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GI 2 > Clin Med - Esophagus > Flashcards

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
Q

LES Mechanisms in severe esophagitis

A

Transient LES relaxation is more common than weak LES

D/t medicines and food

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26
Q

What are the 2 esophageal neoplasms?

A

Adenocarcinoma & squamous cell

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27
Q

What part of the esophagus does adenocarcinoma involve?

A

Distal esophagus

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28
Q

Risk factors for adenocarcinoma

A
  • ETOH
  • Barrett’s Esophagus and GERD
  • H/o colon cancer
  • Obesity
  • Smoking
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29
Q

What part of the esophagus does squamous cell cancer involve?

A

Proximal and mid-esophagus

30
Q

Risk factors of squamous cell

A
  • H/o radiation therapy
  • Smoking
  • Achalasia
  • ETOH
31
Q

Neoplasm clinical manifestations

A
  • Progressive dysphagia
  • Odynophagia
  • Chest pain
  • Weight loss
  • Anorexia
32
Q

Esophageal Cancer Risk Factors

A 
C igarette smoking
A lcoholism
N utritional deficiencies
C arcinogens
E ndemic microorganisms
R egional practices
S oil salinity
33
Q

Define strictures

A

-includes esophageal webs and rings and diverticula

34
Q

Study of choice for strictures

A

EGD

35
Q

Stricture Disorders

A

Cervical esophageal webs - more commonly found in females often associated with iron deficiency anemia (Plummer-Vinson syndrome)

36
Q

Define Schatzki’s Ring

A

Lower esophageal ring circumferential constricting at any level - usually scar

37
Q

Define Zenker’s Diverticulum

A

Outpouching of the esophagus between the inferior pharyngeal constrictor and cricopharyngeal muscles
*unknown pathogenesis

38
Q

Treatment for strictures

A

surgery

39
Q

Esophageal varices

A

Venous collaterals that develop as a result of portal hypertension.

*results in massive upper GI bleeding

40
Q

Gastritis and PUD - relationship

A
  • Gastritis and PUD much alike in etiology
  • Consider gastritis pre-PUD
  • Treat gastritis to avoid conversion to an ulcer
41
Q

Cause of peptic ulcers

A

Increased aggressive factors and/or decreased defensive factors lead to mucosal damage and ulcer formation.

42
Q

Protective Mucosal Factors

A
  • HCO3
  • Mucus
  • Blood flow
  • Growth factors
  • Cell renewal
  • Prostaglandins
43
Q

Damaging Mucosal Factors

A
  • H+
  • Pepsins
  • Smoking
  • ETOH
  • Bile acids
  • Ischemia
  • NSAIDs
  • Hypoxia
  • H. pylori
44
Q

Affect of NSAIDs on prostaglandins

A

Inhibit local prostaglandin synthesis

  • reduces mucus secretion
  • interferes with cell turnover
45
Q

Helicobacter Pylori is both

A

pro aggressive and anti defensive

46
Q

H. pylori directly stimulates acid secretion by…

A

stimulation of the parietal cell’s acid secretion from a submucosal position

47
Q

How does H. pylori decrease defensive factors?

A

uses Urease to cleave Urea into ammonia which directly inhibits prostaglandin synthesis

48
Q

H. pylori leads to…

A

Gastritis which leads to ulcers

49
Q

Treatment of H. pylori

A
  • 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
Q

Define Zollinger-Ellison Syndrome

A
  • Gastric acid hypersecretion
  • Severe peptic ulcer disease
  • Non-beta islet cell tumors of the pancreas
51
Q

Define peptic ulcer disease (PUD)

A

Defect in the gastrointestinal mucosa that extend through the muscularis mucosa

52
Q

PUD is caused by

A

auto-digestion of epithelium by acid and pepsin.

53
Q

When do most ulcers occur?

A

when normal mechanisms are disrupted by superimposed processes such as H pylori infection or NSAIDs

54
Q

Importance of acid in ulcer formation

A

Acid is necessary for ulcer development

*if you find an ulcer without acid, that’s cancer

55
Q

Describe PUD ulcers

A
  • Usually single
  • Less than 1-2cm in diameter
  • Only a small portion of PUD have increased acid secretion
56
Q

PUD - Clinical Features/Triages

A
  • Abdominal pain
  • Hematemesis
  • Melena
  • BRBPR – requires a massive bleed
57
Q

PUD Complications

A
  • Hemorrhage- 15% (elderly, NSAIDS)
  • Perforation / Penetration – 7%
  • Gastric outlet obstruction- 2%
  • Complications more frequent in chronic, fibrosed ulcers
58
Q

PUD Perforation

A
  • 1/3 to 1/2 associated with NSAID use

- Rapid diagnosis- prognosis is excellent within the first 6 hours

59
Q

PUD Hemorrhage

A

Majority of patients will stop bleeding spontaneously and most will not re-bleed

60
Q

Diagnosis-EGD

A

Gold standard

-Used for actively/recently bleeding patients

61
Q

Hiatal Hernia

A

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
Q

Hiatal Hernia MOA

A

Trapping of parietal cells (HCl) of fundus above diaphragm with marked erosions and ulcers - hernia does not empty well

63
Q

Hiatal Hernia Symptoms

A
  • Epigastric burning, dysphagia, and OCC regurg

- High risk for PUD within the hernia itself

64
Q

Hiatal Hernia Diagnosis

A
  • EGD is the gold standard
  • plain films commonly show gas bubble above diaphragm
  • Barium swallow if needed
65
Q

Hiatal Hernia Treatment

A
  • PPI to control erosions/ulcers
  • Surgical repair reserved for volvulus, bleeding, perforation or recurrent PUD in the hernia sac
  • Nissen fundoplication + others
66
Q

Pyloric Stenosis

aka Infantile Hypertrophic Pyloric Stenosis (IHPS)

A

Marked hypertrophy of the pyloris

*Etiology is unknown

67
Q

IHPS classic presentation

A

PROJECTILE vomiting in 3-6 week infant immediately post prandial.

68
Q

IHPS Physical Exam finding

A

Palpable mass in medial RUQ at edge of rectus abdominis.

“The Olive”

69
Q

IHPS Clinical Manifestations

A

Hypo-chloremic metabolic alkalosis- due to massive acid loss.

70
Q

IHPS Diagnosis

A

Abdominal ultrasound is the procedure of choice in most institutions

71
Q

IHPS Treatment

A

PYLOROTOMY- Definitive management

Correct electrolyte abnormalities 1st !!!
- Ramstedt pyloromyotomy- longitudinal incision in pylorus then sewn in the transverse plane (open or laparoscopic)

72
Q

IHPS Other Treatments (“poor outcomes”)

A
  • Balloon dilation
  • Atropine
  • Conservative management

GI 2 (11 decks)

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