down, but sånnsett not painful
  -odynophagia: pain when swallowing
  Causes:
  1. systemic disaeases of skeletal muscle
  2. neurological disaese affecting nerves to skeletal or smooth muscle
  3. peripheral neuropathy associated with diabetes or alcoholism

TYPES
1. achalasia
2. systemic sclerosis cuases fibrosis of esopahgeal wall

Question 13

achalasia/cardiospam

Answer 13

-failure of lower esophageal sphincter to relax when swallowing–>hypertrophy and dilates!!!

ikke viktig
-inflammatory diases–>loss of inhibitory neurons in esopagheal myenteric plecus. CHRONIC infla–>neuritis and ganglionitis–>loss of these nervecells and fibrosis–>esopgaheal function destruction

Etiology:
-unkown
-chagas disease-latin america
- amylodidosis, sarcoidosis, infiltrative malignancies

common sympt: dusphagia, sometime odynophagia+regurgation, squamos cell carcinoma

x-ray: bird-beak

Question 14

systemic sclerosis/scleroderma

Answer 14

-leads to fibrosis by hardenign and thightening of skin and CT. ^coll production
-anywhere in GIT(+organs)-mostly eso
-lower esophgaeal spohincter qne pqeristalisis may be impared

Pathology:
- fibrosis in smooth m in eso
-non specific infla
-small aa and arteriolis-intimal fibrosis

clinical
-dysphagia, regurgation, heartburn caused by peptic esophagtitis, severe refluc changes can occur

Question 15

What is hernia and types of hiatal hernias

Answer 15

protrusion of stomach into chest through enlarged diaphragmatic openeing

Types:
- Sliding(axial)
- paraesophageal (non-axial)

Question 15

Sliding (axial) hernia

Answer 15

-part of stomach moves upward above diaphragm
-95’% av alle hernia
-asymptomaptic eller gastroesopgaheal reflux

Question 16

paraesophageal (non axial) hernia

Answer 16

-fundus through esophageal hiatus og stiller seg vedsiden av
-5% of hernias
-sumtomps: dysphagia, fullnes after meal, shortness of breath, odynophagia, kanskje bledding from peptic ulcers

Question 16

Esophagitits types

Answer 16

1. reflux(peptic)+baretts
2. esosinophilic
3. infective
4. chemical
5. iatrogenic

Question 17

reflux/peptic esophagitis

Answer 17

-most common cause
-reflux of gastric/duodenal contonents bc incompotent lower esophageal sphincter
-frequent and prolonged episodes

risk factors: alchohol, tobaco, obestiy, pregnancy, cns depres, hiatal hernia

endoscopdy: erythrema, edema, lineral ulcers

symptoms: heart burn, dysphgaia

long ter, consequence: bleeding, stricture, baretts esophagus

Question 17

baretts esophague

Answer 17

-from reflux esophagitits
-squamos epi –>columnar aka columanr metaplasia

Barrett’s epithelium (columnar metaplasia) → Dysplasia → carcinoma in situ →
esophageal adenocarcinoma (risk factor)

what we see-macro: red area, hiatal hernia and peptic ulcer at squamocolumnar junction

micro: mataplastic columnar cells, maybe intestinal epi/gastric flands/cardiac mucous glands, dysplastic changess

Question 18

Eosinophilic esophagitis

Answer 18

-chronic, allergic inflammatory disease
-allergies to ingested food and inhaled allergens

symptoms: dysphagia, vomintign and pain, progressing to odynophagia, stenosis and foodd impaciton

who: children mostly

15 esoinophils

Question 19

infective esophgaitiis

Answer 19

-associated with immunosuppresions
-symtpoms: dysphagia and odynophagia

candida esophagitits/mycotic: most comon

who: DM, corticosteroids intakers

other ecamples
-herpetic(herpes simplex virus-HSV): punched out ulcers, see multinucleted cells on biopsy

• cytomegalovirus(CMV): large deep ulcers, see owl’s eye inclusion bodies in infected cell

Question 20

chemical esophagitis

Answer 20

-result form ingestion of corrosive agents -accidentaly with children, cleaning supplies Pathology - Alkaline agents-->liqueafactive necrosis+inflamamtion+ small vv thrombosis - Acidic: coagulative necorsis

Question 21

Iatrogenic esophagitis

Answer 21

-Iatrogenic: illness caused by medical examination or treatment -EX: 1. Nasogastric tube: pressure ulcers and refluc esophagitis 2. external irridation for treatment of thoracic cancers-->esophagitis and stricture

Question 22

what are esophageal varices

Answer 22

-dilated veins benetg mucosa. are prone to rupture and hemorrhages - lower third of esophagus -linked with hepatic cirrhosis and portal hypertension (gastroesophageal anastomooses) -result in life threting hemorrhage

Question 23

what is mallory weiss syndrome

Answer 23

-acute bleeding, secondary to longitudinal mucosal laceration at gastroesophageal junction - non-transmural tears (in contrast to Boerhaave syndrome) - provokes sudden rise in the intragastric pressure symptoms:Most commonly characterized by abdominal pain, history of severe vomiting, hematemesis and the strong involuntary effort of vomit (retching), maybe melena risk facotry:▪ 40-80% of patients have a history of heavy alcohol use leading to vomiting, -good progningsis, bleeding stops in 80-90% of cases basically : tear on agstric side of the gastroesophageal junciton, which may extend to distal esophagues. - hematemesis - tear-->upper GI bleeding -incomplete tear-only affect mucosa and submucosa

Question 24

Boerhaave syndorme

Answer 24

-Perforation or post-emetic rupture (forceful emesis) of the esophagus, results from a sudden increase in intraluminal esophageal pressure due to vomiting -tear occur on esophgael side-typically left lower esopahgus under diaphragm in ADULTS, younger: right pleural cavity POSTEROLATERAL WALL OF LOWER THIRD OF ESO - clinicallt:Sudden onset severe chest pain in the lower thorax and upper abdomen after repeated episodes of retching or vomiting, often with fever typically, acute upper GI bleeding is NOT seen i motsetning til mallory weiss other - hammans sign: cruching sound of heart bc pneumomediastriunum -chest pain and shock -subcutaneous emphysema -complete rupture at lower thoracic esophagus

Question 25

neoplasm of esophagus-benign tumors types

Answer 25

1. leiomyoma 2. squamos papilloma

Question 26

Leiomyoma-bening tumor of eso

Answer 26

-spindle cell(mesenchumal ) tumor along smooth muscle line -most common mesenchymal+bening tumor of eso -bening +indolent course -Who: median 35 y-mostly men -see intramural mass - malignant form is leiomyosarcoma: rare and poor prognosis

Question 27

squamos papilloma-bening tumor of eso

Answer 27

-small nodules of eso w prolif squamos epo -uncommon, distal eso -sometimes associated with Human pappiloma virus(HPV) -rare malignnat tranformation

Question 28

malingnat utmors of esophagus-Types

Answer 28

1. adneocarcinoma 2. squamos cell carcinoma

Question 29

adenocarcinoma-malignant eso

Answer 29

-vesten -galndular differations (baretts) -distal 1/3 of eso -factors: male, white, obesity, tobacco, alcohol -symptoms: dysphagia, odynophagia, weight loss -survival: 5 yeras-dårliggg

Question 30

squamos cell carcinoma

Answer 30

-globally, developing countries -squamos differations+keratinization - middle 1/3 - factors: smoking+alcohol, poor prognisis -clinically: dysphagiam odynophagia, weight looww

Question 31

most comon gastric infection

Answer 31

helicobacter pylori

Question 32

regions of stomach

Answer 32

cardia, funcus, body, pyloric antrum, pylorus

Question 33

congential anomalies of stomach: types

Answer 33

1. pancreatic heteoptia 2. pyloric stenosis

Question 34

pancreatic heteropia(ectopic pancreas

Answer 34

-panceratic tissue foudn outisde the pancreas. no connection to normal pancrea - pancreatic acinin in stomach wall -gastric mass -newborn or loater macro: mass -->gastric lumen in submucosa mostly, antrum/pylorus micro: normal pancreatic and ductal tissue

Question 35

pyloric stenosis

Answer 35

-hypertrophy and narrowing of pyloric luemen -most commen congenital who: male children mostly, in newborn we see vomiting -adult form rarely seen clincially: projectile vomiting onset at 3-12 weeks, visible peristalsis

Question 36

Miscellaneous aquired conditions of stomach: types

Answer 36

1.Bezoars - foreign bodies -mentally ill patient intake this -types: trichobezoars (hair), phytebezoars(fibers, seed, fruit skin), trichophytobezoars-begge 2. acute dilation - by gas or fluid -paralysis of gastric musculature: after abd operation, peritonits and pyloric stenosis 3. gastric rupture - fatal -blutn trauma, intake of heavy metl

Question 37

inflammatory conditions of stomach

Answer 37

-gastritis and peptic ulcer -protective vs hostile factors -hostile åredominating-->peptic ulcers

Question 38

what is gastritis and types

Answer 38

-infla of gastric mucosa - peptic ulcer and gastric cancer - type: acute and chronic(majority)

Question 39

acute gastritic

Answer 39

- pangastritis: entire inner surface of stomach -smaller surfaces like antral adn pyloric gastritis Types 1.erosive:/hemorrhagic/stress: 2.non erosive Etiopathogenesis: -dietal and persoanal habits -infections: bacterial and viral - drugs - chemical and physical agents -streess Pathophysio -imbalanec btw aggressive and defensive factors that maintain intergity of gastric mucosa -symptoms: nondescript epigastric discomfort, nausea, vomiting, loss od appetite, bleching, bloating

Question 40

❖ Acute erosive/hemorrhagic gastritis (stress gastritis)

Answer 40

-reactive -arise in SHOCK state -abdominal pain+bleeding associated with alcohol, NSAIDS, low hemodynamic state after trauma, bile redulc, cocaine!!!!! - See multiple erosions in gastric mucosa by damage to mucosal defenses : reduction in prostaglanding synsthesis -older people: 29-87y -clinically: often asymptomatic, abd pain, vomiting, GI bleeding, dyspepsia, gematemesis, melena acute stress gastritis - form of erosice, 5% - hypoperfusion of GI mucosa-->impaired mucosal defense -can have ^acid secretion

Question 41

❖ Acute non-erosive gastritis

Answer 41

-mostly by HB.pylori-antrum -superficial gastric mucosa -asymptomatic -usually aquired in childhood -associated with 60%gastric ulcers and 80% of duodenal ulcers

Question 42

atrophic grastitis

Answer 42

Intense inflammation due to H. pylori results in the loss of gastric glands responsible for the production of acid →

Question 43

chronic gastritis

Answer 43

-eldre: 45y 1. Etopathogenesis - samme som acute -refluc of duodenal content-bilee -H.pylori inf - associated disese of stomach and duodenum-gastric or duodenal ulcer, gastric carcinoma -chornic hypochormic anemia -autoanitbodies to gastric parietal cells 2. types A. autoimmune gastitis: B. H-pylori releated/hypersecretory gastritis: AB. mixed gastritis:atrophic w mucosal atrophy and metaplasia of intestinal or pseudopyloric type

Question 44

❖ Autoimmune gastritis (autoimmune metaplastic atrophic gastritis) (Type A)

Answer 44

-circulatiing antiparietal cell and IF AB, involve BODY-FUNDIC mucosa - loss of oxyntic cells, hypochloridria, achloridria, vitB12 deficiency -older white women: 50-60y clinically: abd pain, discomfort, weight loss, iron deficiency anemia, pernicious anemia high serium gastrin-->compensatory to hypochlorhydria low serium pepsoinogen

Question 45

❖ Helicobacter infection

Answer 45

- ->infla or ulceration in stomach -contracted in childhood but symptoms come later -longterm inf --

Question 46

Mixed gastritis – TYPE AB gastritis

Answer 46

-most common type of gastritis in all age groups. -environmental gastritis -chronic superficial gastritis to chronic atrophic gastritis, characterized by mucosal atrophy and metaplasia of intestinal or pseudopyloric type

Question 47

Complications of chronic and acute gastritis

Answer 47

1. peptic ulcers: NSAID increase chance of this 2. atrophic gastritis: loss of stomach linign and glands 3. anemia: erosice -->chronci bleeding 4. vit B12 deficiency and pernicious (megaloblastic )anemia: Type a gastritis dont produce enoguh IF to help absorb VITB12

Question 48

Peptic ulcer+etiology

Answer 48

break in the lining of the stomach, duodenum, or occasionally the lower esophagus Etiology of peptic ulcer ➢ 1. Common: ▪ Helicobacter pylori infection ▪ Nonsteroidal anti-inflammatory drugs (NSAIDs) ▪ Stress-related mucosal damage ➢ 2. Uncommon: ▪ Zollinger-Ellison syndrome and other hypersecretory acid states -tumors, viral infection, theraoy 3. rare -chronc disease, idiopahtic

Question 49

pathophysiology of peptic ulcers + types

Answer 49

1. ^vagal activity and stimulation 2. parietal hyperplasia, hyperprpod of HCL Types 1. Acute peptic /stress ulcer - surface ulceration -mutlple small mucosal erosiions -ischemsi hypoxia injur -depletion of gastric mucis/barrier 2. Chronic /stomach) - penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression Histopathologic pictures: ▪ During the active phase, the base of the ulcer shows 4 zones: * 1. Inflammatory exsudate * 2. Fibrinoid necrosis * 3. Granulation tissue * 4. Fibrous base ▪ The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis (see picture below)

Question 50

symtoms /signs of peptic ulcer

Answer 50

-A dull or burning pain in your stomach - pain anywhere between your belly button and breastbone Happens when you stomach is empty – such as between meals or during the night ▪ Stops briefly if you eat or if you take antacids ▪ Comes and goes for several days, weeks or months ▪ Lasts for minutes to hours

Question 51

dudodenal peptic ulcer

Answer 51

symptoms of a duodenal ulcer include burning, gnawing, aching or hunger-like pain, primarily in the upper middle region of the abdomen below the breastbone (the epigastric region) ❖ Pain may occur or worsen when the stomach is empty, usually 2 or 5 hours after a meal. Symptoms may occur at night at 11PM and 2 AM, when acid secretion tends to be greatest ❖ Feel better when you eat or drink and then worse 1 or 2 hours later (duodenal ulcer)

Question 52

diff btw gastric and duodenal ulcer

Answer 52

Gastric: -Symptoms do not follow a consistent pattern -Eating sometimes exacerbates rather than relieves pains Duodenal -Tend to cause more consistent pain -Pain can awaken the patient at night -Pain is relieved by food, but recurs 2 to 3 hours after a meal

Question 53

tumor like lesions

Answer 53

=polyps 1. hyperplastic (inflammatory) polyp 2. Hamartomatous polyp

Question 53

complications of chronic peptic ulcer

Answer 53

-Upper GI bleeding -perforation: communication btw stomach and periotneal space -penetration -gaatric stenosis -malignant transformation

Question 54

zollinger ellison sndrome

Answer 54

-disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. -caused by gastrinoma-->neuroendocrine tumor that secrete gastrin -^prod of HCL-->growth of mucosa and prolif of parietka and ECL cells

Question 55

Gi bleeding presentation

Answer 55

1. Hematemesis: vomiting of blood 2. melena 3. hematochexia: passage of briht red or marron blood from the rectum 4. occult Gi bleeding: not visble to patient/physician, resulting in either a positive fecal occcult blood test or iron deficency anemia w/wo pso fecal occult test 5. symtomps of blood loss or anemia: light headedness, syncope, angina, dyspnea

Question 56

bening tumors

Answer 56

Epithelial – adenomatous or neoplastic polyps Non epithelial – gastrointestinal stromal tumor (GIST)

Question 57

malignant tumors

Answer 57

Epithelial (90%) adenocarcinoma Non-epitheilal (2%) leiomyosarcoma, leiomyoblastoma Carcinoid tumors (3%) Lymphoma (4%)

Question 58

Stomach polyps

Answer 58

- rare -asymptomatic -dont become cancerous but can increase risk

Question 59

Hyperplastic polyps

Answer 59

-75% of gastric polups -H.pylori most commen etiology: hyperregenrative epi bc chronic infla stimulus like atrophic gastritis, H.pylory, pernicious anemia Upper endo: polyps: smooth, dome shaped or stalked, multiple, ANTRUM-body-fundus-cardia Micro: elongated, dilated, cystic, distorted, edematous, congested, chronically inflamed lamina propria other: epi regenerative chnages, dystrophci goblet cells, interstinal metaplasia, pyloric metaplasia, erosina and ulceration

Question 60

hamartomatous polyp

Answer 60

-uncommen, 1% - Mixture: contain mucus-filled glands, with retention cysts, abundant connective tissue, and a chronic cellular infiltration of eosinophils -EX: strawberry naevus -peutx-jeghers syndrome/juvenile polyposis syndrome: polypd+ ^pigmentation around lips, gentalia, buccal mucosa, feet and hands -little maligant potential

Question 61

❖ Adenomatous (neoplastic) polyp (bad polyp) / Gastric adenoma

Answer 61

-bening -tumor galndular tissue but not yet cancer -most common adenomas of stomach and colon: tubular, tubulovillous, villous, sessile serrated Gastric adenoma ➢ Benign epithelial tumor ➢ Localized growth of dysplastic epithelium ➢ Account for 10% of gastric polyps ➢ Related to risk for malignant progression ➢ Incidence increased w/age, peaking at 70 years old

Question 62

❖ When does a polyp become a problem?

Answer 62

Malignant potential is associated with degree of dysplasia in epithelial cells ➢ Type of polyp (e.g. villous adenoma) ▪ Tubular Adenoma: 5% risk of cancer ▪ Tubulovillous adenoma: 20% risk of cancer ▪ Villous adenoma: 40% risk of cancer ➢ Size of polyp: ▪ < 1 cm = < 1% risk of cancer ▪ 1 cm = 10% risk of cancer ▪ 2 cm = 15% risk of cancer ➢ Normally an adenoma which is greater than 0,5 cm is treated

Question 63

❖ Stomach adenocarcinoma

Answer 63

-➢ Precursor lesions are mucosal dysplasia’s -2nd most common cancer worldwide -leading cause of cancer death worldwide, 5y survival rate is 10-15% -who: males more, 70y, -risk factors: diets, smoking, H-pylroi gatsritis, germline mutations in CDH1 -Clinically: usually asymptomatic until late, weight loss, abd pain, nause, vomiting, matasatis to supraclavicular nodes,

Question 64

stomach adenocarcinoma phenotypes

Answer 64

1. Intestinal 2. diffuse -from gastric foveolar epi, -poor progninsis 3. Microsatellite instability phenotype cancers

Question 65

adenocarcinoma classificaiotion

Answer 65

- Early: confined to mucosa or mucosa + submucosa, regardless of perigastric nodal metastases ➢ Advanced: muscularis propria invasion Borman (macroscopic) classification of advanced gastric cancer: ▪ Type 1: Polypoid ▪ Type 2: Fungating ▪ Type 3: Ulcerating ▪ Type 4: Infiltrative ➢ Lauren (histopathologic) classification ▪ Diffuse ▪ Intestinal ▪ Mixed ▪ Indeterminate Adenocarcinoma – WHO classification ➢ Tubular adenocarcinoma ➢ Papillary adenocarcinoma ➢ Mucinous adenocarcinoma, tumor shows >50% mucin ➢ Poorly cohesive carcinomas, including signet ring cell carcinoma ➢ Rare variants:

Question 66

Intestinal-type adenocarcinoma of the stomacH

Answer 66

-PAPILLARY GROWTH PATTERN - chronic gastritis-->interstinal metaplasia, dysplasia, CIS and invasive carcinoma -no know precurson

Question 67

diffuse gastric carcinoma

Answer 67

atypical epi cells contain many masses of mucus

Question 68

❖ Gastric adenocarcinoma: diffuse type (Linitis Plastica; Signet ring cell carcinoma)

Answer 68

-consist of discohesive cells infiltarting through all layers -extensive fibrosis and infla - tumor cells have intracytoplasmic vacoules-->signet ring

Question 69

❖ Gastric carcinoma diffuse type mucinous

Answer 69

Sometimes atypical cells produce large amount of mucus and push out from cytoplasm to interstitium, we see mass of mucinous material and small islets of atypical carcinoid cells

Question 70

Interstitial-type gastric adenocarcinom

Answer 70

arising in chronic atrophic gastritis

Question 71

genrtic risk factor for gastric cancer

Answer 71

CDH1 gene known as hereditary diffuse gastric cancer (HDGC). The CDH1 gene, which codes for E-cadherin, lies on the 16th chromosome

Question 72

❖ Paraneoplastic manifestations

Answer 72

Sometimes it may produce this ➢ Seborrhagic keratosis or acanthosis nigricans – very typical sign for gastric cancer (velvety and darkly pigmented patches on skin folds

Question 73

Grading of gastric cancer

Answer 73

1. Low grade - cancer cell well diff -look and act much like normal -slow growing and less likely to spread 2.2. High grade ▪ cancer cells are poorly differentiated, or undifferentiated ▪ abnormal ▪ Higher grade cancer cells tend to grow more quickly and are more likely to spread ▪ 1 = Low grade, similar to normal mucosa ▪ 2 = High grade solid unglandular mass of carcinomatous cells

Question 74

staging of gastric cancer

Answer 74

-can spread to liver, pancreas, lungs -CT, PET scan, endoscopic ultrasound

Question 75

Krukenbergs tumor

Answer 75

-malignancy in the ovary that metastasized from a primary site, classically from the stomach or GI tract -source: gastric adenoma-PYLORUS mostly

Question 76

most common extranodal lymphoma:

Answer 76

it is gastric lymphoma Most are extranodal marginal zone lymphomas (MALT lymphoma) or DLBCL ➢ Both are associated with Helicobacter infection ➢ Clinically and radiologically mimics gastric adenocarcinoma

Question 77

❖ Neuroendocrine tumors

Answer 77

Neoplasms of the diffuse neuroendocrine system of the gastrointestinal tract ➢ Associated with chronic atrophic autoimmune gastritis (65%), Zollinger Ellis syndrome and MEN-I, sporadic development ➢ Symptoms often vague and non-specific ➢ In general, gastric neuroendocrine tumors have a relatively good prognosis compared with andeocarcinoma

Question 78

Gastrointestinal stromal tumor-GIST

Answer 78

-rare type of neoplasm found in the digestive system, most often in the wall of the stomach -arise form intestinal cells of Cajal - some benign and some malignnat - are tumors of CT aka MESENCHYMAL -70% in stomach, 20 in intestine and <10 in eso -c-KIT for detection/CD117