Dyspepsia pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
 
(6 intermediate revisions by 3 users not shown)
Line 4: Line 4:


==Overview==
==Overview==
The symptoms of functional dyspepsia are directly caused by two major [[Pathophysiology|pathophysiological]] abnormalities in [[Abnormality (behavior)|abnormal]] [[Gastric motility disorder|gastric motility]] and [[visceral]] [[hypersensitivity]]. These [[Mechanism of action|mechanisms]] occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, [[genetic]] abnormalities, [[residual]] [[inflammation]] after [[gastrointestinal]] [[Infection|infections]], or other causes, with the process modified by factors including psychophysiological abnormalities, [[abnormal]] secretion of [[gastric acid]], [[Helicobacter pylori infection]], diet, and lifestyle.
The [[symptoms]] of functional dyspepsia are directly caused by two major [[Pathophysiology|pathophysiological]] abnormalities in [[Gastric motility disorder|gastric motility]] and [[visceral]] sensitivity. These [[Mechanism of action|mechanisms]] occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, [[genetic]] abnormalities, [[residual]] [[inflammation]] after [[gastrointestinal]] [[Infection|infections]], or other causes. The process may be modified by factors including psychophysiological abnormalities, [[abnormal]] secretion of [[gastric acid]], [[Helicobacter pylori infection]], diet, and lifestyle.


==Pathophysiology==
==Pathophysiology==
The pathophysiology of dyspepsia is as follows:<ref name="pmid26535514">{{cite journal |vauthors=Talley NJ, Ford AC |title=Functional Dyspepsia |journal=N. Engl. J. Med. |volume=373 |issue=19 |pages=1853–63 |year=2015 |pmid=26535514 |doi=10.1056/NEJMra1501505 |url=}}</ref><ref name="pmid26901578">{{cite journal |vauthors=Napthali K, Koloski N, Walker MM, Talley NJ |title=Women and functional dyspepsia |journal=Womens Health (Lond) |volume=12 |issue=2 |pages=241–50 |year=2016 |pmid=26901578 |pmc=5375052 |doi=10.2217/whe.15.88 |url=}}</ref><ref name="pmid27048251">{{cite journal |vauthors=Talley NJ |title=Functional dyspepsia: new insights into pathogenesis and therapy |journal=Korean J. Intern. Med. |volume=31 |issue=3 |pages=444–56 |year=2016 |pmid=27048251 |pmc=4855108 |doi=10.3904/kjim.2016.091 |url=}}</ref><ref name="pmid24716560">{{cite journal |vauthors=Ganesh M, Nurko S |title=Functional dyspepsia in children |journal=Pediatr Ann |volume=43 |issue=4 |pages=e101–5 |year=2014 |pmid=24716560 |doi=10.3928/00904481-20140325-12 |url=}}</ref><ref name="pmid21443707">{{cite journal |vauthors=Fock KM |title=Functional dyspepsia, H. pylori and post infectious FD |journal=J. Gastroenterol. Hepatol. |volume=26 Suppl 3 |issue= |pages=39–41 |year=2011 |pmid=21443707 |doi=10.1111/j.1440-1746.2011.06649.x |url=}}</ref><ref name="pmid22327302">{{cite journal |vauthors=Oustamanolakis P, Tack J |title=Dyspepsia: organic versus functional |journal=J. Clin. Gastroenterol. |volume=46 |issue=3 |pages=175–90 |year=2012 |pmid=22327302 |doi=10.1097/MCG.0b013e318241b335 |url=}}</ref><ref name="pmid19663903">{{cite journal |vauthors=Kindt S, Dubois D, Van Oudenhove L, Caenepeel P, Arts J, Bisschops R, Tack J |title=Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia |journal=Neurogastroenterol. Motil. |volume=21 |issue=11 |pages=1183–e105 |year=2009 |pmid=19663903 |doi=10.1111/j.1365-2982.2009.01374.x |url=}}</ref>
The pathophysiology of dyspepsia is as follows:<ref name="pmid26535514">{{cite journal |vauthors=Talley NJ, Ford AC |title=Functional Dyspepsia |journal=N. Engl. J. Med. |volume=373 |issue=19 |pages=1853–63 |year=2015 |pmid=26535514 |doi=10.1056/NEJMra1501505 |url=}}</ref><ref name="pmid26901578">{{cite journal |vauthors=Napthali K, Koloski N, Walker MM, Talley NJ |title=Women and functional dyspepsia |journal=Womens Health (Lond) |volume=12 |issue=2 |pages=241–50 |year=2016 |pmid=26901578 |pmc=5375052 |doi=10.2217/whe.15.88 |url=}}</ref><ref name="pmid27048251">{{cite journal |vauthors=Talley NJ |title=Functional dyspepsia: new insights into pathogenesis and therapy |journal=Korean J. Intern. Med. |volume=31 |issue=3 |pages=444–56 |year=2016 |pmid=27048251 |pmc=4855108 |doi=10.3904/kjim.2016.091 |url=}}</ref><ref name="pmid24716560">{{cite journal |vauthors=Ganesh M, Nurko S |title=Functional dyspepsia in children |journal=Pediatr Ann |volume=43 |issue=4 |pages=e101–5 |year=2014 |pmid=24716560 |doi=10.3928/00904481-20140325-12 |url=}}</ref><ref name="pmid21443707">{{cite journal |vauthors=Fock KM |title=Functional dyspepsia, H. pylori and post infectious FD |journal=J. Gastroenterol. Hepatol. |volume=26 Suppl 3 |issue= |pages=39–41 |year=2011 |pmid=21443707 |doi=10.1111/j.1440-1746.2011.06649.x |url=}}</ref><ref name="pmid22327302">{{cite journal |vauthors=Oustamanolakis P, Tack J |title=Dyspepsia: organic versus functional |journal=J. Clin. Gastroenterol. |volume=46 |issue=3 |pages=175–90 |year=2012 |pmid=22327302 |doi=10.1097/MCG.0b013e318241b335 |url=}}</ref><ref name="pmid19663903">{{cite journal |vauthors=Kindt S, Dubois D, Van Oudenhove L, Caenepeel P, Arts J, Bisschops R, Tack J |title=Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia |journal=Neurogastroenterol. Motil. |volume=21 |issue=11 |pages=1183–e105 |year=2009 |pmid=19663903 |doi=10.1111/j.1365-2982.2009.01374.x |url=}}</ref>
=== Physiology of Digestion ===
=== Physiology of digestion ===
* In humans, digestion begins in the [[mouth]] where food is chewed.  
* In humans, [[digestion]] begins in the [[mouth]] where food is chewed.  
* [[Salivary amylase]] aids in the chemical breakdown of [[polysaccharides]] such as starch into [[Disaccharide|disaccharides]] such as [[maltose]].  
* [[Salivary amylase]] aids in the chemical breakdown of [[polysaccharides]] such as [[starch]] into [[Disaccharide|disaccharides]] such as [[maltose]].  
* The chewed food is pushed down the esophagus to the stomach through [[peristaltic]] [[contraction]] of these [[Muscle|muscles]].  
* The chewed food is pushed down the [[esophagus]] into the [[stomach]] through [[peristaltic]] [[contraction]] of these [[Muscle|muscles]].  
* Food enters the [[stomach]] where it is further broken apart and thoroughly mixed with [[gastric acid]], [[pepsin]], and other digestive enzymes to break down proteins.  
* Food enters the [[stomach]] where it is further broken down and thoroughly mixed with [[gastric acid]], [[pepsin]], and other digestive enzymes to break down [[proteins]], [[fats]] and [[carbohydrates]].  
* After consumption of food, digestive "[[tonic]]" and [[Peristalsis|peristaltic]] contractions begin, which helps break down the food and move it through. Gastric emptying is the release of food from the stomach into the [[duodenum]].  
* After consumption of food, digestive "[[tonic]]" and [[Peristalsis|peristaltic]] [[contractions]] begin, which helps break down the food and move it through the [[gastrointestinal tract]]. Gastric emptying is the release of food from the [[Stomach cancer|stomach]] into the [[duodenum]].  
* [[Gastric emptying]] has attracted medical interest as rapid gastric emptying is related to [[obesity]] and delayed gastric emptying syndrome is associated with [[diabetes mellitus]], [[aging]], and [[gastroesophageal reflux]].  
* Gastric emptying has attracted medical interest as rapid gastric emptying is related to [[obesity]] and [[delayed gastric emptying]] syndrome is associated with [[diabetes mellitus]], [[aging]], [[gastroparesis]] and [[gastroesophageal reflux]].  
* After being processed in the stomach, food is passed to the [[small intestine]]. The majority of [[digestion]] and [[absorption]] occurs here after the milky chyme enters the [[duodenum]]. Here it is further mixed with three different liquids:
* After being processed in the [[stomach]], food is passed to the [[small intestine]]. The majority of [[digestion]] and [[absorption]] occurs here after the milky [[chyme]] enters the [[duodenum]]. Here it is further mixed with three different [[digestive]] juices:
** [[Bile]] which is produced by the [[liver]] and stored in the [[gallbladder]] [[emulsifies]] fats and neutralizes the [[chyme]].
** [[Bile]] which is produced by the [[liver]] and stored in the [[gallbladder]] [[emulsifies]] [[fats]] and neutralizes the [[chyme]].
** [[Pancreatic juice]] made by the [[pancreas]]. It secrete enzymes such as [[pancreatic amylase]], [[pancreatic lipase]], and [[trypsinogen]].
** [[Pancreatic juice]] made by the [[pancreas]]. It secrete [[enzymes]] such as [[pancreatic amylase]], [[pancreatic lipase]], and [[trypsinogen]].
**Intestinal juice secreted by the [[intestinal]] [[glands]] in the [[small intestine]]. It contains [[enzymes]] such as [[enteropeptidase]], [[erepsin]], [[trypsin]], [[chymotrypsin]], [[maltase]], [[lactase]], and [[sucrase]].
**Intestinal juice secreted by the [[intestinal]] [[glands]] in the [[small intestine]]. It contains [[enzymes]] such as [[enteropeptidase]], [[erepsin]], [[trypsin]], [[chymotrypsin]], [[maltase]], [[lactase]], and [[sucrase]].


=== Pathophysiology of Functional Dyspepsia ===
=== Pathophysiology of functional dyspepsia ===
* The symptoms of functional dyspepsia are directly caused by two major [[physiological]] abnormalities   
* The [[symptoms]] of functional dyspepsia (FD) are directly caused by two major [[physiological]] abnormalities   
** '''Abnormal gastric motility'''   
** '''Abnormal gastric motility'''. Gastroparesis and functional dyspepsia may be the same entity<ref name="pmid33548234">{{cite journal| author=Pasricha PJ, Grover M, Yates KP, Abell TL, Bernard CE, Koch KL | display-authors=etal| title=Functional Dyspepsia and Gastroparesis in Tertiary Care are Interchangeable Syndromes With Common Clinical and Pathologic Features. | journal=Gastroenterology | year= 2021 | volume= 160 | issue= 6 | pages= 2006-2017 | pmid=33548234 | doi=10.1053/j.gastro.2021.01.230 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33548234 }} </ref>
** '''Visceral hypersensitivity'''  
** '''Visceral hypersensitivity'''  
* These mechanisms occur in patients who have acquired excessive responsiveness to [[stress]] as a result of the environment during early life, [[genetic]] [[abnormalities]], [[residual]] [[inflammation]] after [[gastrointestinal]] infections, or other causes, with the process modified by factors including psychophysiological abnormalities, abnormal secretion of [[gastric acid]], [[Helicobacter pylori infection]], diet, and lifestyle.  
* These mechanisms occur in patients who have acquired excessive responsiveness to [[stress]] as a result of the environment during early life, [[genetic]] [[abnormalities]], [[residual]] [[inflammation]] after [[gastrointestinal]] infections, or other causes, with the process modified by factors including psychophysiological abnormalities, abnormal secretion of [[gastric acid]], [[Helicobacter pylori infection]], diet, and lifestyle.  
* If the basis of this model of FD [[pathogenesis]] is excessive responsiveness of [[gastrointestinal]] function to stress and external stimuli, [[psychosomatic]] approaches to alter stress [[perception]] could be important treatment options.<ref>{{cite journal |author=Miwa H |title=Why dyspepsia can occur without organic disease: pathogenesis and management of functional dyspepsia |journal=J Gastroenterol |volume= |issue= |pages= |year=2012 |month=July |pmid=22766746 |doi=10.1007/s00535-012-0625-9 |url=}}</ref>
* If the basis of this model of FD [[pathogenesis]] is excessive responsiveness of [[gastrointestinal]] function to stress and external stimuli, [[psychosomatic]] approaches to alter stress [[perception]] could be important treatment options.<ref>{{cite journal |author=Miwa H |title=Why dyspepsia can occur without organic disease: pathogenesis and management of functional dyspepsia |journal=J Gastroenterol |volume= |issue= |pages= |year=2012 |month=July |pmid=22766746 |doi=10.1007/s00535-012-0625-9 |url=}}</ref>
==Gross Pathology==
'''''There are no significant gross or microscopic pathology associated with dyspepsia, however the gross and microscopic pathology of peptic ulcer disease should be kept in mind.'''''
*[[Gastric|Gastric ulcers]] are most often localized on the lesser curvature of the [[stomach]]
*[[Duodenal]] [[ulcers]] are more located at bulb of duodenum
*Characteristic findings of a [[peptic ulcer]] on gross pathology include:
**Round to oval
**Two to four cm diameter
**Smooth base with perpendicular borders.
**Parietal scarring with radial folds may be evident in the surrounding mucosa
<gallery widths="250px">
Benign gastric ulcer 1.jpg|A benign gastric ulcer (from the antrum) of a [[gastrectomy]] ''Source:https://commons.wikimedia.org/wiki/File:Benign_gastric_ulcer_1.jpg#/media/File:Benign_gastric_ulcer_1.jpg''
Duodenal ulcer01 (1).jpg|Duodenal ulcer specimen. ''Source: https://commons.wikimedia.org/wiki/File:Duodenal_ulcer01.jpg#/media/File:Duodenal_ulcer01.jpg''
Gastric ulcer 3.jpg|Gastric ulcer specimen ''Source:https://commons.wikimedia.org/wiki/File:Gastric_ulcer_3.jpg#/media/File:Gastric_ulcer_3.jpg''
</gallery>
==Microscopic Pathology==
'''''There are no significant gross or microscopic pathology associated with dyspepsia however, the gross and microscopic pathology of peptic ulcer disease should be kept in mind.'''''
*A [[peptic ulcer]] is a mucosal defect produced by acid-pepsin aggression which penetrates the [[muscularis mucosae]] and muscularis propria
*There is increased plasma cells, neutrophilic infiltrate, villous blunting
*The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
*During the active phase, the base of the ulcer shows 4 zones:
**[[Inflammatory]] exudate: polymorphonuclear infiltration which along with bacterial products stimulate the production of IL-8 and tumor necrosis factor alpha (TNF-α) and IL-1 released by macrophages in response to bacterial [[lipopolysaccharide]]
**Fibrinoid necrosis
**Granulation tissue
**Fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis<ref name="pathologyatlas">{{cite web | url=http://www.pathologyatlas.ro/Peptic%20ulcer.html| title=ATLAS OF PATHOLOGY|accessdate=2007-08-26}}</ref>
<gallery widths="250px">
Erosive gastric ulcer (1).jpg| [[Erosive gastric ulcer ]]''source: https://commons.wikimedia.org/wiki/File:Erosive_gastric_ulcer.jpg#/media/File:Erosive_gastric_ulcer.jpg''
</gallery>


==References==
==References==


{{Reflist|2}}
{{Reflist|2}}
{{WS}}
{{WH}}


[[Category:Needs overview]]
[[Category:Needs overview]]
[[Category:Gastroenterology]]
[[Category:Gastroenterology]]
[[Category:Primary care]]
{{WS}}
{{WH}}

Latest revision as of 01:20, 25 May 2021

Dyspepsia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Dyspepsia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Dyspepsia pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Dyspepsia pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Dyspepsia pathophysiology

CDC on Dyspepsia pathophysiology

Dyspepsia pathophysiology in the news

Blogs on Dyspepsia pathophysiology

Directions to Hospitals Treating Dyspepsia

Risk calculators and risk factors for Dyspepsia pathophysiology

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

Overview

The symptoms of functional dyspepsia are directly caused by two major pathophysiological abnormalities in gastric motility and visceral sensitivity. These mechanisms occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, genetic abnormalities, residual inflammation after gastrointestinal infections, or other causes. The process may be modified by factors including psychophysiological abnormalities, abnormal secretion of gastric acid, Helicobacter pylori infection, diet, and lifestyle.

Pathophysiology

The pathophysiology of dyspepsia is as follows:[1][2][3][4][5][6][7]

Physiology of digestion

Pathophysiology of functional dyspepsia

Gross Pathology

There are no significant gross or microscopic pathology associated with dyspepsia, however the gross and microscopic pathology of peptic ulcer disease should be kept in mind.

  • Gastric ulcers are most often localized on the lesser curvature of the stomach
  • Duodenal ulcers are more located at bulb of duodenum
  • Characteristic findings of a peptic ulcer on gross pathology include:
    • Round to oval
    • Two to four cm diameter
    • Smooth base with perpendicular borders.
    • Parietal scarring with radial folds may be evident in the surrounding mucosa

Microscopic Pathology

There are no significant gross or microscopic pathology associated with dyspepsia however, the gross and microscopic pathology of peptic ulcer disease should be kept in mind.

  • A peptic ulcer is a mucosal defect produced by acid-pepsin aggression which penetrates the muscularis mucosae and muscularis propria
  • There is increased plasma cells, neutrophilic infiltrate, villous blunting
  • The surface epithelium usually shows mucous cell (pseudopyloric) metaplasia
  • During the active phase, the base of the ulcer shows 4 zones:
    • Inflammatory exudate: polymorphonuclear infiltration which along with bacterial products stimulate the production of IL-8 and tumor necrosis factor alpha (TNF-α) and IL-1 released by macrophages in response to bacterial lipopolysaccharide
    • Fibrinoid necrosis
    • Granulation tissue
    • Fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis[10]

References

  1. ↑ Talley NJ, Ford AC (2015). "Functional Dyspepsia". N. Engl. J. Med. 373 (19): 1853–63. doi:10.1056/NEJMra1501505. PMID 26535514.
  2. ↑ Napthali K, Koloski N, Walker MM, Talley NJ (2016). "Women and functional dyspepsia". Womens Health (Lond). 12 (2): 241–50. doi:10.2217/whe.15.88. PMC 5375052. PMID 26901578.
  3. ↑ Talley NJ (2016). "Functional dyspepsia: new insights into pathogenesis and therapy". Korean J. Intern. Med. 31 (3): 444–56. doi:10.3904/kjim.2016.091. PMC 4855108. PMID 27048251.
  4. ↑ Ganesh M, Nurko S (2014). "Functional dyspepsia in children". Pediatr Ann. 43 (4): e101–5. doi:10.3928/00904481-20140325-12. PMID 24716560.
  5. ↑ Fock KM (2011). "Functional dyspepsia, H. pylori and post infectious FD". J. Gastroenterol. Hepatol. 26 Suppl 3: 39–41. doi:10.1111/j.1440-1746.2011.06649.x. PMID 21443707.
  6. ↑ Oustamanolakis P, Tack J (2012). "Dyspepsia: organic versus functional". J. Clin. Gastroenterol. 46 (3): 175–90. doi:10.1097/MCG.0b013e318241b335. PMID 22327302.
  7. ↑ Kindt S, Dubois D, Van Oudenhove L, Caenepeel P, Arts J, Bisschops R, Tack J (2009). "Relationship between symptom pattern, assessed by the PAGI-SYM questionnaire, and gastric sensorimotor dysfunction in functional dyspepsia". Neurogastroenterol. Motil. 21 (11): 1183–e105. doi:10.1111/j.1365-2982.2009.01374.x. PMID 19663903.
  8. ↑ Pasricha PJ, Grover M, Yates KP, Abell TL, Bernard CE, Koch KL; et al. (2021). "Functional Dyspepsia and Gastroparesis in Tertiary Care are Interchangeable Syndromes With Common Clinical and Pathologic Features". Gastroenterology. 160 (6): 2006–2017. doi:10.1053/j.gastro.2021.01.230. PMID 33548234 Check |pmid= value (help).
  9. ↑ Miwa H (2012). "Why dyspepsia can occur without organic disease: pathogenesis and management of functional dyspepsia". J Gastroenterol. doi:10.1007/s00535-012-0625-9. PMID 22766746. Unknown parameter |month= ignored (help)
  10. ↑ "ATLAS OF PATHOLOGY". Retrieved 2007-08-26.

Template:WS Template:WH

Retrieved from "https://www.wikidoc.org/index.php?title=Dyspepsia_pathophysiology&oldid=1702091"