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Peds GI RC > Esophagus/Stomach > Flashcards

Esophagus/Stomach Flashcards

1
Q

List parameters of the Johnson -DeMeester Score

A

o There are 6 variables in the Johnson-DeMeester or Composite pH score:
1. Percent total time pH <4 (reflux index or esophageal exposure time)
2. Percent upright time pH <4
3. Percent recumbent (supine) time pH <4
4. Number of reflux episodes
5. Number of reflux episodes with pH <4 for ≥ 5 minutes
Duration of single longest reflux (acid exposure) episode (minutes

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2
Q

How does Fundoplication reduce reflux (6)

A
  • Increasing the LES baseline pressure
  • Decreasing the number of TLESRs
  • Decreasing the nadir pressure during swallow induced relaxation
  • Increasing the length of the intra-abdominal esophagus
  • Accentuating the angle of His
  • Reducing a hiatal hernia if present
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3
Q

Side effects of baclofen (5)

A
  • dyspeptic symptoms
  • drowsiness
  • dizziness
  • fatigue
  • lower threshold for seizures
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4
Q

Side effects of metaclopramide

A

-extrapyramidal symptoms (9%)
-diarrhea (6%)
-sedation (6%)
Rare effects: dysrhythmia, resp distress/arrest, neuroleptic malignant syndrome, tardive dyskinesia

Contraindicated in infants < 1 yr due to side effects

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5
Q

Side effects of domperidone

A
  • prolongation of QTc
  • extrapyramidal CNS side effects
  • Small risk of: adverse cardiac effects - serious ventricular arrhythmia and sudden cardiac death
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6
Q

Most common complication of fundo?

A
  • postoperative dysphagia
  • failure of fundo in adults range from 3-16%
  • between 37-62% of patients are taking PPIs a few years after intervention
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7
Q

Indications for antireflux surgery

A
  • life threatening complications of GERD after failure of optimal medical treatment
  • symptoms refractory to optimal therapy after appropriate evaluation to exclude other underlying diseases
  • chronic conditions (neurologically impaired, CF) with sig risk of GERD-related complications
  • need for chronic pharmacothearpy for control of signs and/or symptoms of GERD
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8
Q

What is Strobel formula

A

0.252 x body length (cm) + 5 = length (cm) of infant esophagus

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9
Q

How do you prepare a patient for pH monitoring

A
  • fasting 3-5 hours prior to placement of transnasal probe
  • H2RA stopped 3 days prior, PPI stopped 7 days prior, antacid stopped > 6 hours prior, prokinetics stopped > 48 hours prior

Timing:

  1. pH monitoring performed > 3 hours after barium or nucleotide study
  2. study duration at least 18 - 24 hours spanning day and night
  3. GERD and esophageal acid exposure is highest during the day
  4. More reflux episodes occur during daytime than night time (due to eating and physical activity)
  5. More acid reflux events during fasting; more nonacid events during feeding
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10
Q

RI?

A

RI = reflux time
- % time pH < 4 during study
RI < 3% normal
RI > 4.5 -5 % in children and > 10% in infants = abnormal

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11
Q

How does MII testing work?

A
  • MII detects GER episodes based on changes in electrical resistance to the flow of an electrical current btw 2 electrodes placed on the probe when a liquid, semisolid or gas bolus moves btw them (measured in ohms)
  • reflux episode = impedance >50% fall in intraluminal impedance from baseline that progresses retrograde across 2 or more of the distal-most channels
  • Acidic GER - episode defined by a fall in esophageal pH decreases 4 lasting >/5 sec
  • Nonacidic GER - pH increase, remains unchanged or decreases while remaining >/4
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12
Q

Advantages of pH-MII over standard pH probe

A
  • detects NAGER
  • detects postparandial GER
  • determines height of reflux
  • determines bolus clearance
  • determines superimposed acid reflux
  • determines gas reflux
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13
Q

What is Symptom Index (SI)

A
  • percentage of symptom episodes that are related to reflux (# of reflux-related symptom episodes / total # symptom episodes x 100%)
  • consensus threshold for SI is 50%
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14
Q

What is Symptom Severity Index (SSI)

A
  • percentage of symptom-associated reflux episodes (reflux episodes associated with symptom episodes /total number of reflux episodes) x 100%
  • SSI values >/10% considered positive
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15
Q

What is Symptom Associated Probability (SAP)

A
  • used to address limitations of the SI and SSI both strongly influenced by the frequency of symptoms or reflux
  • SAP determines whether reflux-symptom correlation is statistically significant
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16
Q

What stimulates Gastrin secretion

A
  • components of meal: protein, peptides and AA in lumen of stomach
  • high gastric pH
  • gastrin releasing peptide (GRP)
  • Stomach distention
  • Vagal stimulation (mediated by GRP)
  • hypercalcemia
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17
Q

What inhibits Gastrin secretion

A
  • Fasting
  • Increased gastric acid in the stomach (negative feedback)
  • somatostatin
  • secretin
  • GIP (gastro-inhibitory peptide)
  • VIP (vasoactive intestinal peptide)
  • Glucagon
  • Calcitonin
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18
Q

Name 4 components that maintain a healthy gastric epithelium

A
  • mucus layer
  • HCO3- secretion
  • Epithelial integrity
  • surface of the stomach is hydrophobic and therefore a barrier to acid back-diffusion because of the presence of surfactant-like layer of surface-active phospholipids
  • normal blood flow
  • normal motility-clear acid
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19
Q

3 endogenous factors which stimulate gastric acid from parental cells

A

(1) ACh, released from postganglionic enteric neurons (neurocrine),
(2) gastrin, released from antral G cells (hormonal)
(3) histamine, released from oxyntic ECL cells (paracrine)

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20
Q

4 inhibitors of gastric acid

A

• The main inhibitor of acid secretion is somatostatin (released from oxyntic and antral D cells (paracrine))
• Others:
o ANP, CCK, secretin, neurotensin, glucagon-like peptide 1 (GLP-1), glicentin, oxyntomodulin, peptide YY, adrenomedullin, amylin, glucose-dependent insulinotropic polypeptide (GIP), leptin, epidermal growth factor, and interleukin-1β (IL-1β) inhibit acid secretion

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21
Q

What are 4 functions of acid

A
  • facilitate digestion of protein
  • facilitate absorption of iron
  • calcium
  • Vb12
  • prevent bacteria overgrowth, enteric infection and possibly community acquired pneumonia
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22
Q

Foods/Meds that give the appearance of bloody stools

A
  • red licorice
  • foods or drinks with red dye
  • beets
  • iron
  • pepto bismol
  • cefdinir
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23
Q

False positives of Hemoccult

A
  • red meet
  • aspirin and other NSAIDs
  • corticosteroids, phenylbutazone, reserpine, anticoagulants, antimetabolites, cancer chemotherapeutic drugs
  • alcohol in excess
  • povidone iodine solution
  • plant peroxidases: broccoli, cauliflower, radish, turnips and some melons (eaten raw in in large quantities)
  • dietary iron supplementations DO NOT produce false tests
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24
Q

False negative of Hemoccult

A
  • Ascorbic acid > 250mg/day
  • excessive vit-C enriched foods and other citrus fruits and juices
  • iron supplementation that have excess vit C
  • if intestinal bacteria degrade the Hgb to prophyrin
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25
Q

What receptors does Metaclopramide work on

A

D2 antagonist in at CTZ
5-HT4 agonist in gut

Side effects:

  • irritability
  • extrapyramidal reactions
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26
Q

What receptors does cisapride work on

A

-5-HT4 agonists and Ach release in the gut

Side effects:

  • diarrhea
  • abdo pain
  • headache
  • QT prolongation
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27
Q

What receptors does domperidone work on

A

-D2 antagonist in the gut

Side effects:
-Headache

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28
Q

What receptor does ondansetron work on

A
  • 5-HT3 antagonist at CTZ
  • decrease vagal afferents from gut

Side effect:
Headache

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29
Q

What receptor does Aprepitant work on

A

-NK1 antagonist on emesis program

Side effects:
Fatigue, dizziness and diarrhea

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30
Q

What receptor does Cyproheptadine work on

A
  • H1 antagonist
  • 5-HT2 antagonist

Side effects:

  • Sedation
  • anti-ACH effects
  • weight gain from appetite stimulation
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31
Q

What receptors does Propranolol work on

A

-B1 and B2 adrenergic antagonists

Side effects:

  • hypotension
  • bradycardia
  • fatigability
  • monitor pulse
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32
Q

What receptors does Amitriptyline work on

A
  • 5-HT2 antagonist
  • increased synaptic norepinephrine

Side effects:

  • sedation
  • anti-AcH effects
  • prolong QTc
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33
Q

Reactive gastritis histology

A
  • reactive changes in mucosa secondary to ischemia, chemical changes or trauma
  • foveolar hyperplasia, mucosal edema and paucity of inflammatory cells
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34
Q

How does prostaglandin E affect neonatal stomachs

A
  • focal foveolar hyperplasia

- antral muocsal thickening presenting as gastric outlet obstruction

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35
Q

How does NSAIDs results in gastropathy

A
  • inhibits cyclo-oxygenase-2-mediated prostaglandin production
  • prostaglandins promote gastric mucosal blood flow and secretion of mucous and bicarbonate
  • lack of prostaglandins compromises mucosal integrity and protective barrier
  • increased plt-activating factor –> platelet dysfunction
Younger children - ulceration at incisura
Older children/adults: reactive gastropathy with:
-epithelial hyperplasia
-mucin depletion
-enlarged nuclei
-smooth muscle hyperplasia
-vascular ectasia
-edema
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36
Q

Medications that cause gastropathy

A
  • valproic acid
  • dexamethasone
  • NSAIDs
  • chemotherapy
  • KCl
  • iron
  • long term fluoride ingestion
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37
Q

Causes of granulomatous gastritis

A

Noninfectious causes:

  • Crohns
  • CGD
  • sarcoidosis
  • lymphoma
  • Wegener granulomatosis

Infectious

  • TB
  • syphilis
  • histoplasmosis
  • parasites
  • foreign body granulomas
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38
Q

Causes of Lymphocytic Gastritis

A
  • celiac disease
  • Menetrier disease
  • CMV
  • Chronic varioliform gastritis
  • Crohn disease
  • idiopathic
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39
Q

Features of Menetrier disease

A
  • giant gastric folds
  • increase mucus secretion
  • decrease acid secretion
  • PLE
40
Q

Differential for giant gastric folds

A
  • lymphoma
  • H. pylori, CMV, anisakiasis
  • granulomatous gastritides
  • plasmacytoma
  • SLE
41
Q

What is the histology in Menetrier disease

A
  • elongated tortuous foveolae
  • decreased parietal and chief cell glands
  • cystic dilations
  • edematous lamina propria with increased eosinophils and lymphocytes and round cells
42
Q

What composes PPI gasropathy

A
  • long term or high dose PPI can cause Parietal cell hyperplasia
  • no dysplasia associated with
  • body and antrum studded with small 1-2 mm polyps

-typically resolves with cessation of therapy

43
Q

GI involvement in HSP

A
  • abdo pain
  • N/V
  • GI bleeding
  • intermural hematoma
  • intussusception
  • bowel infarction
  • bowel perforation
  • pancreatitis
  • appendicitis
  • cholecystitis
44
Q

Features of Pernicious anemia

A
  • achlorhydria
  • intrinsic factor deficiency
  • B12 deficiency

Histology: atrophic fundic gland gastritis and absence of parietal cells

45
Q

What are the enzymes that H. pylori release

A
  • Urease: epithelial cell damage, activates host immune system, stimulates inflammation leading to tissue damage
  • bacterial phospholipases: affect the mucosal barrier and cause cell injury
  • catalase: protects the organism from activated neutrophils
  • proteolytic enzymes: degraes mucosa
46
Q

What is CagA

A
  • cytotoxin-associated gene
  • fragment of DNA encoding for components of type 4 secretion system which enable HP to transport proteins to other cells
  • CagA+ straing increase risk of PUD and gastric cancer
47
Q

What is Vacuolating cytotoxin

A
  • pore-forming protein in 50% of H. pylori strains

- associated with severe disease as it helps protect organism from gastric acid

48
Q

What are the proposed benefits of H pylori infection

A
  • stimulation of local and systemic immune system which may help promote host defense to exogenous pathogens
  • protection from diarrheal diseases (particularly bacterial)
  • inverse relationship between incidence of H. pylori infection (CagA+) and diagnosis of allergic asthma
  • associated with increase ghrelin and decreased gastric leptin which may protect against obesity
49
Q

What is associated with adenocarcinomas in children

A

-IgA deficiency
-CVID
-ataxia-telangiectasia
-FAP
-Peutz-Jeghers
familial diffuse gastric carcinoma syndrome

50
Q

What factors allow H. pylori for gastric adaption

A
  • urease
  • motility
  • ability to adhere to gastric epithelium

-Bacteria urease hydrolyzes gastric lumina urea to form ammonia that helps neutralize gastric acid and form a protective cloud around the organism enabling it to penetrate the gastric mucus layer

51
Q

what is the length of the esophagus

A 
Birth = 8-10 cm, doubles in first year
Adult = 18-25 cm long muscular tube; ~25 cm from cricopharyngeus to LES
52
Q

Where is the UES and what is it made of

A
  • at level of cricoid cartilage
  • skeletal muscle
  • 3 structure:
  • muscle of cricopharyngeus muscle
  • lower border of the inferior pharyngeal constrictor
  • upper fibres of the esophagus
  • main muscle = cricopharyngeus
  • enervation= vagal branch of pharyngeal plexus
53
Q

What are the layers of the Esophageal mucosa

A

-three main layers:
Epithelium
Lamina propria
Muscularis mucosae

Majority of the esophagus lined with nonkeratinized stratified epithelium with distal esophagus lined with columnar epithelium

54
Q

What occurs to the basal layer of the squamous epithelium in GERD

A
  • normally Basal layer accounts for 10-15% of the epithelial thickness
  • Hyperplasia > 15% of epithelial thickness occurs in GERD and other inflammatory conditions - especially in distal esophagus
55
Q

How does swallowing occur

A
  • bolus delivered to hypopharynx by tongue and mouth musculature
  • contracted swallow includes :
  • simultaneous elevation of soft palate
  • closure of larynx/epiglottis
  • brief relaxation of cricopharyngeus to admit swallowed bolus through UES

-force applied to bolus by voluntary swallowing and esophageal peristalsis propel it through the esophageal body

56
Q

TLESR relaxations frequency

A
  • increase frequency postprandially due to gastric distention which stimulates subdiaphragmatic nerves
  • afferent sensory fibers from the stomach go to the vagal nuclei which result in efferent vagal-mediated TLESR of LES
  • normally 6x/hr, especially after meals
57
Q

What is the normal resting pressure of LES

A

-20-30 mmHg

pressure < 10 mmHg is abnormally low

58
Q

What is the criteria for dx of esophageal duplication

A
  • lay within the esophageal wall
  • covered by 2 muscle layers
  • lining compatible with that found in embryonic esophagus

-gastric mucosa frequently seen in duplications irrespective of site of origin

59
Q

What are the different variants of esophageal stenosis

A

Intrinsic congenital esophageal stenosis caused by congenital malformation of the esophageal wall

3 variants:

  • esophageal web or diaphragm
  • fibromuscular stenosis
  • cartilaginous tracheobroncial remnants
60
Q

What is the most common cause of stenosis

A

Tracheobronchial rest:

  • abnormal separation of foregut into trachea and esophagus
  • found in distal esophagus usually w/n 3 cm of gastric cardia
61
Q

Where do fibromuscular stenosis and membranous web occur

A

-middle 3rd of esophagus

  • fibromuscular stenosis has smooth wall and 1-4 cm in length; partial obstruction of esophageal lumen
  • membranous diaphragm least common
62
Q

Treatment of esophageal stenosis

A
  • excision with end-to-end anastomosis

- fibromuscular stenosis and esophageal webs are amenable to dilation

63
Q

Associated syndromes related to TEF

A
  • VACTERAL
  • CHARGE
  • Fanconi syndrome
  • T21
  • Potter syndrome
  • McKusick-Kaufman syndrome
64
Q

TEF variants and prevalence

A

Type A - Proximal atresia, distal fistula (86% most common)

Type B - Atresia alone (8%)

Type C - Proximal and distal fistula (1%)

Type D- Proximal atresia and proximal fistula - often long gap, small stomach (1%)

Type E- H type (no atresia) (4%)

65
Q

Postoperative Complications for TEF

A
  • Anastamotic leak (5-20%)
  • Anastamotic strictures (33-50%)
  • Recurrent (1-12%) missed fistula
  • GERD (25-40%) due to poor esophageal motility and altered anatomy
  • tracheomalacia (75%) in TEF
  • Barrett esophagus - long term complication of TEF
66
Q

Location in Esophageal Web

A
  • mucosal membrane occludes esophageal lumen
  • usually in proximal esophagus

Associated with TEF and zenker diverticulum

67
Q

What is Plummer-Vinson syndrome

A

-web associated with:
glossitis
IDA
koilonychias (spoon nail)

68
Q

Conditions associated with Esophageal Web

A

Inflammatory complication of:

  • Epidermolysis bullosa
  • cicatrical pemphigoid
  • SJS
  • Psoriasis
  • Idiopathic eosinophilic gastroenteritis
  • GVHD
69
Q

Esophageal ring types

A

A ring:
asymptomatic caused by hypertrophic circular muscle 1.5 - 2 cm above squamocolumnar junction

B ring: (Schatzki ring)

  • most common type
  • only mucosa
  • associated with hiatal hernia
  • can be associated with EOE

C ring:
indentation of esophagus by diaphragmatic crura

70
Q

What are the 3 phases of deglutition

A
  1. Oral: voluntary activity
    - bolus formed in oral cavity
    - mouth = sensory and motor organ
  2. Pharyngeal: reflexive and complex
    - bolus transferred through upper pharynx into esophagus by pharyngeal peristalsis
    - last for ~1 sec in health individuals
  3. Esophageal
    - peristaltic contractions propel bolus through distal esophagus into stomach
71
Q

Steps of the pharyngeal phase of deglutition

A
  • tongue loading and transport of bolus posterior in solid feeding
  • elevation of pharyngeal tube simultaneous with bolus delivery
  • velopharyngeal closure
  • relaxation of UES
  • closure of laryngeal vestibule followed by peristaltic wave in posterior pharyngeal constrictors that propels bolus past UES
72
Q

What are neurological defects that cause problems with poor motor oral-pharyngeal coordination

A

CNS:

  • head trauma
  • brain injury
  • microcephaly
  • anencephaly
  • myelomeningocele
  • Chiari malformation
  • dysautonomia

Neuromuscular disorders:

  • myotonic dystrophy
  • myasthenia gravis
  • GBS syndrome
  • poliomyelitis
  • Spinal muscular atrophy
73
Q

Differential for cricopharyngeal dysfunction

A
  • cricopharyngeal achalasia
  • muscular hyperplasia
  • cricopharyngeal discoordination
  • central or cranial nerve damage - failure to relax the UES
74
Q

Diffuse/distal esophageal spasm

A
  • simultaneous esophageal contractions after >/20% swallows
  • LES relaxation is normal
  • dysphagia caused by esophageal dilation proximal to transient muscular obstruction
  • treatment with Ca1+ channel blockers or anticholinergics
75
Q

Systemic neuromuscular disorders causing dysphagia

A
  • SLE and scleroderma
  • DM
  • thryoid disorders
  • Amyloidosis
  • Chagas disease
  • GVHD
  • mitochondrial disorders
  • paraneoplastic syndromes
76
Q

Pediatric populations at high risk for severe chronic GERD

A
  • neurologic impairment
  • obesity
  • repaired EA
  • hiatal hernia
  • treated achalasia
  • CF
  • post-lung transplantation
77
Q

Risks of fundoplication

A
  • gas bloat syndrome
  • dysphagia
  • need for reoperation
  • pooling of secretions in the esophagus with worsening aspiration
  • retching
78
Q

Risk of esophageal adenocarcinoma (EA) in barretts

A
  • intestinal-type epithelium associated with high risk of EA

- cardia type metaplasia may also be risk factor for malignancy

79
Q

Adult suggestions for surveillance for Barrett esophagus

A
  • endoscopy every 3-5 years fo Barrett esophagus w/o dysplasia
  • Every 6-12 month with low grade dysplasia
  • every 3 months with high grade dysplasia

-white light endoscopy 4 quadrant bx specimens every 2 cm (or every 1 cm in pts with known or suspected dysplasia)

80
Q

Risk factors for Candida Esophagitis

A

Immunocompromised:
-mucositis, leukopenia, steroid use, severe malnutrition, systemic disorders (HIV, Crohns) congenital or acquired immunodeficiency

Healthy:
-stasis, abnormal motility (scleroderma and achalasia), broad spectrum Abx, underlying esophageal disease (GERD and EOE) PPI use

81
Q

Treatment of Candida Esophagitis

A
  • Oral or IV fluconazole

- Oral itraconazole

82
Q

Histology of Candida Esophagitis

A
  • hyphae and unicellular form invading surface epithelium

- positive silver stain, PAS stain and gram stain

83
Q

Endoscopic findings Histology of HSV esophagitis

A

-Volcano ulcers - distinct round lesion with yellow boarders characteristic of infection after several days

Histology: findings found best at end of ulcers

a) nuclear inclusions
b) multinucleate giant cells
c) prominent mononuclear cell infiltrate

84
Q

Treatment for HSV esophagitis in immunocompromised host

A
  • acyclovir

- if acyclovir resistance = foscarnet

85
Q

Endoscopic and histological findings of CMV esophagitis

A
  • ulcerations similar to HSV but usually more linear and deeper
  • mid to distal esophagus
  • basophilic nuclear inclusions in bx from edge of ulcer
86
Q

Treatment for CMV esophagitis

A
  • ganciclovir

- foscarnet

87
Q

Histology of esophagitis

A

-2 of 3 findings present for dx

  • basal layer hyperplasia > 15% of thickness
  • elongation of stroma papillae into upper 1/3
  • presence of inflammatory cells: eosinophils, lymphocytes and neutrophils
88
Q

Composition of reflux

A
  • HCl
  • pepsin
  • bile
  • pancreatic and intestinal enzymes
89
Q

Endoscopic findings consistent with EOE

A
  • longitudinal furrowing
  • white exudate often in 1-2 mm plaques (eosinophilic microabscesses)
  • Edema
  • friability
  • trachealization/circumferential ridges
  • Tubular midesophgeal stricture –> linear rent on endoscopy
90
Q

Histological findings of EOE

A
  • Esophageal infiltrate > 15/HPF in >1 site
  • basal hyperplasia
  • papillary height increase
  • dilated intracellular spaces
  • superficial eosinophilic micro-abscesses
91
Q

Cytokines involved in EOE

A
  • IL-13

- eotaxin-3

92
Q

What type of injury is caused by:

a) acidic agents
b) alkaline agents

A

a) acidic agents: coagulation necrosis - limits penetration so damage is superficial to mucosa
b) liquefaction necrosis: very rapid transmural inflammation and edema with risk of perf

93
Q

Who and when should endoscopy be performed in caustic injury

A

Who:

  • symptomatic
  • oral burns
  • highly caustic substance

When:

  • within 24 hrs
  • < 6 hrs = may not reveal full extent
  • > 4 days = increase risk of perf
94
Q

Grading system of esophageal injury

A

-Grade 0 - normal mucosa
-Grade 1 (superficial) - muocsa edema and erythema
-Grade 2 (transmural)- friability, hemorrhages, erosions, whitish membrane and superficial ulceration
2A = superficial and noncircumferential ulcers
2B = deep focul or circumferential ulcers
-Grade 3- areas of mltiple ulceration and necrosis with brown/black or grey discoloration
Grade 3A- small scattered areas of focal necrosis
Grade 3B- extensive necrosis

95
Q

Where is the most common location of rupture in Boerhaave

A

-left posteriorlateral wall of lower 1/3 of esophagus

96
Q

Injuries related to button battery esophagus

A
  • TEF
  • esophageal perf
  • esophageal stricture
  • vocal cord paralysis from recurrent laryngeal nerve injury
  • mediastinitis
  • pneumothorax
  • cardiac arrest
  • aortoenteric fistula

Peds GI RC (12 decks)

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