2. Plan of the lecture
• Digestion failure, definition, causes,
consequence
• Syndrome of dysphagia
• Secretory and motility disorders of the
stomach
• Peptic ulcer disease, etiology, pathogenesis
• Disturbances of digestion in intestine
• Etiology and pathogenesis of digestion
disorders at pancreatic insufficiency
• Malabsorption syndrome (MAS), etiology,
pathogenesis
4. Digestion failure
is the pathological state when gastrointestinal
system is unable to absorb and digest the food.
Dys’pepsia - Indigestion, impaired digestion
Early satiety (feeling full earlier than expected when eating)
Abdominal fullness
Heartburn (burning)
Bloating (flatulence)
Nausea
Vomiting
Eructation (burp)
Hiccup
Diarrhea
Constipation
Pain
5. Causes of digestion disorders:
Direct damage to DS
• Chemicals (toxins, products of tobacco
smoking, nutritional supplements, alcohol
• Physical (rough food, excessively cold or hot
food, foreign bodies, ionizing radiation
• Biological (microbes, viruses, helminthes)
• Social
• Indirect damage to DS:
Diseases of heart, kidneys, liver,
endocrine system etc.
6. Disease or
condition
Associated GI
Manifestations
Pathogenesis
Hypothyroidism Esophageal
reflux
Constipation
Malabsorption
Lower esophageal sphincter
dysfunction
Intestinal dysmotility
Villous atrophy and
pancreatic insufficiency
Hyperthyroidism Diarrhea and
weight loss
Intestinal hypermotility
with rapid transit and
malabsorption
Diabetes
mellitus
Esophageal,
gastric, small
and large
intestinal and
rectal
dysfunction
Autonomic neuropathy
7. Disease or
condition
Associated GI
Manifestations
Pathogenesis
Primary
hyper-
parathyro-
idism
Nausea and
vomiting
Pancreatitis
peptic ulcer
disease
Hypercalcemia-induced
alteration in signal
transduction resulting in
gastric atony and
dysmotility
Hypercalcemia-induced
premature activation of
pancreatic enzymes
Hypercalcemia-induced
increased acid secretion
Сhronic renal
failure
Abdominal pain,
GI bleeding,
intestinal
perforation
Gastritis, duodenitis,
pancreatitis
8. Disease or
condition
Associated GI
Manifestations
Pathogenesis
Scleroderma Dysphagia, esophageal
reflux, obstruction,
bleeding, perforation,
pseudo-obstruction,
pancreatitis,
malabsorption
Inflammation,
vasculitis, vascular
obliteration,
villous atrophy
Neurologic
disorders
(including spinal
cord injury,
myotonic
dystrophy, CNS
disease)
Impaired gut motility
with nausea, vomiting,
chronic constipation
Disordered central
and enteric
nervous system
communication
9. Syndrome of dysphagia
Dysphagia is difficulty or discomfort in
swallowing, disorders of swallowing
Dysphagia is classified into three major types:
• Oropharyngeal dysphagia
• Esophageal dysphagia.
• Functional dysphagia (disruption of the
coordinated waves of peristaltic contractions
that follow swallowing: nutcracker
esophagus, diffuse esophageal spasm, and
• hypertensive lower esophageal sphincter.)
10. • Damage to the 5th, 9th, or 10th nerve can
cause paralysis of the significant portions of
the swallowing mechanism.
• Poliomyelitis, encephalitis can prevent
normal swallowing center in the brain.
• Malfunction of the swallowing muscles as
occurs in muscle dystrophy or in failure of
neuromuscular transmission in myasthenia
gravis or botulism
• Mechanical obstruction, which can be caused
by strictures or cancer
11. Acha’lasia means "failure to relax."
It is characterized by three major
abnormalities of the esophagus:
1. Incomplete LES relaxation
2. Increased LES tone
3. Aperistalsis
12. Pathogenesis:
dysfunction of in’hibitory neurons
containing nitric oxide and vasoactive
intestinal polypeptide in the distal
esophagus.
Primary achalasia is the result of distal
esophageal inhibitory neuronal
degeneration.
Secondary achalasia may arise from
destruction of inhibitory neurons by
viruses, antibodies.
14. Disorders of gastric secretion
• Hyposecretion is low production of
gastric juice, often is associated with
hypochlorhydria when pH of the gastric
secretion fails to decrease below 6.5,
following maximal stimulation.
Hypochlorhydria means diminished
acid secretion.
• Achylia - partial or complete absence of
gastric juice (HCl and pepsin)
15.
16. Regulation of gastric acid secretion
by nerves and hormones. During the
cephalic phase of digestion, vagal
cholinergic nerves directly stimulate
parietal cells and induce release of
histamine, which also stimulates
parietal cells. Vagal fibers also
release gastrin-releasing peptide
(GRP) in the antrum to induce
gastrin secretion, which is carried in
the bloodstream to induce release of
histamine and stimulate parietal
cells. During the gastric phase of
digestion, food in the stomach
triggers vagovagal reflexes and also
stimulates gastrin secretion.
Acidification of the gastric antrum
stimulates the release of
somatostatin, which inhibits gastrin
release and thus acid secretion.
17. Causes of hyposecretion:
• The decrease in the mass of secretory cells
(Hypo - and atrophic gastritis, malignant
tumors)
• Reduction of n. vagus effects (neuroses or
constitutional sympathicotonia)
• Central nervous system dysfunction
• Reduced gastrin production
• Deficiency of proteins and vitamins in diet
• Drugs, reducing or eliminating the effects of
n. vagus (cholinergic receptors blockers or
activators of cholinesterase)
• Hypothyroidism
18. Consequences of hypochlorhydria are:
• Low activity of pepsin and depressed digestive
capability by the stomach
• Low bactericidic activity of gastric juice
fermentation, rotting
• Rapid chyme evacuation from the stomach into
duodenum (relaxation of py’lorus)
• Decreased secretion of secretin decreased
secretion of pancreatic juice
• Irritation of intestinal receptors by badly digested
food diarrhea
•
• Hypovitaminoses, hypohydration, metabolic and
functional disorders
19. • Hypersecretion of gastric juice is often
associated with hyperchlohydria when pH is
below 1.5
Causes:
• Hereditary increase in parietal cells
• Stimulation of n. vagus
• Stretching the antrum of the stomach
(impaired emptying).
• Hypergastrinemia, Zollinger-Ellison syndrome
• Increased sensitivity of parietal cells to the
action of stimulants
• Insufficient inhibition of acid secretion (deficit
of secretin, somatostatin)
20. Consequences:
• Pylorospasm slow evacuation of the
food mass from the stomach
fermentation in the stomach ulceration
of the mucosa gastro-esophageal reflux
(heartburn)
• Decreased peristalsis constipation
21. Disorders of gastric motility
1. The increase in motor activity (tone
and peristalsis)
Observed at:
• peptic ulcer, gastritis,
• pathological viscero-visceral reflexes
• the increased acidity of gastric juice
• stimulation of n.vagus
• increased secretion of gastrin, motilin,
serotonin, insulin
pain
22. 1. The decrease in motor activity
Observed at:
• postoperative period (postvagotomy
syndrome)
• alimentary dystrophy
• idiopathic gastroparesis, anorexia nervosa
• diabetic neuropathy
• stimulation of sympathetic nervous system
• increasing secretion of secretin,
cholecystokinin, glucagon
23. appearance of heaviness in the
epigastrium after eating.
Stagnation of food masses in the
stomach processes of fermentation
and rotting infectious-toxic lesions
of the digestive tract, digestion disorders
24. Manifestations of motility disorders
Early satiety syndrome
• Is a result of reduced tone and motility
of the antrum. A small amount of food
causes a feeling of heaviness and
fullness of the stomach.
Heartburn is a burning sensation in the
central chest or upper central
abdomen. It is usually due to
regurgitation of gastric acid (gastric
reflux) into the esophagus due to
decreased tone of cardiac sphincter.
25.
26. Eructationn
esophagus
stomach
liver
Small intestine
colon
Burping (also known as
belching, ructus, erupt or
eructation) is the release of gas
from the digestive tract (mainly
esophagus and stomach) through
the mouth, caused by swallowing
air when eating or drinking
SWALLOWING AIR
eructation
10
27. Vomiting is the involuntary, forceful
expulsion of the contents of one's stomach
through the mouth and sometimes the nose.
Pathogenesis:
• excitation of the vomiting center of the
medulla
• reinforced antistalsis of the stomach
• diaphragm and abdominal wall muscles
contraction
• relaxation of the cardia and esophagus
29. Vomiting of Central origin
• Pathological processes in IV ventricle
• Increased intracranial pressure
• Hypertension
• Increased sensitivity of vestibular system (sea and air
sickness – motion sickness, kinetosis)
Toxic vomiting
• Exogenous and endogenous intoxications
Vomiting of visceral origin
• Irritation of the gastric receptors by bacterial toxins,
chemical substances
• Reflectory vomiting due to irritation of the
peritoneum, bile ducts, kidneys, coronary vessels
30. Consequences:
• Aspiration of vomit aspiration
pneumonia
• Dehydration and electrolyte imbalance,
alkalosis
• Repeated or profuse vomiting may
cause erosions to the esophagus
• Destruction of the tooth enamel due to
the acidity of the vomit
31. Gastric dumping syndrome, or rapid
gastric emptying
is a condition where ingested foods pass
through the stomach very rapidly and
enter the small intestine largely
undigested.
32. Pathogenesis:
• Rapid loading of the small intestine with
hypertonic stomach contents rapid entry
of water into the intestinal lumen. Osmotic
diarrhea, distension of the small bowel
(leading to abdominal pain) hypovolemia,
releasing of BAS Systemic vasodilation
arterial hypotension
• Intensive reabsorption of glucose
hyperglycemia
rapid "dumping" of food triggers the pancreas
to release excessive amounts of insulin
hypoglycemia 1,5-2,0 hours after meal
35. • PEPTIC ULCER DISEASE (PUD) refers
to chronic mucosal ulceration affecting
the duodenum or stomach.
36. PEPTIC ULCER DISEASE (PUD) refers to
chronic mucosal ulceration affecting the
duodenum or stomach.
Etiology
• Helicobacter pylori
• Stress
• Mechanical trauma
• NSAIDs
• Alimentary factors
• Tobacco smoking
• Hereditary predisposition
• Asthenic type of constitution
• Blood group (0)
Multiple stress ulcers of
the stomach, highlighted
by dark digested blood
on their surfaces.
37. Damaging
factors
Pathogenesis
Helicobacter
pylori
1. It induces inflammatory and immune
response. There is increased production of pro-
inflammatory cytokines such as IL-1, IL-6, TNF,
IL-8.
2. H.pylori secretes a urease that breaks down
urea to form toxic compounds such as
ammonium chloride and monochloramine,
elaborates phospholipases that damage surface
epithelial cells. Bacterial proteases and
phospholipases break down the glycoprotein-
lipid complexes in the gastric mucus, thus
weakening the first line of mucosal defense.
3.H. pylori enhances gastric acid secretion and
impairs duodenal bicarbonate production, thus
reducing luminal pH in the duodenum.
38. Damaging
factors
Pathogenesis
Helicobacter
pylori
Hyper
secretion of
HCl and
pepsin
4. Several H. pylori proteins are immunogenic, and
they evoke a robust immune response in the
mucosa. Both activated T cells and B cells can be
seen in chronic gastritis caused by H. pylori. T-cell-
driven activation of B cells may be involved in the
pathogenesis of gastric lymphomas.
5.Thrombotic occlusion of surface capillaries is
promoted by a bacterial platelet-activating factor.
Destruction of gastric mucosa
39. NSAIDs Inhibition of cyclooxygenase
decreased prostaglandins synthesis
decreased blood supply
Glucocorticoids
Smoking
Bile acids
Inhibit reparation
Increase sensitivity to adrenalin
ischemia of gastric wall
Decreases the function of pancreas
concentration of bicarbonates in
duodenum
decreases the tone of pylorus
acidity in duodenum
Increases secretion of pepsinogen-1
Increase secretion of gastrin and
histamine, destruct mucus barrier
40. Mucosal defense
mechanisms
Pathogenesis
Mucus and
bicarbonates
prevents large food particles
from directly touching the
epithelium. The mucus
covering also promotes
formation of an "unstirred"
layer of fluid over the
epithelium that protects the
mucosa and has a neutral pH
41. a continuous
layer of gastric
epithelial cells
forms a physical
barrier
limits back diffusion of acid and
leakage of other luminal
materials, including pepsin, into
the lamina propria
Normal
microvasculature
delivers oxygen and nutrients
while washing away acid that has
back-diffused into the
lamina propria.
Prostaglandins stimulate nearly all of the above
defense mechanisms including
mucus, bicarbonate, and
phospholipid secretion, mucosal
blood flow, and epithelial restitution
while reducing acid secretion.
44. Intestinal dyspepsia
• is due to the violation of intestinal functions:
digestive, absorptive, barrier, motor and protective
Causes:
• Disturbances of pancreatic functions
• Disorders of bile production and excretion
• Gastric dyspepsia
• Damage to the intestinal mucosa
46. Causes of Pancreatic Insufficiency.
Primary
A. Acquired decreased enzyme secretion
Chronic pancreatitis
Pancreatic neoplasms
Pancreatic resection
Severe protein-calorie malnutrition, hypoalbuminemia
B. Congenital decreased enzyme secretion (trypsinogen,
enterokinase, amylase, lipase, protease, and 1-antiprotease
deficiency)
Secondary
Intraluminal enzyme destruction
Decreased pancreatic stimulation
Mistiming of enzyme secretion
47. Acute pancreatitis
is reversible pancreatic parenchymal injury
associated with inflammation. It is initiated
by injuries that lead to autodigestion of the
pancreas by its own enzymes.
Causes
Biliary tract disease and alcoholism account
for approximately 80% of cases of acute
pancreatitis in Western countries
48. Acute pancreatitis
is reversible pancreatic parenchymal injury
associated with inflammation. It is initiated
by injuries that lead to autodigestion of the
pancreas by its own enzymes.
49. The following mechanisms protect the
pancreas from self-digestion by its secreted
enzymes:
1. Most digestive enzymes are synthesized as
inactive proenzymes (zymogens), which are
packaged within secretory granules.
2. Most proenzymes are activated by trypsin,
which itself is activated by duodenal
enteropeptidase (enterokinase) in the small
bowel;
3. Acinar and ductal cells secrete trypsin
inhibitors, which further limit intrapancreatic
trypsin activity.
50. Alcohol consumption
increases contraction of the sphincter of Oddi
secretion of protein-rich pancreatic fluid that
leads to the deposition of protein plugs and
obstruction of small pancreatic ducts
direct toxic effects on acinar cells. Alcohol-
induced oxidative stress may generate free
radicals in acinar cells, leading to membrane
lipid oxidation and free radical production,
which is linked to activation of the proinflam-
matory transcription factors API and NF-kB.
51. Oxidative stress also may promote the fusion of
lysosomes and zymogen granules promoting
the intraacinar activation of trypsin and other
digestive enzymes.
Pancreatic duct obstruction
gallstones and biliary sludge, periampullary
neoplasms, parasites intrapancreatic ductal
pressure accumulation of enzyme-rich fluid
in the interstitium. Most pancreatic enzymes
are secreted as inactive zymogens, lipase is
produced in an active form and has the potential
to cause local fat necrosis release
proinflammatory cytokines by myofibroblasts and
leukocytes local inflammation, interstitial
edema ischemic injury to acinar cells.
52. Pancreatic duct obstruction
gallstones and biliary sludge, periampullary
neoplasms, parasites intrapancreatic ductal
pressure accumulation of enzyme-rich fluid
in the interstitium. Most pancreatic enzymes
are secreted as inactive zymogens, lipase is
produced in an active form and has the potential
to cause local fat necrosis release
proinflammatory cytokines by myofibroblasts and
leukocytes local inflammation, interstitial
edema ischemic injury to acinar cells.
53. Reflux of bile or duodenal contents into the pancreatic
duct leads to parenchymal injury; bacterial toxins or free
bile acids travel via lymphatics from the gallbladder to the
pancreas, giving rise to inflammation.
54. Metabolic disorders
hypertriglyceridemia, hypercalcemic states
Hereditary factors (resistance of trypsin to self-
inactivation, hypersensetivity of trypsinogen to
proteolytic activation.
Medications
More than 85 drugs, including furosemide,
glucocorticoids, thiazide diuretics, estrogens,
immunosuppressants, and cancer
chemotherapeutic agents, etc.
55. Traumatic injury of acinar cells
Ischemic injury of acinar cells (shock, vascular
thrombosis, embolism, and vasculitis)
Infections (mumps, HAV, HIV, cytomegalovirus
etc.) direct acinar cell injury
56. Pathogenesis:
1. Pancreatic duct obstruction
2. Primary acinar cell injury
3. Defective intracellular transport of
proenzymes within acinar cells
57.
58.
59.
60. Acute Respiratory Distress Syndrome
(ARDS):
diffuse alveolar damage
ARDS is characterized by
The widespread damage to endothelium
of lung capillaries
The widespread damage to alveolar
epithelium
Development of noncardiogenic
pulmonary edema
61. • Endothelial
activation
• Adhesion and
extravasation of
neutrophils
• Accumulation
of intraalveolar
fluid and
formation of
hyaline
membranes.
• Resolution of
injury
62. • Profound dyspnea and tachypnea herald ARDS
followed by increasing cyanosis and hypoxemia,
respiratory failure, and the appearance of diffuse
bilateral infiltrates on radiographic examination.
Hypoxemia may be refractory to oxygen therapy due to
ventilation perfusion mismatching. Respiratory acidosis
develops. Early in the course, the lungs become stiff
due to loss of functional surfactant.
63. Clinical
Manifestations
Pathogenesis
Pain is
constant and
intense and is
referred to the
upper back and
occasionally to the
left shoulder.
stretching of the pancreatic capsule by distended
ductules and parenchymal edema, inflammatory exudate,
metabolites may come out into the retroperitoneal space,
irritating the peritoneum
Nausea, Vomiting,
and Ileus
Stretching of the pancreatic capsule, increasing
abdominal pain, peritoneal irritation, and electrolyte
imbalance (especially hypokalemia)
Fever extensive tissue injury, inflammation, and necrosis and
release of endogenous pyrogens, principally IL-1
Hyperamylasemia
and
Hyperlipasemia
marked elevation of serum amylase levels during the first
24 hours, followed by a rising serum lipase level by 72 to
96 hours after the beginning of the attack.
Coagulopathy Tissue factor release and expression during proteolysis,
DIC syndrome development
Clinical manifestations
64. Clinical
Manifestations
Pathogenesis
Hyperkalemia
and
Hypokalemia
The initial phase: tissue necrosis, release of large
amounts of K+ into the circulation.
Later, after fluid repletion and correction of acidosis, the
serum K+ may fall to dangerously low levels.
Hyperlipidemia decreased release and activity of the endothelial
and plasma enzyme lipoprotein lipase.
Hyperglycemia
(25% of patients)
It is thought to be related to a decreased release of
insulin by pancreatic islet cells in combination with
increased levels of circulating catecholamines and
glucocorticoids from the adrenal gland.
Jaundice transient common bile duct obstruction, swelling of the
head of the pancreas
Hypocalcemia Lipolysis of the peripancreatic, retroperitoneal, and
mesenteric fat releases free fatty acids that combine with
Ca2+ to form soaps.
65. Chronic pancreatitis is prolonged
inflammation of the pancreas associated
with irreversible destruction of exocrine
parenchyma, fibrosis, and, in the late
stages, the destruction of endocrine
parenchyma.
Causes:
The most common cause of chronic
pancreatitis is long term alcohol abuse.
66. Causes:
• gallstones (cholelithiasis)
• long-standing obstruction of the
pancreatic duct by calculi or neoplasms
• autoimmune injury to the gland
• hereditary pancreatitis (up to 25% of
chronic pancreatitis has a genetic basis)
Pathogenesis
• Reflux of bile or duodenal contents into
the pancreatic duct
• High viscosity of pancreatic juice and
hyperproduction of proteins
67. Pathogenesis
• Dicreased content of Lithostathines (formerly
called pancreatic stone proteins, or PSPs),
peptides secreted into pancreatic juice that
normally inhibit the formation of protein plugs
and the aggregation of calcium carbonate
crystals to form stones. Acinar cell secretion
of lithostathine may be inherited and acquired,
due to alcohol abuse.
• Increased level of lactoferrin, inducing
formation of protein agregates
• Hypercalcemia (Intraductal precipitation of
calcium and stimulation of pancreatic enzyme
secretion )
• Fibrosis as a result of inflammation
68. Proposed Pathogenetic Mechanisms for Chronic Pancreatitis.
"Big duct" mechanisms
Biliary-pancreatic reflux
Sphincter of Oddi obstruction or hypersecretion
Increased ductal permeability
"Small duct" mechanisms
Increased viscosity or hypersecretion of proteins
Increased lactoferrin
Decreased lithostathine (pancreatic stone protein)
Acinar cell mechanisms
Toxic metabolites
Unopposed free radical injury
Hyperstimulation of leukocytes
Lysosomal hyperactivity
Cholinergic hyperactivity
Abnormal protein trafficking
Stellate cell-induced fibrosis
Necrosis-fibrosis sequence
71. Symptoms Pathogenesis
Weight loss (90%) Malabsorption, increased
catabolic processes, anorexia
Steatorrhea (stool fat > 6 g/d) Decreased activity of lipase
Diarrhea
voluminous or bulky, foul-
smelling, greasy, frothy, pale
yellow, and floating feces
Increased osmotic pressure in
the lumen of the intestine,
cathartic action of
hydroxylated fatty acids
Decreased activity of
pancreatic enzymes
Hypocalcemia,
hypophosphatemia, tetany,
osteoporosis,
hypomagnesemia
Vit D deficiency, binding of
dietary calcium with fatty
acids
72. appearance of
muscle fibers in
the feces
Decreased protein digestion
Malabsorption of
vitamin B12
reduced degradation by pancreatic
proteases of the normal complexes of
vitamin B12 and its binding protein (R
protein), resulting in less free vitamin B12
to bind to intrinsic factor in the small
intestine.
73. .
Digestion & Absorption in the Small
Intestine. Malabsorption syndrome
Malabsorption syndrome is characterized
by impaired intestinal absorption of
nutrients especially of fat, proteins,
carbohydrates, vitamins and minerals. It is
the result of disturbance of the normal
digestive functions.
74. MAS is subdivided into 2 groups:
Primary MAS, which is due to, inherited
deficiency of enzymes. The classic example is
lactose intolerance. The inherited deficiency of
disaccharidase is rare but is of great
consequence because in infants it produces
milk intolerance leading to diarrhea, weight
loss.
Secondary MAS, in which mucosal changes
result secondary to such factors as diseases,
surgery, trauma, drugs (gastritis, enteritis,
atrophy of intestinal mucosa, diarrhea,
pancreatic insufficiency).
75. Symptoms and Signs of Malabsorption.
Clinical Features Pathophysiology Laboratory Findings
Diarrhea Increased secretion and
decreased absorption of water
and electrolytes; unabsorbed
fatty acids and bile salts
Increased fat excretion,
"osmotic gap" in stool
electrolytes
Weight loss with
hyperphagia
Decreased absorption of fat,
protein, and carbohydrate
Increased fat excretion
Bulky, foul-smelling
stools
Decreased fat absorption Increased fat excretion
Flatulence Fermentation of carbohydrates
by intestinal bacteria
Increased fat excretion
Decreased D-xylose
absorption
Abdominal pain Small intestinal stricture,
infiltration of the pancreas,
intestinal ischemia
Increased fat excretion
Paresthesias, tetany Decreased vitamin D and
calcium absorption
Hypocalcemia,
hypomagnesemia
Bone pain Decreased calcium absorption Hypocalcemia, increased
alkaline phosphatase
Muscle cramps,
weakness
Excess potassium loss Hypokalemia, abnormal
ECG
76. Symptoms and Signs of Malabsorption.
Clinical Features Pathophysiology Laboratory Findings
Easy bruisability,
petechiae,
hematuria
Decreased vitamin K
absorption
Prolonged
prothrombin time,
increased fat excretion
Hyperkeratosis,
night blindness
Decreased vitamin A
absorption
Decreased serum
carotene, increased fat
excretion
Pallor Decreased vitamin B12 ,
folate, or iron absorption
Macrocytic anemia,
microcytic anemia
Glossitis,
stomatitis,
cheilosis
Decreased vitamin B12 ,
folate, or iron absorption
Decreased serum
vitamin B12 , RBC
folate, or serum iron
Acrodermatitis Zinc deficiency Decreased serum zinc
Muscle wasting,
edema
Decreased protein absorption Decreased serum
albumin
77. Disturbances of intestine motility
Diarrhea. Constipation
Diarrhea is defined as bowel movements that are
excessive in volume, frequency, or liquidity.
Types:
osmotic
secretory
hyperkinetic
exudative
Consequences of diarrhea
dehydration, acidosis, malabsorption.
78. Mechanisms of Diarrhea and Major Specific Causes.1
Mechanisms of
Diarrhea
Specific Causes
Osmotic Disaccharidase deficiencies (eg, lactase deficiency)
Glucose-galactose or fructose malabsorption
Mannitol, sorbitol ingestion
Lactulose therapy
Some salts (eg, magnesium sulfate)
Some antacids (eg, Maalox)
Generalized malabsorption
Malabsorption Pancreatic enzyme deficiency
Pancreatic enzyme inactivation (eg, by excess acid)
Defective fat solubilization (disrupted enterohepatic
circulation or defective bile formation)
Ingestion of nutrient-binding substances
Bacterial overgrowth
Loss of enterocytes (eg, radiation, infection, ischemia)
Lymphatic obstruction (eg, lymphoma, tuberculosis)
79. Mechanisms of Diarrhea and Major Specific Causes.1
Mechanisms of
Diarrhea
Specific Causes
Secretory Enterotoxins
Tumor products (eg, VIP, serotonin)
Laxatives
Bile acids
Fatty acids
Congenital defects
Motility disorder
Hyperkinetic
Diabetes mellitus, hyperthyroidism
stress
Inflammatory
exudation -
exudative
Inflammatory bowel disease
Infection (eg, shigellosis)
80. Constipation – means slow movement of feces
through the large intestine. A frequent cause of
constipation is irregular bowel habits that have
developed through a lifetime of inhibition of the
normal defecation reflexes.
There are two types of constipation: spastic and
atonic.
Spastic constipation occurs at lead poisoning,
administration of certain drugs (Hg, Fe, Ca,), stress
81. Atonic constipation is due to low tone of
intestine. It occurs at the following
conditions:
• low cellular tissue content
• hypokinesia
• obesity
• Vit B1 deficiency (acetylcholine
metabolism disorders)
• Hirschprung’s disease
82. Constipation may be so severe that
bowel movements occur only once
every weak or so, it cause the colon
sometimes to distend to a diameter as
great as 3 to 4 inches. The condition is
called megacolon or Hirschprung’s
disease. The most frequent cause of
megacolon is lack of ganglion cells in
the mesenteric plexus in a segment of
the sigmoid colon.
84. Neurogenic obstruction due to paralysis of
muscularis of the intestine as a result of shock after
abdominal operation or by acute peritonitis.
Vascular obstruction
Obstruction of the superior mesenteric artery or its
branches may result in infarction causing paralysis. The
causes are:
•thrombosis
•Embolism
Consequences
• Marked distention of the intestine proximal to the
obstructed point
• Increased secretion of the fluid and electrolytes into
the lumen
• Severe vomiting
• Hypohydration, electrolyte disorders, shock
• Intestinal intoxication (acute)
85. Intestinal intoxication (acute)
Rotting and fermentation within intestine
high level of poisons in blood (kadaverin, putriscin, indol,
skatol, phenols) direct and reflectory injury to organs
and systems.
• Low blood pressure
• Low pain sensitiveness
• Low heart contractility
• Inhibition of brain cortex
Chronic intestinal intoxication head ache,
myocardial dystrophy, anemia, anorexia,
impairment of digestion and absorption
Coma
