Motility Disorders Flashcards
etiologies of GI motility disorder
CNS, neuropathic (enteric nervous system), myopathic, abnormalities in interstitial cells of Cajal
is esophagus skeletal or smooth muscle
upper = striated muscle, distal = smooth muscle
voluntary swallowing phase
chewing, bring bolus back with tongue, which raises soft palate and closes off nasopharynx
Dysphagia
difficulty swallowing/discomfort in swallowing
Achalasia
muscles in lower esophagus fail to relax and food can’t get into stomach
Scleroderma
multisystem disorder with obliterative small vessel vasculitis and connective tissue proliferation with fibrosis of multiple organs
Main pathologic abnormalities of GI tract in sclertoderma
smooth muscle atrophy and gut wall fibrosis
Esophageal manifestations of scleroderma
smooth muscle atrophy can cause weak peristalsis –> dysphagia
- can also cause weak LES –> GERD
- unrepentant gerd can lead to esophagitis and stricture
is smooth muscle atrophy and gut wall fibrosis myopathic or neuropathic
MYOPATHIC
how to diagnose esophageal disease
Esophageal manometry (transnasal probe)
Main characteristic of scleroderma patients
PERISTALSIS ABSENT due to atrophy of smooth muscle and weak LES
Main characteristic of spastic disorders of esophagus
PERISTALSIS PRESERVED!!
symptoms of spastic disorders of esophagus
chest pain, dysphagia
postulated pathophys of spastic disorders of esophagus
overactive excitatory nerves (neuropathic) or overreacting smooth muscle response (myopathic)
how are inhibitory nerves distributed in esophagus
fewer proximal and more as you go distal
Jackhammer esophagus
hypercontractile; contractions coordinated but excessive amplitlude
2 main ideas of stomach motility
retropulsion and receptive relaxation
Receptive relaxation
vagally-mediated inhibition of smooth muscle tone of stomach body–maintain low intragastric pressure
what drives liquid emptying
tonic pressure gradient
what drives solid emptying from stomach
vagall-mediated contractions and enteric nervous system
how are residual solids emptied
migrating motor complex every 90-120 minutes
what causes retropulsion
mixing/churning of stomach tries to push food contents along but pyloric sphincter only opens so much/too big of particles get retropulsed back for more digestion
Gastric reservoir function
receptive relaxation and accomodation
gastric accommodation
stomach likes to keep things low pressure, so smooth muscle relaxation due to mechanical distention (gastric mechanoreception from enteric nervous system); vasovagal response
Function of fundus/proximal body of stomach
storage
main function of distal body/antrum
processing/emptying
dyspepsia
syndromic term
- discomfort or pain centered in upper abdomen usually related to eating
symptoms of dyspepsia
postprandial heaviness, early satiety, epigastric pain or burning
organic causes of dyspepsia
PUD, atypical GERD, gastric/esophageal cancer, pancreaticobiliary disorders, food/drug (NSAIDs) intolerance
functional dyspepsia
when no organic causes found
prevalence of dyspepsia
20-25%
alterations in gastric motility in functional dyspepsia
40% have impaired gastric accomodation; 45% have imparied gastric emptying (gastroparesis)
Gastroparesis
impaired transit of food from stomach to duodenum (excludign mechanical obstruction of gastric outlet)
Clinical manifestations of gastroparesis
nausea, vomiting, early satiety, postprandial abdominal distention, postprandial abdominal pain
Major causes of gastroparesis
idiopathic-(postinfectious?), Post surgical, diabetic, med related, paraneoplastic syndrome, rheumatologic, neurologic, myopathic (scleroderma)
Diagnose gastrophoresis
Gastric emptying study
how is a gastric emptying study performed
pt eats low fat EggBeaters radiolabeled with 1 mCi Technetium 99; microwaved/served wtih toast, jam, and water
- take serial lpictures at 0,1,2,3,4 hours and look at percept of emptied food
- abnormal when retention >60% at 2 hr or >10% at 4 hr
- Normally almost gone at 4 hours
How to manage gastrophoresis
small frequent meals, low-fat and low-residue diet, glucose control in diabetes, prokinetic agents, antiemetics, gastric electrical stimulation, surgery (2%)
gastroparesis in funcitonal dyspepsia
up to 45% FD pts have delayed gastric emptying, potential pacemaker cell dysfunction/ineffective muscle function of distal stomach
- ineffective antropyloroduodenal contraction patterns
Small intestine size
21’ long 1” diameter with increased surface area due to villi/microvilli
Small intestine motility
when fed–primary motility is segmentation (mixing)
- when fasting– migrating motor complex
Segmentation
mixing of contents to and fro in different segments of small bowel to increase exposure to mucosa for increasing changes of nutrient absorption; 9-12 contractions per min; total transit 3-5 hrs
Migrating Motor complex
main motility of SI in fasting state; every 90-120 min have sequential orderly peristaltic wave from stomach to ileocecal valve to sweep gut between meals
Main categories of SI motility disorders
Neuropathic and Myopathic; some diseases with features of both
Neuropathic SI motility disorders
normal amplitude but sustained bursts of uncoordinated phasic contractions – not progression down small bowel
- early return of MMC and increased frequency which impairs absorption and can cause diarrhea by overwhelming digestive capacity of colon
Myopathic SI motility disorders
decreased amplitude of contraction or complete lack of any motor activity
Chronic Intestinal Pseudo Obstruction (CIPO)
signs/symptoms of small bowel without lesion obstructing flow of intestinal contents
- have dilation without transition of bowel on imaging
major manifestation of small intestinal dysmotility
Chronic intestinal pseudo obstruction (CIPO)
complication of CIPO
small intestinal bacterial overgrowth
stasis of contents –> bacterial overgrowth –> fermentation adn malabsorption
symptoms of CIPO
nausea/vomiting, abd pain, distention, constipation, diarrhea, urinary symptoms
Neuropathic etiologies of SI motility disorders
degenerative neuropathies(parkinsons), paraneoplastic autoimmune (anti-Hu Ab), Chagas dz, Diabetes associated (neuropathy)
Mixed myopathic and neuropathic etiologies of SI motility disorders
- infiltrative conditions (scleroderma, amyloidosis, eosinophilic gastroenteritis)
- idiopathic
CIPO in kids
mostly congenital, usually a primary condition (visceral neuropathy/myopathy), absent MMC predicts need for IV nutrition
mortality of children with CIPO
1/3 infants born die in 1st year of life
function of colon
transport, store and expel stool after absorbing majority of luminal fluid– try to maintain Intravascular volume
Muscle in colon
smooth and skeletal; circular smooth (internal anal sphincter)– autonomic innervation by pelvic plexus
Internal anal sphincter
circular smooth muscle innervated by pelvic plexus
External anal sphincter
striated skeletal muscle innervated by pudendal nerve
puborectalis muscle
striated-volitional
which muscles to we voluntarily control in rectum
EAS and puborectalis
types of motor activity in colon
Low amplitude tonic and phasic contractions; high amplitude propagated contractions
role of low amplitude phasic and tonic contractions in colon
mix luminal contents (in Haustra) for increasing luminal fluid absorption
role of high amplitude propagated contractions (HAPCs)
propelling contents forward
what increases colonic motility
after a meal (gastrocolonic response) and on awakening
Causes of constipation
drugs, mechanical block,
- Metabolic (DM, hypoK, hyperCa, HypoMg, hypothyroid)
- Myopathy (amyloid, scleroderma)
- Neurogenic (Parkinson’s spinal cord injury, MS, autonomic nneuropathy, Hirschsprung’s)
- Other: pregnancy, immobility
- IBS-C
- Refractory constipation: (normal transit, slow transit, dyssynergic defecation)
colonic transit studies
Sitz marker, Scintography, Wireless capsule
Sitz marker transit study
24 radioopaque makers in capsule given Day 1 – plain abdominal xray on day 5
- 5 markers scattered throughout colon = slow transit (more myopathic or neuropathic motility disorder of colon)
- > 5 markers in recto-sigmoid suggests defecatory disorder
Scintography
Isotope in delayed–release capsule dissolves in alkaline pH of distal ileum
- gamma camera scans in 4, 24, 48 hrs to show colonic distribution
disorders of esophageal peristalsis
achalasia, scleroderma
disorders of LES relaxation
Achalasia
disorders of LES tonic contraction:
scleroderma
Disordered gastric receptive relaxation/accomodation
functional dyspepsia
disorders with impaired gastric emptying
gastroparesis, functional dyspepsia
disorder of impaired SI peristalsis
CIPO (scleroderma)
disorders of impaired colonic transit
slow transit constipation (scleroderma)
disorder of impaired sphincter dysfunciton
Hirschsprung’s, Dyssynergic defecation
Tests for evaluating GI motility
- Esophageal manometry for achalasia, scleroderma
- gastric emptying study for gastroparesis
- Anal manometry for Hirschsprung’s and dyssynergic defecation
anal manometry
- similar to esophageal manometry but diff muscles/probe
- evaluate incontinence (resting/volition squeeze, cough reflex, rectal sensation)
Eval of constipation
anal resting pressure, attempted defecation lying left lateral, simulated defecation , recto-anal inhibitory reflex, rectal sensation
in what disease is recto-anal inhibitory reflex absent
Hirschsprung’s
Hirschsprung’s disease
- congenital absence of myenteric neurons of distal colon (Neuropathic Motility Disorder)
normal recto-anal inhibitory reflex
distended colon –> relaxation of internal anal sphincter
abnormality in Hirschsprungs
- can’t relax internal anal sphincter after distention –> rarely or hard to bypass IAS –> dilated ganglionic segment above segment lacking myenteric neurons
role of puborectalis muscle
- part of pelvic floor muscles
- creates acute angle at rest to help maintain continence
- strain to defecate –> straighten rectal canal and descend pelvic floor – easier to evacuate rectum– wider anorectal angle
Pelvic Floor Dysfunction
inability to coordinate abdominal, rectoanal, and pelvic floor muscles during defecation
symptoms of pelvic floor dysfunction
- anismus (high anal resting pressure)
- incomplete anal relaxation
- paradoxical contraction of pelvic floor and external anal sphincters (dyssyndrgia)
- rectal hyposensitivity
- excessive perineal descent
- rectocoele
causes of pelvic floor distention
bad toilet habits, painful defecation (trauma to canal where relaxing painful), obstetric or back injury, brain gut dysfunction
diagnose dyssynergia
abnormal anorectal manometry, reveals paradixical contraction of pelvic floor and EAS
Treat pelvic floor dysfunction
biofeedback therapy effective
