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

Chapter 17 (Part 1): Esophagus and Stomach Flashcards

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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?

Study These Flashcards
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)?

Study These Flashcards
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
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?
- 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
What are 4 causes of acute blood loss from the stomach? (AG/SRMD/DL/G)
acute gastritis stress-related mucosal disease dieulafoy lesion GAVE (watermelon stomach)
27
What is the difference between Acute Gastritis and Gastropathy?
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
What does Acute Gastritis look like?
- moderate edema with slight vascular congestion; more severe = erosion --> hemorrhage/ulcers - foveolar cell hyperplasia and corkscrew profiles - presence of NEUTROPHILS (abnormal --> means gastritis)
29
Stress-Related Mucosal Disease Stress Ulcers vs Curling Ulcers vs Cushing Ulcers
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
Stress-Related Mucosal Disease What causes it, what do they look like, and how do they present clinically?
- 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
GAVE Syndrome vs Dieulafoy Lesion
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
What are two most common causes of Chronic Gastritis and how can they be differentiated from Acute Gastritis?
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
H. Pylori Chronic Gastritis (Type B) What is it, how is it transmitted, and what are its 4 virulence factors? (F/U/A/C)
- 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
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?
- 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
Autoimmune Chronic Gastritis (Type A) What is it, what does it destroy, and what does it look like?
- 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
What cancers are H. Pylori and Autoimmune Gastritis associated with?
HP: adenocarcinoma, MALToma A: adenocarcinoma, carcinoid tumors
37
Autoimmune Chronic Gastritis (Type A) How does it present clinically and what is it associated with?
C: atrophic glossitis, megaloblastic RBCs with hypersegmented neutrophils, and peripheral neuropathies - most are B12 Deficiency symptoms - associated with AUTOIMMUNE DISEASES`
38
Uncommon Forms of Gastritis Eosinophilic Gastritis vs Lymphocytic Gastritis vs Granulomatous Gastritis
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
Peptic Ulcer Disease What is it, what is its risk of becoming cancer, and how does it present clinically?
- 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
What is Gastritis Cystica?
- exuberant epithelial proliferation with entrapment of epithelium-lined cysts that is associated with chronic gastritis (trauma-induced) - mimics invasive adenocarcinoma
41
What are two common Hypertrophic Gastropathies?
Menetrier Disease and Zollinger-Ellison Syndrome - uncommon diseases characterized by giant "cerebriform" enlargement of rugal folds due to epithelial hyperplasia without inflammation
42
Menetrier Disease What is it, what does it look like, and how does it present clinically?
- 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
Zollinger-Ellison Syndrome What is it, how does it present clinically, and how is it treated?
- 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
What are 3 benign stomach tumors and what are 4 malignant stomach tumors?
B: Hyperplastic (inflammatory) polyps, Fundic Gland Polyps, Gastric Adenoma M: Gastric Adenocarcinoma, Lymphoma, Carcinoid, GIST (gastrointestinal stromal tumor)
45
Hyperplastic (Inflammatory) Polyps
- 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
Fundic Gland Polyps
- 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
Gastric Adenoma
- 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
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?
- 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
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)?
- 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
Intestinal Type Gastric Adenocarcinoma
- 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
What is the best prognostic indicator for gastric cancer?
depth of invasion and extent of nodal/distant metastases at time of diagnosis - local invasion of duodenum, pancreas, retroperitoneum
52
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?
- 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
What is an unusual marker that may be diagnostic for MALTomas?
25% are CD43 (+) - otherwise express CD19/20
54
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?
- 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
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?
- 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
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?
- 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
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?
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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