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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
Esophageal rings
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
26
Achalasia triad
Incomplete relaxation of the LES Increase LES tone Esophageal aperistalsis Vagus and glossopharyngeal nerve
27
What are the S/Sx of Achalasia?
Dysphagia for solids AND liquids Difficulty belching Chest pain
28
Primary Achalasia
Cause unknown Ganglion cell degeneration Rare familial cases Increased tone, and inability to relax LES and esophageal aperistalsis
29
Secondary Achalasia
T. Cruz I = Chagas disease->destroy myenteric plexus, failure of peristalsis, and esophageal dilation
30
What is the treatment for Achalasia?
Overcome mechanical obstruction = laparoscopic myotomy and pneumatic balloon dilation or Botox injection (block LES cholinergic neurons)
31
Nutcracker esophagus
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
32
Diffuse esophageal spasm
Functional obstruction Repetitive, simultaneous contractions of the distal esophageal SM Increased wall stress causes diverticula to form (primarily epiphrenic diverticulum just above the LES)
33
CREST syndrome
Absence of altered patters of esophageal contraction Called hypertensive LES Distinguished from achalasia bc achalasia includes reduced esophageal peristaltic contractions Functional obstruction
34
Zenker diverticulum
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
35
Mallory Weiss tears
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
36
Boerhaave's syndrome
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
37
Esophageal varices: cause and recurrence
``` Portal hypertension -> esophageal varices Can cause esoph bleeding 50% of cirrhosis; 25-40% bleed 30% die initially 50% recur w/i a year ```
38
Treatment of varices
Pharmacologic - splanchnic vasoconstriction Sclerotherapy - injection of thrombotic agents Balloon tamponade Ligation
39
What are the main causes of esophagitis?
``` Radiation Chemical Infectious Eosinophilic Most common cause is GERD ```
40
Radiation esophagitis
Intima L proliferation and luminal narrowing of submucosal and mural blood vessels GI tract injury common
41
Chemical esophagitis symptoms and causes
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
42
In what setting does infectious esophagitis occur? What organisms?
Uncommon in healthy Infections occur more frequently in immunocompromised hosts Most often d/t HSV, CMV, Fungal (MC Candidiasis)
43
Morphology of infectious esophagitis
``` 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
Eosinophilic esophagitis Sx and Patient hx
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
Eosinophilic esophagitis key histology
Large #s of intraepithelial eosinophils, particularly superficially
46
Tx for eosinophilic esophagitis
Diet change to decrease exposure to food allergens and topical or systemic corticosteroids
47
What is the most frequent cause of esophagitis and the most common outpatient GI diagnosis in the US? What is the mechanism?
GERD: reflex of gastric contents | Transient LES relaxation
48
GERD is most common in what pts? What are the complications?
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
Most common Sx of GERD in adults
Dysphagia, heartburn, regurgitation, Fq cough or hoarseness, excessive belching
50
Most common sx of GERD in infants
``` Vomiting often Cough that doesnt go away Refuse eating or trouble eating Crying during or after feeding Gas ```
51
Histology of GERD
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
Describe the classic pt w Barrett esophagus
Chronic GERD with intestinal metaplasia 10-20% of pts with chronic GERD White male 40-60 Sx: heartburn, regurgitation, dysphagia
53
How is Barrett esophagus diagnosed?
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
What is the Treatment of barrett esophagus ?
Esophagectomy Photodynamic therapy Laser ablation Endoscopic mucosal resection
55
What are the most common benign esophageal tumors?
Mesenchymal, Smooth muscle tumors (Leiomyomas) | Arise in the wall of the esophagus (submucosal)
56
What are the most common malignant esophageal tumors?
Adenocarcinoma: US | Squamous cell carcinoma: MC world wide
57
Adenocarcinoma of the esophagus: epidemiology, location, MC histologic type
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
Symptoms of Adenocarcinoma of the esophagus in the setting of Barrett esophagus
Odynophagia, or dysphagia, vomiting with or without hematemesis, chest pain, weight loss* When symptomatic, usually has spread to submucosal lymphatics
59
What lowers the risk of Adenocarcinoma ?
Fruit/veggie diet | Some H. Pylori types that cause gastric atrophy -> decrease acid secretion and reflux
60
Squamous cell carcinoma GI tract: most common location, pts, and risk factors
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
SCC esophagus behavior
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
Prognosis of SCC esophagus
Endoscopy early dx: superficial tumor 5 y sr 75% Lymph node metastasis = Poor Depends on stage and other co-morbidities
63
What inflammatory cells in mucosal inflammatory process are present in acute inflammation vs chronic ?
Acute: neutrophils Chronic: Mo/monocytes and lymph's
64
Describe peptic ulcers in acute injury
Acute: few days after injury, small, stained brown by acid digestion or blood Can be anywhere in stomach and often are multiple
65
Describe stress-related mucosal disease
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
Stress ulcers
Common with shock, sepsis, or severe trauma | Sharply demarcated with essentially normal adjacent mucosa
67
Curling ulcers vs Cushing ulcers
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
2 Non-stress-related gastric bleeding causing acute gastritis
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
What are the etiologies of Chronic gastritis?
Infection with H. Pylori (90%) | Autoimmune gastritis
70
Describe H pylori
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
Pathogenesis and morphology of Helicobacter pylori gastritis
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
Describe key points of autoimmune gastritis
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
Autoimmune gastritis epidemiology
Women, progression occurs over 2-3 decades Median age 60 Associated with other autoimmune diseases: Hashi, TIDM, addison,
74
Pathogenesis of autoimmune gastritis
CD4 T cells directed against parietal cell components, including H, K ATPase, are considered to be principal agents of injury
75
Morphology of autoimmune gastritis
Rural folds are lost Diffuse mucosal damage of parietal cells in mainly body and fundus Lymphs, Mo, plasma cells
76
S/Sx of autoimmune gastritis | Treatment
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
Uncommon forms of gastritis
Eosinophilic, lymphocytic and granulomatous
78
Eosinophilic gastritis
``` Allergies, immune disorders, parasites, H pylori Many eosinophils Antral or pyloric region Allergies Elevate serum IgE possible ```
79
Lymphocytic gastritis
``` Varioliform gastritis Women Celiac disease (40%) T lymphs Idiopathic, non specific sx Entire stomach Thickened folds with central aptthous ulceration ```
80
Granulomatous gastritis
Crohn disease most common Then sarcoidosis and infection Well-formed granulomas or aggregates of epitheliod Mo
81
What is PUD due to?
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
What are the clinical features of PUD?
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
What are the risk factors of PUD?
H pylori Cigarette use (energizes with H pylori for gastric PUD) NSAIDS- older pts
84
Menetrier disease
``` 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
What is gastritis cystica
Exuberant reactive epithelial proliferation with cysts that exhibit reactive changes that mimic invasive adenocarcinoma Associated with chronic gastritis Risk factors: trauma, prior surgery
86
Zollinger-ellison syndrome pearls
Rare 50s Sporadic: gastrin secreting tumors(gastrinomas-90% malignant) in SI or pancreas MEN1: Werner syndrome - parathyroid, pancreas, pituitary Duodenal ulcers, chronic diarrhea
87
Inflammatory and hyperplastic polyps
``` 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
Fundic gland polyps
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
Gastric adenoma
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
Gastric adenocarcinoma: Association, and most common in what settings and people
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
Pathogenesis of diffuse Gastric adenocarcinoma and epidemiology
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
Pathogenesis of intestinal type gastric adenocarcinoma and epidemiology
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
What are the metastatic patterns and outcome?
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
Where is the most common extranodal site for lymphoma?
GI tract, especially stomach
95
How is MALT induced in the stomach?
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
Histology of MALTomas in stomach
Marginal zone B-cell lymphoma Diagnostic lymphoepithelial lesions CD19 and CD20, CD43 in some
97
What is carcinoid tumor?
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
Prognosis of Carcinoid tumor
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
What is the most useful diagnostic marker for GIST?
KIT - detectable in Cajal cells and 95% of gastric GISTs by immunohistochemical stains
100
What is the most common mesenchymal tumor in the abdomen?
GIST
101
Describe GIST
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
Carney triad
Nonhereditary syndrome primarily in young females including gastric GIST, paraganglioma, and pulmonary chondroma
103
Carney-stratakis dead
GIST and paragangliomas = germline loss of SDH function (Mitochondrial succinate dehydrogenase)
104
GIST clinical features and outcome
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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