Peptic ulcer natural history: Difference between revisions

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__NOTOC__
__NOTOC__
{{Peptic ulcer}}
{{Peptic ulcer}}
{{CMG}} ;{{AE}} {{MKK}}
{{CMG}}; {{AE}} {{MKK}}
 
==Overview==
==Overview==
[[Peptic ulcers]] tend to come back if untreated. Cure rates are high and recurrence is low, if patient is compliant to treatment.
''[[Helicobacter pylori]] infection is a'' common cause of [[peptic ulcer disease]] which is acquired usually during childhood but presents in second to fifth decade of life. Patient presents with episodic [[epigastric pain]], [[indigestion]], [[bloating]],[[hematemesis]] and [[melena]]. If not treated, patients can develop [[complications]] like [[bleeding]], [[perforation]], [[obstruction]] or [[stricture]]. Chronic infection of [[helicobacter pylori]] leads to [[gastric cancer]], [[MALT lymphoma|MALT lymphoma,]] [[Iron deficiency anemia|iron deficiency anemia,]] [[Idiopathic thrombocytopenic purpura]][[Peptic ulcers|. Peptic ulcers]] tend to recur if left untreated. Prognosis is good if the eradication therapy of [[Helicobacter pylori]] is taken.The recurrence rate of patients with [[peptic ulcer disease]] is less than 20%.


==Natural History==
==Natural History==
*The infection of ''[[Helicobacter pylori]]'' , common cause of [[peptic ulcer disease]] is acquired usually during the childhood, mainly in those who have low socioeconomic status, increased number of siblings and similar [[infection]] in the mother<ref name="pmid11045838">{{cite journal |vauthors=Opekun AR, Gilger MA, Denyes SM, Nirken MH, Philip SP, Osato MS, Malaty HM, Hicks J, Graham DY |title=Helicobacter pylori infection in children of Texas |journal=J. Pediatr. Gastroenterol. Nutr. |volume=31 |issue=4 |pages=405–10 |year=2000 |pmid=11045838 |doi= |url=}}</ref><ref name="pmid11063492">{{cite journal |vauthors=Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, Swaminathan B, Khanna B, Petersen KM, Fitzgerald MA |title=High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults |journal=Clin. Diagn. Lab. Immunol. |volume=7 |issue=6 |pages=885–8 |year=2000 |pmid=11063492 |pmc=95979 |doi= |url=}}</ref><ref name="pmid11918912">{{cite journal |vauthors=Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, Yamaoka Y, Berenson GS |title=Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to adulthood |journal=Lancet |volume=359 |issue=9310 |pages=931–5 |year=2002 |pmid=11918912 |doi=10.1016/S0140-6736(02)08025-X |url=}}</ref>   
*The infection of ''[[Helicobacter pylori]]'' , common cause of [[peptic ulcer disease]] is acquired usually during the childhood, mainly in those who have low socioeconomic status, increased number of siblings and similar [[infection]] in the mother.<ref name="pmid11045838">{{cite journal |vauthors=Opekun AR, Gilger MA, Denyes SM, Nirken MH, Philip SP, Osato MS, Malaty HM, Hicks J, Graham DY |title=Helicobacter pylori infection in children of Texas |journal=J. Pediatr. Gastroenterol. Nutr. |volume=31 |issue=4 |pages=405–10 |year=2000 |pmid=11045838 |doi= |url=}}</ref><ref name="pmid11063492">{{cite journal |vauthors=Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, Swaminathan B, Khanna B, Petersen KM, Fitzgerald MA |title=High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults |journal=Clin. Diagn. Lab. Immunol. |volume=7 |issue=6 |pages=885–8 |year=2000 |pmid=11063492 |pmc=95979 |doi= |url=}}</ref><ref name="pmid11918912">{{cite journal |vauthors=Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, Yamaoka Y, Berenson GS |title=Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to adulthood |journal=Lancet |volume=359 |issue=9310 |pages=931–5 |year=2002 |pmid=11918912 |doi=10.1016/S0140-6736(02)08025-X |url=}}</ref>   
*The [[duodenal ulcer]] occurs in second to fifth decade of life. where as [[gastric ulcer]] occurs in the 4th decade of life.  
*The [[duodenal ulcer]] occurs in second to fifth decade of life. where as [[gastric ulcer]] occurs in the 4th decade of life.  
*Peptic ulcer disease starts with symptoms such as episodic [[epigastric pain]], [[indigestion]], [[bloating]].  
*Peptic ulcer disease starts with symptoms such as episodic [[epigastric pain]], [[indigestion]], [[bloating]].  
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*'''Bleeding''' is the commonest complication.  
*'''Bleeding''' is the commonest complication.  
**Sudden large bleeding can be life threatening.
**Sudden large bleeding can be life threatening.
**[[Bleeding]] occurs when the ulcer erodes one of the blood vessels around the stomach.<ref name="pmid22095016">{{cite journal |vauthors=Milosavljevic T, Kostić-Milosavljević M, Jovanović I, Krstić M |title=Complications of peptic ulcer disease |journal=Dig Dis |volume=29 |issue=5 |pages=491–3 |year=2011 |pmid=22095016 |doi=10.1159/000331517 |url=}}</ref><ref name="pmid9391242">{{cite journal |author=Cullen DJ, Hawkey GM, Greenwood DC, ''et al'' |title=Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs |journal=Gut |volume=41 |issue=4|pages=459–62 |year=1997 |pmid=9391242 |doi=}}</ref>.
**[[Bleeding]] occurs when the ulcer erodes one of the blood vessels around the stomach.<ref name="pmid22095016">{{cite journal |vauthors=Milosavljevic T, Kostić-Milosavljević M, Jovanović I, Krstić M |title=Complications of peptic ulcer disease |journal=Dig Dis |volume=29 |issue=5 |pages=491–3 |year=2011 |pmid=22095016 |doi=10.1159/000331517 |url=}}</ref><ref name="pmid9391242">{{cite journal |author=Cullen DJ, Hawkey GM, Greenwood DC, ''et al'' |title=Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs |journal=Gut |volume=41 |issue=4|pages=459–62 |year=1997 |pmid=9391242 |doi=}}</ref>
*'''Perforation'''
*'''Perforation'''
**[[Perforation]] is most common occur at the [[duodenal bulb]] (62%), followed by the [[pyloric region]] (20%), and the [[gastric]] body (18%)
**[[Perforation]] is most common occur at the [[duodenal bulb]] (62%), followed by the [[pyloric region]] (20%), and the [[gastric]] body (18%).
**Erosion of the gastro-intestinal wall  by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity leading to fatal consequences
**Erosion of the gastro-intestinal wall  by the ulcer leads to spillage of stomach or intestinal content into abdominal cavity leading to fatal consequences.
**[[Perforation]]  at the anterior surface of stomach  leads to acute [[peritonitis]], initially chemical and later bacterial peritonitis  
**[[Perforation]]  at the anterior surface of stomach  leads to acute [[peritonitis]], initially chemical and later bacterial peritonitis.
**Often first sign is sudden intense [[abdominal pain]]
**Often, the first symptom is a sudden intense [[abdominal pain]].
**Posterior wall [[perforation]] leads to [[pancreatitis]]; pain in this situation often radiates to back
**Posterior wall [[perforation]] leads to [[pancreatitis]], pain in this situation often radiates to back.
**'''Penetration''' is also a form of [[perforation]], when the ulcer continues into adjacent organs such as [[liver]] and [[pancreas]]<ref>{{cite web|url=http://www.merck.com/mmhe/sec09/ch121/ch121c.html |title=Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition|accessdate=2007-10-10 |format= |work=}}</ref><ref>{{cite web|url=http://www.merck.com/mmhe/sec09/ch121/ch121c.html |title=Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition|accessdate=2007-10-10 |format= |work=}}</ref>  
**'''Penetration''' is also a form of [[perforation]], when the ulcer continues into adjacent organs such as [[liver]] and [[pancreas|pancreas.]]<ref>{{cite web|url=http://www.merck.com/mmhe/sec09/ch121/ch121c.html |title=Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition|accessdate=2007-10-10 |format= |work=}}</ref><ref>{{cite web|url=http://www.merck.com/mmhe/sec09/ch121/ch121c.html |title=Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition|accessdate=2007-10-10 |format= |work=}}</ref>  
*'''Obstruction'''
*'''Obstruction'''
**Occurs as a result of [[stricture]] and [[scarring]] narrowing in the [[duodenum]] leading to '''[[gastric outlet obstruction]]'''.
**Occurs as a result of [[stricture]] and [[scarring]] narrowing in the [[duodenum]] leading to [[gastric outlet obstruction]].
 
==== Chronic complications: ====
==== Chronic complications: ====
Chronic Helicobacter pylori infection leads to
Chronic Helicobacter pylori infection leads to:
* [[Gastric cancer]]
* [[Gastric cancer]]
*[[MALT lymphoma]]
*[[MALT lymphoma]]
*[[Iron deficiency anemia]]
*[[Iron deficiency anemia]]
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==Prognosis==
==Prognosis==
*Prognosis is good if the eradication therapy of [[Helicobacter pylori]] is taken.
*Prognosis is good if the eradication therapy of [[Helicobacter pylori]] is taken.
*The recurrence rate of patients with [[peptic ulcer disease]] is less than 20%
*The recurrence rate of patients with [[peptic ulcer disease]] is less than 20%.


==References==
==References==
{{reflist|2}}
{{reflist|2}}
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Latest revision as of 23:37, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]

Overview

Helicobacter pylori infection is a common cause of peptic ulcer disease which is acquired usually during childhood but presents in second to fifth decade of life. Patient presents with episodic epigastric pain, indigestion, bloating,hematemesis and melena. If not treated, patients can develop complications like bleeding, perforation, obstruction or stricture. Chronic infection of helicobacter pylori leads to gastric cancer, MALT lymphoma, iron deficiency anemia, Idiopathic thrombocytopenic purpura. Peptic ulcers tend to recur if left untreated. Prognosis is good if the eradication therapy of Helicobacter pylori is taken.The recurrence rate of patients with peptic ulcer disease is less than 20%.

Natural History

Complications

Acute complications :

Chronic complications:

Chronic Helicobacter pylori infection leads to:

Prognosis

References

  1. Opekun AR, Gilger MA, Denyes SM, Nirken MH, Philip SP, Osato MS, Malaty HM, Hicks J, Graham DY (2000). "Helicobacter pylori infection in children of Texas". J. Pediatr. Gastroenterol. Nutr. 31 (4): 405–10. PMID 11045838.
  2. Parkinson AJ, Gold BD, Bulkow L, Wainwright RB, Swaminathan B, Khanna B, Petersen KM, Fitzgerald MA (2000). "High prevalence of Helicobacter pylori in the Alaska native population and association with low serum ferritin levels in young adults". Clin. Diagn. Lab. Immunol. 7 (6): 885–8. PMC 95979. PMID 11063492.
  3. Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, Yamaoka Y, Berenson GS (2002). "Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to adulthood". Lancet. 359 (9310): 931–5. doi:10.1016/S0140-6736(02)08025-X. PMID 11918912.
  4. Kusters JG, van Vliet AH, Kuipers EJ (2006). "Pathogenesis of Helicobacter pylori infection". Clin. Microbiol. Rev. 19 (3): 449–90. doi:10.1128/CMR.00054-05. PMC 1539101. PMID 16847081.
  5. Milosavljevic T, Kostić-Milosavljević M, Jovanović I, Krstić M (2011). "Complications of peptic ulcer disease". Dig Dis. 29 (5): 491–3. doi:10.1159/000331517. PMID 22095016.
  6. Cullen DJ, Hawkey GM, Greenwood DC; et al. (1997). "Peptic ulcer bleeding in the elderly: relative roles of Helicobacter pylori and non-steroidal anti-inflammatory drugs". Gut. 41 (4): 459–62. PMID 9391242.
  7. "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.
  8. "Peptic Ulcer: Peptic Disorders: Merck Manual Home Edition". Retrieved 2007-10-10.

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