Kembara Xtra - Medicine - Allergic Rhinitis

Kembara Xtra - Medicine - Allergic Rhinitis 
​After being exposed to allergens like pollen, dust, or animal dander, the mucous membranes in the nose, eyes, ears, and throat may experience a variety of symptoms known as allergic rhinitis.
Sneeze, congestion, and rhinorrhea are the early symptoms of IgE-mediated inflammation of the nasal mucosa in response to exposure to an exogenous protein. A persistent late phase is marked by congestion and mucosal hyperreactivity.
Allergic rhinitis can be sporadic or persistent, as well as seasonal or perennial.
Outdoor allergens including tree pollen, flowering shrubs in the spring, grasses and flowering plants in the summer, and ragweed and mildew in the fall, are typically to blame for seasonal reactions.
Perennial reactions, or symptoms that persist throughout the year, are frequently linked to indoor allergens such dust mites, mildew, and animal dander.
Occupational allergens can produce seasonal or year-round allergic rhinitis, which can be intermittent.
It is possible to develop non-allergic rhinitis, such as vasomotor, pregnancy-related, and medicamentosa.

Child Safety Considerations

Sleep problems, dental misalignments, and facial abnormalities can all be caused by chronic nasal blockage.

Pregnant women's issues

All types of rhinitis may become more severe during pregnancy due to physiological changes, especially in the second trimester.

Epidemiology 

The average age of onset is 8 to 11 years, and around 80% of patients have established allergic rhinitis by the time they are 20 years old. Onset often occurs in the first two decades, seldom before 6 months of age, and tends to get worse as people age.


Prevalence
44-87% of patients with allergic rhinitis have mixed allergic and nonallergic rhinitis, which is more common than either pure form. Scandinavian studies have shown a cumulative prevalence rate of 14% in men and 15% in women. 10-25% of U.S. adults and 9-42% of U.S. children are affected.

Pathophysiology and Etiology 

Mucosal inflammation brought on by aeroallergens is brought on by infiltrating and residing inflammatory cells as well as vasoactive and proinflammatory mediators (such as cytokines).
Allergens in inhalants:
- Perennial: indoor molds, animal dander, cockroach and bug debris, home dust mites,
- Temporary: pollen from trees, grass, and weeds; outdoor molds
- For those working in farms and veterinary offices, latex, plant items (like baking flour), sensitizing chemicals, and specific animals
80% of people have a substantial genetic predisposition toward allergy diseases despite complex genetics.

Risk factors include atopy in the family history, with a higher chance if both parents have the condition.
Higher socioeconomic level.Patients with allergic rhinitis who inhale tobacco smoke may have worsening of their symptoms and an increased chance of acquiring asthma.
Uncertain evidence exists on the risk associated with early, recurrent exposure to the offending allergen and early introduction of solid food. Pets in the house and cockroach infestations in the home can also result in perpetual allergic rhinitis.
Another risk factor is male gender. 

Prevention 
Maternal nutrition and allergy avoidance have not been shown to be useful in the primary prevention of atopic illness.
Up to 6 months of age, breastfeeding exclusively reduces the risk of various atopic illnesses.
The "first-line treatment" is the avoidance of trigger environments.
There is insufficient data to back up the use of acaricides along with mite-proof mattress and pillow covers, removing carpet and drapes, removing indoor plants, and controlling pets.
Close doors and windows during allergy season; use a dehumidifier to lower house humidity; air conditioning and minimal outside exposure during allergy season; ineffective HEPA air cleaners and vacuum bags.


Accompanying Conditions 

Asthma, atopic dermatitis, allergic conjunctivitis, and food allergies are further IgE-mediated diseases.

Diagnoses are determined mostly based on the history and physical examination.

Atopic dermatitis and/or food allergies, a history of nasal congestion, rhinorrhea, pruritus of the nose, eyes, ears, and/or palate, sneezing, itching, and watering eyes, a family history of allergic diseases, a history of environmental and occupational exposure, as well as a history of various nasal stimuli, can all be used to distinguish between allergic and vasomotor rhinitis.

clinical assessment 
Numerous characteristics are indicative but not conclusive of allergic rhinitis:
Transverse nasal crease from rubbing nose up; frequently visible in infants; dark circles under eyes; "allergic shiners" (infraorbital venous congestion); and rhinorrhea, generally with clear discharge
Postnasal mucus discharge Oropharyngeal lymphoid tissue hypertrophy Pale, soggy, blue-gray nasal mucosa


Multiple Diagnoses 
Infectious rhinitis, often known as rhinosinusitis, is a viral condition that is frequently accompanied by a subsequent bacterial infection. Between the ages of 2 and 6 years, viral rhinitis typically has six episodes per year.
- Rhinitis medicamentosa (RM) - IgA deficiency with recurrent sinusitis:
Topical decongestant drops and sprays are the most popular treatments that have a rebound effect; other drugs that may cause RM include ACE inhibitors, reserpine, -blockers, oral contraceptive pills (OCPs), guanethidine, methyldopa, Aspirin, and NSAIDs
- Vasomotor (idiopathic) rhinitis brought on by a variety of nasal stimuli, including light or particle matter, cold or warm air, aromas and odors, and both.
- Hormonal: OCPs, thyroid, and pregnancy
- NARES, or nonallergic rhinitis with eosinophilia syndrome
- Gustatory: watery rhinorrhea brought on by food or alcohol; - "Skier's nose": watery rhinorrhea brought on by chilly air
Diseases connected to rhinitis:
- Tumor and nasal polyps
- Adenoidal hypertrophy, especially in children - Septal irregularity or deflected nasal septum (DNS) in adults - Septal/anatomic blockage

Laboratory results and diagnostic tests 

Rarely necessary are lab tests
In order to determine the allergen for immunotherapy, skin testing is performed.
Initial exams (lab, imaging) Testing is infrequently necessary.
If a diagnostic suggests additional factors, take into account:
- Eosinophil counts may be high on a CBC with differential.
Nasal probe smear results may reveal higher eosinophils due to an increased total serum IgE level.
Drugs that may affect lab findings include corticosteroids, which can lower eosinophilia.
- Antihistamine use should be stopped seven days prior to testing since it reduces skin test responsiveness.
Sinuses can be checked for total opacity, fluid level, and mucosal thickening using a CT scan, which is not usually done.


Other/Diagnostic Procedures
If treatment for allergy symptoms is ineffective, only then should testing or immunotherapy be considered.
Radioallergosorbent test (RAST) or allergen skin testing for specific allergen sensitivity; clinical correlation based on history is crucial in interpreting results.
Diagnostic allergy prick tests are used to decide on an agent, choose the best environmental controls, and guide immunotherapy:
- Prick or puncture: abrasion of the skin's surface followed by administration of test antigen or the intradermal
RAST is often utilized in patients for whom skin testing is impractical or where a serious reaction could occur. It is more expensive and less sensitive than skin testing.
Rhinoscopy is helpful for observing posterior pharyngeal structures, such as adenoids, polyps, and the larynx, as well as intranasal architecture.
Eosinophils predominate in nasal washing/scraping, while basophils and mast cells can also be seen.
Nasal mucosa features include goblet cells, eosinophilic infiltration, and submucosal edema without destruction.

Management 

The three mainstays of treating allergic rhinitis are as follows:
Avoiding allergens, taking medication, and using allergy immunotherapy

General Actions 
Limit your contact with the allergen.

Medication 

Intranasal sprays and oral medications are frequently employed.
Initial Line
Mild symptoms: The first-line treatment for mild to moderate allergic rhinitis is 2nd-generation nonsedating antihistamines.
Negative effects include mild drowsiness and slight anticholinergic effects.
Levocetirizine, a second-generation non-sedating antihistamine, is an effective but pricey generic (cetirizine, fexofenadine, loratadine; most to least effective).
Mild to severe signs and symptoms: The first-line treatment for moderate to severe allergic rhinitis is intranasal corticosteroids:
The most effective medicine class for treating allergic rhinitis symptoms is nasal sprays. Use them after a shower and aim them away from the septum to promote mucosal surface deposition.
- Although it can be used as needed, it works best when used frequently. - Negative effects include nosebleeds, perforated nasal septa, and systemic corticosteroid effects.
- When administered via a metered-dose inhaler, the new-generation corticosteroid clesonide has been shown to be effective in the treatment of asthma.
Systemic steroids should only be explored in extreme circumstances and for brief periods of time. Ciclesonide is also currently undergoing clinical research as an intranasal formulation for the treatment of AR.
Next Line
Effective nasal antihistamines with the potential for systemic absorption and sedation olopatadine, azelastine
Decongestants Phenylephrine: 10 mg PO every four hours (PRN) Pseudoephedrine: 60 mg PO every six hours (PRN)
- Oxymetazoline nasal spray (Afrin): q10–12h PRN, 2–3 sprays per nostril, max 3 days. Due of rebound rhinitis, intranasal medications shouldn't be administered for longer than three days.
Patients with heart arrhythmia or hypertension (HTN) should be discouraged from using.
ipratropium nasal spray, 2 sprays per nostril, BID-TID, is an example of an intranasal anticholinergic.
- When combined with steroid use, intranasal anticholinergics can boost effectiveness.
Drugs that block leukotrienes, such as montelukast 10 mg/day PO
- May be used as the first line of treatment in people with concurrent asthma; generally, it should be an adjuvant, not a monotherapy
Mast cell stabilizers, such as cromolyn nasal spray 1 spray per nostril TID-QID, may require 2 to 4 weeks of treatment for best efficacy, and individuals with nonallergic rhinitis and nasal polyps may not benefit from them.
Third-generation antihistamines, including those listed below:
12 to 24 mg PO BID of brompheniramine
Chlorpheniramine: 4 mg PO q4-6h PRN
1 to 2 mg PO BID PRN of clemastine
- Diphenhydramine: 25 to 50 mg PO every 4-6 hours on demand
In men with prostatism and/or hypertrophy, this condition may cause urine retention.
Sedation, a longer QT interval, decreased performance, and an anticholinergic action are some of the negative consequences.
QUESTIONS FOR REFERENCE
Inquire with your allergist about immunotherapy.

Further Therapies 

Nasal saline use has been shown to be effective as a stand-alone or supplementary treatment.
Additional treatment methods Consider commencing intranasal steroids with a "burst," utilizing two sprays in each nostril per day for two weeks, then reducing the dosage to one spray per nostril per day moving forward.
- Consider a "5 days on, 2 days off" plan, with the days off being the days with the least exposure to allergens, to lessen the long-term negative effects of intranasal steroids.
- Allergen immunotherapy (desensitization) - Reserved for symptoms that are unmanageable with medical treatment or have a comorbidity (such as asthma) - Specific allergen extract is injected SC in increasing doses to create patient tolerance.


Take Action 

Patient observation
It's crucial to start the patient education process.
DIET Some people who have a severe allergy to seasonal pollens may develop oral allergy syndrome, which is characterized by mouth itchiness after eating fresh fruit that may react with the allergens.

Prognosis The goal is to achieve an acceptable level of symptom control, and treatment can help lower the risk of concomitant conditions including sinusitis and asthma.


Complications include: Epistaxis; secondary infections such sinusitis or otitis media; nasal lymphoid hyperplasia; airway hyperreactivity from allergen exposure; asthma; facial abnormalities, especially in mouth-breathing children; and sleep disturbances.

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