Transcript 07.Pathophysiology of digestion

Pathophysiology
of digestion
MD, Prof. Yu.I. Bondarenko
INSUFFICIENCY OF DIGESTION.
THE REASONS. MANIFESTATIONS
The basic role of digestive system consists in digestion
of components of food that enter into an alimentary
canal (proteins, fats, carbohydrates), absorption of
formed nutrients and removing from an organism endproducts of metabolism.
Numerous functions of digestive system are regulated
by the central and autonomic nervous system, humoral
and endocrine influences.
Disorders of regulation cause disturbance of normal
course of the processes in an alimentary canal, result in
insufficiency of digestion and promote development of
many diseases.
INSUFFICIENCY OF DIGESTION
It is pathological condition at which the
digestive system does not provide
assimilation of the nutrients that enter in
the organism.
 hereditary insufficiency of digestion
(some kinds malabsorption)
 acquired insufficiency of digestion
CAUSES OF DIGESTION
INSUFFICIENCY DEVELOPMENT
1. Alimentary (food) factors:
a) reception of bad and rough food
b) dry rations
c) irregular reception of food
d) disbalanced meal (for example, reduction of the
contain of vitamins, proteins in diet)
e) abuse in alcohol
2. Physical factors
Greatest role belonge to radiation which damage epithelial
cells of the alimentary channel which have high mitotic
activity
3. Chemical agents: Poisonings with inorganic and
organic compounds.
4. Biological factors:
a) bacterium (for example, v.cholera, dysentery, typhoid,
paratyphoid fever)
b) bacterial toxins (for example, salmonellosis,
staphylococcus infection)
c) viruses (for example, adenoviruses)
d) helminths
5. Organic effects:
a) congenital anomalies of digestive system
b) postoperative conditions
c) tumors of digestive system
6. Disorders of nervous and humoral
regulation:
a) psychoemotional disorders (neurotic and neurosislike conditions)
b) mental diseases (schizophrenia, maniac - depressive
syndrome)
c) organic diseases of the central nervous system
(encephalites)
d) lesions of peripheral structures of autonomal nervous
system
e) reflex disorder (various viscero-visceral reflexes)
Disorders of humoral regulation of digestion may be
connected to disorders of synthesis and secretion
gastrointestinal hormones (gastrine, secretin,
cholecystokinin-pancreazymin etc.)
INSUFFICIENCY OF DIGESTION
MAY MANIFESTS SYNDROMES:
1.
2.
3.
4.
5.
6.
Starvation
Dispeptic syndrome
Dehydratation
Disturbance of the acid-base balance
Intestinal autointoxication
Painful syndrome
DISPEPTIC SYNDROME
Dispeptic syndrome includes different combinations of the
following symptoms:
a) anorexia
b) heartburn
c) eructation
d) nausea
e) vomitting
f) meteorism
g) constipations
h) diarrhea
ANOREXIA
Anorexia is a full absence of appetite while person
need food
Kinds of the anorexia:
а) intoxical - develops during acute and chronic
poisonings (for example, salts of mercury, medical
products, bacterial toxins)
b) dispeptic - arises at diseases of digestive system, has
more often behavior-reflex nature
c) neurodynamic - develops as a result reciprocal
disturbance of the appetite centre after overexcitation
of structures limbic systems (for example, painful
syndrome during heart attacks, colics, peritonitis)
ANOREXIA
d) neurotic - is connected with excessive
excitation of cortex brain and strong emotions
(especialy negative)
e) psychogenic – is connected with conscious
restriction of food (for example, with an aim of
getting thin or as result of mental disorders)
f) neuroendocrinopathy - is caused by organic
lesion of the central nervous system
(hypothalamus) and endocrine diseases
(hypophysial cachexia, Addison’s disease)
MECHANISMS OF ANOREXIA
DEVELOPMENT :
1. Reduction of excitability of the food centre
(intoxical, dispeptic, neuroendocrinopathy
anorexia)
2. Inhibition of neurons of the food centre
(neurodynamic, neurotic, psychogenic anorexia)
The heartburn is a feeling of heat or burnings
long esophagus.
Development is connected with irritation of
receptors of esophagus during pelting
contents of stomach into one (reflux).
It may be caused by:
а) increase forming of gastric juice
b) functional insufficiency of cardial sphincter
The eructation is sudden involuntary allocation into oral cavity
some gas from a stomach or a gullet, sometimes with small
portions of contents of a stomach
The increasing of the contents of gases in stomach may be
caused by two reasons:
а) receipt big quantity of gases with food and a drink (for example,
aerated drinks), siping of air (aerofagia)
b) formation of gases in the stomach, it is especial at a long delay
there peep (at a stomach ulcer, cancer of a stomach)
As a result of increasing of the contents of gases in a stomach it is
increased intrastomach pressure. It reflexly can cause:
а) reduction of muscles of a stomach wall
b) a spasm of the gatekeeper
c) a relaxation of muscles of aesophagal-gastric sphincter
Thereof gases are superseded from a cavity of a stomach in a
gullet, to a drink. And then in an oral cavity
The nausea is a burdensome sensation in epigastric
area breast and in the oral cavities, quite often
previous to vomitting and frequently accompanying
with the general weakness, sweatness, increasing
of salivation, coldness of arms and legs, pallor of a
skin, decrease of arterial pressure that is
connected to activation parasympathic nervous
system. In a basis of a nausea is an excitation of
the emetic centre, but insufficient for occurrence of
vomitting lays.
Vomitting - the complex-reflex act which results to
eruption of contents of a stomach outside through
a mouth is a result of excitation of the emetic
centre which is situated in an oblong brain.
The mechanism of vomitting includes a number of consecutive
stages. His pick out the following pathogenetic variants of
vomitting:
а) central - it is connected with increasing of excitability of the
emetic centre. It happens at diseases of the central nervous
system (meningitises, encephalities, tumours of a brain), at
excitation of cortex of the big hemispheres (behavior-reflex
vomitting) or receptors of a labyrinth (vestibular vomitting);
b) hematogenic-toxic - it is caused by direct action of toxic
substances which are in blood, on receptors that are in emetic
centre. It may be exogenous substances (carbonic oxide,
alcohol, medical products, toxins of bacteria) or toxic products
of an own metabolism which are collected during at a uremia,
hepatic insufficiency, decompensated diabetes and others;
c) visceral (reflex) – is a result of reflexes which are caused from
different receptors of internal organs. Such reflexogenic zones
are in a stomach, a mucous membrane of pharynx, coronal
vessels, peritoneum, biliary duct etc.
Meteorism is a superfluous accumulation of gases in
the digestive channel due to their increased
formation or insufficient removing from intestines
Superfluous formation of gases underlies
development of the following kinds of meteorism:
а) alimentary - develops at reception with food a lot
cellulose, starches (leguminous, cabbage, a
potato)
b) disorders of digestion (pathology of enzymes,
disturbances of absorbtion, intestinal
disbacterioses)
Disturbance of discharge of gases typically for
such meteorism:
а) mechanical - develops as a result of
Disturbance of passableness of intestines
(spasms, solderings, tumours)
b) dynamic - arises at disorders of motor
function of intestines
c) circular – is a result of the general and local
disorders of blood circulation
It is pick out two mechanisms of development of
constipations - spastic and atonic.
The first is caused by long constant reduction of
smooth muscles of guts, the second – because of
their atonia.
To spastic constipations concern:
а) inflammatory - arise owing to local spastic reflexes
with changed of mucous membrane;
b) proctogenic - develop at a pathology anorectal
areas;
c) mechanical - arise at impassability of guts;
d) toxic – is result of poisonings lead, mercury,
thallium.
Atonic constipations are:
а) alimentary - develop at receipt light food
containing(not enough) cellulose
b) neurogenic – is the result of disorders of nervous
regulation of a motility of guts
c) hypodynamic - arise at bed patients, at old men,
people with very low motor activity
d) constipations at anomalies of a thick gut
(Girshprungs disease)
e) constipations in consequensce disorders waterelectrolyte metabolism
Diarrhea
Pathogenetic variants of diarrheas:
а) osmotic diarrhea. Develops when osmotic pressure is increase
because of intestinal contents at intake of substances which are
bad or are not absorbed at all (for example, laxative), and also at
disturbances of digestion and absorbtion (syndromes maldigestion
and malabsorbtion)
b) secretory diarrhea. It is connected with activation of secretion of
ions (Na+ , Cl‾), that causes the strengthened secretion of water
into gap of guts (for example, during cholera)
c) diarrhea, caused by braking of active transport of ions through
cellular membranes in guts (for example, congenital chlordiarrhea genetic defect of absorbtion of anions of chlorine in illeum)
d) diarrhea is caused by increase of permeability of an intestinal wall
(inflammatory)
e) diarrhea at disturbance of an intestinal motility
Intestinal autointoxication, as a rule, is connected with
infringement corelation between bacterias and
formation a plenty of toxic products of fermentation
and putrafaction.
Dysbacteriosis is an infringement of a ratio between
separate kinds of microflora. Thus the quantity of the
bacteria causing processes of putrafaction and
fermentation is frequently increased. As a result
formation in guts of toxic products - hydrogen
sulphide, scatol, indole, phenols, putrescine,
cadaverine grows etc. If formation of these products
exceeds functional ability of a liver on them
detoxifcation, attributes of hepatic insufficiency
develop. Development of intestinal autointoxication is
promoted by reduction of intestinal
peristalsis(constipations), reduction of secretion of
intestinal juice, intestinal obstruction.
PAIN
The pain frequently accompanies with development of
diseases of the alimentary channel. Depending to the
reasons and pathogenesis pain may have different
characters.
Distinguish the following mechanisms of occurrence of pain
at lesions of digestive organs:
The spastic mechanism. The pain is caused by a spasm of
smooth muscles of different parts of the alimentary
channel. In this case the reason of pain is constriction of
the vessels which are located in the wall of hollow organs
owing to that the ischemia develops. It cause appearance
of metabolism products in the working organs, and their
influence on pain receptors. At sharply arising strong
spasm pain on colics type develops
PAIN
The hypotonic mechanism. At reduction of smooth
muscles tone (hypotonia) the pain appears due to
stretching the wall of hollow organs ( stomach, guts, gall
bladder) by their contents. Thus the mechanical
stretching of tissues causes irritation of the nervous
endings;
Influence of biological active substances (histamine,
serotonin, kinines, prostaglandins) on the nervous
endings. These substances are formed and secreted at
damage of cells and inflammation (gastritis, duodenitis,
enteritis, colitis, cholecystitis). Especially a lot of these
substances appear during acute pancreatitis.
FUNCTIONAL DISORDERS OF DIGESTIVE SYSTEM
1. Disturbance of digestive system secretion :
а) hypersecretion states:
1 hypersalivation
2 gastric hypersecretion
3 pancreatic hypersecretion
4 hypercholia
b) hyposecretion states:
1 hyposalivation
2 gastric hyposecretion
3 pancreatic hyposecretion
4 acholia
2. Disturbance of motor function of the alimentary
channel:
1 disturbance of chewing
2 disturbances of swallowing - dysphagia
3 gastric dyskinesia
4 intestinal dyskinesia
5 dyskinesia of gall bladder and biliary ducts
6 disturbances of defecation
3. Disturbance of digestive and absorptive functions syndromes of maldigestion and malabsorption.
HYDROCHLORIC ACID, PEPSIN, MUCUS SECRETION
DISTURBANCE
Hydrochloric acid is secreted with parietal cells of mucous
membrane of stomach. Their number in the healthy person is
about 1 billion.
Phases of secretion:
1.Neurogenic (vagal);
2.Gastric (gastrine);
3.Intestinal that is regulated by intestinal hormones.
In regulation of functional activity of parietal cells takes place
nervous system (through mediator acethylcholine), and also
various hormones (serotonin, insulin). The parietal cell contains
receptors to histamine which is released from
enterochromaphilic cells (ECL), gastrin and cholecystokinin
(CCK-receptors), and also receptors for acethylcholine (M3receptors),
REGULATION OF OUTPUT HCL
Stimulation of H2-histamine receptors is bring on formation cAMP,
and stimulation of CCK-receptors and M3-receptors results to
increasing of level of endocellular calcium (Са++).
Stimulation of M3-receptors increases, not only total Са++ into cell
and due to increasing of level inositolthreephosphate (IP3)
strengthens an output of endocellular Са++.
Gastrin, cholecystokinin and histamine also raise output of Са++ due
to action on IPh3 .
Parietal cell has receptor to prostaglandin E2 (PGE2)) which
stimulation reduces level cAMP and results ihibition of hydrochloric
acid secretion.
Secretion of hydrochloric acid by parietal cell is carried out by
principle of the proton pump in which K+ exchanges on H+, and Cl‾ on HCO3-‾. An important role in this process plays H+, K+ ATPase which, using energy of ATP, provides transport H+ from
parietal cells and K+ into cell.
Hypersecretion of hydrochloric acid plays the important
role in development of several gastroenterologic
illness, may be observed at hereditary conditioned
increasing of weight parietal cells, the increased tone
of a vagal nerve, stretching of antral part of stomach
during disorder of emptying, increasing of secretion of
gastrin, increasing quantity of ECL-cells in the mucous
membrane of stomach (in the patients with carcinoid
syndrome).
The main cells of mucous membrane form pepsin . It is
know seven types of pepsinogen. Disturbance of
pepsin formation take place in the number
gastroenterologic diseases (for example, stomach
ulcer).
Gastric mucus is secreted by stomach mucous cells. Into
structure of gastric musous contain glycosaminoglycans and
glycoproteins.
From sialic acids N-acethylneuraminic acid provides ability of
gastric mucus to form water-insoluble viscose lay of stomach
mucus membrane.
Stimulating influence on formation of mucus result irritation of
adreno- and cholinoreceptors, prostaglandins. Hydrolysis of
lisosoms cause dehydratation of glycoproteins.
Gastric mucus (together with bicarbonates) takes part in
formation of mucus barrier which supports a gradient рН
between hollow of stomach and its mucus membrane and
H+.
Disturbance of this barrier as a result of reduction the synthesis of
prostaglandins in the wall of stomach.
GASTRIC HYPERSECRETION IS CHARACTERIZED :
Increased quantity of gastric juice as after
reception of food and also on the empty
stomach
Hyperaciditas and hyperchlorhydria - is increase
of the common acidity and the maintenance of
free hydrochloric acid of gastric juice
Increasing of digestive ability of gastric juice
The disturbances of digestion connected with gastric
hypersecretion, are caused with long delay food in
the stomach (pylorus is closed, because
neutralization of very acidic contents that goes into
duodenum,it take a lot time).
Consequences:
A little contents that enter into guts lead to reduction
of gut peristaltic and constipation development.
Processes of fermentation and formation gases is
amplified in the stomach. It causes appearance of
eructation and heartburn
Motor activity of stomach is increased as a result
hypertone and hyperkinesis of smooth muscles.
GASTRIC HYPOSECRETION IS CHARACTERIZED:
Reduction the quantity of gastric juice on an
empty stomach and after reception of food
Decreased or zero acidity of gastric juice (hypoor unacidity), reduction of the contents in it or
absence of the free hydrochloric acid (hypo- or
achlorhydria)
Reduction of digesting ability of gastric juice
due to achylia (the full stop formation a
hydrochloric acid and enzymes)
Reduction of gastric secretion stipulated disturbance of
digestion along alimentary channel.
Insufficient formation of gastric juice that keeps pylorus opened
also contents of stomach quickly passes into duodenum where
environment becomes constantly alkaline. It causes inhibition
of formation secretin.
Insufficiently digested components of food irritate receptors of
mucus membrane of guts that results in their strengthening of
peristaltic and diarrhea develop.
Besides an absence of a hydrochloric acid leads to development
of microflora in the stomach.
Activation of processes of rotting and fermentation is connected
appearance such disturbance of digestion, as an eructation, the
impose tongue etc.
DISTURBANCE OF STOMACH MOTOR FUNCTION
Disturbance of stomach motor function is called
gastric diskinesia
Trere are two kinds of gastric diskinesia: hypertonic
and hypotonic
Hypertonic kind is characterized strengthening of
peristaltic(hyperkinesia) and increasing of
stomach muscles tone (hypertonia)
The hypotonic kind, on the contrary, is characterized
hypotonia and hypokinesia
THE REASONS OF MOTOR GASTRIC
DISTURBANCE OF HYPERTONIC TYPE
Some food factors (rough food, alcohol)
Increase of gastric secretion
Increase of vagal nerve tone
Some gastrointestinal hormones (motilin)
Hypertension and hyperkinesia of stomach leads to:
A long time delay of food in stomach that promotes
increase of gastric secretion and development of
ulcers of mucus membrane
Development antiperistaltic of stomach that results in
development of dispeptic disturbances (an eructation,
nausea, vomitting)
One forms of diskinesia of stomach hypertonic type is
pylorospasm
It is observed mainly in babies, especially in the first
weeks and months of life.
Pylorospasm in children is caused by functional
disturbances of the nervous- muscular system of
pylorus part stomach. It is observed mainly at the
excitable children who have transferred intrauterine hypoxia, born in asphyxia with attributes of
a birth trauma of the central nervous system
At pylorospasmis marked weak development of
muscles in cardial parts of stomach and its more
expressed development in the area of pylorus. It
promotes development of vomitting and eructation
CAUSES OF STOMACH MOTOR ACTIVITY REDUCTION
Alimentary factors (fat food)
Reduction of gastric secretion (hypoacidic gastritis)
Reduction of vagal nerve tone
Action gastrointerstitial hormones (gastroinhibiting peptide,
secretine etc.)
Removal of stomach pylorus
The common weakening of organism, an exhaustion, gastroptosis
At hypotonic diskinesia time of staying of food in the stomach
is shortened that lead to disturbance of its digestion. Action
undigested components of food on receptors of mucus
membrane of guts causes increase of peristaltic and diarrhea.
ETIOLOGY OF GASTRIC ULCER
Etiology of ulcer disease now is not established !
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In development of stomach and duodenal ulcers
take place the following risk factors
1. Psychoemotional negative overstrains (negative emotions,
conflict situations, feeling of constant alarm, overfatigue etc.)
2. Stress
3. Hereditary predisposition
4. Nutritional disorder – live on dry ration, irregular reception
of nutriment, eating of rough or pungent food, bad chawing of
food, fast meal, absence of the teeth, the insufficient contents in
food of proteins and vitamins
5. Chronic gastritis and duodenitis with increased secretion
6.The microbic factor - Helicobacter pylori
7. Harmful habits - smoking, abuse of alcohol
Pathogenesis of stomach ulcer in general is reduced to
disturbance of balance between factors acid-peptic
aggressions of gastric contents and elements of protection of
stomach mucus membrane and duodenum.
Sufficient of bicarbonates buffer, good regeneration of epithelial
cells, blood supply of mucus membrane, normal formation of
prostaglandins in wall of stomach are factors that protect
mucus.
Helicobacter pylori. These bacterias produce a lot of enzymes
(urease, protease, phospholipase), damaging protective barrier
of mucus membrane, and also various cytotoxins. The most
pathogenic are Vac A-strains, that produce vacuolizing cytotoxin
which results in formation cytoplasmatic vacuoles and
destructions of epithelial cells, and the Sad A-strains which
express gene associated with cytotoxin. This gene codes
protein which has direct damaging effect on mucus membrane.
Helicobacter pylori promotes liberation in a mucus membrane of
stomach interleukines, lisosomal enzymes, TNFα, that causes
development of inflammatory processes in mucus.
STOMACH PEPTIC ULCER
PEPTIC STOMACH ULCER
STOMACH AND DUODENUM ULCER
HYSTOLOGY OF THE STOMACH ULCER
DUODENUM
ULCERS
ACUTE STOMACH ULCERS
DUODENUM ULCER
INFECTIOUSES AGENTS OF STOMACH
HELICOBACTER PYLORI
DUODENUM
ULCER
Contamination of stomach mucus membrane by Helicobacter is accompanied by
development superficial anthral gastritis and duodenitis and lead to increase
level of gastrin with the subsequent increasing of hydrochloric acid secretion.
Excess of hydrochloric acid, getting into lumen of duodenum, in conditions of
deficiency of pancreatic bicarbonates promotes development of duodenitis
(remodulation of epithelium of duodenal mucus membrane on gastric type)
which are quickly contaminated by Helicobacter.
Further at adverse current, especially when there are additional etiological
factors (hereditary predisposition, 0 (1) group of blood, smoking,
psychological an overstrain etc.), in area of metaplased mucus membrane
ulcer defect is formed.
However connection of occurrence of stomach ulcer with infection of mucus
membrane of stomach by Helicobacter revealed not always. Approximately 5
% of patients with ulcers of duodenum and of 15-20 % patients with stomach
ulcers, disease develops without participation of these microorganisms.
DISTURBANCE OF INTESTINAL FUNCTIONS
Functions of intestines may be disordered owing to many
organic diseases. In some cases these disturbances
arise owing to disturbances of nervous regulation of
small and large intestine motility
Disturbance of digestion and absorbtion in intestines
The complex of disturbances which occur in an organism
as a result of disturbance of digestion and absorbtion
processes, received the name of a syndrome
maldigestion and malabsorption
THE SYNDROME MALDIGESTION
The syndrome of maldigestion is disturbances of primary
digestion, caused by insufficient secretion into guts the
digestive enzymes, in particular at pancreatic hyposecretion.
This syndrome is characterized:
disturbance of digestion of fats (absence of lipase and
phospholipase). About 60-80 % of fat that get into guts is
removed with feces – steatorrhea (fat in feces)
disturbance of absorption of fat-soluble vitamins – cause the
development hypovitaminosis A,D, E and K
disturbance of digestion of proteins (absence of digestive
proteases). About 30-40 % of food protein are not adopted. In
feces there is plenty of muscular fibres
disturbance of digestion of carbohydrates (absence of amylase)
disturbance of nucleinic acids digestion (absence of nucleases)
THE SYNDROME OF MALABSORPTION
It is complex of symptoms which occur in a result of
disturbance absorption of substances in guts.
Disturbance of absorbtion in guts may be caused by
the disturbances that occur at three levels:
Preenterocytic disturbance. Develop as a result of
disturbances of processes of digestion before
absorbtion;
Enterocytic. Disturbance of activity epithelial cells of
intestinal mucus membrane;
Postenterocytic. Disturbance of the processes that
provides utilization of absorbed substances into
internal environment of an organism (blood, lymph).
PREENTEROCYTIC DISTURBANCES:
Disturbances of primary digestion (the syndrome maldigestion).
By origin they may be gastrogenic, pancreatogenic,
hepatogenic, enterogenic, disregulated, iatrogenic (connected
with long usage of antibiotics and other medical drugs)
Disturbance of memrane digestion. More often it is caused by
disturbance of formation and fixation of enzymes in plasmatic
membrane of enterocytic microvillus
Interstitinal enzymopathies- hereditary caused disturbances of
digestive enzymes synthesis by microvillus which provide
processes of membrane digestion. Among interstitial pathology
of enzymes the most often is intolerance to disaccharides
(lactoses, saccharoses, tregaloses) and insufficiency of
peptidase (gluten enteropathy, celiac disease).
THE REASONS OF MALABSORBTION MAY BE
SUCH ENTEROCYTIC DISTURBANCES:
Reduction of absorption area ( condition after resection of gut,
an atrophy of villus and microvillus)
Hereditary and acquired disturbance of proteins formation carriers monosaccharides (intolerance of glucose, galactose,
fructoses), amino acids (tryptophanmalabsorbtion), ions
calcium (hypovitaminosis D)
Disturbances of functioning ions pumps of enterocytes (transport
monosaccharides and amino acids is connected with work of
Na-K-pump)
Deficiency of energy (absorbtion the majority of substances process energydependent)
Disturbance of formation in enterocytes of transport complexes
(chilomicrones, lipoproteids)
THE REASONS OF POSTENTEROCYTIC
DISTURBANCES OF MALABSORPTION :
Disturbances of blood circulation in a wall of guts, may
be caused with disturbances of general
hemodynamic (ischemia, venous hyperemia,
thrombosis, embolism, reaction of vessels in an
inflammation);
Disturbances of lymph flow. Lymph circulation
disorders may be connected to disturbances of
constriction of intestinal wall fibres due to local
reflex and act of villikinin.
DISTURBANCES OF MOTOR FUNCTION OF INTESTINES
Disturbances of motor function of guts is called
intestinal diskinesia.
There are two types of intestinal diskinesia:
hyperkinetic and hypokinetic.
The first type is characterised strengthening of the
peristalties, segmentary and pendulum-like
movements. It manifastates by diarrhea.
The second, on the contrary, is characterized
weakeing of motor activity of guts as a result
constipations appears.
THE REASONS OF INTESTINAL DISKINESIAS OF
HYPERKINETIC TYPE:
Increasing excitability of receptors of guts to adequate irritators,
that accompanies with development of an inflammation of an
intestine mucus membrane (enteritis, colics)
Action on receptors of guts unusual, pathological irritators undigested food (for example, achylia), products of rotting and
fermentation, toxic substances etc.
Increasing of excitability of the vagal nerve centres
Increase of some gastrointerstitial hormones form that
strengthening peristaltics of guts (motilin)
Consequences intestinal diskinesias of hyperkinetic type :
Disturbances of digestion (digestion, absorbtion)
Dehydratation
Development of ungas acidosis (loss of hydrocarbonates)
INTESTINAL DYSKINESIA OF
HYPERKINETIC TYPE
It is manifestated with reduction of guts peristaltics.
That results in appearance of constipations. In
mechanisms of development it pick out two kinds of
constipations: spastic and atonic.
Spastic constipations arise due to long time tonic reduction
of smooth muscles constriction of guts (spasm) and may
be caused by viscero-visceral reflexes, or action of toxic
factors (for example, lead poisoning).
Reason of development atonic constipations connected
with reduction of contractive function of smooth muscles
guts:
a poor feed, the low contents of cellulose in nutritient.
•excessive digestion of food into stomach (for
example, gastric hypersecretion)
•age changes of receptor system of guts in old
men, and also structural changes of an intestinal
wall in obesity
•decrease of tone vagal nerve
•disturbances intraintestinal innervation, for
example, Girshprungs disease - absence of
ganglion cells Auerbachs plexus in sigmoideum
and rectum
CONSEQUENCES OF THE INTESTINAL
DYSKINESIA
Intestinal dyskinesia of hypokinetic type lead to:
 development of intestinal autointoxication
 occurrence meteorism
 formation of feces stones
 in extreme cases intestinal obstruction may
develop