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GI II: Test 2 > Esophageal disorders > Flashcards

Esophageal disorders Flashcards

1
Q

SAD CREaP

A

Solids and liquids: (motility)

  • Scleroderma
  • Achalasia (watch out for “pseudoachalasia”)
  • Diffuse esophageal spasm – “corkscrew esophagus”

Solids only (mechanical)

  • Carcinoma
  • Ring(Schatski’s)*/webs**
  • Eosinophilic esophagitis
  • Peptic stricture

*distal esophagus - associated with HH and reflux symptoms
**mid or upper esophagus – congenital, epidermolysis bullosa, GVHD, pemphigus, pemphigoid,
Plummer-Vinson syndrome

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2
Q

transfer (oropharyngeal dysphagia)

A

problem with food getting from mouth to esophagus.
Causes: stroke, Parkinson’s, corticobulbar problems (ALS, MS)
Treatment:
Thickening agents:

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3
Q

Transmit dysphagia

A

Problem getting food through the esophagus to the stomach: SAD Creap

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4
Q

eosinophilic esophagitis TQ

A

Symptoms: GERD to food impaction

History: allergies/atopy-peripheral eosinophilia

Mucosa: normal to tapered strictures (could see rings)

Biopsy: eosinophilia > 20%/HPF

Treatment: swallowed fluticasone (steroids)

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5
Q

barium swallow showing “birds beak”

A

= achalasia = failure of lower esophageal sphincter to relax and aperistalsis of smooth mm. above it

Diagnosis of achalasia would be made with
- esophagography (Bird’s beak),
- endoscopy
- manometry
(absent peristalsis, elevated LES pressure, and intraesophageal pressure > gastric pressure).

see decreased numbers of neurons (ganglion cells) in m yenteric plexuses

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6
Q

barium swallow shows beading

A

think “esophageal spasm”

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7
Q

pseudoachalasia?

A

could be due to

  1. Chagas disease (Reduviid/kissing but) - Trypanasoma cruzi
    - preferentially attacks the cardiac (causing dysrrhythmias/CHF) and smooth muscle (megaesophagus + megacolon)
  2. cancer (ADCA in lower 1/3, SCC in upper 2/3)
  3. amyloidosis
  4. sarcoidosis]
  5. neurofibromatosis
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8
Q

what is ADCA of esophagus related to?

A

GERD, Barretts, obesity

located in lower 1/3

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9
Q

What is SCC of esophagus related to?

A

mostly men and blacks, mid to lower esophagus, and risk factors = ETOH, smoking, HPV, nitrates, lye, achalasia, hot liquids, tylosis, and PV syndrome.

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10
Q

antineuronal nuclear antibodies (ANNA-1)

A

produced by small cell carcinoma –> destroy the myenteric plexus, simulating achalasia.
(cancer that is a cause of “pseudoahcalasia”)

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11
Q

causes for dysphagia related to esophagitis?

A
  1. GERD with peptic stricture
  2. pills
  3. infections:
    - herpes (CD4< 500)
    - CMV = (CD 4 < 50; look for involvement of CNS, lung, colon and retina).
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12
Q

owl eyes?

A

indicates CMV, a cause of esophagitis seen in HIV+ patients w/ CD4s disease!

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13
Q

A’s of Addison’s disease? CMV is a cause of Addison’s disease…

A 
Anorexia and weight loss
Asthenia and weakness
Arterial hypotension and fatigue
Affect (flat)
Abdominal pain with N, V and D
Anxiety and personality change
Aglycemia, anatremia
Aching muscles
Apigmentation (vitiligo)
Axillary, areolar and anal pigmentation
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14
Q

which bug causes infectious chronic gastritis most often?

A

H. pylori!

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15
Q

noninfectious causes of chronic gastritis?

A
  • autoimmune = pernicious anemia

* chemicals = NSAIDs, ASA, bile reflux

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16
Q

best test for H. pylori?

A

stool antigen

can also used urea breath test

17
Q

what is nonerosive gastritis related to?

A
  1. AI gastritis = Pernicious anemia:
    - associated with parietal cell antibodies (wipes out acid producing cells)
    - achlorhydria (low gastric acid production)
    - gastric gland atrophy
    - intestional metaplasia (probably sets the stage for adenocarcinoma)
    - hypergastrinemia (may stimulate gastric enterochromaffin cells to proliferate into carcinoid tumors).
    * * carcinoid as well as ADCA!
  2. H. pylori:
    74% - mild diffuse pangastritis (acute or chronic)

15% - antral gastritis (duodenal ulcers)

1% - fundic and corpus gastritis (atrophic gastritis, gastric ulcers, metaplasia, adenocarcinoma, and MALT lymphoma)

18
Q

how can H. pylori manifest?

A

74% - mild diffuse pangastritis (acute or chronic)

15% - antral gastritis (duodenal ulcers)

1% - fundic and corpus gastritis (atrophic gastritis, gastric ulcers, metaplasia, adenocarcinoma, and MALT lymphoma)

  • antral gastritis –> stimulates gastrin output, this time the gastrin WILL interact w/ parietal cells and produces HCL –> causes duodenal ulcers
19
Q

What are causes of erosive gastritis?

A

DASH

Erosive, hemorrhagic gastritis =

  • Drugs (NSAID- especially COX-1)
  • Alcohol
  • Stress:
  • Portal Hypertensive Gastropathy (DASH).

see “coffee ground” appearance in NG tube

20
Q

What criteria are used to determine prophylaxis for stress gastritis?

A

set you up to bleed w/ erosive gastritis

Respiratory failure, especially on a respirator.

Platelets < 50,000 or PT > 1.5

Recent NSAID use and alcohol status

21
Q

causes of stress/erosive gastritis?

A 
**Mechanical ventilation (> 48 hrs)
Trauma
Burns
Shock
Sepsis
Liver and kidney disease
CNS injury
Multiorgan failure
**Coagulopathy (platelets < 50,000; INR > 1.5)

Prophylaxis should be used: enteral feeding, H2 blockers

Bleeding: tx w/ PPIs

22
Q

Menetrier’s Disease?

A

“Hypoproteinemic hypertorphic gastropathy” = allows albumin to be secreted

see hypochlorhydria (low stomach acid) as well as xs mucus secretion

see EGFR is increased in this disease –> hypertrophy of folds of stomach

= a rare, acquired, premalignant disease of the stomach characterized by massive gastric folds, excessive mucous production with resultant protein loss, and little or no acid production

tx: cetuximab (EGFR monoclonal Ab)
(note: also think ZE syndrome if see large gastric folds…)

23
Q

what test is used to determine if the protein loss is due to menetrier or liver disease?

A

24 hour feces for α-1-antitrypsin excretion (>13 ml/24 hr = abnormal), since it is not normally absorbed or secreted into the bowel.

In Menetrier disease you will see excretion of alpha1 AT in GI tract (this is not seen in liver problems of hypoalbunemia)

24
Q

portal hypertensive gastropathy

A

(PHG = “snake skin” or “mosaic stomach” - usually in fundus and body) with or without varices.

usually involves the stomach diffusely w/ dilated and twisted blood vessels

  • cause of bleeding and is an early form of portal HTN
25
Q

Triad of cirrhosis?

A
  1. Esophageal and gastric varices
  2. Encephalopathy
  3. Spontaneous Bacterial Peritonitis
26
Q

what is measurement of portal HTN?

A

Normal portal vein to inferior vena cava gradient = 2-6mm Hg. When > 10-12 mmHg = portal hypertension

27
Q

Mallory Weiss Tear

A

seen in alcoholics - d/t vomiting

  • tear is in the mucosal layer at the jn. of the esophagus and the stomach
28
Q

Boerhaave’s syndrome

A

see complete tear in the esophageal tissue

on CXR see pneumonmediastinum w/ pleural effusion

29
Q

Arterio-Venous (AV) malformations

A

can be a cause of GI bleeding:

Hereditary Hemorrhagic
Telangiectasia*, (i.e. osler-webber-rendau disease)
CREST syndrome (calcinoma, raynaud’s, sclerodactyl, esophageal, telengiectasia),
CRD

30
Q

Dieulafoy’s lesion:

A

cause of gastric bleeding

(congenital) – erosion of an ectatic artery or a “persistent caliber vessel” into the stomach - (large and submucosal)
* vessel is congenitally too close to the surface - results in acid eroding the vessel

31
Q

Watermelon stomach** TQ

A

cause of gastric bleeding

= (GAVE – gastric antral vascular ectasia) – older women with ectasia of antrum associated with scleroderma, DM, CRF, and cirrhosis (rarely)

** this is at the ANTRUM, similar to snakeskin, but its fully developed - a bunch of telangiectasia lumped together

an uncommon cause of chronic gastrointestinal bleeding or iron deficiency anemia.
The condition is associated with dilated small blood vessels in the antrum, or the last part of the stomach.[1] The dilated vessels result in intestinal bleeding
- GAVE results in intestinal bleeding similar to duodenal ulcers and portal hypertension

32
Q

Pseudoxanthoma elasticum

A

degeneration and calcification of elastic fibers in connective tissue related to mutations in the ABCC6 – ATP binding cassette which doesn’t allow vitamin K to reach peripheral tissue. Involves midlaminar layer of the dermis, Bruch’s membrane in the eye, and midsized arteries ( premature atherosclerosis).

–> results in esophageal bleeding

  • see “plucked chicken” skin appearance
33
Q

why carcinoid tumors in PA?

A

PA attacks mostly body and fundus sparing the antrum (knocking out chief and parietal cells)- G Cells in antrum are producing gastrin –> gastrinemia –> stimulates enterochromaffin cells which may produce carcinoid tumors

34
Q

causes of hypoalbunemia?

A

ddx of GI disorder should be considered after rule out nephrotic syndrome, malnutrition, and chronic liver disease

35
Q

acanthosis nigricans

A

think ADCA of stomach

36
Q

telengiectasia

A

spots seen in cirrhotic pts. - due to high levels of estrogen due to liver cirrhosis

seen in alcoholic hepatitis along w/ gynecomastia

GI II: Test 2 (6 decks)

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