Lawv tshem tawm qhov mob thiab ua npaws qis. Hauv kev muaj tiag, txawm li cas los xij, NSAIDs tuaj yeem ua rau lub plab zom mov los ntawm ob lub tswv yim

Txhua txhua hnub, ntau lab tus tib neeg thoob plaws ntiaj teb yuav tsum tau tshem tawm qhov mob lossis txo qhov kub taub hau, thiab ua li ntawd lawv noj cov tshuaj uas tsis yog-steroidal anti-inflammatory tshuaj (NSAIDs)

Hmoov tsis zoo, cov haujlwm tseem ceeb ntawm kev kho mob ntawm txhua yam tshuaj yog nrog los ntawm cov kev mob tshwm sim, qee qhov kev mob tshwm sim tsis zoo.

Cov kab mob plab hnyuv loj tshwm sim los ntawm NSAIDs, xws li dyspepsia mus rau peptic ulcer teeb meem, yog tej zaum cov tshuaj feem ntau tshwm sim.

Qhov kev pheej hmoo ntawm acid pathology cuam tshuam nrog kev siv NSAIDs zoo li muaj feem cuam tshuam nrog cov koob tshuaj thiab ntau dua rau cov neeg uas tau noj NSAIDs tsawg dua ib hlis lossis cov uas tau noj ib txhij noj ntau NSAIDs lossis corticosteroids.

Cov neeg laus, uas yog cov neeg siv tseem ceeb ntawm NSAIDs, kuj tshwj xeeb tshaj yog muaj kev pheej hmoo, tej zaum vim yog txo qis metabolisation ntawm cov tshuaj, ua rau muaj kev cuam tshuam ntau dua ntawm cov mucosa vim yog senile atrophy thiab ntev kev sib cuag ntawm NSAIDs thiab gastric mucosa vim qeeb. plab hnyuv.

Thaum noj NSAIDs, cov kab mob dyspeptic tshwm sim txog li 60% ntawm cov neeg mob, 20% ntawm qhov uas tsis muaj kev hloov pauv ntawm kev kuaj mob endoscopic.

Kev pheej hmoo rau kev loj hlob ntawm gastroduodenal ulcers thib ob rau NSAID tau txais yog suav tias:

• Advanced hnub nyoog (> 60 xyoo)
• Keeb kwm ntawm digestive pathology
• Concomitant kho nrog anticoagulants
• Concomitant kho nrog corticosteroids
• Cov kab mob hnyav (xws li kab mob plawv, mob caj dab rheumatoid)
• Kev siv tshuaj ntau lossis ntau dua ib NSAID tib lub sijhawm.

NSAIDs tuaj yeem ua rau lub plab zom mov puas los ntawm ob lub ntsiab lus

Ib qho kev cuam tshuam ncaj qha hauv zos, uas pom tseeb tsuas yog tshwm sim tom qab qhov ncauj tau txais cov tshuaj, thiab cov txiaj ntsig ntawm lub cev, qhov thib ob rau kev nqus ntawm cov tshuaj.

Kev mob tshwm sim tuaj yeem ua rau hauv zos lossis kab mob; rau thawj pab pawg muaj:

• Intracellular diffusion;
• Kev puas tsuaj ncaj qha rau cov hnoos qeev thiab nto phospholipids;
• Direct inhibition ntawm HCO3 ntau lawm thiab ntshav khiav;

Cov teebmeem hauv lub cev muaj xws li:

• Inhibition ntawm cyclooxygenase nrog txo PG synthesis;
• Kev hloov pauv tsis ncaj ntawm cov hnoos qeev, HCO3 thiab cov ntshav ntws;
• Hyperproduction ntawm lipoxygenase derivatives.

Qhov cuam tshuam ncaj qha rau cov tshuaj lom yog vim liposolubility ntawm NSAIDs, uas tso cai rau lawv kom diffuse dawb los ntawm cov cell membranes mus rau hauv cov mucous hlwb.

Qhov no ua rau hloov pauv cell permeability nrog backscattering ntawm hydrogen ions los ntawm lub lumen thiab ua rau kev puas tsuaj rau mucosa.

Tsis tas li ntawd, kev sib cuag ncaj qha ntawm NSAIDs thiab cov mucosa kuj ua rau tsis muaj zog ntawm cov khoom tiv thaiv ntawm cov mucosa (txo cov hnoos qeev thiab bicarbonate secretion thiab ntshav ntws).

Cov nyhuv tsis ncaj ncees tshwm sim los ntawm inhibition ntawm ib qho enzyme, cyclooxygenase, uas yog lub luag haujlwm rau kev sib txuas ntawm prostaglandins.

Prostaglandins yog cov tshuaj uas muaj kev ua haujlwm hauv zos, uas ua rau cov hnoos qeev thiab bicarbonate tsim nyob rau hauv lub plab zom mov thiab ua rau cov ntshav ntws hauv zos, yog li muaj kev tiv thaiv ntawm mucous hlwb (cytoprotection).

Tsis tas li ntawd, inhibition ntawm cyclooxygenase ua rau muaj kev nce hauv kev ua haujlwm ntawm lwm cov enzyme, lipoxygenase, nrog rau qhov nce ntxiv hauv lwm cov tshuaj nrog cov nyhuv hauv zos, leukotrienes, uas ua rau muaj kev puas tsuaj rau lub plab mucosa.

NSAIDs gastroduodenopathy, cov tsos mob

Daim ntawv no ntawm gastroduodenopathy tej zaum yuav asymptomatic kiag li los yog tam sim no nrog dyspepsia, mob thiab / los yog kub hnyiab nyob rau hauv lub epigastric cheeb tsam, kev loj hlob ntawm peptic ulcer teeb meem xws li digestive haemorrhage (uas yog loj heev muaj ib tug tuag ntawm txog 10%), stenosis ntawm lub lumen. thiab perforation ntawm lub plab los yog ntau dua cov phab ntsa duodenal.

Mob ntshav qab zib occult tsis yog qhov tsis tshua muaj, thiab tuaj yeem ua rau mob ntshav qab zib sideropenic.

Nws yog qhov tsis txaus ntseeg seb qhov kev noj cov tshuaj no ua rau muaj kev nce ntxiv hauv plab hnyuv oesophageal reflux thiab / lossis cov tsos mob ntawm tus kab mob reflux.

Nws yog ib qho kev nkag siab ntawm cov kws kho mob hais tias kev siv cov tshuaj uas tsis yog-steroidal anti-inflammatory ua phem rau cov kab mob gastro-oesophageal reflux, tab sis cov kev tshawb fawb soj ntsuam tau lees tias qhov no tsis muaj.

Kev kuaj mob thiab kuaj mob

Qhov kev tshawb nrhiav tseem ceeb los kuaj xyuas kab mob gastroduodenal ntsig txog kev siv cov tshuaj uas tsis yog-steroidal anti-inflammatory yog kev kuaj endoscopic.

Hauv cov tsos mob me me, kev kuaj mob kuj tuaj yeem ua rau ex adiuvantibus, los ntawm kev soj ntsuam cov tsos mob tom qab txiav tawm ntawm NSAIDs thiab noj tshuaj antacids.

Yuav ua li cas

Hauv cov neeg mob uas muaj kab mob gastroduodenal los ntawm cov tshuaj uas tsis yog-steroidal anti-inflammatory siv tshuaj uas tsis siv tshuaj tiv thaiv kab mob, kev kho mob nrog H2 antagonists lossis proton twj tso kua mis inhibitors muaj txiaj ntsig zoo ib yam li cov neeg mob uas muaj kev puas tsuaj lossis cov kab mob tsis yog los ntawm NSAIDs.

Nws tseem tsis tau tsim kho seb puas kho tus kab mob Helicobacter Pylori tuaj yeem txo qhov tshwm sim ntawm gastroduodenal teeb meem los ntawm kev noj cov tshuaj uas tsis yog-steroidal anti-inflammatory.

Noj NSAIDs, qee cov lus qhia

Qhov kev tiv thaiv tseem ceeb yog kom tsis txhob siv ntau dhau, siv ntau dhau thiab noj ntau NSAIDs tib lub sijhawm.

Tsis ntev los no kev tshawb fawb tshawb fawb thaum kawg tau pom qhov ua tau zoo ntawm kev tiv thaiv tshuaj (nrog rau cov tshuaj thaiv cov plab hnyuv) ntawm cov kab mob gastroduodenal tshwm sim los ntawm kev siv NSAIDs ntev.

Lwm cov kev pab kho mob uas yuav pab tau rau kev tiv thaiv cov kab mob NSAID yog antacids, mucosal protectors thiab prostaglandin synthetase analogues.

Kev tiv thaiv kev kho mob yog qhov yuav tsum tau ua nyob rau hauv cov neeg mob uas noj NSAIDs thiab muaj ntau tshaj ib qho ntawm cov kev pheej hmoo.

Tsis ntev los no, ntau qhov kev txaus siab tau tshwm sim los ntawm kev qhia txog cov tshuaj tiv thaiv kab mob tshiab uas cuam tshuam ib feem ntawm cyclooxygenase.

Muaj ob lub isoforms ntawm cyclooxygenase: COX-1 thiab COX-2. COX-1 yog ib qho uas tsim cov tshuaj (prostaglandins) uas tiv thaiv cov hlwb.

COX-2, ntawm qhov tod tes, yog induced nyob rau hauv inflammatory cells thiab yog li ntawd tseem ceeb nyob rau hauv tus txheej txheem ntawm o thiab mob.

Yog li ntawd, kev siv cov tshuaj uas xaiv los thaiv COX-2 yuav tsum txo qhov tshwm sim ntawm gastro-duodenal lesions.

Nyeem kuj:

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Gastric Bypass yog dab tsi?

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