Motility Disorders of the GI Tract Flashcards
What causes motility disorders?
ENS: missing, immature, damaged by infection, influenced by chemical substances; =Neuropathic
Diseased GI muscles: genetic defect (muscular dystrophy) or acquired (progressive systemic sclerosis) =Myopathic
Abnormalities of interstitial cells of Cajal– pacemaker
CNS disorders
Achalasia
seen as absence of esophageal peristalsis and no LES relaxation
Scleroderma/Progressive Systemic Sclerosis (PSS)
Multisystem disorder:
- obliterative small vessel vasculitis
- Connective tiss proliferation w/ fibrosis of multiple organs
GI manifestations in 80-90%
GI abnormalities: smooth muscle atrophy and gut wall fibrosis (thus a myopathic process)
Esophageal manifestations:
smooth muscle atrophy–>weak peristalsis–>dysphagia
SM atrophy–>weak LES–>GERD
Unrepentant GERD–>Esophagitis–>stricture
How do you dx esophageal disease?
esophageal manometry
seen with Scleroderm/PSS
Spastic Disorders of the esophagus
- conditions of uncertain etiology
- peristalsis PRESERVED
- Sx: chest pain, dysphagia
- poss pathophys: overactivity of excitatory nerves or overreactivity of smooth muscle response
physiology of gastric emptying
- receptive relaxation (vagally mediated inhibition of body tone)
- liquid emptying by tonic pressure gradient
- solid emtying by vagally mediated contractions
- residual solids emptied during non-fed state MMC every 90-120 mins
Gastric Motility
Gastric pacemaker:
- interstitial cell of Cajal?
- proximal body along greater curvature
Fundus and proximal body:
storage
Distal body and antrum
-processing and emptying
Receptive relaxation
swallowing induced vagal response
accomodation
- smooth muscle relaxation elicited by mechanical distention of the stomach (Gastric mechanoreceptors)
- vasovagal response
Dyspepsia
- discomfort or pain centered in the upper abdomen usually related to eating
- postprandial heaviness, early satiety, epigastric pain or burning
Organic: PUD, atypical GERD, gastric/esophageal cancer, pancreatico-biliary disorders, food/drug (NSAIDs) intolerance
Functional dyspepsia
dyspepsia without organic etiologies
-40% w/ FD will have impaired gastric accommodation
Gastroparesis
“stomach paralysis”
- impaired transit of food from the stomach to the duodenum
- Mechanical obstruction of the gastric outlet excluded
Clinical Manifestations of gastroparesis
n/v, early satiety, postprandial abdominal distention or pain
Major causes of gastroparesis
idiopathic (?post infectious)
post surgical (vagal nerve injury): gastric, esophageal, thoracic surgical procedures (lung transplant)
Diabetic
Meds (opiates)
Others: paraneoplastic, rheumatologic, neurologic, myopathic (Scleroderma)
Dx of gastroparasis
-Gastric emptying study
gastric scintigraphy
Low fat EggBeaters w/ radiolabel
abnormal: retention >60% at 2 hr or >10% at 4 hr
Management of gastroparesis
Lifestyle/dietary: small and infrequent meals, low fat and low residue diet, glucose control in diabetics
Meds:
Prokinetic agents, antiemetics
Gastric electric stimulation
Surgery ~2%
Small Intestine motility fed vs fasted
-in fed state: primary motility is segmentation
-9-12 contractions/min (pacemaker cells)
-transit time 3-5 hrs
-Fasted state: Migrating motor complex: sequential orderly short peristaltic waves
stomach–>caudally
sweep gut b/t meals
Small bowel motility disorders
Neuropathic:
- normal amplitude, but sustained bursts of uncoordinated phasic contractions
- early return and increased freq of MMC (can be bad because decrease absorption and can overwhelm the colon)
Myopathic:
decreased amp of contractions or lack of any motor activity
some diseases show both
Chronic Intestinal Pseudo-Obstruction (CIPO)
- signs/sx of mech obstruction of SI w/o lesion obstructing flow
- dilation of the bowel on imaging
- major manifestation of SI dysmotility
- SI bacterial overgrowth =complication of CIPO: stasis–> bacterial overgrowth–>fermentation and malabsorption
Sx: n/v, abd pain, distention, constipation, diarrhea, urinary sx
What might you see in myopathic forms of CIPO?
hypoactive motility
Etiology of Small Intestinal Motility Disorders (and CIPO)
Neuropathic:
- degenerative neuropathies (eg Parkinson’s)
- Paraneoplastic Autoimmune (anti-Hu ab)
- Diabetes associated (neuropathy)
- Chagas Disease: parasite Trypanosoma cruzi
Mixed myopathic and neuropathic:
- infiltrative conditions: **Scleroderma, amyloidosis, eosinophilic gastroenteritis
- idiopathic
CIPO in kids
- mostly congenital
- mostly primary condition (visceral neuropathy/myopathy)
- absent MMC predicts need for IV nutrition
- one third of infants born die in 1st year of life
Two types of motor activity in Colon
- low amp tonic and phasic contractions for mixing luminal contents (Haustra)
- high amp propagated contractions (HAPCs) for propelling
Causes of constipation
drugs
mechanical
metabolic: *DM, hyopK, hyperCa, hypoMg, hypothyroid
Myopathy: amyloid, scleroderma
Neurogenic: Parkinson’s, spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s
Other: preg, immob
IBS-C
Normal transit, slow transit, dyssynergic defecation
Colonic Transit studies
Sitz marker (get XR day 5; >5 markers in recto-sigmoid= defecatory disorder; >5 throughout colon =slow transit) Scintigraphy (dissolves in alkaline distal ileum, scans 4, 24, 48 hrs show colonic distrib) wireless capsule
Evaluation of incontinence
-anal manometry
resting and volitional squeeze, cough reflex test, rectal sensation testing
Eval of constip
-anal manometry
anal resting pressure, attempted defectation lying left lateral, simulated defecation w/ 50cc balloon, rectoanal inhibitory reflex (absent in Hirschsprung’s), rectal sensation testing
Hirschsprung’s Disease
- congenital absence of myenteric neurons of the distal colon (Neuropathic motility disorder)
- no reflex inhibition of the IAS following rectal distention (***no recto-anal inhibitory reflex)
internal and external anal sphincter muscle, puborectalis muscle
IAS: circular smooth; autonomic innervation: pelvic plexus
EAS: striated volitional
innervation: pudendal nerve
Puborectalis muscle: striated–volitional
(helps form anorectal angle; w/ contraction and descent of pelvic floor–>decreased angle)
Pelvic floor dysfunction
- inability to coordinate the abdominal, rectoanal, and pelvic floor muscles during defecation
- anismus (high anal resting pressure)
- incomplete anal relaxation
- paradoxical contraction of pelvic floor and EAS (*dyssynergia)
- rectal hyposensitivity
- excessive perineal descent
- rectocoele
Causes: bad toilet habits, painful defecation, obstetric or back injury, brain/gut dysfunction
Dx of Dyssynergia
-abnormal anorectal manometry
-reveals: paradoxical contraction of pelvic floor and EAS
Tx: biofeedback therapy is effective
Alteration of esophageal peristalsis
achalasia
scleroderma
Alteration of LES relaxation
achalasia
Alteration of LES tonic contraction
scleroderma
Alteration of gastric receptive relaxation/accomodation
functional dyspepsia
Alteration of gastric emptying
gastroparesis, functional dyspepsia
Alteration of small bowel motility (peristalsis)
CIPO (scleroderma)
altered SI motility w/ underlying neuropathic cause: DM, primary pediatric visceral neuropathy
w/ underlying myopathic:
scleroderma, amyloidosis, primary pediatric visceral myopathy
Alteration of colonic tranist
slow transit constipation (scleroderma)
Alteration of sphincter function
Hirschsprung’s
Dyssynergic defecation
Esophageal manometry can dx
achalasia
scleroderma
Gastric emptying study (gastric scintigraphy) can dx
gastroparesis
Anal manometry can dx
Hirschsprung’s
Dyssynergic defecation
