Scleroderma (Progressive Systemic Sclerosis) Flashcards

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1
Q

80–90% of patients with scleroderma will develop diminished esophageal peristalsis from

A

atrophy and fibrosis of the esophageal smooth muscle.

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2
Q

What is the Clinical Presentation of Scleroderma?

A

1-dysphagia
2-main clue is GERD symptoms with a history of scleroderma
3-LES will not contract nor relax

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3
Q

what is the most accurate diagnostic test of scleroderma?

A

motility study.

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4
Q

what is the Treatment of scleroderma?

A

1-proton-pump inhibitor e.g. omeprazole.

2- Metoclopramide a promotility agent.

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5
Q

what are the Diffuse Esophageal Spasm and Nutcracker Esophagus?

A

idiopathic abnormalities of the neural processes of the esophagus

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6
Q

what is the difference between Diffuse Esophageal Spasm and Nutcracker Esophagus

A

the manometric pattern

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7
Q

what is the Clinical Presentation of Diffuse Esophageal Spasm?

A

1-Intermittent chest pain and dysphagia
2-pain simulate myocardial infarction but it bears no relationship with exertion
3-no relation with eating, ruling out odynophagia
4-pain triggered by drinking cold liquids.

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8
Q

what is the diagnosis of Diffuse Esophageal Spasm?

A

1-Barium study show a “corkscrew”’ pattern at time of spasm.

2-most accurate test for diagnosis is a manometric study.

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9
Q

what is the Treatment of diffuse esophageal spasm?

A

calcium-channel blocker e.g., nifedipine, or nitrate.

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10
Q

what does Schatzki’s ring leads to?

A

intermittent dysphagia not associated with pain

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11
Q

Schatzki’s ring located at

A

It is more distal at the squamocolumnar junction proximal to the LES.

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12
Q

Plummer-Vinson syndrome (PVS) is located at

A

more proximal and located in hypopharynx

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13
Q

PVS is associated with

A

1-iron-deficiency anemia and squamous cell cancer

2-in middle-aged women.

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14
Q

what is the diagnosis of Schatzki’s ring and Plummer-Vinson syndrome?

A

barium swallow or barium esophagoram.

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15
Q

Treatment of Schatzki’s ring and Plummer-Vinson syndrome

A

1-treated with dilation procedures.

2-PVS may respond to treatment for iron deficiency

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16
Q

Esophagitis is due to

A

infection or inflammation of the esophagus

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17
Q

The most common infection of Esophagitis is

A

Candida albicans.

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18
Q

Candida esophagitis occurs in patients who are

A

HIV-positive with CD4 count <200/mm3

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19
Q

The second most common risk for developing Candida esophagitis is

A

diabetes mellitus

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20
Q

Clinical Presentation of esophagitis

A

1-Candida esophagitis presents with progressive odynophagia
2-swallowing is painful
3-pain in esophagitis is only on swallowing, while the pain in spastic disorders is intermittent without even needing to swallow.
5-Esophagitis pain is from mechanical rubbing of food against an inflamed
esophagus as it passes by.

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21
Q

Treatment of Esophagitis

A

1-If the patient is HIV-positive, assume Candida esophagitis and start fluconazole
2-If symptoms do not improve, perform
endoscopy and biopsy to exclude other causes such as HSV and CMV

22
Q

the treatment for Candida must be

A

fluconazole

23
Q

Diagnosis of patients with Candida esophagitis

A

35% will not have oral thrush

24
Q

esophagitis can also result from

A

ingestion of medication and caustic substances, the direct effect of contact between the mucosa and the pill causes inflammation rather than infection.

25
Q

The most common pills causing esophagitis are

A
1-alendronate, 
2-quinine, 
3-risedronate,
4- vitamin C,
5-potassium chloride, 
6-doxycycline, 
7-NSAIDs, and iron sulfate.
26
Q

Consider pill esophagitis in a young patient who takes……… and who has an……….

A

acne medication

acute onset of odynophagia

27
Q

Pill esophagitis is prevented by

A

swallowing pills in the upright position and drinking enough water to flush them into the stomach

28
Q

Clinical Presentation of Eosinophilic Esophagitis

A

1-infiltration with eosinophils
2- no improvement after an
8-week trial of PPIs
GERD can mimic EE

29
Q

Treatment of Eosinophilic Esophagitis

A

1-fluticasone or budesonide
2-If the biopsy shows eosinophils,
give PPIs before swallowed steroids.

30
Q

define Zenker diverticulum

A

outpocketing of the posterior pharyngeal constrictor muscles at the back of the pharynx

31
Q

Clinical Presentation of Zenker diverticulum

A

1-older patients.
2-Bad breath
3-Difficulty initiating swallowing (due to such a proximal lesion)
4-repeatedly clear the throat
5-Waking up with undigested, regurgitated food on the pillow (food from perhaps several days ago)

32
Q

Treatment of Zenker diverticulum

A

1-surgical resection

2-Endoscopy and the placement of NGtubes are contraindicated because they could perforate the pharynx.

33
Q

define Mallory-Weiss syndrome

A

nontransmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting.

34
Q

Clinical Presentation of Mallory-Weiss Syndrom

A

1-No dysphagia or odynophagia, but rather, painless upper GI bleed
2-Black stool from melena if volume of bleed >100 mL or with hematemesis if there is continued vomiting

35
Q

Diagnosis of Mallory-Weiss Syndrom

A

direct visualization on upper endoscopy

36
Q

Treatment of Mallory-Weiss Syndrome

A

1-will resolve spontaneously

2-inject the tear with epinephrine or perform cauterization

37
Q

causes of epigastric pain

A

1-Pancreatitis (most common reason for epigastric tenderness and pain)
2-Ulcer disease (associated with epigastric tenderness in <20% of patients
3-GERD
4-Gastritis
5-Gastric cancer (rare)

38
Q

Helicobacter pylori is most strongly associated with the development of

A

duodenal ulcers, gastric ulcers, and gastritis.

39
Q

define nonulcer dyspepsia

A

a functional disorder in which there is persistent pain in the epigastric area but all tests are found to be normal.

40
Q

patients with dyspepsia and alarm features require

A

upper endoscopy

41
Q

Alarm features for patients with EPIGASTRIC PAIN

A
  • Onset age >50
  • Anemia
  • Dysphagia
  • Odynophagia
  • Vomiting
  • Weight loss
  • Family history of upper GI malignancy
  • Personal history of peptic ulcer disease
  • Gastric surgery
  • GI malignancy
  • Abdominal mass or lymphadenopathy on examination
42
Q

Treatment of epigastric pain

A

1-Treat young, generally healthy patients empirically with H2 blocker, liquid antacid, or PPI; if no improvement, undergo endoscopy.
2-For patients without duodenal/gastric ulcer or gastritis, do not treat for H. pylori.

43
Q

Gastroesophageal reflux disease (GERD) is caused by

A

abnormal flow of the acid gastric contents backward from the stomach up into the esophagus.

44
Q

number of factors can cause decreased tone or loosening of LES are

A
  • Nicotine, alcohol, caffeine
  • Peppermint, chocolate
  • Anticholinergics
  • Calcium-channel blockers
  • Nitrates
45
Q

Clinical Presentation of GERD

A
1-heartburn (burning substernal pain)
2-sore throat
3-metal-like taste in the mouth
4-hoarseness 
5-cough
6- wheezing.
7-Symptoms are worse after a meal or while lying flat
46
Q

The most accurate diagnostic test for Gastroesophageal Reflux Disease is

A

1-24-hour pH monitor, an electrode is placed several
centimeters above the gastroesophageal junction, and a determination is made of what the
average pH is in that area.

47
Q

What is the order when working up GERD

A

• Initiate PPI; if no improvement, increase PPI to 2x daily (before EGD) for 4–8 weeks and make sure patient is taking properly (30–60 min before meals)
• If no improvement, do EGD: If EGD shows esophagitis, that confirms GERD and 24-hour pH monitoring is not needed. If EGD is normal, do ambulatory 24-hour pH monitoring (while off the PPI) and if results are consistent with GERD, do Nissen
fundoplication.

48
Q

In clear cases of epigastric pain going under the sternum and associated with a respiratory
complaint or bad taste in the mouth, do the following

A

initiate therapy immediately with antisecretory medications such as PPIs.

49
Q

Treatment of GERD is

A

1- Treatment is a PPI and lifestyle modification (avoid nicotine/alcohol/caffeine/
chocolate/late-night meals
2- elevate the head of the bed 6–8 inches with blocks to keep acid in the stomach)
3-Omeprazole,
4-PPI side effects include increased risk for C. difficile infection, aspiration pneumonia, osteoporosis, and hip fracture
5-A few people (<5%) will not respond to PPIs or will have refractory side effects (headaches, diarrhea); those patients will require surgery to tighten the sphincter (traditionally, a Nissen fundoplication is done laparoscopically).
6-Do motility studies prior to surgery to avoid iatrogenic dysphagia.
7-Use H2 blockers only if the patient has very mild, intermittent symptoms, as they are less effective than PPIs.

50
Q

define Barrett Esophagus

A

1-a complication of long-standing reflux disease
2-epithelium of the lower esophagus undergoes histologic change from a normal squamous epithelium to a columnar epithelium.

51
Q

Patients with Barrett esophagus should have

A

repeat endoscopy every 3–5 years to see whether
dysplasia or esophageal cancer has developed:
• If low-grade dysplasia, repeat endoscopy in 6–12 months
• If high-grade dysplasia, do radiofrequency ablation, photodynamic therapy, or
endoscopic mucosal resection
• The usual rate of progression to cancer is about 0.5% per year.

52
Q

Treatment of Barrett esophagus

A

PPIs