Gastric Motility and Function

waves of rhythmic depolarization of intestinal smooth muscle cells propagate along length of gi tract

pacemaker potentials of stomach

basal electric rhythmn

differes in various segments

3 cpm in stomach, 12 cpm in duodenum

pacemaker network of cells in stomach small intestine and large intestine

interstitial cells of Cajal

does the pacemaker potential of BER initiate action potentials of its own in smooth muscle

no, stimulation of ENS or hormonal input is needed

what is receptive relaxation and what triggers it

the drop in gastric pressure after eating

stomach must relax as volume increases → reservoir

persists til all solids emptied

NO and VIP are released when mechanoreceptors triggers intrinsic and vasovagal reflexes

why do we have receptive relaxation

it delays gastric emptying until the duodenum is ready

how does the duodenum contribute to receptive relaxation

fat adn protein in duodenum also distend duodenum → release CCK → binds CCK1 → delay gastric emptying

what reflex induces need to defecate shortly after eating a meal

gastrocolic reflex

what reflex relaxes ileocecal valve in response to gastric distension

gastroileal reflex

rapid phasic contractions of stomach

circumferential, start from gastric pacemaker near antrum and move toward pylorus

fluid and small particles <2 mm empty into duodenum

solid meal gastric lag

1 hr before emptying begins

chronic disorder char by delayed emptying of the stomach after eating in the absence of mechanical obstruction like pyloric stenosis

gastroparesis

neuromuscular dysfunction, derangements in extrinsic control, intrinsic nerve dysfunction, cells in local control of gi muscle function and loss of function of smooth muscles

causes of gastroparesis

idiopathic

DM

iatrogeni/post surg

neurological disorders

viral or bacterial infection

gastroparesis association/causes

gastroparesis sx

postprandial fullness, N/V, belching, bloating

tx for gastroparesis

antiemetics, prokinetic drugs, dietary mods, PPI, pyloric botulinum toxin injection

primary role of small intestine

digest components of meal and absorb nutrients into blood stream or lymphatics

what compoounds stimulate smooth muscle contractions in ENS

ACh, substance P

what stimulates smooth muscle relaxation in ENS

VIP and NO

what is the motility pattern of the small intestine during fed state

not to propel but to mix contents with digestive secretions and prolong exposure to absorptive epithelium

propel it slowly

segmentation and peristalsis

once the meal is absorbed the intestine converts to

MMC, migrating motor complex (house cleaning)

describe the migrating motor complex

occurs between meals, fasting state

pattern of motility repeating every 90 minutes to 2 hours

what stimulates the MMC

motilin from M cells during fasting

surpressed during feeding

role and sinificance of the colon

reabsorb water

process feces

colon in fasting states

not part of MMC

biased toward mixing and retaining contents for prolonged periods of time

periodically have large propulsive contractions to transfer contents to rectum and promote urge to defecate

high amplitude propagating contraction of the large intestine

provides mass movement of chyme and feces

poor motility in colon →

greater absorption and hard feces/constipation

excess motility in colon →

diarrhea or loose feces

contains both circular and longitudinal smooth muscle and is under involuntary control

internal anal sphincter

encircle rectum and contains only striated muscle but is controlled by voluntary and involuntary mechanisms

external anal sphincter

resting tone 40-60 mmHg

if passive distension of rectum is large enough →

triggers active contraction of rectal smooth muscles

triggers relaxation of smooth muscle on internal anal sphincter (rectosphincteral reflex) via VIP and NO

if defecation is not desired

skeletal muscle of external anal sphincter contracts by involuntary reflex

increased tone prevents leakage, involuntary control

slow transit constipation

slow movement of feces through large intestine → large dry hard feces bc excess fluid absorption

hirchsprungs disease

congenital megacolon

ENS fails to develop appropriately

defecation reflexes and strong peristaltic motility cannot occur in area of large intestine

segment remains contracted → functional barrier to passage of feces, dams up area and causes megacolon in ascending transverse and descending colon (ganglion cells in myenteric plexus of sigmoid colon is the problem)

stomach secretions

acid, pesinogen, mucus, bicarb, intrinsic factor, water

stomach humoral agents

gastrin, somatostatin

largest portion of the stomach

corpus

stomach area with no acid secreting parietal cells

cardia

most distal region of the stomach

antrum

between cell types and within cell types there is what

cellular heterogeneity throughout (epithelial in antrum vs body very different)

contains gastric glands with variety of secretory cell types and its secretory products

corpus of the stomach

acid, pepsinogen, intrinsic factor

secrete acid and IF necessary for b12 absorption in the ileum

parietal cells (oxyntic)

secrete pepsinogens that are active as pepsins (active by low ph, intitaie protein digestion)

chief cells

chief cells and parietal cells are found in what part of the stomach

corpus

other cell types in corpus

mucus secreting cells in neck of gastric gland

epithelial cell

endocrine cell

• enterochromaffin like cells to release histamine

water also secreted

antrum cells

glands DO NOT contain parietal cells

chief cells

epitelial cells

enodcrin cells

• g cells → gastrin

• d cells → somatostatin

two pathways for acid secretion

direct

• stimulate parietal cell directly

indirect

• stimulate ECL cell to secrete histamine which acts on parietal cell

Gq → PLC → IP3 and DAG

ACh

CCK2 or CCK1 receptor (Gq)

gastrin

Gs → AC → cAMP → PKA

histamine

stimulation causes cytoskeletal rearrangement of

parietal cells

steps of acid secretion

1. h-k pump activated (p type atpase)

   1. extrusion of h into lumen in exchange for k

2. secretion of Cl into gland lumen

3. results in active secretion of HCL

active secretion of HCL leads to what intracellularly

increased pH → passive uptake of h2o and co2 for conversion to bicarb and h+ by carbonic anhydrase

bicarb gets exchanged for cl- at basolateral surface

gastric acid secretion stimulation summary

Vagus nerve and ENS stimulate parietal directly →ach

ecl cells → histamine

inhibits d cell release of somatostatin (via ach)

stimulates g cells vis GRP

products of protein digestions directly stimulate

g cells to release gastrin

regulation of gastric acid secretion inhibition summary

somatostatin is major

luminal H+ stimulates d cells to release somatostatin

• inhibits gastrin

• inhibits ecl histamine release

• inhibits acid release from parietal cells directly

phase of acid scretoin before food enters stomach

cephalic phase

sights smells and tastes of food

20% of secretion

vagus

phase of secretion after food enters stomach

gastric phase

stimulates vasovagal and enteric reflexes and gastrin

65% of acid secretion

phase pf acid secretion where food is in upper duodenum

intestinal phase

small amounts of gastric acid in stomach

10% acid secreted

what protects the gastric surface

gastric diffusion barrier

what gives gastric diffusion barrier its impermeability to acid

apical membrane and gastric gland tight junctions

3 parts of the gastric diffusion barrier

1. tight junctions that help make it impermeable to acid at apical membrane

2. mucous gel on surface epithelial cells

3. bicarb containing microclimate next to epithelial cells

increased acid secretion due to elevated levels of gastrin usually due to a tumor

zollinger ellison syndrome

what tumors usually cause zollinger ellison syndrome

gastrinoma

pancreatic cell adenoma

what happens with gastrin in zollinger ellison syndrome

gastrin’s release is unregulated/not under phsyiological control

fasting gastrin level is elevated in almost all patients

• leads to ulcers

patients lack parietal cells

cannot secrete ____ and ____

pernicious anemia

H+ and IF

hyperplasia of parietal cells is noted in what

zollinger ellison syndrome

low somatostatin, no D cells stimulated

gastrin secretion is high with almost no H+ secretion

no b12 (cobalamin) absorption

pernicious anemia

no parietal cells