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Clin Med - Esophagus Flashcards

1
Q

Esophagitis occurs principally in…

A

Immunocompromised.

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2
Q

Common agents - esophagitis

A
  • Candida albicans (post antibiotic use)
  • Herpes simplex
  • Cytomegalovirus
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3
Q

Esophagitis clinical manifestations

A
  • Odynophagia may be severe
  • Dysphagia, weight loss, upper GI bleeding
  • Esophageal candidiasis associated with oral candidiasis
  • Herpes esophagitis associated with oral herpetic lesions
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4
Q

MC esophagitis

A

Radiation-induced

Requires symptomatic treatment

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5
Q

Esophageal motility

A

Tubular - made of smooth and striated muscle structure.

  1. Outer muscle layer in longitudinal
  2. Inner layer is circular

Together, if driven with coordination, normal peristalsis occurs.

*Under vagal control

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6
Q

Esophageal Motor Disorders (3)

A
  • Achalasia
  • Diffuse esophageal spasm
  • Nutcracker esophagus
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7
Q

Esophageal Motor Disorders Generally

A

Oropharyngeal vs. Esophageal

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8
Q

Which is the MC esophageal motor disorders?

A

Achalasia

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9
Q

Achalasia Etiology

A

Leads to increase in lower esophageal sphincter (LES) pressure, incomplete relaxation of the LES with swallowing, and dilated aperistalsis of the body of the esophagus

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10
Q

Achalasia Clinical Manifestations

A

Dysphagia of liquids and solids is the primary problem.

Regurgitation is common.

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11
Q

Achalasia Diagnosis

A

Barium swallow shows a dilated esophagus, air fluid level, delayed esophageal emptying, and a smooth tapered “birds-beak” deformity at the LES.

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12
Q

Achalasia treatment

A

Muscle relaxation

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13
Q

Diffuse Esophageal Spasm

A
  • Common disorder
  • Patient presents with chest pain, dysphagia, or both.
  • Associated with degeneration of Auerbach plexus
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14
Q

Diffuse Esophageal Spasm Dx

A
  • Barium swallow shows prominent, spontaneous, non-propulsive, tertiary contractions
  • Gives a “corkscrew” esophagus appearance on barium swallow
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15
Q

Diffuse Esophageal Spasm Tx

A

Supportive and empirical - muscle relaxants, antidepressants, relaxation exercises.

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16
Q

Nutcracker Esophagus

A

-Functional peristaltic motility disorder (no regurgitation)

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17
Q

Nutcracker Esophagus Sx

A
  • Chest pain with no dysphagia

- Association with anxiety and manic state (adrenaline??)

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18
Q

Nutcracker Esophagus Tx

A

Muscle relaxants, nitrates, reassurance, bio feedback

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19
Q

Mallory-Weiss Tear characteristics

A
  • one of the major causes of upper GI bleeding

- occur in the distal esophagus at gastroesophageal (GE) junction

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20
Q

When does Mallory-Weiss Tear occur?

A
  • Typically occurs after a bout of vomiting or retching.
  • Bleeding occurs when tear involves the underlying venous or arterial plexus.
  • Increased risk in patients with portal hypertension.
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21
Q

Mallory-Weiss Tear Dx

A

Endoscopy is the procedure of choice.

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22
Q

Mallory-Weiss Tear Tx

A
  • Most tears stop bleeding spontaneously

- Injection and thermal coagulation may be needed

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23
Q

Mallory-Weiss Tear Complications

A

Re-bleeding and extension to full thickness tear = Boerhaave Tear (Esophageal rupture!)

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24
Q

GERD is due to…

A

Weak lower esophageal sphincter tone

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25
LES Mechanisms in severe esophagitis
Transient LES relaxation is more common than weak LES D/t medicines and food
26
What are the 2 esophageal neoplasms?
Adenocarcinoma & squamous cell
27
What part of the esophagus does adenocarcinoma involve?
Distal esophagus
28
Risk factors for adenocarcinoma
- ETOH - Barrett's Esophagus and GERD - H/o colon cancer - Obesity - Smoking
29
What part of the esophagus does squamous cell cancer involve?
Proximal and mid-esophagus
30
Risk factors of squamous cell
- H/o radiation therapy - Smoking - Achalasia - ETOH
31
Neoplasm clinical manifestations
- Progressive dysphagia - Odynophagia - Chest pain - Weight loss - Anorexia
32
Esophageal Cancer Risk Factors
``` C igarette smoking A lcoholism N utritional deficiencies C arcinogens E ndemic microorganisms R egional practices S oil salinity ```
33
Define strictures
-includes esophageal webs and rings and diverticula
34
Study of choice for strictures
EGD
35
Stricture Disorders
Cervical esophageal webs - more commonly found in females often associated with iron deficiency anemia (Plummer-Vinson syndrome)
36
Define Schatzki's Ring
Lower esophageal ring circumferential constricting at any level - usually scar
37
Define Zenker's Diverticulum
Outpouching of the esophagus between the inferior pharyngeal constrictor and cricopharyngeal muscles *unknown pathogenesis
38
Treatment for strictures
surgery
39
Esophageal varices
Venous collaterals that develop as a result of portal hypertension. *results in massive upper GI bleeding
40
Gastritis and PUD - relationship
- Gastritis and PUD much alike in etiology - Consider gastritis pre-PUD - Treat gastritis to avoid conversion to an ulcer
41
Cause of peptic ulcers
Increased aggressive factors and/or decreased defensive factors lead to mucosal damage and ulcer formation.
42
Protective Mucosal Factors
- HCO3 - Mucus - Blood flow - Growth factors - Cell renewal - Prostaglandins
43
Damaging Mucosal Factors
- H+ - Pepsins - Smoking - ETOH - Bile acids - Ischemia - NSAIDs - Hypoxia - H. pylori
44
Affect of NSAIDs on prostaglandins
Inhibit local prostaglandin synthesis - reduces mucus secretion - interferes with cell turnover
45
Helicobacter Pylori is both
pro aggressive and anti defensive
46
H. pylori directly stimulates acid secretion by...
stimulation of the parietal cell’s acid secretion from a submucosal position
47
How does H. pylori decrease defensive factors?
uses Urease to cleave Urea into ammonia which directly inhibits prostaglandin synthesis
48
H. pylori leads to...
Gastritis which leads to ulcers
49
Treatment of H. pylori
- Many to choose from - Must be used in combination, often 3 antibiotics at one time - You want to make the environment basic - use PPIs to decrease acidity
50
Define Zollinger-Ellison Syndrome
- Gastric acid hypersecretion - Severe peptic ulcer disease - Non-beta islet cell tumors of the pancreas
51
Define peptic ulcer disease (PUD)
Defect in the gastrointestinal mucosa that extend through the muscularis mucosa
52
PUD is caused by
auto-digestion of epithelium by acid and pepsin.
53
When do most ulcers occur?
when normal mechanisms are disrupted by superimposed processes such as H pylori infection or NSAIDs
54
Importance of acid in ulcer formation
Acid is necessary for ulcer development *if you find an ulcer without acid, that's cancer
55
Describe PUD ulcers
- Usually single - Less than 1-2cm in diameter - Only a small portion of PUD have increased acid secretion
56
PUD - Clinical Features/Triages
- Abdominal pain - Hematemesis - Melena - BRBPR – requires a massive bleed
57
PUD Complications
- Hemorrhage- 15% (elderly, NSAIDS) - Perforation / Penetration – 7% - Gastric outlet obstruction- 2% - Complications more frequent in chronic, fibrosed ulcers
58
PUD Perforation
- 1/3 to 1/2 associated with NSAID use | - Rapid diagnosis- prognosis is excellent within the first 6 hours
59
PUD Hemorrhage
Majority of patients will stop bleeding spontaneously and most will not re-bleed
60
Diagnosis-EGD
Gold standard | -Used for actively/recently bleeding patients
61
Hiatal Hernia
Damage to the phreno-esophageal membrane allowing the fundus to herniate through the hiatus of the diaphragm Type I - only GE Junction is above the hiatus Type II,III,IV - Fundus is pulled to paraesophogeal position
62
Hiatal Hernia MOA
Trapping of parietal cells (HCl) of fundus above diaphragm with marked erosions and ulcers - hernia does not empty well
63
Hiatal Hernia Symptoms
- Epigastric burning, dysphagia, and OCC regurg | - High risk for PUD within the hernia itself
64
Hiatal Hernia Diagnosis
- EGD is the gold standard - plain films commonly show gas bubble above diaphragm - Barium swallow if needed
65
Hiatal Hernia Treatment
- PPI to control erosions/ulcers - Surgical repair reserved for volvulus, bleeding, perforation or recurrent PUD in the hernia sac - Nissen fundoplication + others
66
Pyloric Stenosis | aka Infantile Hypertrophic Pyloric Stenosis (IHPS)
Marked hypertrophy of the pyloris | *Etiology is unknown
67
IHPS classic presentation
PROJECTILE vomiting in 3-6 week infant immediately post prandial.
68
IHPS Physical Exam finding
Palpable mass in medial RUQ at edge of rectus abdominis. | “The Olive”
69
IHPS Clinical Manifestations
Hypo-chloremic metabolic alkalosis- due to massive acid loss.
70
IHPS Diagnosis
Abdominal ultrasound is the procedure of choice in most institutions
71
IHPS Treatment
PYLOROTOMY- Definitive management Correct electrolyte abnormalities 1st !!! - Ramstedt pyloromyotomy- longitudinal incision in pylorus then sewn in the transverse plane (open or laparoscopic)
72
IHPS Other Treatments ("poor outcomes")
- Balloon dilation - Atropine - Conservative management

GI 2 (11 decks)

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