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Lectures > Stomach > Flashcards

Stomach Flashcards

1
Q

Motility disorders of the stomach

- Gastroparesis

A

Partial paralysis of the stomach, results in delayed gastric emptying

  • gastric motility normally governed by the vagus nerve –> any nerve injury can cause gastroparesis
  • Diabetic neuropathy is most common cause
  • injury to stomach itself –> connective tissue disorders
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2
Q

Motility disorders of the stomach

- Pyloric stenosis

A

Hypertrophy of muscle of the pylorus

  • may be palpable through the abdominal wall
  • prevents movement of food into the duodenum
  • idiopathic condition
  • presents with projectile vomiting ~2 weeks after birth
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3
Q

Classification of gastritis

A

By presentation –> acute vs. chronic

  • based on the clinical picture
  • histologic features won’t always match
  • classically acute features = “active” gastritis (PMNs)
  • features of active and chronic = “active chronic” gastritis

By cause

  • H. pylori
  • chemical –> bile, iron, etc.
  • autoimmune
  • radiation
  • stress ulcer
  • curling ulcer –> severe burns
  • cushing ulcer –> intracranial disease
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4
Q

H. pylori gastritis

  • pathogenesis
  • histology
  • location of h. pylori
A

Spiral shaped bacterium found in the gastric mucus layer or adherent to the epithelial lining of the stomach

Acute h. pylori is usually asymptomatic –> takes time to develop injury

Pathogenesis –> increased acid production + reduced protection against acid in the stomach and duodenum

Histology –> produces “active” gastritis (PMNs), usually chronic component too = “active chronic”

Organism is present in surface and glandular mucosa –> prefers antrum, but may be pangastritis

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5
Q

Complications of H. pylori infection

A
  1. peptic ulcer disease
  2. intestinal metaplasia –> gastric carcinoma
    - short term is good –> h. pylori can’t live in intestinal type epithelium
    - long term is bad –> the metaplasia is not wide spread enough to eradicate infection, predisposes to adenocarcinoma
  3. lymphoma –> MALToma
    - stimulated by ongoing exposure to h. pylori antigen
    - classic appearance = lymphoepithelial lesion –> destruction of glands
    - may be treated along with h. pylori antibiotics
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6
Q

Autoimmune gastritis

- morphology

A

Pernicious anemia –> autoimmune destruction of intrinsic factor and of parietal cells

  • characterized by circulating autoantibodies, but mediated by T cells
  • associated with other autoimmune diseases

Morphology

  • predominates in gastric body and fundus with relative sparing of the antrum –> disruption of the parietal cells, differs from h. pylori
  • active chronic gastritis –> resembles h. pylori
  • replacement of fundic by antral type mucosa
  • “atrophic gastritis” = gradual destruction of mucosa –> incomplete atrophy with foci of epithelial sparing may mimic polyps
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7
Q

Complications of autoimmune gastritis/pernicious anemia

A
  1. Anemia
  2. Peptic ulcer disease
  3. Intestinal metaplasia
  4. Neuroendocrine tumors
    - loss of acid secretion –> hypergastrinemia –> overgrowth of endocrine cells (ECLs)
    - linear hyperplasia –> nodular hyperplasia (timy tumors) –> neuroendocrine tumors
    - may be monitored with sequential endoscopy
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8
Q

H. pylori vs. autoimmune gastritis

A

Location

  • H pylori –> mostly antrum
  • A.G. –> mostly in fundus/body

Acid production

  • h. pylori = normal/increased
  • A.G. = decreased

Gastrin

  • h. pylori = normal/decreased (due to increased acid)
  • A.G. = increased (due to decreased acid)

Antibodies

  • h. pylori = anti-HP antibodies
  • A.G. = anti-parietal cell antibodies

Associated malignancy

  • h. pylori = adenocarcinoma, lymphoma
  • A.G. = adenocarcinoma, NET
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9
Q

Chemical gastritis

- histology

A

Foveolar hyperplasia –> may resemble vili

  • complex glandular architecture –> “corkscrew”
  • vascular congestion
  • typically mild inflammation
  • erosions may be associated with more inflammation
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10
Q

Gastropathy

A

Mild changes with limited inflammation –> uncertain clinical significance, some asymptomatic

Many causes –> most look exactly the same

  • NSAIDS
  • bile reflux into stomach from duodenum
  • alcohol
  • coffee
  • cocaine
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11
Q

Iron pill gastritis

A

Severe, chronic gastritis associated with oral iron pills –> causes ulceration of the mucosa

  • may have acute features
  • iron apparent in lamina propria and crusted along surface
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12
Q

Lymphocytic gastritis

A

Pain and diarrhea, may present with protein losing enteropathy

  • relatively rare
  • marked lymphocytosis (>25 lymphocytes/100 epithelial cells) –> lymphocytes in the lamina propria

Causes –> descriptive term associated with multiple possible etiologies

  • H. pylori
  • HIV
  • Crohn’s
  • lymphoma
  • Celiac disease –> ~1/.3 of celiac patients, may also have lymphocytic colitis, relatively resistant to gluten free diet
  • idiopathic
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13
Q

Crohn’s gastritis

A

1/3 of crohn’s patients have upper tract disease

  • pain, nausea, vomiting
  • may produce strictures, perforations, etc
  • may produce elucers, but histologic changes may be present even in grossly normal tissue

Histology

  • granulomas –> relatively rare, more common in kids
  • focally enhanced gastritis –> relatively common
  • –> typically focal with normal backgroun
  • –> periglandular inflammation with lymphocytes, histiocytes and often neutrophils
  • –> differential diagnosis includes h. pylori
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14
Q

Zollinger Ellison syndrome

A

Triad of hypergastremia (due to gastrinoma), increased acid, and duodenal ulcers
- hyperplasia of fundic mucosa in response to stimulation

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15
Q

Heterotopia

A

Normal tissue in an abnormal place –> not usually significant

  • antral heteropia –> histologically unremarkable antral type mucosa located in body or fundus
  • pancreatic heterotopia –> umbilicated nodule in stomach; most are submucosal
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16
Q

Fundic gland polyps

A

Most common gastric polyps –> benign

Two major associations

  1. long term PPI use
  2. familial adenomatous polyposis –> polyp itself usually benign, but condition is dangerous
  • often multple
  • small, same color background as stomach
  • histology –> fundic mucosa with cystic dilation
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17
Q

Hyperplastic polyp

A

Overgrowth of foveolar epithelium

  • may be multiple
  • smooth surface
  • large, cystically dilated glands
  • surface inflammation/erosion
  • may hardbor intestinal metaplasia –> dysplasia –> carcinoma –> bigger polyps = increased risk
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18
Q

Polyposis

A

Characterized by multiple gastric polyps

  • associated with APC mutations = familial adenomatous polyposis
  • increased cancer risk –> screen with colonoscopy
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19
Q

Dysplasia

A

“gastric dysplasia” refers to a flat lesion –> often grossly inapparent

  • may arise in background of intestinal metaplasia
  • may regress or progress –> particularly if high grade
  • features like those of esophageal dysplasia
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20
Q

Adenoma

A

Denotes glandular polyp with at least low grade dysplasia

- high grade/malignant potential –> especially >2 cm, most are < 2 cm

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21
Q

Polypnoid

A

Visible growth of dysplastic epithelium

  • often arise in context of inflammation and intestinal metaplasia
  • may be
  • –> intestinal type (goblet cells ) OR
  • –> gastric type (foveolar cells)
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22
Q

Risk factors for adenocarcinoma

A
  • environmental –> diet, h. pylori, smoking
  • genetics –> inherited abnormalities in APC + e-cadherin
  • genetic abnormalities –> e-cadherin, KRAS, p53, APC
23
Q

Intestinal type gastric adenocarcinoma

A
  • cohesive glands
  • typically discrete fungating masses or ulcers
  • associated with intestinal metaplasia
24
Q

Diffuse type gastric adenocarcinoma

A

Particularly bad prognosis

  • individual cells with “signet ring” morphology –> very poorly cohesive, infiltrate extensively
  • generalized thickening of the stomach = “linitis plastic”
  • can be subtle endoscopically and microscopically
  • often younger patients
  • usually sporadic –> rarely associated with e-cadherin mutations
  • poor outcomes
25
Q

Staging of gastric carcinoma

A

Mostly looking at indirect measures of how aggressive the tumor is

  • direct tumor spread –> through muscularis propria, or through serosa
  • lymph node metastases
  • distant metastases

Predictive markers –> markers that predict response to chemo
- overexpression of her2/neu = response to trastuzimab (~20% of intestinal type cancers)

26
Q

Neuroendocrine tumors

A

Classified by associated conditions

  • Type I = autoimmune gastritis –> best prognosis
  • Type 2 = ZES
  • Type 3 = sporadic –> worst prognosis

Hard to predict behavior –> called “tumors” rather than carcinomas unless metastatic

  • grade 1 = carcinoid
  • grade 2 = atypical carcinoid
  • ** grade 1 and 2 are well differentiated –> use mitotic rate to tell them apart
  • grade 3 = high grade, overtly malignant
27
Q

GAVE (gastric antral vascular ectasia)

A

“Watermelone stomach”

  • dilated capillaries with fibrin thrombi
  • mostly antral
  • elderly women
  • bleeding –> acute or chronic
  • autoimmune association –> also cirrhosis and end stage renal disease
28
Q

Caliber persistent artery (CAP)

A

Aka dieulafoy

  • large caliber artery going up to the surface
  • near GEJ, along lesser curvature
  • recurrent bleeding without other symptoms –> may be massive
  • typically managed endoscopically –> if resected, try to find to justify the procedure
29
Q

Causes of peptic ulcer disease

A
  • too much acid –> ZE
  • h. pylori
  • NSAIDS
  • rare causes = CMS, syphillis, lymphocytic gastritis, crohns, granulomatous autoimmune gastritis, cancer
30
Q

Pathogenesis of peptic ulcer disease

A
  • injurants to the lining –> gastric or bile acids, NSAIDS

- impaired mucosal defense mechanism –> impaired mucous bicarb secretion, poor blood flow

31
Q

Stress ulcers

A

Occur with severe physiological stress –> decreased mucsal blood flow = impaired mucus layer

  • ICU patients, intubated patients, post trauma patients
  • increased intracranial pressure = cushings ulcer
  • severe burns = curling ulcer
32
Q

Complications of ulcers

A
  • perforation –> contents of stomach are not sterile –> when they enter peritoneal cavity = surgical emergency
  • bleeding
  • penetration –> penetration posteriorly into the head of the pancreas, can cause pancreatitis
  • obstruction –> when located at the pyloric outlet

major cause of GI morbidity and mortality

33
Q

Epidemiology of h. pylori infection

A
  • ~50-60% of worlds population is infected
  • major cause of duodenal and gastric ulcers + gastric cancer
  • age at acquisition = childhood
  • transmission is likely fecal oral
34
Q

Natural history of infection

A

Initial infection –> chronic gastritis –>

  1. gastric or duodenal cancer (10%)
  2. lymphoproliferative disease = MALToma
  3. gastric atrophy –> gastric cancer
35
Q

Evidence that h pylori causes ulcers and gastric cancer

A

Association with h. pylori infection –> >90% of duodenal ulcers and 80% of gastric ulcers + increased risk of gastric cancer

Eradication of organism results in marked reduction in ulcer relapse + regression of maltoma

36
Q

Diagnosis of H. pylori

A
  • serum antibody test –> will remain positive even after treatment so not very specific for current active infection, other tests are more specific
  • stool antigen test
  • urea breath test
  • upper endoscopy with gastric biopsy
  • Urease test
  • microscopic identification of organism
37
Q

Treatment of h. pylori

A

2 antibiotics + PPI

  • amoxicillin, tetracycline, metronidazole, clarithromycin
  • higher eradication rates with longer treatment –> eradication rate = 90%
  • antibiotic resistance and patient non-adherence to treatment are major reasons for failure
38
Q

NSAID induced ulcers

A

PGs are important for maintaining a healthy mucous lining in the stomach

NSAID gastrophathy

  • superficial erosions
  • ulcers
  • absence of chronic gastritis
  • frequently asymptomatic in elderly
  • usually occur in the antrum
  • very common
39
Q

Risk factors for NSAID complications

A
  • age >60 years
  • past history of ulcers
  • high dose
  • concomitant corticosteroid therapy –> prevents healing of ulcers but does not cause them
  • highly selective COX 2 inhibitors appear to be safer for the stomach but increase risk of CV disease
40
Q

Prevention and tx of NSAID induced ulcers

A

Prevention –> avoid NSAIDS, use less NSAIDS, concomitant H2 blocker of PPI
- misoprostol = PGE1 analog

treatment –> stop NSAID, start PPI

41
Q

Zollinger ellison syndrome

A

Gastrin secreting non-beta islet cell tumor with gastric acid hypersecretion

  • causes gastric and small intestinal ulcers
  • 1/3 have severe esophageal reflux
  • diarrhea is common –> due to high acid load and acid inhibition of pancreatic enyzmes

Multiple endocrine neoplasia type 1 –> 25% of ZE patients

  • autosomal dominant
  • hyperplasia/adenoma of…
    1. parathyroids
    2. pancreatic islets
    3. pituitary glands
42
Q

Epidemiology of ZE

A

1/1 million –> rare

  • male > female
  • mean age at dx ~50 –> range = 7-90
  • ~25% associated with MEN1 –> 60% of MEN1 patients have gastrinomas
43
Q

Diagnosis and tx of ZE

A

Dx

  • gastric hypersecretion
  • hypergastrinemia > 150 pg/mL in face of increased acid secretion –> normally when there is high acid levels there should be neg feedback to inhibit g cells, but this does not occur in ZE
  • –> other causes of hypergastrinemia = H2 blockers, PPIs, gastric atrophy, antral resection
  • secretin provocation test –> gastrin should fall when you give IV secretin, but it rises in ZE
  • CT scan, endoscopic ultrasound to localize tumor –> >50% have multiple tumors
  • octreotide scan

Tx –> high dose PPIs, surgery, chemo

44
Q

Acute gastritis

A

erosive and hemorrhagic –> as opposed to ulcers and erosions where there are breaks in the lining, gastritis is inflammation without breaks

causes

  • toxins and drugs –> ethanol, KCl, aspirin, nsaids, chemo
  • radiation
  • vascular –> ischemia, vasculitis
  • gastroduodenal reflux
  • stress gastritis
45
Q

Chronic gastritis

A
  1. infection –> h. pylori (common), TB, syphilis, viral, funal (rare)
  2. autoimmune –> pernicious anemia
    - vit B1`2 deficiency caused by gastric atrophy and loss of IF production
    - associated with other autoimmune diseases
    - familial tendency
    - corticosteroids may help
    - diagnosis –> low serum B12, IF and parietal cell antibodies, achlohydria, schilling test
  3. generalized GI diseases –> crohn’s, eosinophilic gastroenteritis
  4. systemic –> sarcoidosis, chronic granulomatous and GVHD
46
Q

Benign gastric tumors

A
  • hyperplastic polyp
  • adenomatous poly
  • leiomyoma
  • lipoma
47
Q

Malignant gastric tumors

A
  1. adenocarcinoma –> most common, declining incidence in developed countries
    - distal stomach = associated with h. pylori infection
    - proximal stomach = not associated with h. pylori infection
  2. lymphoma –> second most common
  3. GIST = GI stromal tumor
  4. Carcinoid tumors
  5. Kaposi sarcoma
48
Q

Findings in gastric cancer

A

Symptoms

  • early = none –> presents late = poor prognosis
  • late = anorexia, early satiety, nausea, vomiting, weight loss, anemia, GI bleeding, dysphagia (cardia tumor)

Physical findings

  • early = none
  • late = mass
  • metastasis –> hepatomegaly, supraclavicular, rectal shelf, umbilical
49
Q

Diagnosis of gastric cancer

A
  • indirect –> UGI x ray + CT scan

- UGI endoscopy with biopsy –> optimal

50
Q

Gastric vascular lesions

A
  1. angiodysplasias –> cause of occult GI bleeding
  2. GAVE = gastric antral vascular ectasia –> dilated venules in gastric antrum
    - associated with chronic liver disease –> poral hypertensive gastropathy and gastric varices
51
Q

Vomiting

- GI causes

A

Obstruction

  • Gastric –> tumor, ulcer, volvulus
  • small intestine –> obstruction, ileus
  • large intestine –> obstruction, crohn’s, etc

Inflammation –> infection, crohn’s

Motility disorder = gastroparesis –> delayed gastric emptying when no mechanical obstruction

  • disordered peristalsis
  • diabetes is most common cause –> also autoimmune (scleroderma), post-viral, idiopathic, meds (anti-cholinergics + narcotics)
  • diagnosis –> rule out obstruction + gastric emptying test
  • treatment –> metoclopramide, erythromycin, gastric pacing
52
Q

Upper GI bleeding

  • symptoms
  • causes
A

Symptoms

  • hematemesis
  • –> bright red = vomiting blood
  • –> coffee grounds = acid/pepsin break down blood
  • melena = dark, tarry, foul smelling stool
  • hematochezia = red blood per rectum
  • occult blood loss = heme + stool, can cause iron deficiency anemia

Causes

  • ulcer
  • gastritis
  • esophagitis
  • mallory weiss tear
  • GI varices
  • vascular malformation
  • tumors
  • aortoenteric fistula
53
Q

Evaluation

A
  1. Stabilize the patient
    - two large bore IVs
    - isotonic fluids –> replace lost fluids
    - blood products
  2. check labs
  3. start PPIs
  4. nasogastric lavage
  5. urgent endoscopy
  6. endoscopic therapy –> cautery, hemoclips, epinephrine injection, banding

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