Pathophysiology of Pathophysiology of digestion. Violation of digestion. Violation of

digestion in a oral cavity, digestion in a oral cavity, stomach and intestinestomach and intestine

Plan of the lecturePlan of the lecture

1.1. Insufficiency of digestion. Etiology.Insufficiency of digestion. Etiology.

2.2. Syndromes of digestion Syndromes of digestion insufficiency.insufficiency.

3.3. Disorders of stomach.Disorders of stomach.

4.4. Ulcer disease of stomach.Ulcer disease of stomach.

5.5. Pathogenesis of pancreatitis.Pathogenesis of pancreatitis.

6.6. Bowel obstruction.Bowel obstruction.

7.7. Malabsorbtion. Malabsorbtion.

8.8. Maldygestion.Maldygestion.

Actuality of the lectureActuality of the lecture Number of patients, which suffer the different diseases of stomach of, which Number of patients, which suffer the different diseases of stomach of, which

are accompanied disorders of digestion, grows constantly, resulting in the are accompanied disorders of digestion, grows constantly, resulting in the decline of capacity, invalidity of people. These diseases often cases death. decline of capacity, invalidity of people. These diseases often cases death.

One of important and most early violations of functions of stomach there is One of important and most early violations of functions of stomach there is violation of gastric secretion, which can develop as a result of violation of the violation of gastric secretion, which can develop as a result of violation of the neuroendocrine regulation, and also at pathological processes in a stomach.neuroendocrine regulation, and also at pathological processes in a stomach.

The diseases of liver and bile excretory system take considerable specific The diseases of liver and bile excretory system take considerable specific weight in a general morbidity of the population, and last decade the further weight in a general morbidity of the population, and last decade the further growth of them was increased. growth of them was increased.

Technological revolution and associated with it the negative ecological shifts Technological revolution and associated with it the negative ecological shifts have resulted in useful increase of frequency and spread spectrum of diseases have resulted in useful increase of frequency and spread spectrum of diseases

of liver and cholic tractsof liver and cholic tracts. .

• Insufficiency of digestion is a pathological condition at which the digestive system does not provide assimilation of the nutrients that get inside the organism.

Etiology of digestion Etiology of digestion insufficiency:insufficiency: 1.  1.  Alimentary (food) factors:Alimentary (food) factors:

a) reception of bad and rough food; a) reception of bad and rough food; b) kidney live on dry rations; b) kidney live on dry rations; c) irregular reception of food; c) irregular reception of food; d) disbalanced meal (for example, reduction of the d) disbalanced meal (for example, reduction of the

maintenance of vitamins, proteins in a diet); maintenance of vitamins, proteins in a diet); e) overindulge in alcohol.e) overindulge in alcohol. 2. 2. Physical factorsPhysical factors.. Among factors of this group the greatest Among factors of this group the greatest

role belongs to radiation which effects epithelial cells of the role belongs to radiation which effects epithelial cells of the alimentary channel which have high mitotic activity.alimentary channel which have high mitotic activity.

3. 3. Chemical agentsChemical agents are the reason of digestion  disorders are the reason of digestion  disorders after poisonings with inorganic and organic substances during after poisonings with inorganic and organic substances during manufacture and in life.manufacture and in life.

4. 4. Biological factors:Biological factors: a) a) bacteriabacteria (for example, v.cholera, causative agents of (for example, v.cholera, causative agents of

dysentery, typhoid fever, paratyphus); dysentery, typhoid fever, paratyphus); b) b) bacterial bacterial toxins (for example, at salmonellosis,  toxins (for example, at salmonellosis, 

staphylococcal infection); staphylococcal infection); c) c) virusesviruses (for example, adenoviruses); (for example, adenoviruses); d) d) helminthshelminths..

Etiology of digestion Etiology of digestion insufficiency:insufficiency:

5.5. Organic effects:Organic effects: a) a) congenital congenital anomalies of digestive system; anomalies of digestive system; b) b) postoperativepostoperative conditions; conditions; c) c) tumourstumours of digestive system. of digestive system. 6. 6.  Disorders of nervous and humoral regulation.Disorders of nervous and humoral regulation.

Disorders of digestion can develop during: Disorders of digestion can develop during: a) a) psychoemotional disorderspsychoemotional disorders (neurotic and neurosis-like (neurotic and neurosis-like

conditions);          conditions);          b) b) mental diseasesmental diseases (schizophrenia, a manic - depressive (schizophrenia, a manic - depressive

syndrome); syndrome); c) c) organic diseasesorganic diseases of the central nervous system of the central nervous system

(encephalites); (encephalites); d) d) lesions of peripheral structureslesions of peripheral structures of vegetative nervous of vegetative nervous

system; system; e) e) reflex disordersreflex disorders (various viscero-visceral reflexes). (various viscero-visceral reflexes). Disorders of humoral regulation of digestion may be connected to Disorders of humoral regulation of digestion may be connected to

disorders of synthesis and secretion of gastrointestinal disorders of synthesis and secretion of gastrointestinal hormones (gastrine, secretin, cholecystokinin-pancreazymin hormones (gastrine, secretin, cholecystokinin-pancreazymin etc.).etc.).

Syndromes of Syndromes of digestion digestion

InsufficiencyInsufficiency            • 1) starvation;  • 2) dispeptic syndrome; • 3) dehydratation; • 4) disturbance of the acid-basic balance; • 5) intestinal autointoxication; • 6) the painful syndrome.

Dispeptic syndromeDispeptic syndrome includes different includes different combinations of the combinations of the following symptoms: following symptoms:

a) anorexia, a) anorexia, b) heartburn, b) heartburn, c) eructation, c) eructation, d) nausea, d) nausea, e) vomitting,                  e) vomitting,                   f) meteorism, f) meteorism, g) constipations,g) constipations, h) diarrhea.h) diarrhea.

AnorexiaAnorexia is a full absence of appetite is a full absence of appetite combined with an objective need of combined with an objective need of

foodfoodThere are following kinds of anorexia:There are following kinds of anorexia: аа) ) intoxicalintoxical – develops during acute and chronic poisonings (for example, salts of – develops during acute and chronic poisonings (for example, salts of

mercury, medical products, bacterial toxins); mercury, medical products, bacterial toxins); b) b) dispepticdispeptic –arises at diseases of digestive system, has more often behavior-reflex –arises at diseases of digestive system, has more often behavior-reflex

nature; nature; c) c) neurodynamicneurodynamic –  develops as a result of reciprocal inhibition of the appetite –  develops as a result of reciprocal inhibition of the appetite

centre after overexcitation of separate structures of limbic systems (for example, a centre after overexcitation of separate structures of limbic systems (for example, a painful syndrome during  heart attacks, colics, peritonitis); painful syndrome during  heart attacks, colics, peritonitis);

d) d) neuroticneurotic –  it is connected with excessive excitation of cortex  brain and strong –  it is connected with excessive excitation of cortex  brain and strong emotions (especialy  negative); emotions (especialy  negative);

e) e) psychogenicpsychogenic – is connected with conscious restriction of food (for example, with – is connected with conscious restriction of food (for example, with an aim of getting thin or as result of mental disorders);  an aim of getting thin or as result of mental disorders); 

f) f) neuroendocrinopathyneuroendocrinopathy –  is caused by organic lesions of the central nervous –  is caused by organic lesions of the central nervous system (hypothalamus) and endocrine diseases (hypophysial cachexia, Addison’s system (hypothalamus) and endocrine diseases (hypophysial cachexia, Addison’s disease).disease).

In the basis of development of anorexia two mechanisms may take place: In the basis of development of anorexia two mechanisms may take place:                                         1) 1) reduction of excitability of the food centrereduction of excitability of the food centre (intoxical, dispeptic, (intoxical, dispeptic,

neuroendocrinopathy anorexia); neuroendocrinopathy anorexia); 2) 2) inhibition of food centre neuronsinhibition of food centre neurons  (neurodynamic, neurotic, psychogenic   (neurodynamic, neurotic, psychogenic

anorexia). anorexia).

► The heartburnThe heartburn is a feeling of heat or burnings is a feeling of heat or burnings along the esophagus. Its development is connected along the esophagus. Its development is connected with irritation of receptors of the esophagus during with irritation of receptors of the esophagus during pelting contents of stomach into an esophagus pelting contents of stomach into an esophagus gullet (reflux). gullet (reflux).

It may be caused by: It may be caused by: аа) a large quantity of formed gastric juice; ) a large quantity of formed gastric juice; b) functional insufficiency of cardial sphincter.b) functional insufficiency of cardial sphincter.► MeteorismMeteorism is  surplus accumulation of gases in the is  surplus accumulation of gases in the

digestive channel due to their increased formation digestive channel due to their increased formation or insufficient removing from intestines. or insufficient removing from intestines.

► DiarrheaDiarrhea is a frequent emptying of intestines with is a frequent emptying of intestines with discharging of diluted and plentiful excrements.discharging of diluted and plentiful excrements.

The eructationThe eructation is a sudden involuntary allocation into oral cavity of is a sudden involuntary allocation into oral cavity of gas from a stomach esophagus, sometimes with small portions of  gas from a stomach esophagus, sometimes with small portions of  stomach contents.stomach contents.

The nauseaThe nausea is a burdensome sensation in epigastric area, chest and is a burdensome sensation in epigastric area, chest and in oral cavity, quite often previous to vomitting and frequently is in oral cavity, quite often previous to vomitting and frequently is accompanied general weakness, sweatness, increasing of salivation, accompanied general weakness, sweatness, increasing of salivation, coldness of arms and legs, pallor of skin, decrease of arterial coldness of arms and legs, pallor of skin, decrease of arterial pressure that is connected to activation parasympathetic nervous pressure that is connected to activation parasympathetic nervous system. In the basis of  nausea stays excitation of the emetic centre, system. In the basis of  nausea stays excitation of the emetic centre, which is insufficient for occurrence of vomitting.which is insufficient for occurrence of vomitting.

VomittingVomitting is the is the complex-reflex act complex-reflex act which results to which results to eruption of stomach eruption of stomach contents outside contents outside through the mouth. through the mouth. It is a result of the It is a result of the emetic centre emetic centre excitation which is excitation which is situated in medulla situated in medulla oblongata.oblongata.

Constipations are slowing down, difficulted or regularly insufficient emptying of intestines.• There are two mechanisms of development of constipations - spastic

and atonic. The first is caused by long constant contraction of smooth muscles of intestines, the second – because of their atonia.

Spastic constipations are: • а) inflammatory - arise owing to local spastic reflexes with changed 

mucous membrane; • b) proctogenic - develop in case of anorectal area pathology; • c) mechanical – arise in case of impassability of guts; • d) toxic – is a result of poisonings by lead, mercury, thallium.Atonic constipations are: • а) alimentary – develop with consuming of light food containing (little

quantity of) cellulose; • b) neurogenic – is result of disorders of nervous regulation of intestinal

motility; • c) hypodynamic – arise in bed-patients, old men, people with very low

motor activity; • d) constipations in case of anomalies of thick gut (Girshprungs

disease); • e) constipations as a consequensce of water-electrolyte metabolism

disorders.

The pain frequently accompanies development of the alimentary channel diseases.

There are following mechanisms of pain occurrence at lesions of digestive organs:

• а) the spastic mechanism. The pain is caused by a spasm of smooth muscles of different parts of the alimentary tract. It is considered, that in this case the reason of pain is constriction of the vessels which are laying in the wall of hollow organs owing to what the ischemia develops. It causes appearance of metabolic products from the working organs, and their influence on pain receptors. At sharply arising strong spasm colic pain develops;

• b) the hypotonic mechanism. At reduction of smooth muscles tone (hypotonia) the pain appears from stretching of the wall of hollow organs (stomach, guts, gall bladder) by their contents. Thus the mechanical stretching of tissues causes irritation of the nervous endings;

• c) influence of biological active substances (histamine, serotonin, kinines, prostaglandins) on the nervous endings.

Disturbance of stomach functionsDisturbance of stomach functionsDisturbance of  hydrochloric acidDisturbance of  hydrochloric acidHydrochloric acidHydrochloric acid is excreted by is excreted by parietal cellsparietal cells of mucous membrane of of mucous membrane of stomach which number in a healthy person is about 1 billion. stomach which number in a healthy person is about 1 billion. SecretionSecretion of it is regulated by complicated mechanisms which include of it is regulated by complicated mechanisms which include three interconnected three interconnected phases of secretionphases of secretion: : neurogenicneurogenic (vagal), (vagal), gastricgastric (gastrine) and (gastrine) and intestinalintestinal which is regulated by irritation of receptors and which is regulated by irritation of receptors and intestinal hormones.intestinal hormones.In regulation of functional activity of In regulation of functional activity of parietal cellsparietal cells nervous system (through nervous system (through mediator acethylcholine), and also various hormones (serotonin, insulin) mediator acethylcholine), and also various hormones (serotonin, insulin) take place. take place. The parietal cell contains receptors to histamine which is released from The parietal cell contains receptors to histamine which is released from enterochromaphilic cells (ECL), gastrin and cholecystokinin (CCK-enterochromaphilic cells (ECL), gastrin and cholecystokinin (CCK-receptors), and also receptors for acethylcholine (M3-receptors). receptors), and also receptors for acethylcholine (M3-receptors). Stimulation of H2-histamine receptorsStimulation of H2-histamine receptors promotes formation of cAMP and promotes formation of cAMP and stimulation of CCK-receptors and M3-receptors results to stimulation of CCK-receptors and M3-receptors results to increasing of increasing of endocellular calciumendocellular calcium ( (СаСа++) level. ++) level. Besides the Besides the stimulation of M3-receptors increasesstimulation of M3-receptors increases, in comming of , in comming of СаСа++ ++ into a cell and due to increasing of inositolthreephosphate (IP3) into a cell and due to increasing of inositolthreephosphate (IP3) level strengthens an output of endocellular level strengthens an output of endocellular СаСа++. ++. GastrinGastrin, , cholecystokinincholecystokinin and and histaminehistamine also raise output of also raise output of СаСа++ due to ++ due to action on IP3. action on IP3. Parietal cellParietal cell has a receptor for prostaglandin E2 (PGE2) stimulation which has a receptor for prostaglandin E2 (PGE2) stimulation which reduces  level of cAMP and results to inhibition of hydrochloric acid reduces  level of cAMP and results to inhibition of hydrochloric acid secretion.secretion.

• Secretion of  hydrochloric acid by parietal cell is carried out by a principle of the proton pump in which K+ exchanges on H+, and Cl‾ on HCO3‾. An important role in this process is played by H+, K+ -ATPase which, using energy of ATP, provides transport of H+ from parietal cells and K+ into the cell. The difficult mechanism of regulation of hydrochloric acid production  explains increasing or decreasing of its secretion under the influenece of numerous factors.

• Hypersecretion of  hydrochloric acid which plays an important role in development of several gastroenterologic disease may be observed in hereditary caused increasing of parietal cells weight the increased tone of a vagal nerve stretching of antral part of stomach during disorder of emptying, increasing of gastrin secretion, increasing of ECL-cells quantity in the mucous membrane of stomach (in patients with carcinoid syndrome).

• Besides  hydrochloric acid main cells of  mucous membrane of stomach produce pepsin from pepsinogen. Now there are seven types of pepsinogen distinguished. Disturbance of pepsin formation function of a stomach matters in appearance of number of gastroenterologic diseases (for example, stomach ulcer).

In the basis of indigestion the following disturbances of functions of digestive system

may take place:1. Disturbance of secretion in digestive system: A. Hypersecretion conditions: 1) hypersalivation, 2) gastric hypersecretion,                 3) pancreatic hypersecretion, 4) hypercholia;

B. Hyposecretion conditions: 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 dyskinesias,                      4) intestinal dyskinesias, 5) dyskinesia of gall bladder and biliary ducts,                       6) disturbances of defecation.

3. Disturbance of absorbtive functions -  syndrome of malabsorption.

Disturbance of mucus secretion

• Gastric mucus is secreted by mucous cells of stomach  mucous membrane. The content of gastric musous is formed by glycosaminoglycans and glycoproteins. From sialic acids N-acethylneuraminic acid provides ability of gastric mucus to form  water-insoluble viscose coverings of stomach mucous membrane.

• Secretion of gastric mucus takes place continuously. Irritation adreno- and cholinoreceptors, prostaglandins render stimulating influence on formation of mucus.

• In process of mucus formation the certain role is played by stability of lysosomes. Hydrolases of lysosomes cause dehydratation of glycoproteins.

• Gastric mucus (together with bicarbonates) takes part in formation of a mucus barrier which supports рН gradient between hollow of stomach and its mucous membrane and late H+.

•  Disturbance of this barrier as a result of reduction of prostaglandins synthesis in the stomach wall is one of mechanisms of mucous membrane damage under the action of some medical products (aspirin, not steroid anti-inflammatory drugs). On the contrary, synthetic prostaglandins have cell protective properties, raise mucus formation and prevent damage of stomach.

According to quantity of gastric juice and its According to quantity of gastric juice and its

quality there are gastric hyper- and hyposecretionquality there are gastric hyper- and hyposecretion Gastric hypersecretion is characteristed by: Gastric hypersecretion is characteristed by: 1) increase of the quantity of gastric juice as after reception of food, and also 1) increase of the quantity of gastric juice as after reception of food, and also

on the empty stomach; on the empty stomach; 2) hyperaciditas and hyperchlorhydria 2) hyperaciditas and hyperchlorhydria –– increase of the common acidity increase of the common acidity

and maintenance of the free hydrochloric acid in gastric juice; and maintenance of the free hydrochloric acid in gastric juice; 3) increase of digestive ability of gastric juice.3) increase of digestive ability of gastric juice.The The disturbances of digestiondisturbances of digestion connected with connected with gastric hypersecretiongastric hypersecretion, are caused , are caused

by a long delay of food in the stomach (pylorus is closed, because of by a long delay of food in the stomach (pylorus is closed, because of neutralization of very sour contents that go into duodenum, demands a neutralization of very sour contents that go into duodenum, demands a lot time). lot time).

This circumstance has such consequences: This circumstance has such consequences: 1) 1) small quantity of contentssmall quantity of contents go into intestine, that results in go into intestine, that results in reduction of reduction of

guts peristalticsguts peristaltics and to development of and to development of constipationsconstipations; ; 2) in the stomach processes of 2) in the stomach processes of fermentation and formation gases increasefermentation and formation gases increase. It . It

causes appearance of an causes appearance of an eructation and a heartburneructation and a heartburn; ; 3) 3) motor activity of stomach is increasedmotor activity of stomach is increased, what leads to , what leads to hypertonushypertonus and and

hyperkinesishyperkinesis of smooth muscles. of smooth muscles.Formation of active gastric juice plenty is the important factor promoting Formation of active gastric juice plenty is the important factor promoting

formation of ulcers in stomach and duodenum.formation of ulcers in stomach and duodenum.

Gastric hyposecretion is characterised by: Gastric hyposecretion is characterised by: • 1) reduction of quantity of gastric juice on an empty stomach and

after reception of food; • 2) decreased or zero acidity of gastric juice (hypo- or unacidity),

reduction of the contents in it or absence of free hydrochloric acid (hypo- or achlorhydria);

• 3) reduction of digesting ability of gastric juice due to achylia (the full stop formation of hydrochloric acid and enzymes).

• Reduction of gastric secretion results to disturbances of digestion along alimentary tract. It is caused by insufficient formation of gastric juice that keeps pylorus opened also contents of stomach quickly pass into duodenum where environment becomes constantly alkaline. Thus there is inhibition of secretine formation that results decreased of pancreatic juice secretion and processes of hollow digestion in guts are broken.

• Insufficiently digested components of food irritate receptors of  mucous membrane of guts that result in strengthening of peristaltics and diarrheas. Besides due to the absence of  hydrochloric acid growth of microflora in the stomach increases. Activation of processes of rotting and fermentation in the stomach and appearance of such disturbance of digestion, as eructation, the impose tongue etc. are also connected with.

Disturbance of stomach motor function Disturbance of stomach motor function is called gastric diskinesia. There are two

kinds of gastric diskinesia: hypertonic and hypotonic.• Hypertonic kind is characterised by strengthening of peristaltics (hyperkinesia)

and increasing of stomach muscles tone (hypertonia). • The hypotonic kind, on the contrary, is characterized by hypotonia and

hypokinesia.The reasons of motor gastric disturbance of hypertonic type may be: а) some food factors (rough food, alcohol); b) increase of gastric secretion; c) increase of a tone of vagal nerve; d) some gastrointestinal hormones (motilin).Hypertension and hyperkinesia of stomach leads: 1) to a long delay of food in stomach that promotes increase of gastric secretion and

development of ulcers on  mucous membrane; 2) to development of antiperistaltics of stomach that results in development of

dispeptic disturbances (eructation, nausea, vomitting).• One of the forms of stomach diskinesia of 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 stomach pyloric part. It is observed mainly at the excitable children who have suffered intra-uterine hypoxia, born in asphyxia with attributes of  birth trauma of the central nervous system.

• Pylorospasm is marked by weak development of muscles in cardial part of stomach and its more expressed development in the area of pylorus. It promotes development of vomitting and eructation.

Reduction of motor activity of  stomach may be caused by:

Reduction of motor activity of  stomach may be caused by:

а) alimentary factors (fat food); b) reduction of gastric secretion (hypoacid

gastritis); c) reduction of vagal nerve tone; d) action inhibiting  motility of stomach

through gastrointerstitial hormones (gastroinhibiting peptide, secretine etc.);

e) removal of pyloric part of stomach; f) the common weakening of organism, an

exhaustion, gastroptosis.• At hypotonic diskinesias time of food

staying in the stomach is shortened that conducts to disturbance of its digestion. Action of the undigested components of food on receptors of  guts mucous membrane causes the increase of peristaltics and diarrhea.

STOMACHSTOMACH

CONGENITAL ABNORMALITIESCONGENITAL ABNORMALITIES

• Pyloric stenosisa) males 3:1 vs. femalesb) may occur with Turner

syndrome, trisomy 18, esophageal atresiac) clinical:

1) narrowing of pyloris- hypertrophy and possibly hyperplasia (muscularis)

2) regurgitation (projectile !!)- dehydration of concern

3) oval (“olive”) palpable mass4) surgical splitting is curative

Pathophysiology of gastritis

In gastritis, the gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes superficial erosion. It secretes a

scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage.

ACUTE GASTRITISACUTE GASTRITIS• Gastritis (inflammation of gastric mucosa)

• Transient inflammation (usually)a) bleeding and erosion

) sloughing of mucosa

• Pathogenesis not clear: associationsa) NSAID (e.g., aspirin)b) alcoholc) smokingd) stress (trauma, burns, surgery)e) uremia, infections

• Several factors involved: (1 or more)a) acid secretion with back diffusionb) HCO3

- bufferc) blood flowd) disruption of mucus layere) damage to epitheliumf) lots of patients have idiopathic acute gastritis without any of the

listed disorders !!g) neutrophils above basement membrane active inflammation

GastritisGastritis Chronic gastritis and prolonged inflammation

of the stomach may be caused by either benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori.

Chronic gastritis is sometimes associated with autoimmune diseases such as pernicious anemia; dietary factors such as caffeine; the use of medications, especially NSAIDs; alcohol; smoking; or reflux of intestinal contents into the stomach.

Special forms of GastritisSpecial forms of Gastritis Infectious (Phlegmonous or necrotizing gastritis)Infectious (Phlegmonous or necrotizing gastritis)

Emergency gastric resection, and Abx therapyEmergency gastric resection, and Abx therapy CMV, candidal (fungal) in immunocompromised pt’sCMV, candidal (fungal) in immunocompromised pt’s Larvae ingestion requires endoscopic removalLarvae ingestion requires endoscopic removal

Eosinophilic GastritisEosinophilic Gastritis Giant Cell (Menetrier’s disease) (Hypertrophic Giant Cell (Menetrier’s disease) (Hypertrophic

Gastropathy) Gastropathy) only found on biopsyonly found on biopsy

Lymphocytic GastritisLymphocytic Gastritis Granulomatous GastritisGranulomatous Gastritis

TuberculosisTuberculosis SyphilisSyphilis FungalFungal SarcoidSarcoid Crohn’sCrohn’s

Gastritis SymptomsGastritis SymptomsClinical features of gastritis generally reflects the Clinical features of gastritis generally reflects the underlying syndrome rather than the gastric injury itselfunderlying syndrome rather than the gastric injury itselfAcute:Acute:– Dyspepsia and abdominal pain are common indicators of Dyspepsia and abdominal pain are common indicators of

gastritisgastritis– Mild epigastric discomfortMild epigastric discomfort– Occasional N/VOccasional N/V– Headache, excessive salivation, flatusHeadache, excessive salivation, flatus

Chronic:Chronic:– Non specific symptoms c/ chronic abdominal discomfortNon specific symptoms c/ chronic abdominal discomfort

Key signs: (usually none)Key signs: (usually none)– Hematemesis, bloody nasogastric aspirateHematemesis, bloody nasogastric aspirate– Abdominal tendernessAbdominal tenderness– BloatingBloating– EmesisEmesis

SYMPTOMS

Burning painBurning pain bloating bloating

NauseaNausea water brashwater brash

Unexplained weight lossUnexplained weight loss hematemesis (vomiting of blood)hematemesis (vomiting of blood)

Appetite changes  Appetite changes   MelenaMelena

vomitingvomiting Blood in the stoolsBlood in the stools

low blood cell count (anemia)low blood cell count (anemia) Stomach pain wakes you up at nightStomach pain wakes you up at night

frequent burping or hiccuppingfrequent burping or hiccupping An early sense of fullness with eatingAn early sense of fullness with eating

The reasons and pathophysiologic

mechanisms of stomach ulcer 1. Psychoemotional negative overstrains (negative emotions, disputed situations, feeling

of constant alarm, strain etc.) 2. Stress.3. Hereditary predisposition. Value of this factor proves to be true concerning high (40-50

%) frequency of disease in parents and relatives of the patients, especially of the young age. It is established, that patients with the burdened heredity mucous membrane of stomach have 1.5-2 times bigger of parietal cells than in healthy person. Characters of genetic predisposition are also 0(1) group of blood, deficiency of α1-antitripsin and fucoglycoproteins.

4. Errors in nutrition meal lice dry ration, irregular consumption of food, eating of rough or spicy (hot) food, bad chewing, fast meal, absence of the teeth, the insufficient maintenance (contents) in food of proteins and vitamins.

5. Chronic gastritis and duodenitis with increased secretion of glands of mucus membrane.6. Microbic factor – Helicobacter pylori.7. Harmful habits – smoking, overindulge of alcohol • According to modern representations, pathogenesis of stomach ulcer in general is

reduced to disturbance of balance between factors of acid-peptic aggressions of gastric contents and elements of protection of stomach mucous membrane and duodenum. Sufficient formation of bicarbonates, good regeneration of epithelial cells, constant blood supply of mucous membrane, normal formation and maintenance of prostaglandins in wall of stomach, sufficient gastric formation of mucus are factors that protect mucous membrane.

• During last years an important role in weakening of protective properties of stomach mucus membrane and duodenum is given to microorganisms Helicobacter pylori.

Pathogenesis of Ulcers

Aggressive Factors Acid, pepsin Bile salts Drugs (NSAIDs) H. pylori

Defensive Factors Mucus, bicarbonate layer Blood flow, cell renewal Prostaglandins Phospholipid Free radical scavengers (Antyoxidants!)

Therapy is directed at enhancing host defense or eliminating aggressive factors; i.e., H. pylori.

Gastric UlcerGastric Ulcer

Duodenal Peptic UlcerDuodenal Peptic Ulcer

Peptic Ulcer DiseasePeptic Ulcer Disease

ADVERSE EFFECTS OF SMOKINGADVERSE EFFECTS OF SMOKING 1. Interferes c/ action of H2 antagonists1. Interferes c/ action of H2 antagonists 2. Increases rate of gastric emptying2. Increases rate of gastric emptying 3. Increases duodenogastric reflux3. Increases duodenogastric reflux 4. Decreases pancreatic bicarb secretion4. Decreases pancreatic bicarb secretion 5. Decreases mucosal blood flow5. Decreases mucosal blood flow 6. Depresses gastric mucosal 6. Depresses gastric mucosal

prostaglandin synthesisprostaglandin synthesis

Helicobacter pyloriHelicobacter pylori   These bacterias produce a These bacterias produce a lot enzymeslot enzymes ( (urease, protease, phospholipaseurease, protease, phospholipase), ),

damaging protective barrier of mucous membrane, and also various damaging protective barrier of mucous membrane, and also various cytotoxins. The most pathogenic are cytotoxins. The most pathogenic are Vac A-strainVac A-strain, that produce vacuolizating , that produce vacuolizating cytotoxin which results in formation of cytoplasmatic vacuoles and destructions cytotoxin which results in formation of cytoplasmatic vacuoles and destructions of epithelial cells, and the Cag A-strain which of epithelial cells, and the Cag A-strain which expresses gene associated expresses gene associated with cytotoxinwith cytotoxin. This gene codes protein which has direct damaging effect . This gene codes protein which has direct damaging effect on mucous membrane. Helicobacter pylori promotes liberation in mucous on mucous membrane. Helicobacter pylori promotes liberation in mucous membrane of stomach interleukines, lysosomal enzymes, TNFmembrane of stomach interleukines, lysosomal enzymes, TNFαα, that causes , that causes development of inflammatory processes in the mucous membrane of stomach. development of inflammatory processes in the mucous membrane of stomach. Pathophysiologic mechanismsPathophysiologic mechanisms of duodenum ulcer development in 95 % of of duodenum ulcer development in 95 % of cases is associated with cases is associated with HelicobacterHelicobacter. .

Contaminating the mucous membrane of the stomach by Helicobacter is Contaminating the mucous membrane of the stomach by Helicobacter is accompanied by development of superficial anthral gastritis and duodenitis accompanied by development of superficial anthral gastritis and duodenitis and and leads to increase of gastrin levelleads to increase of gastrin level with the subsequent increase with the subsequent increase of of hydrochloric acid secretionhydrochloric acid secretion. The plenty quantity of hydrochloric acid getting . The plenty quantity of hydrochloric acid getting into a lumen of duodenum in conditions of into a lumen of duodenum in conditions of deficiency of pancreatic deficiency of pancreatic bicarbonatesbicarbonates promotes development of duodenitis and besides causes promotes development of duodenitis and besides causes appearance of gastric sites metaplasia in duodenumappearance of gastric sites metaplasia in duodenum (reorganization of (reorganization of epithelium of duodenal mucous membrane on gastric type) which are quickly epithelium of duodenal mucous membrane on gastric type) which are quickly contaminated by Helicobacter. contaminated by Helicobacter.

Further in case of unfavourable course especially when there are additional Further in case of unfavourable course especially when there are additional ethiology factors (hereditary predisposition, ethiology factors (hereditary predisposition, 0 (1) group of blood0 (1) group of blood, smoking, , smoking, psychological overstrain etc.). In sites of metaplased mucous membrane ulcer psychological overstrain etc.). In sites of metaplased mucous membrane ulcer defect is formed. However connection of stomach ulcer occurrence with defect is formed. However connection of stomach ulcer occurrence with infection of stomach mucus membrane by Helicobacter is not always revealed. infection of stomach mucus membrane by Helicobacter is not always revealed. Approximately in Approximately in 5 % of patients with ulcers of duodenum5 % of patients with ulcers of duodenum and in  and in 15-20 % of 15-20 % of patients with stomach ulcerspatients with stomach ulcers, disease , disease develops without participation of these develops without participation of these microorganismsmicroorganisms..

To To gastroduodenal ulcersgastroduodenal ulcers which have been not associated with Helicobacter which have been not associated with Helicobacter belong, to erosion-ulcer defects and are caused by using of aspirin and other belong, to erosion-ulcer defects and are caused by using of aspirin and other non steroid anti-inflammatory drugs, stress ulcers etc.non steroid anti-inflammatory drugs, stress ulcers etc.

Tests For Initial Diagnosis

of Infection Urea Breath TestUrea Breath Test and

Stool AssayStool Assay Non-invasive, sensitive

and specific SerologySerology

O.K. for initial diagnosis

Fair sensitivity and specificity

Endoscopy Not necessaryEndoscopy Not necessary for diagnosis

How is How is H. pyloriH. pylori infection diagnosed? infection diagnosed? Several methods may be used to diagnose Several methods may be used to diagnose H. pylori H. pylori infection.infection. Serological testsSerological tests that measure specific that measure specific H. pylori H. pylori IgG IgG antibodies can determine if a person has been infected. antibodies can determine if a person has been infected. – The sensitivity and specificity of these assays around 80% The sensitivity and specificity of these assays around 80%

Fecal Antigen AssayFecal Antigen AssayUrea Breath testUrea Breath test – In this test, the patient is given either 13C- or 14C-labeled urea to In this test, the patient is given either 13C- or 14C-labeled urea to

drink. drink. – H. pylori H. pylori metabolizes the urea rapidly, and the labeled carbon is metabolizes the urea rapidly, and the labeled carbon is

absorbed. absorbed. – This labeled carbon can then be measured as CO2 in the patient's This labeled carbon can then be measured as CO2 in the patient's

expired breath to determine whether expired breath to determine whether H. pylori H. pylori is present. is present. – The sensitivity and specificity of the breath test ranges from 94% The sensitivity and specificity of the breath test ranges from 94%

to 98%. to 98%. – PPI’s can give false negative resultsPPI’s can give false negative results

Tests for Detection of Tests for Detection of H. pyloriH. pylori

TestTestSensitivity/Sensitivity/Specificity, Specificity,

%%CommentsComments

Invasive (Endoscopy/Biopsy Required)Invasive (Endoscopy/Biopsy Required)  

Rapid ureaseRapid urease 80–95/95–80–95/95–100100

Simple, false negative with recent use of Simple, false negative with recent use of PPIs, antibiotics, or bismuth compoundsPPIs, antibiotics, or bismuth compounds

HistologyHistology 80–90/>9580–90/>95 provides histologic informationprovides histologic information

CultureCulture ——/—/— Time-consuming, expensive ; antibiotic Time-consuming, expensive ; antibiotic susceptibilitysusceptibility

Non-invasiveNon-invasive  

SerologySerology >80/>90>80/>90 Inexpensive, convenient; not useful for Inexpensive, convenient; not useful for early follow-upearly follow-up

Urea breath Urea breath testtest

>90/>90>90/>90 Simple, rapid; useful for early follow-up; Simple, rapid; useful for early follow-up; false negatives with recent therapy ; false negatives with recent therapy ; exposure to low-dose radiation with exposure to low-dose radiation with 1414C C test test 

Stool antigenStool antigen >90/>90>90/>90 Inexpensive, convenient; not established Inexpensive, convenient; not established for eradication but promisingfor eradication but promising

Gastric and Duodenal Ulcers

A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus (opening between stomach and duodenum), in the duodenum (first part of small intestine), or in the esophagus.

A peptic ulcer is frequently referred to as a gastric, duodenal, or esophageal ulcer, depending on its location, or as peptic ulcer disease.

Perforation:Perforation:

PEPTIC ULCER DISEASEPEPTIC ULCER DISEASE

• chronic, most often solitary lesionsa) duodenum (initial portion) 4:1b) stomach (antrum)c) gastroesophageal junction

i) Barrett esophagusd) duodenum, stomach and/or jejunum

i) Zollinger-Ellison syndrome• in USA, ~ 4 million; 3:1 male:female• middle age to older adults

Zollinger-Ellison Syndrome

• Ulcers-associated with the Zollinger-Ellison (ZE) Syndrome are caused by gastrin-releasing islet cell tumors (gastrinomas), & are also considered a form of peptic ulcer.

Zollinger-Ellison SyndromeZollinger-Ellison Syndrome A tumor of the pancreas that secretes A tumor of the pancreas that secretes

gastrin (gastrin (Gastrinoma)Gastrinoma)

Usually found in head of pancreas but can Usually found in head of pancreas but can also be found in duodenum, liver & lungalso be found in duodenum, liver & lung

75-80% of ulcers produced develop in the 75-80% of ulcers produced develop in the duodenal bulbduodenal bulb

Suspect in any patient with:Suspect in any patient with:– Multiple or recurring duodenal ulcersMultiple or recurring duodenal ulcers– Post bulbar or jejunal ulcersPost bulbar or jejunal ulcers– Ulcers associated with diarrheaUlcers associated with diarrhea– Elevated serum gastrin levelsElevated serum gastrin levels

Usually only tested when suspect ZE syndromeUsually only tested when suspect ZE syndrome

Clinical Manifestations of UlcerClinical Manifestations of Ulcer

Gastric:Gastric: Burning or gassy sensation Burning or gassy sensation

in high epigastric area in high epigastric area Occurs within ½ hr. after Occurs within ½ hr. after

eating, food can worsen eating, food can worsen symptomssymptoms

Rarely occurs at nightRarely occurs at night Vomiting may ease Vomiting may ease

discomfortdiscomfort May lose weightMay lose weight Pyrosis Pyrosis

Duodenal:Duodenal: More cramplike discomfortMore cramplike discomfort Occurs on empty stomach, Occurs on empty stomach,

food relieves symptomsfood relieves symptoms Often occurs at nightOften occurs at night Vomiting uncommonVomiting uncommon May gain weightMay gain weight PyrosisPyrosis

Gastric ulcer

Duodenal ulcer

Disturbance of intestinal functions

• Functions of intestines may be broken Functions of intestines may be broken owing to many organic diseases. In owing to many organic diseases. In some cases these disturbances arise some cases these disturbances arise owing to disorders of nervous owing to disorders of nervous regulation of small and large intestine regulation of small and large intestine motility.motility.

Disturbance of digestion and absorbtion in intestines

• The complex of disturbances which appear in an organism as a result of disturbance of digestion processes and absorbtion, has received the name of syndrome of maldigestion and malabsorbtion.

Syndrome of MalabsorbtionSyndrome of Malabsorbtion The syndrome of malabsorbtion is a complex of The syndrome of malabsorbtion is a complex of

symptoms whichsymptoms which appearsappears result ofresult of absorbtion absorbtion disturbancedisturbance of substances in guts. Disturbance of of substances in guts. Disturbance of absorbtion in guts may be caused by disturbances absorbtion in guts may be caused by disturbances that appear on three levels:that appear on three levels:

1) 1) preenterocyticpreenterocytic disturbance. Develop as a result disturbance. Develop as a result of disturbances of digestion processes before of disturbances of digestion processes before absorbtion;absorbtion;

2) 2) enterocyticenterocytic from disturbance of intestinal from disturbance of intestinal mucous membrane epithelial cells activity; mucous membrane epithelial cells activity;

3) 3) postenterocyticpostenterocytic disturbance. There are disturbance. There are consequences of the processes disturbance that consequences of the processes disturbance that provide reception of absorbed substances into provide reception of absorbed substances into internal environment of an organism (blood, lymph).internal environment of an organism (blood, lymph).

Preenterocytic disturbances:Preenterocytic disturbances: Preenterocytic disturbances:Preenterocytic disturbances: ► 1. Disturbances of motor function of the alimentary 1. Disturbances of motor function of the alimentary

channel. channel. ► 2. Disturbances of primary digestion (a syndrome of 2. Disturbances of primary digestion (a syndrome of

maldigestion). By origin they may be gastrogenic, maldigestion). By origin they may be gastrogenic, pancreatogenic, hepatogenic, enterogenic, pancreatogenic, hepatogenic, enterogenic, disregulated, iatrogenic (connected with long usage disregulated, iatrogenic (connected with long usage of antibiotics and other medical products). of antibiotics and other medical products).

► 3. Disturbance of membrane digestion. More often 3. Disturbance of membrane digestion. More often they are caused by disturbances of formation and they are caused by disturbances of formation and embedding of enzymes into plasmatic membrane of embedding of enzymes into plasmatic membrane of enterocytic microvillis.enterocytic microvillis.

► Interstitial pathology of enzymes are hereditary Interstitial pathology of enzymes are hereditary caused disturbances of digestive enzymes synthesis  caused disturbances of digestive enzymes synthesis  by microvillis which provide processes of membrane by microvillis which provide processes of membrane digestion. Among the interstitial pathologies of digestion. Among the interstitial pathologies of enzymes intolerance to disaccharides (lactoses, enzymes intolerance to disaccharides (lactoses, saccharoses, tregaloses) and insufficiency of saccharoses, tregaloses) and insufficiency of peptidase (gluten enteropathy, celiac disease) occur peptidase (gluten enteropathy, celiac disease) occur the most often.the most often.

► 1. Disturbances of motor function of the alimentary 1. Disturbances of motor function of the alimentary channel. channel.

► 2. Disturbances of primary digestion (a syndrome of 2. Disturbances of primary digestion (a syndrome of maldigestion). By origin they may be gastrogenic, maldigestion). By origin they may be gastrogenic, pancreatogenic, hepatogenic, enterogenic, pancreatogenic, hepatogenic, enterogenic, disregulated, iatrogenic (connected with long usage disregulated, iatrogenic (connected with long usage of antibiotics and other medical products). of antibiotics and other medical products).

► 3. Disturbance of membrane digestion. More often 3. Disturbance of membrane digestion. More often they are caused by disturbances of formation and they are caused by disturbances of formation and embedding of enzymes into plasmatic membrane of embedding of enzymes into plasmatic membrane of enterocytic microvillis.enterocytic microvillis.

► Interstitial pathology of enzymes are hereditary Interstitial pathology of enzymes are hereditary caused disturbances of digestive enzymes synthesis  caused disturbances of digestive enzymes synthesis  by microvillis which provide processes of membrane by microvillis which provide processes of membrane digestion. Among the interstitial pathologies of digestion. Among the interstitial pathologies of enzymes intolerance to disaccharides (lactoses, enzymes intolerance to disaccharides (lactoses, saccharoses, tregaloses) and insufficiency of saccharoses, tregaloses) and insufficiency of peptidase (gluten enteropathy, celiac disease) occur peptidase (gluten enteropathy, celiac disease) occur the most often.the most often.

The reasons of malabsorbtion may be such enterocytic disturbances:           1) reduction of absorbtion area (a condition after resection

of a gut, an atrophy of villi and microvillis); 2) hereditary caused and acquired disturbances of

formation of proteins – carriers monosaccharides (intolerance to glucose, galactose, fructose), amino acids (tryptophanmalabsoption), ions of calcium (hypovitaminosis D);          

3) disturbances of functioning ion pumps of enterocytes (transport of monosaccharides and amino acids is connected with the work of Na-K-pump);

4) deficiency of energy (absorption of the majority of substances – energy-dependent process);

5) disturbance of assembly of convey complexes (chilomicrones, lipoproteids) in enterocytes.

The reasons of The reasons of malabsorption may be malabsorption may be such postenterocytic such postenterocytic

disturbances:disturbances:    

The reasons of The reasons of malabsorption may be malabsorption may be such postenterocytic such postenterocytic

disturbances:disturbances:       1) 1) disturbances of blood circulationdisturbances of blood circulation in wall of in wall of

intestines, may be caused by disturbances of intestines, may be caused by disturbances of general haemodynamics in system of v. porta and general haemodynamics in system of v. porta and local disturbances (ischemia, venous local disturbances (ischemia, venous hyperaemia, thrombosis, embolia, reactions of hyperaemia, thrombosis, embolia, reactions of vessels on inflammation);   vessels on inflammation);  

  2) 2) disturbances of lymph flowdisturbances of lymph flow. Besides general . Besides general disorders of lymph circulation they may be disorders of lymph circulation they may be connected to disturbances of villis contraction of connected to disturbances of villis contraction of intestinal wall. Such contraction is usually intestinal wall. Such contraction is usually carried out due to local reflexes with a part of carried out due to local reflexes with a part of submucous nervous plexus and due to submucous nervous plexus and due to participation of hormone villikinin.participation of hormone villikinin.

•        The syndrome of maldigestion is disturbances of primary digestion, caused by insufficient reception of digestive enzymes into guts in particular in case of pancreatic hyposecretion.

•        This syndrome is presented by:

1) disturbance of digestion of fats (absence of lipase and phospholipase). About 60-80 % of fat that gets into intestines is deduced with feaces – steatorrhea (fat in feaces);

2) disturbance of absorbtion of fat-soluble vitamins – causes the development of hypovitaminosis A, E and K;

3) disturbance of proteins digestion (absence of digestive proteases). About 30-40 % of food proteins are not acquired. In feaces there is a plenty of muscular fibres;

4) disturbance of digestion of carbohydrates (absence of amylases);

5) disturbance of decomposition of nucleinic acids (absence of nucleases).

Disturbances of intestine motor function Disturbances of intestine motor function • Disturbances of motor function of guts refer to intestinal diskinesia.

There are two types of intestinal diskinesia: hyperkinetic and hypokinetic. The first type is characterized by strengthening of the peristaltics, segmentary and pendulum-like movements, and is manifastatied as diarrheas.

•         The second, on the contrary, is characterized by weakening of motor activity of guts which result to development of constipations.

•         The reasons of intestinal diskinesias of hyperkinetic type may be: а) increase excitability of guts receptors to adequate irritators that

accompanies development of inflammation of intestines mucous membrane (enteritis, colics);

b) action unusual, pathological irritators undigested food (for example, for achylia), products of rotting and fermentation, toxic substances etc. on receptors of guts.;

c) increase of the centres of vagal nerve excitability; d) increase of some gastrointerstitial hormones formation that strengthen

peristaltics of guts (motilin).•        Consequences of intestinal dyskinesias of hyperkinetic type are: а) disturbances of digestion (digestion, absorption); b) dehydratation; c) secretory non gas acidosis (loss of hydrocarbonates).

Disturbances of intestine motor Disturbances of intestine motor functionfunction

    Intestinal dyskinesias of hypokinetic type are manifestated by reduction Intestinal dyskinesias of hypokinetic type are manifestated by reduction intestinal peristaltics. That results in appearance of constipations. According to intestinal peristaltics. That results in appearance of constipations. According to mechanisms of development there are two kinds of constipations: mechanisms of development there are two kinds of constipations: spastic and spastic and atonicatonic..

                SpasticSpastic constipations result from long tonic contraction of smooth muscles of constipations result from long tonic contraction of smooth muscles of guts (spasm) and may be caused by viscero-visceral reflexes, or action of toxic guts (spasm) and may be caused by viscero-visceral reflexes, or action of toxic factors (for example, poisoning with lead).factors (for example, poisoning with lead).

          The reason of The reason of atonicatonic constipations development connected with reduction of constipations development connected with reduction of

contractive function of guts smooth muscles may be: contractive function of guts smooth muscles may be: аа) malnutrition low contents of cellulose in consumed food; ) malnutrition low contents of cellulose in consumed food; b) excessive digestion of food in the stomach (for example, in gastric hypersecretion); b) excessive digestion of food in the stomach (for example, in gastric hypersecretion); c) age changes of receptor system of guts in old men, and also structural changes of c) age changes of receptor system of guts in old men, and also structural changes of

an intestinal wall during obesity; an intestinal wall during obesity; d) decrease of vagal nerve tone; d) decrease of vagal nerve tone; e) disturbances of intraintestinal innervation, for example, during Girshprungs disease e) disturbances of intraintestinal innervation, for example, during Girshprungs disease

- absence of ganglion cells of Auerbachs plexus in sigmoideum and rectum.- absence of ganglion cells of Auerbachs plexus in sigmoideum and rectum.

        Intestinal dyskinesis of hypokinetic type lead to: Intestinal dyskinesis of hypokinetic type lead to: 1) development of intestinal autointoxication; 1) development of intestinal autointoxication; 2) occurrence of meteorism; 2) occurrence of meteorism; 3) formation of feces stones; 3) formation of feces stones; 4) in extreme cases intestinal obstruction may develop.4) in extreme cases intestinal obstruction may develop.

PathogenesisPathogenesis The common end pathway is The common end pathway is inflammation of the inflammation of the

mucosal liningmucosal lining of the intestinal tract, causing ulceration, of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss.edema, bleeding, and fluid and electrolyte loss.

Persons with IBD have a Persons with IBD have a genetic predispositiongenetic predisposition (or (or perhaps susceptibility) for the disease. perhaps susceptibility) for the disease.

The triggering event for the activation of the immune The triggering event for the activation of the immune response has yet to be identified. response has yet to be identified.

Possible factors related to this event include a Possible factors related to this event include a pathogenic organism (as yet unidentified), an immune pathogenic organism (as yet unidentified), an immune response to an intraluminal antigen (egg, protein from response to an intraluminal antigen (egg, protein from cow milk), or an autoimmune process whereby an cow milk), or an autoimmune process whereby an appropriate immune response to an intraluminal antigen appropriate immune response to an intraluminal antigen and an inappropriate response to a similar antigen is and an inappropriate response to a similar antigen is present on intestinal epithelial cells (alteration in barrier present on intestinal epithelial cells (alteration in barrier function).function).

ULCERATIVE COLITISULCERATIVE COLITIS Ulcerative colitisUlcerative colitis ( (Colitis ulcerosaColitis ulcerosa, , UCUC) is a ) is a

form of form of inflammatory bowel disease inflammatory bowel disease (IBD). (IBD). Ulcerative colitis is a form of colitis, a disease Ulcerative colitis is a form of colitis, a disease

of the intestine, specifically the large intestine of the intestine, specifically the large intestine or colon, that includes characteristic or colon, that includes characteristic ulcers, ulcers, or open sores, in the colon. or open sores, in the colon.

The main symptom of active disease is usually The main symptom of active disease is usually diarrhea mixed with blood, diarrhea mixed with blood, of gradual of gradual onset. onset.

however, a systemic disease that affects however, a systemic disease that affects many parts many parts of the body outside the intestine of the body outside the intestine

Crohn’s (Crohn’s () & Ulcerative Colitis () & Ulcerative Colitis () )

Small IntestineSmall Intestine Skip LesionsSkip Lesions Full thicknessFull thickness Narrow lumenNarrow lumen Granulomatous infl.Granulomatous infl. Large IntestineLarge Intestine Continuous, MucosalContinuous, Mucosal Thin wall Thin wall Dilatation.Dilatation.

Fibrous, granulomatousFibrous, granulomatous Thick wall, narrow lumen.Thick wall, narrow lumen. Transmural – full thick.Transmural – full thick. Skip Lesions commonSkip Lesions common

Acute inflammationAcute inflammation Mainly mucosalMainly mucosal Ulceration, dilated lumen.Ulceration, dilated lumen. Continuous lesionContinuous lesion

Crohn’s (Crohn’s () - vs - Ulcerative Colitis () - vs - Ulcerative Colitis () )

Patients with ulcerative colitis can occasionally have aphthous ulcers involving the tongue, lips, palate and pharynx

 

Endoscopic image of ulcerative colitis showing loss of vascular pattern of the sigmoid colon, granularity and some friability of the mucosa.

Ulcerative colitis Ulcerative colitis involves only the mucosa; it is involves only the mucosa; it is characterized by the formation of characterized by the formation of crypt abscessescrypt abscesses and a coexisting depletion of and a coexisting depletion of goblet cell mucingoblet cell mucin..

In severe cases, the In severe cases, the submucosa may be involvedsubmucosa may be involved; ; in some cases, the deeper muscular layers of the in some cases, the deeper muscular layers of the colonic wall is also affected.colonic wall is also affected.

Increased intensity of the cellular infiltrate in the Increased intensity of the cellular infiltrate in the lamina propria with alterations of the composition. lamina propria with alterations of the composition.

Infiltrate is more extensive and extends diffusely Infiltrate is more extensive and extends diffusely towards the deeper part (transmucosal) towards the deeper part (transmucosal)

Accumulation of Accumulation of plasma cells near the mucosal plasma cells near the mucosal basebase, in-between the crypt base and the muscularis , in-between the crypt base and the muscularis mucosae (basal mucosae (basal plasmacytosisplasmacytosis)

Pathological Feature Pathological Feature

MCC of GI Bleeding MCC of GI Bleeding 2006 Current2006 Current

Upper GIUpper GI PUDPUD Portal HTNPortal HTN Mallory WeissMallory Weiss Vascular abnVascular abn Gastric NeoplasmsGastric Neoplasms Erosive gastritisErosive gastritis othersothers

Lower GILower GI Under 50 y/oUnder 50 y/o

• Infectious colitisInfectious colitis• Anorectal dsAnorectal ds• Inflammatory bowel dsInflammatory bowel ds

Over 50 y/o c Major BleedOver 50 y/o c Major Bleed• DiverticulosisDiverticulosis• Vascular ectasiasVascular ectasias• MalignancyMalignancy• ischemiaischemia

Bowel motility disorders:Bowel motility disorders:

Ileus is a disruption of the normal Ileus is a disruption of the normal propulsive gastrointestinal motor activity propulsive gastrointestinal motor activity from non-mechanical mechanismsfrom non-mechanical mechanisms

Motility disorders that result from structural Motility disorders that result from structural abnormalities are termed mechanical abnormalities are termed mechanical bowel obstruction.bowel obstruction.

Paralytic (ileus)Spastic

Mechanical

Bowel Obstruction

Dinamic

ObturativeStrangulative

IntestinalIntestinal mechanicalmechanical obstructionobstructionPathogenesisPathogenesis

StenosisStenosis Obstruction Obstruction CompressionCompression InvaginationInvagination TorsionTorsion AngulationAngulation StrangulationStrangulation

Pathogenesis Pathogenesis Obstruction Bowel distention (increased secretion

reduced absorption, hypomotility)

Gas production, lack of absorption

Progressive distention, fluid accumulation, emesis

Systemic dehydration

Reduced venous return

Poor tissue perfusion

Obstruction of venules and lymphatics in bowel wall

Edema of bowel wall

Ischaemia of bowel wall

Necrosis of bowel wall

Enterotoxemia

Death

Rupture of bowel wall

Peritonitis

Accumulation of fluids and gas proximal to Accumulation of fluids and gas proximal to the obstructionthe obstruction

Simple mechanicalSimple mechanical obstructionobstructionPATHOGENESISPATHOGENESIS

Distention of the intestine (self Distention of the intestine (self perpetuating)perpetuating)

Increase intestinal secretionIncrease intestinal secretionLosses of water, Na, Cl, K, HLosses of water, Na, Cl, K, HDehydratation, hypokalemia, hypochloremiaDehydratation, hypokalemia, hypochloremiaMetabolic alkalosisMetabolic alkalosis

Circultory changesCircultory changes

Low central venous pressureLow central venous pressure Reduced cardiac outputReduced cardiac output HypotentionHypotention Hypovolemic shockHypovolemic shock

Rapid proliferation of intestinal bacteriaRapid proliferation of intestinal bacteria ToxiemiaToxiemia

Simple mechanicalSimple mechanical obstructionobstruction

PATHOGENESISPATHOGENESIS

Paralytic IleusParalytic Ileus

MechanicalMechanical obstructionobstruction

Paralytic Ileus

After abdominal surgery (laparotomy) Electrolyte imbalances (hypokalemia) Abdominal thrauma Spine fracture Retroperitoneal hemorrhage Ureter distension – Acute pancreatitis Ischemia of the intestine Drugs (Narcotics, Psychotropics) Peritonitis (ex. Gangrenous cholecystitis) Diabetic coma Extra abdominal infections (Lung) – Sepsis IBD (ulcerative colitis)

Ischemia of the bowel

Strangulation obstructionPATHOGENESIS

Loss of blood and plasma into the strangulated segment

Gangrene

Perforation

Peritonitis

Sistemic absorption of toxic materia

Strangulation ObstructionStrangulation Obstruction

Simple Simple MechanicalMechanical obstructionobstruction

SurgicalSurgicaltimingtiming

Intestinal obstructionIntestinal obstructionSiteSite

Proximal s.b. Proximal s.b. obstructionobstruction

Greather vomitimg and less Greather vomitimg and less intestinal distention than distal intestinal distention than distal obstructionobstruction

Colon obstructionColon obstruction Less fluid and electrolyte Less fluid and electrolyte

disturbancedisturbance Large distension and perforation Large distension and perforation

riskrisk

Intestinal obstructionIntestinal obstructionClinical aspectsClinical aspects

Abdominal painAbdominal pain VomitingVomiting ObstipationObstipation Abdominal distentionAbdominal distention Failure to pass flatusFailure to pass flatus FeverFever DehydratationDehydratation Hypotention – hypovolemic shockHypotention – hypovolemic shock

Intestinal obstructionIntestinal obstructionPainPain

Typical Typical crampy paincrampy pain in paroxysm at 4 to in paroxysm at 4 to 5 minute intervals in proximal obstruction 5 minute intervals in proximal obstruction

Less frequently in distal occlusionLess frequently in distal occlusion After a long period of mechanical After a long period of mechanical

obstruction the obstruction the crampy pain may subsidecrampy pain may subside A strangulation should be suspected A strangulation should be suspected

when when continuus severe paincontinuus severe pain replace replace crampy paincrampy pain

Intestinal obstructionIntestinal obstructionVomitingVomiting

ProximalProximal obstruction produce profuse obstruction produce profuse vomiting and little abdominal distension vomiting and little abdominal distension

DistalDistal obstruction is less frequent but obstruction is less frequent but feculentfeculent

Initial phaseInitial phase byliary aspect byliary aspect Late phaseLate phase feculent feculent

BUTBUT

Intestinal obstruction - LevelIntestinal obstruction - LevelHIGHHIGH LOWLOW

PAINPAIN Crampy pain in Crampy pain in paroxismparoxism

Less intensityLess intensity

VOMITINGVOMITING Early, profuse, biliaryEarly, profuse, biliary Late, feculent may be Late, feculent may be absentabsent

METEORISMMETEORISM ++ ++++++

BEGINNINGBEGINNING AcuteAcute Slow, insidiousSlow, insidious

ABDOMINAL ABDOMINAL DISTENTIONDISTENTION

Moderate, upper Moderate, upper quadrantquadrant

Early, intenseEarly, intense

GENERAL CONDITGENERAL CONDIT Early compromissionEarly compromission preservedpreserved

ELECTOLYTESELECTOLYTES Cl, K, Na rapid lossCl, K, Na rapid loss Late hydro electrolytic Late hydro electrolytic imbalanceimbalance

Intestinal obstruction Clinical examinationIntestinal obstruction Clinical examination

PalpationPalpation abdominal masses can suggest abdominal masses can suggest neoplasms, intussusception, abscess neoplasms, intussusception, abscess

Incarcerated herniasIncarcerated hernias may be obscure (obese) may be obscure (obese)

Surgical scarsSurgical scars can suggest adhesions can suggest adhesions

Abdominal auscultationAbdominal auscultation period of increasing period of increasing separated by periods of quite bowel sounds (high separated by periods of quite bowel sounds (high pitched, tinkling or musical) in mechanical pitched, tinkling or musical) in mechanical obstructionobstruction

Rectal examinationRectal examination to seek luminal masses. Blood to seek luminal masses. Blood in the feces suggest mucosal lesion (cancer, in the feces suggest mucosal lesion (cancer, intussusception, infarction)intussusception, infarction)

Key pointsKey points

Intestinal obstruction Clinical examinationIntestinal obstruction Clinical examination

Young children and Young children and babies babies

AtresiaAtresia

VolvolusVolvolus

Anal imperforationAnal imperforation

Meconial ileusMeconial ileus

Intestinal DuplicationIntestinal Duplication

MalrotationMalrotation

IntussusceptionIntussusception

Ascaris infestationAscaris infestation

HerniaHernia

Patient age and sexPatient age and sex

Adults Adults

HerniaHernia

AdhesionsAdhesions

NeoplasmNeoplasm

InflammationInflammation

RT RT

EndometriosisEndometriosis

Gynecological Gynecological pathologypathology

Intestinal obstructionIntestinal obstruction

GasGas abnormally large quantities of gas in the abnormally large quantities of gas in the bowel bowel

Multiple gas-fluid levelsMultiple gas-fluid levels in the upright or in the upright or lateral decubitus positionlateral decubitus position

Abdominal direct X ray exhaminationAbdominal direct X ray exhamination

Proximal or Distal?

Symptom Proximal(open loop)

Distal(open loop)

Closed loop

Pain I ntermitt ent,colicky, relieved

by vomiting

I ntermitt entto constant

Progressive,rapidlyworsens

Vomiting Large volumes,bilious

Low volume,feculent over

time

May beprominent(refl ex)

Tenderness Epigastric, mildunless

strangulated

Diff use andprogressive

Diff use,progressive

Distention Absent Moderate tomarked

Of ten absent

Obstipation May not bepresent

Present May not bepresent

It is the commonest abdominal emergency between 3 months and 2 yearsIt is the commonest abdominal emergency between 3 months and 2 years Peak incidence is between 6 and 9 monthsPeak incidence is between 6 and 9 months Most cases are idiopathic with the lead point due to enlarged Peyer's Most cases are idiopathic with the lead point due to enlarged Peyer's

patches patches Usually due to a viral infectionUsually due to a viral infection 5% are due to polyp, Meckel's diverticulum, duplication cyst or tumour5% are due to polyp, Meckel's diverticulum, duplication cyst or tumour Commonest site involved is the ileocaecal junctionCommonest site involved is the ileocaecal junction

Barium study showing the filling defect in the jejunum with claw-like appearance suspicious of intussusception. The bowel loop distal to the filling defect is collapsed (arrow).

CT scan of the abdomen showing the intraluminal hypodense filling defect with mottled appearance (arrow).

• Occurs when one part of bowel invaginates Occurs when one part of bowel invaginates (intussusceptum) into an adjacent section (intussusceptum) into an adjacent section (intussuscipiens) (intussuscipiens)

• Results in intestinal obstruction and venous compressionResults in intestinal obstruction and venous compression• If uncorrected it can result in arterial insufficiency and If uncorrected it can result in arterial insufficiency and

necrosisnecrosis

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