Adenoiditis pathophysiology

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Adenoiditis Microchapters

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Patient Information

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

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

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

Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. They can be infected by either bacterial and viral pathogens and develop to adenoiditis.[1]

Normal adenoid development

  • 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 include adenoids and tonsils.
  • 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.

Pathophysiology

  • 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.[1]
  • 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.[2][3]
  • 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.[4]
  • 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).
  • On gross pathology, characteristic findings of adenoiditis, include:
  • Enlarged adenoids
  • Soft greasy yellow areas within capsule
Pathogen Symptoms Treatment
Viral Tonsillitis[11][12][13][14] 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

  • Incubation period: 1-2 months
  • Common symptoms include:
treating symptoms and complications of the infection.
Human adenovirus

Symptoms

treating symptoms and complications of the infection.
Enterovirus treating symptoms and complications of the infection.
Rhinovirus Symptoms include sore throatrunny nosenasal congestionsneezing and cough; sometimes accompanied by muscle achesfatiguemalaiseheadachemuscle weakness, or 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:
  • Other symptoms that have been described in patients with EBV infection include:
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 blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals.[1] Acyclovir

Valacyclovir

Famcyclovir

Cytomegalovirus (CMV) mononucleosis like presentation.

Retinitispresents with blurred vision and floatersColitis presents with abdominal pain and bloody diarrheaPneumonitis

Ganciclovir

Foscarnet 

Cidofovir 

Acute Bacterial Tonsillitis[5][15][16][17] Haemophilus influenzae bacteremia, and acute bacterial meningitis. Occasionally, it causes cellulitisosteomyelitisepiglottitis, and joint infections

(otitis media) and eye (conjunctivitis)

sinusitis

pneumonia

Group A β-hemolytic streptococcus strep throat, acute rheumatic feverscarlet fever, acute glomerulonephritis and necrotizing fasciitis

rheumatic fever

Staphylococcus aureus

Atopic dermatitis

Toxic shock syndrome

Moraxella catarrhalis otitis media and sinusitis

tracheobronchitis and pneumonia 

beta lactamase inhibitor antibiotics
Streptococcus pneumoniae pneumonia

sinusitis

otitis media

Endocarditis

Flouroquinolones

Macrolide

Penicillin and Beta lactamase inhibitors

Recurrent Bacterial Tonsillitis Usually due to normal flora pathogen:
  • Sore or dry throat from breathing through the mouth
Chronic Bacterial Tonsillitis
Non-infectious Tonsillitis[11][12][13] Allergies Allergic sinusitis

Redness and itching of the conjunctiva (allergic conjunctivitis)

Sneezing, coughing, bronchoconstrictionwheezing and dyspnea, sometimes outright attacks of asthma, in severe cases the airway constricts due to swelling known as angioedema

Antihistamines

Cosrticosteroids

Decongestants

Asthma fast-acting bronchodilators (LABA)

Short-acting selective beta2-adrenoceptor agonists

Anticholinergic medications

GERD Heartburn

esophagitis

strictures, difficulty swallowing (dysphagia)

vomiting, effortless spitting up, coughing, and other respiratory problems

Lifestyle Modifications

Proton pump inhibitors

Antacids 

Alginic acid (Gaviscon)

References

  1. 1.0 1.1 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.
  2. 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.
  3. 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.
  4. 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.
  5. 5.0 5.1 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.
  11. 11.0 11.1 Sadeghi-Shabestari M, Jabbari Moghaddam Y, Ghaharri H (2011). "Is there any correlation between allergy and adenotonsillar tissue hypertrophy?". Int J Pediatr Otorhinolaryngol. 75 (4): 589–91. doi:10.1016/j.ijporl.2011.01.026. PMID 21377220.
  12. 12.0 12.1 Akcay A, Tamay Z, Dağdeviren E, Guler N, Ones U, Kara CO; et al. (2006). "Childhood asthma and its relationship with tonsillar tissue". Asian Pac J Allergy Immunol. 24 (2–3): 129–34. PMID 17136878.
  13. 13.0 13.1 Proenca-Modena JL, Pereira Valera FC, Jacob MG, Buzatto GP, Saturno TH, Lopes L; et al. (2012). "High rates of detection of respiratory viruses in tonsillar tissues from children with chronic adenotonsillar disease". PLoS One. 7 (8): e42136. doi:10.1371/journal.pone.0042136. PMC 3411673. PMID 22870291.
  14. Endo LH, Ferreira D, Montenegro MC, Pinto GA, Altemani A, Bortoleto AE, Vassallo J (2001). "Detection of Epstein-Barr virus in tonsillar tissue of children and the relationship with recurrent tonsillitis". Int. J. Pediatr. Otorhinolaryngol. 58 (1): 9–15. PMID 11249975.
  15. Wessels MR, Bronze MS (1994). "Critical role of the group A streptococcal capsule in pharyngeal colonization and infection in mice". Proc. Natl. Acad. Sci. U.S.A. 91 (25): 12238–42. PMC 45412. PMID 7991612.
  16. Cunningham, M. W. (2000). "Pathogenesis of Group A Streptococcal Infections". Clinical Microbiology Reviews. 13 (3): 470–511. doi:10.1128/CMR.13.3.470-511.2000. ISSN 0893-8512.
  17. Ellen RP, Gibbons RJ (1972). "M protein-associated adherence of Streptococcus pyogenes to epithelial surfaces: prerequisite for virulence". Infect. Immun. 5 (5): 826–30. PMC 422446. PMID 4564883.