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Pathology 3 > quiz 3- Esophagus, stomach, bowel 1 > Flashcards

quiz 3- Esophagus, stomach, bowel 1 Flashcards

1
Q

• What is the esophagus? d/os?

A

o Muscular tube, 20-24 cm, pharynx to stomach
o 3 segments: cervical, thoracic, and abdominal.
o Cervical: near midline, bw trachea and vertebrae. Narrow → easy trauma perforation
o Thoracic: posterior and left of trachea. Next to left primary bronchus, left lung, aorta, heart. Contacts right pleura, aorta left. Ends at diaphragm: anterior to aorta, left of midline
o Infection, inflammation, abnormalities in swallowing, trauma w or w/o perforation, tumors (benign and malignant). 2nd Thoracic and pulmonary complications → high morbidity and mortality.

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2
Q

• What are the developmental disorders of the esophagus?

A

o Esophageal atresia

o Esophageal webs

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3
Q

• What is esophageal atresia?

A

o Congenital, E dead-ends, not connected to stomach
o Includes variety of anatomic/developmental defects
o 1:30,000. >60% assoc w chromosomal or developmental syndromes: Edwards’ (trisomy 18), VATER (Vertebral defects, Anal atresia, TracheoEsophageal fistula, Renal dysplasia).

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4
Q

• What are esophageal webs?

A

o thin (2-3 mm) membranes (normal E tissue, mucosa, submucosa) in lumen of E
o congenital or acquired.
o Congenital: middle and inferior 1/3; circumferential, central orifice
o Acquired: cervical area (post-cricoid). Most common
o Sxs: odynophagia, dysphagia (esp liquids)

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5
Q

• What are the esophageal motility disorders?

A

o Achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal spasm
o All may present w varying degrees of solid and liquid dysphagia.

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6
Q

• What are odynophagia and dysphagia?

A

o Odyno: painful swallowing; oropharynx or upper chest pain; most common cause is E candidiasis; very hot/cold food/drink, drugs, ulcers and mucosal destruction, URI, immune dos, CAs, motor dos. → weight loss
o Dys: difficulty swallowing

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7
Q

• What is achalasia? Ssx?

A

o ↑ tone and P at LES
o no peristalsis distally
o no LES relaxation after swallowing → distal dilation
o ssx: dysphagia, regurgitation, chest pain

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8
Q

• Describe the Muscularis externa (aka muscularis propria) of E:

A

o 2 layers: circular and longitudinal, bw is Auerbach’s plexus w ganglia (aka myenteric=motor innervation, para- and sympathetic; Meissner’s has only para=secretomotor to lumen)
o Upper 1/3: striated muscle; voluntary
o Middle 1/3: smooth and striated; autonomic
o Inferior 1/3: predominantly smooth; autonomic

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9
Q

• What causes achalasia?

A

o Unknown
o Mb lymphocytic infiltration of Auerbach’s plexus, destruction of ganglion cells
o This mb AI, or dt toxin or infection agent

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10
Q

• What are factors in etio of idiopathic achalasia?

A

o esophageal gastric junction obstruction, degeneration of Auerbach´s plexus, virus, congenital, AI, toxin. The achalasia diagnosis is reached after excluding Chaga’s disease possibilities
o mb dysfunction of NO
o study: **emotion, **AI dz, phsychiatric, child infxns, chemicals, herbicides, GI dz, genetic, nervous system, sz

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11
Q

• How is achalasia diagnosed? Tx?

A

o Dx: manometry, barium swallow esophagram (x-ray) (classic “bird’s beak” finding)
o Must r/o Chaga’s dz: sero-negative Trypanosoma cruzi, no megacolon
o Tx: various, no cure, botox; more permanent relief w esophageal dilatation, surgical incision of the muscle (Heller myotomy)

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12
Q

• Describe histo of diff inflammation stages of myenteric plexus in achalasia:

A

o Normal: multiple ganglion cells, minimal lymphocytic infiltration
o Mild: lymphocytes, ganglion cells can still be identified.
o Mod: more lymphocytes (2 ganglion cells visible)
o Severe: lymphocytes densely clustered, no ganglion cells

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13
Q

• What are the types of esophageal spasms?

A

o Diffuse E spasm: aka corkscrew E; contractions uncoordinated, several segments contract simultaneously.
o Nutcracker E: contractions coordinated, but too much P

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14
Q

• What is nutcracker E?

A

o No histopathology; mb dt neurotransmitter dysfunction (NO)
o Mb asx, Dysphagia (solid and liquid), chest pain. GERD
o any age, more 50-70.
o Dx: esophageal motility study (esophageal manometry: eval pressure of E at diff points). ↑ P during peristalsis (↑ 2 SD), >180 mmHg (P of a nut cracker)
o Unknown complications
o Tx: sxs only

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15
Q

• What is corkscrew E (DES)? Esophagram?

A

o No propagative waves (bolus doesn’t travel)
o Sxs: st dysphagia and chest pain
o DES, non-peristaltic contractions, short segment of tapered narrowing in distal E dt incomplete opening of LES. mb small hiatal hernia

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16
Q

• What are causes and assoc of Mallory–Weiss syndrome?

A

o E trauma; bleeding from tears (a Mallory-Weiss tear) in mucosa at junction of stomach and E
o tear involves mucosa, submucosa but not muscular layer
o cause: severe coughing, retching, vomiting, Hyperemesis gravidarum (severe prego morning sickness)
o assoc: alcoholism (disc 1929 by Mallory and Weiss), eating dos, hiatal hernia, NSAID abuse
o >60, 80% are men.

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17
Q

• What are ssx of Mallory–Weiss syndrome? Dx? Tx? Px?

A

o episode of hematemesis after violent retching or vomiting; old blood in stool (melena) no hx vomiting, bleeding usu stops after 24–48 hours,
o dx: endoscopy
o tx: mb cauterization, injection of epinephrine, embolization of arteries, high gastrostomy to stop bleeding (all progressively rare). SB tube not effective bc arterial pressure too hi
o px: rarely fatal

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18
Q

• what is Boerhaave’s syndrome?

A

o full thickness tear or rupture of esophageal wall (sub/mucosa, muscular)
o Dt sudden↑ intra-esophageal P w negative intra-thoracic P: strain, cough, vomit.
o causes: severe retching or vomiting, chicken bone, perforation of esophageal ulcers. caustic ingestion (lye poisoning). upper endoscopy or esophageal surgery. pill esophagitis, Barrett’s ulcer, AIDS infectious ulcers, after dilation of esophageal strictures
o Common: tear at left posterio-lateral distal E, several cm.
o high morbidity and mortality (esp w E dz), fatal w/o tx. Mb delay in dx, poor outcome. Cervical rupture more benign
o 18th-century, by Boerhaave

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19
Q

• What is esophagitis?

A

o inflammation of E. acute or chronic
o usu dt GERD (aka reflux esophagitis), chemical injury (alkaline or acid, esp in kids accidental ingestion, adults suicide)
o dt Candida albicans, CMV, HSV infxn uncommon in immunocompetent (no chemo, AIDS, immunosuppressants)

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20
Q

• how may Candida esophagitis present? Imaging?

A

o Odynophagia, ↓ appetite → weight loss
o W thrush
o Mb first sign of systemic infxn
o Should get endoscopy (raised white plaques, easily removed; severe=erosive)
o Brushings or bx: yeast and pseudohyphae

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21
Q

• What is GERD?

A

o Gastroesophageal reflux disease: damaged esophageal mucosal lining dt stomach acid into E
o Cause: abn relaxation of LES, hiatal hernia, any ↑ intra-abdominal P
• Sx: heartburn
• Endoscopy: erythema; severe: friable mucosa, narrowing

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22
Q

• What is a hiatal hernia? 2 major types?

A
  • protrusion of upper stomach into thorax thru tear/weak diaphragm.
  • Type 1 (“Sliding” 95%): GE junction moves above diaphragm w stomach
  • Type 2 (“Rolling” Para-esophageal, 5%): stomach herniates thru diaphragm, beside E, w/o moving GE junction.
  • 3rd: combo of sliding and rolling
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23
Q

• What is a Schatzki ring?

A
  • Seen in hiatal hernia; narrow lower E → dysphagia, or completely blocked E
  • Ring/web of sub/mucosa
  • A rings: above GE junction
  • B rings (most common): lower E at SC junction (proximal margin of a hiatal hernia)
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24
Q

• What is Barrett’s esophagus?

A
  • Transformation/metaplasia at lower E from normal squamous to columnar epithelium.
  • Columnar can better withstand acid (↑ goblet cells), but more likely to develop adenocarcinoma
  • Dt damaged esophageal lining from chronic acid exposure (GERD)
  • 5-15% who seek help for heartburn; mb asx
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25
Q

• What are the warning signs of dysplasia/premalignancy in Barrett’s E? Imaging?

A
  • Change mb asx
  • Frequent and longstanding heartburn, dysphagia (& weight loss), Vomiting blood
  • Endoscopy: pink area=metaplastic; white=squamous
  • Dx: bx; columnar may look more gastric or colonic, or mix
  • Colonic: ↑ malignancy, mb genetic
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26
Q

• What are risks factors for esophagus adenocarcinoma? Work-up?

A
  • Barrett’s type mucosa → dysplasia
  • Caucasian M > 50, > 5 yrs sxs; rare in African-American men
  • routine endoscopy and bx
  • If 2 endoscopies and bx in 12 mos are negative for dysplasia → surveillance every 3 yrs, control GERD w PPI, prevention
  • Any dysplasia → close observation by gastroentrologist, repeat endoscopy and bx
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27
Q

• Tx for esophagus adenocarcinoma dt Barrett’s?

A
  • PPI may not prevent CA
  • Laser for severe dysplasia
  • overt malignancy may require surgery, radiation, chemo
  • photodynamic tx w Photofrin better than PPI to eliminate dysplasia
  • no way to predict dev’t of cancer from Barrett’s (mb genetic assoc w 79% chance in 6 yrs)
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28
Q

• what are esophageal varices?

A
  • dilated sub-mucosal veins in lower 1/3 E (→ L gastric v →portal v)
  • usu in pts w cirrhosis, dt portal HTN (portal P norm 9mmHg, IVC 2-6; if portal >12, gradient >5 = portal HTN, so if portal >10-12; grad >10 blood redirected (collateral circ in lower esophagus, abdominal wall, stomach, rectum) → varicosities
  • 1-2 cm (norm 1mm)
  • (most blood of E→ azygnos vein →SVC; no risk of varices)
  • ↑ risk develop severe hemorrhage
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29
Q

• What is caput medusa?

A

• appearance of distended, engorged peri-umbilical veins, radiate from umbilicus across abdomen to join systemic veins.

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30
Q

• What are the benign esophageal tumors?

A
  • Fibrovascular polyp
  • Granular cell tumor
  • Hemangioma
  • Inflammatory fibroid polyp (eosinophilic granuloma)
  • Leiomyoma (2/3 of benign E tumors)
  • Lipoma
  • Lymphangioma
  • Neurofibroma
  • Squamous cell papilloma
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31
Q

• What are sxs of esophageal leiomyoma?

A
  • Mb hx of dysphagia, or an E polyp

* Mb asx, found on incidental endoscopy

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32
Q

• What are granular cell tumors?

A
  • neural origin, from Schwann cells
  • yellow lesion in E
  • Anywhere in body, incl skin, oral cavity, breast, GI
  • E most common GI site, also occur in colon
  • Assoc: GERD, Barrett’s
  • Found on endoscopy, dx w bx
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33
Q

• What are the two main forms of esophageal cancer? Sxs? Dx? Tx? Px?

A
  • SCC (90-95% world): from cells that line upper 2/3 E; look like head and neck CA, assoc w tobacco and alcohol
  • Adenocarcinoma (50-80% US): from glandular cells at GE junction (lower 1/3 E); assoc hx GERD, Barrett’s
  • Sxs: dysphagia, odynophagia, weight loss, heartburn, hoarse cough, N/V, regurg, hematemesis, SVC syndrome, upper airway obstruction, TE fistula (fix w stent)
  • Dx: bx, usu late stage (asx b/f tumor really large))
  • Tx: small w surgery (cure); large palliative, mb chemo, radio
  • Px: fairly poor
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34
Q

• What are risk factors for E CA?

A
  • Avg age 67, M>F, FHx CA
  • US: Tobacco smoking (A & SCC), heavy alcohol (SCC), synergistic (90% E SCC)
  • GERD → Barrett’s (adeno)
  • Chronic esophagitis (non-reflux)
  • HPV (SCC), cervix, larynx
  • swallow strong alkaline (lye) or acids.
  • China: nitrosamines (diet), fungus, vitamin/mineral def
  • Hx other head and neck CA
  • Plummer-Vinson syndrome (anemia and E webbing)
  • Tylosis and Howell-Evans syndrome (hereditary, keratosis of skin of palms, soles)
  • Radiation tx nearby
  • Celiac dz (SCC)
  • Obesity (A 4x), ↑ reflux
  • Drinks too hot
  • Alcohol, w flush reaction (Asian, def ALDH2), SCC
  • Achalasia
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35
Q

• What may decrease risk of E CA?

A
  • Aspirin, NSAIDs
  • Helicobacter pylori , mb protective, but may cause GERD???
  • cruciferous (cabbage, broccoli, cauliflower, Brussels sprouts), green, yellow vegetables, fruits
  • Moderate coffee
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36
Q

• What are “Barrett’s cancer columns?”

A
  • Seen on endoscopy

* Cancer protrudes into lumen, progresses down E wall in columns

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37
Q

• Where may E CA spread to, and sxs?

A
  • Liver: jaundice, ascites

* Lung: SOB, pleural effusions, etc

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38
Q

• What does histo of E adenocarcinoma look like? SCC?

A
  • A: Glands; variable nuclear size, staining, shape; lots of mitoses (neoplastic cells)
  • SCC: full thickness replacement of epithelium with severely dysplastic cells. basement membrane intact, no invasion to lamina propria
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39
Q

• How is alcohol metabolized? Why do Asians have “glow”? How does this cause E CA?

A
  • Ethanol →(ADH) acetaldehyde →(ALDH) acetate
  • Many Asians have def ALDH2 → too much acetaldehyde →histamine release (facial flush, nausea, HA, tachycardia)
  • Acetaldehyde = animal carcinogen, mutagen → inc risk E SCC
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40
Q

• What is the pathogenesis of E SCC?

A
  • increasingly severe degrees of dysplasia to carcinoma-situ to invasive carcinoma
  • chronic inflammatory state (↑cell turnover) → dysplasia (cervix, colon in IVD)
  • unclear assoc oncogenes, tumor suppressor genes, gene replication (as w colon CA)
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41
Q

• what is epidemiology of E CA?

A
  • M:F 5:1
  • 4X more in blacks in the US (blacks rising, whites stable or declining)
  • Men age 60 (slow evolution of dysplasia to carcinoma)
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42
Q

• What is congenital diaphragmatic hernia (CDH)?

A
  • Anatomic defect in diaphragm, usu left side (90%), 1:2000 births (8% all major congenital anomalies), 50% survival
  • mb genetic, 40% assoc w other abnormalities (trisomy 18 and 21)
  • No dev’t of postero-lateral diaphragm (persistence of foramen of Bochdalek).
  • herniation of abdominal contents into thorax → pulm hypoplasia, HTN
  • mb asx; mb life threatening respiratory distress by compressing one or both lungs (degree affects px)
  • If R: mb structural lung lesion (congenital cystic adenomatous malformation, CCAM)
  • Antenatal detection st assoc w worse px
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43
Q

• What are the 3 types of CDH?

A
  • Bochdalek: L (posterior defect), MC (85%), S/L I and organs → thoracic cavity; liver gets tilted vertically
  • Morgagni: R, only liver and small part of LI tend to herniate
  • bilateral diaphragmatic: uncommon, usu fatal
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44
Q

• describe presentation and CXR of infant w R CDH?

A
  • Tachypnea
  • CXR: irregular air pockets in R hemithorax, compressive atelectasis of R lung, mediastinal shift to L
  • ddx: CDH, CCAM
  • contrast: bowel loops in R hemithorax
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45
Q

• what is congenital hypertrophic pyloric stenosis (HPS)? Histo?

A
  • Smooth mm hypertrophy of pylorus →thickened wall, ↓lumen size
  • Pylorus → firm, resistant to relaxation
  • ↑gastric peristalsis → ↑gastric P →backflow into E and mouth
  • ↓ gastric emptying, but complete blockage rare
  • histo: mucosal hyperplasia w elongated, branched, mildly distorted pits; abundant lamina propria somewhat edematous
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46
Q

• How does HPS present?

A
  • presents at 2 – 3 wks, vomit (mb projectile, non-bilious), regurg food
  • Distended abdomen, visible gastric peristalsis
  • Mb “spitting”
  • ↓ weight over time, although very hungry →vomit
  • ↓defecation, no urination
  • “olive”= palpable enlarged pyloric mm
  • Breast milk better off than formula (smaller curds)
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47
Q

• what is incidence of HPS? Etio?

A
  • 3/1000 births, and increasing
  • M:F 4:1, first-borns
  • More in causasians
  • Unknown etio, but affected M 8x more likely to have affected offspring, F 4x
  • B and O blood types more
  • Risk: if mom took erythromycin in 3rd tri or nursing
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48
Q

• How is HPS dx?

A
  • Dx in utero, or presents at 2 – 3 wks

* US, barium swallow and xray

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49
Q

• what may cause gastric varices? Appearance?

A
  • end-stage liver dz 2nd to alcoholic cirrhosis →recurrent episode bleeding from gastric and esophageal varices. In cardia and fundus, covered w fresh appearing blood
  • colonic carcinoma metastatic to liver →portal HTN. Varices course through gastric fundus
50
Q

• how may gastric volvulus present with work-up?

A
  • protracted vomiting
  • Abd x-ray: large hiatal hernia w 1-2 air-fluid levels
  • Endoscopy: confirm dx
  • May require surgical correction
51
Q

• What may cause acute gastritis? Gross and histo appearance?

A
  • alcoholism, drugs, infections
  • gross: diffusely hyperemic gastric mucosa.
  • Histo: gastric mucosa w N infiltration
52
Q

• What is H pylori? Assoc?

A
  • spiral flagellated rod g(-) bacterium found in surface epithelial mucus; makes urease
  • 90% duodenal ulcers (mc assoc)
  • 70% gastric ulcers
  • 60% gastric CA
  • Gastritis usu have h pylori infx
53
Q

• What tests can detect h pylori infx (Sn; Sp %)?

A
  • Rapid urease (90; 90-95); color changes dt pH change
  • Culture (80; 100); difficult, requires special technique
  • Microscopy (90 ; 90); silver or Giemsa staining of antral biopsies
  • Carbon breath test (95; 95); C13 or C14, ingest radioactive urea, broken down to CO2
  • Serology (98; 100); immunologic w ELISA
54
Q

• How can you differentiate benign from malignant peptic ulcers?

A
  • B: smooth, regular, rounded edges, flat, smooth base, radiating mucosal folds
  • M: irregular, heaped, overhanging margins, nodular, irregular mass mb ulcerated, protrudes into stomach lumen
55
Q

• What are peptic ulcer ssx?

A
  • Signs: hx heartburn, GERD, certain meds (NSAIDs inhibit COX and glucocorticoids)
  • abdominal pain, usu epigastric, severity relating to mealtimes, ~3 hrs after (duodenal ulcers relieved by food)
  • Bloating, abdominal fullness; water brash (↑ saliva after regurg to dilute E acid, more assoc w GERD)
  • N/V, loss appetite, weight loss, hematemesis, melena
  • bleeding directly from gastric ulcer or E damage from severe vomiting
  • > 45 and 2+ wks sxs: get esophagogastroduodenoscopy
56
Q

• what are complications of gastric ulcer?

A
  • Rare: →gastric or duodenal perforation →acute peritonitis. extremely painful, requires immediate surgery.
  • If malignant → resect stomach
57
Q

• What is prevalence of duodenal ulcers? Cause?

A
  • 2x common as gastric
  • usu benign
  • 4.5 million per year in US, significant morbidity and mortality (5%)
  • M=F
  • 90% dt H pylori, 10% NSAIDs
58
Q

• What are potential complications of PUD?

A
  • GI bleeding- mc; mb life-threatening; when ulcer erodes blood vessel (gastroduodenal a)
  • 10%: Perforation of gastric or duodenal (mc duodenal cap) wall (erosion → spillage); detect w air/fluid on imaging; anterior →acute peritonitis → bacterial, intense pn; posterior → GD a bleed
  • Penetration to adjacent organs (LV, PN)
  • Scarring and swelling → gastric outlet obstruction dt narrowing; severe vomit
  • Ulcer transformation into cancer, dx by bx, usu dt h pylori (3-6x risk of stomach CA)
  • Omental patch repair
59
Q

• What is Zollinger–Ellison syndrome?

A
  • Triad: gastric acid hypersecretion, severe peptic ulceration, gastrinoma (non-beta cell islet pancreas tumor)
  • ↑ gastrin → ↑parietal cells → ↑stomach HCl → GI ulcers, diarrhea, malabsorption
  • Usu gastrinoma in pancreas, duodenum, abd LNs, mb other
  • Peptic ulcers in 95% cases
60
Q

• How does ZES lead to malabsorption?

A
  • direct mucosal damage by acid
  • inactivate pancreatic enzymes
  • precipitated bile salts.
61
Q

• What causes the gastrinoma of ZES? Incidence?

A
  • Sporadic (75%) or genetic (25%, MEN 1)
  • MEN 1= AD, w hyperparathyroidism, pancreatic endocrine tumors, pituitary tumors
  • US: 0.1-1% of all pts w duodenal ulcers
  • Freq = insulinoma (mc functioning pancreatic endocrine tumor)
62
Q

• How does ZES present?

A
  • Abdominal pain, in75%, mc sx, usu upper, like PUD, more in men and sporadic
  • 73% have diarrhea, mc sx w MEN 1 and female
  • 50%: abd pain + diarrhea
  • Heartburn, like GERD
  • N/A, GI bleed (25%, duodenal ulcer), weight loss
  • P/FHx: nephrolithiasis, hypercalcemia, hyperparathyroidism, gastrinoma, pituitary dos
63
Q

• What is PE for ZES?

A
  • Mb norm
  • pale if GI bleeding
  • Jaundice if tumor compressescommon bile duct (rare)
  • Epigastric tenderness
  • Dental erosions if GERD
  • HM suggests liver metastasis
64
Q

• What is Menetrier’s dz?

A
  • Aka hyperplastic hypersecretory gastropathy = gastric rugae enlarged
  • → ↑ mucus, stomach glands atrophy → ↓acid, protein loss (albumin) → ↓plasma protein
  • tissue mb inflamed, ulcers
65
Q

• what are the 2 forms of Menetrier’s dz?

A
  • Childhood: usu after viral illness (CMV) or bacterial (H. pylori) infx; not genetic; better px
  • Adult: assoc w overexpression transforming growth factor alpha (TGF-a) protein; M:F 4:1 (age 30-60) (3:1 all ages)
  • TGF-a binds epidermal growth receptor, ↑ gastric mucus, cell renewal, inihibit acid secretion
66
Q

• How is menetrier’s dz dx? Ddx?

A
  • Gross: giant folds, polypoid appearance, in body and fundus
  • Histo: marked hyperplasia, atrophy of glands, ↑ mucosal thickness
  • ↑ mucus, ↓ acid, hypoproteinemia
  • Ddx: ZES, H pylori, gastric lymphoma, CMV, gastric CA, eosinophilic gastritis
67
Q

• What is atrophic gastritis? Causes?

A
  • chronic inflamed stomach mucosa →lose gastric glandular cells → replaced by intestinal-type epithelium (metaplasia), pyloric-type glands, fibrous tissue
  • ↓ HCl, pepsin, IF
  • Histo: Mild chronic inflammation in lamina propria (N’s)
  • Atrophy=endpoint of chronic processes (chronic gastritis & H pylori, environmental factors, AI against gastric glandular cells)
68
Q

• What are consequences of atrophic gastritis?

A
  • → B12 def (abs in ileum w IF), megaloblastic anemia, pernicious anemia, other malabsorption
  • AI: more likely to develop achlorhydria and gastric carcinoma; may → IF def
69
Q

• What is Autoimmune metaplastic atrophic gastritis (AMAG)?

A
  • Genetic, AI against parietal cells and IF (serum Abs)
  • Triggered by H pylori (molecular mimicry)
  • → hypochlorhydria → G cell (gastrin) hyperplasia → hypergastrinemia
  • → trophic effect on enterochromaffin-like cells (histamine secretion), may → carcinoid tumors in AMAG
70
Q

• What is EMAG?

A
  • Environmental MAG
  • Diet, H pylori
  • Usu stomach body only
  • ↑ risk gastric carcinoma
71
Q

• What is presentation of AMAG? Endoscopy?

A
  • Dyspepsia, (+) H pylori

* Patchy intestinal metaplasia, paler than surrounding mucosa, in pre-pyloric antrum

72
Q

• What is gastric adenocarcinoma? Histo and gross?

A
  • Intestinal cell type
  • Histo: mitoses, ↑ N:C, hyperchromatism, desmoplastic stromal reaction to infiltrating glands; poorly diff, glands not visible, clear vacuoles of mucin
  • SIGNET RING: cells filled with mucin vacuoles push nucleus to one side
  • Gross: granular white appearance
73
Q

• What may cause gastric adenocarcinoma?

A
  • Mb nitroso-compounds, strong implication as carcinogens
  • Diet: ↑ nitrates/nitrites, or ↓ in reducing agents (prevent nitrates →nitrites)
  • Nitrite-forming bacteria common in gastric atrophy, intestinal metaplasia, hypochlorhydria
74
Q

• What is incidence of gastric CA? ssx? Labs?

A
  • US: distal has ↓, proximal ↑
  • > 50, intestinal M:F=2:1, M=F for mucus secreting type
  • Asx until late, abd pn, weight loss, obstruction w late distal tumors
  • Melena, hematemesis rare
  • metastasis to Virchow’s node, ovary (Krukenberg tumor), liver, peritoneum
  • labs not useful for dx
75
Q

• what is linitis plastic?

A
  • Aka Brinton’s dz, leather bottle stomach
  • Rare, diffuse infiltrative gastric adenocarcinoma originates in glandular tissue lining stomach walls
  • walls → leather-like scar tissue, shrunken, can’t swell or contract
  • extensive mucosal erosion, markedly thickened gastric wall
  • → ↓ digestion, metabolism of vital nutrients
  • Poor px
76
Q

• Another name for gastric lymphoma? Ssx? Gross appearance:

A
  • malignant lymphoma of mucosa-associated lymphoid tissue (MALT)
  • ssx: IDA, loss of appetite, early satiety, weight loss, no abd pn
  • several small antral gastric ulcers with raised surrounding mucosa, bleeding
77
Q

• what is primary gastric lymphoma?

A
  • rare < 5% of primary gastric neoplasms
  • MC stomach malignancy after adenocarcinoma
  • MALT type 40-50% of all gastric lymphomas
  • Usu dt H pylori. St tumor regresses w h pylori eradication (Less likely if large cells, perigastric LN, depth of infiltration, bcl-10 gene translocation
78
Q

• What are Gastrointestinal stromal tumors (GISTs)???

A
  • rare, 10/million per yr, benign to malignant
  • MC mesenchymal tumors in GI tract
  • Usu surgery tx
  • nearly absolute resistance to chemo and radiation
79
Q

• Histology of gastric lymphoma:

A
  • dense lymphoid infiltrate, lymphoepithelial lesions w atypical lymphoid (B) cells permeating glandular epithelium,
  • often H pylori
  • monomorphic, composed of spindle-shaped cells. (+) CD34 and CD117, (-) smooth-muscle actin
80
Q

• Example of Gastric leiomyoma in pylorus?

A
  • Smooth tumor, sxs of gastric outlet obstruction
  • lesion extended into duodenum, deep ulceration, obstructed lumen.
  • Histo: benign, epithelioid leiomyoma
81
Q

• What are carcinoid tumors?

A
  • Uncommon (2/100,000 per yr)
  • neuro-endocrine neoplasms from enterochromaffin cells
  • ~70% in GI tract
  • range from small, benign in stomach, appendix to classic 5HT producing to CT highly malignant, undifferentiated carcinoid small cell carcinomas (endocrine and glandular)
82
Q

• what is carcinoid syndrome?

A
  • < 10% pts w CT
  • Tumor produces vasoactive substances → systemic circulation wo metabolic degradation
  • MC in pts w ileal carcinoid and hepatic or retroperitoneal metastases.
  • Ssx: cutaneous flushing, sweating, bronchospasm, abd colic, diarrhea, right-sided cardiac valvular fibrosis. Alcohol, stress, exercise may precipitate or exacerbate sxs
83
Q

• What are type 1 gastric carcinoid tumors?

A
  • 70 - 80%, dt trophic effect of gastrin on ECL cells
  • Assoc w AI chronic atrophic gastritis → ↓ HCl → stimulates antral G-cells → hypergastrinemia → growth of ECL cells
  • Usu mult, small (< 2cm)
  • MC F >50 (AI), assoc B12 malabsorption, pernicious anemia.
  • Usu asx, incidental dx
  • Usu benign, st metastasis, high recurrence, st tx w somatostatin analog (↓gastrin)
84
Q

• What are type 2 gastric carcinoid tumors?

A
  • 5%, M=F
  • are gastrin dependent, mult (like 1)
  • 2nd to gastrinoma, assoc w MEN I
  • ↑ gastric acid, ssx like ZES
  • Histo like 1, greater malignant potential (regional LN, liver)
  • Tx=remove gastrinoma and carcinoid
85
Q

• What are type 3 gastric carcinoid tumors?

A
  • =sporadic, 20%, not assoc w ↑ gastrin
  • solitary, large (>2cm), M >50
  • high malignancy, 5yr survival 50%
  • 5-10% → ‘atypical’ carcinoid syndrome; releases histamine; patchy bright red flush, cutaneous edema, salivary gland swelling, increase lacrimation.
  • Tx like adenocarcinoma, resection
86
Q

• Carcinoid tumor histology?

A
  • “Endocrine pattern” (nests of cells separated by thin-walled vessels)
  • < 2 mitoses/10 HPF
  • Uniform cells and nuclei, normal N:C ratio, small nucleoli, stippled chromatin. No necrosis
87
Q

• How might a trichobezoar present?

A
  • Girl 12, 6-month hx abd pn, vomiting. intermittent episodes severe epigastric pn. 23 episodes of vomiting every day, non-bilious w food particles. Anorexic, lost weight. normal developmental milestones. Stress at home, long hx of trichophagia
  • PE: 5% ht/wt, Tanner stage 2, scaphoid abd, palpable oblong-shaped hard mass in epigastrium, extending to RUQ
  • Hb 11.7 g/dL. Abd x-ray stomach dilated no air-fluid level, abd CT distended stomach filled w heterogenous areas mixed with contrast. US hyperechoic mass in epigastric.
  • →laparotomy. giant trichobezoar removed by anterior gastrostomy. 125 g 8.5 x 22 cm. pt fine
88
Q

• What is intestinal atresia? Types? Tx?

A

o Congenital malformation (usu vascular in utero → ischemia), narrowing or absence of part of S/L I
o duodenal, jejunal, ileal, colonic
o duodenal (MC): strong assoc w Down’s; ileal 2nd MC
o tx: fetal/neonatal w laparotomy after birth. Mb easy resect if short, or temporary stoma (ileostomy or colostomy tube) if longer

89
Q

• what is Hirshsprung’s dz?

A

o Aka Congenital aganglionic megacolon, dt failure of neural crest cells (enteric ganglion cells) to migrate completely
o No ganglion cells → nerve over-stimulation →Colon can’t relax→ constipation, obstruction
o Usu short segment affected; 5% entire colon
o 1/5000 live births. M:F (4: 1), 9% Down’s

90
Q

• What are ssx of hirshsprung’s dz? Dx? Tx? Px?

A

o Baby not passed meconium in 48 hours (Normally 99% do so)
o green or brown vomitus, swelling abdomen, gas and bloody diarrhea
o dx by bx of distally narrowed segment (proximal seg is enlarged)
o tx: surgical resection, re-anastomosis (Swenson in 1948)
o 25-30% mortality

91
Q

• What is intestinal volvulus?

A

o complete twisting of loop of intestine (any spot) around its mesenteric attachment site.
o Like malrotation (when rotation and fixation of mid-gut fails to normally occur)
o ↑ risk if have intestinal malrotation (esp kids)
o Any age, not usu congenital
o Mid-gut: entire mid-gut around axis of superior mesenteric artery
o Sigmoid: MC elderly

92
Q

• What is intussusception?

A

o part of intestine migrates into another section (telescopic), st ischemia and necrosis
o ssx: triad of abd colic, bilious vomiting, red “currant jelly” stool (blood and mucous, necrotic bowel)
o early: N/V, colic
o late: rectal bleeding, lethargy → emergency, death w/o tx
o PE: palpable “sausage-shaped” mass in abd
o Age: usu 5 mos- 1 yr, or any age, M:F (2:1)

93
Q

• What are 2 variants of intussusception? Other causes? Sign on x-ray?

A

o Idiopathic: at ileocolic junction, esp young kids (MC overall)
o non-ileocolic locations: older kids; assoc w CF, Henoch-Schönlein purpura
o ½ adult cases dt malignant lead points
o Crescent sign: crescent-shaped lucency, usu LUQ, w soft tissue mass adjacent
o CT: “coiled spring” sign

94
Q

• What is tx for intussusception?

A

o Kids: contrast enema to dx may also reduce, 5-10% recur in 24 hrs
o Laparoscopy, or st Surgical reduction, mb resection;
o 80% success rate

95
Q

• What is meckel’s diverticulum

A

o out pouching of intestine in distal ileum, usu within 60–100 cm (~2 ft) of ileocecal valve, 3-5 cm in lenght
o = vestigial remnant of vitelline duct (yolk stalk), MC malformation of GI tract, 2% of pop
o Either true or false diverticula
o True: involve all layers of the structure, including muscularis propria and adventitia
o False: only sub/mucosa and mucosa

96
Q

• What are ssx of meckel’s diverticulum?

A 
o	Usu asx
o	Usu before age 2
o	painless rectal bleeding, either bright red or melenic black; usu stops spontaneously. 
o	Severe epigastric abd pain, bloating
o	Mb like appendicitis
97
Q

• How is meckel’s diverticulum treated?

A

o surgical. Resection of diverticulum
o Mb resection of both diverticulum and adjacent bowel segment (if sxs of bleed, strangulation, perforation, obstruction)

98
Q

• What is diverticulosis? Sxs?

A

o type of diverticular dz (w diverticulitis)
o outpocketings of colonic sub/mucosa dt weak muscle in colon wall
o MC in sigmoid colon (common ↑ P)
o Usu sxs >40; mb ↓ dietary fiber
o Improper motility → spasm → low abd pain, small pellet-like stools and slime relieve pain.
o Sxs: bloating, changes in BMs (diarrhea, constipation), Non-specific chronic discomfort, low abd pain after meals

99
Q

• What is diverticulitis? Ddx?

A

o Inflamed diverticula
o Mb infected →abscesses → perforate (serious)
o classic triad: LLQ pain, fever, ↑ WBC (rare RLQ)
o some: nausea, diarrhea, constipation
o may bleed, either rapidly (thru rectum) or slowly (causing anemia)
o rectal bleeding ddx: colon CA, colonic polyps, IBD

100
Q

• how is diverticulitis treated?

A

o Bowel rest, abx
o W recurrent peritonitis, abscess, or fistula may require surgery (elective or emergency)
o low residue diet (low-fiber) for colon to heal. Later, high-fiber diet

101
Q

• what is Intestinal/Bowel obstruction? Small vs large?

A

o emergency
o mechanical or functional, prevent normal transit of digested material
o any level of Intestine
o ssx: mid-abd colic, distension, vomiting (including fecal vomiting), constipation
o small: colic few mins, vomit first
o large: last longer, lower, constipation first

102
Q

• what are complications of obstruction?

A

o dehydration and electrolyte abnormalities due to vomiting
o respiratory compromise from pressure on diaphragm by distended abdomen
o aspiration of vomitus
o bowel ischemia or perforation

103
Q

• what can cause obstruction?

A 
o	Adhesions
o	Cancer
o	Diverticular disease
o	Hernias
o	Infectious colitis
o	Intussusception
o	Volvulus
104
Q

• What might be seen on xray of intestinal obstruction? Severity? Tx?

A

o Upright, mult air fluid levels in SI
o Less severe: simple
o More: surgical emergies, mb fatal, volvulus, closed-loop obstructions, ischemic bowel, incarcerated hernias
o Tx: nasogastric tube to decompress dilated bowel, relieves sxs

105
Q

• What is volvulus?

A

o complete twisting of a loop of intestine around its mesenteric attachment site
o stomach, SI, cecum, transverse or sigmoid colon
o not congenital
o acute= emergency!

106
Q

• what is malrotation?

A

o Embryologic, Congenital, 1/500 births
o Not confused w mobile/high cecum (RUQ), 10% pop
o Unknown etio
o Assoc: Trisomy 13, 18, 21, VACTERL (vertebral, anal, cardiac, tracheal, esophageal, renal, limb), congenital heart dz, Ileal/jejunal atresia/duplication, Duodenal/pyloric atresia/stenosis, Diaphragmatic hernia, Meckel’s diverticulum, Esophageal atresia, Situs inversus and asplenia, Intussusception, CF, Meconium ileus, Hirschsprung’s dz, Duodenal web

107
Q

• How might a case of intestinal volvulus present? imaging? tx

A

o Severe abd pn, distension, 3 days constipation, intestinal wall injury, gas/fluid accumulation → necrosis, acidosis, death
o Supine: distended loop of bowel, “coffee-bean” contour, in RUQ; cecum not identified in RLQ; distended centrally-located loops.
o Erect: air-fluid level in RUQ, several small bowel air-fluid levels.
o Abd CT: confirmed findings. peritoneal free fluid
o Tx: volvulus was reduced at laparotomy.

108
Q

• What is incidence of volvulus?

A

o Adult to elder men
o Rare comp w redundant colon (variant, extra loops)
o 11% cecal volvulus, 30-60, hx surgery, mass, requires surgery
o sigmoid volvulus (MC, 8% all intestinal obstruction), elder, constipated

109
Q

• what is celiac dz? Ssx?

A

o Aka celiac sprue; non-tropical sprue, endemic sprue, gluten enteropathy, gluten-sensitive enteropathy, gluten intolerance
o AI of SI, rxn to gliadin (gluten protein in wheat, barley, rye); diff from wheat allergy
o → enzyme tissue transglutaminase (TGT) modifies the protein, and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction
o Ssx: chronic diarrhea, failure to thrive (kids), fatigue, mb asx, or sxs in other organ systems

110
Q

• Incidence of celiac? Dx? Tx?

A

o between 1/1,500 and 1/100 in US
o dx: increased screening → ↑ dx in asx;
o tx: only known effective tx life long gluten-free diet

111
Q

• what is pathophysiology of celiac and sxs?

A

o →villous atrophy → ↓absorption
o Can’t absorb nutrients, minerals, fat-soluble vitamins A, D, E, K (abn coagulation)
o Can’t absorb carbs and fats → weight loss, fatigue
o Anemia: iron malabsorption → IDA; folate, B12 malabsorption → megaloblastic anemia
o Ca, vit D malabsorption (and compensatory 2nd hyperparathyroidism) → osteopenia, osteoporosis
o A small proportion have abnormal coagulation due to vitamin K deficiency and are slightly at risk for abnormal bleeding

112
Q

• What are some assoc/comp of celiac?

A

o SIBO: malabsorption, despite celiac tx
o IgA deficiency in 2.3% (alone has 10X risk for celiac), risk infx, AI dz
o Dermatitis herpetiformis: transglutaminase enzyme in skin, sxs like celiac
o Growth failure/delay
o recurrent miscarriage and unexplained infertility
o hyposplenism (1/3 cases)
o abn LFTs
o AI: DM type AI thyroiditis, primary biliary cirrhosis, microscopic colitis
o A-gliadin Abs: cerebellar ataxia, peripheral neuropathy, schizophrenia, autism

113
Q

• Compare normal and celiac histology of intestine:

A

o Normal: villi w microvilli, goblet cells, ducts
o Celiac: blunting and flattening of villi; sever: loss of villi with flattening of mucosa
o >95% have DQw2 histocompatibility Ag, suggests genetic

114
Q

• What is idiopathic inflammatory bowel dz?

A

o group of inflammatory conditions of S/L I
o major: Crohn’s dz, ulcerative colitis
o other: Collagenous colitis, Lymphocytic colitis, Ischemic colitis, Diversion colitis, Behçet’s disease

115
Q

• what is difference bw crohn’s and UC? Dx?

A

o C: any part of GI from mouth to anus, many in terminal ileum; skip lesions (patchy areas on inflame), entire bowel wall (“transmural lesions”)
o UC: colon and rectum only, mucosa only
o Dx: colonoscopy w lesion bx

116
Q

• What are ssx of Crohn’s and UC?

A

o Common to both
o abd pn, vomit, diarrhea, rectal bleed, severe internal cramps/muscle spasms in pelvis, weight loss
o many other non-GI ssx

117
Q

• what is gross appearance of bowel w Crohn’s?

A

o thickened wall, mucosa has lost the regular folds, irregular nodular, hyperemia, focal superficial ulceration
o serosal surface: reddish indurated adipose tissue
o Serosal inflammation → adhesions
o Patchy inflamed areas throughout
o Endoscopic: mucosal erythema and erosion

118
Q

• Crohn’s histology:

A

o transmural inflammation. inflammatory cells extend from mucosa thru submucosa and muscularis → nodular infiltrates on serosal surface w pale granulomatous centers
o granuloma: epithelioid cells, giant cells, many lymphocytes
o Special stains for organisms are negative

119
Q

• Gross appearance of UC:

A

o Hyperemia, ulcers, erythema, granularity
o Inflammation continuous along mucosal surface, tends to begin in rectum.
o mucosa becomes eroded → remaining islands of mucosa called “pseudopolyps”
o pseudopolyps: seen clearly as raised red islands of inflamed mucosa, w only remaining muscularis bw them
o mucosal erosions → linear ulcers undermine remaining mucosa

120
Q

• UC histology:

A

o characteristic mucosal alteration = “crypt abscess”, neutrophilic exudate in glandular lumens
o Sig inflam of sub/mucosa, loss of goblet cells, exudative surface
o Both acute and chronic inflammatory cells
o hyperchromatic nuclei w inflammatory atypia

121
Q

• what has an ↑ risk w UC?

A

o adenocarcinoma

o dysplasia of glands (histo), first indication of neoplasia

Pathology 3 (6 decks)

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