Physio Ii - Gi Motility

Front 1

four basic layers of GI tract from inside to out

Back 1

Mucosa (epithelium, lamina propria, muscularis mucosa)
Submucosa
Muscularis Externa
Serosa

Front 2

epithelium

Back 2

inner most layer of mucosa.

single layer of specialized cells that vary from one part of GI to another

Front 3

Lamina Propria

Back 3

2nd layer of mucosa

layer of loose CT to which epithelia attach.

Contains blood vessels, lymph nodes, and some glands

Front 4

Muscularis mucosa

Back 4

3rd outermost layer of mucosa

thin layer of smooth muscle, contraction causes folds and helps to mix luminal contents, as well as expose different mucosal surfaces

Front 5

Submucosa

Back 5

Loose connective tissue. Has blood & lymphatic vessels, major nerve tracts, enteric plexus

submucosal plexus controls secretions

Front 6

Muscularis externa

Back 6

inner circular layer of muscle and an outer longitudinal layer.

Contraction mixes contents and moves it along GI tract

Front 7

Serosa

Back 7

outermost layer of GI tact, consists mainly of CT

Front 8

GI innervation

intrinsic and extrinsic innervation

Back 8

Intrinsic - enteric nervous system, comprised of Myenteric plexus (Auerbach's) and Submucosal (Meissners) plexus.

Extrinisc - from ANS
Sympathetic, PS, and Afferent fibers

Front 9

Myenteric plexus

Back 9

AKA Auerbach's plexus.

Part of intrinsic enteric nervous system

larger of the two plexuses, located b/w circular and longitudinal muscles layers from esophagus to rectum

concerned primarily with control of motility

Front 10

Submucosal plexus

Back 10

AKA Meissner's

in the submucosa of the small intestine

concerned primarily with control of secretion from glands of the GI

Front 11

Sympathetic innervation of GI

Back 11

Extrinsic from ANS

-postganglionics from cells in the paravertebral and prevertebral ganglia.
most postganglionics end in myenteric and submucosal plexuses where they act to inhibit activity.

a few fibers end on gland cells and blood bessels where they inhibit secretion and produce vasoconstriction

Activation: inhibits contraction in muscularis externa, stimulates contraction of sphincters and the muscularis mucosa.

Front 12

Parasympathetic Innervation of GI

Back 12

supplied preganglionic (cholinergic) fibers from the vagus (GI tract to level of transverse colon) and pelvic nerves (descending colon to rectum)

fibers terminate on ganglion cells in the myenteric and submucosal plexuses, the axons of the ganglion cells (postganglionics) innervate the smooth muscle and glands of the GI tract

Activation increases contraction and secretion

Front 13

Afferent fibers

Back 13

about 75% of vagal fibers are afferents and about 50% of fibers in sympathetic nerves to the gut are afferents.

intrinsic and extrinsic aff fibers.

receptors include chemoreceptors, mechanoreceptors, and nociceptors.

cell bodies in local reflex arcs or central reflex arcs

visceral nociceptive fibers to CNS via sympathetic, non-nociceptive sensory via parasympathetic

Front 14

Local reflex arcs

Back 14

cell bodies of sensory nuerons in submucosal and myenteric plexuses

Front 15

Central reflex arc

Back 15

cell bodies of the sensory nuerons located in dorsal root ganglia or cranial ganglia.

Front 16

GI smooth muscle characteristics

Back 16

single unit type. neighboring cells connected by gap junctions so electrical activity can spread easily.

membrane potential -40 to -80 mV

has slow waves aka basical electric rhythm

nueromuscular junctions

Front 17

GI smooth muscle membrane potential

Back 17

-40 to -80 mV

determined mainly by K conductance, but resting Na conductance is higher than in skeletal making the potential less negative than skeletal.

eletrogenic Na/K pump makes a significant contribution (1/3rd to 1/2 of resting potential)

Front 18

Slow waves of GI smooth muscle

Back 18

AKA basical electrical rhythm

low frequency fluctuations in membrane potential found from stomach to colon.

different regions have diff frequencies

generated by pacemaker cells (intersitial cells) located b/w longitudinal and circular smooth msc of mscularis externae

Front 19

Modulation of slow waves in GI smooth muscle

Back 19

slow wave amplitude modulated by homones and extrinsic and intrinsic innervation.
-Sym - decreases amp
-PS - increases amp

Front 20

Slow waves and contraction in GI smooth muscle

Back 20

Slow waves can elicit contractile activity

-in the stomach and small intestine, if slow waves are sufficient amplitude, contraction occurs

-in colon, relationship not clear

- in stomach and SI the frequency represents max freq of contractions

Front 21

Nueromuscular junctions in GI smooth muscle

Back 21

do not involve postjunctional specializations like endplate in skeletal muscle

circular smooth layer recievees extensive innervation and nerve terminals form a close association (20nm gaps) with muscle cells

longitudinal muscle layer receives much less dense innervation and the gaps b/w nerve and muscle are large (80nm)

Front 22

Length-tension curve

Back 22

GI smooth muscle has a much broader length tension curve than skeletal muscle meaning that it can develop force effectively over a wider range of muscle length

Front 23

Contraction time

Back 23

about 10X slower than that for skeletal muscle: contractile response to a burst of action potentials appears as smoothly increasing tension instead of individual twitches

Front 24

Tone

Back 24

GI smooth muscles has a resting tension which results from slightly elevated levels of intracellular Ca2+. Can be modified by nuerotransmitters, hormones, or drugs.

Front 25

Mastication

Back 25

chewing. Fx is enjoyment, reduction of particle size, breakdown cell wall, mix food with salivary

Front 26

amylase function

Back 26

salivary mucus lubricates food,

alpha-amylase begins digestion of starches

Front 27

control of mastication

Back 27

both voluntary and involuntary. brain stem has masticatory center which is responsible for basic oscillatory pattern.

cortex - initiate and modify movements

sensory from oral cavity terminates primarily in trigeminal sensory and mesencephalic nuclei and acts to modify chewing movements

Front 28

Deglutination (swallowing)

Back 28

initiated voluntarily but then is under control of the swallowing reflex mediated by nuerons of the swallowing center in the medulla and pons

2 phases, voluntary and involuntary

Front 29

Voluntary phase of deglutination

Back 29

oral phase.

tongue moves a bolus of food upward and backward in the mouth eventually forcing it against the pharynx

the bolus of food in the pharynx stimulates mechanoreceptors and initiates the swallowing reflex

Front 30

Involuntary (reflex) phase of deglutination

Back 30

pharyngeal phase

soft palate pulled upward closing off nasopharynx

respiration is inhibited, the vocal cords are pulled together, the epiglottis covers the opeing of the larynx and the larynx is moved upward against the epiglottis

upper esophageal sphincter relaxes and a peristaltic wave of contraction begins in the superior constrictior muscles of the pharynx an forces the bolus of food into the esophagus

Front 31

deglutination control

Back 31

voluntary phase - initiated in motor cortex, primarily involves motor activity in CNXII

involuntary - swallowing center in medulla and lower pons, afferent input comes from sensory receptors in pharynx, once intitiated the reflex produces an orderly sequence of pharyngeal muscles conteactions and relaxations mediated by various cranial nerves

Front 32

Fx of esophagus

Back 32

conduit to get food from mouth to stomach

sphincters act as barriers
-upper ES keeps air out of GI
-Lower ES prevents reflux of avid and gastric contents into esophagus

Front 33

anatomy of esophagus

Back 33

-follows general scheme of an inner circular layer and an outer longitudinal layer

-Upper Circular Schp and upper 1/3rd esophagus is skeletal

-iower sphc and distal 1/3 is smooth

-intermediate is mixed

Front 34

Esophageal peristalsis

Back 34

2 types
-primary - wave that began in phaynx during swallowing continues through esophagus taking about 10 s to go from upper esophagus to stomach
-controlled mainly by swallowing center

-secondary - if primary wave fails a secondary occurs, controlled by intrinsic nervous system

Front 35

Upon what does the intensity of peristalsis depend?

Back 35

size of the bolus, not required for liquid in the upright position

also regulated by the rate of swallowing
1) if second swallow occurs within 5 sec, first bolus inhibited til second catches up
2) if a series of rapid swallows occurs peristalsis is inhibited until the last swallow

Front 36

Lower esophageal sphincter (LES) tone

Back 36

during non-peristaltic periods LES tone is high due to myogenic mechanisms (remained of esophagus is flacid) however, resting tone can be increased by both nueral (ACh) and hormonal (gastrin) influences

relaxation of LES is mediated by the vagus through vasoactive intestinal peptide (VIP) and nitric oxide (NO)

Front 37

Achalasia

Back 37

disturbance of esophageal function

-insufficient relaxation of LES to allow food into stomach

-is attributed to abnormal enteric nervous function

Front 38

Gastroesophageal reflux disease (GERD)

Back 38

disturbance of esophageal f(x)


normally LES transiently relaxes and closes (permits belching) but in people with GERD the relaxations occur more frequently or be more prolonged in duration allowing reflux of gastric contents (acid and pepsin) into the esophagus which can eventually produce ulcerations

Front 39

diffuse esophageal spasm

Back 39

disturbance of esophageal f(x)

prolonged painful contraction of esophagus instead of normal peristalsis after swallowing

Front 40

Functions of the stomach

Back 40

reservoir for food
digestion - fragment food (homogenization) and mix with gastric secretions (chyme)

empty gastric contents into duodenum at a controlled rate

Front 41

Anatomy of stomach (layers)

Back 41

three layers of smooth muscle
outer - longitudinal
middle - circular (most prominent)
inner - oblique (present on anterior and posterior sides)

Front 42

Innervation of stomach

Back 42

extrinisic motor
-PS from vagus stimulates motility and secretion
-S from splanchnic inhibits

intrinsic motor via submucasal and myenteric plexuses

numerous sensory (afferent) fibers which respond to gastric distenstion, intragastric pressure, pH, and pain

Front 43

Anatomical divisions of stomach

Back 43

Cardia - region surrounding LES aka cardiac schpincter

Fundus - superior portion of stomach above the cardia

Body or Corupus - main portion of stomach

Antrum - inferior region, 2 parts
1) pyloric antrum - continuous with body of stomach
2) pyloric canal - leads to doudenum

Front 44

Receptive relaxation

Back 44

response to gastric filling
1) fundus and body relax
-initiated as part of reflex of LES induced by primary esophageal peristalsis
-can also be indced by directly filling of stomach with gas or liquid (vagovagal reflex involves stretch receptors)

reflex dependent on intact vagal innervation

allows accommodation of 1L-2L without a significant increase in intragastric presssure

Front 45

Why does so little mixing happen in the fundus of the stomach?

Back 45

The muscle layers are thin and the contractions are weak

contents form layers based on their densities

fats form an upper oily layer and are therefore emptied last

Front 46

Rate of emptying (what does it depend on) of the stomach

Back 46

depends on physical and chemical characteristics of its contents

-inert, isotonic solutions (glucose) leave the stomach rapidly
-solutions with nutrients (AAs) empty more slowly, reflects feedback from receptors in SI (caloric density)
-emptying of solids even slower (half time 1-2 hours)
----emptying of solids preceeded by a lag time of up to 1 hour for retropulsion and mixing
---larger swallowed piece = longer lag time

Large >2mm indigestible fragments remain in stomach until period of fasting (see MMC)

Front 47

Where does most mixing occur in the stomach? Why here?

Back 47

Antrum
produce vigorous persistaltic contractions
food broken down and mixed with gastric juices

Front 48

How do contractions work in relation to stomach emptying

Back 48

strong peristaltic waves

contractions produced by slow waves originate in middle of the body and move towards pylorus, increasing in force and velocity

the antrum and pylorus contract almost simultaneously, and a small fraction of chyme with particles <2mm is pushed into duodenum (these contractions are pyloric pump)

pyloric schpincter closes and pushes rest back into proximal antrum (retropulsion)

frequency is about 3/min
duration ranges from 2 to 20 sec

Front 49

Pyloric pump

Back 49

the peristaltic contractions that eject a small amount of chyme with particles <2mmsquared into the duodenum

Front 50

Retropulsion

Back 50

when the pyloric schpincter closes and forces the rest of the antral contents back towards the proximul antrum

Front 51

Duodenal factors that delay gastric emptying

Back 51

1. hypertonicity of DUO contents
2. decrease in DUO pH
-normally near 5.0
-pH < 3.5 inhibits empyting
3. fatty acids or mono- or diglycerides in DUE
4. peptides and amino acids (esp tryptophan)
5. DUO distension

Front 52

Mechanisms regulating gastic emptying

Back 52

receptors in DUO and JEJ involed in reflex control, both nueronal and hormonal pathways

nueral pathways involve ENS reflex arcs as well as inhib and excite vagal input
-ENS works in concert with vagus
-vagotomy delays gastric emptying

homones involved are released from DUO and JEJ
-secretin in response to acid
-CCK and GIP in response to fats
-Gastrin in response to AAs
-unknown hormone in response to hypertonicity

Front 53

Hormones involved in gastric emptying

Back 53

Secretin - Acid

Cholecystokinin (CCK) and glucose-dependent insulinotropic peptide (GIP) ---fats

Gastrin - AAs

unknown - hypertonicity

Front 54

Non- duodena factors affecting gastric concentration

Back 54

"Illeal break" - glucose of fats in the ileum reduces gastric contractions

colonic distension causes relaxation of gastric muscle

Front 55

Migrating Myoelectric Complex (MMC)

Back 55

1. occurs during fasting
2. antrum quiescent for 1-2 hr
3. this period followed by period of intense electrical and motor activity lasting 10-20 minutes
4. strong antral contractions occur but pylorus is relaxed
5. allows for emptying of large chunks of undigested materials
6. triggered by the hormone motilin released by enteroendocrine cells

Front 56

Motilin

Back 56

released by enteroendocrine cells, triggers the migrating myoelectric complex aka MMC

Front 57

Gastroduodenal junction (pylorus)

Back 57

regulates emptying of gastric contents to a rate at which chyme can be processed by duodenum

prevents regurgitation of duodenal contents back into stomach
-gastric mucosa resistant to acid, damaged by bile
-duodenal mucose resistant to bile, dmg by acid
-too rapid gastric empyting produces DUO ulcers
-regurgitation of bile into stomach = gastric ulcers

Front 58

Vomiting (emisis)

Back 58

causes ejection of gastric (and sometimes DUO and JEJ) contents through the esophagus and mouth, usually preceeding by retching in which some of the stomach content is forced into esophagus but does not reach pharynx

Front 59

reflex behavior of vomiting
-medullary centers

Back 59

controlled by medullary centers
1. vomiting center- stimulation = vomiting with no prior retching
2. stimulation of another site = retching and no vomiting
3. chemoreceptor trigger zone
-rostal medulla
-outside of BBB, reached by chemicals in blood
4. Nucleus tractus solitarius
-input from vagal, labyrinths, and chemoreceptor trigger
-coordinates somatic motor response in response to vomiting

Front 60

stimulations for vomiting

Back 60

1. distension of stomach and DUO
2. tickling back of throat
3. noxious stimuli to genitourinary system
4. certain smells and sights
5. semicircular canal stimulation (motion sickness) - impulses sent to vomiting center, blocked by antihistamines (H1)
6. emetic agents - 2 types
A. ipecac - receptors in stomach or duo
B. chemo trigger zone - morphine, hormones, etc

Front 61

Events occuring during vomiting

Back 61

central coordination of contraction of thoracic, diaphragmatic and abdominal musculature

basic electrical rhythm of intestinal smooth muscle is suspended and replaced with bursts of electrical activity that are propagated orally
-results in retrograde giant contractions
-retrograde propulsion during emesis is entirely extrinsic nerves

Front 62

Retrograde propulsion during emesis is driven by ________

Back 62

Extrinsic nerves only

Front 63

Clinical consequences of vomiting

Back 63

1. metabolic alkalosis from loss of HCL
2. dehydration
3. hypokalemia because K+ is higher in gastric juice than in blood

Front 64

stimulations for vomiting

Back 64

1. distension of stomach and DUO
2. tickling back of throat
3. noxious stimuli to genitourinary system
4. certain smells and sights
5. semicircular canal stimulation (motion sickness) - impulses sent to vomiting center, blocked by antihistamines (H1)
6. emetic agents - 2 types
A. ipecac - receptors in stomach or duo
B. chemo trigger zone - morphine, hormones, etc

Front 65

Events occuring during vomiting

Back 65

central coordination of contraction of thoracic, diaphragmatic and abdominal musculature

basic electrical rhythm of intestinal smooth muscle is suspended and replaced with bursts of electrical activity that are propagated orally
-results in retrograde giant contractions
-retrograde propulsion during emesis is entirely extrinsic nerves

Front 66

Retrograde propulsion during emesis is driven by ________

Back 66

Extrinsic nerves only

Front 67

Clinical consequences of vomiting

Back 67

1. metabolic alkalosis from loss of HCL
2. dehydration
3. hypokalemia because K+ is higher in gastric juice than in blood

Front 68

Characteristics of Small Intestine (SI)

Back 68

length is about 5 m (16 ft)

takes about 2 hr for chyme to go through

major portion of digestion and absorption

intestinal motility mixes chyme with digestive enzymes and moves chyme in an aboral direction

Front 69

alcohol, aspirin, and a small amount of fat are absorbed in the ______

Back 69

stomach

Front 70

How do the structural features of SI increase digestion and absorption

Back 70

1. folds of mucosal and submucosal layers (circular folds - plicae circularis) triples surface area

2. projections of mucosa form finger-like villi

3. apical portion of cells lining villi have extensions called microvilli

Front 71

villi vs microvilli of SI

Back 71

villi are projections of mucosa
-covered with absorptive epithelial cells
-each one contains a blood capillary network and a lymphatic capillary (lacteal)
-villi increase surface area 10-fold

microvilli are extensions of the absorptive cells on villi, contain enzymes that further hydrolyze carbs and peptides into simple sugars and amino acids
-increase SA by 20 fold
-collective term for whole epithelia surface of microvilli is BRUSH BORDER

Front 72

how are digestive products drained in the SI

Back 72

blood supply and lymphatics
-blood capillaries in the villi take up AAs and simple sugars and drain into veins that empty in the portal vein to the liver
-lacteals take up lipids and the lymphatic drainage of the lipids from SI empties into the venous circulation at the left subclavian vein to the heart

Front 73

Electrical acivity of SI

Back 73

Slow waves - up to 12/min in DUO ----> 8/9/min in ILE

frequency determines max contraction frequency

basic electrical rhythme independent of extrinsic innervation

Front 74

Factors that influence amplitude of SI contraction

Back 74

1. hormnones both enhance and inhibit
2. ANS via intramural plexuses
-PS enchances
-S inhibits
3. enteric nuerons enhance or inhibit

Front 75

Segmentation in SI

Back 75

fed state behavior of SI
-most common type of movement
-contractions of circular muscle layer divide SI in segments
-11-12/min in DUO 8-9/min in ILE
-sites of contraction alternate
-mixes chyme with digestive juices
-contractions at adjacent sites occur in prox-->distal sequence propelling chyme in arboral direction
-due to action of the enteric nervous system, vagotomy DOES NOT STOP segmental contractions

Front 76

Peristalsis in SI

Back 76

behavior in a fed state
-occur much less frequently than segmentation
-waves travel less than 5cm in SI
-produce net movement of chyme in aboral direction

Front 77

Local intestinal reflex (Law of the Intestine)

Back 77

placing a bolus of material in SI produces a contraction oral to the bolus and relaxation aboral, propelling it forward

mediated by intramural plexuses

Front 78

Intestinointestinal reflex in SI

Back 78

over distension of one segment relaxes the rest of the intestine

requires intact extrinsic innervation

Front 79

Gastroileal reflex in SI

Back 79

increased secretory and motor activity in the stomach increases motility in the terminal part of the ileum and quickens movement of chyme through the ileocecal sphincter

probably mediated hormonally and by extrinsic innervation

Front 80

Migrating Myoelectrical Complex in the SI

Back 80

behavior in a fasted state
1. occurs several hours after a meal
2. SI shows bursts of intense electrical and contractile activity seperated by longer quiescent periods
3. usually propogated from the MMC in antrum but can originate anywhere
-ENS and hormone motilin are responsible
-extrinsic innervation not required
4. During parts of MMC contractions are stronger than those during a meal
-cleans and empties SI
-inhibits migration of colonic bacteria
5. disrupted by psychological stress, ends promptly when eating

Front 81

Illeocecal Sphincter

Back 81

1. seperates ileum from cecum and prevents retrograde flow of chyme from cecum to ileum
2. opened by peristalsis in distal ileum allowing chyme to enter cecum
3. distenseion of distal ileum also causes sphincter to relax
4. distention of cecum causes scphincter to constrict further

Front 82

Colon - general characteristics

Back 82

recieves 1500 ml of chyme/day from ileum

most salts/h20 that enter colon are absorbed so feces contains only about 50 to 100 ml of H20

movement of contents is slow (5-10cm/h)
-majority of transit time
-takes 1-3 days after entering colon to be evacuated but is highly variable

Front 83

7 subdivisions of colon in aboral direction

Back 83

1. cecum
2. ascending
3. transverse
4. descending
5. sigmoid
6. rectum
7. anal canal

Front 84

Extrinsic innervation of colon

Back 84

PS - stimulates motility
--vagus innervates proximal colon (cecum-transverse)
--pelvic nerves (from sacral) innervate descending-anal canal

SYM -
--postganglionics from mesenteric and hypogastric ganglia
--sympathetic activity inhibits motility

Front 85

Intrinsic innervation of colon

Back 85

plays a major role in control of colonic motiliy (both propulsive and non-propulsive contractile activity) occur in absense of extrinsic

Front 86

Hirschsprung's disease

Back 86

most often a result of congenital abnormality in which the enteric nervous system does not develop properly, but can also be caused by radiation damage during chancer therapy

colon becomes constricted in the region where the intraural plexuses is absent

Front 87

2 types of contractions in the colon

Back 87

NO MMC!!!!!!

Haustral and Mass movements

Front 88

Haustral contractions

Back 88

colon is divided into bag-like sacs called haustra

fluctuations in contractions and relaxations cause back anf forth movements of chyme (haustral shifting) with a net, slow orthograde propulsion of chyme

Front 89

Mass movements

Back 89

in colon, occur 1 to 3 times/day

haustra disappear and are replaced by waves of contraction resembling intense peristaltic waves which progress in aboral direction

pushes contents of long lengths of colon toward rectum

Front 90

2 reflexes of the colon

Back 90

Colocolonic - over distention in one part relaxes the rest - mediated by sympathetic innervation

Gastrocolic
- frequency of mass movements and motility of proximal and distal colon increase after meal ingestion
-mediated by ext and intr innervation
-occurs only weakly without ext
-initiated by stretching of stomach
may also have hormonal component involving CCK or gastrin

Front 91

Sphincters involved in defecation

Back 91

Internal Anal - a thickening of the intestinal circular smooth - under reflex control by enteric and PS nervous systems

External anal - striated voluntary muscle, innervated by somatic motor nerves (from pudendal), under voluntary and reflex control

Front 92

Events of defecation

Back 92

1. rectum is normally empty because frequency of contractions is greater than in sigmoid colon
2. mass movement forces feces into rectum
3. distension of rectum occurs and signals urge to defecate, initiates intrinsic and extrinsic (PS only) reflexes
-peristaltic waves in descending colon, sigmoid colon, and rectum forcing feces towards anus
-internal sphincter relaxes
4. stool moves into anal canal
5. relaxation of external sphincter
-under voluntary control in toilet trained individuals
-voluntary constriction overrides reflex relaxation

Front 93

Osmotic diarrhea

Back 93

produced by the presence of a poorly absorbable solute in the GI tract
-example is presence of lactose in lactase deficient individuals
-osmotically active solute draws water into intestine

Front 94

Secretory Diarrhea

Back 94

produced by an elevation in endogenous fluid and electrolyte secretion
-bacterial enterotoxins increase fluid secretion via activation of second messenger systems
-i.e. cholera toxin from Vibrio cholerae increase cAMP levels
---this stimulats excessive h20/electrolyte secretion via intestinal walls
fluid loss can amount to 12L/day and colon can only absorb 6L/day

-also E. Coli toxins increase cAMP, while others increase cGMP

also enteritis and ulcerative colitis (seperate flash cards)

Front 95

Enteritis

Back 95

form of Secretory Diarrhea produced by infection by non-toxin producing bacteria, protozoans, or viruses

1) infection irritates and inflames mucosa
2) inflammation leads to dysfunction of motility and secretion
3) produces a low volume often blood diarrhea

Front 96

Ulcerative colitis

Back 96

form of secretory diarrhea

1) causes unknown but mabe immune or allergic effect
2) colon becomes inflamed and ulcerated
3) secretion from colon high and absorption reduced
4) irritation produces very frequent mass movements
5) low volume often blood diarrhea

Front 97

Constipation

Back 97

results from feces remaining in colon for prolonged periods usually as a result of decreased GI motility

Front 98

causes of constipation

Back 98

A) irregular bowel habits
1- continuous voluntary suppression of defecation weakens reflexs
2- voluntary initiation of reflexs not as strong as natural ones
B) overuse of stimulant laxatives - weakens reflexs
C) Opiods - act on receptors on enteric nuerons
1- decrease aboral peristaltic movment thus increase transit time
2 - tone of rectal sphincter also increased

Front 99

Aspirin absorption

Back 99

optimum absorption occurs in stomach at pH 2 -4, via passive diffusion across gastric epithelia

presence of food slows rate by elevating pH

also absorbed in proximal small intestine at a faster rate

enteric coating is used to reduce gastric bleeding in susceptible individuals, delays absorbtion and reduces effectieness of aspirin to platelet aggregation.