Adenoiditis pathophysiology

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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

X Ray

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Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

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 3993046Freely accessible. 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. ISSN 0886-4470. doi:10.1001/archotol.131.5.383. 
  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. PMC 2785020Freely accessible. PMID 17426506. doi:10.1097/AIA.0b013e318034194e. 
  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. PMC 2830486Freely accessible. PMID 20209109. doi:10.1371/journal.pone.0009452. 
  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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