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