Allergic Rhinitis IP3

Inflammation of the nasal mucous membrane, causing symptoms like nasal congestion, runny nose, sneezing, and itching.

An IgE-mediated inflammatory response in the nasal mucous membranes triggered by inhaled allergens.

Inflammation of the conjunctiva (the membrane lining the eyelid and covering the white of the eye) caused by IgE-mediated response, leading to itching, redness, and tearing.

Allergic rhinitis that occurs year-round due to constant exposure to allergens like mold spores, house dust mites, animal dander, and cockroaches.

Allergic rhinitis that happens seasonally due to exposure to specific allergens, such as tree, grass, or weed pollens.

Allergic rhinitis that occurs after infrequent exposures to allergens not usually encountered in the patient's environment.

The nasal cavity serves as the airway for breathing, moistens and warms inhaled air, filters and cleans incoming air, helps with speech resonance, and houses smell receptors.

A protective layer that lines various body cavities exposed to the external environment, such as the respiratory, digestive, and urinary tracts.

Mucosa-covered projections in the nasal cavity that increase surface area, helping warm, moisten, and filter inhaled air.

A thin, transparent mucous membrane that lines the eyelids and covers the visible surface of the eye, secreting oils and mucus to lubricate it.

An exaggerated immune response that's harmful to the body, often triggered by allergens.

A type of hypersensitivity reaction involving IgE antibodies, mast cells, and basophils, leading to rapid symptoms like sneezing, itching, and swelling. Examples: allergies

A type of hypersensitivity reaction involving antibodies against self-antigens, leading to tissue damage. Examples: autoimmune diseases

A type of hypersensitivity reaction involving immune complexes that deposit in tissues, causing inflammation. Examples: lupus

A type of hypersensitivity reaction involving T cells and delayed reactions, often seen in autoimmune diseases. Examples: type 1 diabetes

A substance that triggers an allergic reaction in a sensitized individual, usually a protein.

The initial response to an allergen, happening within minutes, involves mast cell degranulation, releasing histamine, prostaglandins, and leukotrienes. This causes immediate symptoms like sneezing, runny nose, and itching.

The secondary response to an allergen, occurring 4-8 hours after initial exposure. This phase involves recruitment of eosinophils and TH2 cells, causing prolonged inflammation and symptoms like congestion and nasal polyps.

The activation of the parasympathetic nervous system leads to increased mucus secretion, causing a runny nose.

Histamine, a powerful chemical released during the allergic reaction, binds to H1 receptors on sensory nerves, causing itching and sneezing.

Histamine, released during the allergic reaction, causes the blood vessels to widen (vasodilation) and become leaky, leading to congestion and stuffy nose.

Allergens trigger vasodilation and swelling (edema) in the conjunctiva (the membrane lining the eye), leading to itchy, red, and watery eyes.

TH2 cells, specialized immune cells, play a crucial role by secreting cytokines like IL-4 and IL-13. These cytokines promote the production of IgE antibodies and recruit more eosinophils, contributing to the allergic response.

Histamine, a chemical released during the allergic reaction, binds to H1 receptors. This causes vasodilation, increased vascular permeability, smooth muscle contraction, and stimulation of sensory nerves, ultimately leading to symptoms like sneezing, itching, and nasal congestion.

Allergic rhinitis causes symptoms such as clear rhinorrhea, sneezing, nasal congestion, itchy ears, nose, and palate, and allergic conjunctivitis. Physical examination findings include a crease across the nose, dark circles under the eyes, and pale nasal mucosa.

Complications of allergic rhinitis include sleep disruption, fatigue, impaired work/school performance, postnasal drip with cough, loss of smell or taste, high-arched palate, persistent crease across the nose, dark circles under the eyes, asthma, chronic sinusitis, nosebleeds, nasal polyps, and sleep apnea.

Ethanolamine Ether, Alkyl Amine, and Phenothiazine are chemical classes that first-generation antihistamines belong to.

Loratadine is metabolized by CYP3A4 to form Desloratadine, which is the active ingredient.

Activation of peripheral α-adrenergic receptors causes vasoconstriction, reducing blood flow and congestion. This effect is used to treat conditions like nasal congestion.

α-1 adrenergic agonists work by binding to α-1 receptors in vascular smooth muscle, causing vasoconstriction and reducing nasal swelling. This reduces congestion.

Pseudoephedrine and phenylephrine act as mimics of norepinephrine and epinephrine, selectively activating α-1 receptors to reduce nasal congestion. This design strategy is effective because it specifically targets the desired effect.

Keeping household humidity below 50% can help prevent mold growth, a common allergen for people with allergic rhinitis.

Wearing a mask during pollen season, especially during outdoor activities, can help reduce exposure to allergens.

Intranasal drug delivery delivers medication directly to the site of inflammation in the nasal passages, minimizing systemic drug exposure and side effects.

Before using intranasal medication, clear nasal passages to ensure the medication reaches the intended area and is absorbed properly.

Second-generation antihistamines, like loratadine and cetirizine, do not cross the blood-brain barrier as easily, resulting in less sedation and milder anticholinergic effects compared to first-generation antihistamines.

First generation antihistamines like diphenhydramine and chlorpheniramine can cross the blood-brain barrier, leading to sedation and drowsiness due to their central nervous system effects.

Cromolyn sodium is a mast cell stabilizer that prevents the release of histamine and other inflammatory mediators from mast cells, reducing allergic symptoms.

Intranasal corticosteroids, such as fluticasone and mometasone, work by reducing inflammation in the nasal lining, effectively treating allergic rhinitis symptoms.

Pseudoephedrine and phenylephrine are sympathomimetic decongestants that constrict blood vessels in the nasal passages, relieving congestion.

Montelukast is a leukotriene receptor antagonist that blocks the action of leukotrienes, chemicals involved in the inflammatory response associated with allergic rhinitis.

Inflammation of the conjunctiva, the membrane lining the eyelid and covering the white of the eye, caused by an infection or an irritant, such as an allergen.

Allergic conjunctivitis is caused by an allergic reaction in the conjunctiva. It is characterized by itchy, red, and watery eyes.

It's a common bacterial infection of the conjunctiva, often referred to as 'pink eye'.

It refers to an immune response that goes into overdrive and causes harm to the body, often triggered by allergens.

Maintaining household humidity below 50% and removing visible mold with bleach or disinfectant can significantly reduce mold growth, a common allergen for people with allergic rhinitis. This helps prevent further sensitization and aggravation of symptoms.

Wearing a face mask, especially during outdoor activities, can reduce exposure to pollen, a major trigger for seasonal allergies. This helps minimize symptoms and maintain a comfortable lifestyle.

First-generation antihistamines, like diphenhydramine and chlorpheniramine, can cross the blood-brain barrier, leading to sedation and drowsiness due to their central nervous system effects. This can be a significant drawback for some individuals.

Prolonged (more than 10 days) use of these eye drops can lead to rebound redness of the eyes. This happens because the vasoconstrictors have shrunk the blood vessels, and when the medication is stopped, they rebound (become bigger) causing redness.

These medications can raise pressure inside the eye, which could be harmful for people who already have glaucoma.

Systemic decongestants (taken by mouth) are most likely to cause unwanted side effects. Intranasal (sprayed in the nose) decongestants are less likely to cause these side effects.

These medications can cause a problem called 'rhinitis medicamentosa.' This is like rebound hyperemia, but in the nose. It's when the decongestant is stopped, the blood vessels in the nose rebound, and the congestion actually gets worse.

Ophthalmic vasoconstrictors are not effective for reducing allergic inflammation. They only reduce the redness of the eyes.

They can be helpful for reducing nasal congestion, but they should only be used when symptoms are present.

Pseudoephedrine and phenylephrine are both decongestants. They act on the same type of receptors, but pseudoephedrine is typically more effective and longer-lasting.

Oral decongestants, like pseudoephedrine, are more likely to cause systemic side effects. Intranasal decongestants are less likely to be absorbed into the bloodstream and cause these side effects.

These are more effective for treating allergic rhinitis symptoms than decongestants. They reduce the overall inflammation and swelling instead of just addressing the congestion.

Intranasal corticosteroids are often the first-line treatment for allergic rhinitis. This is because they are effective, safe, and convenient.

Immunotherapy aims to increase the body's tolerance to allergens by gradually exposing the patient to increasing doses of the allergen, leading to decreased IgE production, increased IgG production, and changes in T-lymphocytes.

Subcutaneous immunotherapy (SCIT) involves injecting increasing doses of allergen extracts under the skin, often administered one to two times a week until the maximum tolerated dose is reached.

Sublingual immunotherapy (SLIT) involves placing allergen extracts under the tongue, allowing for gradual absorption into the bloodstream.

Some allergens can cause more severe reactions than others, and specific allergens can also trigger serious side effects such as anaphylaxis. Patients with severe, uncontrollable symptoms or a history of significant allergic reactions may not be suitable candidates for immunotherapy.

Common side effects of immunotherapy include local reactions at the injection site, such as swelling and redness, as well as more serious reactions like urticaria, bronchospasm, laryngospasm, vascular collapse, and anaphylaxis.

Corticosteroids, when delivered intranasally, directly target the nasal tissue, reducing inflammation by blocking the release of inflammatory mediators, suppressing neutrophil chemotaxis, reducing cell swelling, causing mild vasoconstriction, and inhibiting mast cell-mediated reactions.

Ophthalmic corticosteroids, like loteprednol, are used to reduce inflammation in the conjunctiva, providing temporary relief from allergic conjunctivitis symptoms. It's important to remove contact lenses before instilling these medications.

Oral corticosteroids are rarely used for allergic rhinitis due to their potential for significant side effects. However, a short course might be used to treat severe or persistent nasal symptoms.

Intranasal corticosteroids, such as fluticasone and mometasone, are frequently used to treat allergic rhinitis. They work by reducing inflammation in the nasal lining, effectively managing symptoms.

Topical corticosteroids like loteprednol are preferred for allergic conjunctivitis because they have a lower risk of increasing intraocular pressure compared to other ocular corticosteroids.

Ophthalmic antihistamines, due to their mast cell stabilizing effect, are the preferred agents for allergic conjunctivitis. They help reduce inflammation and allergic symptoms in the eye.

Corticosteroids, like all steroids, have a characteristic chemical structure with a specific arrangement of rings and functional groups. This specific structure is essential for their biological activity.

Corticosteroids work by regulating gene expression, influencing the production of proteins involved in inflammation. They modulate the immune response, suppressing inflammation.

Intranasal corticosteroids are delivered directly to the nasal tissue, minimizing systemic exposure and potential side effects. This targeted delivery helps reduce inflammation in the nose.

Contact lenses can absorb and trap eye drops, affecting the medication's effectiveness. Therefore, it's recommended to remove lenses before instilling ophthalmic corticosteroids and wait 10 minutes before reinserting.

Intranasal corticosteroids are the most effective first-line treatment for persistent or moderate-to-severe allergic rhinitis symptoms.

Oral second-generation antihistamines like loratadine or cetirizine are good options for mild intermittent symptoms or patients who prefer not to use nasal sprays.

Intranasal antihistamines like azelastine provide rapid symptom relief, especially for seasonal rhinitis.

Leukotriene receptor antagonists like montelukast are another option for second-line therapy.

Combination therapies like azelastine/fluticasone (Dymista) or olopatadine/mometasone (Ryaltris) combine an antihistamine and a corticosteroid for synergistic effects.

First-generation antihistamines, like diphenhydramine, can cause sedation and drowsiness due to their effects on the central nervous system.

Ophthalmic antihistamines, such as ketotifen, olopatadine, and bepotastine, are preferred for treating allergic conjunctivitis as they directly target the eye inflammation.

Cromolyn sodium is a mast cell stabilizer that prevents the release of histamine and other inflammatory mediators from mast cells, reducing allergic reactions.

Intranasal corticosteroids effectively reduce inflammation in the nasal lining, making them a valuable treatment option for allergic rhinitis.

Montelukast, a leukotriene receptor antagonist, blocks the action of leukotrienes involved in the inflammatory response associated with allergic rhinitis.