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M2 GI > 9. Conf 1: GERD, Pelv Ulcer Dz, Esop Cancer > Flashcards

9. Conf 1: GERD, Pelv Ulcer Dz, Esop Cancer Flashcards

1
Q

Pt with substernal chest burning, x10yrs, worst at night, brought on by exertion or lying supine. what is your most immediate concern/questions you will ask first?

A

-biggest concern for cardiac problems, ask about cardiac risk factors

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2
Q

what is the DDx for: substernal chest burning, x10yrs, worst at night, brought on by exertion or lying supine.

A 
GERD 
infectious esophagitis
pill esophagitis
peptic ulcer disease
nonulcer dyspepsia
biliary tract disease
coronary artery disease
esophageal motility disorders
eosinophilic esophagitis
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3
Q

what is pyrosis?

A

heartburn

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4
Q

what is the definition of GERD?

A

any symptomatic clinical condition, or histo alteration resulting from reflux of irritant gastric juices from stomach into the esophagus

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5
Q

most common presenting sx of GERD are what?

A

pyrosis, acid regurg, dysphagia

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6
Q

what can cause dysphagia?

A

peptic stricture, Schatzki’s ring, peristaltic dysfunction, adenocarcinoma, eosinophilic esophagitis, or abnormal sensitivity

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7
Q

what is water brash?

A

unusual symptom of GERD, where esop acidification triggers an excessive reflex leading to hypersalivation. patients can literally foam at the mouth, producing 10ml saliva per minute.

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8
Q

what is odynophagia?

A

painful swallowing.

uncommonly associated with GERD< usually due to infectious esophagitis or pill esophagitis

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9
Q

what extra-esophageal sx can be caused by GERD?

A

posterior laryngitis due to acid reflux
chronic sore throat
chronic cough
bronchospasm/nonseasonal asthma

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10
Q

what is the biggest problem leading to GERD (once thought to be low resting pressure of the LES - but now thought to be what)?

A

transient relaxation of the LES, that is not associated with a swallow or other normal stimuli.

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11
Q

what muscle fibers that are external to the LES help maintain pressure?

A

the crural fibers of the diaphragm, at the point where the esophagus crosses through it

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12
Q

in addition to the biggest problem leading to GERD (which is transient relaxation of the LES), what are the other 2 major mechanisms that predispose a pt to GERD?

A
  • hypotensive LES (just in general)

- hiatal hernia

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13
Q

best initial therapy for a pt with GERD for 5 years and solid food dysphagia?

A

Esophagoscopy, and biopsy if it appears necessary. However, mucosal changes may not be visible, and this is subject to observer skill
Note that we don’t scope everyone with heartburn: the duration of his sx and the dysphagia make this more concerning

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14
Q

Beyond endoscopy, what is a good initial diagnostic tool for detecting GERD?

A

esophageal pH monitoring. useful to confirm a diagnosis, also useful to monitor adequacy of treatment.

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15
Q

how do we perform esophageal pH monitoring?

A

either trans-nasal catheter that hangs down to the LES, or a wireless capsule device that is placed in the esophag mucosa.
to determine whether reflux is physiological or pathological, use the % of time the pH in area of concern is below 4.

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16
Q

Lifestyle modifications that can treat/help GERD?

A
  • elevation of the head of the bed
  • avoiding certain foods (chocolate, onions)
  • not eating 2 h before sleep
  • weight loss
  • avoiding smoking, EtOH
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17
Q

medical therapy for GERD: three general categories?

A
  • antacids
  • H2 blockers
  • PPIs
18
Q

H2 blockers vs PPI: which is more effective?

A

PPIs: more effective at healing esophagitis, more symptom relief.

19
Q

what is the difference between GERD and NERD?

A

NERD is Non-Erosive gastroesophageal Reflux Disease; most patients actually have this instead of GERD since the majority do not have esophagitis. may have sx despite normal pH levels at the LES. may have not yet developed mucosal injury.
these pts respond to PPIs anyhow.

20
Q

what are options for managing peptic stricture?

A

mechanical dilation - basically like a stent.

pneumatic balloon dilators are often used.

21
Q

what is the basic pathway that causes peptic stricture?

A

repeated episodes of reflux:

edema -> inflammation -> ulceration -> fibrosis -> stricture

22
Q

Barrett’s epithelium: what is it, how common, what is the risk, how to manage?

A
  • pre-malignant condition of the esop: squamous epithelium of esop has been replaced by columnar mucosa of stomach.
  • seen in 10% GERD patients
  • increases risk for adenocarcinoma
23
Q

Principles of anti-reflux surgery? (from ppt deck accompanying this conference)

A

Basically, this surgery reinforces the LES by wrapping the stomach around itself! Procedure is called Nissen fundoplication.

  • restore the intra-abdominal esophagus
  • restore the diaphragmatic crurae which may have moved/been damaged
  • reduce any hiatal hernia
  • fundoplication
24
Q

Is PPI therapy safe for the long term? what are possible risks?

A

maintenance antisecretory therapy is the RULE now. generally safe and effective

  • possible risks: pneumonia (changing pH alters reaction to bacteria, may allow bact overgrowth)
  • enteric infections (C Diff) since stomach acid is protective
  • Vit B12 malabsorption
  • Hip fracture, Ca/Mg absorption
  • hypergastrinemia (tumors seen in rats, not yet in humans)
  • atrophic gastritis (-> gastric cancer), possibly due to H Pylori infection?
25
Q

Pt with 3 months of dysphagia, 15# weight loss, cough, alcoholism. Differential? What is most likely?

A 
Esophageal neoplasm
Peptic stricture
Esophageal Web/Ring
Motility disorder
(Wt loss & progressive solid food dysphagia points to cancer)
26
Q

For a patient with suspected esophageal cancer, what studies would you get?

A
  • Barium swallow (check for narrowing)
  • Endoscopy (assess for SCC)
  • Manometry (function of esop nerves/muscles)
27
Q

Risk factors for esophag carcinoma?

A
  • alcohol, cigs
  • other carcinogens like nitrates, smoked opiates, fungal toxins)
  • physical insults (hot tea, silica, lye)
  • host susceptability: (another flashcard for this)
28
Q

Host susceptability to esophag carcinoma: what are demographics of SCC vs adenocarcinoma in terms of race, gender?

A

SCC: blacks > whites; males > females
adeno: whites > blacks, 70% of esop ca in US is adeno.

29
Q

treatment for esop carcinoma?

A

Lecture says Esophagectomy is standard treatment: conference answers say that most of these cancers don’t present until they are surgically unresectable. Jen emailed Benson.

  • surgery
  • radiation
  • chemo
30
Q

treatment for esop carcinoma?

A

Poor. usually don’t present until late in the progression

31
Q

what are some causes of peptic ulcer disease?

A

-injury to mucosa: NSAIDs, H pylori

32
Q

anatomically, where do peptic ulcers occur?

A

in the stomach! we are no longer in the esophagus.

33
Q

how does antrectomy help pts with peptic ulcer disease?

A

removes antrum, where G cells are located. thus eliminates gastrin stimulation/production

34
Q

how does the vagotomy component of the antrectomy help pts with peptic ulcer disease?

A

removes Ach stimulation of parietal cells.

35
Q

What are Bilroth I and Bilroth II procedures?

A

types of gastrojejunostomy? performed prior to discovery of PPI, seldom performed today.

36
Q

what are risks or reaasons for recurrent PUD?

A
  • continued presence of H Pylori
  • NSAID use
  • smoking
37
Q

what is Zollinger Ellison syndrome?

A

gastrinoma: so levels of gastrin would be high even after antrectomy.

38
Q

what is a provacative test for Zollinger Ellison syndrome?

A

secretin stimulation test: give IV secretin. Normally will suppress gastrin levels.
If gastrinoma, will paradoxically cause tumor to secrete gastrin → levels will be high

39
Q

where are most gastrinomas located?

A

Most commonly in side wall of duodenum.
Gastrinoma triangle:
-junction of cystic duct & common bile duct
-junction of neck& body of pancreas
-junction of 2nd/3rd parts of the duodenum

40
Q

Treatment options for Zollinger Ellison?

A
  • High dose PPIs
  • omeprazole (SMS analog, suppresses gastrin)
  • resection of gastrinoma

M2 GI (41 decks)

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