Therapy for acute/chronic asthma that inhibits mast cell degranulation
Chromolyn and nedocromil. Note that these are not really used anymore.
Therapy for acute/chronic asthma that inhibits leukotrienes
Zileuton: 5-lipoxygenase inhibitor prevents synthesis of leukotrienes. Montelukast/Zafirlukast: LTD4 receptor antagonists prevent activation of leukotriene receptors.
Therapy for acute/chronic asthma that dilates the bronchioles.
Albuterol, terbutaline, metaproterenol, pirbuterol: beta-2 selective agonists causes smooth muscle relaxation in airways. Salmeterol, formoterol: long-acting beta-2 selective agonists. Theophylline: methylxanthine that inhibits PDE? and relaxes smooth muscle. Ipratropium: muscarinic receptor antagonist and prevents bronchospasm.
Therapy for acute/chronic asthma that reduce inflammation.
Inhaled corticosteroids: beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone, triamcinolone.
Anti-IgE antibody that targets the Fc portion of the IgE molecule that prevents it from binding to the mast cell and thus prevents mast cell degranulation.
Omalizumab. Note that it is important that it binds to the Fc region, because if it cross-linked IgE molecules you would have massive anaphylaxis.
Why is omalizumab reserved for people who do not have results from bronchodilators and inhaled corticosteroids?
Although it is a great drug, it is very expensive and it thus not first line therapy.
Treatment for someone in anaphylaxis
1) Non-selective alpha/beta agonist epinephrine 2) Antihistamines diphenhydramine (H1R antagonist) + Cimetidine/ranitidine (H2R antagonist) to prevent mast cell degranulation 3) Corticosteroids to block late-phase cytokine response. 4) IV fluids to account for fluid loss from increased vascular permeability from vasoactive amines.
How do you administer definitive therapy to a patient who has a type 1 hypersensitivity?
Desensitization by allergen-specific immunotherapy. This involves repeated increasing doses of the allergen that results in stimulation of regulatory T-cells, inhibition of the immune response and decreased sensitivity on re-exposure.
Treatment to prevent erythroblastis fetalis
Administration of Rhogam (anti-Rh antibody) < 72 hrs after delivery to clear fetal RBCs from maternal circulation and prevent her immune system from mounting an antibody response that could cause erythroblastis fetalis in a future baby.
How do people have a type II hypersensitivity to penicillin and sulfa drugs?
The drug metabolite (happen) binds covalently to a carrier protein that stimulates an immune response against the hapten-carrier complex, typically on an RBC (which causes hemolytic anemia, thrombocytopenia etc). Note that often the immune response against penicillin is driven by IgE.
A patient presents with joint pain, fatigue, fever, serositis and labs positive for anti-nuclear antibodies and anti-histone antibodies. She has a history of hypertension and takes hydralazine and procainamide. What is likely causing her condition? How do you treat her?
Hydralazine and procainamide can cause drug-induced Lupus, a type III hypersensitivity. If you remove the drug she will go back to normal.
How does poison ivy cause a type IV hypersensitivity reaction?
Haptens complex with carrier proteins in the dermis and are then swallowed up by dendritic cells. Langerhans cells go back to the lymph nodes to elicit a T-cell response. The T-cells go back to the site of contact and initiate an inflammatory reaction.
Treatment for contact dermatitis
Topical corticosteroids and tacrolimus to suppress inflammation. Antihistamines can also be given to control itching.
How does carbamazepine induce Stevens-Johnson syndrome (toxic epidermal necrolysis)? What group of people are at higher risk for this?
Carbamazepine binds directly to HLA-B*1502 on the surface of keratinocytes -> the carbamazepine-HLA complex triggers CTL response in keratinocytes. Greater risk for east asians.