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GI, Liver, GallBladder, Pancreas > CM- Approach to Stomach Disease > Flashcards

CM- Approach to Stomach Disease Flashcards

1
Q

What is the primary purpose of the stomach?

A
  1. store ingested nutrients and dispense them into the small intestine in an orderly fashion
  2. HCl prevents pathogens from causing enteric infections [it is NOT necessary for digestion]
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2
Q

What kind of cells are found in the glands of the cardia?

A

mucous cells that secrete mucus and pepsin

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3
Q

What type of gland is found in the body and fundus of the stomach?
What cells make up this gland?

A

Oxyntic glands made of:

  1. parietal cells
  2. chief cells
  3. enterochromaffin cells (ECL)
  4. endocrine
  5. mucus
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4
Q

What types of glands are found in the antrum of the stomach? What cells make up this gland?

A

Pyloric glands made of:

  1. mucous cells
  2. G cells (gastrin)
  3. D cells (somatostatin)
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5
Q

What glands are found in the duodenum? What is their role?

A

Brunner’s glands are located in the submucousa. They are a source of bicarbonate

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6
Q

As food enters the proximal stomach, what process occurs?

A

Receptive relaxation-

vagus efferents inhibit fundus and body muscular tone to allow volume expansion without pressure

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7
Q

How are liquids emptied from the stomach?

A

Once in the stomach, liquids rapidly redistribute and are emptied by a tonic pressure gradient from the proximal stomach and duodenum

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8
Q

How are solids emptied from the stomach?

A
  1. After storage for 30 minutes, they move to the antrum
  2. vagally mediated segmental contractions in the greater curve of the body mix the food
  3. when the food is 1mm or less, it is emptied into the pylorus
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9
Q

What 2 problems arise with the stomach if there is vagal nerve dysfunction/destruction?

A
  1. there is no receptive relaxation -> early satiety

2. there is no mixing–>delayed emptying

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10
Q

What happens to non-digestible (over 1mm) retained gastric solids?

A

Interdigestive Migrating Motor Complex contracts and pushes out undigested particles every 1.5-2 hours in the non-fed state.

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11
Q

How does the small intestine keep from being overwhelmed during digestion?
What 4 things are sensed?
What are suggested hormones that play a role in these reflexes?

A

There are receptors that respond to :

  1. low pH
  2. osmolarity
  3. fatty acids
  4. high caloric density

that signal back to slow gastric emptying

Suggested: CCK, secretin, GIP

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12
Q

At what concentration do parietal cells secrete HCl? What is the tonicity?
What happens when the patient vomits?

A

Parietal cells secrete HCl at a concentration of 160mmo/L and a volume determined by the number of partietal cells secreting.

It will be isotonic with NO sodium ions.

If the patient vomits, they lose [H+] but must keep the same concentration so there will be more Na in the gastric juices. This leads to Na depletion

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13
Q

What determines the volume and acidity of gastric juice?

A

The relative proportion of parietal and non-parietal secretions

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14
Q

What is the most important stimulant of gastric acid secretion?
What 2 cells is it released from?
What 2 receptors does it interact with?

A

Histamine is released from:

  1. ECL
  2. mast cells in the lamina propria

It acts on :
1. H2 receptor on parietal cells to release acid
2, H3 receptors on D cells to block somatostatin release
[somatostatin inhibits parietal AND ECL cells]

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15
Q

What are the 3 things Ach controls in gastric acid secretion?

A
  1. M3 receptor on parietal cells
  2. ECL to release histamine
  3. D cells to inhibit somatostatin release
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16
Q

What are the 3 things that stimulate acid release from parietal cells?

A
  1. Histamine
  2. Ach
  3. Gastrin
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17
Q

What 2 things stimulate the release of gastrin?

What 2 cells does gastrin act on?

A

Gastrin release from G cells in the atrum is stimulated by:

  1. presence of food
  2. neural release of gastrin releasing peptide (GRP)

It acts on:

  1. parietal cells to release acid
  2. ECL to release histamine (** more accepted scenario)
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18
Q

How does somatostatin regulate gastrin release?

What turns D cells on and off?

A

Somatostatin released from D cells can act in a paracrine manner on adjacent G cells to inhibit the release of gastrin.

Hydrogen in the gastric lumen turns on D cells which inhibit gastrin release.

Ach turns off D cells inhibiting somatostatin release

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19
Q

How do parietal cells release acid after Ach or Histamine has bound to it?

A

Ach–> Ca
Histamine->Gs->adenylate cyclase->cAMP

cAMP and Ca open the tubulo-vesicles that had been storing acid. They open into canaliculi with microvilli to increase the surface area from which acid is excreted into the lumen

H goes in the lumen in exchange of K by a proton pump. The protein pump relies on K in the lumen however.
Transcellular pathways for K and Cl must be open

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20
Q

What are the 2 proposed mechanisms of H3 receptors?

A
  1. on D cells to inhibit somatostatin release (pro acid)

2. on ECL to inhibit more histamine release (antacid)

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21
Q

What are the 2 MAIN inhibitors of acid secretion from parietal cells?
What are some others?

A
  1. Prostaglandins & somatostatin inhibit adenylate cylase which stops cAMP production in parietal cells
  2. Somatostatin also inhibits ECL directly stopping histamine release

Others: secretin, GIP, peptide YY

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22
Q

What are the mucosal defense factors against acid?

A

It is hypothesized to be prostaglandins because: 1. NSAIDS (which block COX) leads to ulcers.
2. In experiments, when prostaglandins were inhibited, ulcers developed as well.

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23
Q

What are the 3 means by which PGs protect gastroduodenal mucosa?

A
  1. secretion of mucus
  2. stimulation of bicarb secretion
  3. maintaining mucosal blood flow during periods of potential injury
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24
Q

Describe the process of vitamin B12 (cobalamin) absorption.

A
  1. B12 is separated from food by pepsin and acid
  2. B12 attaches to R proteins present in saliva
  3. In the alkaline duodenum, pancreatic enzymes hydrolyze the R protein-B12 complex
  4. Free cobalamin binds IF
  5. IF-cobalamin complex passes through the intestines to the ileum where it is actively absorbed.
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25
Q

What are the 4 things that can lead to failure to absorb cobalamin?

A
  1. IF deficiency
  2. pancreatic exocrine insufficiency (rare)
  3. small intestine bacterial overgrowth (achlorhydria)
  4. ileal disease (Crohn’s)
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26
Q

Why does deficiency of B12 not occur in a timely manner to pathology (failure to absorb)?

A

Liver stores of B12 can last up to 5 years with NO absorption

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27
Q

Who is the Schilling test performed on? What are the steps?

A

If is performed on people with low serum cobalamin after parenteral repletion of the vitamin.

  1. Radiolabeled B12 alone. If urine B12 is low,
  2. Radiolabeled B12 AND IF
    - if it normalizes–> pernicious anemia
    - if it is still low,
  3. Radiolabeled B12 + antibiotics
    - if normalizes–> bacterial overgrowth
    - if not …
  4. Radiolabeled B12 + pancreatic enzymes
    - if normalizes = pancreatic exocrine insufficiency
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28
Q

Little digestion takes place under the influence of pepsin in the stomach. How does pepsin indirectly aid in digestion?

A

The release of AA and peptides by pepsin trigger the release of important digestive hormones like gastrin and CCK.

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29
Q

What are major symptoms of delayed gastric emptying?

A
  1. early satiety
  2. epigastric fullness/bloating
  3. nausea
  4. vomiting
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30
Q

A patient present with early satiety, epigastric fullness, nausea and vomiting. You are not sure if they have delayed emptying [motility disorder] or a mechanical obstruction. What test should you do?

A

Endoscopy

You CANNOT do a barium swallow in a patient suspected of mechanical obstruction

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31
Q

What is the only diagnostic study that can confirm delayed gastric emptying?

A

Radionucleotide scan using labeled mixed meal.

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32
Q

What are major causes of gastoparesis?

A
  1. post-surgical state
  2. diabetes, hypothyroidism
  3. muscular disorder (systemic sclerosis, ALS)
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33
Q

What are 2 situations that lead to rapid gastric emptying or “dumping syndromes”?

A
  1. gastric surgery

2. abnormal myoelectric function

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34
Q

Describe the difference between early dumping syndrome and late dumping syndrome,

A

Early- 30 to 60 minutes after eating. Rapid movement of food into the duodenum causes fluid shifts leading to faintness.

Late = 2-3 hours after eating. It is associated with excessive insulin secretion and rebound hypoglycemia

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35
Q

What is the relationship between severity of body gastritis and acid secretion?

A

The more severe the gastritis in the body of the stomach, the LESS acid is secreted.
Some subjects may be hypo or achlorhydric.

36
Q

What is the effect of H. pylori on acid secretion?

A

H. pylori causes inflammation.
Cytokines from the inflammation suppress somatostatin which increases gastrin levels in fasting and fed states.

Despite higher gastrin, healthy subjects with h. pylori infections have decreased mean basal acid output (BAO).

37
Q

What is Zollinger-Ellison Syndrome?

A

a tumor of pancreatic islet cells causes overproduction of gastrin –> gastric acid.

38
Q

What is the effect of a vagotomy with or without antrectomy on secretion of acid?

A

It will result in 75% decrease in acid secretion with just the vagotomy.
The antrectomy will decrease acid secretion even more.

39
Q

What is the basis of the urease breath test?

A

H. pylori makes urease to make ammonium to provide a more stable environment for itself in the stomach.
The body does not make urease anywhere so this distinction allows H. pylori to be detected non-invasively

40
Q

How does H. pylori escape the effects of acidic gastric juice?

A

It has chemotactic properties and flagella that help it burrow through the mucus layer covering to the epithelial cells.
It also has adhesins to attach to the epithelial cells.
It uses urease to break down urea to ammonia and then uses an H+ to make ammonium.

41
Q

What have several studies shown to correlate with the prevalence of H. pylori of adults in developed nations? Why?

A

It correlates with socioeconomic status and crowded living conditions in childhood.

It is likely that H. pylori spreads person to person especially among children

  1. oral-oral
  2. fecal-oral
42
Q

What the the mucosal biopsy for H. pylori show?

A
  1. demonstration of the organism
  2. determination of the presence of urease
    - if present it will split urea into ammonia and CO2 which will raise the pH. the test medium has a color change pH indicator and it will change yellow to red.
43
Q

What three things can give false negatives on the rapid urease test?

A
  1. presence of PPI (raises pH)
  2. blood in the stomach
  3. high dose H2 antagonist
44
Q

What is the least sensitive of the direct techniques for diagnosing H. pylori?

A

Culture so it is generally not done

45
Q

What are the 3 non-invasive tests used for H. pylori?

A
  1. blood antibody test
  2. urea breath test
  3. stool antigen test
46
Q

What are the pros and cons of blood antibody tests?

A

Pros:
-almost as specific and sensitive as biopsy-based studies

Cons:

  • high number of false positives
  • cannot confirm eradication because IgG titers decrease very slowly over time
47
Q

How does urea breath test work?

What are the pros and cons?

A

In UBT, the person ingests a liquid meal with radioactively labeled c13 or c14.
If urease is present, labeled CO2 will be split off and absorbed into circulation and exhaled.

Pros
100% positive predictive, 95% negative predictive

Cons
false negatives with PPIs and H2 antagonists

48
Q

What is the histological marker for H. pylori even in the absence of being able to specifically identify the organism?

A

CAG
Chronic active gastritis - lymphocytes and neutrophils in the mucosa.

This is associated with cytokine release and increased cell proliferation that can lead to:

  • ulcers
  • lymphoma
  • carcinoma
49
Q

What are the 3 choices for initial therapy for chronic gastritis?

A
  1. Triple therapy: PPI, amoxicillin, clarithromycin
  2. Quad therapy: PPI, tetracycline, metronidazole, pepto bismol
  3. Sequential therapy: 5 days PPI and amoxicillin followed by 5 days PPI and clarithromycin and tinadazole
50
Q

What is salvage therapy for chronic gastritis?

A

Quadruple therapy (PPI, pepto, metro, tetra) is a good therapy for triple

or

esomeprazole, amoxicillin, levofloxacin

51
Q

When should you be looking for H. pylori infection in patients?

A
  1. peptic ulcer disease
  2. low grade gastric lymphoma
  3. family history of gastric carcinoma
  4. dyspepsia
  5. gastritis found on EGD for another reason
52
Q

What are the 4 gastrides?

A
  1. infectious gastritis
  2. lymphocytic gastritis
  3. eosinophilic gastritis
  4. gastritis associated with systemic disease
53
Q

What is the only way you can determine something to be gastritis?

A

it is defined histologically as diffuse mucousal infiltration by inflammatory cells

54
Q

What are the 3 mucousal divisions?

A
  1. gastrides
  2. hypertrophic fold syndromes
  3. non-inflammatory
55
Q

With the exception of H. pylori, what are the bacteria causes of gastritis?

A

syphilis and TB

56
Q

What are the 4 ways lymphocytic gastritis can present on endoscopy?

What disease is it associated with? What is treatment?

What in the DDx for lymphocytic gastritis must you exclude?

A
  1. normal folds
  2. hypertrophic lymphocytic (giant folds)
  3. nodular with erosions
  4. volcano-like

It is associated with celiac sprue and can be treated with corticosteroids

You must exclude lymphoma

57
Q

What determines how eosinophilic gastritis will present? What are a few presentations?
What must be excluded?
What is treatment?

A

The layer involved determines the presentation.

  1. mucousal ulceration
  2. obstruction – delayed gastric emptying

Parasitic infestation must be excluded.

Treatment is corticosteroids and occasionally surgery

58
Q

What are the 3 hypertrophic fold syndromes?

A
  1. Menetrier Disease
  2. lymphocytic gastritis
  3. acid hypersecretory states
59
Q

What is seen on endoscopy and histology of Menetrier disease?

A

Endoscopy:

  • giant gastric rugal folds
  • spared antrum

Histology

  • massive foveolar hyperplasia
  • cystic dilation that penetrates into submucosa
  • in extreme cases, absent parietal cells and hypochlorhydria
  • little inflammation (which differentiates it from a similar presentation with CAG from H. pylori)
60
Q

In addition to Menetrier disease and lymphocytic gastritis (with foveolar hyperplasia) what are other causes of hypertrophic fold syndrome?

A
  1. parietal mass causing hypersecretory states
  2. gastric lymphoma
  3. gastric adenocarcinoma
61
Q

What 2 types of mucousal injury do NSAIDs produce?

A
  1. suppression of endogenous PGs + local damaging effect : hyperemia, erosion, subepithelial hemorrhage
  2. Ulceration (>5mm in diameter with histology breaching muscularis mucosa) as the result of overall PG depletion [these lesions can occur with IV/rectal suppository]
62
Q

What 3 types of NSAID do NOT cause initial damage to the epithelium of the stomach?
What are some drawbacks?

A
  1. Enteric coated
  2. NO-NSAID
  3. COX2 specific or salsalaste
    - expensive
    - coronary artery disease (because of increased aggregation and vasoconstriction)
63
Q

What is treatment for gastric ulcers due to NSAID use?

A
  1. PPI
  2. Misoprostol
  3. H2r antagonist- duodenal ulcers only
64
Q

Who should receive prophylactic treatment for NSAID ulcers?

What is the treatment?

A
  1. documented prior history of peptic ulcer
  2. increased risk like the elderly

Prophylactic drugs are the same as treatment.
H2r antag = duodenum only
PPI, misoprostol = gastric/duodenum

65
Q

What do ethanol-induced stomach lesions look like?

A
  1. erosions
  2. sub-epithelial hemorrhage
  3. erythema
66
Q

What is the main problem that leads to peptic ulcers?

A

Mucousal integrity failure NOT excess acid/pepsin

with the exception of ZES

67
Q

What is the MOST effective way to treat an ulcer caused by H. pylori?
NSAIDs?

A

H. pylori:

  1. PPI (to lower acid)
  2. treat infection (to return mucousal integrity)

NSAIDs

  1. PPI (to lower acid)
  2. stop NSAID use (to return mucosal integrity)
68
Q

What is the clinical presentation of peptic ulcer disease?

A

Usually it is asymptomatic, however, if the patient presents with symptoms it will be burning epigastric pain (usually nocturnal&intermittent) that can be relieved with food and antacids

69
Q

What are the 3 main complications of a peptic ulcer?

A
  1. Bleeding
  2. perforation/penetration
  3. obstruction
70
Q

What are 3 factors associated with a poor outcome from a bleeding ulcer?

A
  1. age/concomitant disease
  2. bleeding fails to stop or recurs at the hospital
  3. hemodynamic instability from the bleed
71
Q

What areas of the gastroduodenum are most prone to ulcer bleeds?

A
  1. large deep ulcers on the lesser gastric curve
  2. posterior duodenal bulb

because these in these areas the ulcer is more likely to erode a major vessel

72
Q

What is treatment for gastric ulcers? What determines the speed of ulcer healing?

A

Antisecretory medications and the speed of recovery is determined by:

  1. duration gastric pH is >3
  2. number of weeks of therapy
73
Q

What are the 5 types of gastric neoplasms?

A
  1. adenocarcinoma
  2. gastric polyps
  3. stromal tumors and GISTs
  4. neuro-endocrine tumors
  5. lymphoma
74
Q

What are the 2 types of gastric adenocarcinoma? What histology is associated with each?

What is thought to be a major factor in the cause of both types?

A
  1. Diffuse- signet cells, excess mucin production, undifferentiated
  2. Intestinal- form glands and are found in association with atrophic gastritis, intestinal metaplasia–>dysplasia

H. pylori is a cause of both (along with other factors)

75
Q

What determines the prognosis of gastric adenocarcinoma?

A

The depth of the primary invasion regardless of lymph node metastases.

Mucosa/submucosa has better prog. than those that have penetrated the muscular layer.

76
Q

What is treatment for gastric adenocarcinoma?

A

After diagnosing, staging is determined on CT and with EUS. If there is no distal mets, surgical resection will be attempted.

Chemo regimens are being tested in patients with unresectable cancer

77
Q

What are the three types of gastric polyp? Which show progression to malignancy?

A
  1. hyperplastic
  2. adenoma (–>carcinoma)
  3. fundic gland (if related to FAP –> carcinoma)
78
Q

Why do hyperplastic polyps form?

A

Hypergastrinemia and is associated with autoimmune body gastritis

79
Q

Describe the distribution of adenoma polyps in the stomach.

A

They are more likely to occur in patients with familial adenomatous polyposis (FAP)

They are LESS common in the duodenum and are villus instead of tubular, but there is a predilection for the ampulla of Vater.

80
Q

Who is at increased risk of developing fundic gland polyps?

A
  1. people on long term PPI therapy

2. FAP

81
Q

What are the 2 main stromal gastric tumors?
What is their location/appearance?
What usually differentiates benign/malignant?
What is treatment?

A

Leiomyomas and lipomas that arise:
1. submucosal bulging into the lumen
2. subserosal bulging extraluminally
3, Both –> dumbbell appearance

Usually the larger, the more malignant (leiomyosarcoma or liposarcoma) but to confirm malignancy there must be invasion or metastases

Treatment is surgical resection

82
Q

What determines prognosis of GIST?
How is GIST identified?
What is treatment?

A

The size and number of mitoses/50 high power field determines the prognosis.

It is identified by cKIT
It is treated with Gleevec

83
Q

How do neuroendocrine tumors look histologically? Where do carcinoid tumors typically arise in the intestinal tract?

A

They are small nests of bland looking cells.

They arise in enterochromaffin and enterochromaffin-like cells

84
Q

What are the 2 types of carcinoid tumors that arise in the stomach?
What is treatment?

A
  1. Sporadic- single/few in number. Surgical resection
  2. Secondary to atrophic gastritis- smaller/more numerous. Atrophic gastritis causes and increase in gastrin which is tropic for ECL in the body/fundus. Treat with antrectomy
85
Q

What is the cause of lymphoma in the stomach?

What is treatment at each stage?

A

H. pylori induces low grade clonal B-cell proliferation in MALT (mucosa associated lymphoid tissue) which leads to low grade–> high grade stages.

Low grade- eradicate H. pylori
high grade- surgery/radiation/chemo

GI, Liver, GallBladder, Pancreas (24 decks)

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