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OSD_GI > Stomach > Flashcards

Stomach Flashcards

1
Q

Diff. between deep layer cells of the mucosa in the proximal vs. distal stomach?

A

Proximal stomach contains acid-secreting cells:

  • Chief cells
  • Parietal cells
  • Enterochromaffin-like cells (ECL)

Distal stomach contains neuroendocrine cells that secrete regulatory peptides:

  • Gastrin
  • Somatostatin
  • Glucagon
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2
Q

Difference between muscular layer in stomach vs. esophagus?

A

Stomach has a 3rd layer of oblique fibers that provide more muscular support for the function of the organ

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3
Q

During meals, the ____ nerve seems to promote receptive relaxation of the proximal stomach, gastric acid secretion and the grinding and mixing of food with gastric acid secretion in the distal stomach

A

Vagus

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4
Q

What is the process called that relaxes the proximal stomach to enable it to accommodate food and allow it to promote its storage without raising intra-gastric pressure?

A

Receptive Relaxation

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5
Q

What 4 things does the stomach secrete during meals?
For each, give the cell that secretes it & where in the stomach these cells are located.

A
  1. Hydrochloric (Gastric) Acid
    - Parietal cells in proximal stomach (active energy-dependent; H/K+ATPase)
  2. Intrinsic factor
    - Parietal cells in proximal stomach
  3. Pepsinogen
    - Chief cells in proximal stomach
  4. Mucus
    - Mucous cells in all parts of stomach
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6
Q

Hydrochloric (Gastric) Acid: Function?

Activated by? Inhibited by?

A

Fx:

  • Activates pepsinogen –> pepsin
  • Breaks down proteins
  • Provides a protective barrier against ingested microorganisms

Activated by:

  • Gastrin
  • Acetylcholine
  • Histamine

Inhibited by:
- Somatostatin

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7
Q

Intrinsic Factor: Function?

A

Binds vitamin B12 to form a complex that can be absorbed in the terminal ileum

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8
Q

Pepsin: Function? Activated by?

A

Fx:
- Breaks down protein for digestion

Activated by:
- Gastric acid (pepsinogen –>
pepsin)

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9
Q

Mucus: Function in stomach?

A

It consists of a glycoproteins and mucopolysaccarides that form a thin gel lining the stomach and protecting it from digestion by pepsin and acid injury

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10
Q

What is the inter-digestive migrating motor complex (IMMC)?

A

Periodic bursts of peristalsis that occur every 90 minutes between meals.

It is triggered by Motilin, which is released during long periods of inactivity (fasting).

(this results in the emptying of large indigestible solids, bacteria and debri, getting the stomach empty and ready for the next meal)

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11
Q

When are UGI series used?

A
  • Detection of mucosal lesions such as ulcers or cancers

- They’re less sensitive than endoscopy, but also less invasive (still at times used)

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12
Q

When are CT scan, MRI, & endoscopic ultrasonography (EUS) used on the stomach?

A

Evaluation & staging of malignant gastric disorders

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13
Q

Name of procedure?
Patients are fed a test meal that is labeled with radioactive technetium. They are then scanned to determine the emptying rate of the stomach using a gamma camera.

A

Radionuclide Gastric Emptying Scan

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14
Q

Which test is the most commonly used to evaluate gastric motility disorders?

A

Radionuclide Gastric Emptying Scan
(patients are fed a test meal labeled w/ radioactive technetium, then scanned to determine emptying rate of the stomach using a gamma camera)

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15
Q

What is “Dyspepsia”

A

A term for epigastric pain associated with peptic injury of the stomach

  • Burning discomfort
  • Relieved by ingestion of foods or antacids
  • May also present w/ nausea, w/ or w/out vomiting, early satiety, or postprandial fullness
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16
Q

What might upper GI

bleeding represent?

A
  1. Peptic ulcer disease
  2. Neoplastic disorders:
    - - Polyps
    - - Adenocarcinoma
    - - Lymphoma
    - - Carcinoid
    - - Gastrointestinal stromal tumors (GIST)
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17
Q

Where in the stomach do ulcers usually form?

A

Antrum (specifically @ junction w/ fundus)

  • normally lined by columnar epithelium that does not secrete acid
  • suggests non-acid secreting cells are more susceptible to ulceration
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18
Q

When are Fasting Serum Gastrin Levels useful for diagnosis?

A

In evaluating hypergastrenimic states associated with peptic ulcer disease such as suspected:
1) Gastrinoma (Zollinger-Ellison syndrome)
2) Retained antrum syndrome, following antrectomy
3) G cell hyperplasia

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19
Q

Dyspepsia: first dDx thoughts?

A
  • Acute gastritis
  • Chronic gastritis (H pylori, autoimmune)
  • Complications of chronic gastritis:
    peptic ulcer disease
  • Hypertrophic gastropathies
  • Gastroparesis (motor disorder)
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20
Q

Acid-secreting cells of the stomach are located where w/in the stomach?

A

Fundus & body
(parietal cells)

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21
Q

Symptom presentation of gastric vs. duodenal ulcers?

A

Gastric:

  • More severe pain, soon after meals
  • Less frequent relief by antacids or food
  • Older patient
  • Lower gastric acid levels
  • (ass’d w/ risk of gastric cancer)

Duodenal:

  • Pain/discomfort 3-5 hrs after meals or on empty stomach, also during night @ peak acid secretion (11p-2a)
  • Younger age patient
  • higher gastric acid levels
  • (also no risk of gastric/duodenal cancer)
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22
Q

Likely explanation for ulcers formed in acid-secreting parts of the stomach?

A

Infection (H. pylori) can cause atrophy of acid- secreting cells, leaving the region susceptible to ulceration once they’re gone

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23
Q

Major worldwide cause of Peptic Ulcer Disease?

A

H. pylori infection

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24
Q

Most frequent site of duodenal ulcer?

A

Duodenal bulb or pyloric channel crossing into the bulb
(aka close to the stomach)

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25
Q

Are duodenal ulcers typically single or multiple?

A

Single
(multiple or large ulcers prompt an investigation for other causes, like Zollinger Ellison Syndrome)

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26
Q

T or F?
Up to 40% of patients w/ healed ulcers (on endoscopy) will have persistent symptoms.

A

True

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27
Q

Describe the host immune response to H. pylori infection.
(or at least that which is linked to disease & possible progression to cancer)

A

Th1 immune response, specifically with elevated levels of IL-1, TNF-alpha, & low levels of IL-10

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28
Q

Following H. pylori infection, inflammatory cells trigger the Fas Ag/CD95 pathway, which has what direct effect on the stomach?

A

Triggers apoptosis of gastric mucosal cells – parietal & chief cells are most susceptible
(“how does H. pylori cause infection?”)

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29
Q

H. pylori infection: Symptoms/presentation?

A

Most asymptomatic or w/ mild symptoms. Those w/ symptoms, have:
- Dyspepsia (40-50%)
- Ulcer disease (20-30%)
- Gastric adenocarcinoma (<1.0%)

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30
Q

Risk factors for GI toxicity due to NSAIDs?

A

History of Ulcers = most important! Others:
- Dose
- Duration
- Age >75
- Co-morbidity (esp. cardiovascular)
- Concurrent use of: Steroids, Anticoagulants, Aspirin, Alendronate, Clopidogrel

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31
Q

Ulcer complications?

A
  • Bleeding
  • Perforation
  • Obstruction
  • Penetration into surrounding organs (most notably a DU penetrating into the pancreas)
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32
Q

How do penetrating ulcers typically present?

A

A shift from the typical vague visceral discomfort to a more localized and intense pain that radiates to the back and is not relieved by food or antacids

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33
Q

The sudden development of severe, diffuse abdominal pain in a patient with a GI ulcer may indicate ______

A

perforation

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34
Q

______ is the cardinal feature present in most cases of pyloric outlet obstruction.

A

Vomiting

35
Q

Presentation of hemorrhage as a complication from a GI ulcer?

A

Nausea, hematemesis, melena, or dizziness

36
Q

What is a “Giant Ulcer?”
Are these more or less prone to hemorrhage? Penetration into surrounding organs? Cancer?

A

It is an ulcer >2cm in diameter
(normal ulcers btwn 1 & 2 cm).
These are more prone to severe hemorrhage, penetration into surrounding organs, & cancer.

37
Q

When do Giant ulcers usually occur (i.e. in what setting)?

A

Giant ulcers commonly occur in association with NSAID use.

also in association with end-stage renal failure, orthotopic lung transplantation, and Crohn’s disease

38
Q

Endoscopically, what type of lesion has a shallow, “skinned knee” type of appearance?

A

Erosion

39
Q

4 “layers of defense” against ulcers?

A

Mucous layer
Bicarbonate
Lipid rich epithelium
Blood flow to remove ions and dilute insult

40
Q

Duodenal ulcer- classic presentation?

A
  • occurs 2-5 hours after a meal occur

- at night between 11 and 2 ( high acid)

41
Q

Gastric ulcer- classic presentation?

A
  • More severe pain (than duodenal ulcer)

- occurring soon after a meal

42
Q

Ulcer- type/description of pain?

A

Burning Gnawing- hunger like
Can be vague or cramping
Many may be asymptomatic

43
Q

H. pylori- description of pathogen?

A

Gram negative microaerophilic rod

WHO class 1 carcinogen

44
Q

Diseases H. pylori is linked to?

A
  • chronic atrophic gastritis
  • gastric and duodenal ulcer disease
  • gastric adenocarcinoma
  • gastric lymphoma
  • mucosa associated lymphoid tissue of the stomach (MALT)
45
Q

NSAIDs inhibit _____, reducing prostaglandin production.

A

COX-1

46
Q

Normal COX-1 present in stomach tissue produces prostaglandins which do what?

A
  • increase mucous and bicarbonate production,
  • inhibit stomach acid secretion
  • increase blood flow within the stomach wall.

(By acting on COX-1, NSAIDs restrict these self- protection mechanisms, allowing stomach ulcers to develop. It is primarily through this mechanism, NOT a local acid effect, that NSAIDs cause stomach ulcers.)

47
Q

Autoimmune Gastritis

A
  • < 10% of cases of chronic gastritis.
  • Antibodies to parietal cells and intrinsic factor (likely not the cause. CD4+ T cell mediated)
  • Reduced serum pepsinogen 1
  • Antral endocrine cell hyperplasia
  • vit B12 deficiency (anemia rare)
  • Defective gastric acid secretion (achlorhydria and hypergastrinemia)
48
Q

Reactive gastropathy:
Caused by..?
Characterized by..?

A 
- caused by chemical injury, NSAIDs, bile
or trauma (prolapse)
  • characterized by foveolar hyperplasia, glandular regeneration and mucosal edema.
49
Q

Eosinophilic Gastritis - Cause?

A
  • Allergic reaction (most commonly soy and milk in children and drugs in adults)
  • Collagen vascular diseases
  • Infection (Hp or parasites)
50
Q

Lymphocytic Gastritis:
Sex distribution?
Cause?
Type of inflammatory cells?

A
  • women > men
  • 60% idiopathic
  • 40% associated with celiac disease
  • CD8+ lymphocytes.
51
Q

Granulomatous Gastritis is ass’d w/ what 4 diseases/infections?

A
  • Crohn’s disease
  • Sarcoidosis
  • CMV
  • H. pylori
52
Q

Menetrier Disease:

  • Describe
  • Treatment?
A
  • excessive TGF-alpha secretion.
  • diffuse hyperplasia of the foveolar epithelium
  • treatment- supportive, TGF blockers, surgery

(rare)

53
Q

Zollinger-Ellison Syndrome (ZE)

  • Ass’d w/ ____?
  • What is it?
  • Cause?
  • Presentation
A
  • 20-25% associated with MEN1
  • acid hypersecretion
  • caused by gastrin secreting tumors (SI)
  • most common presentation is DU +/- diarrhea DU= acid, diarrhea+ insoluble bile acids/malabsorption.
54
Q

Zollinger-Ellison Syndrome (ZE):

- Diagnosis?

A

Dx:
- pH 1000 - secretin stimulation test

Imaging:

  • gastrinomas express the somatostatin receptor. This receptor binds octreotide.
  • somatostatin receptor scintigraphy (SRS)
  • endoscopic ultrasound- preoperative tumor localization
55
Q

T or F? Fundic gland polyps are secondary to PPI therapy.

A

True

56
Q

90% of all gastric malignancy is ______

A

adenocarcinoma

STRONGLY associated with helicobacter infection

57
Q

Gastrointestinal Stromal Tumor (GIST) - involves what anatomy?

A

Involves GI tract, omentum, mesentery
– Stomach (60-70%)
– Small intestine (20-30%)
– Colorectum and esophagus (<10%)

58
Q

Gastric adenocarcinoma: important mutations?

A 
CDH1 – encodes E-cadherin 
IL1-beta 
THF 
IL-10 
IL-8 
TLR4 
p53

(STRONGLY associated with helicobacter infection)

59
Q

GIST: microscopy?

A
  • Spindle cell tumor
  • Resemble smooth muscle tumors
  • Focal nuclear palisading like nerve sheath tumors
  • Epithelioid pattern in ~1/3 of gastric GIST’s
  • Positive for KIT- or PDGFRA-activating mutation
60
Q

Adenocarcinoma- Sx & Tx?

A

Symptoms are non specific and range from No symptoms to dyspepsia, ulcer like pain, early satiety, obstruction, perforation.

Tx: Surgical resection

61
Q

Gastric adenocarcinoma: Prognosis?

A
  • High rate of malignancy

- Overall survival at 1 year after diagnosis is 63%

62
Q

Diagnosis:

  • Involves GI tract, omentum, mesentery
  • Origin proposed to be Cajal cells
A

Gastrointestinal Stromal Tumor (GIST)

63
Q 
Diagnosis?
Microscopy includes:
• Spindle cell tumor
• Resemble smooth muscle tumors
• Positive for KIT tyrosine kinase receptor
A

Gastrointestinal Stromal Tumor (GIST)

64
Q

Most common extranodal site of lymphoma?

A

Lymphoma of the GI tract

• Stomach involved most often, followed by small intestine and colon

(Diffuse large B-cell lymphoma is most common, followed by marginal zone lymphoma)

65
Q

Lymphoma of the GI Tract: Most common type of lymphoma?

A

Diffuse large B-cell lymphoma is most common, followed by marginal zone lymphoma

(stomach involved most often, followed by small intestine and colon)

66
Q

Diagnosis?
• Solitary or multiple mass lesions
• Some more diffuse, ill defined
• Large, ulcerated, exophytic or polypoid
• Diffuse or vaguely nodular infiltrate of lymphoma cells

A

Lymphoma of GI tract

67
Q

What is a Carcinoid Tumor?

A

Well differentiated neuroendocrine tumor

• Arise from gastrointestinal endocrine system

68
Q

What is Carcinoid Syndrome?

What percent of patients w/ Carcinoid Tumor have this?

A

Flushing, diarrhea, & asthma

Less than 10%

69
Q

Benign or Malignant?

_____ ulcers have a smooth, regular edge.

_____ tends to be ragged and irregular

A

Benign ulcers have a smooth, regular edge

Malignant (adeno) tends to be ragged and irregular

70
Q

T or F?

Gastric ulcers MUST be biopsied to determine if cancer is present.

A

True.

6 biopsies will detect cancer accurately in greater than 98% of cases

71
Q

T or F?

Delayed gastric emptying can sometimes be associated with structural obstruction.

A

False.
Delayed gastric emptying NOT associated with structural obstruction.

(would be Gastroparesis- dysfunctional coordination of muscles of 4 regions of the stomach)

72
Q

Gastroparesis- Etiologies?

A

Idiopathic- viral, GERD, NUD

Diabetic – acute vs chronic hyperglycemia

Post surgical

73
Q

Gastroparesis- presentation?

A
  • postprandial nausea, vomiting belching early satiety, bloating, discomfort or pain

May have weight loss and symptoms from various forms of malabsorption

74
Q

Medication options for Gastroparesis?

A

prokinetics- erythromycin, metoclopramide

Antiemetics

Tricyclic antidepressants- control pain

75
Q

Type of Gastritis ass’d w/ the following:

  • 85% have parietal cell pseudohypertrophy with snouting
  • Often extensive intestinal, antral or pancreatic acinar metaplasia
  • Linear or nodular neuroendocrine (enterochromaffin cell-like/ECL) hyperplasia on chromogranin immunostains
A

Autoimmune Gastritis

76
Q

What is the etiology of chronic gastritis that is described to have the following:

Foveolar hyperplasia, sparse inflammation, mucin depletion, vascular congestion, edema, smooth muscle hyperplasia

A

Chemical/Reactive Gastropathy

  • Bile reflux
  • NSAID
  • Acid, Alkali
  • Ethanol
77
Q

Type A vs. Type B Gastritis?

A

Type A = Autoimmune
Type B = non-Autoimmune

(most cases are type B)

78
Q

Etiology of Gastritis that presents w/ Pernicious anemia?

A 
Autoimmune Gastritis
(Anti-intrinsic factor (IF) antibodies --> IF deficiency)
79
Q

Clopidogrel - MOA? Risks?

A

MOA: Anti-platelet agent

Risks: Bleeding (moreso than Aspirin)

80
Q

GIST - origin cells?

A

Origin proposed to be Cajal cells (interstitial pacemaker cells)

81
Q

Most common primary mesenchymal tumor of the GI tract?

A

Gastrointestinal Stromal Tumor (GIST)

82
Q 
Diagnosis?
Immunohistochemical study shows 1 of these:
- C-Kit (CD117)
- DOG1
- CD34
A

Gastrointestinal Stromal Tumor (GIST)

83
Q

What is true of patients w/ GIST that have KIT exon 11 mutations?

A

They show improved response to therapy w/ imatinib mesylate

84
Q

cagA genotype – risk factor for..?

A

Developing cancers & ulcers if you have H. pylori

OSD_GI (13 decks)

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