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Welcome
Pc:-Waking up at night
with Upper
abdominal pain
or upper abdominal
pain that
improves with eating ?
PEPTIC ULCER DISEASE
By
Dr.Shubhanshi Bhasin
(BHMS)
Learning Objectives
• On completion of this lecture participants will be
able to:
• Recognize the typical clinical presentation and
risk factors for peptic ulcer disease
• Understand pathophysiology of PUD focusing
on H. pylori
• Describe an appropriate diagnostic plan based
on individual risk factors
• Prescribe an appropriate therapeutic regimen
Peptic Ulcer Disease
DEFINITION
• Break in the gastrointestinal mucosa exposed to
the aggressive action of acid peptic juices.
• An ulcer in the lining of the stomach,duodenum,
or esophagus.
• OPEN SORES ARE CALLED ULCERS AND THE WORD
PEPTIC MEANS THAT ACID IS THE CAUSE OF
ULCERS
• Gastric
• Duodenal
GASTRIC MUCOSAL DEFENCE
MECHANISMS
• SEVERAL MUCOSAL DEFENCE MECHANISM
PROTECT THE GASTRIC MUCOSA AGAINST
ACID AND NOXIOUS AGENTS
• MAINLY A THREE-TIER SYSTEM OPERATES :
• 1. PRE EPITHELIAL PROTECTION IS PROVIDED BY
THE MUCUS-BICARBONATE BARRIER.
• MUCUS AND BICARBONATE , SECRETED BY MUCUS
CELLS IS AN ACTIVE PROCESS UNDER VAGAL
INFLUENCE
• IT MAINTAINS A NEUTRAL pH AT THE EPITHELIAL
SURFACE
• 2. AT THE EPITHELIAL LEVEL THE SURFACTANTS,
NON PROTEIN –SH, RAPID CELL TURN OVER AND
THE PROCESS OF RESTITUTION PLAY THE ROLE IN
KEEPING THE INTEGRITY OF INTACT EPITHELIUM
• 3. IN SUB EPITHELIAL LEVEL PROSTAGLANDINS
AND MUCOSAL BLOOD FLOW KEEPS THE MUCOSA
HEALTHY AND HELPS IN DISPOSAL OF HYDROGEN
IONS AND NOXIOUS AGENTS.
MECHANISM OF INJURY
• DIRECT MUCOSAL DAMAGE DUE TO TOXINS ,ETHANOL,
NSAIDS, BILE, AND H.PYLORI
• WHEN WE CONSIDER THE PEPTIC ULCER DISEASE OF
STOMCH IT IS ACTUALLY NOT DUE TO EXCESS ACID
PRODUCTION.
• STOMACH LINING IS EFFECTIVELY PROTECTED
NATURALLY FROM THE ACID ATTACK BY THE
BICARBONATES AND PROSTAGLANDINS.
• HOWEVER THIS NATURAL PROTECTION OFFERED BY
THE PROSTAGLANDINS IS OFTEN
• COMPROMISED WHEN NSAIDS INHIBIT THE
PRODUCTION OF PGs THROUGH COX PATHWAY.
• STEROIDS KNOCK OUT THE PHOSPHOLIPASE A2
THEREBY BLOCK THE PGs PRODUCTION
• WHEN THE BILE REGURGITATES BACK INTO THE
STOMACH IT MAY CAUSE DAMAGE TO THE STOMACH
LINING
H.PYLORI RESIDING AT THE ANTRUM OF THE
STOMACH IS CAPABLE OF SPLITTING UREA INTO
AMMONIA WITH THE HELP OF THE ENZYME
UREASE
AT SOME POINT OF TIME THE BACTERIA CAN BURROW INTO THE
LINING OF STOMACH AND WEAKEN THE LINING WHERE THE ACID
CAN PRODUCE FURTHER DAMAGE RESULTING PEPTIC ULCER
DISEASE .
INCREASED ACID PRODUCTION IS THE MAJOR
CAUSE OF PEPTIC ULCERATION IN THE DUODENAL
MUCOSA
MUCOSAL ISCHAEMIA IS ALWAYS A POSSIBILITY
WHICH CAN COMPROMISE THE INTEGRITY OF
MUCOSAL LINING OF STOMACH AND DUODENUM
THEREBY LEADING TO EROSIONS AND ULCERATIONS
• H. Pylori Infection
• NSAIDs
• Smoking & Alcohol
• Acid Hypersecretion
• Stress
• Family History of PUD.
The gastroduodenal
mucosal integrity is
determined by
protective (defensive) &
damaging (aggressive)
factors
Defensive
• Bicarbonate
• Mucus layer
• Prostaglandins
• Mucosal blood flow
• Epithelial renewal
Aggressive
• Helicobacter pylori
• NSAIDs
• Pepsins
• Bile acids
• Smoking and alcohol
Mucosal damage erosions & ulcerations
EPIGASTRIC PAIN,NAUSEA AND EMESIS
GI BLEEDING:
 MELENA,
• HAEMATEMESIS,HEMATOCHEZIA,
IRON DEFICIENCY ANEMIA
 PERFORATION POSTERIORLY INTO THE
PANCREAS (ONLY GASTRIC ULCERS)
• GASTRIC OUTLET OBSTRUCTION DUE TO
PERIPYLORIC SCAR FORMATION
• GASTRIC ULCERS MAY BE MALIGNANT
WHILE DUODENAL ULCERS ARE NOT
Symptoms
• POST PRANDIAL EPIGASTRIC PAIN,
• EPIGASTRIC PAIN THAT AWAKENS THE
PATIENT AT NIGHT,
• “HEART BURN” THAT DOESN’T RESPOND
TO ANTACIDS,
ALARM SYMPTOMS
• HISTORY: FREQUENT NSAID USE.
• ROUGHLY EQUAL BETWEEN MEN AND
WOMEN
ALARM SYMPTOMS
• WEIGHT LOSS OF MORE THAN 10% IN 3
MONTHS
• ANEMIA
• HEME POSITIVE STOOL OR HAEMATEMESIS
• EARLY SATIETY
• ODYNOPHAGIA OR DYSPHAGIA
• OLDER THAN AGE 45 YEARS
• ABNORMAL PHYSICAL EXAMINATIONS
Duodenal Ulcer Gastric ulcer
Age Any age specially 30-40 middle age 50-60
Sex More in male More in male
Occupation Stress job eg. Manager Same
Pain Epigastric , discomfort Epi. Can radiate to
back
Onset 2-3 hours after eating &
midnight
Immediately after
eating
Agg.by Hunger Eating
Relived by Eating Lying down or vomiting
Duodenal Ulcer Gastric ulcer
Duration 1-2 months Few weeks
Vomiting Uncommon Common(to relieve the
pain)
Appetite Good , eat to relieve the pain Pt. afraid to eat
Avoid fried food
Weight No wt. loss wt. Loss
Hematemesis 40% 60%
Melena 60% 40%
Gastric and Duodenal Ulcers
GASTRIC ULCER
• Pain occurs 1-2 hours after meals
• Pain usually does not wake patient
• Accentuated by ingestion of food
• Risk for malignancy
• Deep and penetrating and usually
occur on the lesser curvature of
the stomach
Duodenal Ulcers
• Pain occurs 2-4 hours after
meals
• Pain wakes up patient
• Pain relieved by food
• Very little risk for malignancy
 Lifestyle
•Smoking
•Acidic drinks
•Medications
H. Pylori infection
•90% have this bacterium
•Passed from person to person (fecal-oral route or
oral-oral route)
Age
• Duodenal 30-50
• Gastric over 60
Gender
•Duodenal: are increasing
in older women
Other factors:
stress can worsen but not the
cause
Stool fecal occult blood
CBC CBL
Rapid Urease test,
urea breath test H. Pylori
Upper GI Endoscopy
Barium meal X-Ray.
Any patient >50 y/o with new
onset of symptoms
In all patients with “Alarming
symptoms” endoscopy is required.
Dysphagia.
Weight loss.
Vomiting.
Anorexia.
Hematemesis or Melena.
Homoeopathic Medicines used for
treatment
• 1. Argentum nit—Small spot between
xyphoidnaval sensitive to pressure; pain radiate
in all directions. Gnawing, ulcerative pain is
epigastrium.
• Pain below and to the left of the xyphoid process
in a small spot extending to a corresponding
point in spine, where pressure aggravates it.
• Looks as if dying .
2.Hydrastis—Vomits all she eats, expect
milk and water mixed. Backache (maybe
severe); Tired aching across small of
back.Excessive sweat of armpits and
genitalia which is offensive. Sinking, gone
feeling in stomach and Obstinate
constipation.
3.Ignatia—Pain is located in a small
circumscribed spot, relief from eating. Pains
may appear gradually and subside suddenly;
or appear as suddenly as they disappear.
4.Lycopodium—Yellowish-gray color of face.
Pit of stomach swollen and sensitive to touch.
Aching in stomach in evening and after eating.
5.Arsenic alb—Great prostration and weakness:
Restlessness with tossing about.
Vomiting is present immediately after eating or
drinking and Great burning in the stomach.
6.Carbo veg—Burning in the stomach spreading
down to small back and up to the shoulders. Pain
paroxys¬mal, takes away the breath. Vomiting of sour
bloody masses. Ameliorates from cold drink.
Peptic ulcer disease by dr shubhanshi

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Peptic ulcer disease by dr shubhanshi

  • 2. Pc:-Waking up at night with Upper abdominal pain or upper abdominal pain that improves with eating ?
  • 4. Learning Objectives • On completion of this lecture participants will be able to: • Recognize the typical clinical presentation and risk factors for peptic ulcer disease • Understand pathophysiology of PUD focusing on H. pylori • Describe an appropriate diagnostic plan based on individual risk factors • Prescribe an appropriate therapeutic regimen
  • 6. DEFINITION • Break in the gastrointestinal mucosa exposed to the aggressive action of acid peptic juices. • An ulcer in the lining of the stomach,duodenum, or esophagus. • OPEN SORES ARE CALLED ULCERS AND THE WORD PEPTIC MEANS THAT ACID IS THE CAUSE OF ULCERS • Gastric • Duodenal
  • 8. • SEVERAL MUCOSAL DEFENCE MECHANISM PROTECT THE GASTRIC MUCOSA AGAINST ACID AND NOXIOUS AGENTS • MAINLY A THREE-TIER SYSTEM OPERATES : • 1. PRE EPITHELIAL PROTECTION IS PROVIDED BY THE MUCUS-BICARBONATE BARRIER. • MUCUS AND BICARBONATE , SECRETED BY MUCUS CELLS IS AN ACTIVE PROCESS UNDER VAGAL INFLUENCE • IT MAINTAINS A NEUTRAL pH AT THE EPITHELIAL SURFACE • 2. AT THE EPITHELIAL LEVEL THE SURFACTANTS, NON PROTEIN –SH, RAPID CELL TURN OVER AND THE PROCESS OF RESTITUTION PLAY THE ROLE IN KEEPING THE INTEGRITY OF INTACT EPITHELIUM • 3. IN SUB EPITHELIAL LEVEL PROSTAGLANDINS AND MUCOSAL BLOOD FLOW KEEPS THE MUCOSA HEALTHY AND HELPS IN DISPOSAL OF HYDROGEN IONS AND NOXIOUS AGENTS.
  • 9. MECHANISM OF INJURY • DIRECT MUCOSAL DAMAGE DUE TO TOXINS ,ETHANOL, NSAIDS, BILE, AND H.PYLORI • WHEN WE CONSIDER THE PEPTIC ULCER DISEASE OF STOMCH IT IS ACTUALLY NOT DUE TO EXCESS ACID PRODUCTION. • STOMACH LINING IS EFFECTIVELY PROTECTED NATURALLY FROM THE ACID ATTACK BY THE BICARBONATES AND PROSTAGLANDINS. • HOWEVER THIS NATURAL PROTECTION OFFERED BY THE PROSTAGLANDINS IS OFTEN • COMPROMISED WHEN NSAIDS INHIBIT THE PRODUCTION OF PGs THROUGH COX PATHWAY. • STEROIDS KNOCK OUT THE PHOSPHOLIPASE A2 THEREBY BLOCK THE PGs PRODUCTION • WHEN THE BILE REGURGITATES BACK INTO THE STOMACH IT MAY CAUSE DAMAGE TO THE STOMACH LINING
  • 10. H.PYLORI RESIDING AT THE ANTRUM OF THE STOMACH IS CAPABLE OF SPLITTING UREA INTO AMMONIA WITH THE HELP OF THE ENZYME UREASE AT SOME POINT OF TIME THE BACTERIA CAN BURROW INTO THE LINING OF STOMACH AND WEAKEN THE LINING WHERE THE ACID CAN PRODUCE FURTHER DAMAGE RESULTING PEPTIC ULCER DISEASE . INCREASED ACID PRODUCTION IS THE MAJOR CAUSE OF PEPTIC ULCERATION IN THE DUODENAL MUCOSA MUCOSAL ISCHAEMIA IS ALWAYS A POSSIBILITY WHICH CAN COMPROMISE THE INTEGRITY OF MUCOSAL LINING OF STOMACH AND DUODENUM THEREBY LEADING TO EROSIONS AND ULCERATIONS
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  • 12. • H. Pylori Infection • NSAIDs • Smoking & Alcohol • Acid Hypersecretion • Stress • Family History of PUD.
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  • 14. The gastroduodenal mucosal integrity is determined by protective (defensive) & damaging (aggressive) factors
  • 15. Defensive • Bicarbonate • Mucus layer • Prostaglandins • Mucosal blood flow • Epithelial renewal Aggressive • Helicobacter pylori • NSAIDs • Pepsins • Bile acids • Smoking and alcohol Mucosal damage erosions & ulcerations
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  • 19. EPIGASTRIC PAIN,NAUSEA AND EMESIS GI BLEEDING:  MELENA, • HAEMATEMESIS,HEMATOCHEZIA, IRON DEFICIENCY ANEMIA  PERFORATION POSTERIORLY INTO THE PANCREAS (ONLY GASTRIC ULCERS) • GASTRIC OUTLET OBSTRUCTION DUE TO PERIPYLORIC SCAR FORMATION • GASTRIC ULCERS MAY BE MALIGNANT WHILE DUODENAL ULCERS ARE NOT
  • 20. Symptoms • POST PRANDIAL EPIGASTRIC PAIN, • EPIGASTRIC PAIN THAT AWAKENS THE PATIENT AT NIGHT, • “HEART BURN” THAT DOESN’T RESPOND TO ANTACIDS, ALARM SYMPTOMS • HISTORY: FREQUENT NSAID USE. • ROUGHLY EQUAL BETWEEN MEN AND WOMEN
  • 21. ALARM SYMPTOMS • WEIGHT LOSS OF MORE THAN 10% IN 3 MONTHS • ANEMIA • HEME POSITIVE STOOL OR HAEMATEMESIS • EARLY SATIETY • ODYNOPHAGIA OR DYSPHAGIA • OLDER THAN AGE 45 YEARS • ABNORMAL PHYSICAL EXAMINATIONS
  • 22. Duodenal Ulcer Gastric ulcer Age Any age specially 30-40 middle age 50-60 Sex More in male More in male Occupation Stress job eg. Manager Same Pain Epigastric , discomfort Epi. Can radiate to back Onset 2-3 hours after eating & midnight Immediately after eating Agg.by Hunger Eating Relived by Eating Lying down or vomiting
  • 23. Duodenal Ulcer Gastric ulcer Duration 1-2 months Few weeks Vomiting Uncommon Common(to relieve the pain) Appetite Good , eat to relieve the pain Pt. afraid to eat Avoid fried food Weight No wt. loss wt. Loss Hematemesis 40% 60% Melena 60% 40%
  • 25. GASTRIC ULCER • Pain occurs 1-2 hours after meals • Pain usually does not wake patient • Accentuated by ingestion of food • Risk for malignancy • Deep and penetrating and usually occur on the lesser curvature of the stomach
  • 26. Duodenal Ulcers • Pain occurs 2-4 hours after meals • Pain wakes up patient • Pain relieved by food • Very little risk for malignancy
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  • 28.  Lifestyle •Smoking •Acidic drinks •Medications H. Pylori infection •90% have this bacterium •Passed from person to person (fecal-oral route or oral-oral route) Age • Duodenal 30-50 • Gastric over 60 Gender •Duodenal: are increasing in older women Other factors: stress can worsen but not the cause
  • 29. Stool fecal occult blood CBC CBL Rapid Urease test, urea breath test H. Pylori Upper GI Endoscopy Barium meal X-Ray.
  • 30. Any patient >50 y/o with new onset of symptoms In all patients with “Alarming symptoms” endoscopy is required. Dysphagia. Weight loss. Vomiting. Anorexia. Hematemesis or Melena.
  • 31. Homoeopathic Medicines used for treatment • 1. Argentum nit—Small spot between xyphoidnaval sensitive to pressure; pain radiate in all directions. Gnawing, ulcerative pain is epigastrium. • Pain below and to the left of the xyphoid process in a small spot extending to a corresponding point in spine, where pressure aggravates it. • Looks as if dying .
  • 32. 2.Hydrastis—Vomits all she eats, expect milk and water mixed. Backache (maybe severe); Tired aching across small of back.Excessive sweat of armpits and genitalia which is offensive. Sinking, gone feeling in stomach and Obstinate constipation. 3.Ignatia—Pain is located in a small circumscribed spot, relief from eating. Pains may appear gradually and subside suddenly; or appear as suddenly as they disappear.
  • 33. 4.Lycopodium—Yellowish-gray color of face. Pit of stomach swollen and sensitive to touch. Aching in stomach in evening and after eating. 5.Arsenic alb—Great prostration and weakness: Restlessness with tossing about. Vomiting is present immediately after eating or drinking and Great burning in the stomach. 6.Carbo veg—Burning in the stomach spreading down to small back and up to the shoulders. Pain paroxys¬mal, takes away the breath. Vomiting of sour bloody masses. Ameliorates from cold drink.