Ch. 17 pt 1 Flashcards
What are the histological features of GERD
mild GERD - unremarkable
if significant dz - eosinophils recruited into squamous mucosa followed by neutrophils –> basal zone hyperplasia exceeding 20% total epithelial thickness & elongation of lamina propria papillae –> cause extension into upper 1/3 of epithelium
What are the etiologies of chronic gastritis
MCC: H. pylori
Autoimmune (MCC - diffuse atrophic gastritis & MCC chronic gastritis W/O H. pylori)
less common: radiation injury, chronic bile reflux, mechanical injury (NGT), systemic dz (ie Crohns), amyloidosis, GVH dz
What is the morphology of PUD
classic = round-oval, sharply punched-out defect
usually level w/ surrounding BUT may have mucosal margins that overhang the base slightly (particularly upstream)
Heaped-up margins = CA characterisitic = depth of ulcer may be limited by thick gastric muscularis propria or adherent pancreas, omental fat or liver
hemorrhage & fibrin deposition on gastric serosa
Perforation- into peritoneal cavity = SRG emergency; identified by detecting free air under diaphragm on upright radiographs of abs
when do tracheoesophageal (TE) fistulas form?
what are they associated with?
abnormal septation of the caudal foregut during the 4th and 5th wk
-trachea forms a diverticulum of the forgut & develop a complete septum that seperates the esophagus and trachea
associated w/ other congenital malformations, esp cardiac defects
what is the prognosis of esophageal SCC
5 yr survival rate
75% in pts w/ superficial esophageal SCC
lower if advanced or if LN metastases
What are the prevelance and RF esophageal SCC
> 45 yo male AA
location: Iran, central China, Hong Kong
RF: alc, tobacco, poverty, caustic esophageal injury, achalasia, tylosis (RHBDF2 mutation = howel-evans syndrome), radiation, Plummer-Vinson, fruit/veggie deficiency, very hot drinks & mursik ( = fermented milk, kenya)
HPV (high risk areas) ; HIV
How do you Dx and Tx H. pylori gastritis
- non-invasive serologic tests for Ab to H. pylori
- fecal bacterial detection
- urea breath test - form ammonia
- *Bx - analyze by rapid urease test, bacterial culture or DNA dectection by PCR
Tx: combo if ABx & PPI (make sure completely eradicated after treatment bc if not - relapse)
What are examples of structural/mechanical esophageal obstruction
Not cancer: (benign stricture- maintain wt & appetite) & Cancer (malignant stricture = wt loss!)
- esophageal web
- esophageal rings
- achalasia
- MC = inflam & scarring = esophagitis
What esophageal causes can lead to hematemesis
what is the presentation & prognosis of GIST
presentation: mass effect, anemia/bleeding 50%, incidental
depends on tumor size, mitotic index, location
gastric GIST < aggressive thatn intestinal GIST
What is the most common extranodal site for MALTomas?
what genetic mutation may be causing the these marginal zone B-cell lymphomas
GI tract = MC extranodal site
3 possible translocations - MC = t(11;18)(q21;21) ==> constitutively active NF-kB –> B cell growth & prolif
What type of gastric CA has a decrease in incidence
only Intestinal type
bc intestinal type is more closely associated w/ atrophic gastritis & intestinal metaplasia
What is the epidemiology of H. pylori gastritis
poverty, household crowding, limited education, African/Mexican American, rural area, born outside US
acquired in childhood & persist throughout life if not treated
<12 yo = < 15% (cohort effect due to improved sanitization) & >60 yo = 50-60%
colonization rates = <10 - 80% depending on age & geography
what are the epigemiological factors, pathogenesis & morphological features of GIST
peak age 60 yo
Carney syndrome triad & Carney-Stratakis dyad when present in kids w/ neurofibromatosis type 1 - increased risk for GIST & paraganglioma
pathogenesis: KIT tyrosine kinase GOF 75-80; mutation of KIT or PDGFRA = early event in sporadic GISTs
Morphology = whorled appearancearise from interstitial cells of Cajal
what is diffuse esophageal spasm
=repetitive, simultaneous contractions of distal esophageal Sm. M
chest pain when swallowing cold food
(barium swallow- pic)
what are “clues” that youre dealing w/ a carcinoid tumor
cutaneous flushing, sweating, bronchospasm, colicky abd pain, diarrhea, R-sided cardiac valvular fibrosis
circumscribed yellow mass
“salt & pepper” chromatin
(+) for synapophysin, chromogranin, NSE by immunohistochemistry (neuroendocrine differentiation)
neurosecretory granule
what is the VACTERL association
Vertebral
Anal-abnormalities (imperforate anus - MC congenital intestinal atresia; cloacal membrane doesnt involate)
Cardiac
Tracheo-Esophageal fistula
Renal anomalies
Limb anomalies
*congenital prob in one organ - check for probs in other organs*
What are common settings of gastric adenoCA
linked to chronic gastritis & H. pylori, dietary carinogens
More common in setting of=
- gastric atrophy
- intestinal metaplasia
- gastric dysplasia (precursor lesion)
- gastric adenoma (precursor lesion)
- Menetrier dz
- partial gastrectomy
What is Mallory-weiss syndrome
tears at mucosa at GE-jxn bc severe retching of vomiting
(2ndary to binge drinking)
relaxation of LES reflex fails –> esophageal stretching & tearing –> hematemesis
What are the divisions of the stomach
what cells are present in each
cardia - mucin-secreting foveolar cells
antrum: mucin-secreting foveolar cells & endocrine cells (G-cells - release gastrin)
fundus & body: parietal cells (acid secretion) & chief cells (digestive enzymes)
What is the MCC of esophagitis
list other characterisitics
GERD (reflux esophagitis) - also MC outpt GI dx in US
MC = >40 yo
heartburn, dysphagia, regurg of sour taste (water brash), if chronic - severe chest pain
Tx: PPI _(_previously H2 antagonists)
What is the pathogenesis & morphology of H. pylori gastritis
Pathogenesis: fecal-oral transmission;
most often predom antral gastritis w/ normal/increased acid production ==> increase risk for DU
Morphology: mucosa = red & nodular stomach; lamina propria has plasma cells, macrophages & lymphoctyes; urease generate ammonia –> increase pH, so h. pylori survives; CagA toxin - for adherence
*look for H. pylori w/ Warthrin-Starry stain*
what are non-stress related causes of causes of bleeding
- dieulafoy lesions: submucosal A that doesnt branch properly; increase in diameter; MC in lesser curve near GE jxn
- GAVE: endocopically = longitudinal stripes of edematous erythematous mucosa (pic); present w/ occult bleeding/Fe def anemia
what are fxnal causes of esophageal obstruction? & what is the general presentation
(fxnal = disruption in coordinate peristalsis)
- nutcracker esophagus
- diffuse esophageal spasm
- systemic scleroderma (CREST) syndrome
- Zenker diverticulum
dysphagia, odynophagia, globus, regurg, mimic MI
what is the difference btn primary and secondary achalasia
primary = distal inhibitory neuron, ganglion cell, degeneration
secondary = other cause
- chagas - T. cruzi = destruction of myenteric plexus, failure of peristalsis & esohageal dilatation
- diabetic autonomic neuropathy
- HSV1
- autoimmune (sjogrens or thyroid dz)
what is the morphology of Barret esophagus
patches of red, velvety muscosa - extend cephalad from GE jxn
dysplasia may be low or high grade (high = more severe cytologic/architectural changes)
where do MC forms of PUD present?
w/i gastric antrum & duodenum
-as a result of chronic, H. pylori-induced antral gastritis - associated w/ increased gastric acid secretion (hyperchlorhydria), and decreased duodenal HCO3- secetion
what are the associations and presentation of pyloric stenosis
M > F
monozygotic twins >
Turner syndrome & Trisomy 18 (Edward’s syndrome)
increased incidence w/ exposure to erythromycin & azithromycin in 1st 2 wks (orally or mom’s milk)
present btn 3rd & 6th wk of life
regurg/new onset regurg, projectile, nonbilious vomit after feeding, freq need for refeeding
PE = palpable, firm, 1-2 cm ovoid abd mass
What are complications of PUD
most freq = bleeding: 15-20% pt; maybe lifethreatening, 25% of ulcer death, may be 1st indication of an ulcer
perforations: rarely 1st indication, 2/3 ulcer deaths
obstruction (acquired pyloric stenosis),
mucosal atrophy & intestinal metaplasia,
dysplasia,
gastritis cystica
Most gastric adenocarcinomas involve which part of the stomach
antrum
lesser curve > greater
what is the vascular anatomy of esophageal varicies
venous blood from GI tract –> liver via portal V –> heart
portal V = first pass effect
if flow impeded = portal HTN
consequence of portal HTN –> develop collateral channels at sites wheren portal and caval systems communicate –> develop congested subepithelial and submucosal venous plexi w/i distal esophagus & proximal stomach = varices
What is the fxn of gastrin
peptide hormone primarily responsible for enhancing gastric mucosal growth, motility & HCl (luminal acid) secretion by parietal cells within the gastric fundus & body
released in response to vagal & GRP
inhibited by somatostatin & decreased stomach pH
How can eosinophilic esophagitis varying w/ age
what will it look like of examination
children: food intolerance (infants) & common cause of GERD like symptoms in children of developing countries
adults: food impaction + dysphagia
most pts have food/seasonal allergies - asthma, allergic rhinitis, atopic dermatitis (everywhere in kids, hands and feet in adults)
upper EGD: esophagus looks like trachea (rings)
Bx: >25 eosinophils for high power
when evaulating a newborn, you find the pt has a congenital GI disorder. What is your next step
check other organs!
bc organs develop simultaneously during embryogenesis
What are characteristics of esophageal webs
>40 yo, F
associated w/ GERD, chronic graft vs host dz or celiac dz
seen in paterson-brown-kelly** AKA **plummer-vinson syndrome (cheliosis, glossitis & Fe def, increase risk for SCC!)
= nonprogressive dysphagia w/ incomplete chewing of food
SEMI-circumferential lesions, <5 mm (thin)
What is the MC esophageal tumor?
benign :
mesenchymal w/ Sm M tumor (=leiomyoma)
What is barrett esophagus
complication of chronic GERD
intestinal columnar metaplasia w/i esophageal squamous mucosa (stratified squamous –> columnar)
=precursor lesion –> increased risk for esophageal adenocarcinoma (not all pts will develop Ca!)
=esophagitis w/ heartburn, regrug, dysphagia
explain how radiation can cause esophagitis
tx for CA but
long-term effects = fibrosis, mutagenesis, carcinogenesis and teratogenesis
fibrosis –> change perstalsis
what dz is due to the NCCs failing to migrate from the cecum, leading to abnormal migration/premature death of enteric ganglion cells?
list other characterisitcs and presentation
hirschsprung dz -(RET gene) 10% occur in pt w/ down’s syndrome and 5% have serious neurologic abnormalities
–> fxnal obstruction - proximal colon dilation –> massive distention - to point of rupture
rectum ALWAYS affected
F have longer length of colonic involvement
=fail to pass meconium; obstruction/constipation w/ ineffective peristalsis; bilous vomiting
what are examples of UGI polyps (found in 5% UGI endoscopies)
& what are the association of each w/ adenocaricoma
- inflam & hyperplastic polyps - MC associated w/ H. pylori
- fundic gland polyp = sporadic (PPI) or syndrome (FAP)
- gastric adeoma- freq adenoCa (FAP), risk of CA related to size
FAP = familial adenomatous polyposis
compare & contrast Menetrier dz & zolinger-ellison syndrome
- age
- location
- predominant cell type
- inflam infiltrate
- sxs
- RFs
- associations**
What is Zenker diverticulum
increased P w/i distal pharynx due to impaired relaxation & spasn of cricopharyngeus M after swallowing
immediately above UES
Elderly MIKE has Bad breath:
Elderly (>50)
Male
Inferior pharyngeal constrictor
Killian triangle
Esophageal dysmotility - dysphagia, regurg, fxnal obstruction
Halitosis -bad breath
It is NOT uncommon to diagnose gastic CA in advanced stages, where will you find a mass that may lead you to the Dx?
=areas of metastasis
virchow node
sister mary jospeh nodule
irish node
krukenberg tumor
pouch of douglas
What are the malignant tumors of stomach
gastric adenoCA
lymphoma - (MALToma)
carcinoid
GIST (GI stromal tumor)
Where are PGs found and what are their fxns
gastric mucosa & juice
exogenous PG -
- (-) acid secretion
- stimulate mucus & HCO3- secretion
- alter mucosal blood flow
- protection against wide variety of agents
define:
gastritis
gastropathy
gastritis = mucosal inflam process
gastropathy =inflam cells rare/absent (ie. diabetic gastropathy)
what enzymes are secreted by the pancreas to help with digestion
secretion = pancreatic juice & act in duodenum
pancreatic amylase - starch => maltose
trypsin & chymotrypsin - protein => peptide
pancreatic lipase - fats => FA + glycerol
what can longstanding chronic gastritis lead to
What is a mechanism for on of the effects
if longstanding H.pylori –> atrophic gastritis (multifocal)
if involves body/fundus –> mucosal atrophy &/or intestinal metaplasia ==> BOTH RF for adenoCA
(expose epithelium to inflam related free radical damage & prolif stimuli lead to gastric dysplasia -> accumulate genetic alterations –> carcinoma)
what are upper GI symptoms and potential/likely causes of each
obstruction/inflam
- dysphagia/ odynophagia
- “food/liquid gets stuck”
incompetence of LES/reflux of gastric acid
- CHEST PAIN (rule out MI)/heartburn
- coughing, choking, sour taste
blood loss/anemia
- fatigue, lightheaded, fainting
- pallor
inadequate nutrition or CANCER
- wt. loss
what major Vs drain the GI tract (stomach and beyond) & associated accessory organs
portal v
splenic V
superior mesentric V
inferior mesentric V
what is the blood supply and innervation of the esophagus
BS:
upper 1/3 = inferior thryoid A
middle 1/3 = branches of thoracic aorta
lower 1/3 = L. gastric A
N = sym trunk & vagus N (parasym)
what are hypertrophic gastropathies
=uncommon
=giant “cerebriform” enlargement of rugal folds due to epithelial hyperplasia w/o inflam
What is the importance of gastric blood flow
sustain normal phys fxn
& help protect gastric mucosa from ulcer formation
What is an esophageal atresia (EA)
how can it present w/ a TE-fistula
EA= may present w/ or w/o fistula ; commonly at tracheal bifurcation
pic 1= MC - blind upper w/ fistula btn lower and trachea
-pic 2 = blind upper & lower esophagus w/ thin cord of CT linking 2 segments
what is the presentation of a pt with TE-fistula
aspiration, (swallowed material/gastric fluid into resp tract)
suffocation,
pneumonia, severe fluid/electrolyte imbalance
What are symptoms and causes of esophagitis (cause of stuctural and mechanical obstruction)
=self limited pain (odynophagia) to hemorrhage, stricture, or perforation
- radiation
- chemical
- infxous: MC in immunocompromised pts
- eosinophilic-strongly associated w/ food allergy, allergic rhinitis, asthma
- reflux: most prevelant cause of esophagitis = GERD
where and when does the development of the esophagus begin
from cranial portion of foregut
3rd week of gestation
How does the common form of esophageal obstruction w/ presentation of “bird beak” upon barium swallow form?
Achalasia
triad! = incomplete LES relaxation, increased LES tone & aperistalsis of esophagus
sxs = dysphagia (solid & liquids), chest pain
what is the difference btn omphalocele & gastroschisis
omphalocele = abd M. is incomplete & herniate into ventral membranous sac (look for other birth defect (40%)); repair w/ SRG
gastroschisis: ALL layers of the abd wall FAIL to develop, from peritoneum to the skin
both = ventral herniation of abd organs
what is the clinical presentation & morphology of esophageal SCC
= dysphagia, odynophagia, obstruction; diet = soft foods –> nutrient def (often Fe def) & wt loss; hemorrhage/sepsis (if ulcerationg)
ocassionaly, 1st sxs = arpiration of food via TE-fistula
begins as squamous dysplasia
50% in middle 1/3 of esophagus –> metastasis: mediastinal, paratracheal &/or tracheobronchial LNs
early = small, gray-white, plaque like thickenings
later (months-yrs) - mass may be polypoid or exophytic and protrude into/obstruct lumen
may ulcerate/diffusely infiltrative lesions -spread to esophageal wall and cause thickening, rigidity, and luminal narrowing
What are clinical features of PUD
=epigastric burning/aching pain - 1-3 hrs after meals/night
may have relief w/ milk or OTC meds
-referred pain to the back LUQ or chest w/ penetrating ulcers
What is the presentation of Fundic gland polyps
develop in gastic body & fundus
sporadic -increased incidence w/ PPI –> PPI inhibit acid production –> increase gastin secretion –> trophic effects of oxyntic glands
or
FAP
what is the morphology of acute gastritis
surface epithelium intact
foveolar cell hyperplasia
neutrophils in epithelial cells or w/i mucosal glands (if present above BM & in contact w/ epithelial cells = sign for inflam –> gastritis, NOT gastropathy)
Pt presents w/ chest pain & hematemesis & upon auscultation you hear crunching bc of pneumomediastinum, what is your Dx?
Boerhaave syndrome
Hamman’s sign: crunching upon auscultation bc of pneumomediastinum
chest pain, tachypnea & shock
What are the types of Esophageal rings (schatzki rings)
A: distal esophagus above GE jxn; covered w/ squamous mucosa (chronic acid reflux)
B: at squamocolumnar jxn at lower esophagus
=CIRCUMFERENTIAL w/ all layers of esophagus (thick)
Dx = barium swallow
what is Nutcracker esophagus
=jackhammer esophagus
=high amp contraction of distal esophagus due to loss of normal coordination btn inner circular and outer longitudinal Sm M contraction
how can TE-fustula be acquired later in life
esophageal SCC or lung cancer
(e-SCC = dysphagia, odynophagia, change diet: solid –> liquid; hemorrhage & sepsis –> tumor ulcerate –> form TEF)
which congenital defect has the rules of 2’s?
What are its characteristics?
= Merkel diverticulum (true diverticulum)
= vitelline duct persists - (which connects lumen to the developing gut to yolk sac)
=presence of all 3 layers of bowel wall (mucosa, submucosa & muscularis propria)
may contain ectopic gastric –> present in occult bleeding, abd pain mimicking appendicitis or obstruction
may contain pancreatic tissue –>secrete exocrine secretions –> perforate
rules of 2 = 2 yo, 2% population, 2 ft f_rom ileocecal valve_, 2 inches thick, 2x > in Males
What are the genetic associations and epidemiology of intestinal gastric CA
=sporadic & FAP pt due to APC mutations
increased signaling via Wnt path - LOF of APC (adenomatoous polyposis coli) & tumor suppressor (5q21)
GOF = beta-catenin
higher risk geographic (ie Japan); 55 yo Male
What are the causes and examples of stress ulcers that may cause bleeding
how do they present
-pt w/ shock, sepsis, severe trauma (present in critically ill pt in ICU)
curling ulcer: proximal duodenum & associated w/ severe burns/trauma
cushing ulcer: gastric, duodenal, esophageal due to increased intracranial P ;high incidence of perforation
stress-related= range from shallow erosions due to superficial epithelial damage or deep lesions
What is Autoimmune gastritis characterized by & how does it present?
- Ab to parietal cells & IF -detect in serum & gastric secretions
- reduced serum pepsionogen I concentration (bc loss of chief cells (collateral damage)
- endocrine hyperplasia
- Vit B12 def (megaloblastic pernicious anemia; hypersegmented neutrophils; atrophic gastritis)
- defective gastric secretion (achlorhydria) (h. pylori has hypo)
(gastric atrophy over 2-3 decades & anemia only in few pts; slow onset & variable progression -diagnose after being affect many yrs; median age 60 yo, F>M (slightly)
What are histological characteristics of MALTomas
dense lymphocytic infiltrate in the lamina propria
the neoplastic lymphocytes infiltrate the gastric glands focally to create diagnostic lymphepithelial lesions
-reactive-appearing B cell follicles may be present & 40% tumors, plasmacytic differentiation is observed
at other sites GI lymphoma may disseminate as discrete small nodules OR infiltrate the wall diffusely
What are epidemiologic factors & characterisitics of gastric adenoCA
20x greater incidence in Japan, Chile, Costa Rica, & E. Europe
MC malignancy of stomach
gastric CA in US dropped by more than 85% bc change in environmental & dietary factors & decrease in H. pylori
how has the treatment for PUD evolved
SRG- anterctomy (remove gastrin producing cells) & vagotomy (prevent acid stimulatory effects mediated by vagus N)
found PPI and H. pylori eradication works well, so only use SRG for bleeds/perforations
how does esophageal adenoCa present & what is it’s morphology?
what is the survival rate?
- initally = flat/raised patch in otherwise intact mucosa, large masses of >= 5 cm may develop
- tumor may infiltrate diffusely or ulcerate & invade
- location: usually distal 1/3 esophagus (can invade adjacent cardia!)
clinically = dysphagia, odynophagia, progressive wt. loss, hematemesis, chest pain or vomiting (by the time sxs appear the tumor has spread to submucosal lymphatic vessels)
- occasionally discovered in evaluation of GERD or Barrett esophagus surveillence
5 yr survival <25% in high stage dz BUT if CA limited to mucosa or submucosa = 80% survival rate (only few people)
what is the Dx & Tx for Hirschsprung dz
Dx: scope & Bx - absence of ganglion cells w/ H/E stain and immune staining for AChE - confirm w/ intraop frozen section analysis
submucosal plexus (Meissner) - regulate digestive secretions & react to presence of food & myentric plexus (Auerbach) - in muscularis layer, responsible for motility (force & rhythm)
BOTH ABSENT in distal segments
Tx: remove aganglionic part & anastamose normal proximal colon to rectum
What is the MC mesenchymal tumor of the abd
GIST
=50% in the stomach
what are the prevalence and RFs for esophageal adenocarcinoma
white, male
>50% esophageal Ca in US (increased since 1970 - increase in white & hispanic men & white women in US)
highest rate = US, UK, Canada & Australia
RF: barrett esophagus, tobacco, radiation, reduced H. pylori (some strains cause gastric atrophy and reduce acid secretion/reflux = if less of these strains, more likely to get adenoCa)
What is the common presentation of hyperplastic polyp
= MC polyp
associated w/ chronic gastritis & H. pylori
50-60 yo
occasional transformation to adenoCA
What are uncommon forms of gastritis
Eosinophilic: allergies (MC in kids =cow’s milk/soy), immune disorders, parasites, H. pylori
Lymphocytic (varioliform gastritis)- women, celiac dz (40%), T lymph’s; endoscopy: thickened folds covered by small nodules w/ central aphthous ulcerations; affect entire stomach
Granulomatous: MC =Crohn’s dz, then sarcoidosis & infxn
What is the pathogenesis of esophageal adenocarcinoma
progression of barrett esophagus over an extended period of time by genetic and epigenetic changes
early mutations of TP53, CDKN2A (p16/INK4a)
late mutation = amplification of EGFR, ERBB2, MET, cyclin D1, cyclin E
Compare & contrast the following for H. pylori gastritis vs autoimmune gastritis
- location
- inflam infiltrate
- acid production
- gastrin levels
- other lesions
- serology
- sequelae
- associations
What is the morphology, pathogenesis, epidemiology and clinical features of diffuse gastric CA
=sporadic & familial (hereditary forms)
Pathogenesis: loss of E-cadherin development
morphology: infiltrates the wall diffuses, thickens it & typically composed of signet ring cells (=large intracell mucin vacuoles that push nucleus to the periphery)
Linitis plastica (pic) = leather bottle- diffuse rugal flattening & rigid thickened wall
no geographic or gender preference or precursor lesion
Complications fo GERD can lead to…
ulceration
hematemesis
melena
strictures
and development of barretts esophagus - jxn of esophagus & stomach –> squamous to columnar
what it the most powerful prognostic indicator in gastric CA?
depth of invasion & extent of nodular & distant metastases at time of Dx
What is the pathogenesis of esophageal SCC
amplification of SOX2
overexpression of cyclin D
LOF of TP53, E-cadherin & NOTCH1
what is the most important prognostic factor for carcinoid tumors
-compare the types based on the imp factor
location
What are damaging and protective factors of the gastric mucosa
normally = balance btn damage (acid/enzymes) & protection (HCO3-, mucus, blood flow, barrier, regeneration and PG (prostaglandins))
injury - outside factors:
- H. pylori ((-) HCO3-),
- NSAIDS (inhibit COX dep PG production),
- tobacco/alc,
- hyperacid,
- duodenal-gastric reflux,
- decreased O2 deliver (high altitudes; acute gastritis)
direct cellular damanging factors: ischemia, shock, chemo, radiation
Ulcers: layers of necrosis, inflam, granulation tissue & fibrotic scar (chronic gastritis)
how can chemical esophagitis occur
damage by alc, corrosive acids/alkalis, hot fluids, smoking, medication
caustic:
- kids: accidental - often household products
- adults: more severe damage following attempted suicide
Pills: med gets stuck, dissolves and irritates esophagus
What does autoimmune gastritis look like in endoscopy & histology
& what is its pathogenesis
- endoscopy: rugal folds are lost (looks smooth)
- = diffuse mucosal damge of oxyntic (acid producing) mucosa (aka parietal cell mucosa) w/i the body & fundus
- see BVs bc mucosa is so thin
pathogenesis: CD4-T cell destruction of parietal cells (including H/K ATPase; spares antrum & has hyper gastrinemia (unlike H. pylori!)
What is the presentation and histological features of infxous esophagitis
immunocompromised pts!
pathogen invade lamina propria & cause necrosis
HSV: punched out ulcer w/ viral inclusion & rim of epithelial cells
CMV- shallow ulceration w/ nuclear/cytoplasmic inclusion
Candidiasis: grey-white psuedomem of hyphae & inflam cells
What are the precursor lesions for intestinal type gastric CA
metaplasia
atrophy
dysplasia
adenoma
menetrier
What are RFs/associations for PUD?
(PUD =chronic mucosal ulceration affecting duodenum/stomach)
nearly all peptic ulcers associated w/ H. pylori, NSAIDS, or cig smoking
what is the histology of the esophagus
=stratified squamous epitheloum
- mucosa = epithelium, lamina propria & muscularis mucosa
- submucosa: Fat, Ns, BVs, ganglion cells & CT
- muscularis propria: inner circular & outer longitudinal Ms
What is ectopic pancreatic tissue
ectopic tissues = developmental rests
ectopic pancreatic tissue - found in esophagus or stomach
if present in pyloris - may lead to obstruction ; rests may be present in any layer w/i gastric wall - mimic invasive CA
What is an example of referred pain & what is the mechanism
pancreatic pain felt in back
pain in internal organs can be referred to sites distant
=innervations of organs by afferent pain fibers, follow similar paths as the sympathetic NS
What is acute gastritis
& what can be the clinical presentation
=mucosal inflam w/ neutrophils present
=hyperemia & no blood loss
epigastric pain, N/V
if severe: ulcers, hemorrhage, hematemesis, melana, blood loss = emergency!
Finish the sentence-
- Gastric adenoCA are classified by….
- Most gastric adenoCA involve … (location)
- A mass may be difficult to appreciate in _____
- classified according to location, gross & histological morphology
- located in gastric antrum (lesser curve > greater curve)
- mass difficult to appreciate in diffuse gastric CA, but these infiltrative tumors often evoke a desmoplastic reaction that stiffens the gastric wall & may provide a valuable diagnostic clue
what is the morphology of acute ulcers
round & less 1 cm diameter
base = stained brown-black by acid digestion of extravasated blood & may be associated w/ transmural inflam/local serostitis
anywhere in stomach and often in multiples
What is the prevalence of esophageal varices?
how do they present & how do you treat
prognosis?
majority = 50% cirrhotics (25-40% of these bleed = emergency!) ; 2nd MC = hepatic schistosomiasis
silent until - Variceal hemorrhage - hematemesis = emergency ==> Tx = splanchnic vasoconstriction or endoscopically by sclerotherapy (injection of thrombotic agents), balloon tamponade or variceal ligation
Prognosis:
>= 30% die bc hemorrhage- shock, hepatic coma or other complication
>= 50% have recurrent hemorrhage w/i 1 yr
(treat prophylactically in high risk pt w/ beta blocker & endoscopic variceal ligation)
What is the pathogenesis of LES relaxation
LES relaxation usually present w/ release of NO and vasoactive intestinal peptides from inhibitory neurons, along w/ interruption of normal cholinergic signaling
==> if LES tone is decreased or abd pressure is increased –> reflux
