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GI II Midterm > Chapter 17 - Esophagus, Stomach > Flashcards

Chapter 17 - Esophagus, Stomach Flashcards

1
Q

When do atresia, fistula and duplications of the GI tract usually present?

A

Shortly after birth
Any part of GI tract
Regurgitation during feeding

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2
Q

What is the most common form of congenital intestinal atresia?

A

Imperforate anus

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3
Q

What is agenesis?

A

Without formation, failure of development, absent

Absent esophagus extremely rare

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4
Q

What is esophageal atresia?

A

Incomplete development or closure of a normal orifice - general definition
Thin, noncanalized cord replaces a segment of esophagus, causing a mechanical obstruction
Most common at or near tracheal bifurcation - usually associated with fistula

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5
Q

What defects are associated with esophageal atresia?

A

Genital heart defects, genitourinary malformations, and neurologic disorders
Presence of congenital GI disorders should prompt evaluation of other organs

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6
Q

What can fistula lead to?

A

Aspiration, suffocation, pneumonia, and sever fluid and electrolyte imbalances

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7
Q

Describe stenosis

A

Incomplete form of atresia in which the lumen is markedly reduced in caliber as a result of fibrous thickening of the wall
Can be acquired as a consequence of inflammatory scarring (GER, irradiation, systemic sclerosis, caustic injury)
Esophagus and Small intestines most often affected

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8
Q

What is imperforate anus due to? What is it usually associated with?

A 
D/t failure of cloacal diaphragm involute 
V - Vertebral anomalies
A - Anus atresia
C - Cardiac anomalies
TE - Tracheoesophageal fistula 
R - Renal anomalies 
L - Limb anomalies
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9
Q

Globus = ?

A

Feeling like something stuck in the back of the throat

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10
Q

What are the functional causes of obstruction in the esophagus ?

A

Nutcracker esophagus (jackhammer esophagus)
Diffuse esophageal spasm
Hypertensive LES
CREST syndrome

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11
Q

What are the mechanical causes of obstruction of esophagus

A

Stricture and stenosis
Esophageal webs, Esophageal rings, Achalasia
Inflammation and scarring - Esophagitis

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12
Q

What is meckel diverticulum?

A

True diverticulum: blind pouch of alimentary tract, communicates with lumen, all three layers of bowel wall
Remnant of Vitelline duct (failed involution)
Rule of 2’s: 2% of pop, 2 ft from iliocecal, 2 in, 2x male, age 2 symptomatic
95% asymptomatic

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13
Q

What is the most common true diverticulum?

A

Meckel diverticulum

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14
Q

When does meckel diverticulum resemble acute appendicitis or obstruction?

A

When ectopic pancreatic or gastric tissue is present
Gastric secretes acid-> peptic ulcer of SI presents with occult bleeding or abdominal pain resembling acute appendicitis or obstruction

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15
Q

Describe the occurrence of Pyloric stenosis and the epidemiology

A

Congenital hypertrophic pyloric stenosis occurs 1:500 births
Male
Association with Turner syndrome and trisomy 18
Exposure to erythromycin or analogues in first 2 weeks of life
Monozygotic twins HIGH concordance rate

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16
Q

Describe symptoms and typical pt with pyloric stenosis

A

New-onset regurgitation, projectile, nonbilious vomiting after feeding
FAQ demand re-feeding
PE: firm, ovoid, 1 - 2 cm abdominal mass
3rd and 6th weeks of life presentation

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17
Q

Describe acquired pyloric stenosis?

A

Adults
Consequence of antral gastritis or peptic ulcers close to pylorus
Carcinomas of the distal stomach and pancreas may also narrow the channel due to fibrosis or malignant infiltration

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18
Q

What does Hirschrpung Dz result from?

A

Aganglionic megacolon
Results when the normal migration of neural crest cells from cecum to rectum is arrested prematurely or when the ganglion cells undergo premature death

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19
Q

Describe the epidemiology and genetics of Hirschprung Dz

A

1 in 5000
Familial and sporadic with heterozygous loss fan RET mutation chr 10
Penetrance incomplete
Isolated or combined with other abnormalities (10% w Down syndrome)
Males>F but more extensive aganglionic segments in F
4% of pts siblings affected (genetic component)

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20
Q

What is the Pathogenesis of Hirschrpung disease?

A

Disease of lack of peristalsis leading to a functional obstruction
Abnormal neuronal migration (meissner submucosal and Auerbach myenteric plexus) and ganglion cell death
Genetic component in most cases
RET

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21
Q

Describe the clinical features of Hirschrpung Dz

A

Neonatal failure to pass meconium stool
Progressive dilation and hypertrophy of unaffected proximal colon
RECTUM always affected
Abdominal distension/bilious vomiting
Can stretch near point of rupture, most likely at cecum

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22
Q

What does the diagnosis of Hirschrpung disease require?

A

Documenting the absence of ganglion cells within the affected segment

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23
Q

Describe acquired megacolon?

A

May occur at any age as a result of CHAGAS disease, bowel obstruction
Only in Chagas are ganglia actually lost

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24
Q

Esophageal webs

A

non cancerous mechanical obstruction
Ledgelike protrusions of mucosa->obstruction
Semi-circumferential lesions: fibrovascular CT
Most common in upper esophagus
Women over 40
Patterson-Brown-Kelly or Plummer-Vinson syndrome: webs associated with iron deficiency anemia (microcytic hypochromic) glossitis, cheilosis, koilonychia

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25
Q

Esophageal rings

A

Schatzki rings
Similar to webs but are circumferential and thicker and made of mucosa, submucosa, and hypertrophic muscularis propria
Distal esophagus - called A rings; squamous

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26
Q

Achalasia triad

A

Incomplete relaxation of the LES
Increase LES tone
Esophageal aperistalsis

Vagus and glossopharyngeal nerve

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27
Q

What are the S/Sx of Achalasia?

A

Dysphagia for solids AND liquids
Difficulty belching
Chest pain

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28
Q

Primary Achalasia

A

Cause unknown
Ganglion cell degeneration
Rare familial cases
Increased tone, and inability to relax LES and esophageal aperistalsis

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29
Q

Secondary Achalasia

A

T. Cruz I = Chagas disease->destroy myenteric plexus, failure of peristalsis, and esophageal dilation

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30
Q

What is the treatment for Achalasia?

A

Overcome mechanical obstruction = laparoscopic myotomy and pneumatic balloon dilation or Botox injection (block LES cholinergic neurons)

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31
Q

Nutcracker esophagus

A

Jackhammer esophagus
High-amplitude contractions of the distal esophagus that are, in part, due to loss of the normal coordination of inner circular layer and doubter longitudinal layer SM contractions

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32
Q

Diffuse esophageal spasm

A

Functional obstruction
Repetitive, simultaneous contractions of the distal esophageal SM
Increased wall stress causes diverticula to form (primarily epiphrenic diverticulum just above the LES)

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33
Q

CREST syndrome

A

Absence of altered patters of esophageal contraction
Called hypertensive LES
Distinguished from achalasia bc achalasia includes reduced esophageal peristaltic contractions
Functional obstruction

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34
Q

Zenker diverticulum

A

Pharygoesophageal diverticulum
Occur immediately above the UES
Impaired relaxation and spasm of cricopharyngeus m after swallow->increased pressure ->small out pouches/herniation
Age 50 or above

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35
Q

Mallory Weiss tears

A

Longitudinal mm tear near GE jxn
Due to severe vomit 2* to acute EtOh into—> hematemesis
Relaxation fails during prolonged vomiting -> stretch and tear
Incomplete tear

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36
Q

Boerhaave’s syndrome

A

Less common than Mallory-Weiss
Serious disorder
Transmural tearing and rupture of distal esophagus
Produces severe mediastinitis
Emergency
Chest pain, Shock, Hamman’s sign (crunching sound of heart due to pneumomediastinum), tachypnea
Diff Dx: MI

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37
Q

Esophageal varices: cause and recurrence

A 
Portal hypertension -> esophageal varices
Can cause esoph bleeding 
50% of cirrhosis; 25-40% bleed 
30% die initially 
50% recur w/i a year
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38
Q

Treatment of varices

A

Pharmacologic - splanchnic vasoconstriction
Sclerotherapy - injection of thrombotic agents
Balloon tamponade
Ligation

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39
Q

What are the main causes of esophagitis?

A 
Radiation 
Chemical
Infectious
Eosinophilic 
Most common cause is GERD
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40
Q

Radiation esophagitis

A

Intima L proliferation and luminal narrowing of submucosal and mural blood vessels
GI tract injury common

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41
Q

Chemical esophagitis symptoms and causes

A

Self-limited pain, odynophagia to hemorrhage, stricture or perforation in severe cases
Corrosives, alcohol, tobacco, hot liquids, medications
Children= cleaning product
Adult = suicide
Pill-induced: lodged in esop, dense infiltrates of neutrophils, necrosis, ulceration, eventual fibrosis

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42
Q

In what setting does infectious esophagitis occur? What organisms?

A

Uncommon in healthy
Infections occur more frequently in immunocompromised hosts
Most often d/t HSV, CMV, Fungal (MC Candidiasis)

43
Q

Morphology of infectious esophagitis

A 
Dense infiltrates of neutro present in most cases (may be absent in injury induced by chemical) 
Nonpathogenic oral bacteria are frequently found in ulcer beds 
Photogenic organisms (10%) may invade lamina propria and cause necrosis

HSV: punched out ulcer
Candidiasis: pseudomembranes
CMV: more shallow ulcers

44
Q

Eosinophilic esophagitis Sx and Patient hx

A

Increased incidence since 1978
Sx: food impaction, dysphagia or feeding intolerance, or GERD sx in infants/children
Most pts have food or seasonal allergies (Atopic) -> asthma, allergic rhinitis, atopic dermatitis
Unlike GERD, acid reflux is not prominent: high doses of proton pump Is dont work

45
Q

Eosinophilic esophagitis key histology

A

Large #s of intraepithelial eosinophils, particularly superficially

46
Q

Tx for eosinophilic esophagitis

A

Diet change to decrease exposure to food allergens and topical or systemic corticosteroids

47
Q

What is the most frequent cause of esophagitis and the most common outpatient GI diagnosis in the US? What is the mechanism?

A

GERD: reflex of gastric contents

Transient LES relaxation

48
Q

GERD is most common in what pts? What are the complications?

A

MC > 40 YOA
Peds = hiatal hernia
MC etiologies: alcohol, tobacco use, obesity, CNS depressants (vagal), pregnancy, increased intra-abdominal pressure, gastroparesis

Complications from chronic reflux: surface ulceration/inflammation, hematemesis/Elena, stricture, metaplasia

49
Q

Most common Sx of GERD in adults

A

Dysphagia, heartburn, regurgitation, Fq cough or hoarseness, excessive belching

50
Q

Most common sx of GERD in infants

A 
Vomiting often
Cough that doesnt go away
Refuse eating or trouble eating
Crying during or after feeding
Gas
51
Q

Histology of GERD

A

Mild: redness d/t simple hyperemia
Severe: Scattered intraepithelial eosinophils then neutrophils and mild basal zone expansion (hyperplasia)
Chronicity - changes in epithelium of esophagus

52
Q

Describe the classic pt w Barrett esophagus

A

Chronic GERD with intestinal metaplasia
10-20% of pts with chronic GERD
White male 40-60
Sx: heartburn, regurgitation, dysphagia

53
Q

How is Barrett esophagus diagnosed?

A

Biopsy by endoscopy to yield tissue for histology
Metaplastic columnar mucosa above GE junction
Intestinal-type metaplasia seen as replacement of squamous esophageal epithelium w goblet cells

54
Q

What is the Treatment of barrett esophagus ?

A

Esophagectomy
Photodynamic therapy
Laser ablation
Endoscopic mucosal resection

55
Q

What are the most common benign esophageal tumors?

A

Mesenchymal, Smooth muscle tumors (Leiomyomas)

Arise in the wall of the esophagus (submucosal)

56
Q

What are the most common malignant esophageal tumors?

A

Adenocarcinoma: US

Squamous cell carcinoma: MC world wide

57
Q

Adenocarcinoma of the esophagus: epidemiology, location, MC histologic type

A

White males (7x), highest risk groups
Rate increase possible d/t increase obesity related reflux and barrett esophagus
Usually distal third of esophagus d/t gastric reflux
MC histo: mucinous

58
Q

Symptoms of Adenocarcinoma of the esophagus in the setting of Barrett esophagus

A

Odynophagia, or dysphagia, vomiting with or without hematemesis, chest pain, weight loss*
When symptomatic, usually has spread to submucosal lymphatics

59
Q

What lowers the risk of Adenocarcinoma ?

A

Fruit/veggie diet

Some H. Pylori types that cause gastric atrophy -> decrease acid secretion and reflux

60
Q

Squamous cell carcinoma GI tract: most common location, pts, and risk factors

A

Middle third of esophagus -> strictures
Adults > 45 males
African americans 8x
Iran, china, Hong Kong, brazil, south africa
Risk factors: tobacco and alcohol, Tylosis (RHBDF2 mutation) - Howel-Evans syndrome

61
Q

SCC esophagus behavior

A

Insidious onset: dysphagia/odynophagia/obstruction, WL
Can invade local structures (trachea, aorta)
Most well-moderate differentiated SCCs
Like oral SCC, begins as precancerous dysplastic lesion akin to leukoplakia endoscopically
Progressive growth to ulcerative and infiltration tumor or exophytic polyploid obstructive lesion

62
Q

Prognosis of SCC esophagus

A

Endoscopy early dx: superficial tumor 5 y sr 75%
Lymph node metastasis = Poor
Depends on stage and other co-morbidities

63
Q

What inflammatory cells in mucosal inflammatory process are present in acute inflammation vs chronic ?

A

Acute: neutrophils
Chronic: Mo/monocytes and lymph’s

64
Q

Describe peptic ulcers in acute injury

A

Acute: few days after injury, small, stained brown by acid digestion or blood
Can be anywhere in stomach and often are multiple

65
Q

Describe stress-related mucosal disease

A

Focal, acute mucosal defects
Typically a consequence of NSAIDs or severe physiologic stress
Alterations in local blood flow->ischemia
Stress, curling and cushing ulcers

66
Q

Stress ulcers

A

Common with shock, sepsis, or severe trauma

Sharply demarcated with essentially normal adjacent mucosa

67
Q

Curling ulcers vs Cushing ulcers

A

Curling: proximal duodenum, occur in association with severe burns or trauma
Cushing: esophagus, stomach, duodenum; arise in pts with increased intracranial pressure and carry a high incidence of perforation

68
Q

2 Non-stress-related gastric bleeding causing acute gastritis

A

Dieulafor lesion: rare, lesser curve near GE jxn, abnormal branching of artery
Gastric antral vascular ectasia: watermelon stomach, ecstatic mucosal vessels, ass. Cirrhosis and systemic sclerosis, longitudinal stripes, can have fecal blood or iron deficiency anemia

69
Q

What are the etiologies of Chronic gastritis?

A

Infection with H. Pylori (90%)

Autoimmune gastritis

70
Q

Describe H pylori

A

Spiral-shaped or curved bacilli, flagella, urease, adhesions, CagA toxin,
Dx: antibody serologic test, urea breath test, bacterial culture
Humans 1* carrier
Epidemiology: poverty, overcrowding, limited education, ethnicity, rural, birth outside US,
Fecal-oral transmission

71
Q

Pathogenesis and morphology of Helicobacter pylori gastritis

A

Predominantly antral gastritis w/ normal or increased acid
Infected mucosa erythematous
Variable #s of intraepithelial and luminal neutrophils forming pit abscesses
Lamina propria: many plasma cells, Mo and lymphs
Warthin starry stain positive
May create thickened rural folds
Lymphoid aggregates: MALT that can become lymphoma
Multifocal atrophic gastritis - hypochlohydria

72
Q

Describe key points of autoimmune gastritis

A

Diffuse mucosal damage of oxyntic mucosa w/i body and fundus
Serum abs to parietal cells (gastric atrophy in 2-3 decades) and intrinsic factor (B12 deficiency)
Achlorhydria

73
Q

Autoimmune gastritis epidemiology

A

Women, progression occurs over 2-3 decades
Median age 60
Associated with other autoimmune diseases: Hashi, TIDM, addison,

74
Q

Pathogenesis of autoimmune gastritis

A

CD4 T cells directed against parietal cell components, including H, K ATPase, are considered to be principal agents of injury

75
Q

Morphology of autoimmune gastritis

A

Rural folds are lost
Diffuse mucosal damage of parietal cells in mainly body and fundus
Lymphs, Mo, plasma cells

76
Q

S/Sx of autoimmune gastritis

Treatment

A

B12 deficiency: atrophic glossitis, malabsorption, peripheral neuropathy, spinal cord lesions, cerebral dysfunction, megaloblastosis of RBCs and epithelial cells (pernicious anemia)
Sx may present over a few weeks with subacute combine degeneration of cord: initially bilateral numbness, and ataxia in LE but may progress to spastic weakness of LE
Treatment: vitamin replacement therapy, once complete paraplegia developed, recovery is poor

77
Q

Uncommon forms of gastritis

A

Eosinophilic, lymphocytic and granulomatous

78
Q

Eosinophilic gastritis

A 
Allergies, immune disorders, parasites, H pylori 
Many eosinophils 
Antral or pyloric region 
Allergies
Elevate serum IgE possible
79
Q

Lymphocytic gastritis

A 
Varioliform gastritis 
Women
Celiac disease (40%) 
T lymphs 
Idiopathic, non specific sx
Entire stomach
Thickened folds with central aptthous ulceration
80
Q

Granulomatous gastritis

A

Crohn disease most common
Then sarcoidosis and infection
Well-formed granulomas or aggregates of epitheliod Mo

81
Q

What is PUD due to?

A

Imbalances btw mucosal defense mechanisms and damaging factors-> chronic gastritis
Chronic mucosal ulceration affecting proximal duodenum(most) or stomach( lesser curve jnx of body and antrum)

82
Q

What are the clinical features of PUD?

A

Sx of epigastric burning or aching pain: 1-3 hours after meals/at night, or relieved with milk or OTC meds
Nausea, vomiting, bloating, belching, significant WL
Complications - chronic blood loss, hemorrhage, or perforation, obstruction (acquired pyloric stenosis) metaplasia, dysplasia
Referred pain to back, LUQ, or chest with penetrating ulcers

83
Q

What are the risk factors of PUD?

A

H pylori
Cigarette use (energizes with H pylori for gastric PUD)
NSAIDS- older pts

84
Q

Menetrier disease

A 
Rare; hypertrophic gastropathy 
30-60
Hypertrophy of rural folds 
Hyperplasia of foveolar mucous* cells 
TGF-a
Antrum spared; body and fundus location 
Precancerous - risk of gastric adenocarcinoma 
In children: self-limited and follows respiratory infection
Sx: hypoproteinemia, WL, Diarrhea
85
Q

What is gastritis cystica

A

Exuberant reactive epithelial proliferation with cysts that exhibit reactive changes that mimic invasive adenocarcinoma
Associated with chronic gastritis
Risk factors: trauma, prior surgery

86
Q

Zollinger-ellison syndrome pearls

A

Rare
50s
Sporadic: gastrin secreting tumors(gastrinomas-90% malignant) in SI or pancreas
MEN1: Werner syndrome - parathyroid, pancreas, pituitary
Duodenal ulcers, chronic diarrhea

87
Q

Inflammatory and hyperplastic polyps

A 
Benign gastric tumor
Antrum>body
75% of gastric polyps of these types
d/t chronic inflammation - H. Pylori prevalence 
Mucous cells
MC age 50-6
Complication of chronic gastritis - similar sx 
Remove if greater than 1.5 cm
88
Q

Fundic gland polyps

A

Benign gastric tumor
Sporadic (women over 50) and syndromic (FAP - only one ass with adenocarcinoma)
Increasing with PPI use–> increase gastric secretion
Asymptomatic or N/V or epigastric pain
Parietal and chief cells
Gastric body and fundus, well-circumscribed lesions with smooth surface

89
Q

Gastric adenoma

A

Benign Gastric tumor
10% of all gastric polyps
Increases with age (50-60)
Males
Antrum
Chronic gastritis with atrophy and intestinal metaplasia
Increased in FAP
Precancerous/premalignant lesions (bad if >2cm)
Solitary lesions, MC in antrum
HG dysplasia: more severe cytology atypia

90
Q

Gastric adenocarcinoma: Association, and most common in what settings and people

A

Linked to chronic gastritis and H pylori, and dietary carcinogens
More common in lower socioeconomic groups
MC setting: gastric atrophy, intestinal metaplasia (precursor), gastric adenoma (precursor), and Menetirer disease

91
Q

Pathogenesis of diffuse Gastric adenocarcinoma and epidemiology

A

Infiltrates wall diffusely, thickens it, discohesive w/ vacuoles expand cyto and nucleus pushed aside = Signet rings cells
Sporadic and familial forms
LOF CDH1 -> encodes E-Catherine on ch 16
TP 53 mutation also present
No precursor lesion***
Desmoplastic rxn that stiffens gastric wall
Leather bottle appearance - Lin itis plastic d/t large areas of infiltration, diffuse rural flattening and rigid wall
M=F, uniform across countries

92
Q

Pathogenesis of intestinal type gastric adenocarcinoma and epidemiology

A

Bulky masses composed of glandular structures, grow along cohesive fronts -> exophytic mass or ulcerated tumor
Apical mucin vacuoles w/ abundant mucin present
Sporadic and FAP
Sporadic: increased signaling via Wnt -> LOF APC -> GOF of B-catenin
Precursor lesion*** -> metaplasia, atrophy, dysplasia, adenoma, Menetrier
Male, japan, 55
Decreased incidence d/t decreased H pylori

93
Q

What are the metastatic patterns and outcome?

A

These are diagnosed in advance stage:
Virchow node: supraclavicular sentinel LN
Sister Mary Joseph nodule: periumbilical LN
Irish node: left axillary LN
Krukenberg tumor: tumor of ovary
Blumer shelf

94
Q

Where is the most common extranodal site for lymphoma?

A

GI tract, especially stomach

95
Q

How is MALT induced in the stomach?

A

Typically as a result of chronic gastritis.
H pylori infection is the most common induce in the stomach and, is found in association w most gastric MALToma
Translocations: 11,18 MC

96
Q

Histology of MALTomas in stomach

A

Marginal zone B-cell lymphoma
Diagnostic lymphoepithelial lesions
CD19 and CD20, CD43 in some

97
Q

What is carcinoid tumor?

A

Neuroendocrine tumor
Enteroendocrine cell origin (gastrin secreting cells ex)
Most in GI (SI)
Indolent course compared to adenocarcinoma
Arise de novo or with some syndromes
Peak age 60
Yellow-tan mass with chromagranin A and synptophysin

98
Q

Prognosis of Carcinoid tumor

A

Depends on site
Midgut carcinoids: ilium and jejunum - multiple and tend to be aggressive. Greater depth of local invasion, increased size, and the presence of necrosis and mitosis are associated with worse outcome
Foregut: rare metastasis
Hindgut: found incidentally (colonic can metastasize)

99
Q

What is the most useful diagnostic marker for GIST?

A

KIT - detectable in Cajal cells and 95% of gastric GISTs by immunohistochemical stains

100
Q

What is the most common mesenchymal tumor in the abdomen?

A

GIST

101
Q

Describe GIST

A

Most common mesenchymal tumor of the abdomen
Arise from interstitial cells of Cajal, or pacemaker cells or the GI muscularis propria
Half occur in stomach
Peak age 60
Carney triad, Carney-stratakis dead, NF type 1 association
Sx related to mass effect
Tyrosine kinases receptors - imitinib RX
KIT or PDGFRA mutations respond to therapy

102
Q

Carney triad

A

Nonhereditary syndrome primarily in young females including gastric GIST, paraganglioma, and pulmonary chondroma

103
Q

Carney-stratakis dead

A

GIST and paragangliomas = germline loss of SDH function (Mitochondrial succinate dehydrogenase)

104
Q

GIST clinical features and outcome

A

Sx related to mass effect
Prognosis related to tumor size (<5 cm), mitotic index, and location
Gastric GISTs are less aggressive than those in small intestine

GI II Midterm (5 decks)

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