Gastritis 22 sep 14

7/24/2019 Gastritis 22 sep 14

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Definition:Inflammation of the gastric mucosa

-group of disorders with inflammatory changes

in the gastric mucosa (G.M.) that have different

clinical features, histological characteristicsand pathogenesis.

A. ACUTE GASTRITISB. CR!"IC GASTRITIS


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A. ACUTE E#!RAGIC GASTRITIS

$ER!SI%E&E'a(inationsho)s:

EDE#A#UC!SA* +RIABI*IT

ER!SI!"S: li(ited to the (ucosa -SITES !+ B*EEDI"G: diffusel through the G. #.locali/ed to the 0od, antru( of the sto(ach

IST!*!GIC E1A#I"ATI!" of the G.#. re2eals infiltration of

the la(ina propria )ith: 3 (ononuclear cells

3 4#" leu5octes3 e'tra2asations of 0lood in the (ucosa


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ETI!*!G 6 4AT!GE"ESIS:Erosive gastritis 8 - ! " of critically ill hospitali#ed patients

(medical) surgical intensive care units

$tress induced gastritis

#echanis(:a) ischemia of the G.M.%) acid diffusion from the gastric lumen into gastric mucosal tissues

c) %ile acid & duodenal pancreatic secretions reflu'ed into the gastric

lumen

a % *+I, in the ethiopathogenesis of the $*E$$ I/0+E0 G,$*II$

AGE"TS in7ure the G.#.8 aspirin3in7ure the s(all 2essels in the G.#. 0:

3inhi0itor of prostacclin in the )alls of 2essels

3snthesis of tro(0o'ane 0 platelets8 "SAIDS8 0ile acids8 pancreatic en/(es8 ethanolReduction in tissue 4G 3 principal in da(age the G.#.


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C*I"ICA* +EATURES 4SICA* E1A#I"ATI!"1e(ate(esis 9 (elena 4allor 1Ane(ia Tachcardia1Epigastric pain potension

1"ausea1%o(iting

BI!*!GICA* AS4ECTS8 leucoctosis 9 leu5openia


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DIAG"!SIS-0lood in the stool 9 gastric aspirate

Upper GI endoscop:

1mucosal hemorrhages1fria%ility congestion1erosions1superficial & deep ulcerations in the fundus & %ody of the stomach

Radiographic e'a(ination 3 much less relia%le in detecting acutehemoragic erosive gastritis

TREAT#E"TA. General supporti2e (easures

8 (aintenance of o'gen, 0lood 2olu(e, fluid and electroltereuire(ents

B. ; 3 R antagonist $i.2.& = (g9daEm%oli#ation & vasopressin infusion of the left gastric artery

I22 ontroloc 3! mg i.v.$urgical treatment should not %e performed unless is a%solutely necessary.


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ACUTE GASTRITIS ? E*IC!BACTER

4*!RI8 short spiral 3 shaped, (icroaerophitic gra( 8 0acillus8 in gastric sa(ples 0 histological e'a(ination, culture,

increase acti2it, 0 endonuclease analsis.8 he(ato'lin 3 positi2e8 UBT @C, @>C8 anti0odies $Ig G, Ig A& to .4.

90 100 % Hp + antral biopsy specimens of DU patients

70 % - G.U.80 % - chronic astritis in!ol!in the antral m"cosa

#0 % - non "lcer $yspepsia


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CR!"IC GASTRITISDefinition4 hronic inflammatory cells5 predominately lymphocytes andplasma cells.

IST!*!GIC C*ASSI+ICATI!"

I. SU4ER+ICIA* GASTRITIS- Inflammatory changes in the lamina propia of the superficial mucosa of

the upper half of G.M. and the glands are preserved

II. ATR!4IC GASTRITIS- the inflammatory infiltrate e'tends to the deep positions of the mucosa

- profound loss of the glandular structures which are separated widely %y

connective tissue5 with a greatly reduced & a%sent inflammatory infiltrate.

- the mucosa is thin5 revealing the prominence of its underlying vessels %yendoscope e'amination.

Gastritis progresses changes in the morphology of the gastric glandular

elements.

Intestinal metaplasia conversion of gastric glands to the small-intestinal

mucosal glands with go%let cells.


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CR!"IC GASTRITIS 3 T4ES A 6 B

Tpe A3 in2ol2es the 0od and fundus of the sto(ach 3 fro( that (a lead to pernicious ane(ia

Anti0odies to parietal cells, intrinsec factor in seru( i((uno 9 autoi((unopathogenesis

4arietal cell Anti0odies ;= of patients o2er age = ;= of patients )ith 3 hpoparathroidis(

3 Addisons disease

3 2itiligoAnti0odies to intrinsec factor >= of those )ith pernicious ane(ia.The ris5 of sto(ach cancer in patients )ith tpe A gastritis and perniciousane(ia is three ti(es than the general population

Tpe B:In ounger patients in2ol2es the antru(In elderl patients in2ol2es entire sto(achThe incidence increases )ith age8 Strong associations of . plori )ith tpe B gastrities8 Chronic reflu' of: pancreatic 3 0iliar secretions

0ile acidslsolecithin


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DIAG"!SIS

- 6iopsy of the G.M. provides the most relia%le means of

identifying and classifying gastritis.-$everal %iopsies of suspected areas5 when safe and

possi%le5 are recommended.

TREAT#E"T

In type ,.G. pernicious anemia

7it. 69 indefinite regular parental administration


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#"TRIERS DISEASE

- large tortuoces gastric mucosal folds in gastric %ody and fundus.- hyperplasia of surface and glandular mucous cells5 which replace most of

the chief and parietal cells.- the lamina propria may contain an increased num%er of lymphocytes andintestinal metaplasia may %e present.

S(pto(sepigastric pain

anore'ianausea5 vomitingweight lossgastric %leeding unusualGastric ulcer & gastric carcinoma many develop :

Gastric acid secretion is reduced & a%sent.

6arium e'amination4 large gastric foldsEndoscopic e'amination4 confirm gastric folds

Diagnostic4deep mucosal %iopsy

Treat(ent4 ,*;9 decrease protein losshigh protein diet to replace protein losesgastrectomy in severe disease


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C!RR!SI%E GASTRITIS

- corrosive chemicalsantrum in


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I"+ECTI!US GASTRITIS

2hlegmonous G necrosis5 sepsis

- streptococci5 staphylococci5 2roteus5 Escherichia coli

TREAT#E"T i.v. anti%iotics

fluids electrolyte replacement

gastrectomy in lac> of response

It can occur in immuno-compromised patientscytomegalovirus


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E!SI"!4I*IC GASTRITIS

-e'tensive eosinophilic infiltration (e.i) of the wall of the stomach

-%iopsy reveals e.i.

- antrum is more fre?uently involved than G %ody fundus.

S#4T!#S: epigastric painnausea5 vomiting

TREAT#E"T:glucocorticoids


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GRA"U*!#AT!US GASTRITIS

Chrons diseaseproduce: ulcerationgranulo(atous infiltrationstricture for(ation

!thers: histoplas(osiscandidosissphilistu0erculoses

Diagnostic: 0iopsies ? ctolog to e'clude (alignancsurgical e'ploration if the diagnostic is not

esta0lished 0 0iops at endoscop.


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DU!DE"A* U*CER

hronic and recurrent disease

ETI!*!G- Genetic +actors4increase of %lood !

- increase ;, 6@ antigen in white male su%


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C*I"ICA* +EATURES

@. Epigastric pain: sharp, 0urning, gna)ing@= 8 right epigastriu(

;. !ccurs fro( = 8 hours after eating

a)a5ens the patients at night8 pain is usuall relie2ed 0 food or antacids8 nausea, 2o(iting8 )eight loss8 ane(ia $occult 0lood loss& 3 iron deficienc

8 constipation8 4enetration8 4erforation 9 co(plications8 e(orrhage: @H )ith >= reccurence


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DIAG"!SIS

@. Bariu( e'a(ination+GI A! 8! " discrete crater in the

pro'imal portion of the duodenal %ul%

;. Endoscopic e'a(ination

- si#e- shape- location

- in detecting 0.+. in the a%sence of *' image

- in identifying ulcers too small & superficial to %erecogni#ed %y B-ray- e'cluding an ulcer as the source of active GI;emorrhage


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#EDICA* TREAT#E"T

. Antacids: ,luminum hydro'ide

Magnesiumalcium car%onate

$odium %icar%onate

;. ; 3 R antagonists

imetidine C!! mg ' 3 & days 3 wee>s,dverse effects4 increase transaminase5 creatinine5 gynecomastia

Ranitidine: @! mg ' 9 & dayC!! mg at %edtime

"i/atidine: C!! mg month@! mg %edtime for reduction of 0+ recurrence

+a(otidina: ;= 3 >= (g 9 da > )ee5s

. Anticholinergic agents4atropine decrease gastric acid secretion(g.a.s.)

2iren#epine ad


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>. Coating agentsSucralfate increase (ucosal defense-Colloidal 0is(uth

H. 4rostaglandins reduce 0asal and sti(ulated g.a.s. enhances(ucosal resistance to tissue in7ur.

. 4roton 4o(p Inhi0ition8 !#E4RA!*E ;= (g 1 ; 9 DA > 3 )ee5s8 *A"S!4RA!*E = (g 9 da8 4A"T!4RA!*E >= (g 9 da8 ES!#E4RA!*E ;= 3 >= (g 9 da

DIET8 free of spices, fruit 7uices8 a2oid coffee, alcohol inta5e8 eli(ination of s(o5ing8 eli(ination stress

eat H ti(es 9 da in s(all (eals


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GASTRIC U*CER $G.U.&-the pic> incidence for G.+. is in the si'th decade

ETI!*!G,cid- pepsin appears important in the pathogenesis

- Gastric emptying is delayed- *egurgitation of duodenal contents (%ile) induce gastric mucosal

in


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DIAG"!SIS. 6arium e'amination

9. Endoscopy4 si#e5 location5 histological characteristics

+lcer C cm diameter are often malignant

3" of G+ appears %enign on B-*ay plane to %e malignant %y

endoscopic %iopsy & surgery:

#EDICA* TREAT#E"T

;9*,$ulcralfate 3& 8 wee>s

,ntacids

6enign G.+. should heal completely within C months of vigorous

therapy.

,void - /$,I0& glucocorticoides- coffee

- smo>ing

- spices foods

Gastroscopy after 3 wee>s of treatment reveal healing of %enign

ulcers.


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Surger in D.U.8 %agoto( ? antrecto(

8 2agoto( ? ploroplast8 truncal or selecti2e 2agoto(8 Bilroth IA: sto(ach ? pro'i(al duodenu(-Bilroth IIA: sto(ach ? loop of the 7e7unu(

Surger GU: Antrecto( ? G.D. Anasto(osis in those )ho do notrespond to (edical theraph9co(plications.

GASTRIC ADE"!CARCI"!#A

= are adenocarcino(as@= non99 odg5inJs l(pho(as and leio(osarco(as.


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ETI!*!G*ong9ter( ingestion of high concentrations of nitrates indried, s(o5ed,salted foods8 higher ris5. Serial endoscopic e'a(ination of the sto(ach in

patients )ith atrophic gastritis8 replace(ent of the gastric (ucosa 0intestinal tpe cells9 cellular atpia9 neoplasia8 Adeno(atous polposis8 Gastric ulcers8 #enetrierJs disease-Group AII patients

C*I"ICA* +EATURES8 Upper a0do(inal disco(fort8 stead pain8 Anore'ia8 Keight loss8 "ausea ? 2o(iting 8 tu(or of the plorus

8 Disphaga 8 tu(or of cardia8 4alpa0le a0do(en (ass8phsic e'a(ination8 Iron 8 deficienc ane(ia8 #igrator thro(0ophle0itis8 (icroangiopathie he(oltic ane(ia8 Achantosis nigricans.

DIAG"!SIS


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DIAG"!SISDou0le8contrast radiographic e'a(ination.Deep Gastroscopic 0iops and 0rush ctolog.

TREAT#E"TSurgical re(o2al of the co(plete T, )ith resection of ad7acent l(ph nodesoffers the onl chance for cure.Su0total gastrecto( 8 distal carcino(as.Total gastrecto( 8 pro'i(al tu(ors.

4R!G"!SIS8 degree of tu(or penetration into the sto(ach )all.8 regional l(ph node in2ole(ent9 2ascular in2asion.Che(otherap and9or radiotherap 8 (etastatic disease $H +U? Do'oru0icin,#to(icin ? G cisplatin&

4RI#AR GASTRIC *#4!#A-L of gastric (alignancies9 ; of all l(pho(as.

GASTRIC SARC!#A8 @8 of all gastric neoplas(s

8 anterior ? posterior )alls of the gastric fundusd t th li d l

Gastritis 22 sep 14

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