GASTROINTESTINAL PHYSIOLOGY
GENERAL PRINCIPLES OF GASTROINTESTINAL FUNCTION
-motility, nervous control and blood circulation
TRANSPORT AND MIXING OF FOOD IN THE ALIMENTARYTRACT
SECRETORY FUNCTION OF ALIMENTARY TRACT
DIGESTION AND ABSORPTION
PHYSIOLOGY OF GI DISORDER
GENERAL PRINCIPLES OF GI FUNCTION
GIT PROVIDES – water, elctrolytes and nutrients
Requirements
1. movement of food thru GIT
2. secretion digestive juices and digestion of food
3. absorption of digestive products
4. circulation of blood thru GIT
5. control of all functions by nervous/hormonal system
TYPICAL INTESTINAL WALL
1. serosa
2. longitudinal muscle layer
3. circular muscle layer
4. submucosa
5. mucosa
THE GIT SMOOTH MUSCLE
Function as a syncytium – when action potential is elicited anywhere within the muscle mass it travels in all directions in the muscle
electrical activity – 2 basic types
1. slow waves – not action potentials
- slow undulating change in membrane potential
- undulating activity of sodium potassium pump
- control the appearance of spike potentials
2. spike potential – true action potentials
- occurs when membrane potentials is 40millivolt more
positive
Factors that depolarize the mambrane
1. stretching of the muscle
2. stimulation by acetylcholine
3. stimulation by parasympathetic nerves secreting aceytylcholine
4. stimulation by specific GIT hormones
Factors that make the membrane more negative
1. effect of norepinephrine or epinephrine
2.stimulation of sympathetic nerves secreting norepinephrine
CALCIUM IONS AND MUSCLE CONTRACTION
Muscle contraction occurs in response to entry of calcium ions
in muscle fibers
In slow waves calcium ions do not enter the membrane but instead only sodium ions thus no contraction occur
causes of tonic contraction of GIT smooth muscle
1. repetitive series of spike potentials
2. hormones
3. continuous entry of calcium ions
ENTERIC NERVOUS SYSTEM
1. myenteric plexus or aurbach’s plexus
- between longitudinal and circular muscular layers
- controls GIT movement
2. submucosal or Meissner’s plexus
- located in the mucosa
- control secretion and local blood flow
AUTONOMIC CONTROL OF GIT
Parasympathetic innervation – cranial and sacral divisions
- cranial part-transmitted almost entirely by vagus nerve
- covers esophagus, stomach, pancreas, first part of large intestine
- sacral part originates from 2nd 3rd 4th segment of spinal cord pass
thru pelvic nerves – distal large intestine
Sympathetic innervation
- originate between T5 and L2
- from cord enter the sympathetic ganglia and pass thru celiac ganglion
- generally inhibitory effect on GIT
Many afferent nerve fibers arise in the gut
Some may have their cell bodies in the enteric nervous
system itself
These nerves can be stimulated by
1. irritation of the gut mucosa
2. excessive distention of the gut
3. specific chemical substances in the gut
Signals transmitted thru these may cause excitation or
inhibition
THE GIT REFLEXES
The anatomical arrangement of the enteric nervous system
and its connection to the sympathetic and parasympathetic
nervous systems support 3 types of GIT reflexes
1. reflexes that occur entirely wihtin the enteric nervous system
- control of GI secretion, peristalsis, mixing contraction
2. reflexes from the gut to the prevertebral sympathetic ganglia then
back to the GIT
- gatrocolic reflex, enterogastric reflex,colonoileal reflex
3. reflexes from the gut to the spinal cord or brainstem and then back
to the GIT
- pain inhibition, defecation reflex,
HORMONAL CONTROL OF GIT MOTILITY
Cholecystokinin – from the jejunum in response to the presence of
fatty substance in the intestinal contents
- increase contractility of gallbladder
- slows stomach emptying
Secretin – from doudenum in response to acidic gastric juice
- mild inhibitory effect on motility of GIT
Gastric inhibitory peptide – from upper small intestine in response to
fat and carbohydrate
- slows gastric emptying
FUNCTIONAL TYPES OF MOVEMENTS IN THE GIT
Two basic types of movements
1. propulsive - move cause food to move forward
- peristalsis- contractile ring appears around the . gut and then moves forward
- usual stimulus is distention
- function of myenteric plexus
- peristaltic reflex or law of the gut
. mixing movements – peristaltic contraction can cause mixing contractions if forward movement of the intestinal is blocked by a sphincter
- local constrictive rings occur at regular interval-
relaxes- reappear at other points- chopping effect
Splanchnic circulation- blood flow thru the alimentary tract, spleen
pancreas and liver
Anatomy of GI blood supply- superior mesenteric artery
- inferior mesenteric artery
- supply small and large intestine
-enters the wall by circling in both directions around the gut
- penetrates into the wall and spread along
1. villi
2. muscle bundles
3.submucosal vessels beneath the epithelium
EFFCT OF GUT ACTIVITY AND METABOLIC FACTORS ON GI BLOOD FLOW
Under normal conditions GI blood flow is directly related to
level of local activity
After a meal the motor, secretory,absorptive activities all increase- blood flow likewise increases by 100-150%
Possible causes of increased blood flow
1.release of vasodilator substances:
cholecystokinin,vasoactive intestinal peptides,gastrin,secretin
2. release of kallidin and bradykinin by gastrointestinal glands
3.decrease in O2 concentration
COUNTERCURRENT BLOOD FLOW MECHANISM IN THE VILLI
Opposite direction of arterial flow into the villi and venous flow out of the villi
Blood O2 diffuses out of the arterioles directly into the venules without being carried to the tip of the villi
Shunting of blood in disease condition can cause ischemia
or disintegration of villus
NERVOUS CONTROL OF GIT BLOOD FLOW
Stimulation of parasympathetic nerves increase blood flow
Stimulation of sympathetic nerves cause vasoconstriction-
last for few minutes because of autoregulatory escape
Major value of sympathetic vasoconstriction is the shutting
off of GI blood flow to the brain and heart during exercise
and shock
CHEWING REFLEX
Presence of food in the mouth reflex inhibition of muscle of mastication dropping of lower jaw
stretch reflex of jaw muscles rebound contraction
raises the jaw that cause closure of the teeth
compresses the food again
SWALLOWING
1.voluntary stage
– food is voluntarily rolled into posterior pharynx by action of tongue
- hence the process becomes almost entirely automatic
2. pharyngeal stage
– receptors around the pharynx(tonsils) send impulses to the brainstem initiating as series of pharyngeal muscular contractions
a soft palate is pulled upwards to close the post. nares
b. palatopharyngeal folds are pulled medially
c. vocal cords of the larynx are approximated, pull of larynx
upwards and anteriorly
d. enlarging of the pharyngeal opening,relaxation of upper
esophageal sphincter
e. contraction of esophageal muscle
Entire process occurs in 1 to 2 seconds
NERVOUS CONTROL OF THE PHARYNGEAL STAGE OF SWALLOWING
Tonsillar pillars – most sensitive tactile area of the pharynx
- impulses from this area are transmitted to trigeminal and glossopharyngeal nerves into medulla oblongata—deglutition center
motor impulses from the swallowing center to the pharynx
and esophagus are transmitted by 5th, 9th,10th and 12th cn
Pharyngeal stage of swallowing is a reflex act
1 – 2 seconds in duration, interrupting respiration for only a fraction
of a second
3. ESOPHAGEAL STAGE OF SWALLOWING
Esophagus has 2 types of peristalsis:
1.primary peristalsis – continuation of pharyngeal peristalsis
2. secondary peristalsis – carries food left behind by primary
peristalsis to distal esophagus
- initiated partly by intrinsic neural circuit
Function of lower esophageal sphincter – thickening of circular
muscle in GE junction
- prevents reflux of acidic gastric juice
MOTOR FUNCTION OF THE STOMACH
1. storage of large quantities of food – vagal reflex can reduce
muscle tone of the stomach for accomodation- 1.5 liters
2. mixing of food with gastric juice – chyme
3. slow emptying into the small intestine – intensity of antral
contraction determines the rate of gastric emptying
- role of pylorus- contracted almost at all times
Hunger contractions – strong tetanic contractions of the body of the
stomach when it is empty for sometime
REGULATION OF STOMACH EMPTYING
Regulated by signals coming from the
stomach and duodenum
Stomach signals are
1. nervous signals caused by distention of the stomach
2. hormone gastrin released from antral mucosa
- both increase pyloric pumping force
- promote gastric emptying
Duodenal signals
- could also be nervous and hormone
- depress pyloric pumping
- increase pyloric tone
GASTRIC FACTORS THAT PROMOTE EMPTYING
Increased food volume in the stomach increased emptying
Gastrin from antral mucosa – potent effect on secretion of acid
-enhance pyloric pumping
Duodenal factors that inhibit emptying
- inhibitory effect of enterogastric nervous reflex –
GASTRIC FACTORS THAT PROMOTE EMPTYING
Factors that excite
1.degree of distention of duodenum
2. degree of irritation of duodenal mucosa
3. degree of acidity of duodenal chyme
4. degree of osmolality of chyme
5. presence of breakdown products
HORMONAL FEEDBACK FROM THE DUODENUM IN INHIBITING GASTRIC EMPTYING
Not only nervous reflex from duodenum inhibits gastric emptying hormones from duodenum do as well
Stimulus for secretion of these hormone is mainly FAT
HORMONAL FEEDBACK FROM THE DUODENUM IN INHIBITING GASTRIC EMPTYING
1. cholecystokinin – from jejunal mucosa
2. secretin – from duodenal mucosa
3. gastric inhibitory peptide
- inhibit pyloric pump activity
- increase the strength of pyloric sphincter contraction
MOVEMENTS OF THE SMALL INTESTINE
As with elsewhere in the GIT – mixing and propulsive
Mixing contraction(segmentation contractions)
- distention with chyme stretch of intstinal wall concentric
contraction spaced at interval
propulsive contraction
- contractile ring appears then moves forward squeezing contents
towards the ileocecal sphincter
Function of ileocecal valve – prevent back flow of fecal content to the small intestine
MOVEMENTS OF THE COLON
Principal functions
1. absorption of water and elctrolytes
2.storage of fecal matter
Mixing movements and propulsive movements
Mass movement - a modified type of peristalsis – constrictive ring
occurs at area of distention then rapidly 20 cm of colon distal
to this point contract as a unit forcing fecal material en mass
down the colon
Initiation of mass movemenet – gastrocolic and duodenocolic
reflexes
MOVEMENTS OF THE COLON
Mixing movements and propulsive movements
Mass movement
- a modified type of peristalsis – constrictive ring occurs at area of distention then rapidly 20 cm of colon distal to this point contract as a unit forcing fecal material en mass
down the colon
Initiation of mass movement
gastrocolic and duodenocolic reflexes
Rectum is empty most of the time
Reasons - presence of weak sphincter at the junction
between sigmoid and rectum
- sharp angulation also at the same area
Dribbling of fecal matter to the anus is prevented tonic constriction of 1. internal anal sphincter
2. external anal sphincter
DEFECATION REFLEXES
Feces enter the rectum distention of rectal wall
initiate afferent signals myenteric plexus
peristaltic waves descending colon, sigmoid and rectum
forcing feces toward the anus
SECRETORY FUNCTIONS OF GIT
Primary functions 1. secretion of digestive enzymes
2. secretion of mucus – lubrication and
protection
Anatomical types of glands
1. single cell mucus glands
2. crypts of lieberkuhn- pits- invaginated epithelium
3. tubular glands – in stomach and duodenum
4. complex glands- salivary, pancreas, liver
BASIC MECHANISMS OF STIMULATION OF THE GIT GLANDS
EFFECT OF LOCAL CONTACT AND ENTERIC NERVOUS STIMULI
-types of stimuli 1. tactile
2. chemical irritation
3. distention of gut wall
Parasympathetic stimulation – increase secretion
Sympathetic stimulation – increase/decrease secretion
Regulation of secretion by hormones
DAILY SECRETION OF INTESTINAL JUICES
Saliva 1000
Gastric secretion 1800
Pancreatic secretion 1000
Bile 1000
Small intestine 1800
Brunners gland 200
Large intestine secretion 200
total 8700
SECRETION OF SALIVA
Principal glands- parotid, submandibular,sublingual glands
2 major types of proteins in the saliva
1. serous secretion – ptyalin –enzyme
2. mucous secretion – mucin – lubrication
Functions of saliva –
1. flow – washes away bacteria
2. contains factors that destroy bacteria
- thiocyanate ions, proteolytic enzyme
GASTRIC SECRETION
ESOPHAGEAL SECRETION –entirely mucoid for lubrication
Mucus glands lined the entire surface of the stomach
2 tubular glands
1.oxyntic(gastric) glands – hcl, pepsinogen, intrinsic fator, mucus
2. pyloric glands – gastrin – mucus, pepsinogen
Secretions from oxyntic glands
3 different types of cell 1. mucus neck cells – mucus
2.peptic(chief)cells – pepsinogen
3. parietal cells – hcl and intrinsic factor
REGULATION OF GASTRIC SECRETION BY NERVOUS AND HORMONAL MECHANISMS
Basic neurotransmitters or hormones that stimulate gastric
secretion
1. acetylcholine – stimulates all types glands
2. gastrin- parietal cell- acid
3. histamine- parietal cell- acid
All function by binding first to the receptor in the secretor cell
REGULATION OF GASTRIC SECRETION BY NERVOUS AND HORMONAL MECHANISMS
Stimulation of acid secretion
Nervous stimulation- half of signal for gastric secretion comes from
the brain and other half from local reflexes within the enteric n.s.
-reflexes are stimulated by
1. distention of stomach
2.tactile stimulation of stomach surface
3.chemical stimuli
REGULATION OF ACID SECRETION
Stimulation of acid secretion by gastrin
- signals from vagus and local reflexes stimulates antral stomach to
secret gastrin from G- cell in the pyloric gland
- gastrin itself can then stimulate parietal cell to strongly secrete hcl
Role of histamine in controlling gastric secretion
-histamine is continuously produced in gastric mucosa
- by itself it causes little secretion
-in the presence of acetylcholine and gastrin it can enhance acid secretion significantly
PANCREATIC SECRETION
Pancreas is located parallel and beneath the stomach
Secretions 1. insulin by islet of Langerhans
2. digestive enzymes – pancreatic acini
3. sodium bicarbonate solution from the ducts
-- secreted to presence of food or chyme in the
upper small intestine
Digestive enzymes of pancreas
For PROTEIN
trypsin
chemotrypsin
carboxypetidase
For CARBOHYDRATE
amylase
dissacharidases
For FATS
lipase
phospholipase
cholesterol esterase
Trypsin inhibitor – prevents activation of enzymes inside the
glandular cell
Bicarbonates – serve to neutralized acid being emptied into
the duodenum
REGULATION OF PANCREATIC SECRETION
Basic stimuli –
1.acetylcholine –from parasympathetic
nerve ending to enteric n.s.
2.gastrin – from stomach
3. CCK – from jejunal and duodenal mucosa
4.secretin – jejunal mucosa
SECRETION OF BILE AND FUNCTION OF BILIARY TREE
One of the function of the liver- secretion of bile
1. fat digestion- a. emulsify large fat particles to smaller ones
b. aid in transport and digestion of fat
2. excretion of several waste products from blood
- bile, excess of cholesterol
- bilirubin, end product of hemoglobin destruction
PHYSIOLOGIC ANATOMY OF BILIARY SECRETION
bile- secreted by hepatocytes into bile canaliculi bile flows to
bigger ducts- terminal bile ducts reaching hepatic ducts
common bile duct cystic duct gallbladder
Composition of bile 1. bile salts – from cholesterol
2. bilirubin
3. cholesterol
4. lecithin
Emptying of the gallbladder – CCK
Bile salts – detergent or emulsifying function
--form micelles lipids to facilitate absorption
SECRETIONS OF SMALL INTESTINE
Brunners gland- mucus gland located in the duodenum
- secretes mucus in response to
1. tactile stimuli
2.vagal stimulation
3. gastrointestinal hormones
- mucus for protection of duodenal wall from gastric juice
crypts of Lieberkuhn – entire surface of small intestine
- secretions by epithelial cells – 1000cc/day
enzymes in the epithelial cells 1. peptidases
2. dissacharidases
3. lipase
SECRETIONS FROM LARGE INTESTINE
Crypts of Lieberkuhn - secrete mucus
-- no enzymes , no villi
mucus protects wall against excoriations
--provides an adherent medium for holding fecal material
together
-- protects wall from bacteria
Secretion of water and electrolytes – in response to irritations to dilute the irritating factors causing raid movement of feces towards anus
DIGESTION AND ABSORPTION IN GIT
Food on which the body lives: carbohydrates
fats
proteins
-- not absorbed in their natural form
Hydrolysis– basic process of digestion
Carbohydrates– large polysaccharides that are made up of
monosaccharide
-- monosaccharides are bound together by the process condensation
--condensation- one hydrogen ion has been removed from one mono -saccharide and one hydroxyl ion from another
During digestion one enzyme return the hydrogen and hydroxyl ions back:
resulting in seperation of the polysaccharide to monosccharide
Triglycerides– consists of free fatty acids condensed with
glycerolmolecules
condensation – 3 molecules of water
digestion- fat enzyme returns the 3molecules of water
(hydrolysis)
Proteins– formed from amino acids that are bound together by peptide linkages
-- hydroxyl ion is removed from one amino acid
and hydrogen ion from another
-- digestion- reverse effect of hydrolysis
DIGESTION OF CARBOHYDRATES
3 major sources of carbohydrates:
1. lactose – galactose and glucose
2. sucrose – fructose and glucose
3. starch – polysaccharide
digestion in mouth and stomach
ptyalin
-from saliva– hydrolyze starch into maltose
- amylase is blocked by acid in the stomach
small intestine
amylase
- pancreatic secretion
- starches almost totally converted to maltose
disacharidases from intestinal epithelial membrane
monosacharides
Final products of carbohydrate digestion
goes to portal blood
DIGESTION OF PROTEIN
pepsin
-peptic enzyme in the stomach is active in acid
- pepsin digest collagen(collagen tissue component in meat)
-making digestive enzymes able to digest meat
Digestion by pancreatic secretion
- mostly occuring in the upper small intestine-
duodenum,jejunum
- partially digested protein will be digested by
trypsin
chemotrypsin
carboxypeptidase
Cleaves the a.a. from polypeptide
peptidase
-digestion of peptides
-occurs in the epithelial lining of the small intestinal villi
- peptidases protrude thru microvilli of brush border membrane
-final digestion to a.a. occurs in the cytosol of the epithelial cell
- this a.a. then passes to the other side of the membrane and
into the portal blood
DIGESTION OF FATS
triglycerides
neutral fat that is most abundant in diet
Phospholipds, cholesterol esters and fatty acid
Cholesterol – no fatty acid component but with same characteristics with fatty acid
lipase
Digestion of triglycerides by pancreatic lipase
Pancreatic lipase is enough to digest all triglycerides
End product of fat digestion is free fatty acid and
monoglyceride
bile + agitation pancreatic lipase
Fat emulsified fat free fatty acid
monoglycerides
BASIC PRINCIPLE OF GASTRO INTESTINAL ABSORPTION
Total quantity that must be absorbed each day is equal to the
ingested fluid(1.5liters) + GI secretions(7 liters)= 8-9liters
All but 1.5 is absorbed in the small intestine
1.5 is pass on to the large intestine
The absorptive surface of the intestinal mucosa- villi
-valvulae conniventes(folds of kerckring)
basic mechanism of absorption
active transport
diffusion
ABSORPTION IN THE SMALL INTESTINE
Several hundred gms of carbohydrates
50-100gm of amino acid
50- 100 gms of ions
7-8 liters of water
Absorption of water
- entirely by diffusion
- when chyme is dilute-water is absorbed thru
intestinal mucosa and into blood supply of villi
by osmosis
-hyperosmolar chyme-water is transferred to the lumen to make it isosmotic with plasma
ABSORPTION OF IONS
Active transport of sodium
30 gms secreted into the lumen each day
5 – 8 gms from diet
Total of 25 – 35 gms absorbed each day
Absorption of chloride ions – follow the electrogradient created by
sodium absorption
Absorption of bicarbonate –large quantities must be reabsorbed form pancreatic secretion
-sodium absorption results in excretion of hydrogen ion- bicarbonate would combine with this forming carbonic acid CO2 and H2O. Water remains with chyme but CO2 is reabsorbed
ABSORPTION OF NUTRIENTS
Absorption of carbohydrates
- all in the monosaccharide form
- absorbed thru the cell membrane by active
transport
- selective
- sodium co-transport for glucose and galactose
Absorption of protein
- absorbed in the form of dipeptides,
tripeptides, amino acid
- needs transport protein thus facilitated diffusion
- some thru sodium co-transport
Absorption of fat
-dissolved in the central liquid portion of a miscelle -ferried t owards brush border diffuse inside the epithelial cell
endoplasmic reticulum triglyceride – chylomicron central lacteal
ABSORPTION IN THE LARGE INTESTINE
Formation of feces
1000- 1500 cc of chyme pass thru ilececal valve each day
- water and electrolytes are absorbed, <100 cc is left in
in the feces
- absorption – proximal half of the colon
- storage – distal half of the colon
Bacteria in the colon
- numerous colon bacilli- digestion of cellulose
- substances formed by bacterial activity- vit K, B12,
thiamin and gases
Composition of feces
-3/4 water and ¼ solid matter
- 30% dead bacteria
30% roughage
- 10-20% fat
-10-20% inorganic matter
- 2-3% protein
PHYSIOLOGY OF GASTROINTESTINAL DISORDER
Disorder of swallowing and esophagus
-paralysis of 5,9 and 10th cranial nerves
-diseases like poliomyelitis or encephalitis-destroy
swallowing center in the brain
-muscle dystrophy – destroy swallowing muscles
-myasthenia gravis or botulism – failure of neurotrans
mission
Abnormalities
1. complete failure of swallowing
mechanism
2. failure of glottis to close
3. failure of soft pallate to close
Anesthetic patients--
ACHALASIA
Lower esophageal sphincter fails to relax thus food
fail to pass to the stomach
Pathology is nonfunctioning of myenteric plexus in
the lower third of the esophagus
Esophageal stasis
Substernal pain- rupture causing death
Treatment – esophageal baloon
- antispasmodic drugs
DISORDER OF THE STOMACH
Gastritis – inflammation of gastric mucosa
- very common
- superficial-not very harmful but deep
involvement can lead to complete atrophy
- acute severe form- ulcerative excoriations
- cause is unknown
- mostly due to foods that are damaging to
mucosal barrier –alcohol and aspirin
Gastric barrier and its penetration in gastritis
- gastric mucosal barrier -cause of poor absorption
in the stomach
1. mucus cell secreting viscid and adherent mucus
2. tight junction between cells
Gastric barrier becomes inflammed in gastritis
increasing permeability to peptic digestion
ulcer formation
Chronic gastritis – gastric atrophy
-mucosa gradually becomes atrophic until
little or no gastric gland activity remains
-autoimmune
- leads to achlorhydria and pernicious
anemia
Peptic ulcer – excoriated area of the mucosa caused
by digestive action of gastric acid
- most common site – first few cm. of duodenum
Basic cause of peptic ulcer:
1. imbalance between rate of secretion of gastric
juice and degree of protection by gastroduodenal
mucosal barrier
2. degree of neutralization of gastric acid by duodenal
juice
Peptic ulcer
treatment 1. reduction of stressful condition
2. antacid drugs
3. H2 blocker
4. stop smoking
5. removal of specific cause like
aspirin and alcohol
surgical treatment—vagotomy antrectomy
DISORDER OF SMALL INTESTINE
Abnormal digestion of food in the small intestine is due to pancreatic failure
1. pancreatitis
2. blockage of pancreatic duct
3. after surgical removal of pancreatic
head
Malabsorption of the small intestine mucosa
1. non tropical sprue -results from toxic effects of
gluten
present in certain grains destruction of
microvilli decreasing absorptive capacity
2. tropical sprue -inflammation of the mucosa,
3. malabsorption sprue- impaired fat absorption
initially
in severe case absorption of other nutrients
are also impaired
DISORDER OF LARGE INTESTINE
Constipation – slow movement of feces
- large quantities of hard and dry feces in
descending colon
- causes- irregular bowel habit
- inhibition of the defecation reflex weakens the
reflex leading to atony of the bowels
Megacolon- hirschsprung disease
- lack or deficiency of ganglionic cells in the
myenteric plexus
-no defecation reflex
-no peristaltic motility
-severe constipation- accumulation of feces-
distention and rupture
Diarrhea—rapid movement of fecal material thru large intestine
Causes--
1.enteritis-virus and bacteria in the intestine
-irritation of the mucosa- increase in
secretion and motility
- defense mechanism
2. psychogenic—periods of nervous tension
- excites parasympathetic nervous
system increasing secretion and
motility
PARALYSIS OF DEFECATION REFLEX IN SPINAL CORD INJURY
DEFECATION –normally is initiated by movement of feces to
the rectum
-this causes cord mediated defecation reflex
passing from the rectum to the spinal cord and
back to descending,sigmoid colon, rectum and anus
Spinal cord injury
—blocks defecation reflexthis reflex
- destruction of conus medullaris of the spinal cord
destroy the sacral center in which the reflex is
integrated—paralyzing defecation reflex
Support measures for loss of defecation reflex
-cathartics and enemas
GENERAL DISORDERS OF THE GIT
VOMITING—means by which GIT rids itself of its contents
when it is irritated over distended or over excitable
-impulse is transmitted by vagal and sympathetic
afferent fibers to the vomiting center in the medulla
-motor response via 5,7,9,10 and 12th cn
Antiperistalsis—prelude to vomiting
-abdominal contents can be pushed back to the
duodenum –the resulting distention excites vomiting
relfex
The vomiting act:
1.deep breath
2.raising of the hyoid bone and larynx-opening of lower
esophageal sphincter
3.closure of glottis
4. lifting of soft pallate-closing the post. Nares
5.strong donwward contraction of the diaphragm
6.contraction of abdominal muscle-building intragastric
pressure
7.relaxation of lower esophageal sphincter
8.expulsion of gastric contents
NAUSEA—conscious recognition of a subconscious
excitation in an area closely associated with
or a part of vomiting center
causes
1. impulses from the GIT
2. impulses from the lower brain
3. impulses from cerebral cortex
GASTROINTESTINAL OBSTRUCTION
Can occur at any point along the course of GIT
Causes
1. malignancy
2. fibrotic constriction from ulceration or peritoneal
adhesion
3. spasm of a segment of GIT
4. paralysis
Abnormal consequence depends on point of obstruction
--obstruction of small intestine
losses of electrolytes and water—plasma loss
circulatory shock
GASSES IN THE GIT AND FLATUS
From swallowed air
From bacterial action
Diffusion from blood
Stomach—swallowed air
-nitrogen, oxygen
-belching
Large intestine—bacterial action
-carbon dioxide,methane and hydrogen
-certain food act as substrate for bacteria
thus more air production
Saturday, February 28, 2009
slides on reflexes, DTR
Muscle spindle
• A small, complex spindle-shaped sensory receptor located in skeletal muscle
• senses muscle stretch
• consists of several modified muscle fibres, called intrafusal fibres
• The ends of these fibres are contractile
• central portion is non-contractile and innervated by special neurones/gamma motor neurones).
Basic reflexes:
The myotatic(stretch) reflex
The inverse myotatic reflex
The flexion withdrawal-crossed extensor reflex
Motor outputs
Involuntary
Stereotyped
Elicited by specific sensory inputs
The stretch reflex
Designed to maintain muscle length
-by countering a muscle stretch
-with a muscle contraction
Provides the basis for muscle tone
Also called deep tendon reflexes
-rapid, passive muscle stretch activates muscle spindles
-spindle afferents (oarticularly Ia) send impulses to the spinal cord
-connections to homonymous muscle alpha neurons: Monosynaptic
-connections to synergistic muscle alpha motor neurons; monosynaptic
--cause the stretched muscle to contract
Connection to the antagonist muscle thru inhibitory neuron—decreases activity of the antagonist muscle
Inverse myotatic reflex
Designed to control muscle tension
-by countering a muscle contraction with relaxation
-plus contraction of the antagonist mmuscle
Allows controlof muscle force
The flexion withdrawal and crossed extensor reflexs
Designed to withdraw one limb from a painful stimulus, while extending the cnotralateral limb for support
Reflexes ;window into the nervous system
- is sensory pathwayintact?
- -is motor output pathway intact?
deep tendon reflexes:
-present normally
-weak of absent with posterior root, LMN, or anterior root lesion,
-weak or absent with acute UMN lesion
-increased with chromic UMN lesion
Some DTRs often tested;
-biceps(C5-6)
-triceps(C7)
Patellar (knee jerk;L3-4)
-achilles (ankle jerk reflex;S1)
Superficial reflexes;
Present normally
-weak or absent with posterior root, LMN< or anterior root lesion,
-weak of absent with UMN lesion
-relfexes testet; abdominal and cremasteric
Plantar reflex
Present normally
Absent with posterior root, LMN, or anterior root lesion
With UMN lesion, plantar flexion is replaced by extensor plantar response(up-going-toes)
-called babinski reflex
Indicates damage to corticospinal tract
-a remnant nociceptive avoidance reflex
Clonus
-rythmic contractions and relaxations of amuslce grup
-often accompanies increased DTRs seen with UMN damage
bIceps brachii(C5)
=purpose – to provoke a root (C5) or cord(cns)sign
-positive response
-hypoactive (root)
Hyperactive (cord-cns)
Brachioradialis(c6)
Positiveresponse
-hypoactive- root
Hyperactive – cord- cns
Triceps (c7)
Hypoactive root
Hyperactive – cord –cns
Quadriceps(L4)
Hypoactive –root
Hyperactive—cord—cns
Gastroc-soleus(S1)
Hypoactive –root
Hyperactive—cord –cns
In general
reflexes are not pathological if symmetric unless they are absent or hyperreflexic
Assymetry of reflexes and absent reflexes tend to localize to a peripheral nervous system process
Increased reflexes tend to indicate a problem of the central nervous system
Reflexes are routinely tested on neuro exam and are nonspecific as to the etiology of the disease process if abnormal.
They provide information to help localize the problem
the pupillary reflex or pupillary light reflex
is the reduction of pupil size in response to light.
It is a normal response and dependent on the function of the optic nerves and oculomotor nerves
Lack of the pupillary reflex or an abnormal pupillary reflex
can be caused by
optic nerve damage
oculomotor nerve damage
brain death
and depressant drugs
such as barbiturates
The optic nerve is responsible for the afferent limb of the pupillary reflex, or in other words, senses the incoming light.
The oculomotor nerve is responsible for the efferent limb of the pupillary reflex; in other words, it drives the muscles that constrict the pupil.
Dependent on how the pupils constrict or do not constrict one can determine which of the cranial nerves is damaged.
• A small, complex spindle-shaped sensory receptor located in skeletal muscle
• senses muscle stretch
• consists of several modified muscle fibres, called intrafusal fibres
• The ends of these fibres are contractile
• central portion is non-contractile and innervated by special neurones/gamma motor neurones).
Basic reflexes:
The myotatic(stretch) reflex
The inverse myotatic reflex
The flexion withdrawal-crossed extensor reflex
Motor outputs
Involuntary
Stereotyped
Elicited by specific sensory inputs
The stretch reflex
Designed to maintain muscle length
-by countering a muscle stretch
-with a muscle contraction
Provides the basis for muscle tone
Also called deep tendon reflexes
-rapid, passive muscle stretch activates muscle spindles
-spindle afferents (oarticularly Ia) send impulses to the spinal cord
-connections to homonymous muscle alpha neurons: Monosynaptic
-connections to synergistic muscle alpha motor neurons; monosynaptic
--cause the stretched muscle to contract
Connection to the antagonist muscle thru inhibitory neuron—decreases activity of the antagonist muscle
Inverse myotatic reflex
Designed to control muscle tension
-by countering a muscle contraction with relaxation
-plus contraction of the antagonist mmuscle
Allows controlof muscle force
The flexion withdrawal and crossed extensor reflexs
Designed to withdraw one limb from a painful stimulus, while extending the cnotralateral limb for support
Reflexes ;window into the nervous system
- is sensory pathwayintact?
- -is motor output pathway intact?
deep tendon reflexes:
-present normally
-weak of absent with posterior root, LMN, or anterior root lesion,
-weak or absent with acute UMN lesion
-increased with chromic UMN lesion
Some DTRs often tested;
-biceps(C5-6)
-triceps(C7)
Patellar (knee jerk;L3-4)
-achilles (ankle jerk reflex;S1)
Superficial reflexes;
Present normally
-weak or absent with posterior root, LMN< or anterior root lesion,
-weak of absent with UMN lesion
-relfexes testet; abdominal and cremasteric
Plantar reflex
Present normally
Absent with posterior root, LMN, or anterior root lesion
With UMN lesion, plantar flexion is replaced by extensor plantar response(up-going-toes)
-called babinski reflex
Indicates damage to corticospinal tract
-a remnant nociceptive avoidance reflex
Clonus
-rythmic contractions and relaxations of amuslce grup
-often accompanies increased DTRs seen with UMN damage
bIceps brachii(C5)
=purpose – to provoke a root (C5) or cord(cns)sign
-positive response
-hypoactive (root)
Hyperactive (cord-cns)
Brachioradialis(c6)
Positiveresponse
-hypoactive- root
Hyperactive – cord- cns
Triceps (c7)
Hypoactive root
Hyperactive – cord –cns
Quadriceps(L4)
Hypoactive –root
Hyperactive—cord—cns
Gastroc-soleus(S1)
Hypoactive –root
Hyperactive—cord –cns
In general
reflexes are not pathological if symmetric unless they are absent or hyperreflexic
Assymetry of reflexes and absent reflexes tend to localize to a peripheral nervous system process
Increased reflexes tend to indicate a problem of the central nervous system
Reflexes are routinely tested on neuro exam and are nonspecific as to the etiology of the disease process if abnormal.
They provide information to help localize the problem
the pupillary reflex or pupillary light reflex
is the reduction of pupil size in response to light.
It is a normal response and dependent on the function of the optic nerves and oculomotor nerves
Lack of the pupillary reflex or an abnormal pupillary reflex
can be caused by
optic nerve damage
oculomotor nerve damage
brain death
and depressant drugs
such as barbiturates
The optic nerve is responsible for the afferent limb of the pupillary reflex, or in other words, senses the incoming light.
The oculomotor nerve is responsible for the efferent limb of the pupillary reflex; in other words, it drives the muscles that constrict the pupil.
Dependent on how the pupils constrict or do not constrict one can determine which of the cranial nerves is damaged.
Friday, February 27, 2009
spinal myotatic reflexes
reflexes are the most objective part of neurologic examination and are very helpful in determining the level of damage in the nervous system
http://www.brainviews.com/abFiles/AniPatellar.htm
copy-paste this link on your address bar for the lecture slides on reflexes
https://rcpt.yousendit.com/658035026/428c6f678387972cd4136a3e69aa4e82
link to animation of stretch reflex for further info:
http://trc.ucdavis.edu/biosci10v/bis10v/media/ch25/stretch_reflex_v2.html
http://www.brainviews.com/abFiles/AniPatellar.htm
copy-paste this link on your address bar for the lecture slides on reflexes
https://rcpt.yousendit.com/658035026/428c6f678387972cd4136a3e69aa4e82
link to animation of stretch reflex for further info:
http://trc.ucdavis.edu/biosci10v/bis10v/media/ch25/stretch_reflex_v2.html
Thursday, February 19, 2009
its GIT tutorial
The physiology of Gastrointestinal tract can easily be studied and reviewed in these sites/links
Copy paste this link into your address bar cause the web prompter of this blog seemed to have conked out. Once in the webpage scroll to GIT or digestive system and open the specific topic to take the online test. It is advisable to review the animation of the same topic before proceeding to the test question. You will learn and have fun too!
www.mhhe.com/biosci/ap/vdghumananatomy/student/olc2/ap_animation-quizzes.html
digestion and absorption of fats
http://bcs.whfreeman.com/thelifewire/content/chp50/5002001.html
more animation on digestion
http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter26/animation__organs_of_digestion.html
Tuesday, February 3, 2009
Botulinum toxin
Mr Gaitano during the discussion of Clostridium botolinum, a gm+ bacilli has asked about the use of this toxin medically.
The popular use of BOTOX treatment must be the subject Gaitano was asking about. Botox is afterall botulinum toxin and is used for its capacity to block acetylcholine release at motor-end-plate. If we could recall, the acetylcholine vesicles in the nerve terminal need to bind with the presynatic membrane so that it can be released by exocytosis. This is the precise process that is being block by the toxin. The inhibition of acetylcholine release then results in loss of impulse conduction to the sarcolemma and thus lost of muscular contractility or tone. This is seen as flaccid paralysis in the affected musculature.
Thus it is this action that the toxin is used for treatment of spastic muscular conditions.
http://emedicine.medscape.com/article/325451-overview
Monday, February 2, 2009
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