peptic ulcer disease diagnosis and treatment.pdf

Pud

1. 1
Lecturer :Dr.mazullahZahid (internal medicine specialist )
Subject : internal medicine (GIS and nephrology )
Semester : 10
th
University : bost
لاسا ناتسناغفادتلود يروهمج يم
ترازو وړک هدز وړولد
نوتنهوپ تسب
يځنهوپ بط
Dr.maullah zahid

2. Dr.maullah zahid 2
•Disease of esophagus
•Gastritis
•PUD
•Complication of PUD
•ZES
•IBS
•IBD
•Gastric cancer
•Disease of liver
•Disease GB
•Disease of pancreases
Outline
•UTI
•Nephritic syndrome
•Nephrotic syndrome
•Good posture
syndrome
•Post streptococcus GN
•Minimal change
disease
•Acute renal failure
•Chronic renal failure

3. 3
•Definition :
•Peptic ulcer :یلاوخارپ یچ ییاو هت ودیک یریڅ یقبط یطاخمد رشعانثا وا یدعمد
یو یروپ یدنلا ازوکویمرت یی یلاوروژوا تایز هخڅورتم یلموځنپد یی
•ب هپ یقبط یطاخمرشعانثا وا یدعمد هلما هل یریتو یباهتلاد هک ترابع لب هپ ای لوډ هړپش
د یسړلاو هځنم هلpeptic ulcer یږیدای همان هپ
•Erosion :ک مویلیت یپا هپ یقبط یطاخمد یزاوی هندیړاجیو یچ ییاو هت تلااح هغه ی
یو
Characters :
oEpigastric burning pan
Peptic ulcer (PU)
Dr.mazullah zahid

4. 4
Stomach :more then 90% of gastric ulcer occur in the lesser
curvature
Duodenum :90-95% of duodenal ulcer occur the first portion of
duodenum
Esophagus: in efflux esophagitis
Jejunum : in zollinger-elisonsyndrome
Location of ulcer
Dr.mazullah zahid

5. 5
•500000 American people new cases per year
•Decrease range of peptic ulcer with treatment in 50% in last 30years
•Decrease recurrence with treatment
•Increase range of duodenal ulcer to gastric ulcer 5:1
•95% common in pyloric channel
•Duodenal ulcer increase 30-55years more in female 1,3 :1
•Gastric ulcer increase in 55-70 years more in male
Epidemiology :
Dr.mazullah zahid

6. 6
 یدعمد هخڅ ورجحد یغهد یچ یوس لښوپ هطساوپ هپ مویلیت یپا هراد فورد هدعم
یوسړوج تاودغ
 یرل یرجح ینیارکودناوا یطاخم تاودغ هغد
Fundus and antrum : parietal cell : secretion HCL and IF
Body : chief cell : secretion pepsinogen
Antrum : G cell : secretion gastrin
D cell : somatostatin
Mucus cell : mucus
Important secretion of stomach : HCL and pepsinogen
Physiology of stomach
Dr.mazullah zahid

7. 7
Cephalic phase :
1.Visual of food
2.Smell of food
3.Taste of food
Gastric phase :this phase of two mechanism
When food inter to stomach
amino acid of Food can secretion of gastrin
Duodenal phase :
•When food enter to intestine this can stretch and distension of
intestine
Stage of HCL secretion
Dr.mazullah zahid

8. 8Dr.mazullah zahid

9. 9
Endogenous factors :
1.HCL
2.Pepsin
3.Pepsinogen
4.Bile salt
Exogenous factors:
Drugs
Alcohol
Bacteria
Smoking
Destruction factors of gastric and duodenum
Dr.mazullah zahid

10. 10
Free epithelial :
1.Mucus
2.Bicarbonate
3.phospholipid
د هخرب ادHCL واpepsin یوک یولق ریالیپاچ وا یوک یوینخم هخڅ نژوفید ایبد
Stimulant factor of bicarbonate secretion : calcium , prostaglandin ,
cholinergic nerve and acid
Inhibitor of bicarbonate :NASIDs
Defensive and repairing system of mucus
membrane
Dr.mazullah zahid

11. 11
Epithelial
Increase cellular resistant
Prevention of HCL diffusion by mucus surpece
Repairing : by stomach epithelium
Growth factors :secretion of GH factors for increasing epithelial cell
Angiogenesis
Increase epithelial tissue in effect area
Prostaglandin :function of prostaglandin
1.Stimulation of mucus and bicarbonate
2.Increase blood flow of mucus
3.Inhibition of HCL secretion
4.Increase repairing of epithelial cell
Con…
Dr.mazullah zahid

12. 12Dr.mazullah zahid

13. 13
Sub epithelial :
هراپل یدد یږیتایز ریهب ینیود یک ازوکویم بس هپ یدنلا طاخمد
Increase bicarbonate
Increase supply of effect area
Increase oxygen delivery to effect area
Removing of toxic agent from effect
Con…
Dr.mazullah zahid

14. 14
Helicobacter pylori and peptic ulcer
NSAIDs and peptic ulcer
Cigarette smoking
Hereditary
Resistant of mucus membrane about HCL and pepsin
Psychological pressure
Foods
Chronic disease
Etiology of peptic ulcer
Dr.mazullah zahid

15. 15
•It is a gram negative bacteria
•It has Flagel and movement
•Live between mucus membrane and epithelial layer
Epidemiology :
1.Seen in every age but increase in old age
2.In poor country patient 90% infection take in child age
3.90% duodenal ulcer patient has H-Pylori
4.70% gastric ulcer patient has H-pylori
5.30% gastric ulcer due to NSAIDs
Helicobacter pylori and peptic ulcer
Dr.mazullah zahid

16. 16
Poor economic condition
Low education level
Increasing delivery of new born in poor developmental country
Poor hygiene
Drink of unclean water
Touch with effected patient stomach contain
Rout of transmission :
•Fecooral
•oral
Predisposing factor for H-pylori
Dr.mazullah zahid

17. 17
Belong to two factors bacterial and host factors
Bacterial factors:
Pathogen virulence factor :vaculatingcytotoxin–A ( VaCA)
Cytotoxinassociated gen (Cag-A)
Urease : bacteria producing ammonia by urease enzyme
یړک یولق هراپد ودیسواد ریالیپاچ اوخواش لپخ ناتناوڅرت
Superficial factors :
ح لیلیت یپاوڅرت یومک زیساتسومیکورجح تیاسونوموا لیفورتندروتکفاد ینمزیغا یرج
یړک
Pathogenesis and pathophysiology
Dr.mazullah zahid

18. 18Dr.mazullah zahid

19. 19Dr.mazullah zahid

20. 20
Adherence :
یولښن ناځ یروپورجح لیلیت یپاد هطساوپ یدد
Protease and phospholipase :
یوک یریڅ ړوپ یمحشوا نیتورپوکیلاګد
Con…
Dr.mazullah zahid

21. 21
Reaction of host abut H-pylori: increase supply of neutrophil ,
lymphocyte and macrophage to effected area
Increase level of cytokine in effected area : interleukin alpha and
beta , IL2 ,IL6 , TNF alpha and IL Gama
Active humoral reaction in human but not benefit
Reactive oxygen and nitrogen : this can damage epithelium
Host factors
Dr.mazullah zahid

22. 22
oThis drugs can fined 10-20% gastric ulcer and 2-5% duodenal ulcer
oIncrease complication of ulcer
oApirinis the most common drugs
oThis drugs can inhibition of underling enzyme
1.Cyclooxygynase-1 (stomach , kidney , thrombocyte )
2.Cyclooxgynase-2 ( macrophage , leukocyte , fibroblast , synovial )
Inhibition of mucosal cytoprotection due to inhibition of
prostaglandins
NSAIDs and peptic ulcer
Dr.mazullah zahid

23. 23
Age above 60years
Past History of peptic ulcer
Past History of this drug side effect
Combine with corticosteroids and anti coagulant
High dose intake or combination of two NSAIDs
Sever internal disease
Increase with paroxicamand ketoprofen
Risk Factors that increase complication of NSAIDs
Dr.mazullah zahid

24. 24
Factors can cause peptic ulcer
Increase in smoker people
Delayed repairing of ulcer
Destruction of treatment response
Increase complication of ulcer
Decrease duodenal bicarbonate secretion
Increase risk of H-pylori
Cigarette smoking
Dr.mazullah zahid

25. 25
Mean mechanism is unknown
Increase in people which has O group of blood
increase parietal cell number
Increase in non secretory people
Resistant of mucus membrane about HCL and pepsin
Psychologic pressure :
Foods :
Alcohol
Caffeine
Hereditary
Dr.mazullah zahid

26. 26
Specific Chronic disorder :
Systemic mastocytosis (increase mast cell)
Chronic pulmonary disease
Nephrolithiasis
Advance age
Chronic renal failure and liver cirrhosis
Chronic pancreatitis
Alcohol use and obesity
Alpha 1 anti terpsine deficiency
Hyper parathyroidism
Coronary artery disease
Polycythemia
Con…
Dr.mazullah zahid

27. 27
•Mean clinical symptom epigastric pain 80-90% :
Character of pain
Location : 2/3 epigastric area me be some time right UQ or
hypoquindrium
Radiation back ,
pointing sign
2/3 night time 1-2 AM
Rhythmicity and periodicity
Pain after meal 1-3hrs
Decreasing factors :eating , anti acid , yawn , vomiting
Sharpe pain , burning pain , gnawing ,dull aching and hunger-like
Duodenal ulcer

28. 28
Uncomplicated ulcer : no finding
Palpation : tenderness of epigastric area
Complicated sign :
1.Tachycardia
2.Orthostatic hypotension
3.Caffee ground emesis
4.Malana
5.Hematochezia
6.Chronic bleeding
7.Iron deficiency anemia
8.If abdis tenderadand painful : peritonitis due to perforation
9.If sever and continuous pain radiation to back no response with anti acid
and eating : penetration of ulcer
10.Succussionsplash
Physical finding :
Dr.mazullah zahid

29. 29
Anemia : due to acute bleeding
Leukocytosis : due to perforation or penetration
Increase serum amylineand sever epigastric pain : perforation of ulcer to
pancreases
Increase level of gastrin in starvation : zolingerelison syndrome
Endoscopy :for DX of gastric and duodenal ulcer
If needed biopsy :
Test for H-pylori :
1.biopsy
2.rapid urease test
3.histologic test
4.Serologic test
Diagnosis and investigation
Dr.mazullah zahid

30. 30
Barium swallow:
Biopsy :
Con…
Dr.mazullah zahid

31. 31
Age : 60 years or above 60 years
Increase in male
This ulcer is very deep then duodenal ulcer
Common in antrum junction
2/3 involve minor curvature
1/3 involve greater curvature
Gastric ulcer
Dr.mazullah zahid

32. 32
HCL and pepsin
H-pylori
NSAIDs
Bile reflux
Clinical feature :
Epigastric pain
Nausea
Vomiting
Anorexia
Food aversion
Weight loss
Cause of death :high age , GI bleeding and late diagnosis
Etiology
Dr.mazullah zahid

33. 33
Non ulcer dyspepsia
GERD
Biliary disease
Pancreatitis
Acute cholisystitis
Esophageal perforation
Biliary tract stones
Gastric valvolus
Aortic aneurysm perforation
Gastric or intestinal ischemia
DDX
Dr.mazullah zahid

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Acid anti secretory agent
Mucosal protective agent
Drugs use to treat H-pylori
Treatment of peptic ulcer
Dr.mazullah zahid

35. 35
Proton pump inhibitor :
Omeprazole 20-4mg
Esomeprazole 40mg
Phentoprazole40mg
Lensoprazole30mg
Rabiprazole20mg
Dexlenzoprazole30-60mg
90% inhibition of HCL for 24hrs
PPI should use before 0,5 or 1 hrof meal
Treat of 90% duodenal ulcer for 4weeks and 90% gastric ulcer for
8weeks
Acid anti secretory agent
Dr.mazullah zahid

36. 36
Cimetidine 800mg
Famotidine 40mg
Nazetidine 300mg
Ranitidine 300mg
•Once in a day night time
•Treat duodenal ulcer in 6weeks and gastric ulcer 8weeks 85-90%
H2-receptor blocker
Dr.mazullah zahid

37. 37
Sacralfat: 1gr 1*4
Basmothagent :
1.Colloidal bismuth sub citrate
2.Bismothsubsalicylate 120mg 1*4
Prostaglandin analog :
Misoprostol 200mg 1*4
Anti acid :
Almonium hydroxide
Magnesium hydroxide
Calcium carbonate
Mucosal protective agent
Dr.mazullah zahid

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Duration 7-14days
Effect 85-90%
Regime for H-pylori :
First regime :
PPI 1*2
Clarithromycin 500mg 1*2
Amoxicillin 500mg 1*3 or 1gr 1*2
H-pylori eradication therapy
Dr.mazullah zahid

39. 39
Second regime :
1.PPI 1*2
2.Bismothsubsalicylate 120mg 1*4
3.Tetracycline 500mg 1*4
4.Metronidazole 250mg 1*4 or 500mg 1*3
Third regime :
PPI
Amoxicillin 1gr 1*2
metronidazole 500mg 1*2
Clarithromycin 500mg 1*2
Con…
Dr.mazullah zahid

40. Dr.mazullah zahid 40
Standard nonbismuthquadruple therapy :
Proton pump inhibitor orally twice daily
Amoxicillin 1000mg orally twice daily
Metronidazole 500mg orally twice daily
Clarithromycin 500mg orally twice daily
Levofloxacin triple therapy
oPPI 1*2
oLevofloxacin 500mg 1*2
oAmoxicillin 1gr 1*2
Con…

41. 41
Peptic ulcer
Gastric metaplasia
Peptic ulcer +active infection
Resistant iron deficiency anemia
Indication of H-pylori treatment
Dr.mazullah zahid

42. 42
Active ulcer :
PPI : for non complicated duodenal ulcer 4weeks and gastric ulcer 8weeks
H2-receptor blocker :for non complicated duodenal ulcer once in a day
FOR 6weeks and gastric ulcer BID for 8weeks
Prevention of complication :
High risk patient :
PPI 1*1
Celecoxib
Misoprostol 200 1*3
For along time treatment :PPI or H2-receptor antagonist
Treatment of peptic ulcer due to NSAIDs
Dr.mazullah zahid