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GI II Exam 1 > Chapter 17 (Part 1): Esophagus and Stomach > Flashcards

Chapter 17 (Part 1): Esophagus and Stomach Flashcards

1
Q

What are 4 common congenital abnormalities of the GI tract? (EA/MD/PS/HD)

A
  1. Esophagela Atresia
  2. Meckel Diverticulum
  3. Pyloric Stenosis
  4. Hirschsprung Disease
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2
Q

What is Esophageal Atresia with Tracheoesophageal Fistula?

A
  • thin, noncanalized cord causes mechanical obstruction, usually presents with fistula
  • commonly blind upper segment with fistula connecting lower segment of esophagus to trachea
  • swallowed material/gastric fluids can enter respiratory tract = aspiration, suffocation, pneumonia, severe electrolyte imbalance
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3
Q

What is the most common form of congenital intestinal atresia?

A

Imperforate Anus

  • failure of cloacal membrane to involute during development
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4
Q

What is Meckel Diverticulum?

What is an acquired Diverticula?

A
  • a true diverticulum (all 3 layers of bowel wall are present); persistant vitelline duct connecting lumen of developing gut (ileum) to yolk sac
  • can have ectopic pancreatic/gastric tissue that can perforate = symptomatic; ulceration of mucosa with bleeding and abdominal pain (RESEMBLES APPENDICITIS)

AD: common occurs in sigmoid colon (NO muscularis propria, might have attenuated muscularis propria)

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5
Q

What are the Rule of 2’s for Meckel Diverticulum?

A

occurs in 2% of population, within 2 feet of ileocecal valve, usually 2 inches long and 2x more common in MALES, and symptomatic by age 2

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6
Q

What is Pyloric Stenosis?

What 4 things is it associated with, what does it look like, and how is Acquired Pyloric Stenosis different?

A
  • congenital hypertrophic pyloric stenosis (hyperplasia of muscularis propria blocking outflow tract)
  • 3-5x more common in MALES, associated with Turner Syndrome/Trisomy 18, erythromycin/azithromycin exposure in first 2 weeks of life, or monozygotic twins
  • regurgitation and projectile nonbillous vomiting (after feeding) with palpable olive-sized mass in RUQ (MUST SURGICALLY SPLIT MUSCLES)

APS: in adults with antral gastritis or peptic ulcers
- carcinomas of distal stomach/pancreas can cause

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7
Q

What is Hirschsprung Disease?

What is a common clinical sign and what are the genetics associated with the disease?

A
  • congenital aganglionic megacolon (both submucosal and myenteric plexuses are absent –> neural crest cells fail to migrate from cecum or undergo premature death)
  • no rhythmic peristalsis = distension that can RUPTURE; Rectum always affected
  • associated with Down Syndrome; failure to pass meconium in immediate post-natal period and potentially billous vomiting

Familial: LOF in RET (RTK)
Sex-linked: more likely in males, females have longer length of involvement

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8
Q

How can Hirschsprung Disease be diagnosed and what treatment options are available?

What is Acquired Megacolon?

A

D: stain for ganglion cells with H/E and immune stain for acetylcholinesterase (GET BIOPSY)

T: surgical resection of aganglionic segment

AM: occurs at any age due to loss of ganglion cells
- associated with CHAGAS disease

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9
Q

What are three forms of Esophageal Dysmotility and what kind of pain do they commonly mimic?

A

Nutcracker Esophagus, Diffuse Esophageal Spasm, and Hypertensive Lower Esophageal Sphincter

  • mimic MI pain
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10
Q

What is the difference between:

Nutcracker Esophagus
Diffuse Esophageal Spasm
Hypertensive Lower Esophageal Sphincter

A

NE: high amplitude contractions of distal esophagus
- loss of normal coordination between inner/outer SM

DES: repetitive, simultaneous contract. of distal eso.

  • diffuse “corkscrew” appearance
  • chest pain when swallowing cold food

HLES: high resting pressure OR incomplete relaxation
- present in two above conditions

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11
Q

What is a Zenker Diverticulum?

A
  • functional obstruction located immediately above the upper esophageal sphincter in pts. after age 50
  • accumulate significant amounts of food and can lead to regurgitation and halitosis (“bad breath”)
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12
Q

What are 4 common causes of mechanical esophageal obstruction? (EMW/ER/A/E)

A

esophageal mucosal webs
esophageal rings (Schatzki rings)
Achalasia
Esophagitis

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13
Q

Esophageal Mucosal Webs vs Esophageal Rings

What syndrome is associated with esophageal mucosal webs?

A

EMW: idiopathic. mucosa ledges that are SEMI-circumferential

  • females > 40
  • associated w/GERD, Celiacs, graft vs host disease
  • *Plummer Vinson (Paterson-Brown-Kelly) Syndrome**
    • upper esophageal mucosal webs
    • iron deficiency, glossitis, cheilosis (corners of mouth)

ER: circumferential; mucosa/submucosa/muscularis propria; usually in DISTAL esophagus (SCHATZKI)

  • CAN involve all layers of esophagus
  • A type (above GE junction; squamous mucosa)
  • B type (gastric-cardia mucosa)
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14
Q

Achalasia

What is it, what triad is associated with it, and what is a common sign associated with it?

A
  • inc. tone of lower esophageal sphincter due to impaired SM RELAXATION

Triad: incomplete LES relaxation, inc. LES tone, lack of esophageal peristalsis

Sign: “bird-beak” appearance on Barium Swallow

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15
Q

What is the difference between Primary and Secondary Achalasia?

A

P: idiopathic

  • distal esophageal inhibitory neuron degeneration
  • neurons cannot induce LES relaxation

S: Chagas disease (Trypanosoma cruzi)

  • destruction of myenteric plexus
  • also lesions of dorsal motor nuclei, Downs, Allgrove syndrome, or immune mediate destruction (HSV1)
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16
Q

What is the difference between Mallory-Weiss Tears and Boerhaave Syndrome?

What sign is associated with Boerhaave?

A

MW: longitudinal lacerations near GE junction mucosa

  • severe retching 2nd to ALCOHOL INTOXICATION
  • MOST common Non-Cancerous structural problem
  • NOT FATAL

BS: transmural tearing and rupture of distal esophagus

  • severe mediastinitis presenting like heart attack
  • full thickness tear = FATAL
  • HAMMAN’S SIGN

Hammans Sign = crackling/crunching on auscultation of mediastinum due to pneumoperitoneum

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17
Q

How do radiation, chemicals, and infectious microbes cause esophagitis?

A

stratified squamous epithelial damage

R: luminal narrowing that can take years to develop fibrosis following radiation therapy

C: pill-induced (pills become stuck and dissolve in esophagus) or ingestion of caustic agents (children)

I: invade lamina propria and cause necrosis of mucosa

  • HSV: punched-out ulcers w/viral inclusions
  • dense neutrophilic infiltrates (granulation)
  • also candidiasis and CMV (immunocompromised)
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18
Q

Reflux Esophagitis (GERD)

What is it, what are 4 common symptoms, and how is it treated?

What is its most common cause?

A
  • mucosal injury due to reflux of gastric juices (most common cause of esophagitis and outpatient GI diagnosis) in pts > 40 yo
  • heartburn, dysphagia, regurgitation of SOUR tasting contents, and inc. saliva (severity NOT related to histological damage)

T: symptomatic relief with PPIs

  • commonly caused by transient LES relaxation
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19
Q

Eosinophilic Esophagitis

What is it, what disorders is it commonly associated with, and how is it treated?

A
  • large numbers of intraepithelial eosinophils (superficially) and is associated with Food/Seasonal allergies
  • patients usually have ATOPIC disorders, such as atopic dermatitis

T: dietary restriction +/- topical/systemic corticosteroids

D: see > 25 eosinophils per high powered field

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20
Q

Esophageal Varices

What are they, what are the two most common causes, and how do they present clinically?

How is it treated? (3)

A
  • distension of subepithelial/submucosal venous vessels in DISTAL esophagus and PROXIMAL stomach due to collateral channel formation

CC: 50% of pts w/liver cirrhosis and hepatic schistosomiasis (“snail fever” - 2nd MC cause)

C: silent until rupture –> catastrophic hematemesis (30% die due to direct consequence and 50% recur within a year with SAME mortality rate)
- hypovolemic shock and hepatic coma

T: splanchnic vasoconstriction, balloon tamponade, variceal ligation (prophylactically with beta blockers)

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21
Q

Barrett Esophagus

What is it, what does it put a pt at increased risk for development of, and how is it diagnosed?

What is a key histological structure that can help diagnose this condition?

A
  • chronic GERD complication causing change from stratified squamous epithelium –> columnar epithelium in the esophagus (GOBLET CELLS and SALMON COLORED MUCOSA)
  • inc. risk of esophageal ADENOCARCINOMA (BE is a precursor lesion, but most do NOT develop it)

D: BIOPSY and ENDOSCOPY (requires intestinal-type columnar epithelium - GOBLET CELL PRESENCE)

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22
Q

What are the two most common forms of esophageal tumors?

What are most benign esophageal tumors?

A

Squamous Cell Carcinoma or Adenocarcinoma

  • most benign tumors are LEIOMYOMAS (mesenchymal origin) from submucosa and can cause OBSTRUCTIONS
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23
Q

Esophageal Adenocarcinoma

What causes it (3), who is at risk (2), and what does it look like?

A
  • most from Barrett Esophagus or obesity GERD (also tobacco and radiation exposure); also H. pylori

Risk: US/Australia/Canada; caucasian men (7x inc)

  • mostly in DISTAL esophagus and can invade adjacent cardia (tumors produce mucin –> GLANDS)

**by times symptoms appear, most have likely spread to submucosal lymphatic vessels)

24
Q

What are the genetics for Esophageal Adenocarcinomas (5) and Squamous Cell Carcinomas (5)?

A

AC: early (TP53, CDKN2A) and late (EGFR, Cyclin D1/E, MET)

SCC: HPV infection, SOX2 amp., Cyclin D1 overexpression, tumor suppressors (TP53, NOTCH1 LOF)

25
Q

Esophageal Squamous Cell Carcinoma

What is it, who is at risk (5), and how does it present clinically?

What syndrome is associated with it and what does it look like?

A
  • squamous dysplasia (gray-white plaque) that can invade deep into adjacent structures; usually well differentiated with HALF occuring in MIDDLE esophagus

Risk: Iran/China/Hong Kong; black men (8x inc), alcohol-tobacco synergy, Tylosis (RHBDF2 mutation), hot drinks, poverty

C: insidious onset: hemorrhage, sepsis (ulceration), iron deficiency, tracheoesophageal fistula formation

Howel-Evans Syndrome (Tylosis) = marked squamous hyperplasia of hands and feet

26
Q

What are 4 causes of acute blood loss from the stomach? (AG/SRMD/DL/G)

A

acute gastritis
stress-related mucosal disease
dieulafoy lesion
GAVE (watermelon stomach)

27
Q

What is the difference between Acute Gastritis and Gastropathy?

A

AG: transient mucosal inflammation w/NEUTROPHILS
- usually self-limited; can become more severe

G: mucosal inflammation with scant inflammatory cells
- due to NSAIDS, alcohol, bile, stress, portal HTN

28
Q

What does Acute Gastritis look like?

A
  • moderate edema with slight vascular congestion; more severe = erosion –> hemorrhage/ulcers
  • foveolar cell hyperplasia and corkscrew profiles
  • presence of NEUTROPHILS (abnormal –> means gastritis)
29
Q

Stress-Related Mucosal Disease

Stress Ulcers vs Curling Ulcers vs Cushing Ulcers

A

SU: common in pts with shock, sepsis, severe trauma

Curling: severe burns or trauma
- in PROXIMAL DUODENUM

Cushing: inc. intracranial pressure; inc. perforation

  • direct stimulation of vagal nuclei = acid secretion
  • can occur in stomach, duodenum, esophagus
30
Q

Stress-Related Mucosal Disease

What causes it, what do they look like, and how do they present clinically?

A
  • related to local ischemia
  • multiple, shallow ulcers found anywhere in the stomach with a brown base and NO adjacent mucosal damage

C: healing takes days-weeks and is determined by ability to correct underlying conditions (correction = normal re-epithelialization)

31
Q

GAVE Syndrome vs Dieulafoy Lesion

A

GAVE: longitudinal stripes of edematous, erythematous mucosa alternating with paler mucosa

  • “Watermelon” stomach appearance
  • fecal blood or iron deficiency anemia

DL: improperly branched submucosal artery in wall of stomach, usually along lesser curvature
- diameter can reach 10x greater than capillary

32
Q

What are two most common causes of Chronic Gastritis and how can they be differentiated from Acute Gastritis?

A

H. Pylori infection and Autoimmune Gastritis

  • H. Pylori most common cause
  • AG most common cause of diffuse atrophic gastritis
  • mainly see lymphocytes and macrophages in these two conditions, versus neutrophils presence in Acute Gastritis

hematemesis is RARE

33
Q

H. Pylori Chronic Gastritis (Type B)

What is it, how is it transmitted, and what are its 4 virulence factors? (F/U/A/C)

A
  • curved/spiral Gram (-) bacilli causing ANTRAL gastritis with normal/inc. acid production and can evolve to multifocal atrophic gastritis (involves body and fundus)
  • transmitted fecal-orally, usually in low income areas or rural locations; inc. risk if Hispanic or African American

VF: flagella, urease (elevates gastric pH), adhesins, CagA (cytotoxin –> inc. risk of gastric cancer –> multifocal atrophic gastritis)

34
Q

H. Pylori Chronic Gastritis (Type B)

What does it look like, what two stains can be used to visualize infection, and how can it be diagnosed?

A
  • bugs located in superficial mucosa (ANTRUM) of surface/neck epithelium and lamina propria w/macrophages and lymphocytes
  • mucosa is erythematous and coarse –> nodular; use Warthrin-Starry Stain or Giemsa-Wright to see bugs

D: antibodies (serology), fecal bacteria detection, UREA BREATH TEST, BIOPSY (gold standard)

35
Q

Autoimmune Chronic Gastritis (Type A)

What is it, what does it destroy, and what does it look like?

A
  • antibodies to PARIETAL cells (H/K ATPase) and INTRINSIC FACTOR that SPARES the ANTRUM; associated with hypergastrinemia (NOT H. PYLORI)
  • CHIEF cells are collateral damage; can cause B12 deficiency –> Pernicious Anemia w/hypersegmented neutrophils (60 yo)
  • mainly atrophy in BODY/FUNDUS; rugal folds are lost giving stomach smooth appearance; can see blood vessels because mucosa is THIN
36
Q

What cancers are H. Pylori and Autoimmune Gastritis associated with?

A

HP: adenocarcinoma, MALToma

A: adenocarcinoma, carcinoid tumors

37
Q

Autoimmune Chronic Gastritis (Type A)

How does it present clinically and what is it associated with?

A

C: atrophic glossitis, megaloblastic RBCs with hypersegmented neutrophils, and peripheral neuropathies
- most are B12 Deficiency symptoms

  • associated with AUTOIMMUNE DISEASES`
38
Q

Uncommon Forms of Gastritis

Eosinophilic Gastritis vs Lymphocytic Gastritis vs Granulomatous Gastritis

A

EG: heavy eosinophilic infiltrate (mucosa/muscularis)

  • antral and pyloric regions
  • history of food/environmental allergies

LG: idiopathic, mainly FEMALES (CELIAC DISEASE)

  • inc. in intraepithelial CD8 T-Cells (entire stomach)
  • thick folds with small nodules (central ulceration)

GG: any gastritis with granulomas or macrophages agg.

  • gastric involvement by Crohn Disease MC
  • narrowing/rigidity of gastric antrum
39
Q

Peptic Ulcer Disease

What is it, what is its risk of becoming cancer, and how does it present clinically?

A
  • chronic mucosal ulcerations of lesser curvature of stomach or proximal duodenum (inc. acid secretion and H. pylori/NSAIDs) –> develops due to chronic gastritis
  • sharply punched out defect (usually solitary) most commonly found in proximal duodenum (heaped peripheral margins = MALIGNANCY, but otherwise rarely transforms to cancer)

C: epigastric pain/burning (night, after meals, LUQ/chest/back), referred pain (rule out MI), relief with milk

perforation is rarely first indication

40
Q

What is Gastritis Cystica?

A
  • exuberant epithelial proliferation with entrapment of epithelium-lined cysts that is associated with chronic gastritis (trauma-induced)
  • mimics invasive adenocarcinoma
41
Q

What are two common Hypertrophic Gastropathies?

A

Menetrier Disease and Zollinger-Ellison Syndrome

  • uncommon diseases characterized by giant “cerebriform” enlargement of rugal folds due to epithelial hyperplasia without inflammation
42
Q

Menetrier Disease

What is it, what does it look like, and how does it present clinically?

A
  • foveolar cell hyperplasia of BODY/FUNDUS (overexpression of TGF-a)
  • irregular enlargement of gastric rugae with elongated glands in “corkscrew” appearance with cystic dilations

C: weight loss, diarrhea, peripheral edema (hypoproteinemia); inc. risk of adenocarcinoma in adults

T: IV albumin and TGF-a blockers

43
Q

Zollinger-Ellison Syndrome

What is it, how does it present clinically, and how is it treated?

A
  • gastrinoma of small intestine/pancreas (gastrin-secreting tumor) leading to proliferation of gastric parietal cells
  • leads to doubling of oxyntic mucosal thickness due ot 5x inc. in parietal cells and hyperplasia of mucous neck cells

C: duodenal ulcers and/or chronic diarrhea, with inc. risk of gastric endocrine cell proliferation

T: PPI (blocks acid), allow ulcers to heal, then treat tumor

44
Q

What are 3 benign stomach tumors and what are 4 malignant stomach tumors?

A

B: Hyperplastic (inflammatory) polyps, Fundic Gland Polyps, Gastric Adenoma

M: Gastric Adenocarcinoma, Lymphoma, Carcinoid, GIST (gastrointestinal stromal tumor)

45
Q

Hyperplastic (Inflammatory) Polyps

A
  • most common polyp and is associated with chronic gastritis (H. Pylori)
  • pts 50-60 yo
  • multiple ovoid polyps with smooth surface and edematous lamina propria
46
Q

Fundic Gland Polyps

A
  • develop in BODY and FUNDUS, and occur sporadically or in pts with Familial Adenomatous Polyposis (FAP)
  • inc. incidence associated with PPI use
  • well-circumscribed lesions with smooth surface, FAP mutations, little/no inflammation; cystically dilated with flattened Parietal/Chief Cells

Sporadic = no cancer risk/FAP = dysplasia/cancer

47
Q

Gastric Adenoma

A
  • associated with FAP and chronic gastritis; are pre-malignant neoplastic lesions (transformation risk MUCH higher with larger size)
  • MALES; occurs solitarily on ANTRUM
  • dysplasia resembles intestinal type columnar epithelium
48
Q

Gastric Adenocarcinoma

Who does it commonly affect, what mutation is present in both forms, and what are two sites of metastases that are commonly detected at diagnosis?

A
  • most common malignancy of the stomach (ANTRUM)
  • high risk in JAPAN, China, Costa Rica, Eastern Europe; common in lower socioeconomic groups and w/H. Pylori infection
  • gastric dysplasia and adenomas are precursor lesions; most have TP53 mutations
  • metastases usually present at time of diagnosis (Virchow Node and Krukenberg Tumor - ovary)
49
Q

Diffuse Type Gastric Adenocarcinoma

What does it look like, what are the two genetic components of it (C/B), and what are two characteristic morphological features (SR/LP)?

A
  • sporadic and familial forms that infiltrate stomach walls, causing them to thicken (LOSS OF E-CADHERIN)
  • early satiety (stomach cannot expand); uniformly across globe with NO gender preference
  • loss of CDH1 and BRCA2
  • “Signet Ring” cells (large intracellular vacuoles that push nucleus to periphery) and Linitis Plastica (diffuse rugal flattening and thickened walls –> leather bottle appearance)
50
Q

Intestinal Type Gastric Adenocarcinoma

A
  • sporadic and FAP forms causing bulky masses that develop from precursor lesions
  • 55 yr old at presentation with MALE predominance (mainly in high risk areas)
  • inc. Wnt signaling, LOF in APC/CDKN2A/TGFb, and GOF in B-catenin
  • grow on broad cohesive fronts to form exophytic mass or ulcerated tumor; early symptoms resemble chronic gastritis and PUD
51
Q

What is the best prognostic indicator for gastric cancer?

A

depth of invasion and extent of nodal/distant metastases at time of diagnosis

  • local invasion of duodenum, pancreas, retroperitoneum
52
Q

Gastric MALToma (Lymphoma)

Where does it occur, what is it commonly caused by, and what does it look like?

What is the most common translocation associated with it?

A
  • extranodal lymphoma commonly arising in sites devoid of organized lymphoid tissue (lamina propria) in the setting of CHRONIC INFLAMMATION (most commonly due to H. Pylori); atypical lymphocytes
  • failure to eradicate infection (combination AB therapy) can cause it to transform to Large, Diffuse B Cell Lymphomas (p53/p16 mutations) that are NOT responsive to H. pylori eradication
    translocation: t(11;18)(q21;q21)
53
Q

What is an unusual marker that may be diagnostic for MALTomas?

A

25% are CD43 (+)

  • otherwise express CD19/20
54
Q

Carcinoid Tumor of Stomach

What is it and where is it most commonly found, what does it look like (3), and what markers is it positive for?

A
  • well-differentiated neuroendocrine tumor that occurs most commonly in the small intestine (40% - jejunum/ileum and aggressive)
  • yellow-tan intramural or submucosal mass that creates small polypoid lesions; “salt-pepper” chromatin, neurosecretory granules
  • (+) for neuroendocrine makers - 5-HIAA (serotonin metabolized by liver); typically see serotonin in portal circulation
55
Q

Carcinoid Tumor of Stomach

What molecule is inc. due to tumor and what are some of the clinical presentations of having the tumor?

What is the most important prognostic feature?

A
  • ileal tumor leads to inc. systemic serotonin
  • cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, RIGHT-SIDED Cardiac Valvular Fibrosis
  • LOCATION is most important prognostic feature
56
Q

GIST (Gastrointestinal Stromal Tumor)

What is it, where does it arise from, what two things are seen in children with it, and what 2 mutations does it commonly have?

A
  • most common mesenchymal tumor of the abdomen (arise from interstitial cells of CAJAL - pacemaker for peristalsis)
  • children present with CARNEY TRIAD and inc. risk if have NF-1 (neurofibromatosis type 1); peak age is 60 yo
  • due to KIT Tyrosine Kinase GOF or PDGFRA activating mutation (both are early events in sporadic GISTs)
57
Q

GIST (Gastrointestinal Stromal Tumor)

What does it look like, how does it present clinically, and what is its prognosis?

What is the diagnostic marker for this tumor?

A

M: solitary, well-circumscribed fleshy masses with “whorled” appearance (either spindle or epitheloid cells)

C: mass effects or blood loss (anemia)

P: imatinib treatment; determined by tumor size, mitotic index, and location

Diagnostic Marker = KIT in Cajal and 95% of gastric GISTs

GI II Exam 1 (12 decks)

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