Clinical Presentation of Esophageal Diseases Flashcards Preview

Gastrointestinal 1 > Clinical Presentation of Esophageal Diseases > Flashcards

Flashcards in Clinical Presentation of Esophageal Diseases Deck (74)
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1
Q

What is GERD?

A

Gastro-Esophageal Reflux Disease= chronic symptoms of mucosal damage produced by the abnormal refulx of grastric contents into the esophagus

2
Q

What are the 2 types of GERD?

A
  1. Erosive esophagitis

2. Nonerosive Reflux Disease (NERD) or endoscopy negative reflux disease (ENRD)

3
Q

How does GERD present clinically?

A

upper epigastric pain that radiates to the chest and may worsen when lying flat.

4
Q

Do you need any diagnostics or imaging studies to diagnose GERD?

A

NO. If you give an antacid and the problem resolves, then you have diagnosed and treated GERD.

5
Q

Is there any correlation with the severity of GERD symptoms and what you will find in the esophagus?

A

NO! This is a problem bc the more erosion you have the more esophagitis you will have, and this can predispose you to some bad things.

6
Q

Is daytime or nocturnal reflux more injurious to the esophagus?

A

nocturnal because you are lying supine (removing gravity from the equation)

7
Q

A 55 y.o. white male presents with frequent heartburn symptoms, 3-4 times weekly, for the past 20 years. Has taken OTC antacids intermittently when needed. No red flags or alarm symptoms. His doctors told him to lose some weight, and avoid spicy, acidic, and caffeine products such as coffee and tea. He also complains of nocturnal reflux.
How COULD you treat this patient?

A
  1. Lifestyle and dietary modifications= weight loss if needed, elevation of the head of the bed (without flexing at the waist, which would increase intra-abdominal pressure and worsen reflux), and avoidance of trigger foods (fatty foods, caffeine, spicy, acidic, carbonated beverages, spearmint/peppermint).
    * avoid tight fitting clothes, avoid tobacco/alcohol, and no eating within 3 hours of bedtime.
  2. Antacids
  3. Surface agents (sucralfate or sodium alginate)= create barrier on the top of the gastric juice to help prevent reflux.
  4. Histamine 2 receptor antagonists (H-2 blockers)= inhibits the histamine-2 receptor on the gastric parietal cell.
  5. Proton pump inhibitors (PPIs)= most potent of all the acid inhibitors, which irreversibly bind to the hydrogen-potassium ATPase pump on the gastric parietal cell.
8
Q

*** What GERD intervention is proven to most effectively heal erosive esophagitis (all grades A-d) and provide symptom relief?

A

Proton pump inhibitors (PPIs)

*ex. Prilosec

9
Q

What was a problem with H-2 blockers?

A

tachyphylaxis= tolerance to drug occurs

10
Q

What is the main reason why you will see GERD?

A

LES (lower esophageal sphincter) dysfunction
*to a lesser degree: hiatal hernia, increased abdominal pressure, defective esophageal clearance, or delayed gastric emptying.

11
Q

What are the 3 main symptoms of GERD?

A
  1. Heartburn
  2. Regurgitation
  3. Difficulty swallowing
12
Q

What are atypical symptoms of GERD?

A
  • chronic cough
  • sore throat
  • lump in throat (globus)
  • cavities
  • chest pain
  • nausea
  • hoarsness
  • throat clearing
  • asthma/wheezing
13
Q

What is the mildest form of GERD?

*diagnosis made via upper endoscopy

A

grade A= one or more mucosal breaks no longer than 5 mm, not bridging the tops of mucosal folds.

14
Q

What are mucosal breaks?

A

an area of slough or erythema with a discrete line of demarcation from the adjacent, more normal looking mucosa.

15
Q

What is grade B esophagitis?

A

one or more mucosal breaks longer than 5 mm, but not bridging the tops of mucosal folds.

16
Q

What is grade C esophagitis?

A

one or more mucosal breaks bridging the tops of mucosal folds involving less than 75 percent of the circumference of the lumen.

17
Q

What is grade D esophagitis?

A

one or more mucosal breaks bridging the tops of mucosal folds involving more than 75 percent of the circumference of the lumen.

18
Q

What are the complications of GERD?

A
  • bleeding
  • stricture
  • ulceration
  • Barrett’s (ONLY comes from long-standing acid refulx)
  • cancer
19
Q

Is Barrett’s esophagus a PRE-malignant condition?

A

YES, meaning you have a higher predisposition of acquiring cancer of the esophagus.

20
Q

What patient’s are most likely to develop Barrett’s esophagus?

A

middle-aged white males

21
Q

What is an upper GI?

A

a barium swallow.

* This is NOT an upper endoscopy.

22
Q

** What is Barrett’s Esophagus?

A

metaplastic columnar epithelium that predisposes to cancer development by replacing the stratified squamous epithelium that normally lines the distal esophagus.

23
Q

What is important to remember about Barrett’s esophagus?

A

it is a condition acquired as a consequence of chronic GERD!

24
Q

What is the only way to diagnose Barrett’s?

A

biopsy! Look at the Z line= transition line between esophagus and stomach separating stratified squamous epithelium from columnar epithelium.

25
Q

What is the gastroesophageal junction?

A

the imaginary line at which the esophagus ends and the stomach begins. It corresponds to the most proximal extent of the gastric folds. This should correspond with the Z line.
* When the Z line moves more proximal, then this is Barrett’s esophagus.

26
Q

What are the risk factors for Barrett’s esophagus?

A
  • increased acid exposure (especially nocturnal)
  • older age
  • male
  • white
  • obese
  • hiatal hernia
27
Q

What do we do if we find H. pylori?

A

treat it

28
Q

After how many years should you wait to do an upper endoscopy?

A

5 years. If a patient has had at least 5 years of GERD, you scope them.

29
Q

If there is no dysplasia on a biopsy of Barrett’s esophagus, how often should you follow up with another endoscopy?

A

every 3-5 years to see if there is a progression to cancer. Remember that we can’t reverse Barrett’s. We can just control the progression with PPIs.

30
Q

How many new cases of Barrett’s esophagus will occur this year?

A

18,000 and of this, 15,000 will die, bc it is picked up so late and esophageal cancer has already spread.

31
Q

What are the 2 types of esophageal cancer?

A
  1. squamous cell carcinoma

2. adenocarcinoma

32
Q

*** For which cancer type are you most at risk if you have Barrett’s esophagus?

A

adenocarcinoma

33
Q

What are the risk factors for squamous cell carcinoma?

A
  • smoking, excessive alcohol use, low intake of fruits and vegetables, or ingesting high temperature liquids.
  • underlying esophageal diseases (achalasia and alkali ingestion like Drain-O).
34
Q

What is Tylosis? (board question)

A

rare disease of hyperkeratosis of palms and feet associated with squamous cell carcinoma.
Autosomal dominant mode of inheritance.

35
Q

Can bisphosphonates cause severe acid reflux?

A

YES. These are used to decrease bone resorption in elderly patients with osteoporosis.

36
Q

How do we treat squamous cell carcinoma?

A

after staging using CT or MRI for distant metastasis or Endoscopic ultrasound (if CT or MRI are negative), you can do chemo or radiation. If too far, then palliative care.

37
Q

*** What is the most common esophageal cancer?

A

adenocarcinoma of the lower 1/3rd of esophagus

38
Q

Has the incidence of adenocarcinoma severely increased over the past 10-15 years?

A

YES :(

39
Q

How do you treat adenocarcinoma?

A

similar to squamous cell carcinoma (chemo, radiation, surgery, palliation)

40
Q

Where is the most common place to find gastrointestinal stromal tumors (GIST)?

A

stomach or proximal small bowel

41
Q

What are some other much less common esophageal tumors?

A

leiomyomas, leiomyosarcomas, lymphangiomas, hemangiomas, fibrovascular polyps, granular cell tumors, adenomas, papillomas…

42
Q

** What is eosinophilic esophagitis (EoE)?

A

allergic inflammatory condition of the esophagus that involves eosinophils. 54% are associated with food impactions.

43
Q

What are the adult symptoms of eosinophilic esophagitis?

A

dysphagia, food impaction, heartburn, regurg, chest pain, odynophagia (painful swallowing).

44
Q

What are the child symptoms of eosinophilic esophagitis?

A

abdominal pain, heartburn, regurg, nausea/vomiting, dysphagia, failure to thrive

45
Q

** What are the 3 types of endoscopic appearances of EoE? (know pictures for test)

A
  1. trachealization of esophagus (concentric rings)
  2. longitudinal linear furrows
  3. white exudates (clumps of eosinophils)
46
Q

What will often happen when you dilate the esophagus due to EoE?

A

you will tear the mucosa (esophageal rent).

47
Q

Can we assume that all esophageal eosinophilia is EoE?

A

NO.

48
Q

Is there a possible complex interaction between GERD and EoE?

A

YES, but we don’t know which is causing which.

49
Q

** What is the first line treatment of EoE?

A

PPI and if that fails, use swallowed steroids (gulp your Flonase)
*also incorporate dietary restrictions on foods that may cause the reaction for pediatric patients.

50
Q

What is achalasia?

A
  • greek for “does not relax”
  • loss of peristalsis in the distal esophagus and failure of LES relaxation due to degeneration of neurons in the esophageal wall (loss of inhibitory interneurons).
51
Q

What causes achalasia?

A
  • primary= unknown
  • secondary causes may be due to Chagas disease (South America), Trypanosoma cruzi infection, or malignancy (amyloid, sarcoid, neurofibromatosis).
52
Q

** What type of cancer does achalasia cause?

A

squamous cell carcinoma

*remember bc the sphincter is too tight and acid cannot reflux like in GERD.

53
Q

What is the biggest symptom of achalasia?

A

dysphagia of both solids and liquids occurring over many years

54
Q

How do you diagnose achalasia?

A
  • barium swallow. Will see beak like narrowing at Z line.

- manometry to look for elevated LES resting pressures

55
Q

** What will you see in late stage achalasia?

A

dilated esophagus (sigmoid esophagus)

56
Q

** How do you treat achalasia?

A
  • nitrates
  • calcium channel blockers
  • botulinum toxin injection
  • dilation of the LES (pneumatic balloon)
  • surgical myotomy
57
Q

** What is Boerhaave’s syndrome?

A
  • spontaneous esophageal perforation due to sudden increase in intraesophageal pressure combined with negative intrathoracic pressure by vomiting or straining
58
Q

What are some causes of esophageal perforation other than Boerhaave’s syndrome?

A

caustic ingestion, pill esophagitis, Barrett’s ulcer, infectious ulcers (AIDS)

59
Q

What are the symptoms of Boerhaave’s syndrome?

A
  • severe retching/vomiting
  • severe retrosternal chest and upper abd pain
  • quick onset of more severe symptoms including fever, odynophagia, tachypnea, dyspnea, cyanosis, shock
60
Q

How do you diagnose Boerhaave’s syndrome?

A
  • CXR looking for free air (mediastinal or peritoneal)
  • CT
  • Gastrografin swallow (water soluble)
61
Q

Should you do and endoscopy with a perforation?

A

NO bc you are introducing positive pressure and can make the perforation worse.

62
Q

What is the treatment of Boerhaave’s syndrome?

A
  • conservative= NG suction, IV abx, and parenteral nutrition.
  • surgical if thoracic perforation
  • SEMS= endoscopically placed self-expandable metal stents (if you can’t get pt to surgery).
63
Q

** What is the most common esophageal infection and how do you treat?

A

esophageal candidiasis (especially HIV pts with CD4

64
Q

What is the most common symptom of esophageal candidiasis?

A

dysphagia

65
Q

What are some other less common infections of the esophagus?

A
  • CMV

- Herpes

66
Q

What are esophageal varices?

A

extremely dilated sub-mucosal veins in the lower third[1] of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding.
*each bleeding episode carries a 20% risk of death!

67
Q

What will esophageal varices look like on endoscopy?

A

will see red wale marks (erythematous raised red marks).

68
Q

Who should be screened for esophageal varices?

A

all pts with cirrhosis

69
Q

How do you prevent esophageal varices from bleeding? (these are very dangerous and severe bleeds)

A
  • nonselective beta blockers (nadolol or propranolol) for SMALL varices.
  • Endoscopic varices ligation (put rubber bands on them) for LARGE varices.
70
Q

How do we treat an active bleeding varix?

A
  • hemodynamic resuscitation= IVF, packed RBCs, clotting factors (fresh frozen plasma), and 2 large bore peripheral IV’s or central line.
  • octreotide/somatostatin IV to decrease portal pressures.
  • EVL is a must
  • prophylactic abx (ceftriaxone)
71
Q

What happens if EVL fails an actively bleeding varix?

A
  • balloon tamponade
  • surgery
  • TIPSS= transjugular intrahepatic portosystemic stent shunt
72
Q

What are the 3 types of esophageal dysmotility? (very rare)

A
  1. diffuse esophageal spasm (DES)= low amplitude
  2. nutcracker esophagus= high amplitude pressures
  3. hypertensive lower esophageal sphincter
73
Q

What may be related to nutcracker esophagus?

A

hypercholinergic state (thus anticholinergic like atropine may be helpful).

74
Q

How do we treat esophageal dysmotility?

A
  • calcium channel blockers
  • antidepressants due to decreased sensation to pain.
  • peppermint oil (remember this is a smooth muscle relaxant; but DON’T use for GERD).