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Rosens > 75. Esophagus, stomach, duodenum > Flashcards

75. Esophagus, stomach, duodenum Flashcards

1
Q

What are the 3 phases of swallowing?

A

oral
pharyngeal
esophageal

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2
Q

Dysphagia meaning

A

difficuklty swallowing

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3
Q

Dysphagia two types - differentiate?

A

oropharyngeal and esophageal
oro - difficultt food bolus oro to esoph vs esoph difficulty transporting material down esoph

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4
Q

Oropharyngeal dysphagia: what is mc cause?

A

neurom disease

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5
Q

Oropharyngeal dysphagia: biggest diffiuclty with what at first?

A

liquids
intermittent

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6
Q

Oropharyngeal dysphagia: how does stroke manifest?

A

failure at cricopharyngeal m to relax
can also have weak tongue, weak buccal muscles

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7
Q

Oropharyngeal dysphagia: second mc cause?

A

inflamm myopathy like polymyositis or dermatomyositis

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8
Q

Oropharyngeal dysphagia: what disease causes progressive worsening with repeat swallowing attempts, temporarily reversible with edrophonium

A

MG

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9
Q

Oropharyngeal dysphagia: 2 main categories of disease

A

NM disorders
structural

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10
Q

Structural disorders causing Oropharyngeal dysphagia: examples?

A

congenital anomaly of aortic arch
anomalous R subclavian vein (known as dysphagia lusoria) - sx as of 40s
aneurysm of aortic arch and great vessels
bronchogenic carcinoma

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11
Q

Two main categories of esophageal dysphagia?

A

mechanical
motor

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12
Q

Mechanical esophageal dysphagia: instrinsic lesions?

A

stricutre, web, ring, tumor, esophagitis, postsurg change, esophageal FB

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13
Q

Mechanical esophageal dysphagia: extrinsic lesions?

A

osteophytes
mediastinal mass
aortic aneurysm

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14
Q

Mechanical esophageal dysphagia: what is a Plummer vinson syndrome finding?

A

anterior web in esophagus

with dysphagia
IDA
cheilosis
spooning ofnails
glossitis
thin firable mucosa of mouth, pharynx and upper esophagus

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15
Q

Mechanical esophageal dysphagia: worse with what foods?

A

solids

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16
Q

Mechanical esophageal dysphagia: Extrinsic Zenker diverticulum findings?

A

progresive outpouching of pharyngeal mucosa due to failure proper relax cricopharyngeal m: noisy chewing, dysphagia, halitosis, palpable compresible mass in neck

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17
Q

Motor disorders esophageal dysphagia: DDX?

A

achalasia, diffuse esophageal spasm, nutcracker esophagus, and hypertensive lower esophageal sphincter (LES).

Systemic connective tissue diseases, such as scleroderma or CREST (calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, Chagas disease, or a paraneoplastic syndrome may cause secondary motor disorders.

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18
Q

Achalasia: what is this?

A

resting presssure LES markedly increase and peristalsis is absent in body of esophagus

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19
Q

What is nutcracker esophagus?

A

diffuse esophageal spasm - severe and prolonged with high peristaltic wafves

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20
Q

Key hx points for dysphagia

A

anatomic level
types of food
intermittent or progressive sx
GI hx
family hx

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21
Q

Oropharyngeal dysphagia vs esophgeal key points

A

oro early, aspiration, moreso liquids

vs esoph: 2-4s post swallow, substernal or retrostenal, equal f s and l

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22
Q

Dysphagia dx testing?

A

hx and pe for testing: nasopharyngoscopy if upper, decision and timing: ask consultants but barium swallows, manometry, iopedence monitoring

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23
Q

Achalasia tx

A

prior nitrates, ccb
surgical: peroral endoscopic myotomy (POEM)
?endoscopic botulinum toxin

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24
Q

4 types of pt with FB

A

ped
prisoner/psych
underlying esoph disease
edentulous pt

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25
Q

Where does esophagus begin? ie what level

A

hypopharynx at level of cricoid cartilage

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26
Q

Where are the four natural areas where FB become entrapped?

A

1, cricopharyngeus m
2. aortic arch
3. L mainstem bronchus
4. LES at diaphragmatic hiatus

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27
Q

Ped mc entrapment FB?

A

crichopharyngeal m in UES

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28
Q

How do the muscles change throughout the esophagus?

A

two main bands of muscle, an inner circu- lar layer and outer longitudinal layer. The resting tone of these muscles causes the inner epithelium to fold in on itself, effectively obliterating the lumen. Elastic fibers enable the esophageal lumen to expand and allow passage of a food bolus. The upper third of the esophagus, includ- ing the cricopharyngeus muscle, contains striated muscle to allow for the voluntary initiation of swallowing. The middle portion of the esophagus is a mixture of skeletal and smooth muscle, and the distal third is composed only of smooth muscle. Although it is relatively fixed at its origin, the esophagus becomes mobile as it traverses the medias- tinum and can be easily displaced by adjacent structures.

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29
Q

What preexisting structural abnormalities may cause worsening of FB?

A

strictures
distal esophageal mucosal rings
eoisinophilic esophagitis

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30
Q

Best imaging for FB to start?

A

upright CXR

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31
Q

When is a ct useful for FB?

A

fishbone, chicken, other nonorganic objects

also can see perf

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32
Q

Typical tx of FB?

A

flexible endoscopy

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33
Q

When do FB need to be taken out asap? (ie within 2-4 hours)

A

button batteries
magnets
large or sharp objects
coins in proximal esophagus
impactions causing difficulty secretion
food bolus with signs of high grade esoph obstruction

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34
Q

Upper esophagus - how to remove oroph FB?

A

foley past, catheter into esophagus and then inflate and pull back

bougienage also possible: esoph dilater to advance coin into stomach and then dilator removed

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35
Q

Upper esophagus - how to remove oroph FB with foley - when can i not use this technique?

A

fb impact >1 week
objects not smooth
imaging evidence of esophageal perf
underlying structural abnormality

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36
Q

What are the 3 ways FB button batteries do bad things?

A

leakage of alkaline electrolyte
pressure necrosis
generates external current causing damage to mucosa

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37
Q

What size of objects in the stomach rarely pass in the duodenum and need to be surgically removed?

A

longer than 5cm or wider than 2.5cm in diameter

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38
Q

What objects need to be surgically removed?

A

longer 5cm or wider than 2.5cm in diameter
sharp and pointy as can perf
longer than 3-4 weeks or same intestinal location x1 week

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39
Q

Esophageal perforation: where does this typically happen in esophagus?

A

distal, at pharyngoesophageal junction as wall so thin, no serosal layer to reinforce, force frewqnetly used to pass tube/scope beyond level of cricopharyngeas

or at esophagogastric junction as subject to iatrogenic injury

40
Q

Esophageal perforation: Mackler triad for spontaneous rupture?

A

subcut emphysema
chest pain
vomiting

41
Q

Esophageal perforation: complications to look out for?

A

abdo pain
hydropneumothorax
pneumomediastinum

42
Q

Esophageal perforation: pathognomonic sign?

A

Hamman
crunching on auscultation - mediastinal/cervical emphysema

43
Q

Esophageal perforation: imaging?

A

upright CXR

44
Q

Esophageal perforation: signs on CXR

A

pneumomediastinum +/- pleural effusion
subcutaneous emphysema
mediastinal widening
pulmonary infiltrates
can also look N early

45
Q

Esophageal perforation: studies?

A

barium sulfate or gastrografin (not ieal as not as dense)
*if not at risk of aspiration can start with gastrograffin - if still high risk and neg - go barium

46
Q

Esophageal perforation: tx

A

npo
abx: IV vancomycin 15 mg/kg q8h to q12h plus IV piperacillin- tazobactam 3.375 g q6h, with consideration to add empiric antifungal coverage (fluconazole 400 mg IV daily
early surgical consult

47
Q

Esophagitis causes

A

gerd
infiltration eosinophilic
infection
FB
toxic ingestion
radiation

48
Q

How does GERD occur?

A

inappropriate relaxation of LES

49
Q

Meds RF for GERD

A

nitrate
ccb
antichol
albuterol

50
Q

RF for GERD

A

meds
pregnancy, obesity
NM disorder, gastroparesis

51
Q

What is most consequential issue of gerd?

A

barrett metaplasia (risk to adeno): changes in normal stratified squamous epithelium to metaplastic columnar

52
Q

Eosinophilic esophagitis: assoc disorder?

A

atopy
eczema

53
Q

Eosinophilic esophagitis: diagnostic criteria

A

clinical sx esoph dysfunction and >15 eosinophils in one high power field on bx
lack responsiveness to high dose PPI

54
Q

Concerning infections for infective esophagitis

A

candida (ie in immuncomp hosts)
hsv
cmv
trypanosoma cruzia
cryptosporidium
PCP

55
Q

MC pill esophagitis offending meds

A

tetracycline/abx
NSAID, aspirin
antivirals
Kcl
quinidine
ferrous sulfate
alendronate
pamidronate

56
Q

Name 8 agents decreasing lower esophageal sphincter pressure causing GERD?

A

Anticholinergic drugs Benzodiazepines Caffeine
Calcium channel blockers Chocolate
Estrogen Ethanol Fatty foods Nicotine Nitrates Peppermint Pregnancy Progesterone

57
Q

Name 3 diseases that cause gerd by decreasing esophageal motility?

A

achalasia
dm
scleroderma

58
Q

Name 3 diseases that cause gerd by increasing gastric empyting time

A

anticholinergic drugs
diabetic gastroparesis
gastric outlet obstruction

59
Q

MC sx of eosinophilc esophagitis?

A

solid food dysphagia

60
Q

Lifestyle recommendations for GERD

A

avoidance of foods that can precipitate reflux (e.g., caffeine, alcohol, chocolate, fatty foods) and avoidance of acidic foods that can cause heartburn (e.g., cit- rus products, spicy foods)

w loss, smoking cessation, elevate hob, avoid recumbant several hrs after eating

**only evidence based ones

61
Q

PPI vs H2 blocker for gerd?

A

ppi better but h2 accetable if mild mod gerd (reduce potency of reflux)

62
Q

dose of famotidine for gerd

A

20 or 40mg bid vs pud 40mg qhs or 20mg bid

63
Q

dose eso for gerdd vs pud/nsaid induced ulcer

A

20 or 40 mg qd
40 mg PO qd

64
Q

dose pantoprazole gerd vs pud/nsaid induced ulcer

A

40 mg qd or 20 bid
40 mg PO qd

65
Q

Tx of eosinophilic esophagitis

A

empirical treat- ment by initiation of a daily PPI and referral to a gastroenterolo- gist for urgent endoscopy is recommended.

add therapies: eukotriene receptor antagonists, mast cell stabilizers, azathioprine, 6-mercaptopurine, and bio- logic immunomodulators.

66
Q

Oropharyngeal candidiasis tx

A

clotrimazole tro- ches (10 mg dissolved in the mouth, five times daily for 1 week) or nystatin (400,000 to 600,000 million units orally [PO] four to five times/day for 2 weeks). Patients with moderate to severe esophageal candidiasis should be treated with oral fluconazole (400 mg as a loading dose and then 100 to 400 mg daily for 14 to 21 day

67
Q

Oropharyngeal HSV1 vs cmv tx

A

Immunocompromised patients should be treated with antivirals, such as acyclovir (400 mg PO, five times/day for 7 to 14 days, or 5 to 10 mg/kg IV tid for 10 to 14 days), famciclovir (500 mg PO, tid for 10 to 14 days), or valacyclovir (1 g tid for 10 to 14 days). For CMV, initial treatment can begin with ganciclovir (5 mg/kg IV bid) or foscarnet (60 mg/kg IV tid or 90 mg/kg IV bid

68
Q

Gastritis vs PUD differentiation

A

histologic diagnosis denoting inflammation of the gastric mucosa. Hence the diagnosis of gastritis can be made only by endoscopy and biopsy. However, it is common practice for clinicians to use the term gastritis to refer to symptoms of dyspepsia

69
Q

MC cause gastritis

A

H pylori

70
Q

What is h pylori?

A

spiral, flagellated gram negative rod normally living in human stomach

71
Q

H pylori increases risk of what 2 cancers?

A

gastric carcinoma
lymphoma

72
Q

Suppurative gastritis/acute phlegmonous gastritis: what is this?

A

strep bacteria often culprit: acute infection of stomach wall

73
Q

second mc cause PUD

A

aspirin, nsaid

74
Q

top 3 highest risk NSAID for GI complication

A

indomethacin
naproxen
diclofenac

75
Q

What substances and conditions damage gastric mucosal barrier? Name 7

A

Bile
Cigarette smoke
Ethanol
Glucocorticoids
Helicobacter pylori
Nonsteroidal antiinflammatory drugs Pancreatic secretions
Shock conditions
Stress

76
Q

How do PG help GI?

A

romote mucosal integ- rity by maintaining mucosal blood flow, promoting mucosal mucus and bicarbonate formation, and reducing mucosal acid secretion

77
Q

Who is most at risk for NSAID induced gastroduodenal toxicity?

A

Patients older than 60 years, those with a prior history of an ulcer or hemorrhage, those receiving higher doses of NSAIDS, and patients concurrently taking glucocorticoids or anticoagulants

78
Q

1% of PUD is caused by acid hypersecretion - what is Zollinger-Ellison sndrome?

A

hypersecrtion caused by gastrin tumor - stimulates parietal cells for more acid

79
Q

PUD pain

A

burning or gnawing pain 2-5 hours post meal
awaken at night particular midn to 3am as gastric acid highest output 2am
relief with eating
antacid relief

80
Q

Name 4 serious complications of PUD

A

hemorrhage
perforation
penetration
GOO

81
Q

which ulcer most often causes hemorrhage?

A

dudoenal > gastric antral > gastric body

82
Q

Therapies for treating h pylori - triple

A

Clarithromycin, 500 mg bid
Plus
Amoxicillin, 1 g bid
Or
Metronidazole, 500 mg bid (if penicillin-allergic)
Plus
A PPI

83
Q

Therapies for treating h pylori - quad therapy

A

Bismuth subsalicylate (Pepto-Bismol), 525 mg PO qid
Plus
Metronidazole, 250 mg PO qid
Plus
Tetracycline, 500 mg PO qid
Plus
A PPI

84
Q

issues with mag vs aluminum vs calcium containing antacids

A

mag - diarrhea
alum - constipation
ca - milk alkali, can actually incr rebound of acid reflux

85
Q

What meds can antacids decrease absorption of ? list 3

A

warfarin
dig
some anticonvulsants
abx

86
Q

H2 blocker SE

A

central nervous system effects, such as somnolence, dizziness, and confusion. Transient increases in liver enzyme levels may be noted. Some patients may exhibit abnormalities in cardiac con- duction as the heart contains H2 receptors. Cimetidine has been shown to cause gynecomastia.

87
Q

how do ppi work?

A

H, K atpase - work by irreversibly binding to stimulated proton pumps to block the secretion of hydrogen ions.

88
Q

how do h2 blockers work?

A

Histamine is the primary stimulus to gastric acid secretion. It binds to the histamine-2 (H2) receptor located on the basolateral portion of the parietal cell to stimulate the release of hydrochloric acid

highly selective com- petitive inhibitors of histamine for the H2 receptor on parietal cells and reduce the volume of gastric juice and its hydrogen ion concentration.

89
Q

Red flag sx in PUD dx to send to gastroenterology

A

Age 55 years or older with new-onset dyspep- sia, dysphagia, progressive unintentional weight loss, persistent vomit- ing, iron deficiency anemia, or an epigastric mass.

90
Q

Which of the follow drug regimens is appropriate first-line treat- ment for Helicobacter pylori infection?
a. Bismuth subsalicylate, famotidine, and clarithromycin
b. Metronidazole and sucralfate
c. Omeprazole, amoxicillin, and clarithromycin
d. Omeprazole and bismuth subsalicylate
e. Famotidine, omeprazole, and amoxicillin

A

c

91
Q

What percentage of esophageal foreign bodies require a nonopera- tive intervention to facilitate removal?
a. <5%
b. 10% to 20%
c. 50%
d. 75%
e. >90%

A

b Most foreign bodies pass spontaneously. Approximately 10% to 20% require intervention, but less than 1% require surgery for removal.

92
Q

A 5-year-old child is brought to the emergency department (ED)
by his mother after a possible ingestion of a plastic Lego piece. He has had no pulmonary symptoms but reports difficulty swallowing and declines to drink liquids that are offered. What would be the intervention of choice?
a. Contrast-enhanced CT scan of the chest
b. Endoscopy
c. Non–water-solublebariumswallow
d. Posteroanterior and lateral chest radiography e. Water-solublebariumswallow

A

b

93
Q
  1. Which of the following statements regarding the use of glucagon in esophageal obstruction from a food bolus is true?
    a. Glucagon should be administered by the oral route.
    b. Glucagon has antiemetic properties.
    c. Glucagon can facilitate passage of a food bolus localized any- where in the esophagus.
    d. Glucagon is relatively contraindicated with sharp-edged foreign bodies.
    e. The success rate of glucagon approaches 90% when used with a few hours of food bolus impaction.
A

d

94
Q
  1. Which of the following is an indication for urgent endoscopy? a. Button battery in the stomach
    b. Chest pain due to foreign body
    c. Coin in the proximal esophagus
    d. Nausea and vomiting
    e. Object failing to pass out of the esophagus after 12 hours
A

c

95
Q
  1. Ulcers in which portion of the upper GI tract are most likely to
    perforate?
    a. Hypopharyngeal b. Esophageal
    c. Gastric—antrum d. Gastric—body
    e. Duodenal
A

e

96
Q
  1. A 32-year-old otherwise healthy man presents with acute onset of epigastric pain radiating to his chest that woke him from sleep at 2 am. It was a burning pain associated with water brash. There were no associated pulmonary symptoms. His past medical history is unremarkable except for tobacco use and heartburn. His electrocar- diogram and upright chest radiograph are normal. Vital signs and physical examination findings are unremarkable. He is currently pain free. His troponin level is normal. What is the most appropri- ate intervention?
    a. Cardiology consultation for catheterization b. Contrast-enhanced CT scan of the chest
    c. Discharge on aspirin, 325 mg once daily
    d. Serial troponins
    e. Trial of twice-daily proton pump inhibitor therapy
A

e

97
Q

A 45-year-old woman presents several hours after an upper endos-
copy with severe chest pain and neck discomfort. She is awake and alert, but rates pain as “10 of 10.” What is the most appropriate test to confirm the diagnosis?
a. Abdominalx-ray
b. Barium contrast esophagography
c. Gastrografin (water-soluble) contrast esophagography d. Ultrasound
e. Upperendoscopy

A

c

as long as awake and not risk aspiration

Rosens (48 decks)

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