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DERS (GIT) > L4- GIT Pathology II (stomach) > Flashcards

L4- GIT Pathology II (stomach) Flashcards

1
Q

discuss the distribution of cells in different areas of the gastric mucosa

A

Cardia, Antrum: mucus secreting cells

Corpus, Fundus (oxyntic): chief cells (pepsinogen) and parietal cells (acid, IF)

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2
Q

list the causes of Pyloric Stenosis

A

Congenital

Acquired: chronic antral gastritis, peptic ulcers, malignancies

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3
Q

Congenital hypertrophic pyloric stenosis:

  • (1) defect/definition
  • (2) associated Syndromes
  • affects (males/females) more
A

1- concentric hypertrophy of circular muscle coat

2- Turner syndrome, Trisomy 18, Esophageal atresia

3- males (3:1)

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4
Q

Congenital hypertrophic pyloric stenosis:

  • (1) clinical presentation
  • (2) Tx
A

1- regurgitation, projectile vomiting, palpable epigastric mass, visible peristalsis

2- surgery: myotomy

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5
Q

list the categories of gastritis

A

Erosive:

  • acute gastritis
  • NSAID injury, EtOH gastritis, oral Fe, KCl

Chronic, non-erosive:

  • H. pylori
  • pernious anemia
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6
Q

describe acute gastritis (what occurs, how long it occurs, occurs in response to what)

A
  • acute mucosal process transient nature
  • occurs in severe stress (burns, shock)

-inflammation associated with hemorrhage, in severe cases erosion => GI bleed

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7
Q

how does EtOH affect the stomach

A
  • direct injury
  • inc acid secretion

-may lead to acute gastritis

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8
Q

list the clinical features (and complications) of gastritis

A

-maybe asymptomatic

  • epigastric pain, n/v
  • hematemesis, melena

-bleeding may be fatal

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9
Q

list some causes of Acute Gastritis

A
  • NSAIDs
  • excess EtOH
  • heavy smoking
  • ischemia, shock
  • severe stress (burns, surgery)
  • chemotherapy drugs
  • systemic infections
  • uremia
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10
Q

Acute Gastritis:

  • can either be (1) or (2) type
  • (3) is obvious on endoscopy, and they can lead to (4)
A

1- superficial mucosal injury = erosions (loss of surface epithelium)
2- full thickness mucosal injury = ulcer

3- erosions and hemorrhage
4- hyperemia, punctate areas of hemorrhage

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11
Q

Acute Gastritis, on histology:

  • (1) in lamina propria
  • (2) in epithelium, glands
A

1- edema, congestion (lamina propria)

2- neutrophil infiltration (surface epithelium, glands)

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12
Q

Chronic Gastritis:

  • (1) definition
  • (2) are the common causes
  • (3) are the less common causes
A

1- chronic inflammation of gastric mucosa associated with epithelial injury, mucosal atrophy, or epithelial metaplasia

2- H. pylori, autoimmune disease
3- chronic bile reflux, post-surgical (antrectomy), Crohn’s, sarcoidosis, radiation

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13
Q

Chronic Gastritis appearance on endoscopy

A
  • variable: from normal to patchy/diffuse erythema

- w/ or w/o hemorrhage to boggy with thick mucosal folds

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14
Q

Chronic Gastritis appearance on microscopy

A
  • inflammatory infiltrates in lamina propria: lymphocytes, plasma cells
  • PMNs / neutrophils in surface epithelium, glandular lumen
  • reactive lymphoid aggregates (mainly superficial, marks H. pylori infections)
  • intestinal metaplasia, glandular atrophy, dysplasia
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15
Q

H. pylori: classic bacterial features (hint- 5 important distinguishing features)

A 
Gram-
curvilinear shape
motile: flagella
non-invasive
urease+
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16
Q

list the diseases associated with H. pylori

A

-Chronic gastritis: diffuse antral, multifocal atrophic

  • peptic ulcer
  • gastric adenocarcinoma
  • gastric lymphoma
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17
Q

describe the basic progression of H. pylori infections into its associated diseases

A

1:

  • enzymes: proteases, ureases, phospholipases
  • -> direct mucosal damage
  • -> induces inflammatory response (+ attraction of inflammatory cells)
  • -> chronic gastritis, peptic ulcer

2:

  • attracts PMNs + other inflammatory cells
  • uncontrolled B cell proliferation
  • lymphoma
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18
Q

list the diagnostic testing for H. pylori, indicate the most commonly used test

A

Non-Invasive:

  • **urea breath test
  • serology: IgG, IgA
  • PCR in saliva, feces

Endoscopic based invasive:

  • rapid urease test
  • histopathology + culture
  • PCR
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19
Q

Autoimmune gastritis:

  • (1) definition
  • destruction of (2), leading to (3) changes
  • inc risk for (4), (5)
A

1- Ig’s against parietal cell Ags/IF
2- oxyntic glands
3- achlorhydria (dec HCl in stomach) + inc gastrin levels

4- gastric carcinoma
5- neuroendocrine tumors / carcinoids

20
Q

Autoimmune gastritis has the presence of (1) to cause gland destruction and (2) in the (3) part of the stomach. As a result of the destruction / (2), there is a loss of (4) and a loss of (5), where (5) leads to (6).

A 
1- Ig's against parietal cells +/- Ig against IF
2- atrophy
3- stomach body, fundus
4- acid production (= achlorhydria)
5- Intrinsic Factor
6- vitB12 def --> pernicious anemia
21
Q

Autoimmune gastritis histology:

-list the 3 main features and describe their individual presentations

A
  • chronic inflammation: deep inflammatory infiltrates composed of lymphocytes
  • gastric atrophy
  • intestinal metaplasia: goblet cells in foveolar pits
22
Q

Gastric Ulcers:

  • (1) definition
  • (2) common locations
  • heals (better/worse) than an erosion
A

1- loss of mucosa that extends thru muscularis mucosa or deeper
2- antrum (gastric), duodenal
3- worse, longer healing time

23
Q

Acute gastric ulcers:

  • (1) major causes
  • Curling ulcers via (2)
  • Cushing ulcers via (3)
  • can develop while in (4), 5-10% of the time
A

1- severe trauma, major surgeries
2- extensive burns
3- head injury, intracranial lesions
4- ICU

24
Q

Acute gastric ulcers:
-usually presents with (1), although can present as (2)

-pathogenesis is related to (3) and (4)

A

1- multiple ulcers, asymptomatic
2- massive upper GI bleed

3- systemic acidosis, hypoxia (trauma, burns)
4- vagal stimulation (intracranial lesions)

25
Q

describe the appearance of an acute gastric ulceration

A
  • multiple, small, circular
  • normal gastric rugae (folds)
  • base is not usually indurated (fibrotic changes)

-adjacent gastric mucosa is either normal or has reactive changes

26
Q

list the sites of Peptic Ulcer Disease (by decreasing popularity)

A
  • duodenum
  • stomach
  • gastroesophageal junction
  • margins of gastrojejunostomy
  • Meckel’s diverticulum
  • stomach, duodenum, jejunum in Zollinger-Ellison syndrome (gastric tumor / gastroma)
27
Q

Peptic Ulcer Disease appearance:

  • (1) usual size
  • (2) shape
  • (3) edges / margins
  • (4) depth
  • (5) base appearance
  • (6) surroundings
A

1- 50% <2cm
2- round/oval, punched out, straight walls
3- sharp, raised (not everted)
4- variable, may penetrate entire wall
5- smooth, clean base
6- radiating surrounding mucosal folds – typical features of chronic gastritis

28
Q

peptic ulcer disease zones

A

(4 zones)

  • necrotic fibrinoid debris
  • nonspecific inflammatory infiltrate (predominately neutrophilic)
  • granulation tissue
  • fibrosis, collagenous scar
29
Q

list the many causes of peptic ulcer disease (hint- 6)

A
  • H. pylori: 70% gastric, 90% duodenal
  • NSAIDs (inhibits PGs)
  • smoking (impairs mucosal blood flow)
  • alcohol
  • psychological stress
  • Zollinger Ellison syndrome (multiple ulcers via gastric tumor)
30
Q

list the clinical features seen in Peptic ulcer disease

A
  • burning epigastric pain 1-3 hours after meals
  • relieved by food, alkali
  • worse at night
  • associated with weight loss
  • gastric outlet obstruction
31
Q

list the clinical complications seen in Peptic ulcer disease

A
  • bleeding
  • perforation
  • gastric outlet syndrome
  • malignant transformation (unknown reason in duodenal, rare in gastric)
32
Q

H. pylori
Gastric Ulcer:
-epigastric pain (1) after meals
-pain (worse/better) with food

Duodenal Ulcer:

  • epigastric pain (3) after meals
  • pain (worse/better) with food

-(gastric/duodenal) is worse at night

A

1- 1-3 hrs
2- worse

3- 3-5 hrs
4- relieved with food

5- duodenal is worse at night

33
Q

list the causes of reactive gastropathy (+ definition)

A

Defn: minimal inflammatory reaction of stomach in response to chemicals

  • NSAIDs
  • other meds: Fe, kayexalate
  • alcohol, acid, alkali
  • duodenopancreatic reflux (bile into stomach)
34
Q

NSAID gastric injury:

  • inhibition of (1) limits production of (2) which is responsible for (3- include all functions)
  • NSAIDs are also considered (4), causing (5) in the stomach upon ingestion
A

1- COX / cyclo-oxygenase
2- PGs
3- (gastric mucosa protection) maintain blood flow, inc mucus / HCO3 production, augment epithelial defenses

4- direct irritant
5- denudation of surface epithelial (removal of layers), inc mucosal permeability to ions

35
Q

(1) is the most common malignant tumor of the stomach, with highest occurrence in (2) geographic areas. It generally has a (good/bad) prognosis and comes in (4) subtypes.

A

1- adenocarcinoma
2- Japan, South Korea
3- bad
4- intestinal, diffuse types

36
Q

intestinal gastric adenocarcinoma:

  • (1) basic definition
  • mainly associated with (2)
  • neoplastic cells form (3), which is not seen in diffuse type
A

1- chronic gastritis with intestinal metaplasia
2- H. pylori infections
3- glands

37
Q

diffuse gastric adenocarcinoma:

  • (1) is the only known risk factor
  • (2) are the hallmark upon investigation
  • it has (3) or lack of (3) appearance in comparison with the intestinal type
A

1- E-cadherin mutation
2- signet ring cells (peripheral nucleus with mucin vacuoles)
3- no glands —- linitis plastica / Brinton’s disease

38
Q

intestinal gastric adenocarcinoma:

  • (1) gross appearance
  • (2) histological appearance
A

1- elevated mass, raised borders with central ulcer

2- columnar gland forming cells infiltrating thru desmoplastic stroma (back-to-back glands)

39
Q

diffuse gastric adenocarcinoma:

  • (1) gross appearance
  • (2) histological appearance
A

1- thickened gastric wall, loss of rugae (folds)

2- signet ring cells: mucin vacuoles, peripherally displaced crescent shaped nuclei

40
Q

gastric adenocarcinoma prognostic classifications (indicate what it is based off of)

A

(based on depth of infiltration)
Early gastric CA:
-confined to mucosa, submucosa, regardless of regional LN involvement

Advanced gastric CA:
-invades beyond submucosa, +/- LN involvement

41
Q

gastric adenocarcinomas:

  • (1) common involved sites
  • (2) growth patterns
  • (3) routes of metastasis
A

1- pylorus/antrum 50-60%, cardia 25%

2- exophytic, excavated/ulcerative, flat/infiltrative

3- regional, transcoelomic, lymphatic, hematogenous

42
Q

Gastric adenocarcinomas:

  • usually present with (1)
  • (2) nonspecific Sxs
  • (3) is a common complication
  • prognosis is based on (4)
A

1- asymptomatic
2- weight loss, anorexia, abdominal pain
3- pyloric outlet syndrome
4- depth of invasion, nodal status

43
Q

_______ results from the spread of gastric adenocarcinomas to both ovaries

A

Krukenberg tumor

44
Q

define Virchow node

A

L supraventricular lymph node

-can indicate metastasis of a gastric adenocarcinoma

45
Q

(1) is a mesenchymal tumor of the GIT (anywhere), previously misdiagnosed as (2) tumors. (1) derives from (3) cells and is usually (benign/malignant).

A

1- GIST (GI stromal tumor)
2- leiomyoma or nerve sheath tumor
3- cells of Cajal (pacemaker cells)
4- either, based on size and mitoses

-found anywhere in GIT, but often in stomach

46
Q

GIST = (1):

  • (2) gross appearance
  • often due to (3) mutation
  • (4) histological appearance
A

1- GI stromal tumor
2- whorls / bundles of spindle shaped / epitheliod cells (protruding mass / fleshy tumor covered by intact mucosa)
3- Kit mutations
4- spindle shaped tumors cells in whorled pattern, high rate of angiogenesis (plenty of blood supply noted)

47
Q

GIST = (1):

  • malignancy is based on (2)
  • (3) Tx
A

1- GI stromal tumor
2- site, size, mitotic count
3- imatinib/Gleevec, KIT inhibitor

DERS (GIT) (21 decks)

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