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GI > Disorders of the Esophagus - Exam 3 > Flashcards

Disorders of the Esophagus - Exam 3 Flashcards

1
Q

What is the technical term for heartburn?

A

pyrosis

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2
Q

Describe heartburn. Where does it radiate?

A

The feeling of substernal burning

often radiates into the neck

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3
Q

What is the process for swallowing?

A

elevation of the tongue

closure of the nasopharynx

relaxation of the upper esophageal sphincter

closure of the airway

pharyngeal peristalsis

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4
Q

What is Oropharyngeal Dysphagia? What are some s/s? What will the pt complain of/ characterized by?

A

Problems with the oral phase of swallowing cause

drooling or spillage of food from the mouth, inability to chew or initiate swallowing, or dry mouth

an immediate sense of the bolus catching in the neck, the need to swallow repeatedly to clear food from the pharynx, or coughing / choking during meals

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5
Q

What are the 2 different types of esophageal dysphagias? How can you tell the difference between the 2?

A

mechanical obstruction: usually just solids
-> recurrent and predictable

motility disorders: BOTH solids and liquids
-> episodic and unpredictable

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6
Q

What is odynophagia? What does it reflect?

A

Sharp substernal pain on swallowing that may limit oral intake

Usually reflects severe erosive disease

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7
Q

odynophagia is most commonly associated with infectious esophagitis due to _________, _______ or _______. especially in ______pt

A

Candida, herpes viruses, or CMV

especially in immunocompromised patients

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8
Q

Odynophagia that is not infectious can also be due to _______. What was the example Adkins gave in class? What medication?

A

corrosive injury due to caustic ingestions and by pill-induced ulcers

button batteries are especially known for causing this!

fosfomax

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9
Q

What are the 2 MC complaints associated with GERD? What is the timing?

A

heartburn and regurgitation

occurs 30–60 minutes after meals and upon reclining

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10
Q

What are the 3 most common pathophys reasons GERD happens?

A
  1. Transient lower esophageal sphincter relaxation

aka increase in relaxation leads to increase in acid that comes into esophagus

  1. Anatomic disruption if GE Junction

aka the junction does NOT close properly

  1. Hypotensive lower esophageal sphincter

aka disruption of normal pressure

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11
Q

Which mechanism is responsible for the action of belching?

A

Transient lower esophageal sphincter relaxation that allows gas to leave

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12
Q

What factors reduce the lower esophageal sphincter pressure?

A

gastric distention
smoking
certain foods
medications

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13
Q

GERD severity is ______ with the degree of tissue damage

A

NOT correlated

aka pt can have minor symptoms with SEVERE disease

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14
Q

What are some atypical or extraesophageal manifestations of GERD?

A

Asthma, chronic cough, chronic laryngitis, sore throat, non-cardiac chest pain, and sleep disturbances

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15
Q

**What are the alarm features that would require additional work-up for GERD?

A
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16
Q

What is the diagnostic imaging for GERD? When NOT on PPI therapy, what can be seen?

A

Esophagogastroduodenoscopy or EGD

visible mucosal damage (known as reflux esophagitis

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16
Q

What is the pt education needed before a pt has an EGD?

A

Need to stop PPI 1 week before EGD

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17
Q

_____ are found in 3/4 of patients with severe erosive esophagitis and over 90% with _______

A

Hiatal Hernia

barrett esophagus

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18
Q

What are hiatal hernias caused by?

A

Caused by movement of the lower esophageal sphincter above the diaphragm which results in dysfunction of the gastroesophageal junction reflux barrier

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19
Q

What are the 2 different types of hiatal hernias? briefly describe each. Which one is MC?

A

**sliding hiatal hernia: Widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophageal membrane allow a portion of the gastric cardia to herniate upward

aka it slides UP in the same direction of the esophagus

Paraesophageal Hernias: Are associated with abnormal laxity of the gastrosplenic and gastrocolic ligaments, which normally prevent displacement of the stomach

aka it slides up to the SIDE of the esophagus

**sliding hernia is MC of the 2- 95% of the hernia as this kind

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20
Q

Paraesophageal Hernias are associated with abnormal laxity of the ______ and _____ ligaements that hold the stomach in place. What part of the stomach is displaced?

A

gastrosplenic and gastrocolic ligaments

As the hernia enlarges, the greater curvature of the stomach rolls up into the thorax

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21
Q

What are the risk factors for a hiatal hernia? **What are the 2 major ones?

A

age 50 and older

obesity

injury to the area

being born with an unusually large hiatus

persistent and intense pressure on the surrounding muscles (coughing, vomiting, straining, pregnancy)

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22
Q

_____ are common and may cause no symptoms and are associated with higher amounts of _____ and delayed ________. What does it lead to?

A

Sliding Hiatal Hernia

acid reflux

delayed esophageal acid clearance

leading to more severe esophagitis and Barrett esophagus

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23
Q

Paraesophageal Hernia may be asymptomatic or present with s/s including ????? GERD symptoms (more/less) prevalent when compared to pts with sliding hiatal hernias

A

epigastric or substernal pain, postprandial fullness, nausea, and retching

paraesophageal have LESS GERD s/s than sliding

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24
Q

In Barrett’s esophagus ,______ of the esophagus is replaced by _______ from the stomach

A

squamous epithelium

metaplastic columnar epithelium

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25
Q

What will Barrett’s esophagus look like on endoscopy? How do you confirm dx?

A

presence of salmon-orange colored, gastric type epithelium that extends upward from the stomach into the distal tubular esophagus in a circumferential fashion

bx obtained during endoscopy

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26
Q

In patients known to have Barrett esophagus, but no dysplasia, how often do you need to do an EGD?

A

surveillance endoscopy every 3–5 years

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27
Q

What is the f/u requirements for patients with low-grade dysplasia?

A

Resect any areas of dysplasia, then repeat endoscopic surveillance in 6 months to exclude any areas of dysplasia, then endoscopic surveillance should be repeated yearly until non-dysplastic Barrett’s exist

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28
Q

What is the f/u requirements for patients with high-grade dysplasia?

A

Resect all areas, then repeat EGD as soon as possible to exclude any other areas

Repeat at 3, 6, and 12 months

then yearly for 5 years, then every 3-5 years

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29
Q

What is considered mild, intermittent GERD? What is the tx?

A

fewer than 2 episodes per week, no esophagitis)

lifestyle modifications

antacids or oral H2 receptor antagonists (cimetidine, nizatidine, famotidine) all found OTC

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30
Q

What are the GERD lifestyle modifications?

A

eating smaller meals

eliminating acidic foods or trigger foods

weight loss

avoid lying down within 3 hours after meals

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31
Q

**______ MOA decrease gastric acid secretion by reversibly binding to _____ receptors located on gastric parietal cells

A

oral H2 receptor antagonists

histamine H2

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32
Q

When oral H2 receptors are taken for active heartburn, how long does it take to go into effect? How long do they provide relief for?

A

these agents have a delay in onset of at least 30 minutes

provide heartburn relief for up to 8 hours.

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33
Q

When is PPI therapy warranted?

A

when a patients fails BID H2RA therapy/Lifestyle modifications by consistently having 2-3 more episodes per week and symptoms that impair quality of life

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34
Q

**______ MOA inhibit gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium ATPase pump

A

PPI

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35
Q

What is the pt education for PPIs?

A

Taken 30 minutes before breakfast for approx 4-8 weeks

needs to be taking once daily

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36
Q

In those who achieve good symptomatic relief with a course of empiric once-daily proton pump inhibitor, therapy may be discontinued ______. More than likely will come back within ______

A

after 8–12 weeks

within 3 months

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37
Q

How do you tx patients whose GERD symptoms relapse? What about in patients who do NOT have erosive esophagitis?

A

continuous proton pump inhibitor therapy, in intermittent 8 week courses

twice daily H2-receptor antagonists may be used to control symptoms

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38
Q

When should long-term PPI therapy (QD or BID) be initiated indefinitely?

A

pts with severe erosive esophagitis

or

pts with Barrett’s esophagus

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39
Q

**What are the potential risks of long-term PPI use?

A

Increased risk of infectious gastroenteritis (including C difficile)

Iron and vitamin B12 deficiency

Hypomagnesemia

Hip fractures (possibly due to impaired insoluble calcium absorption)

Dementia ??

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40
Q

What is the name of the new GERD drug that was just approved in July 2024?

A

Vonoprazan

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41
Q

When should surgical treatment be considered an option for pts with GERD?

A

(1) patients with extraesophageal manifestations of reflux, may be more effectively controlled with antireflux surgery;

(2) those with severe reflux disease unwilling to accept lifelong medical therapy

(3) patients with large hiatal hernias and persistent regurgitation despite PPI therapy

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42
Q

What is a surgical fundoplication?

A

passage of the gastric fundus behind the esophagus to encircle the distal 6cm of esophagus

helps to restore a physiologic equivalent to the normal LES

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43
Q

Who is the linx system a good option for?

A

For patients with a hiatal hernia less than 3 cm in size

magnets open with pressure to to act like a lower esophageal sphincter

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44
Q

When do you need to refer a pt with GERD to GI?

A

Typical GERD whose symptoms do not resolve with empiric management with a twice-daily proton pump inhibitor.

Suspected extraesophageal GERD symptoms that do not resolve with 3 months of twice-daily proton pump inhibitor therapy.

Significant dysphagia or other alarm symptoms for upper endoscopy.

Barrett esophagus with dysplasia or early mucosal cancer.

Surgical fundoplication is considered

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45
Q

_____ is the most serious complication of Barrett Esophagus. What type? What part of the esophagus is involved?

A

Esophageal Carcinoma

adenocarcinoma

distal third of the esophagus

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46
Q

Chronic alcohol and tobacco use more than likely will get _______ carcinoma. In what part of the esophagus?

A

squamous cell carcinoma

middle esophagus

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47
Q

How does esophageal cancer present?

A

Over 90% have solid food dysphagia, with some odynophagia,

significant weight loss is common

coughing, chest or back pain

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48
Q

_______ establishes the diagnosis of esophageal carcinoma with a high degree of reliability

A

Endoscopy with biopsy

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49
Q

What are the 2 general classifications for esophageal cancer?

A

Therapy for “Curable” Disease

Therapy for Incurable Disease

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50
Q

What is the tx for Therapy for “Curable” Disease esophageal cancer?

A

Surgery with or without chemoradiation therapy

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51
Q

What is the tx for Therapy for Incurable Disease for esophageal cancer?

A

Chemotherapy or chemoradiation; Local therapy for esophageal obstruction

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52
Q

What is the overall 5 year survival rate of esophageal carcinoma? What are the 2 most important predictors of poor survival?

A

less than 20%

adjacent mediastinal spread
lymph node involvement

53
Q

What is Zenker’s diverticulum?

A

A sac-like outpouching of the mucosa and submucosa through Killian’s triangle

54
Q

What is Killian’s triangle?

A

An area of weakness between the transverse fibers of the cricopharyngeus muscle and the oblique fibers of the lower inferior constrictor muscles

55
Q

What is the underlying cause of Zenker’s diverticulum?

A

The cause is believed to be loss of elasticity of the UPPER esophageal sphincter, resulting in restricted opening during swallowing

56
Q

What are 5 things that generally are present in a pt with Zenker’s diverticulum?

A

Altered upper esophageal sphincter function

Abnormal esophageal motility

Esophageal shortening

hiatal hernia

reflux

57
Q

Dysphagia
regurgitation
coughing
throat discomfort
halitosis
spontaneous regurgitation of undigested food
gurgling in the throat

What am I?
What are 6 complications?

A

Zenker’s diverticulum

-Aspiration pneumonia
-bronchiectasis
-lung abscess
-Ulceration and bleeding due to retained medication
-Fistula between the diverticulum and trachea lumen formation
-Focal cord paralysis due to the pressure from retained food

58
Q

How do you dx ZD? What is the tx?

A

barium swallow study

upper esophageal myotomy

59
Q

What is an upper esophageal myotomy? When is it used?

A

Surgical procedure to restore the opening of the upper esophageal sphincter

The standard treatment consists of eliminating the functional obstruction at the UES level (myotomy of the cricopharyngeus muscle and the upper 3 cm of the posterior esophageal wall) and excision or suspension of the diverticulum

Zenker’s diverticulum

60
Q

What is achalasia? What does it result from?

A

narrowing of the distal esophagus

Results from progressive degeneration of ganglion cells in the myenteric plexus in the esophageal wall

61
Q

What does the loss of ganglion cells in achalasia lead to? What does that lead to?

A

This loss of cells leaves inflammatory cells of lymphocytes and eosinophils

leads to failure of relaxation of the LES and loss of peristalsis

62
Q

**What is the cause of the inflammation seen in achalasia?

A

**The cause of the inflammation is not known

63
Q

What does the narrowing of the LES in achalasia lead to ?

A

narrowing causes dilation of the esophagus above the LES

64
Q

-gradual onset of dysphagia for solid foods and liquids
-Many patients eat more slowly and adopt specific maneuvers to help emptying
-regurgitation of undigested food is common
-substernal chest pain
-nocturnal regurgitation
-weight loss

What am I?
**What is the diagnostic tool of choice?

A

achalasia

**Esophageal manometry (#1)

65
Q

What is an Esophageal manometry?

A

pressure sensing catheter in esophagus
measures LES sphincter pressure during swallowing
measures esophageal peristaltic contractions

66
Q

What will a CXR show in a pt with achalasia?

A

may show an air-fluid level in the enlarged, fluid-filled esophagus

67
Q

** What is the classic Barium esophagography finding associated with achalasia?

A

**and a smooth, symmetric “bird’s beak” tapering of the distal esophagus

68
Q

What is the tx for achalasia? How many treatments does it usually take?

A

PNEUMATIC DILATION #1

1-3 sessions

69
Q

What is happening in pneumatic dilation? Once the first episode has resolved, when do pts need additional treatment?

A

Forceful Dilation with pneumatic balloon dilation of the LES weakens the LES by circumferential stretching or tearing of its muscle fibers

Symptoms recur following pneumatic dilation in up to 35% within 10 years but usually respond to repeated dilation

70
Q

Name 2 additional treatments for achalasia.

A

BOTULINUM TOXIN INJECTION directly into the LES

surgery: Heller myotomy

71
Q

When are botox injections used in achalasia tx? How often do they need them?

A

This therapy is most appropriate for patients with comorbidities who are poor candidates for more invasive procedures

symptom relapse occurs in over 50% of patients within 6–9 months and in all patients within 2 years.

72
Q

What is a Heller myotomy? What is a common complication? How do you fix it?

A

cut LES muscle fibers, only the OUTER muscles of the esophagus are cut. Incisions will reduce the force of the contracting muscles and relax the LES, thereby, allowing food to pass easily.

makes it easy for the stomach acid to recede into the esophagus. Hence, a fundoplication is often performed along with myotomy.

73
Q

**_____ confirms diagnosis of achalasia

A

esophageal manometry

74
Q

What does diffuse esophageal spasms present as? ** What is the classic finding on barium swallow?

A

Episodes of dysphagia and chest pain

**“corkscrew esophagus” with barium swallow #1

75
Q

What is diffuse esophageal spams defined as on manometry?

A

uncoordinated (“spastic”) activity in the distal esophagus

spontaneous and repetitive contractions

Or, high-amplitude and prolonged contractions

76
Q

What is the running theory as to why diffuse esophageal spasms occur?

A

thought to be a consequence of impaired inhibitory innervation, leading to premature and rapidly propagated contractions

77
Q

for diffuse esophageal spasm pts, will the dysphagia be present for solids and liquids? The dysphagia will occur in association with: (3 things)

A

YES! both solids and liquids

retrosternal, noncardiac chest pain
heartburn
regurgitation

78
Q

What are the top 2 MC treatment options for DES? What are 3 additional options?

A

CCB: Diltiazem 60-90mg QID for 3 months, then prn

or

TCA

_________
NTG
sildenafil
botulinum toxin

79
Q

What is scleroderma? What are the 5 limited symptoms?

A

Autoimmune disorder that can involve skin, lungs, heart, and GI tract

CREST (see picture)

80
Q

What is scleroderma esophagus? _____ is the often the only identifiable association

A

Hypotensive LES and absent esophageal peristalsis

Reflux disease

81
Q

What is the pathogenesis of Scleroderma esophagus? What are these pts at severe risk for?

A

Infiltration and destruction of the esophageal muscularis with collagen deposits and fibrosis

high risk for severe GERD due to inadequate LES barrier

82
Q

What is the tx for scleroderma?

A

PPI for GERD

metoclopramide for dymotility

83
Q

What is a mallory weis tear? What is it characterized by? What is it caused by?

A

a tear in the mucosal layer at the junction of the esophagus and stomach

Characterized by a nonpenetrating mucosal tear at the gastroesophageal junction

suddenly raise transabdominal pressure due to lifting, retching and vomiting

84
Q

______ is a strong predisposing factor for a mallory weis tear

A

alcoholism

85
Q

What are s/s of a mallory weis tear?

A

Acute onset of GI bleeding with hematemesis

may have epigastric or back pain

history of vomiting/retching

86
Q

How do you dx a mallory weis tear? What will it look like? What are the 2 MC sites?

A

EGD

0.5- to 4-cm linear mucosal tear

usually located either at the gastroesophageal junction or, more commonly, just below the junction in the gastric mucosa

87
Q

What is the tx for a mallory weis tear? What happens if the bleeding does NOT stop?

A

fluid resuscitation and blood transfusions because most pts stop bleeding spontaneously and require no therapy

Endoscopic hemostatic therapy

88
Q

What are the 3 options for Endoscopic hemostatic therapy in a mallory weis tear?

A

Injection with epinephrine (1:10,000)

Cautery with a bipolar or heater probe coagulation device

Or mechanical compression of the artery by application of an endoclip or band is effective in 90–95% of cases

89
Q

_______ or operative intervention is required in patients who fail endoscopic therapy for a mallory weis tear

A

Angiographic arterial embolization

90
Q

What are esophageal webs? **Where are they located in the esophagus?

A

Esophageal webs are thin, diaphragm-like membranes of squamous mucosa that cause narrowing in the esophagus

**mid or upper esophagus

91
Q

What are 4 causes of esophageal webs?

A

Congenital

Esophagitis

Pemphigoid: (autoimmune disorder)

Iron deficiency anemia ( called Plummer-Vinson syndrome)

92
Q

What are “Schatzki” rings? **Where are they located within the esophagus? ______ is suggestive that might contribute to the cause of schatzki rings

A

smooth, circumferential, thin (less than 4 mm in thickness) mucosal structures located in the distal esophagus at the squamocolumnar junction

GERD

93
Q

Most webs and rings are over _____ in diameter and are asymptomatic. Solid food dysphagia most often occurs with rings less than _____ in diameter

A

20 mm

13 mm

94
Q

What is the tx for esophageal webs and rings?

A

passage of dilators to disrupt the lesion
or

endoscopic electrosurgical incision of the ring

often repeat dilations are required

should be on PPI therapy

95
Q

What are esophageal varices caused by? Is it considered an emergency? Why or why not?

A

portal hypertension due to cirrhosis

YES!! because it may result in serious upper gastrointestinal bleeding - life threatening

96
Q

Where is bleeding from an esophageal
varices more likely to occur? What is the pathogenesis?

A

most commonly occurs in the distal 5 cm of the esophagus

When the portal vein and IVC gradient exceeds 10–12 mm Hg, significant portal hypertension exists

97
Q

What is the normal portal vein to IVC pressure gradient?

A

Under normal circumstances, there is a 2–6 mm Hg pressure gradient between the portal vein and the inferior vena cava

98
Q

What is the MC cause of esophageal varices? Why do varices develop?

A

Cirrhosis

due to increased portal pressure that results from increased resistance to outflow through obstruction of hepative portal vein

Varices develop in order to decompress the hypertensive portal vein and return blood to the systemic circulation

99
Q

What is the MC cause of portal hypertension? _____ will stop bleeding spontaneously. What is likely to happen in the future?

A

cirrhosis

roughly 50%

60% chance of recurrent variceal bleeding, usually within the first 6 weeks

100
Q

What are the bleeding risk factors for esophageal varices?

A

(1) the size of the varices (>5 cm)

(2) the presence at endoscopy of red wale markings (longitudinal dilated venules on the varix surface)

(3) the severity of liver disease (as assessed by Child scoring)

(4) active alcohol abuse—patients with cirrhosis who continue to drink have an extremely high risk of bleeding

101
Q

What is the scoring system that evaluates liver disease?

A

Child scoring

102
Q

What are red wale markings?

A

longitudinal dilated venules on the varix surface)

aka red marking on top of esophageal varices

103
Q

How will esophageal varices usually present?

A

hematemesis (bright red vomiting of blood)
coffee ground emesis: brown/red blood
melena (dark stools)
retching
dyspepsia
hypovolemic shock

USUALLY VERY SEVERE!!

104
Q

What is this? What disease? what does it increase your risk for?

A

Red Whale Markings

esophageal varices

increased risk of bleeding

105
Q

What is the INITIAL management of esophageal varices?

A

ACUTE resuscitation!!!

fluids and blood products (fresh frozen plasma or platelets) as necessary

supplemental O2 or intubation as necessary

pts with liver disease need to go to ICU

106
Q

When do fresh frozen plasma or platelets need to be given in esophageal varices?

A

fresh frozen plasma or platelets should be administered to patients with INRs greater than 1.8–2.0 or with platelet counts less than 50,000/mcL in the presence of active bleeding

107
Q

For esophageal varices, once the pt is stable, what do you do next?

A
  1. abx: IV Ceftriaxone for 5-7 days
    or fluoroquinolones if allergy
  2. Octreotide (Sandostatin)
  3. vitamin K
  4. lactulose
108
Q

Why do you give esophageal varices pts Octreotide (Sandostatin)?

A

nfusions reduce splanchnic and hepatic blood flow, therefore reducing portal pressure

Inhibits release of vasodilator hormones such as glucagon, indirectly causing splanchnic vasoconstriction and decreased portal blood inflow

109
Q

Why do you give esophageal varices pts Vitamin K?

A

In cirrhotic patients with an abnormal prothrombin time, vitamin K (10 mg) should be administered intravenously

110
Q

Why do you give esophageal varices pts lactulose? What is the dosing?

A

decreasing the intestinal production and absorption of AMMONIA to reduce the risk of Encephalopathy (increased ammonia leads to encephalopathy)

30 mL orally every 1–2 hours until evacuation occurs then reduced to 15–45 mL/h every 8–12 hours as needed to promote two or three bowel movements daily

111
Q

_____ needs to be performed in esophageal varices once the pt is stable and usually within ____ hours of admission. What happens next?

A

EMERGENT ENDOSCOPY

usually within 12 hours of admission

Immediate endoscopic treatment of the varices generally is performed with BANDING

112
Q

How many treatments are needed? How often do you need to repeat banding in EV? How long does it take for the varices to slough off? What medication is given to prevent rebleeding?

A

usually 2-6 treatments

Repeat every 2–4 weeks, until the varices are obliterated or reduced in size

a few days

BB: propranolol, nadolol

113
Q

What is the prevention of rebleeding?

A

COMBINATION BETA-BLOCKERS AND VARICEAL BAND LIGATION

114
Q

**patients with cirrhosis should undergo _______ to look for ______

A

diagnostic endoscopy

varices are present

115
Q

All patients with acute upper gastrointestinal bleeding and ______ should be admitted to _____

A

suspected cirrhosis

an ICU

116
Q

EV are found on EGD, give _______ to reduce the risk of first variceal hemorrhage

A

Beta- blockers

117
Q

________ only used when EV bleeding cannot be stopped by pharmacologic/endoscopic procedures. How does it work? How long is it kept in for?

A

Balloon Tamponade

A balloon is inflated within the esophagus or stomach to apply pressure on bleeding blood vessels, compress the vessels, and stop the bleeding

24 hours

118
Q

_______ is used in EV when pharmacologic/endoscopic procedures fail and is not a balloon. How does it work?

A

Transvenous Intrahepatic Portosystemic Shunts (TIPS)

Wire that is passed through a catheter inserted in the jugular vein
an expandable wire mesh stent (8-12 mm in diameter) is passed through the liver parenchyma

119
Q

Transvenous Intrahepatic Portosystemic Shunts (TIPS) creates a shunt from the _____ vein in the ____ vein

A

portal vein in the hepatic vein

120
Q

When does infectious esophagitis most often occur in ______ patients. What are the 3 MC pathogens?

A

immunosuppressed

Candida albicans, herpes simplex, and CMV

121
Q

______ may occur also in patients who have uncontrolled diabetes and those being treated with systemic corticosteroids, radiation therapy, or systemic antibiotic therapy. ______ can affect normal hosts, in which case the infection is generally self-limited

A

Candida infection

Herpes simplex

122
Q

How will infectious esophagitis present?

A

Odynophagia and dysphagia

Substernal chest pain occurs in some patients

may have CMV infection at other sites such as colon and retina

oral ulcers might also be present with herpes simplex esophagitis

123
Q

How do you dx infectious esophagitis?

A

endoscopy with biopsy and brushings (for microbiologic and histopathologic analysis)

124
Q

What is the tx for CANDIDAL ESOPHAGITIS? CYTOMEGALOVIRUS ESOPHAGITIS? HERPETIC ESOPHAGITIS?

A

CANDIDAL ESOPHAGITIS: systemic fluconazole

CYTOMEGALOVIRUS ESOPHAGITIS: In patients with HIV infection, immune restoration with antiretroviral therapy

HERPETIC ESOPHAGITIS: oral acyclovir

125
Q

What kind of sedation is given during an EGD? What organs are being assessed?

A

Intravenous conscious sedation

through the mouth into the esophagus, stomach, and duodenum

126
Q

Barium swallow evaluates ______ and ______. What is the liquid called?

A

pharynx and the esophagus

barium sulfate (barium)

127
Q

What does Esophageal Manometry
measure? When is it commonly used?

A

Motility testing- examines the coordinated muscle movement (motility) of the esophagus. A pressure-sensing catheter placed within the esophagus and then observe the contractility following test swallows

achalasia and diffuse esophageal spasms

128
Q

The upper and lower esophageal sphincters appear as zones of high ______ that relax on ______, while the intersphincteric esophagus exhibits _______. All are assessed during ______

A

pressure

swallowing

peristaltic contractions

Esophageal Manometry

129
Q

What is Ambulatory Esophageal pH Monitoring do? When is it commonly used?

A

The recording provides information about the amount of esophageal acid reflux and the correlations between symptoms and reflux

aka info about acid reflux

130
Q
A

GI (12 decks)

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