prepared by By M.D., PhD Marta R. Gerasymchuk Department of Pathophysiology Ivano-Frankivsk National Medical University

1. Pathophysiology ofPathophysiology of
digestion. Violation ofdigestion. Violation of
digestion in a oral cavity,digestion in a oral cavity,
stomach and intestinestomach and intestine

2. Plan of the lecturePlan of the lecture
1.1. Insufficiency of digestion. Etiology.Insufficiency of digestion. Etiology.
2.2. Syndromes of digestionSyndromes 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.

3. Actuality of theActuality of the
lecturelectureNumber of patients, which suffer the different diseases of stomachNumber of patients, which suffer the different diseases of stomach
of, which are accompanied disorders of digestion, grows constantly,of, which are accompanied disorders of digestion, grows constantly,
resulting in the decline of capacity, invalidity of people. Theseresulting in the decline of capacity, invalidity of people. These
diseases often cases death.diseases often cases death.
One of important and most early violations of functions of stomachOne of important and most early violations of functions of stomach
there is violation of gastric secretion, which can develop as a result ofthere is violation of gastric secretion, which can develop as a result of
violation of the neuroendocrine regulation, and also at pathologicalviolation of the neuroendocrine regulation, and also at pathological
processes in a stomach.processes in a stomach.
The diseases of liver and bile excretory system take considerableThe diseases of liver and bile excretory system take considerable
specific weight in a general morbidity of the population, and lastspecific weight in a general morbidity of the population, and last
decade the further growth of them was increased.decade the further growth of them was increased.
Technological revolution and associated with it the negativeTechnological revolution and associated with it the negative
ecological shifts have resulted in useful increase of frequency andecological shifts have resulted in useful increase of frequency and
spread spectrum of diseases of liver and cholic tractsspread spectrum of diseases of liver and cholic tracts..

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

6. Etiology of digestion insufficiency:Etiology of digestion 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 maintenance ofd) disbalanced meal (for example, reduction of the maintenance of
vitamins, proteins in a diet);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 roleAmong factors of this group the greatest role
belongs to radiation which effects epithelial cells of the alimentarybelongs to radiation which effects epithelial cells of the alimentary
channel which have high mitotic activity.channel which have high mitotic activity.
 3.3. Chemical agentsChemical agents are the reason of digestion disorders afterare the reason of digestion disorders after
poisonings with inorganic and organic substances during manufacturepoisonings with inorganic and organic substances during manufacture
and in life.and in life.
 4.4. Biological factors:Biological factors:
 a)a) bacteriabacteria (for example, v.cholera, causative agents of dysentery,(for example, v.cholera, causative agents of dysentery,
typhoid fever, paratyphus);typhoid fever, paratyphus);
 b)b) bacterialbacterial toxins (for example, at salmonellosis, staphylococcaltoxins (for example, at salmonellosis, staphylococcal
infection);infection);
 c)c) virusesviruses (for example, adenoviruses);(for example, adenoviruses);
 d)d) helminthshelminths..

7. Etiology of digestionEtiology of digestion
insufficiency:insufficiency:
 5.5. Organic effects:Organic effects:
 a)a) congenitalcongenital 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 (encephalites);of the central nervous system (encephalites);
 d)d) lesions of peripheral structureslesions of peripheral structures of vegetative nervous system;of vegetative nervous system;
 e)e) reflex disordersreflex disorders (various viscero-visceral reflexes).(various viscero-visceral reflexes).
Disorders of humoral regulation of digestion may be connected toDisorders of humoral regulation of digestion may be connected to
disorders of synthesis and secretion of gastrointestinal hormonesdisorders of synthesis and secretion of gastrointestinal hormones
(gastrine, secretin, cholecystokinin-pancreazymin etc.).(gastrine, secretin, cholecystokinin-pancreazymin etc.).

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

9. Dispeptic syndromeDispeptic syndrome
includes differentincludes different
combinations of thecombinations 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.

10. AnorexiaAnorexia is a full absence of appetite combinedis a full absence of appetite combined
with an objective need of foodwith an objective need of food
There 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, acentre 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’ssystem (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).

11. ► The heartburnThe heartburn is a feeling of heat or burnings along theis a feeling of heat or burnings along the
esophagus. Its development is connected with irritation ofesophagus. Its development is connected with irritation of
receptors of the esophagus during pelting contents of stomachreceptors of the esophagus during pelting contents of stomach
into an esophagus gullet (reflux).into an esophagus 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 digestiveis surplus accumulation of gases in the digestive
channel due to their increased formation or insufficient removingchannel due to their increased formation or insufficient removing
from intestines.from intestines.
► DiarrheaDiarrhea is a frequent emptying of intestines with dischargingis a frequent emptying of intestines with discharging
of diluted and plentiful excrements.of diluted and plentiful excrements.

12.  The eructationThe eructation is a sudden involuntary allocation into oral cavity ofis a sudden involuntary allocation into oral cavity of
gas from a stomach esophagus, sometimes with small portions ofgas from a stomach esophagus, sometimes with small portions of
stomach contents.stomach contents.
 The nauseaThe nausea is a burdensome sensation in epigastric area, chest andis a burdensome sensation in epigastric area, chest and
in oral cavity, quite often previous to vomitting and frequently isin 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 arterialcoldness of arms and legs, pallor of skin, decrease of arterial
pressure that is connected to activation parasympathetic nervouspressure 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 theis the
complex-reflex actcomplex-reflex act
which results towhich results to
eruption of stomacheruption of stomach
contents outsidecontents outside
through the mouth. It isthrough the mouth. It is
a result of the emetica result of the emetic
centre excitation whichcentre excitation which
is situated in medullais situated in medulla
oblongata.oblongata.

14. 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.

16. 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.

17. Disturbance of stomach functionsDisturbance of stomach functions
Disturbance of hydrochloric acidDisturbance of hydrochloric acid
Hydrochloric acidHydrochloric acid is excreted byis excreted by parietal cellsparietal cells of mucous membrane ofof 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 includeof it is regulated by complicated mechanisms which include
three interconnectedthree interconnected phases of secretionphases of secretion:: neurogenicneurogenic (vagal),(vagal), gastricgastric
(gastrine) and(gastrine) and intestinalintestinal which is regulated by irritation of receptors andwhich is regulated by irritation of receptors and
intestinal hormones.intestinal hormones.
In regulation of functional activity ofIn regulation of functional activity of parietal cellsparietal cells nervous system (throughnervous 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 fromThe 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 andpromotes formation of cAMP and
stimulation of CCK-receptors and M3-receptors results tostimulation of CCK-receptors and M3-receptors results to increasing ofincreasing of
endocellular calciumendocellular calcium ((СаСа++) level.++) level.
Besides theBesides 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 endocellularlevel strengthens an output of endocellular СаСа++.++.
GastrinGastrin,, cholecystokinincholecystokinin andand histaminehistamine also raise output ofalso 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 whichhas a receptor for prostaglandin E2 (PGE2) stimulation which
reduces level of cAMP and results to inhibition of hydrochloric acidreduces level of cAMP and results to inhibition of hydrochloric acid
secretion.secretion.

18. • 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).

19. 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.

20. 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.

21. According to quantity of gastric juice and itsAccording 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 also1) 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 hyperchlorhydria2) hyperaciditas and hyperchlorhydria –– increase of the common acidityincrease 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.
TheThe disturbances of digestiondisturbances of digestion connected withconnected with gastric hypersecretiongastric hypersecretion, are caused, are caused
by a long delay of food in the stomach (pylorus is closed, because ofby a long delay of food in the stomach (pylorus is closed, because of
neutralization of very sour contents that go into duodenum, demands aneutralization 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 ingo into intestine, that results in reduction ofreduction of
guts peristalticsguts peristaltics and to development ofand to development of constipationsconstipations;;
 2) in the stomach processes of2) in the stomach processes of fermentation and formation gases increasefermentation and formation gases increase. It. It
causes appearance of ancauses 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 andand
hyperkinesishyperkinesis of smooth muscles.of smooth muscles.
Formation of active gastric juice plenty is the important factor promotingFormation of active gastric juice plenty is the important factor promoting
formation of ulcers in stomach and duodenum.formation of ulcers in stomach and duodenum.

22. 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.

23. 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.

24. 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.

25. STOMACHSTOMACH

26. CONGENITAL ABNORMALITIESCONGENITAL ABNORMALITIES
• Pyloric stenosis
a) males 3:1 vs. females
b) may occur with Turner syndrome,
trisomy 18, esophageal atresia
c) clinical:
1) narrowing of pyloris
- hypertrophy and possibly
hyperplasia (muscularis)
2) regurgitation (projectile !!)
- dehydration of concern

27. 3) oval (“olive”) palpable mass
4) surgical splitting is curative

28. 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.

29. ACUTE GASTRITISACUTE GASTRITIS
• Gastritis (inflammation of gastric
mucosa)
• Transient inflammation (usually)
a) bleeding and erosion
) sloughing of mucosa
• Pathogenesis not clear: associations
a) NSAID (e.g., aspirin)
b) alcohol
c) smoking
d) stress (trauma, burns, surgery)
e) uremia, infections

31. • Several factors involved: (1 or more)
a) ↑ acid secretion with back
diffusion
b) ↓ HCO3
-
buffer
c) ↓ blood flow
d) disruption of mucus layer
e) damage to epithelium
f) lots of patients have idiopathic
acute gastritis without any of the
listed disorders !!
g) neutrophils above basement
membrane → active inflammation

32. 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.

33. 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) (HypertrophicGiant 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

34. Gastritis SymptomsGastritis Symptoms
Clinical features of gastritis generally reflects the underlyingClinical features of gastritis generally reflects the underlying
syndrome rather than the gastric injury itselfsyndrome rather than the gastric injury itself
Acute:Acute:
– Dyspepsia and abdominal pain are common indicators ofDyspepsia 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

37. SYMPTOMS
Burning painBurning pain bloatingbloating
NauseaNausea water brashwater brash
Unexplained weight lossUnexplained weight loss hematemesis (vomiting of blood)hematemesis (vomiting of blood)
Appetite changesAppetite 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

38. 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.

39. 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.

40. Gastric UlcerGastric Ulcer

41. Duodenal Peptic UlcerDuodenal Peptic Ulcer

42. 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 prostaglandin6. Depresses gastric mucosal prostaglandin
synthesissynthesis

43. Helicobacter pyloriHelicobacter pylori
 These bacterias produce aThese bacterias produce a lot enzymeslot enzymes ((urease, protease, phospholipaseurease, protease, phospholipase),),
damaging protective barrier of mucous membrane, and also variousdamaging protective barrier of mucous membrane, and also various
cytotoxins. The most pathogenic arecytotoxins. The most pathogenic are Vac A-strainVac A-strain, that produce vacuolizating, that produce vacuolizating
cytotoxin which results in formation of cytoplasmatic vacuoles and destructionscytotoxin which results in formation of cytoplasmatic vacuoles and destructions
of epithelial cells, and the Cag A-strain whichof epithelial cells, and the Cag A-strain which expresses gene associatedexpresses 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 mucouson 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 % ofof duodenum ulcer development in 95 % of
cases is associated withcases is associated with HelicobacterHelicobacter..
 Contaminating the mucous membrane of the stomach by Helicobacter isContaminating the mucous membrane of the stomach by Helicobacter is
accompanied by development of superficial anthral gastritis and duodenitisaccompanied by development of superficial anthral gastritis and duodenitis
andand leads to increase of gastrin levelleads to increase of gastrin level with the subsequent increasewith the subsequent increase
ofof 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 ofinto a lumen of duodenum in conditions of deficiency of pancreaticdeficiency of pancreatic
bicarbonatesbicarbonates promotes development of duodenitis and besides causespromotes 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 quicklyepithelium 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 additionalFurther 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 ulcerpsychological overstrain etc.). In sites of metaplased mucous membrane ulcer
defect is formed. However connection of stomach ulcer occurrence withdefect 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 inApproximately in 5 % of patients with ulcers of duodenum5 % of patients with ulcers of duodenum and inand in 15-20 % of15-20 % of
patients with stomach ulcerspatients with stomach ulcers, disease, disease develops without participation of thesedevelops without participation of these
microorganismsmicroorganisms..
 ToTo gastroduodenal ulcersgastroduodenal ulcers which have been not associated with Helicobacterwhich have been not associated with Helicobacter
belong, to erosion-ulcer defects and are caused by using of aspirin and otherbelong, 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.

44. 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

45. How isHow is H. pyloriH. pylori infection diagnosed?infection diagnosed?
Several methods may be used to diagnoseSeveral methods may be used to diagnose H. pyloriH. pylori
infection.infection.
Serological testsSerological tests that measure specificthat measure specific H. pyloriH. pylori IgGIgG
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 Assay
Urea Breath testUrea Breath test
– In this test, the patient is given either 13C- or 14C-labeled urea toIn this test, the patient is given either 13C- or 14C-labeled urea to
drink.drink.
– H. pyloriH. pylori metabolizes the urea rapidly, and the labeled carbon ismetabolizes the urea rapidly, and the labeled carbon is
absorbed.absorbed.
– This labeled carbon can then be measured as CO2 in the patient'sThis labeled carbon can then be measured as CO2 in the patient's
expired breath to determine whetherexpired breath to determine whether H. pyloriH. 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

46. Tests for Detection ofTests for Detection of H. pyloriH. pylori
TestTest
Sensitivity/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 ofSimple, 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 ; antibioticTime-consuming, expensive ; antibiotic
susceptibilitysusceptibility
Non-invasiveNon-invasive
SerologySerology >80/>90>80/>90 Inexpensive, convenient; not useful forInexpensive, convenient; not useful for
early follow-upearly follow-up
Urea breathUrea 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 withexposure to low-dose radiation with 1414
CC
testtest
Stool antigenStool antigen >90/>90>90/>90 Inexpensive, convenient; not establishedInexpensive, convenient; not established
for eradication but promisingfor eradication but promising

47. 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.

48. Perforation:Perforation:

49. PEPTIC ULCER DISEASEPEPTIC ULCER DISEASE
•chronic, most often solitary lesions
a) duodenum (initial portion) 4:1
b) stomach (antrum)
c) gastroesophageal junction
i) Barrett esophagus
d) duodenum, stomach and/or
jejunum
i) Zollinger-Ellison syndrome
•in USA, ~ 4 million; 3:1 male:female
•middle age to older adults

50. 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.

52. Zollinger-Ellison SyndromeZollinger-Ellison Syndrome
 A tumor of the pancreas that secretes gastrinA tumor of the pancreas that secretes gastrin
((Gastrinoma)Gastrinoma)
 Usually found in head of pancreas but can alsoUsually found in head of pancreas but can also
be found in duodenum, liver & lungbe found in duodenum, liver & lung
 75-80% of ulcers produced develop in the75-80% 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

53. Clinical Manifestations of UlcerClinical Manifestations of Ulcer
Gastric:Gastric:
 Burning or gassy sensationBurning or gassy sensation
in high epigastric areain high epigastric area
 Occurs within ½ hr. afterOccurs within ½ hr. after
eating, food can worseneating, food can worsen
symptomssymptoms
 Rarely occurs at nightRarely occurs at night
 Vomiting may easeVomiting may ease
discomfortdiscomfort
 May lose weightMay lose weight
 PyrosisPyrosis
Duodenal:Duodenal:
 More cramplikeMore cramplike
discomfortdiscomfort
 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

54. Gastric ulcer
Duodenal
ulcer

55. Disturbance of intestinal functions
• Functions of intestines may be brokenFunctions of intestines may be broken
owing to many organic diseases. Inowing to many organic diseases. In
some cases these disturbances arisesome cases these disturbances arise
owing to disorders of nervousowing to disorders of nervous
regulation of small and large intestineregulation 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.

56. Syndrome of MalabsorbtionSyndrome of Malabsorbtion
 The syndrome of malabsorbtion is a complex ofThe syndrome of malabsorbtion is a complex of
symptoms whichsymptoms which appearsappears result ofresult of absorbtionabsorbtion
disturbancedisturbance of substances in guts. Disturbance ofof substances in guts. Disturbance of
absorbtion in guts may be caused by disturbancesabsorbtion in guts may be caused by disturbances
that appear on three levels:that appear on three levels:
 1)1) preenterocyticpreenterocytic disturbance. Develop as a resultdisturbance. Develop as a result
of disturbances of digestion processes beforeof disturbances of digestion processes before
absorbtion;absorbtion;
 2)2) enterocyticenterocytic from disturbance of intestinalfrom disturbance of intestinal
mucous membrane epithelial cells activity;mucous membrane epithelial cells activity;
 3)3) postenterocyticpostenterocytic disturbance. There aredisturbance. There are
consequences of the processes disturbance thatconsequences of the processes disturbance that
provide reception of absorbed substances intoprovide reception of absorbed substances into
internal environment of an organism (blood, lymph).internal environment of an organism (blood, lymph).

57. Preenterocytic disturbances:Preenterocytic disturbances:
► 1. Disturbances of motor function of the alimentary1. Disturbances of motor function of the alimentary
channel.channel.
► 2. Disturbances of primary digestion (a syndrome of2. Disturbances of primary digestion (a syndrome of
maldigestion). By origin they may be gastrogenic,maldigestion). By origin they may be gastrogenic,
pancreatogenic, hepatogenic, enterogenic, disregulated,pancreatogenic, hepatogenic, enterogenic, disregulated,
iatrogenic (connected with long usage of antibiotics andiatrogenic (connected with long usage of antibiotics and
other medical products).other medical products).
► 3. Disturbance of membrane digestion. More often they are3. Disturbance of membrane digestion. More often they are
caused by disturbances of formation and embedding ofcaused by disturbances of formation and embedding of
enzymes into plasmatic membrane of enterocyticenzymes into plasmatic membrane of enterocytic
microvillis.microvillis.
► Interstitial pathology of enzymes are hereditary causedInterstitial pathology of enzymes are hereditary caused
disturbances of digestive enzymes synthesis by microvillisdisturbances of digestive enzymes synthesis by microvillis
which provide processes of membrane digestion. Amongwhich provide processes of membrane digestion. Among
the interstitial pathologies of enzymes intolerance tothe interstitial pathologies of enzymes intolerance to
disaccharides (lactoses, saccharoses, tregaloses) anddisaccharides (lactoses, saccharoses, tregaloses) and
insufficiency of peptidase (gluten enteropathy, celiacinsufficiency of peptidase (gluten enteropathy, celiac
disease) occur the most often.disease) occur the most often.

58. 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.

59. The reasons ofThe reasons of
malabsorption may be suchmalabsorption may be such
postenterocyticpostenterocytic
disturbances:disturbances:
 1)1) disturbances of blood circulationdisturbances of blood circulation in wall of intestines,in wall of intestines,
may be caused by disturbances of general haemodynamicsmay be caused by disturbances of general haemodynamics
in system of v. porta and local disturbances (ischemia,in system of v. porta and local disturbances (ischemia,
venous hyperaemia, thrombosis, embolia, reactions ofvenous hyperaemia, thrombosis, embolia, reactions of
vessels on inflammation); vessels on inflammation);
 2)2) disturbances of lymph flowdisturbances of lymph flow. Besides general disorders. Besides general disorders
of lymph circulation they may be connected toof lymph circulation they may be connected to
disturbances of villis contraction of intestinal wall. Suchdisturbances of villis contraction of intestinal wall. Such
contraction is usually carried out due to local reflexes withcontraction is usually carried out due to local reflexes with
a part of submucous nervous plexus and due toa part of submucous nervous plexus and due to
participation of hormone villikinin.participation of hormone villikinin.

60. • 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).

61. 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).

62. Disturbances of intestine motorDisturbances of intestine motor
functionfunction
 Intestinal dyskinesias of hypokinetic type are manifestated by reductionIntestinal dyskinesias of hypokinetic type are manifestated by reduction
intestinal peristaltics. That results in appearance of constipations. According tointestinal 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 andspastic and
atonicatonic..
 SpasticSpastic constipations result from long tonic contraction of smooth muscles ofconstipations result from long tonic contraction of smooth muscles of
guts (spasm) and may be caused by viscero-visceral reflexes, or action of toxicguts (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 ofThe reason of atonicatonic constipations development connected with reduction ofconstipations 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 ofc) 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 diseasee) 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.

63. PathogenesisPathogenesis
 The common end pathway isThe common end pathway is inflammation of the mucosalinflammation of the mucosal
lininglining of the intestinal tract, causing ulceration, edema,of the intestinal tract, causing ulceration, edema,
bleeding, and fluid and electrolyte loss.bleeding, and fluid and electrolyte loss.
 Persons with IBD have aPersons with IBD have a genetic predispositiongenetic predisposition (or perhaps(or perhaps
susceptibility) for the disease.susceptibility) for the disease.
 The triggering event for the activation of the immune responseThe triggering event for the activation of the immune response
has yet to be identified.has yet to be identified.
 Possible factors related to this event include a pathogenicPossible factors related to this event include a pathogenic
organism (as yet unidentified), an immune response to anorganism (as yet unidentified), an immune response to an
intraluminal antigen (egg, protein from cow milk), or anintraluminal antigen (egg, protein from cow milk), or an
autoimmune process whereby an appropriate immuneautoimmune process whereby an appropriate immune
response to an intraluminal antigen and an inappropriateresponse to an intraluminal antigen and an inappropriate
response to a similar antigen is present on intestinal epithelialresponse to a similar antigen is present on intestinal epithelial
cells (alteration in barrier function).cells (alteration in barrier function).

64. ULCERATIVE COLITISULCERATIVE COLITIS
 Ulcerative colitisUlcerative colitis ((Colitis ulcerosaColitis ulcerosa,, UCUC) is) is
a form ofa form of inflammatory bowel diseaseinflammatory bowel disease (IBD).(IBD).
 Ulcerative colitis is a form of colitis, a diseaseUlcerative colitis is a form of colitis, a disease
of the intestine, specifically the large intestineof the intestine, specifically the large intestine
or colon, that includes characteristicor colon, that includes characteristic ulcers, orulcers, or
open sores, in the colon.open sores, in the colon.
 The main symptom of active disease is usuallyThe main symptom of active disease is usually
diarrhea mixed with blood,diarrhea mixed with blood, of gradualof gradual
onset.onset.
 however, a systemic disease that affectshowever, a systemic disease that affects manymany
partsparts of the body outside the intestineof the body outside the intestine

65. 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 wallThin wall
Dilatation.Dilatation.

66.  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 ( ))

67. 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.

68.  Ulcerative colitisUlcerative colitis involves only the mucosa; it isinvolves only the mucosa; it is
characterized by the formation ofcharacterized by the formation of crypt abscessescrypt abscesses and aand a
coexisting depletion ofcoexisting depletion of goblet cell mucingoblet cell mucin..
 In severe cases, theIn severe cases, the submucosa may be involvedsubmucosa may be involved ; in; in
some cases, the deeper muscular layers of the colonic wall issome cases, the deeper muscular layers of the colonic wall is
also affected.also affected.
 Increased intensity of the cellular infiltrate in the lamina propriaIncreased intensity of the cellular infiltrate in the lamina propria
with alterations of the composition.with alterations of the composition.
 Infiltrate is more extensive and extends diffusely towards theInfiltrate is more extensive and extends diffusely towards the
deeper part (transmucosal)deeper part (transmucosal)
 Accumulation ofAccumulation of plasma cells near the mucosal baseplasma cells near the mucosal base ,,
in-between the crypt base and the muscularis mucosae (basalin-between the crypt base and the muscularis mucosae (basal
plasmacytosisplasmacytosis)
Pathological FeaturePathological Feature

69. MCC of GI BleedingMCC 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

71. Bowel motility disorders:Bowel motility disorders:
 Ileus is a disruption of the normalIleus is a disruption of the normal
propulsive gastrointestinal motor activitypropulsive gastrointestinal motor activity
from non-mechanical mechanismsfrom non-mechanical mechanisms
 Motility disorders that result from structuralMotility disorders that result from structural
abnormalities are termed mechanicalabnormalities are termed mechanical
bowel obstruction.bowel obstruction.

72. Paralytic (ileus)Spastic
Mechanical
Bowel Obstruction
Dinamic
ObturativeStrangulative

73. IntestinalIntestinal mechanicalmechanical obstructionobstruction
PathogenesisPathogenesis
 StenosisStenosis
 ObstructionObstruction
 CompressionCompression
 InvaginationInvagination
 TorsionTorsion
 AngulationAngulation
 StrangulationStrangulation

74. PathogenesisPathogenesis
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

75.  Accumulation of fluids and gas proximal toAccumulation of fluids and gas proximal to
the obstructionthe obstruction
Simple mechanicalSimple mechanical obstructionobstruction
PATHOGENESISPATHOGENESIS
 Distention of the intestine (selfDistention of the intestine (self
perpetuating)perpetuating)
 Increase intestinal secretionIncrease intestinal secretion
 Losses of water, Na, Cl, K, HLosses of water, Na, Cl, K, H
 Dehydratation, hypokalemia, hypochloremiaDehydratation, hypokalemia, hypochloremia
 Metabolic alkalosisMetabolic alkalosis

76.  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

77. Paralytic IleusParalytic Ileus
MechanicalMechanical
obstructionobstruction

78. 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)

79. Ischemia of the bowel
Strangulation obstruction
PATHOGENESIS
Loss of blood and plasma into the
strangulated segment
Gangrene
Perforation
Peritonitis
Sistemic absorption of toxic materia

80. Strangulation ObstructionStrangulation Obstruction
SimpleSimple
MechanicalMechanical
obstructionobstruction
SurgicalSurgical
timingtiming

81. Intestinal obstructionIntestinal obstruction
SiteSite
Proximal s.b. obstructionProximal s.b. obstruction
 Greather vomitimg and less intestinalGreather vomitimg and less intestinal
distention than distal obstructiondistention than distal obstruction
Colon obstructionColon obstruction
 Less fluid and electrolyte disturbanceLess fluid and electrolyte disturbance
 Large distension and perforation riskLarge distension and perforation risk

82. Intestinal obstructionIntestinal obstruction
Clinical aspectsClinical aspects
 Abdominal painAbdominal pain
 VomitingVomiting
 ObstipationObstipation
 Abdominal distentionAbdominal distention
 Failure to pass flatusFailure to pass flatus
 FeverFever
 DehydratationDehydratation
 Hypotention – hypovolemic shockHypotention – hypovolemic shock

83. Intestinal obstructionIntestinal obstruction
PainPain
 TypicalTypical crampy paincrampy pain in paroxysm at 4 toin paroxysm at 4 to
5 minute intervals in proximal obstruction5 minute intervals in proximal obstruction
 Less frequently in distal occlusionLess frequently in distal occlusion
 After a long period of mechanicalAfter a long period of mechanical
obstruction theobstruction the crampy pain may subsidecrampy pain may subside
 A strangulation should be suspectedA strangulation should be suspected
whenwhen continuus severe paincontinuus severe pain replacereplace
crampy paincrampy pain

84. Intestinal obstructionIntestinal obstruction
VomitingVomiting
 ProximalProximal obstruction produce profuseobstruction produce profuse
vomiting and little abdominal distensionvomiting and little abdominal distension
 DistalDistal obstruction is less frequent butobstruction is less frequent but
feculentfeculent
 Initial phaseInitial phase byliary aspectbyliary aspect
 Late phaseLate phase feculentfeculent
BUTBUT

85. Intestinal obstruction - LevelIntestinal obstruction - Level
HIGHHIGH LOWLOW
PAINPAIN Crampy pain inCrampy pain in
paroxismparoxism
Less intensityLess intensity
VOMITINGVOMITING Early, profuse, biliaryEarly, profuse, biliary Late, feculent may beLate, feculent may be
absentabsent
METEORISMMETEORISM ++ ++++++
BEGINNINGBEGINNING AcuteAcute Slow, insidiousSlow, insidious
ABDOMINALABDOMINAL
DISTENTIONDISTENTION
Moderate, upperModerate, upper
quadrantquadrant
Early, intenseEarly, intense
GENERAL CONDITGENERAL CONDIT Early compromissionEarly compromission preservedpreserved
ELECTOLYTESELECTOLYTES Cl, K, Na rapid lossCl, K, Na rapid loss Late hydro electrolyticLate hydro electrolytic
imbalanceimbalance

86. Intestinal obstruction Clinical examinationIntestinal obstruction Clinical examination
PalpationPalpation abdominal masses can suggestabdominal masses can suggest
neoplasms, intussusception, abscessneoplasms, intussusception, abscess
Incarcerated herniasIncarcerated hernias may be obscure (obese)may be obscure (obese)
Surgical scarsSurgical scars can suggest adhesionscan suggest adhesions
Abdominal auscultationAbdominal auscultation period of increasingperiod of increasing
separated by periods of quite bowel sounds (highseparated by periods of quite bowel sounds (high
pitched, tinkling or musical) in mechanicalpitched, tinkling or musical) in mechanical
obstructionobstruction
Rectal examinationRectal examination to seek luminal masses. Bloodto 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

87. Intestinal obstruction Clinical examinationIntestinal obstruction Clinical examination
Young children andYoung children and
babiesbabies
AtresiaAtresia
VolvolusVolvolus
Anal imperforationAnal imperforation
Meconial ileusMeconial ileus
Intestinal DuplicationIntestinal Duplication
MalrotationMalrotation
IntussusceptionIntussusception
Ascaris infestationAscaris infestation
Patient age and sexPatient age and sex
AdultsAdults
HerniaHernia
AdhesionsAdhesions
NeoplasmNeoplasm
InflammationInflammation
RTRT
EndometriosisEndometriosis
GynecologicalGynecological
pathologypathology

88. Intestinal obstructionIntestinal obstruction
 GasGas abnormally large quantities of gas in theabnormally large quantities of gas in the
bowelbowel
 Multiple gas-fluid levelsMultiple gas-fluid levels in the upright orin the upright or
lateral decubitus positionlateral decubitus position
Abdominal direct X ray exhaminationAbdominal direct X ray exhamination

89. Proximal or Distal?
Symptom Proximal
(open loop)
Distal
(open loop)
Closed loop
Pain Intermittent,
colicky, relieved
by vomiting
Intermittent
to constant
Progressive,
rapidly
worsens
Vomiting Large volumes,
bilious
Low volume,
feculent over
time
May be
prominent
(reflex)
Tenderness Epigastric, mild
unless
strangulated
Diffuse and
progressive
Diffuse,
progressive
Distention Absent Moderate to
marked
Often absent
Obstipation May not be
present
Present May not be
present

91.  It is the commonest abdominal emergency between 3 months and 2It is the commonest abdominal emergency between 3 months and 2
yearsyears
 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'sMost cases are idiopathic with the lead point due to enlarged Peyer's
patchespatches
 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

92. 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).

93. • Occurs when one part of bowel invaginates (intussusceptum)Occurs when one part of bowel invaginates (intussusceptum)
into an adjacent section (intussuscipiens)into an adjacent section (intussuscipiens)
• Results in intestinal obstruction and venous compressionResults in intestinal obstruction and venous compression
• If uncorrected it can result in arterial insufficiency andIf uncorrected it can result in arterial insufficiency and
necrosisnecrosis

94. Literature:Literature:
 General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: NovaGeneral and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova
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 Handbook of general and Clinical Pathophysiology / Edited by prof.A.V.Kubyshkin. –Handbook of general and Clinical Pathophysiology / Edited by prof.A.V.Kubyshkin. –
CSMU. – 2005. – p. 142–144.CSMU. – 2005. – p. 142–144.
 Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. – p.125–133, 145–153.Pathophysiology / Edited by prof. Zaporozan. – OSMU. – 2005. – p.125–133, 145–153.
 Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams &
Wilkins), Trade paperback (2003)Wilkins), Trade paperback (2003) // Carol Mattson Porth, Kathryn J. GaspardCarol Mattson Porth, Kathryn J. Gaspard
 Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing.
– 2010. – p. 413-459.– 2010. – p. 413-459.
 General and clinical pathophysiology/ Workbook for medical students and practitioners //General and clinical pathophysiology/ Workbook for medical students and practitioners //
Gozhenko A.I., Makulkin R.F., Gurcalova I.P. [at al.]-Odessa, 2001.- P.203-210.Gozhenko A.I., Makulkin R.F., Gurcalova I.P. [at al.]-Odessa, 2001.- P.203-210.
 Gozhenko A.I. General and clinical pathophysiology/ Study guide for medical studentsGozhenko A.I. General and clinical pathophysiology/ Study guide for medical students
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Copenhagen, 1994.Copenhagen, 1994.
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