GASTROESOPHAGEAL REFLUX DISEASE Flashcards
(122 cards)
1
Q
What pressure gradient exists between the abdomen and thorax?
A
A positive pressure gradient.
2
Q
What would occur without a barrier in the presence of this pressure gradient?
A
GER (Gastroesophageal Reflux).
3
Q
Name three factors that can increase intra-abdominal pressure and contribute to GER.
A
Changes in gravitational position, events associated with abdominal muscle contraction, increase intraabdominal pressure
4
Q
List examples of events associated with abdominal muscle contraction that can lead to GER.
A
Coughing, sneezing, straining, exercise, bending.
5
Q
What is the function of the LES?
A
To maintain a high-pressure tone, preventing reflux.
6
Q
What is the normal resting LES pressure?
A
10-30 mmHg.
7
Q
What can cause transient LES relaxation?
A
Drugs, smoking, foods (fat, chocolate, peppermint, caffeine, alcohol), hormones (progesterone, VIP, glucagon), gastric distension.
8
Q
What can decrease LES pressure?
A
Drugs, smoking, foods (fat, chocolate, peppermint, caffeine, alcohol), hormones (progesterone, VIP, glucagon), gastric distension.
9
Q
What structure at the gastroesophageal junction helps prevent reflux?
A
The distal esophageal mucosal flap.
10
Q
Which part of the diaphragm contributes to the anti-reflux barrier?
A
The diaphragmatic crus.
11
Q
What happens to the abdominal segment of the esophagus in a hiatal hernia?
A
it is lost
12
Q
How does a hiatal hernia impair esophageal clearance?
A
It acts as a reservoir of refluxate.
13
Q
What are three conditions that can lead to increased gastric volume, promoting reflux?
A
After meals, gastric outlet obstruction, hypersecretory disorders.
14
Q
What are three conditions that can lead to increased gastric pressure, promoting reflux?
A
Ascites, pregnancy, obesity.
15
Q
What is a major factor in diabetic patients with autonomic neuropathy that promotes reflux?
A
Delayed gastric emptying.
16
Q
How does the location of gastric volume near the esophagogastric junction promote reflux?
A
Recumbency after meals and bending.
17
Q
What are the two main types of reflux mentioned as aggressive factors?
A
Gastric reflux and Duodenogastric reflux.
18
Q
What are the two aggressive components of gastric reflux?
A
Gastric acid and Pepsin.
19
Q
What are the two aggressive components of duodenogastric reflux?
A
Bile salts and Pancreatic enzymes.
20
Q
What is the primary effect of bile salts in duodenogastric reflux?
A
Dissolution of lipids.
21
Q
What is the primary effect of pancreatic enzymes in duodenogastric reflux?
A
Proteolytic injury.
22
Q
What are the two main mechanisms of esophageal defense against reflux?
A
Esophageal clearance and Tissue resistance of the esophageal mucosa.
23
Q
How does esophageal clearance work?
A
Esophageal distension by reflux triggers esophageal motor activity (peristalsis) and esophageal emptying into the stomach.
24
Q
What are the two types of tissue resistance in the esophageal mucosa?
A
Pre-epithelial defense and Post-epithelial defense.
25
What constitutes the pre-epithelial defense of the esophageal mucosa?
The layer of mucus and the unstirred water layer.
26
What is the function of the unstirred water layer in pre-epithelial defense?
**Neutralizing H+ ions with its rich bicarbonate content.**
27
What is the key component of post-epithelial defense in the esophageal mucosa?
Adequate blood flow.
28
What does adequate blood flow provide for post-epithelial defense?
Oxygen, nutrients, and bicarbonate.
29
What are two key structural components of epithelial defense?
Cell membranes and tight intercellular junctions.
30
What are two functional components of epithelial defense?
Cellular and intercellular buffers, and cell membrane ion transporters.
31
What process is essential for repairing the esophageal epithelium?
Epithelial regeneration
32
What is the normal turnover rate for epithelial repair?
5-8 days.
## Footnote
Increases to 2-4 days with injury
33
What is the primary role of saliva in esophageal defense?
Contributes to esophageal clearance.
34
What are two causes of diminished salivation?
**Primary (Sjogren's syndrome)** and secondary (anticholinergic drugs).
35
How does diminished salivation affect acid clearance and esophageal health?
Causes delayed acid clearance and promotes esophageal injuries.
36
What do damaged esophageal epithelial cells secrete?
Chemokines.
37
What type of inflammatory cells are attracted to the esophagus by chemokines?
PMN (polymorphonuclear neutrophils) and eosinophils.
38
List some potential consequences of reflux on the esophageal mucosa.
Mucosal breaks, erosions, ulcers, strictures, columnar metaplastic epithelium (Barrett's esophagus).
39
What are the classic symptoms described by a patient that can lead to a clinical diagnosis of GERD?
Recurrent retrosternal burning and regurgitation that worsen after eating or bending and are relieved with antacids.
40
When is further testing required to diagnose GERD?
When the presentation is atypical and GERD is suspected.
41
What is the gold standard for diagnosing acid GERD?
Prolonged pH monitoring.
## Footnote
12-24 h time
42
What factors are considered in relation to reflux during prolonged pH monitoring?
Meals, body position, activity, and sleep.
43
At what pH level is reflux defined in pH monitoring?
Less than 4.
44
What reflux characteristics are measured during pH monitoring?
Total number of reflux episodes and number of episodes longer than 5 minutes.
45
What substance is used in a Gastroesophageal Scintiscan?
Technetium-99m sulfur colloid.
46
Where is the Technetium-99m sulfur colloid placed during the Gastroesophageal Scintiscan?
Into the stomach.
47
What are two radiologic studies used in GERD diagnosis?
Barium swallow and upper GI series.
| can detect moderate to severe esophagitis, strictures, hiatal hernia
## Footnote
poor sensitivity in milder forms of GERD
48
How does the sensitivity and specificity of radiologic studies compare to upper endoscopy?
Less sensitive and specific.
49
What can upper endoscopy detect and grade in GERD?
The severity of GERD-induced esophagitis.
50
What complications of GERD can upper endoscopy evaluate?
Strictures and Barrett's esophagus.
51
When is esophageal manometry considered helpful in GERD evaluation?
For patients with atypical symptoms (chest pain), when medical therapy has failed, or those considered for antireflux surgery.
52
How effective is esophageal manometry in predicting GER?
It is a poor test unless the LES pressure is <5 mmHg.
53
In what situations are endoscopy and mucosal biopsies recommended for GERD?
Patients with refractory symptoms, odynophagia, dysphagia, atypical symptoms, and when Barrett's esophagus is suspected (especially in those with GER symptoms for more than 5 years).
54
For what types of patients are pH monitoring and manometry reserved?
Patients with atypical symptoms.
55
What is the test of choice for evaluating complicated GERD patients?
Esophageal biopsy.
56
What are the signs of mild esophagitis?
Erythema, edema of the mucosa, mild friability, increased irregularity of the Z line.
57
What are the signs of moderate-severe esophagitis?
Round and longitudinal superficial ulcers or erosions, diffusely hemorrhagic mucosa with exudates and deep punched-out ulcers and strictures.
58
What causes peptic strictures in GERD?
Inflammation extending below the mucosa, which is replaced by fibrosis.
59
Where are peptic strictures typically located?
**In the distal third of the esophagus.**
60
At what esophageal diameter does dysphagia typically occur?
12 mm
61
What is the initial symptom of dysphagia?
Difficulty swallowing solids.
62
How do peptic strictures appear on a barium esophagogram?
Smooth, tapered appearance, with variable lengths.
63
What diagnostic tool is very useful for evaluating peptic strictures?
endoscopy
64
What are the potential consequences of esophageal ulcers?
Perforation or massive bleeding.
65
What is Barrett's esophagus?
Replacement of the normal squamous epithelium with metaplastic specialized columnar epithelium.
## Footnote
it is a severe reflux
66
How is Barrett's esophagus subclassified?
Short segment or long segment, depending on the length of the abnormal tissue.
67
Through what intermediate stages does Barrett's metaplasia progress to adenocarcinoma?
Low and high grade dysplasia.
68
List some respiratory problems that can be attributed to GERD.
Laryngitis, hoarseness, chronic cough, asthma, bronchitis, aspiration pneumonia
69
How much should the head of the bed be elevated for nighttime heartburn?
15 cm.
70
How long before bed should eating be avoided?
3-4 h
71
List some drug classes that reduce LES pressure and should be avoided in GERD.
Anticholinergics, sedatives/opiates, tranquilizers, theophylline, β-adrenergic agonists, nitrates, calcium channel blockers.
72
What class of drugs is most efficient in decreasing gastric acid output for GERD?
PPIs (Proton Pump Inhibitors).
## Footnote
first line treatment
73
How do PPIs work?
They inhibit acid secretion by forming a covalent bond within the pump, the final step of gastric acid secretion.
74
What effect do PPIs have on gastric pH?
They raise the gastric pH above 4-5.
75
What is the effect of raising gastric pH above 4-5?
Eliminating pepsin activity.
76
List the five PPIs mentioned with their respective dosages.
Omeprazole 20-40 mg/day
Lansoprazole 15-30 mg/day (30 mg - 12/24h)
Rabeprazole 20 mg/day
Pantoprazole 20-40 mg/day (40 mg - 12/24h)
Esomeprazole 20-40 mg/day (20-40 mg/24h
77
For what types of GERD symptoms are H2 blockers recommended?
Intermittent or mild symptoms.
78
How do H2 blockers work?
They bind the histamine receptor on the parietal cell, preventing histamine from binding and stimulating acid secretion.
79
What happens when the concentration of H2 blockers decreases?
Histamine unbinds to the receptor, and acid secretion is resumed.
80
List the four H2 blockers mentioned with their respective dosages.
Cimetidine 400 mg × 4/day, 800 mg × 2/day (300mg × 4)
Ranitidine 150 - 300 mg × 2/day (50 mg × 3)
Famotidine 20 - 40 mg × 2/day (20 mg × 2)
Nizatidine 150 mg × 2/day
81
Name a dopamine antagonist used to increase LES pressure in GERD.
Metoclopramide.
82
What are the potential side effects of metoclopramide?
Somnolence, restlessness, anxiety, extrapyramidal reactions (because it crosses the blood-brain barrier).
83
Name a prokinetic drug that does not cross the blood-brain barrier.
Domperidone.
84
What drug enhances mucosal resistance in GERD?
Sucralfate
85
What is sucralfate's mechanism of action?
Aluminum sucrose polysulfide with cytoprotective action.
| not highly effective
86
What is a potential side effect of long-term PPI use?
Increased susceptibility to enteric infections, such as Clostridium difficile.
87
What is the most common surgical procedure for GERD?
Laparoscopic Nissen fundoplication.
88
What is done in a laparoscopic Nissen fundoplication?
The proximal stomach is wrapped around the distal esophagus.
89
What are some endoscopic antireflux procedures?
Stapling or suturing devices.
## Footnote
many complications
90
How are esophageal strictures managed?
Esophageal dilatation.
## Footnote
Wire-guided dilators (Savary-Gilliard) and balloon dilators.
91
What is the surveillance recommendation for low-grade dysplasia in Barrett's esophagus?
Biopsies every 3-6 months.
92
What are the management options for high-grade dysplasia in Barrett's esophagus?
Endoscopic mucosal resection, endoscopic ablation techniques (photodynamic therapy, radiofrequency, cryoablation), standard esophagectomy.
93
What are the most common types of esophageal infections?
Viral (herpes simplex, CMV), fungal (candida albicans), or a combination
94
What are the most common symptoms of esophageal infections?
Dysphagia and odynophagia.
95
What might be observed on a double-contrast esophagogram in a patient with an esophageal infection?
Superficial or deep ulcerations, diminished peristalsis, occasional spasm, or esophageal strictures.
96
What are the endoscopic findings in fungal esophageal infections?
Raised white plaques.
97
Where does pill-induced esophagitis typically occur?
In the mid-esophagus, near the crossing of the aorta.
98
What causes pill-induced esophagitis?
A swallowed pill lodging within the esophageal lumen.
99
What factors contribute to pill-induced esophagitis?
Inadequate liquid with the pill, lying down after taking it.
100
List some of the most common medications implicated in pill-induced esophagitis.
Doxycycline, quinidine, potassium chloride, NSAIDs, ferrous sulfate, phenytoin, tetracycline, bisphosphonates.
101
What are the typical symptoms of pill-induced esophagitis?
Sudden onset of chest pain and odynophagia.
102
What are the endoscopic findings in pill-induced esophagitis?
Localized ulceration or inflammation.
103
What can develop in severe cases of pill-induced esophagitis?
Strictures.
104
How long does it typically take for pill-induced esophagitis to resolve?
Days to weeks.
105
What is the defining characteristic of Eosinophilic Esophagitis (EoE)?
Esophageal squamous epithelial infiltration with eosinophils.
106
List some secondary etiologies of EoE.
GERD, drug hypersensitivity, connective tissue disorders.
107
What type of disorder is EoE?
An allergic disorder induced by antigen sensitization in atopic individuals (often triggered by dietary allergens).
108
What are the common symptoms of EoE?
Dysphagia and food impactions.
109
How does heartburn in EoE respond to PPI therapy?
It is refractory (unresponsive) to PPI therapy.
110
What are the endoscopic findings in EoE?
Multiple esophageal rings, linear furrows, and punctate exudates.
111
What are some potential complications of EoE?
Fibrosis, strictures, food impaction, and esophageal perforation.
112
What are the first-line medications for EoE treatment?
Topical glucocorticoids (fluticasone or budesonide).
## Footnote
considered in severe cases
113
What is Achalasia?
A disorder of esophageal smooth muscle function.
114
What are the three diagnostic prerequisites for Achalasia?
1. Absence of peristalsis in the smooth muscle of the esophagus (skeletal muscle function is normal). 2. LES does not relax completely with swallowing. 3. The resting LES pressure is usually high.
115
What is the cause of Achalasia?
Neuronal abnormalities; lesions have been found in the dorsal vagal nucleus, vagal trunks, and myenteric ganglia in the esophagus
116
What is secondary Achalasia ("pseudoachalasia")?
Results from tumor invasion of LES, constriction from malignant nodes, or paraneoplastic syndromes.
117
What are the symptoms and signs of Achalasia?
Dysphagia to both solids and liquids, regurgitation of esophageal contents (often with tracheal aspiration), chest pain (occurs in vigorous achalasia).
118
What might be seen on a chest x-ray in a patient with achalasia?
Widened mediastinal shadow (dilatation of the esophagus) with an air-fluid level made up of food and secretions held up by the tight LES.
119
What is the characteristic finding on a barium swallow in achalasia?
A dilated esophagus with a **"parrot beak"** appearance of the gastroesophageal junction.
120
What is the role of upper endoscopy in achalasia diagnosis?
To differentiate "pseudoachalasia" (secondary to tumor infiltration) from primary achalasia.
121
What is the most sensitive diagnostic test for achalasia?
Esophageal manometry.
122
What are the manometric findings in achalasia?
Impaired LES relaxation and absence of peristalsis.
