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GI DRx > 01a: Esophageal Disease, Ulcers > Flashcards

01a: Esophageal Disease, Ulcers Flashcards

1
Q

Which symptom(s) indicate an abnormality in the pharyngeal phase of swallowing?

A
  1. Difficulty initiating swallowing (transfer dysphagia)
  2. Nasal regurg
  3. Pulmonary aspiration
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2
Q

T/F: Unlike the striated
muscle portion of the esophagus, the esophageal smooth muscle can
function independently from the CNS.

A

True

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3
Q

Multiple swallows (chugging) is possible due to (X) phenomenon in which there is (stimulation/inhibition) to which parts of the esophagus?

A

X = deglutitive inhibition
Inhibition (complete)
The entire esophagus (becomes relaxed tube)

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4
Q

Achalasia: (stimulatory/inhibitory) mechanisms mediated by (X) are central to the pathophysiology.

A

Inhibitory;

X = NO and VIP (myenteric neurons post-synaptic NTs acting on LES)

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5
Q

Chocolate, caffeine, and alcohol (increase/decrease) LES tone.

A

Decrease

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6
Q

Gastrin (increases/decreases) LES tone.

A

Increases

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7
Q

List a few etiologies of oropharyngeal dysphagia.

A
  1. Stroke
  2. Parkinson’s
  3. MS
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8
Q

Dysphagia for solid food only is usually a symptom of (obstruction/motility) issue.

A

Obstruction

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9
Q

T/F: Diffuse Esophageal Spasm (DES) will present with dysphagia for solids and liquids.

A

True

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10
Q

Pain on swallowing is called:

A

Odynophagia

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11
Q

T/F: Odynophagia is a common symptom of esophageal dismotility or obstruction.

A

False - usually result of acute inflammation/ulceration

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12
Q

T/F: Nearly 80% of patients with GERD symptoms have mucosal damage.

A

False - only 30-40%

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13
Q

T/F: Majority of GERD patients have very low baseline LES pressure (under 10 mmHg).

A

False

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14
Q

Sjogren’s patients are at (increased/decreased) risk for GERD. Why?

A

Increased;
Due to decreased saliva production;
Saliva pH is 6.4-7.4 and can neutralize the acid

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15
Q

Patient with chronic GERD now presents with dysphagia of solid food. Endoscopy reveals severe scarring. Which complication has occurred?

A

Stricture formation (luminal narrowing)

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16
Q

T/F: Gold standard for detecting episodes of GERD is barium swallow.

A

False - 48h ambulatory intra-esophageal pH monitoring

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17
Q

Phase I of GERD treatment.

A
  1. Lifestyle modifications

2. Antacids

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18
Q

Phase II of GERD treatment.

A
  1. H2-R blockers (decrease gastric acid secretion)

2. Prokinetic drugs (increase LES tone and gastric motility)

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19
Q

Phase III of GERD treatment.

A

PPIs

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20
Q

Cimetidine given for (mild/severe) esophagitis works via which mechanism?

A

Mild/moderate;

H2-R blocker (blocks His receptor and decreases gastric acid secretion)

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21
Q

Lansoprazole given for (mild/severe) esophagitis works via which mechanism?

A

Moderate/Severe;

PPI (specific inhibition of H/K ATPase in parietal cell)

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22
Q

T/F: a single dose of PPIs lasts 24 hours.

A

True - very potent/long-lasting

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23
Q

Phase IV of GERD treatment.

A

Surgical/endoscopic options (aimed at increasing LES strength)

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24
Q

Achalasia: how are peristalsis/LES affected?

A

Peristalsis absent; LES fails to completely relax (BIRD BEAK)

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25
Q

Autopsy of patient with achalasia will show degeneration of which neuron(s)?

A
  1. Intramural ganglion cells (esophagus)
  2. Vagi
  3. Dorsal motor nucleus
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26
Q

T/F: Dysphagia is common in scleroderma due to absent peristalsis.

A

True - as well as GERD-induced strictures

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27
Q

“Steak-house syndrome” is (upper/mid/lower) esophageal stricture composed of which tissue?

A

Lower;
Ring-shaped thin projection of mucosa and submucosa
(also called “Schatzki” or “B” ring)

28
Q

A smoothly tapered stricture of the distal esophagus is a consequence of (X) disease.

A

X = GERD (stricture)

29
Q

Dominant stimulant of acid secretion in stomach is (X), produced by (Y) cells.

A 
X = Histamine
Y = ECL
30
Q

ACh (stimulates/inhibits) acid secretion from stomach by binding (X).

A

Stimulates;

X = M3 receptors

31
Q

Over 99% of all duodenal ulcers are due to one of which three mechanisms?

A
  1. H. pylori infection
  2. NSAID use
  3. Hyper-secretory states
32
Q

List the mechanisms by which prostaglandin mediate GI mucosal defensive factors.

A
  1. Mucus/HCO3 secretion
  2. Stimulate mucosal blood flow
  3. Mediate surface epithelial cell restitution
  4. Inhibit acid secretion
33
Q

Key systemic effect of NSAIDs on gastric mucosa that lead to GI issues.

A

Inhibition of prostaglandin synthesis

34
Q

Combo of NSAIDs and (X) drugs enhances rate of GI complications 10-fold than just NSAIDs alone.

A

X = corticosteroids

35
Q

Patient over 70 has (X)-fold (increase/decrease) in risk of GI complications from NSAIDs than younger patient.

A

X = 5-6

Increase

36
Q

T/F: H. pylori infection increases with age in all western countries.

A

True

37
Q

T/F: Infection with H. pylori is increasing in Western countries.

A

False - decreasing (esp in US)

38
Q

H. pylori transmitted via (X) and human must be in contact with (Y).

A 
X = fecal-oral route
Y = another human
39
Q

List some “tools” H. pylori has to survive in the GI tract.

A
  1. Urease (production of ammonia, neutralizing gastric pH)

2. Spiral morphology, flagella, actin polymer (resists peristalsis and adheres to mucosa)

40
Q

List the “weapons” H. pylori has to cause disease.

A
  1. Toxins (cytotoxin, anti-secretory toxin)
  2. Toxic enzymes (esp urease; also protease, catalase)
  3. Chemoattractants (promote inflammation)
41
Q

H. pylori is capable of producing which three disorders?

A
  1. MALToma
  2. Adenocarcinoma
  3. Peptic ulcer
42
Q

With regard to environmental factors on H. pylori infection outcome, smoking increases risk of:

A

Duodenal ulcer and gastric carcinoma

43
Q

T/F: Most patients who develop H. pylori infection are carriers for life.

A

True - asymptomatic

44
Q

Patient who acquired H. pylori infection at 1 y.o. is more likely to develop (X) disease, whereas a teen is more likely to develop (Y) disease.

A 
X = gastric adenocarcinoma
Y = peptic ulcer
45
Q

Gold standard for H. pylori diagnosis:

A

Endoscopic gastric biopsy

46
Q

You biopsy patient to test for H. pylori. Which tests could you run using the biopsied specimen?

A
  1. Giemsa or Warthin-Starry stain (ideally) or H&E
  2. Rapid urease test
  3. Culture
47
Q

A rapid (X) test for H. pylori is positive if the agar turns (Y) color.

A 
X = urease
Y = red (pH increases)
48
Q

List some non-invasive tests for H. pylori.

A
  1. Serology (anti-bac IgG)
  2. Stool sample Ag
  3. Breath tests (using urea)
49
Q

List the (mono/combo) drug Rx used to eradicate H. pylori.

A

Combo (triple-drug)

  1. Bismuth subsalicylate
  2. Antibiotics (metronidazole and clarithromycin)
  3. PPIs/H2 antagonists
50
Q

You prescribe treatment for eradication of H. pylori in your patient with peptic ulcer disease. You remember to stress that (X) drug must be taken (before/after) dinner and breakfast!

A

X = PPI

Before

51
Q

Zollinger-Ellison Syndrome (ZES) is characterized by (hyper/hypo)-(X) due to (Y) most often located in (Z).

A

Hyper;
X = gastrinemia
Y = gastrinoma (gastrin-secreting tumors)
Z = pancreas or duodenum

52
Q

T/F: Vast majority of patients with ZES have pancreatic tumors.

A

False - 2/3 have extra-pancreatic (although it’s traditionally considered a pancreatic tumor)

53
Q

ZES: How does the gastric mucosa architecture change?

A

Hypertrophy of mucosa and increase in parietal cells

54
Q

Patient with ZES may secrete as much as (X) L of (Y) per day, which is much higher than the normal 1.5 L.

A 
X = 10
Y = gastric acid (from parietal cells)
55
Q

T/F: Gastrinomas (in ZES) are benign and confined.

A

False - 1/3 metastasize (liver, bone)

56
Q

List the three most common clinical manifestations of ZES. Star the one that may be the only initial sign in almost half ZES patients.

A
  1. Duodenal ulcer
  2. GERD
  3. Diarrhea*
57
Q

You realize your patient has multiple gastrinomas, causing symptoms of (X), likely due to (sporadic/genetic) cause.

A

X = ZES
Genetic (multiple endocrine neoplasia-type I or MEN-I)

Pts with sporadic ZES likely only have solitary gastrinoma

58
Q

How could you distinguish between a case of sporadic ZES versus MEN-I associated ZES?

A

Check elevations in other hormones (likely in MEN-I), such as hCG, PTH, prolactin, etc.

59
Q

List treatment options for ZES.

A
  1. PPI (long-term)

2. Surgical excision of gastrinoma

60
Q

Which dietary restrictions are absolutely essential in peptic ulcer disease?

A

None - but can tell patient to avoid food that causes dyspepsia

61
Q

One of the most important pieces of advise for patient with peptic ulcer disease is to avoid:

A

SMOKING (diminishes effectiveness of almost all anti-ulcer drugs and enhances ulcer recurrence)

62
Q

Antacids have been shown to heal ulcers. What are some issues with them?

A
  1. Compliance (multiple doses per day)
  2. Constipation (Ca/Al-containing antacids)
  3. Diarrhea (Mg-containing antacids)
63
Q

Your patient with peptic ulcer disease reports that, since starting his meds, he’s been drowsy and falling asleep at work. What is a potential explanation for this?

A

He’s taking H2 blockers during the day (should be taken at bedtime)

64
Q

T/F: PPI anti-secretory and ulcer healing rates are significantly superior to H2 blockers.

A

False - only super potent anti-secretory rates, but healing rates are only modestly superior to H2-R blockers

65
Q

T/F: Virtually all drugs used for duodenal ulcers will heal 80% of ulcers in just one month.

A

True

GI DRx (11 decks)

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