Stomach Disorders Flashcards

1
Q

Stomach Disorders

A

Gastritits

Peptic Ulcer Disease

Gastric Resection

Gastric Malignancy

Functional Dyspepsia

Gastroparesis

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2
Q

Gastritis

A

Histological finding of injury and inflammation

Diagnosed by “Fab Five:” 5 biopsies from 5 different parts of stomach

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3
Q

Acute Gastritis

A
  • Development of hemorrhagic or erosive lesions soon after exposure of gastric mucosa to toxic substances or reduced blood flow; compromised mucosal lining then allows for further damage
  • MC causes NSAIDs, EtOH, bile acids
  • MC scenarios: trauma, burns, hypothermia, sepsis
  • Tx: treat underlying injury/remove offending agent; aggressive acid suppression to limit mucosal injury
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4
Q

Chronic Gastritis

A

Many types:

  • Atrophic: associated with loss of glands, mucosal thinning, and metaplastic changes. Two types:
    • Autoimmune Atrophic Gastritis: immune response against parietal cells and intrinsic factor leading to severe atrophy, inflammation and metaplasia
    • Multifocal Atrophic Gastritis: Directly due to H. pylori
  • Chronic reactive
  • Infectious
  • Lymphocytic/Eosinophilic
  • Granulomatous
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5
Q

PUD Disease Definitions

A

Ulcer: a break in mucosal lining with appreciable depth on endoscopy; involvement of submucosa

Erosion: break in surface epithelium without depth

PUD: erosions and ulcers in stomach and duodenum

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6
Q

PUD

A

**Pathophysiology: **

  • Imbalance between mucosal insults and mucosal defense mechanisms
  • “Stress” ulcers= disease states like shock, CV, liver, and renal disease

MC cause: H. pylori and NSAIDs

Other causes: EtOH, illicit drugs, chemo/radiation, Crohn’s, sarcoidosis

Smoking= RF b/c decreases blood flow

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7
Q

H. pylori PUD

A

Helicobacter pylori

  • Gram Negative, produce urease, generates ammonia which neutralizes acid
  • Produces protease that allows to break mucous layer

Most commonly progresses to chronic gastritis which is asymptomatic. Leads to atrophic gastritis–>more likely to develop gastric cancer

Dx: Urease Breath Testing (inexpensive and accurate), “Fab Five” bxs

Tx: Antibiotics with PPI

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8
Q

PUD

(Clinical features, dx, complications, tx)

A

**Clinical features: **

  • Gnawing, burning, aching pain which may be accompanied by nausea, vomiting, hematemesis, or melena
  • Gastric ulcer: pain is worse with eating
  • Duodenal ulcer: pain initially improves with eating, then painful 2-4hrs after meal

Dx: Endoscopy most sensitive test and can control bleeding if present

Complications:

  • GI bleeding (coffee ground hematemesis/melena)
  • penetration (pain more severe, longer duration)
  • perforation (sudden, severe abdominal pain
  • Gastric outlet obstruction

Tx: Avoid ulcer causing medications, use PPI’s, tx H. pylori if present

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9
Q

High Risk Ulcers that Require F/U

A
  • Endemic groups–Asians or Latinos
  • FHx of gastric CA
  • No recent Hx of NSAID use
  • H. pylori
  • Over 50y.o.
  • Size greater than 2 cm
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10
Q

Non-healing ulcer causes

A

Ongoing NSAID use

Smoking

Refractory H. pylori

Zollinger-Ellison Syndrome (neoplasm causes gastric acid hypersecretion)

Crohn’s

Malignancy

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11
Q

Stress ulcers/gastritis

A

Risk factors: critically ill patients

  • mechanical ventilation
  • coagulopathy
  • trauma
  • burns
  • shock
  • liver/kidney failure
  • major surgery

Most common presentation is GI bleeding

Treatment:

  • IV PPI therapy
  • Endoscopy with epi injection or clipping if indicated
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12
Q

Most common type of gastric CA

A

Gastric Adenocarcinoma

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13
Q

Gastric Adenocarcinoma

A

Pathogenesis: Chronic gastritis–>intestinal metaplasia–>dysplasia–>adenocarcinoma (similar to Barrett’s)

**Risk factors: **

  • Diet: ingestion of nitrates and high salt diets (less common in US b/c refridgerators so less cured meats)
  • Smoking
  • Gastric Disorders or Surgery
  • Infection: H. pylori and EBV
  • Genetics

Clinical features: usually vague

  • epigastric pain
  • early satiety
  • meal induced dyspepsia
  • weight loss, nausea, anorexia when advanced

B/c sxs are vague until advanced disease, poor prognosis. Will invade adjacent structures including pancreas, colon, spleen, kidney and liver.

Tx: surgery–Roux-en-y bypass MC (chemo/rad relatively ineffective)

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14
Q

Functional Dyspepsia

A

MC cause of chronic dyspepsia

Sxs may arise from visceral hypersensitivity, impaired accomodation (doesn’t stretch to accomodate food), psychosocial stress

R/O other conditions. If have alarm symptoms (weight loss, GIB, dysphagia, vomiting, anemia, abnormal imaging) get endoscopy

Tx: Food diary may indicate triggers. Acupuncture, cognitive behavioral therapy, or hypnosis work well. Reassurance.

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15
Q

Gastroparesis

A

Delayed gastric emptying in the absence of mechanical obstruction b/c dysfunction in nervous system coordination

Not very common. MC causes–idiopathic, DM

Sx: early satiety, N/V, epigastric pain, bloating and fullness

Dx: Gastric emptying scintigraphy

Tx:

  • dietary mod: small frequent meals that are easy to digest
  • medications: promotility agents, anti-emetics, acupuncture, hypnosis, cognitive behavioral therapy
  • devices/procedures: venting G tube, J tube

Complications: bacterial overgrowth, constipation, reflux

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