01a: Esophageal Disease, Ulcers Flashcards by Nuna H

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

Difficulty initiating swallowing (transfer dysphagia)
Nasal regurg
Pulmonary aspiration

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

True

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

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

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

Inhibitory;

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

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

Decrease

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Gastrin (increases/decreases) LES tone.

Increases

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List a few etiologies of oropharyngeal dysphagia.

Stroke
Parkinson’s
MS

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

Obstruction

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

True

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Pain on swallowing is called:

Odynophagia

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

False - usually result of acute inflammation/ulceration

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

False - only 30-40%

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

False

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

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

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

Stricture formation (luminal narrowing)

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

False - 48h ambulatory intra-esophageal pH monitoring

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Phase I of GERD treatment.

Lifestyle modifications

2. Antacids

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Phase II of GERD treatment.

H2-R blockers (decrease gastric acid secretion)

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

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Phase III of GERD treatment.

PPIs

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

Mild/moderate;

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

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

Moderate/Severe;

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

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

True - very potent/long-lasting

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Phase IV of GERD treatment.

Surgical/endoscopic options (aimed at increasing LES strength)

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Achalasia: how are peristalsis/LES affected?

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

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

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

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

True - as well as GERD-induced strictures

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

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

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

X = GERD (stricture)

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

``` X = Histamine Y = ECL ```

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

Stimulates; | X = M3 receptors

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

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

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

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

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

Inhibition of prostaglandin synthesis

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

X = corticosteroids

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

X = 5-6 | Increase

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

True

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

False - decreasing (esp in US)

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

``` X = fecal-oral route Y = another human ```

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

1. Urease (production of ammonia, neutralizing gastric pH) | 2. Spiral morphology, flagella, actin polymer (resists peristalsis and adheres to mucosa)

List the "weapons" H. pylori has to cause disease.

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

H. pylori is capable of producing which three disorders?

1. MALToma 2. Adenocarcinoma 3. Peptic ulcer

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

Duodenal ulcer and gastric carcinoma

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

True - asymptomatic

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.

``` X = gastric adenocarcinoma Y = peptic ulcer ```

Gold standard for H. pylori diagnosis:

Endoscopic gastric biopsy

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

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

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

``` X = urease Y = red (pH increases) ```

List some non-invasive tests for H. pylori.

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

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

Combo (triple-drug) 1. Bismuth subsalicylate 2. Antibiotics (metronidazole and clarithromycin) 3. PPIs/H2 antagonists

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!

X = PPI | Before

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

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

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

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

ZES: How does the gastric mucosa architecture change?

Hypertrophy of mucosa and increase in parietal cells

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

``` X = 10 Y = gastric acid (from parietal cells) ```

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

False - 1/3 metastasize (liver, bone)

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

1. Duodenal ulcer 2. GERD 3. Diarrhea*

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

X = ZES Genetic (multiple endocrine neoplasia-type I or MEN-I) Pts with sporadic ZES likely only have solitary gastrinoma

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

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

List treatment options for ZES.

1. PPI (long-term) | 2. Surgical excision of gastrinoma

Which dietary restrictions are absolutely essential in peptic ulcer disease?

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

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

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

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

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

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?

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

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

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

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

True