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GI Week 2 > ICL 3.3: Pathology of the Upper GI Tract II > Flashcards

ICL 3.3: Pathology of the Upper GI Tract II Flashcards

1
Q

mallory weiss syndrome

A

alcoholic binge drinking

longitudinal tears in the esophagus

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2
Q

plumer vinvent syndrome

A
  1. iron deficiency anemia
  2. glossitis
  3. cracked lips
  4. esophageal webs
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3
Q

neck mass and foul breath

A

Zenker’s diverticulum

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4
Q

chagas disease

A
  1. dilated cardiomyopathy
  2. megacolon
  3. achalasia in esophagus
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5
Q

Barret esphagus

A

metaplasia to intestinal columnar cells

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6
Q

what are rugae?

A

longitudinal infoldings of both mucosa and submucosa on the inner surface of the stomach

they’re important because in some diseases they’re gone!

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7
Q

what are the components of the gastric wall?

A
  1. mucosa
  2. submucosa
  3. muscular propria
  4. serosa
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8
Q

what are the 7 different cell types in the stomach? what do they produce?

A
  1. G cells = gastrin*
  2. EcL = enterochromaffin-like produce histamien
  3. D cells = somatostatin
  4. X cells = endothelin
  5. mucous cells = mucus and pepsinogen II*
  6. parietal cells = intrinsic factor and acid*
  7. chief cells = pepsinogen I and II*
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9
Q

what are the 3 phases of HCl secretion?

A
  1. cephalic phase
  2. gastric phase
  3. intestinal phase
    * all of these converge to activate the proton pump –> people with GERD or ulcers get put on PPI to inhibit some HCl release
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10
Q

what happens during the cephalic phase of HCl secretion?

A

mediated by vagal activity initiated by the sight, taste, smell chewing and swallowing of food

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11
Q

what happens during the gastric phase of HCl secretion?

A

mediated by vagal impulses caused by stimulation of stretch receptors

gastrin is released

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12
Q

what happens during the intestinal phase of HCl secretion?

A

initiated when food containing digested protein enters the proximal small intestine more gastrin

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13
Q

what are the congenital anomalies of the stomach?

A
  1. heterotopic rests

2. diaphragmatic hernia

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14
Q

what are heterotopic rests?

A

congenital anomaly of the stomach = stomach has pancreatic tissue instead of being lined by stomach mucosa which can cause inflammation and obstruction

pancreatic rests located in the pylorus become inflamed leading to obstruction

gastric rests in duodenum or more distal sites undergo peptic ulceration, leading to bleeding

gastric rests in upper esophagus lead to inflammation and discomfort

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15
Q

what is a diaphragmatic hernia?

A

results from defective closure of the diaphragm, usually on the left which means part of the stomach can be sitting in the chest…

may be asymptomatic or cause respiratory problems for newborns

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16
Q

3 week old infant present with projectile vomiting after nursing

PE reveals an olive like mass in the epigastric

diagnosis?

A

congenital hypertrophic pyloric stenosis

projectile vomiting every time after eating

he’s 3 weeks old

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17
Q

what is the incidence of pyloric stenosis?

A

1/300-900 live births

M:F = 3-4:1

may be associated with Turner Syndrome*, Trisomy 18 and esophageal atresia

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18
Q

what is clinical presentation of pyloric stenosis?

A

presents as regurgitation and persistent projectile vomiting at 2-3 weeks of age

PE= palpable mass in the region of pylorus

it feels like an olive which is also visible peristalsis noted.

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19
Q

what is the cause of pyloric stenosis?

A

results from congenital hypertrophy and possibly hyperplasia of muscularis propria of pylorus

the hypertrophy is what presents as the mass and you can see it when the baby swallows during peristalsis

pyloric stenosis can also be acquired in adults as a complication of antral gastritis, peptic ulcer, carcinoma, or prolonged pyloric spasm

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20
Q

what is gastritis?

A

inflammation of the gastric mucosa

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21
Q

what is acute gastritis?

A

an acute mucosal inflammatory process, with neutrophilic infiltrate, that is usually transient

there may be hemorrhage into the mucosa or sloughing of the mucosa

severe erosive form is an important cause of severe GI bleeding

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22
Q

what causes acute gastritis?

A
  1. heavy use of NSAIDS, especially aspirin*
  2. excessive alcohol consumption*
  3. heavy smoking*
  4. severe stress e.g. trauma, burns, surgery
  5. ischemia
  6. systemic infection

often idiopathic though

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23
Q

what is the pathogenesis of acute gastritis?

A
  1. increased acid secretion
  2. decreased bicarbonate buffer
  3. decreased blood flow

these all lead to disruption of the mucus layer and direct mucosal injury which ultimately causes acute gastritis

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24
Q

what is the clinical presentation of acute gastritis?

A

broad range of signs and symptoms that depend on the severity of the the condition

  1. asymptomatic
  2. epigastric pain, nausea and vomiting
  3. hemorrhage, massive hematemesis, melena, or fatal blood loss
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25
Q

which people are at higher risk for acute gastritis?

A

one of the major causes of massive hematemesis, particularly in alcoholics.

~25% patients taking aspirin for rheumatoid arthritis will develop acute gastritis, and some will bleed

papillary necrosis due to chronic interstitial nephritis in the kidney too

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26
Q

what is the morphology of acute gastritis?

A
  1. edema of the lamina propria
  2. slight congestion
  3. neutrophils within the epithelial space
  4. severe erosion and hemorrhage of mucosa

ranges from edema with neutrophil infiltration, vascular congestion, and an intact epithelium, to erosion (mucosal defect that does not cross the muscularis mucosa) and hemorrhage

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27
Q

what is chronic gastritis?

A

chronic mucosal inflammatory changes leading to atrophy and metaplasia (usually without erosions)

dysplasia and ultimate neoplasia are complications…huge risk factor for carcinoma of the stomach

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28
Q

what is the etiology of chronic gastritis?

A
  1. H. pylori

this is the cause of 90% of chronic gastritis!!

  1. autoimmune
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29
Q

what type of bacteria is H. pylori?

A

motile, gram negative curvilinear rods

urease positive = buffers gastric acid because it forms NH4+ and leads to inflammation

produces toxins and has adhesins to bind to the epithelium of gastric mucosa

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30
Q

what is the presentation of an H. pylori infection?

A

most infected persons have gastritis, but are asymptomatic

hypochlorhydria, but NOT achlorhydria and pernicious anemia (parietal cells never completely destroyed)

gastrin normal to slightly elevated

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31
Q

how do you treat H. pylori? why is it important to treat them?

A

antibiotics

you have to treat them because prolonged infections increase risk of gastric carcinoma and lymphoma

also, H. pylori predisposes people to peptic ulcers in the duodenum and stomach –> most patients with a peptic ulcer are infected

32
Q

45 year old female with a past medical history of hypothyroidism presents to her PCP office with dyspepsia and frequent bouts of nausea for the last 6 months

PE: large thyroid gland, hyperpigmentation of the skin, upper endoscopy reveals gastritis.

A

autoimmune chronic gastritis

6 months = chronic

hypothyroidism = endocrine system involvement

hyperpigmentation of skin = another organ involved; probably Addison’s disease

stomach, thyroid and skin involved!

33
Q

what is autoimmune chronic gastritis?

A

antibodies to parietal cells, gastrin receptor, intrinsic factor, and H+, K+ ATPase

pernicious anemia due to loss of intrinsic factor!

antibodies lead to glad destruction and mucosal atrophy –> decreased acid and intrinsic factor which leads to pernicious anemia

since there’s decreased acid production, you’ll have hypergastrinemia that’s trying to compensate!

34
Q

which conditions are associated with autoimmune chronic gastritis?

A
  1. Hashimoto thyroiditis
  2. Addison idesase
  3. type I diabetes
35
Q

what is the risk associated with autoimmune chronic gastritis?

A

significant risk for the development of gastric carcinoma (2-4%) and endocrine tumors (carcinoid tumor)

36
Q

A 45 year old female with problems with her balance for six months and numbness of her fingers.

PE: pale, loss of vibratory sensation

diagnosis?

tests?

What would you expect to see on upper endoscopy?

What other tests?

A

pernicious anemia!

check anti-parietal cell and anti-intrinsic cell antibodies and gastric levels

upper endoscopy would show atrophy of the gastric mucosa from chronic gastritis! so then you also need to get a biopsy to check for carcinoma since there’s atrophy which is a precursor

37
Q

what is the morphology of chronic gastritis?

A
  1. varying degrees of mucosal damage possible
  2. mucosal lesions are reddened, with thickened rugae
  3. atrophied rugae in long-standing cases
  4. lymphocytes and plasma cell infiltrate; neutrophils indicate “active” inflammation (may or may not be present)
  5. regeneration; constant feature
  6. metaplasia of mucosa of antral and body-fundic regions converts to columnar absorptive cells and goblet cells (intestinal metaplasia)
  7. atrophy; marked loss of glands
  8. dysplasia; precursor lesion to gastric cancer in atrophic gastritis
38
Q

a 51 year old bipolar patient present with loss of appetite and sense of gastric fullness. Abdominal x ray reveals a large mass in his stomach.

diagnosis?

endoscopy?

what else can you do?

A

gastric dilation

he’s a psych patient so he’s probably swallowing random things

39
Q

what is the etiology of gastric dilation?

A
  1. pyloric stenosis
  2. paralytic ileus
  3. intralumenal concretions like bezoars (balls of materials)

the stomach is the primary site for development of luminal concretions of indigestible ingested material

40
Q

what are the different types of bezoars associated with gastric dilation?

A
  1. phytobezoars = concretions of plant matter
  2. trichobezoars = AKA “hairballs”
  3. bizarre bezoars associated with illicit drug takers, glue swallowers, and neuropsychiatric patients (pins, nails, razor blades, etc.)
41
Q

12 year old boy presents with puffy eyes , pedal edema & early satiety for 6 months.

PE: edema and puffy eyes

UA: negative, stool analysis negative, liver function negative serum albumin 2.

diagnosis?

A

hypertrophic gastropathy

he’s making albumin but he’s losing it! it’s not nephrotic syndrome

42
Q

what is hypertrophic gastropathy?

A

characterized by cerebriform enlargement of the gastric rugal folds –> the huge rugae have a lot of mucus glands so lots of mucin and mucus are excretes which leads to low protein, decreased oncotic pressure and edema!

caused by mucosal epithelial hyperplasia, without inflammation

these conditions may mimic infiltrative carcinoma or lymphoma on examination

excess acid secretion associated with these disorders predisposes to peptic ulcers

43
Q

what are the types of hypertrophic gastrophathy?

A
  1. Menetrier’s disease*
  2. hypertrophic-hypersecretory gastropathy
  3. gastric gland hyperplasia
  4. parietal cell hypertrophy without excess acid seen in chronic use of acid secretion inhibitors
44
Q

what is Menetrier’s disease?

A

a type of hypertrophic gastropathy that occurs in males in the 4th-6th decades

it’s hyperplasia of mucous cells with atrophy of glands

so gastric secretions contain excessive mucus and very little acid!! this leads to protein loss and hypoproteinemia = protein-losing gastropathy = low oncotic pressure = edema

the stomach becomes smaller!

45
Q

what is hypertrophic-hypersecretory gastropathy?

A

a type of hypertrophic gastropathy

there’s hyperplasia of parietal and chief cells in gastric glands

46
Q

what is gastric gland hyperplasia?

A

a type of hypertrophic gastropathy

secondary to excessive gastrin secretion from gastrinoma (Zollinger-Ellison Syndrome)

47
Q

which cancers are benign cancers of the stomach?

A
  1. hyperplastic polyps
  2. adenomas

hyperplastic and adenomatous polyps cannot be differentiated endoscopically—they must be biopsied!!

48
Q

what are hyperplastic polyps?

A

mucosal masses that project above the level of the surrounding mucosa, single or multiple

majority in patients with achlorhydria, atrophic gastritis and pernicious anemia

most often seen with chronic gastritis

no malignant potential

49
Q

what are adenomas of the stomach?

A

true neoplasms with proliferative dysplastic epithelium so they have malignant potential!

oncidence goes up with age, especially the 70s

M:F 2:1

40% have malignant foci when removed and risk of malignancy in adjacent mucosa as high as 30%

associated with chronic gastritis with intestinal metaplasia and autoimmune gastritis

50
Q

what is the epidemiology you gastric carcinoma?

A

90-95% of malignant tumors of the stomach are carcinoma

it’s the second most common tumor in the world –> ncidence particularly high in Japan, parts of South America, China, Portugal, Russia, and Bulgaria; but 4-6X less common in the US, UK, Canada, Australia –> lower socioeconomic groups!

M:F = 2:1

incidence has declined in most countries

2.5% of all cancer deaths in U.S. and leading cause of cancer death worldwide

5 year survival = < 20% in the US

51
Q

what are the risk factors for developing gastric carcinoma?

A
  1. environmental: nitrites* (from food preservatives), smoked and salted foods, pickled vegetables, deficiency of fresh fruits and vegetables, cigarette smoking
  2. host factors: chronic atrophic gastritis*, adenomatous polyps, partial gastrectomy and H. pylori infection (risk increased 5-6X)
  3. genetic factors: more common in persons with blood group A*, family history of gastric cancer
52
Q

what are the genes associated with gastric carcinoma?

A
  1. germline mutations in CDH1 which encodes E-Cadherin
  2. loss of E-Cadherin function is associated with diffuse gastric carcinoma
  3. BRCA2 mutations are also associated with diffuse gastric cancer
53
Q

where are gastric carcinomas usually located?

A

lesser and greater curvatures

also the pylorus

54
Q

how are gastric carcinomas classified?

A
  1. according to macroscopic growth pattern

2. lintis plastica

55
Q

what are the different macroscopic growth patterns of gastric carcinomas?

A
  1. exophytic = mass protrudes into lumen of the stomach
  2. flat/depressed = no obvious tumor mass
  3. excavated (ulcerative) = shallow or deeply erosive crater

not well circumscribed! so they’re malignant, not benign

56
Q

what is lintis plastica?

A

a specific morphology of gastric carcinomas

the tumor infiltrates the entire thickness of the wall of the stomach

broad portion of gastric wall or entire stomach is extensively infiltrated with malignancy, creating a rigid, thickened appearance like a “leather bottle”

57
Q

what is early vs. late gastric carcinoma?

A

early = defined as being confined to the mucosa and submucosa
regardless of lymph node metastasis

late = defined as extending below the submucosa into muscle
regardless of lymph node metastasis

58
Q

what is the morphology of excavated gastric carcinoma?

A

heaped-up, beaded margins and necrotic base differentiate this cancer from chronic peptic ulcer which are benign

59
Q

what are the 2 histological patterns that can be seen with gastric carcinomas?

A
  1. intestinal type

2. gastric type

60
Q

what is the intestinal type of gastric carcinoma histology?

A

glandular, expansile growth pattern

histology is composed of glands resembling colonic adenocarcinoma; glands everywhere

predominates in high-risk areas and develops from precursor lesions associated with mutations in β catenin and APC

61
Q

what is the gastric type of gastric carcinoma histology?

A

diffuse infiltrating pattern of poorly differentiated cells; “signet ring” conformation = mucin expansion in cells puts nuclei at the periphery

there are gastric-type mucus cells that don’t form glands but rather permeate the wall as individual cells or clusters

incidence the same everywhere and no known precursor lesion

62
Q

what are the clinical features of gastric carcinoma?

A

insidious disease; asymptomatic until late in the course when they develop:

  1. weight loss
  2. abdominal pain
  3. anorexia
  4. vomiting
  5. altered bowel habits
  6. sometimes dysphagia, anemia and hemorrhage
63
Q

how important is detection of gastric carcinomas?

A

early detection is SO important because it’s an aggressive disease

Japan uses endoscopic screening programs, resulting in 35% of newly diagnosed gastric carcinoma being found in an early stage –> this is because they have high incidence of gastric carcinoma

US and Europe only catch 10-15% in the early stage

64
Q

what are the clinical complications of gastric carcinoma?

A
  1. local invasion of pancreas, duodenum, and retroperitoneum
  2. at death, peritoneum is seeded and there are often mets to liver and lungs
  3. metastasis to regional and distant nodes –> frequently mets to Virchow’s node* (left supraclavicular node) as the first clinical manifestation
  4. mets to ovaries = Krukenberg Tumors*
65
Q

what is the prognosis of gastric carcinoma?

A

determined by depth of penetration and extent of nodal involvement, not histology

you can treat with surgical resection w/ or w/out adjuvant chemotherapy and radiation

66
Q

what are some of the less common gastric neoplasms other than gastric carcinoma?

A
  1. lymphomas (5%); but the stomach is the most common site for extranodal lymphoma (20%)
  2. EBV positive lymphomas seen in immunocompromised patients = MALT (lymphomas of mucosa-associated lymphoid tissue) (11;18 translocation)
  3. GI stromal tumors
  4. neuroendocrine cell tumors—carcinoids (rare)
  5. lipomas
  6. metastatic cancers (unusual)
  7. gastrointestinal stromal tumor (mutation of the gene encoding tyrosine kinase [cKIT])**
67
Q

what is the clinical presentation of carcinoid tumors?

A
  1. flushing
  2. diarrhea
  3. asthma
68
Q

what is Zollinger-Ellison syndrome?

A

patients have multiple ulcers in their stomach and duoedenum

associated with gastrin-producing tumor in the tails of the pancreas

they have ulcers because gastrin stimulates the production of HCl in the stomach so there’s lots of acid in the stomach!

they also have diarrhea because gastrin stimulates the motility of the small intestine

69
Q

Virchow’s lymph nodes

A

left supraclavicular lymph nodes

associated with gastric carcinoma

70
Q

protein losing gastropathy

A

Menetrier’s disease = hypertrophic gastropathy

71
Q

melena

A

upper GI bleeding causing blood in the stool

black stool since bleeding is in the upper GI = gastric ulcers/tumors, esophageal bleeding, etc.

72
Q

11/18 translocation

A

MALT

lymphoma of the stomach!

73
Q

signet ring cells

A

diffuse type gastric carcinoma

74
Q

Krukenberg Tumors

A

mets to the ovaries in gastric carcinomas

75
Q

lintis plastica

A

involvement of the whole stomach wall

76
Q

olive like mass

A

hypertrophic pyloric stenosis

77
Q

anti-HK ATPase

A

autoimmune gastritis

atrophic! risk factor for gastric cancer

GI Week 2 (10 decks)

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