Adenoiditis pathophysiology: Difference between revisions

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* After the birth adenoids begin to enlarge.
* After the birth adenoids begin to enlarge.
* By the time children are aged 6 months, [[lactobacilli]], [[Anaerobic bacteria|anaerobic streptococci]], [[actinomycosis]], [[Fusobacterium species]], and [[Nocardia]] species are present.
* By the time children are aged 6 months, [[lactobacilli]], [[Anaerobic bacteria|anaerobic streptococci]], [[actinomycosis]], [[Fusobacterium species]], and [[Nocardia]] species are present in the mucosal flora.
* Normal flora found in the mature adenoid tissue consists:
* Normal flora found in the mature adenoid tissue consists:
** [[Streptococcus|Alpha-hemolytic streptococci]]
** [[Streptococcus|Alpha-hemolytic streptococci]]
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* Adenoids start to shrink by the age 6-7.
* Adenoids start to shrink by the age 6-7.
* By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.
* By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.
=== Pathogenesis ===
== Pathogenesis ==
* [[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface providing local [[immune]] protection. Studies suggest that a reduction in [[IgA]] will happen postoperative of [[adenoidectomy]].<ref name="pmid12117336">{{cite journal |vauthors=Havas T, Lowinger D |title=Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy |journal=Arch. Otolaryngol. Head Neck Surg. |volume=128 |issue=7 |pages=789–91 |year=2002 |pmid=12117336 |doi= |url=}}</ref>
* [[Adenoid|Adenoids]] are involved in the production of mostly secretory [[IgA]], which is transported to the surface providing local [[immune]] protection. Studies suggest that a reduction in [[IgA]] will happen postoperative of [[adenoidectomy]].<ref name="pmid12117336">{{cite journal |vauthors=Havas T, Lowinger D |title=Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy |journal=Arch. Otolaryngol. Head Neck Surg. |volume=128 |issue=7 |pages=789–91 |year=2002 |pmid=12117336 |doi= |url=}}</ref>


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***Colonization begins when the [[bacteria]] adheres to the adenoid surface [[proteins]] through [[lipoteichoic acid]] (LTA), depositing [[fibronectin]] molecules that bind to the adenoidal [[epithelium]].<ref name="pmid3317744" /><ref name="pmid17426506">{{cite journal |vauthors=Zhang JM, An J |title=Cytokines, inflammation, and pain |journal=Int Anesthesiol Clin |volume=45 |issue=2 |pages=27–37 |year=2007 |pmid=17426506 |pmc=2785020 |doi=10.1097/AIA.0b013e318034194e |url=}}</ref>
***Colonization begins when the [[bacteria]] adheres to the adenoid surface [[proteins]] through [[lipoteichoic acid]] (LTA), depositing [[fibronectin]] molecules that bind to the adenoidal [[epithelium]].<ref name="pmid3317744" /><ref name="pmid17426506">{{cite journal |vauthors=Zhang JM, An J |title=Cytokines, inflammation, and pain |journal=Int Anesthesiol Clin |volume=45 |issue=2 |pages=27–37 |year=2007 |pmid=17426506 |pmc=2785020 |doi=10.1097/AIA.0b013e318034194e |url=}}</ref>
*Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).
*Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).
== Gross pathology ==
*On gross pathology, characteristic findings of adenoiditis, include:
*On gross pathology, characteristic findings of adenoiditis, include:
:*Enlarged adenoids
:*Enlarged adenoids
:*Soft greasy yellow areas within capsule
:*Soft greasy yellow areas within capsule
== Microscopic Pathology ==
*On microscopic histopathological analysis, characteristic findings of adenoiditis  
*On microscopic histopathological analysis, characteristic findings of adenoiditis  
*Recurrent [[bacterial]] tonsillitis is caused primarily by ''[[Staphylococcus aureus]]''.<ref name="pmid20209109">{{cite journal |vauthors=Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A |title=Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis |journal=PLoS ONE |volume=5 |issue=3 |pages=e9452 |year=2010 |pmid=20209109 |pmc=2830486 |doi=10.1371/journal.pone.0009452 |url=}}</ref>
*Recurrent [[bacterial]] tonsillitis is caused primarily by ''[[Staphylococcus aureus]]''.<ref name="pmid20209109">{{cite journal |vauthors=Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A |title=Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis |journal=PLoS ONE |volume=5 |issue=3 |pages=e9452 |year=2010 |pmid=20209109 |pmc=2830486 |doi=10.1371/journal.pone.0009452 |url=}}</ref>
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**Following invasion, ''[[S. aureus]]'' is internalized by non-[[phagocytic]] cells through [[fibronectin]]-binding [[protein]] and beta-[[integrins]].<ref name="pmid11549002">{{cite journal |vauthors=Alexander EH, Hudson MC |title=Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans |journal=Appl. Microbiol. Biotechnol. |volume=56 |issue=3-4 |pages=361–6 |year=2001 |pmid=11549002 |doi= |url=}}</ref>
**Following invasion, ''[[S. aureus]]'' is internalized by non-[[phagocytic]] cells through [[fibronectin]]-binding [[protein]] and beta-[[integrins]].<ref name="pmid11549002">{{cite journal |vauthors=Alexander EH, Hudson MC |title=Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans |journal=Appl. Microbiol. Biotechnol. |volume=56 |issue=3-4 |pages=361–6 |year=2001 |pmid=11549002 |doi= |url=}}</ref>
**Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in adenoiditis
**Invasion of non-eukaryotic cells results in the up-regulation of [[cytokines]], resulting in adenoiditis
{| class="wikitable"
!
!Pathogen
!Symptoms
!Treatment
|-
| rowspan="9" |Viral adenoiditis<ref name="pmid21377220">{{cite journal| author=Sadeghi-Shabestari M, Jabbari Moghaddam Y, Ghaharri H| title=Is there any correlation between allergy and adenotonsillar tissue hypertrophy? | journal=Int J Pediatr Otorhinolaryngol | year= 2011 | volume= 75 | issue= 4 | pages= 589-91 | pmid=21377220 | doi=10.1016/j.ijporl.2011.01.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21377220  }}</ref><ref name="pmid22870291">{{cite journal| author=Proenca-Modena JL, Pereira Valera FC, Jacob MG, Buzatto GP, Saturno TH, Lopes L et al.| title=High rates of detection of respiratory viruses in tonsillar tissues from children with chronic adenotonsillar disease. | journal=PLoS One | year= 2012 | volume= 7 | issue= 8 | pages= e42136 | pmid=22870291 | doi=10.1371/journal.pone.0042136 | pmc=3411673 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22870291  }}</ref><ref name="pmid11249975">{{cite journal |vauthors=Endo LH, Ferreira D, Montenegro MC, Pinto GA, Altemani A, Bortoleto AE, Vassallo J |title=Detection of Epstein-Barr virus in tonsillar tissue of children and the relationship with recurrent tonsillitis |journal=Int. J. Pediatr. Otorhinolaryngol. |volume=58 |issue=1 |pages=9–15 |year=2001 |pmid=11249975 |doi= |url=}}</ref>
|[[Epstein Barr virus|Epstein-barr virus]] (EBV)
|
==== Asymptomatic ====
In small children, the course of the disease is frequently asymptomatic. Majority of adults infected with ''mono'' also remain asymptomatic with serological evidence of past infection.
====Initial Prodrome====
Common symptoms include: low-grade [[fever]] without chills is seen in nearly all cases, [[Sore throat]], white patches on the tonsils and back of the throat are often seen, [[Muscle weakness]] and sometime extreme [[fatigue]], tender [[lymphadenopathy]], particularly the posterior [[cervical lymph nodes]] are involved
|Treating symptoms and complications of the infection.
|-
|[[Adeno virus|Human adenovirus]]
|Common cold syndrome, [[Pneumonia]], [[Croup]], [[Bronchitis]]
|Treating symptoms and complications of the infection.
|-
|[[Enterovirus]]
|Mild respiratory illness ([[common cold]]), [[Hand, foot and mouth disease]], acute [[hemorrhagic]] [[conjunctivitis]], [[Aseptic meningitis]], [[Myocarditis|myocarditis,]] severe [[neonatal]] [[sepsis]]-like disease, acute [[flaccid paralysis]].<sup>[[Enterovirus|[2]]]</sup>
|Treating symptoms and complications of the infection.
|-
|[[Rhinovirus]]
|[[Pharyngitis|Sore throat]], [[Rhinitis|runny nose]], [[nasal congestion]], [[Sneeze|sneezing]] and [[cough]]; sometimes accompanied by [[Myalgia|muscle aches]], [[Fatigue (medical)|fatigue]], [[malaise]], [[headache]], [[muscle weakness]], or [[Anorexia (symptom)|loss of appetite]].
|[[Interferon]]-alpha
[[Pleconaril]]
|-
|[[Respiratory syncytial virus]]
|[[Bronchiolitis]] (inflammation of the small airways in the lung) and [[pneumonia]] in children under 1 year of age
Recurrent wheezing and [[asthma]]
|Treating symptoms and complications of the infection.
[[Ribavirin]]
|-
|[[Mononucleosis]]
|Common symptoms include: Low-grade [[fever]] without chills is seen in nearly all cases, [[Sore throat]]: white patches on the tonsils and back of the throat are often seen, [[Muscle weakness]] and sometime extreme [[fatigue]], tender [[lymphadenopathy]], particularly the posterior [[cervical lymph nodes]] are involved
Other symptoms that have been described in patients with [[EBV|EBV infection]] include: unable to swallow due to [[Tonsils|enlarged tonsils]], [[Cough|dry cough]], [[Loss of appetite]], [[Anorexia]], [[Nausea]] without [[vomiting]], [[Abdominal pain]]- a possible symptom of a potentially fatal rupture of the spleen<sup>[[Mononucleosis history and symptoms|[1]]]</sup> [[Diarrhea]]
|Treating symptoms and complications of the infection.
|-
|[[Toxoplasmosis]]
|Symptoms are often [[influenza]]-like: Cervical lymphadenopathy, sore throat, muscle aches and pains that last for a month or more, fever, malaise, night sweats
|[[Pyrimethamine]]
[[Sulfadiazine]]
[[Leucovorin]] ([[Folinic acid]])
|-
|[[Herpes virus]]
|Watery [[Blister|blisters]] in the [[skin]] or [[mucous membranes]] (such as the mouth or lips) or on the [[Genital|genitals]].<sup>[[Herpes simplex virus|[1]]]</sup>
|Acyclovir
Valacyclovir
Famcyclovir
|-
|[[Cytomegalovirus|Cytomegalovirus (CMV)]]
|[[Mononucleosis]] like presentation.
[[Retinitis]]<nowiki/>presents with [[blurred vision]] and [[floaters]]. [[Colitis]] presents with [[abdominal pain]] and [[bloody diarrhea]]. [[Pneumonitis]]
|Ganciclovir
[[Foscarnet]] 
[[Cidofovir]] 
|-
| rowspan="5" |Acute Bacterial adenoiditis<ref name="pmid9804015" /><ref name="pmid7991612">{{cite journal |vauthors=Wessels MR, Bronze MS |title=Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=91 |issue=25 |pages=12238–42 |year=1994 |pmid=7991612 |pmc=45412 |doi= |url=}}</ref><ref name="Cunningham2000">{{cite journal|last1=Cunningham|first1=M. W.|title=Pathogenesis of Group A Streptococcal Infections|journal=Clinical Microbiology Reviews|volume=13|issue=3|year=2000|pages=470–511|issn=0893-8512|doi=10.1128/CMR.13.3.470-511.2000}}</ref><ref name="pmid4564883">{{cite journal |vauthors=Ellen RP, Gibbons RJ |title=M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence |journal=Infect. Immun. |volume=5 |issue=5 |pages=826–30 |year=1972 |pmid=4564883 |pmc=422446 |doi= |url=}}</ref>
|[[Haemophilus influenzae]]
|[[Bacteremia]], and acute bacterial [[meningitis]]. Occasionally, it causes [[cellulitis]], [[osteomyelitis]], [[epiglottitis]], and joint infections
([[otitis media]]) and eye ([[conjunctivitis]])
Sinusitis
Pneumonia
| rowspan="5" |Beta lactamase inhibitor antibiotics
|-
|[[Streptococcus|Group A β-hemolytic streptococcus]]
|[[Strep throat]], acute [[rheumatic fever]], [[scarlet fever]], acute [[glomerulonephritis]] and [[necrotizing fasciitis]]
[[rheumatic fever]]
|-
|[[Staphylococcus aureus]]
|[[Atopic dermatitis]], [[Toxic shock syndrome]]
|-
|[[Moraxella catarrhalis]]
|Otitis media and sinusitis, tracheobronchitis and [[pneumonia]]
|-
|[[Streptococcus pneumoniae]]
|Pneumonia, sinusitis, otitis media, endocarditis
|-
|Recurrent Bacterial adenoiditis<ref name="pmid21377220" /><ref name="Cunningham2000" />
| rowspan="2" |Usually due to normal flora pathogens:
* [[Staphylococcus aureus]]
* [[Streptococcus|Group A β-hemolytic streptococcus]]
| rowspan="2" |
Nasal [[airway obstruction]], [[Snoring]], [[sleep apnea]], oral breathing, sore or dry throat from breathing through the mouth, [[Rhinorrhea|purulent rhinorrhea]], nasal obstruction, fever, ear pain, [[Headache]], [[Sore throat]]
| rowspan="3" |[[Angioedema|Antihistamines]]
[[Angioedema|Cosrticosteroids]]
[[Angioedema|Decongestants]]
|-
|Chronic Bacterial adenoiditis<ref name="pmid17136878">{{cite journal| author=Akcay A, Tamay Z, Dağdeviren E, Guler N, Ones U, Kara CO et al.| title=Childhood asthma and its relationship with tonsillar tissue. | journal=Asian Pac J Allergy Immunol | year= 2006 | volume= 24 | issue= 2-3 | pages= 129-34 | pmid=17136878 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17136878  }}</ref><ref name="Cunningham2000" />
|-
| rowspan="3" |Non-infectious adenoiditis<ref name="pmid21377220" /><ref name="pmid17136878" /><ref name="pmid22870291" />
|Allergies
|Allergic [[sinusitis]]
Redness and [[Itch|itching]] of the [[conjunctiva]] (allergic conjunctivitis)
Sneezing, coughing, [[bronchoconstriction]], [[Wheeze|wheezing]] and [[dyspnea]], sometimes outright attacks of [[asthma]], in severe cases the airway constricts due to swelling known as [[angioedema]]
|-
|[[Asthma]]
|[[Cough]] with or without [[sputum]] ([[phlegm]]) production, pulling in of the skin between the ribs when breathing (intercostal retractions), [[Shortness of breath]] that gets worse with [[Exercise induced asthma|exercise or activity]], [[Wheezing]]
|[[LABA|Fast-acting bronchodilators]] ''([[LABA]])''
[[SABA|Short-acting selective beta<sub>2</sub>-adrenoceptor agonists]]
[[Asthma anticholinergic therapy|Anticholinergic medications]]
|-
|[[GERD]]
|[[Heartburn]], [[esophagitis]]''',''' [[Stenosis|strictures]], difficulty swallowing ([[dysphagia]]), [[vomiting]], effortless spitting up, [[coughing]], and other respiratory problems
|Lifestyle Modifications
[[Proton pump inhibitor]]s
[[Antacid]]s 
[[Alginic acid]] ([[Gaviscon]])
|}


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Disease]]
[[Category:Up-To-Date]]
[[Category:Otolaryngology]]
[[Category:Pediatrics]]
[[Category:Pulmonology]]
[[Category:Emergency medicine]]
[[Category:Infectious disease]]
[[Category:Surgery]]

Latest revision as of 20:18, 29 July 2020

Adenoiditis Microchapters

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Adenoiditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

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Treatment

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Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

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

Overview

The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1] Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface where it provides local immune protection. Adenoids can be infected by either bacterial and viral pathogens leading to adenoiditis.[2]

Pathophysiology

  • Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the Waldeyer's ring of lymphoid tissue, which is a ring of lymphoid tissue and includes adenoids and tonsils.
  • Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx during the 16th week of gestation.
  • Adenoids start to shrink by the age 6-7.
  • By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.

Pathogenesis

  • Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. Studies suggest that a reduction in IgA will happen postoperative of adenoidectomy.[2]
  • Adenoiditis can happen as a result of infection and harbor pathogenic bacterial activity, which may lead to the development of disease of the ears, nose, and sinuses. Adenoiditis can progress to chronic disease if remain untreated for a long term.
  • Parental history of tonsillectomy and atopy hold significant predictive power in pediatric adenoiditis.[3][4]
  • The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.[1]
  • The persistence of tonsillitis beyond 3 months is known as chronic tonsillitis. In case of chronic bacterial tonsillitis the bacteria persist in the tonsils and lead to chronic inflammation. This persistent infection and inflammation leads to chronic tonsillitis. Manifestations appear whenever the patient has decline in immunity.
  • The immune response between the antigen and lymphocyte that leads to cellular proliferation and enlargement of the adeoid especially in paracortex area which lead to excess enlargement of the adenoids.
  • Bacterial adenoiditis is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.[5]
  • Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).

Gross pathology

  • On gross pathology, characteristic findings of adenoiditis, include:
  • Enlarged adenoids
  • Soft greasy yellow areas within capsule

Microscopic Pathology

References

  1. ↑ 1.0 1.1 Mohseni S, Shojaiefard A, Khorgami Z, Alinejad S, Ghorbani A, Ghafouri A (2014). "Peripheral lymphadenopathy: approach and diagnostic tools". Iran J Med Sci. 39 (2 Suppl): 158–70. PMC 3993046. PMID 24753638.
  2. ↑ 2.0 2.1 Havas T, Lowinger D (2002). "Obstructive adenoid tissue: an indication for powered-shaver adenoidectomy". Arch. Otolaryngol. Head Neck Surg. 128 (7): 789–91. PMID 12117336.
  3. ↑ Capper R, Canter RJ (2001). "Is the incidence of tonsillectomy influenced by the family medical or social history?". Clin Otolaryngol Allied Sci. 26 (6): 484–7. PMID 11843928.
  4. ↑ Kvestad, Ellen; Kværner, Kari Jorunn; Røysamb, Espen; Tambs, Kristian; Harris, Jennifer Ruth; Magnus, Per (2005). "Heritability of Recurrent Tonsillitis". Archives of Otolaryngology–Head & Neck Surgery. 131 (5): 383. doi:10.1001/archotol.131.5.383. ISSN 0886-4470.
  5. ↑ Lilja M, Räisänen S, Stenfors LE (1998). "Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes". Int. J. Pediatr. Otorhinolaryngol. 45 (1): 15–20. PMID 9804015.
  6. ↑ 6.0 6.1 Beachey EH, Courtney HS (1987). "Bacterial adherence: the attachment of group A streptococci to mucosal surfaces". Rev. Infect. Dis. 9 Suppl 5: S475–81. PMID 3317744.
  7. ↑ Gibbons RJ (1989). "Bacterial adhesion to oral tissues: a model for infectious diseases". J. Dent. Res. 68 (5): 750–60. PMID 2654229.
  8. ↑ Zhang JM, An J (2007). "Cytokines, inflammation, and pain". Int Anesthesiol Clin. 45 (2): 27–37. doi:10.1097/AIA.0b013e318034194e. PMC 2785020. PMID 17426506.
  9. ↑ 9.0 9.1 Zautner AE, Krause M, Stropahl G, Holtfreter S, Frickmann H, Maletzki C, Kreikemeyer B, Pau HW, Podbielski A (2010). "Intracellular persisting Staphylococcus aureus is the major pathogen in recurrent tonsillitis". PLoS ONE. 5 (3): e9452. doi:10.1371/journal.pone.0009452. PMC 2830486. PMID 20209109.
  10. ↑ Alexander EH, Hudson MC (2001). "Factors influencing the internalization of Staphylococcus aureus and impacts on the course of infections in humans". Appl. Microbiol. Biotechnol. 56 (3–4): 361–6. PMID 11549002.
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