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GI Exam 2 > Disorders of the stomach > Flashcards

Disorders of the stomach Flashcards

1
Q

Gastroesophageal Reflux Disease

A

Also known as GERD or Reflux Esophagitis, this is the
recurrent reflux of gastric contents into the esophagus
secondary to Gastroesophageal junction incompetence

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2
Q

GERD affects about ____% of the adult
population, with over half of the population
experiencing heartburn at least once in their lives

A

10-20

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3
Q

Pathophysiology of GERD

A

○ Most episodes of gastric reflux occur during transient relaxation of
the LES (TLESR), triggered by gastric distention and/or being in an
upright position. Some degree of reflux occurs in all persons
○ A smaller portion of GERD patients have an weak LES that results in gastric reflux when lying supine or with increase in abdominal pressure (lifting or bending)

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4
Q

The presence of a _____ can also be a causal factor in GERD and increase the complications

A

Hiatal Hernia

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5
Q

Other factors that contribute to the presence and severity of
GERD include

A

■ Increased intragastric pH
■ Impaired esophageal motility
■ Decreased salivation
■ Increased Intra-abdominal pressure

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6
Q

Factors that increase intra-abdominal pressure

A

■ Obesity
■ Pregnancy
■ Smoking

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7
Q

Foods or drugs can also decrease LES tone:

A

■ Chocolate, Peppermint
■ Alcohol and Smoking
■ Onions, citrus, and tomatoes
■ Caffeine
■ Certain Medications (Calcium Channel Blockers, Anticholinergics)

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8
Q

Characteristic Signs and Symptoms of GERD

A

○ Heartburn (pyrosis) is the hallmark symptom
○ Regurgitation: Refluxed gastric content into mouth/throat. Sour,
acidic taste in mouth
○ “Atypical” or “Extraesophageal” symptoms of GERD may occur: Dysphagia, chronic cough, wheezing, etc.

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9
Q

Diagnosis of GERD

A

○ Initial diagnostic studies are generally not required for patients with
typical GERD symptoms suggesting uncomplicated reflux
○ Upper Endoscopy (EGD) is the study to definitively diagnose GERD

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10
Q

T/F Barium Swallow Esophagram is not used in the diagnosis of GERD

A

T

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11
Q

Esophageal pH Monitoring

A

■ Unnecessary in most patients.
■ May be used to document significant
esophageal acid exposure in those with
atypical symptoms, or those being considered for anti-reflux surgery

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12
Q

Plain radiographs help Identify hiatal hernias but can’t Dx _____

A

GERD

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13
Q

Management of MILD GERD

A

○ Treatment of mild, intermittent symptoms:
■ May be treated sufficiently with a trial of antacids and lifestyle modifications (diet changes, weight loss, don’t eat 3 hours
before bed, avoid overeating and tight clothes, etc).
■ Other recommendations: Avoid caffeine, chocolate, tomatoes, carbonation, smoking, alcohol, etc, raise head of bed.

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14
Q

Management of moderate to severe GERD

A

○ Pharmacologic therapies are indicated with moderate to severe
disease, or when lifestyle modification have failed.
■ Proton Pump Inhibitors, treatment of choice in severe disease

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15
Q

T/F You can never discontinue a GERD treatment plan once one is started

A

F - In those who achieve good symptomatic relief with a course of PPI,
treatment may be discontinued after 4-12 weeks

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15
Q

Barrett’s Esophagus

A

● The most significant complication of GERD.
● It is believed that the chronic
epithelial injury (by the gastric acid),
leads to replacement of esophageal
squamous cells with gastric columnar
cells (a process called Metaplasia).
○ These cells are considered
dysplastic and precancerous.

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15
Q

The most significant complication of GERD

A

Barrett’s Esophagus

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16
Q

Paradox of Barrett’s esophagus and GERD

A

The development of Barrett’s does not necessary mean the GERD
symptoms will increase.
○ Interestingly, a paradoxical effect is often seen, where Barrett’s patients often have less symptoms, suggesting decreased acid sensitivity of Barrett epithelium.

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17
Q

The most common complication of Barrett’s is _____

A

Esophageal Adenocarcinoma

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18
Q

Endoscopic screening with biopsy for Barrett’s esophagus is indicated in
______

A

patients with multiple risk factors for adenocarcinoma (age over 50, hiatal
hernia, male, obesity, caucasian, cigarette smoking, chronic GERD, or
family history of Barrett’s or esophageal adenocarcinoma).

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19
Q

If nondysplastic Barrett’s is discovered, surveillance with _____

A

an EGD is recommended every 3-5 years

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20
Q

If dysplasia is discovered with barretts:

A

○ Low grade- Endoscopic Radioablation or annual EGD surveillance.
○ Moderate to High grade- Endoscopic Radioablation

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21
Q

Treatment of barretts esophagus:

A

● First line therapy: Treat the GERD! (indefinite sure of PPIs)
● If dysplasia present: Endoscopic Radiofrequency Ablation is a treatment
that ablates dysplastic cells in the epithelial lining of the esophagus.
○ Eradication of high-grade Barrett’s can be
achieved in as many as 91% of patients.

22
Q

Hiatal Hernia

A

When a portion of the stomach prolapses through the Esophageal Hiatus of the diaphragm.
● These hernias are often associated
with GERD, as the LES is displaced
upward and gastric contents are more
likely to move into the esophageal
lumen. Diaphragm normally provides
strength to the LES.

23
Q

Hiatal Hernia diagnosis

A

Barium Swallow is the historical gold standard for diagnosis

24
Q

Management of hiatal hernia

A

○ Treatment is generally conservative, focusing on postural adjustments,
antacids, H2 blockers, and PPIs.
○ Weight control can often times significantly improve or fix the condition
○ In severe cases (usually with large hernias or persistent symptoms), surgical intervention can be performed.
■ A Laparoscopic Fundoplication (Nissen) is
the procedure of choice.

25
Q

Gastritis

A

●Gastritis is inflammation, irritation, or erosion of the stomach epithelium
secondary to an irritant
●Superficial inflammation and erosion of mucosa without penetration into muscularis

26
Q

Gastritis be caused by several different factors

A

○ Infection (especially H pylori)
○ Physiologic and social stress
○ Medications (such as NSAIDs)
○ Heavy alcohol use
○ Portal hypertension

27
Q

Gastritis pathophysiology

A

○ Stress gastritis can occur in critically ill
patients, which is likely histamine and
inflammatory mediator-driven
○ NSAIDs diminish prostaglandin production in the stomach. Prostaglandins ↓HCL and are
cytoprotective (↑mucus)

28
Q

Gastritis Signs and Symptoms

A

○ Epigastric pain
○ Abdominal tenderness
○ Bloating
○ Anorexia
○ Nausea with or without vomiting
○ May be aggravated by eating
○ Foul-smelling breath
○ Hematemesis (rare and minimal, often “coffee
ground”)
○ Melena may occur

29
Q

Diagnosis of Gastritis

A

○ Upper Endoscopy (EGD) with biopsy
■ Testing is not usually needed, but if the patient presents with
hematemesis, EGD is required.
GI-STOM-1
■ EGD will reveal classic mucosal erythema,
possible subepithelial hemorrhages, and
mucosal erosions.

30
Q

Gastritis Management

A

Proton Pump Inhibitors and H2 Blockers are important in the prevention and treatment of gastritis

31
Q

H. Pylori infection

A

●Helicobacter pylori is a Gram negative bacteria that can live comfortably in the acidic stomach
●H. pylori infection is commonly found in patients having duodenal ulcers (80-95%) gastric ulcers (65-95% percent), dyspepsia (20-60%), and gastric cancer (70-90%)

32
Q

S&S of H. Pylori infection

A

○ Most patients with H pylori infection are asymptomatic.
○ If they do develop symptoms, this may include:
■ Epigastric abdominal pain
■ Nausea with or without vomiting
■ Dyspepsia
■ Diarrhea
■ Halitosis
○ The patient may present with Chronic Gastritis, Atrophic Gastritis, Peptic Ulcer Disease, or Gastric Adenocarcinoma

33
Q

Testing for H. Pylori infection

A

○ H pylori Fecal Antigen Test- The preferred test with sensitivity of 94% and specificity of 98%. Only positive if acute, so useful to confirm eradication too.
○ Carbon-13 Urea Breath Test- Not as common. Can only be positive if H pylori is present in the stomach.
○ H pylori serum Serology Testing- High sensitivity and Specificity (>90%), but expensive and positive if history
of infection. NOT useful to confirm eradication.
○ Tissue Biopsy during EGD - Commonly performed

34
Q

Management of H. Pylori infection

A

■ PBMT Quadruple Therapy (14 days): PPI
(omeprazole or pantoprazole), Bismuth
Subsalicylate, Metronidazole, and Tetracycline.
■ PAMC Quadruple Therapy (14 days): PPI
(omeprazole or pantoprazole), Amoxicillin,
Metronidazole, and Clarithromycin
○ Additionally, the FDA has approved several “Triple Therapy” regimens, although resistance is a concern now. While FDA approved, these are not 1st line

35
Q

Peptic Ulcer Disease

A

● PUD is a common disorder that includes Gastric and Duodenal ulcers.
● It is the most common cause of acute upper GI bleeding.
● Duodenal ulcers are 4-5 times more
common than Gastric Ulcers

36
Q

The most common cause of acute upper GI bleeding

A

PUD

37
Q

Pathophysiology of PUD

A

○ Peptic ulcers result from disruption of
gastric or duodenal mucosa secondary to
an overproduction of acid or defects in
the protective mucous barrier of the
stomach lining.
○ Three major causes have been
implicated: NSAIDs, H pylori infection,
Zollinger-Ellison Syndrome

38
Q

S&S of PUD

A

○ Epigastric pain is the hallmark symptom
○ Nausea
○ Anorexia
○ Abdominal bloating
○ Hematemesis or Melena

39
Q

If the pain is relieved with eating food, suggestive of _____

A

duodenal ulcer
(Gastric ulcers may be aggravated by food.)

40
Q

Peptic Ulcer Disease diagnosis

A

○ Upper Endoscopy (EGD) provides great visualization of the pathology
and is the diagnostic test of choice
○ H pylori testing should be strongly considered.
○ Ordering lab tests to rule out Zollinger-Ellison Syndrome (ZES) should also be considered (more to come).
○ Anemia may be present if slowly bleeding peptic ulcer.
○ Also order an X-ray or CT scan if concern for perforation

41
Q

Medical Management of PUD

A

■ PPIs are the treatment of choice
■ H2 blockers also help and can be added to PPI if needed
■ Sucralfate, Antacids, and Bismuth enhance mucosal barrier
defense and promote ulcer healing

42
Q

Perforation of Peptic Ulcer - presentation

A

Patient will present with acute
increase in abdominal pain, board-like abdomen, rebound tenderness, and possibly hypotension and pallor.
X-ray or CT may reveal
pneumoperitoneum (surgical emergency!)

43
Q

Zollinger-Ellison Syndrome

A

A hypergastrinemic state caused by a Gastrin-secreting tumor

44
Q

About 1/3 of all Gastrinomas are part of ____

A

the autosomal dominant
Multiple Endocrine Neoplasia

45
Q

S&S of Zollinger-Ellison Syndrome

A

○ Most patients present with symptoms
indistinguishable from regular PUD
○ Anemia may be present secondary to
bleeding of peptic ulcers.
○ Abdominal pain with accompanying
secretory diarrhea is common, often
improved with PPI treatment.

46
Q

Diagnosis of Zollinger-Ellison Syndrome

A

○ Fasting serum Gastrin level greater than 150 pg/mL indicates hypergastrinemia (normal is 0-100 pg/mL)
○ A secretin stimulation test confirms the presence of a gastrin secreting mass

47
Q

Management of Zollinger-Ellison Syndrome

A

○ Use of PPIs are the mainstay of controlling gastric acid secretion.
○ If the tumor is found, surgical resection of the gastrinoma should be attempted if possible

48
Q

Gastric Neoplasm

A

● Adenocarcinoma is the most common stomach cancer (>90%) and arises from
the glandular cells of the stomach (goblet and Paneth cells).
● Gastric adenocarcinoma is among the most common cancers worldwide (4th
most common), but is less common in the US
● Because early gastric cancer is usually
asymptomatic, this cancer is difficult to cure
because it is most often in advanced stages by the time the diagnosis is made

49
Q

Pathophysiology of a Gastric Neoplasm

A

○ Chronic H pylori Gastritis has been strongly associated with the
development of Gastric cancer
○ Other risk factors include:
■ Tobacco and/or alcohol consumption
■ Possibly food additives and carcinogens
■ Possibly occupational exposures to heavy metals
■ Genetic mutations may play a role

50
Q

S&S Gastric Neoplasm

A

○ Dyspepsia and weight loss associated with anemia and fecal occult GI
bleeding in a patient over 40 is gastric cancer until proven otherwise.
○ Progressive dysphagia may develop
○ Classic signs of metastatic spread:
■ Virchow’s Node- An enlarged, firm node in the left supraclavicular
region is strongly associated with Gastric cancer.
■ Sister Mary Joseph Node- Palpable node bulging into the umbilicus
is often seen with metastatic gastrointestinal cancers.

51
Q

Classic signs of metastatic spread for gastric neoplasm

A

■ Virchow’s Node- An enlarged, firm node in the left supraclavicular
region is strongly associated with Gastric cancer.
■ Sister Mary Joseph Node- Palpable node bulging into the umbilicus
is often seen with metastatic gastrointestinal cancers

52
Q

Gastric Neoplasm Diagnosis

A

○ EGD is the diagnostic study of choice, as
biopsy is possible.
○ Biopsy
○ CT and Endoscopic Ultrasound are used to determine the depth of
spread and likelihood of metastatic disease. (chest X-ray also 4 mets)
○ CBC and CMP are important lab studies as well.

53
Q

Management of a Gastric Neoplasm

A

○ Treatment generally involves palliative or curative resection of the
tumor, depending on size, depth, and location.
○ Chemotherapy is often utilized after surgery.
○ Radiation plays more of a palliative role.

54
Q

Prognosis of Gastric neoplasm

A

■ Only a small percentage of people who undergo surgery will
be cured and most experience a recurrence.
■ The overall 5-year survival rate is 29.3% in the US.
● Much more grim if widespread metastatic disease

GI Exam 2 (6 decks)

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