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GI motility disorder Cecil chap 132(p694-702 )

1. Normal motility in stomach, small intestine and colon

1) smooth muscle

stomach¿¡¼­ distal colon±îÁö luminal content°¡ À̵¿Çϱâ À§Çؼ­´Â phasic & tonic

contractions & intrinsic stomach muscle toneÀÇ relaxation(peristaltic reflex)»çÀÌÀÇ Á¶È­°¡

ÇÊ¿äÇÏ´Ù.

smooth muscle cellÀÇ slow wave frequency´Â cell¾È¿¡ ÀÖÀ¸³ª ÀÎÁ¢¼¼Æ÷ÀÇ activity¿¡ ÀÇÇØ

modifyµÉ ¼ö ÀÖ´Ù. pacemaker regionÀÌ GIT °¢ ºÎºÐÀÇ dominant frequency¸¦ Á¶ÀýÇÑ´Ù.

* interstitial cell of Cajal

: GITÀÇ ´Ù¸¥ ºÎºÐ¿¡ ´ëÇÑ pacemaker·Î ÀÛ¿ëÇϸç ÀÌ ¼¼Æ÷ÀÇ Á¸Àç´Â proto-oncogene c-ki

tÀÇ Á¸Àç·Î ¾Ë¼ö ÀÖ´Ù.

proto-oncogene c-kit´Â tyroine kinase receptor¸¦ codeÇÑ´Ù.

slow wave˂ progressive propagation˼ gastric smooth muscle cell˂ tight electrical

couplingÀ¸·Î ÀÌ·ç¾îÁö¸ç, higher contraction frequency´Â mean pressure¸¦ Áõ°¡½ÃÄÑ

intraluminal contents¸¦ lower pressure area ¹× distal·Î À̵¿½ÃŲ´Ù.

discending colon¿¡ intraluminal pressure°¡ ³ôÀ¸¸é intraluminal pressure¸¦ µÚ·Î´Â

transverese colonÀ¸·Î, ¾ÕÀ¸·Î´Â sigmoid colonÂÊÀ¸·Î À̵¿½ÃŲ´Ù.

±×·¯¹Ç·Î frequency gradientº¸´Ù´Â pressure amplitude gradient°¡ colonic transitÀ» °áÁ¤

ÇÑ´Ù.

colon¿¡¼­ proximal descending colon & splenic flexure¿¡ ¼öÃàÀÌ ¿ì¼¼Çϸé Àå³» ³»¿ë¹°À»

¼¯´Â ÀÛ¿ëÀ» Çϰí, transverse colonÀº storage areaÀÇ ¿ªÇÒÀ» ÇÑ´Ù.

´Ù¸¥ motility patternÀÎ propagating contractionÀº neural controlÇÏ¿¡ ÀÌ·ç¾îÁö¸ç fecal

content¸¦ T-colon¿¡¼­ distalÂÊÀ¸·Î propagationÇÏ¿© sigmoid colon¿¡ º¸´Ù ¸¹ÀÌ ÀúÀå

µÈ´Ù.

circular contractionÀº lumenÀ» ±¸È¹È­ÇÏ¿© Á¡¸·¿¡ ³ëÃâµÈ contents¸¦ ¼¯´Â ¿ªÇÒÀ» ÇÑ´Ù.

longitudinal muscleÀÌ Âª¾ÆÁ® luminal contents°¡ Àü¹æÀ¸·Î À̵¿ÇÑ´Ù.

sphincter contraction & relaxationÀº ÁÖÀ§ bowel pressure or physiologic stimuli¿¡ ¹ÝÀÀ

ÇÏ¿© enteric neurotransmitter or circulating peptide hormone¿¡ ÀÇÇØ Á¶ÀýµÈ´Ù. GI smooth

muscle contractionÀ» À§Çؼ­´Â intracellular Ca³óµµÀÇ Áõ°¡°¡ ÇÊ¿äÇÏ´Ù.

GIT¸¦ ÅëÇÑ intraluminal content transport¿¡´Â smooth muscle relaxationµµ ¶È°°ÀÌ Áß¿ä

ÇÏ´Ù.

cAMP»ý»êÀº smooth m. cell membrane receptorÀÇ ligand activation¿¡ ÀÇÇØ ½ÃÀ۵ǰí SR

·Î CaÀÌ À̵¿ÇÔÀ¸·Î½á intraluminal Ca³óµµ°¡ °¨¼ÒÇÑ´Ù.

(1) enteric nervous system

enteric neuron¿¡´Â ¸¹Àº excitatory & inhibitory neurotransmitter°¡ ÇÔÀ¯µÇ¾î ÀÖ´Ù(Tab

132-1).

ÀϺΠneurotransmitters´Â stimulatory(¿¹, Ach)ÀÌ°í ´Ù¸¥ °ÍµéÀº inhibitory(¿¹, VIP)ÀÌÁö¸¸,

ÀϺΠneurotransmitter ´Â nerve¿Í muscle¿¡ ´Ù¸¥ ÀÛ¿ëÀ» ³ªÅ¸³¿À¸·Î½á motility patternÀ»

Á¶ÀýÇÑ´Ù.(¿¹, opiates´Â muscle¿¡´Â stimulation, Ach release´Â inhibition)

ȤÀº ´Ù¸¥ regional effect¸¦ ³ªÅ¸³»±âµµ ÇÑ´Ù(¿¹, neurotensinÀº gastric muscleÀº relax,

small intestinal & colon muscle˼ stimulation).

NO´Â myenteric neuron, smooth muscle cells & cells of Cajal¿¡¼­ »ý»êµÇ¸ç, intracellular

cGMP¸¦ À¯µµÇÔÀ¸·Î½á GI smooth muscle relaxation½ÃŰ´Â final mediatorÀÌ´Ù.

intrinsic enteric neuronÀº ¼­·Î ¿¬°áµÇ¾î ÀÖ´Ù(Fig 132-2).

(2) enteric peptide hormones

peptides´Â ½Ä»çÈÄ GI mucosa¿¡¼­ Ç÷ÁßÀ¸·Î À¯¸®µÇ¾î hormoneó·³ ÀÛ¿ëÇÏ¿© gastric,

small intestinal, and colonic smooth muscle contraction¿¡ ¿µÇâÀ» ¹ÌÄ£´Ù.

enteric nervous systemó·³ stimulating peptides(gastrin, CCK, motilin)¿Í inhibitory

peptides(enteroglucagon & peptide YY)»çÀÌÀÇ counterbalance°¡ motility¸¦ Á¶ÀýÇÑ´Ù.

½Ä»çÈÄ 30-60ºÐ¿¡ ÃÖ°í Ç÷Á߳󵵿¡ µµ´ÞÇÑ´Ù.

(3) GI transit

¨ç stomach

liquid emptying(T12=15min)ÀÌ solid(T12=45-90min)º¸´Ù ºü¸£´Ù.

glucose solutionÀÇ gastric emptyingÀº 2 kcal/min·Î salineº¸´Ù ºü¸£´Ù.

fundus: liquid emptying

antrum: solid emptying

¨è small intestine

transit time: small intestine¿¡¼­ cecum±îÁö 40-180min

* MMC(migrating motor complex)

°øº¹½Ã ¹ß»ýÇÏ¿© indigestible luminal content¸¦ Á¦°ÅÇÏ´Â ¿ªÇÒÀ» ÇÑ´Ù.

3 phases·Î ÀÌ·ç¾îÁö¸ç

phase 1 : inactivity period

phase 2 : intermittent phasic contractions

phase 3 : continous periods of contractions that propels the remaining intestinal

contents during fasting

phase 3 MMC´Â stomach(3 cycle/min)¿¡¼­ duodenum(11 cycles/min)À¸·Î ÁøÇàÇÑ´Ù.

2. GI motility disorder

1) delayed gastric emptying Tab 132-3

typical sx: early satiety, nausea, vomiting

¿¹> postvagotomy, DM, viral infections, reflux esophagitis, brain stem lesions,

anorexia nervosa, tachygastria

¨ç diabetic gastroparesis

diabetic hyperglycemia or ketoacidosis¿¡ ÇÕº´µÇ¾î ³ªÅ¸³ª´Â delayed gastric emptyingÀº

´ë»ç»óŰ¡ È£ÀüµÇ¸é ȸº¹µÈ´Ù. ±×·¯³ª ¶§·Î´Â À§°¡ ½ÉÇÏ°Ô ÆØ¸¸Çϰí Á¡¸·ÃâÇ÷À» º¸¿© NG

tube decompressionÀÌ ÇÊ¿äÇÒ¼öµµ ÀÖ´Ù.

chronic delayed gastric emptyingÀº long-standing IDDM°ú µ¿¹ÝµÇ¸ç ÀÓ»óÀû ¹®Á¦°¡ Å©´Ù.

±×·± ȯÀÚµéÀº ¹Ýº¹ÇÏ¿© nausea, vomitingÀ» º¸À̰í À½½Ä¼·ÃëÀÇ Àå¾Ö ¹× insulin¿ä±¸¸¦

º¹ÀâÇÏ°Ô ÇÑ´Ù.

retinopathy, nephropathy, peripheral neuropathy ¹× ´Ù¸¥ ÇÕº´ÁõÀÌ ÈçÈ÷ Á¸ÀçÇÑ´Ù.

1mmÀÌ»óÀÇ non-digestible materialÀÇ emptying¿¡ ÇÊ¿äÇÑ MMC°¡ ¾ø¾î¼­ diabetic patient

´Â bezoar°¡ Àß »ý±ä´Ù.

autonomic neuropathy°¡ Ç×»ó Á¸ÀçÇÏ´Â °ÍÀº ¾Æ´ÏÁö¸¸ vagal neuropathy´Â DM¿¡¼­

gastric stasis¸¦ ÀÏÀ¸Å°´Â º´ÀÎÀ¸·Î »ý°¢µÈ´Ù.

metoclopramide°¡ gastric emptyingÀ» ÃËÁø½Ã۰í, nausea and distension¿¡ ´ëÇÑ CNS

recognitionÀ» °¨¼Ò½ÃÅ´À¸·Î½á Áõ»óÀ» È£Àü½ÃŲ´Ù. Bethanechol¶ÇÇÑ gastric motility¸¦

Áõ°¡½Ã۰í, diabetic gastric stasisȯÀÚÀÇ Áõ»óÀ» È£Àü½ÃŲ´Ù.

erythromycinÀº antral contraction°ú fundal toneÀ» Áõ°¡½ÃÅ´À¸·Î½á gastroparesisÁõ»óÀ»

È£Àü½ÃŲ´Ù. clonidineµµ gastric emptying & sxÀ» È£Àü½Ãų¼ö ÀÖ´Ù.

¨è anorexia nervosa

anorexia nervosaȯÀÚ¿¡¼­ liquid°¡ ¾Æ´Ñ solid gastric emptying°¡ Áö¿¬µÇ´Â °ÍÀÌ °üÂû

µÈ´Ù.

À̰ÍÀÌ bulimia ȯÀÚ¿¡¼­´Â °üÂûµÇÁö ¾Ê´Â´Ù.

delayed gastric emptying˼ antral dysrhythmia, fundal hypotonia, decreased

postprandial plasma concentrations of norepinephrine and neurotensin and impaired

autonomic function(decreased resting diastolic blood pressure and skin conductance)

°ú °ü·ÃÀÖ´Ù.

underlying psychiatric disturbance reversalÀÌ complete sx resolution¿¡ ÇÊ¿äÇÏ´Ù.

2) rapid gastric emptying

¿¹> dumping syndrome, pancreatic insufficiency, celiac sprue,

Zollinger-Ellison syndrome, duodenal ulcer