Scleroderma (Progressive Systemic Sclerosis) Flashcards

(52 cards)

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

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
The most common pills causing esophagitis are
``` 1-alendronate, 2-quinine, 3-risedronate, 4- vitamin C, 5-potassium chloride, 6-doxycycline, 7-NSAIDs, and iron sulfate. ```
26
Consider pill esophagitis in a young patient who takes......... and who has an..........
acne medication | acute onset of odynophagia
27
Pill esophagitis is prevented by
swallowing pills in the upright position and drinking enough water to flush them into the stomach
28
Clinical Presentation of Eosinophilic Esophagitis
1-infiltration with eosinophils 2- no improvement after an 8-week trial of PPIs GERD can mimic EE
29
Treatment of Eosinophilic Esophagitis
1-fluticasone or budesonide 2-If the biopsy shows eosinophils, give PPIs before swallowed steroids.
30
define Zenker diverticulum
outpocketing of the posterior pharyngeal constrictor muscles at the back of the pharynx
31
Clinical Presentation of Zenker diverticulum
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
Treatment of Zenker diverticulum
1-surgical resection | 2-Endoscopy and the placement of NGtubes are contraindicated because they could perforate the pharynx.
33
define Mallory-Weiss syndrome
nontransmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting.
34
Clinical Presentation of Mallory-Weiss Syndrom
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
Diagnosis of Mallory-Weiss Syndrom
direct visualization on upper endoscopy
36
Treatment of Mallory-Weiss Syndrome
1-will resolve spontaneously | 2-inject the tear with epinephrine or perform cauterization
37
causes of epigastric pain
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
Helicobacter pylori is most strongly associated with the development of
duodenal ulcers, gastric ulcers, and gastritis.
39
define nonulcer dyspepsia
a functional disorder in which there is persistent pain in the epigastric area but all tests are found to be normal.
40
patients with dyspepsia and alarm features require
upper endoscopy
41
Alarm features for patients with EPIGASTRIC PAIN
* 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
Treatment of epigastric pain
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
Gastroesophageal reflux disease (GERD) is caused by
abnormal flow of the acid gastric contents backward from the stomach up into the esophagus.
44
number of factors can cause decreased tone or loosening of LES are
* Nicotine, alcohol, caffeine * Peppermint, chocolate * Anticholinergics * Calcium-channel blockers * Nitrates
45
Clinical Presentation of GERD
``` 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
The most accurate diagnostic test for Gastroesophageal Reflux Disease is
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
What is the order when working up GERD
• 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
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
initiate therapy immediately with antisecretory medications such as PPIs.
49
Treatment of GERD is
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
define Barrett Esophagus
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
Patients with Barrett esophagus should have
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
Treatment of Barrett esophagus
PPIs