peptic ulcer disease - russian state medical...
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Peptic ulcer disease
Bogush N.L.
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Definition
Peptic ulcer disease (PUD) -
it is a chronic intermittent and recurrent
disease with a defect in the mucosa of
stomach or duodenum that extends through
the muscularis mucosa into the submucosa
or deeper.
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Symptomatic ulcers
A breach in the mucosa arise:
• By stress
• By intake of some medical drugs
• As complications at:
Cushing disease, Wakesa disease, leukemias,
diabetes mellitus, chronic diseases of the liver,
kidneys, brain, atherosclerosis.
• By Zollinger-Ellison syndrome
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Etiology of PUD
Theories:
• 1. Mechanical (Ashoff)
• 2. Inflammatory
• 3. Vascular (Virchov)
• 4. Peptic, autodigestion (Quinke)
• 5. Cortex-visceral
• 6. Infectious
• 7. Inherited
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Outward signs of hereditary
predisposition
• 1. Asthenic constitution
• 2. Blond hair
• 3. Blue eyes
• 4. Hand type – radial, foot type –
intermediate
• 5. Blood type – 0 (I), Rh “-”.
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Hereditary predisposition
Such persons can have:
- level of maximal HCl secretion,
- content of pepsinogen I in the serum,
- gastrin secretion after meal
+
glycoproteins (GAG) in the mucus
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Pathogenesis of PUD
• PUD arises as an imbalance between local
gastroduodenal protective mechanisms and
the aggressive damaging factors (exogenous
and endogenous).
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I. Local protective mechanisms
• 1. The mucosa (with the mucus)
• 2. The mucus
• 3. The mechanism of antro-duodenal
inhibition or damping, that HCl secretion
• 4. Intensive blood circulation
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Protective features of the mucus
• 1. A gel-like mucus film with thickness 0,1-0,5
mm thick.
• 2. Protects from mechanical injury.
• 3. Compounds:
acid GAG – fucose; neutral GAG –
N-acetylneuraminic acid (salic acid) = NANA.
• 4. Can’t be digested by pepsin.
• 5. Prevents direct contact of the juice, acid with
the epithelium.
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Protective mechanisms of the mucosa -1
• 1. A mucus production.
• 2. Tight cells junctions (keep H+ in the lumen).
• 3. Bicarbonate production ( HCl within mucosa).
• 4. Prostaglandin E production.
• 5. Synthesis of IgA antibodies (due to plasma
cells).
• 6. High ability of regeneration important for
epithelial repair and wound healing.
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Epithelial repair and wound healing.
• Healing of light epithelial arrosion – through
sideward epithelial cells migration along the basal
membrane. Takes 30 min.
• Healing of more deep defects – through
proliferation, which takes more time. Growth
factors are: EGF-like growth factor, TGF, IGF-1,
gastrin-releasing peptide.
• Healing of big defects – through the inflammation.
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Protective mechanisms of the mucosa -2
• 7. Intensive blood circulation (sympathetic N.S.).
• 8. Many mast cells – regulate the blood flow.
• 9. Antro-duodenal inhibitory reflex – regulates
HCl production: pH in antrum to 2-2,5 or pH in
duodenum to 4,0 inhibition of HCl secretion.
• 10. Neuro-endocrine regulation of gastric juice
secretion: synthesis of gastrin, secretin,
somatostatin; innervation with n.vagus endings.
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Protective role of prostaglandins E2 and I2.
• 1. Stimulate the mucus synthesis.
• 2. They synthesis of GAG (mucopolysaccharides) and hydrophobic properties of the mucus.
• 3. They synthesis of bicarbonates.
• 4. They intensity of the blood flow.
• 5. They HCl secretion.
So, they act as potent gastroprotectors.
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II. Endogenous damaging
factors.
• 1. Acid-peptic factor.
• 2. Motordisfunction of stomach and
duodenum.
• 3. Disorders of neuro-humoral regulation
(n.vagus).
• 4. Disorders of cells and humoral immunity.
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The STOMACH
Esophagus
Cardia
Fundus
Parietal cells (H+)
Body
Chief cells (pepsin)
Duodenum
Pyloric
canal
Pylorus Antrum
G-cells
(gastrin)
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Carbonic anhydrase
CO2 HCO3¯ Cl¯
H20
Diffusion
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Ach
M1-r
M2-r Ach
G-cell
Hist prod.
cell
Parietal
cell
Ganglion
Intramural
neuron
G-r
gastrin
H2-r
Histamin
Ca++
H+
Ach –acetylcholin;
r - receptor
Stimulators of HCl secretion
Proton
pump
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Functions of the stomach .
• 1. Reservoir
• 2. Secretory
• 3. Motility
• 4. Evacuatory
• 5. Excretory
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Morfofunctional types of gastric secretion.
• 1. Normal – N HCl and pepsin in gastric
juice.
• 2. Hyperchlorhydremic - HCl, N pepsin.
• 3. Hyperpepsinogenic – N HCl, pepsin.
• 4. Pyloric - HCl, pepsin.
• 5. Hypochlorhydremic - HCl, N pepsin.
• 6. Hypopepsinogenic – N HCl, pepsin.
• 7. Achylic - HCl, pepsin.
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Gastric juice secretion.
During an intubation 3 portion of the juice:
I portion – the juice from the empty stomach.
II portion – juice secretion as a response on the tube mechanical irritation – the basal secretion. Depends from neuro-humoral regulation!
III portion - juice secretion as a response on chemical stimuli: injection of histamin or pentagastrin. Depends from amount of the parietal cells (hereditary).
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Regulation of gastric juice
secretion.
• The stimulators are: n. vagus tonicity,
gastrin, histamin, glucocorticoids,
parathyroid hormone, bombesin,
enkephalins…
• The inhibitors are: mineralcorticoids,
sectretin, glucagon, somatostatin…
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Proteolytic activity of gastric
juice
The coefficient of proteolytic activity =
PEPSIN â (active)
common PEPSIN - PEPSIN â
= 0,3
The high concentration of H+ activates
pepsinogen into pepsin.
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Acid-peptic factor – harmful action of
gastric juice.
1.Pathogenesis of ulcer at HCl hypersecretion.
HCl damage of mucosal barrier back
diffusion of H+ damage of endothelium
in the vessels occlusion of vessels
ischemia necrosis + pepsin action
fixation of the damage the ulcer.
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2. Motordisfunction of the stomach and the
duodenum
• motor activity of the stomach rapid evacuation of acid contents duodenal ulcer(?)
• motor activity of the stomach long contact of stomach mucosa with acid contents stomach ulcer(?)
• The duodenal-gastric reflux, backward flow bile acids with lysolecitin appear in the stomach removing of mucus, epithelium damage stomach ulcer(?), mucous cells metaplasia (precancerous condition).
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III. External damaging factors.
• 1. Nutritional factors.
• 2. Harmful, pernicious habits.
• 3. Helicobacter pylori.
• 4. Medicine.
• 5. Stress.
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1.Nutritional factors.
• 1. Irregular meal fasting hypersecretion.
• 2. Starvation fasting hypersecretion, stress, negative nitrogen balance and bad mucosa regeneration.
• 3. Irritating food – spicy food, fruit juices, coffee, beer, wine…. gastric juice hypersecretion.
• 4. Empty stomach or refined products in the meal bad gastric juice absorption and HCl neutralization.
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2. Harmful, pernicious habits.
• 1. Smoking blood flow, HCl-
secretion, motility, bicarbonate
secretion, Prgl E synthesis and mucosal
regeneration.
• 2. Alcohol intake moderate drinking of
wine and beer HCl-secretion, gastrin
production; alcohol in large quantities or in
high concentration damages the mucosa.
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3. Helicobacter pylori (HP).
S-shaped gram “-” rod, lives under mucus. It has: 1) enzyme UREASE that produce NH3 from the urea, which defends the rod from HCl (+ C02, HCO3); 2) enzyme CATALASE which defends the rod from phagocytes.
HPs produce from the urea the toxic monochlora-mine; secret toxic lipases, proteases, phospho-lipases, produce toxic oxygen radicals and destroy the mucus and cells; excrete CO2 meteorism;
stimulate chemotaxis and secretion of Il-1, IL-6, Il-8, TNF; HCl-secretion; thrombus formation.
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4. Medicine.
Aspirin, NSAiDs Prgl synthesis, bicarbonate
secretion, mucus formation +damage the
mucosa locally by nonionic diffusion into the
mucosal cells.
Reserpin Histamin secretion and so HCl
secretion.
Catecholamines spasm of vessels and ischemia.
Glucocorticoides HCl secretion, mucus
formation, regeneration, food evacuation.
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5. Stress.
STRESS
Hypothalamus vegetative N.S.
ACTH cortisol vagus+symphat N.S.
Acch + Norepin
HCl, pepsin ( gastrin, histamin)
blood flow, regeneration
mucus formation; motordisfunction
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Principles of Phatogenetic Therapy –1.
• The diet. Refuse from harmful habits.
• activity of acid-peptic factor: blockers of
1) M2-cholinoreceptors = cholinolytics; 2) gastrin
receptors; 3) H2-histamin receptors; 4) blockers of
proton pump; 5) antacids (HCl).
• growth of HP: 1) AB; 2) metronidasol; 3) drugs
with bismuth.
• Immunocorrectors.
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Principles of Phatogenetic Therapy –2.
• Cell protectors: 1) drugs that defensive
mucus layer = polysaccharides + sulfur; 2)
drugs that mucus secretion = Prgl E.
• Sedatives.
• Analgetics.
• Surgery.
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The dumping syndrome -1.
A stump from the stomach reservoir and motility function.
A meal I. Too rapid emptying distension + mechanical irritation of the gut (the pieces of food > 2 mm) nausea, bloating, flushing, pain in the abdomen; hypertonicity of chyme - H2O secretion and diarrhea; activation of kallikrein-kinine system (dilation of mesenterical vessels + their permeability) CBV activation of sympathetic N.S. ( catecholamines) cardiovascular reactions: palpitation,weakness...
[ 30-60 min after food intake – early D.S.]
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The dumping syndrome -2.
II. glucose in the blood (especially when
sugar is in the food) secretion of
insulin 90-180 min after food intake
hyperglycemia changes into hypoglycemia:
confusion, loss of consciousness – late D.S.
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