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Medicine and surgery
Antihistamines for allergies
Glucocorticoids
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Hypertension: Clinical (To be retired)
Hypercholesterolemia: Clinical (To be retired)
Peripheral vascular disease: Clinical (To be retired)
Leg ulcers: Clinical (To be retired)
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Antiplatelet medications
Hypersensitivity skin reactions: Clinical (To be retired)
Eczematous rashes: Clinical (To be retired)
Papulosquamous skin disorders: Clinical (To be retired)
Alopecia: Clinical (To be retired)
Hypopigmentation skin disorders: Clinical (To be retired)
Benign hyperpigmented skin lesions: Clinical (To be retired)
Skin cancer: Clinical (To be retired)
Diabetes mellitus: Clinical (To be retired)
Hyperthyroidism: Clinical (To be retired)
Hypothyroidism and thyroiditis: Clinical (To be retired)
Dizziness and vertigo: Clinical (To be retired)
Hyperthyroidism medications
Hypothyroidism medications
Insulins
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Gastroesophageal reflux disease (GERD): Clinical (To be retired)
Peptic ulcers and stomach cancer: Clinical (To be retired)
Diarrhea: Clinical (To be retired)
Malabsorption: Clinical (To be retired)
Colorectal cancer: Clinical (To be retired)
Diverticular disease: Clinical (To be retired)
Anal conditions: Clinical (To be retired)
Cirrhosis: Clinical (To be retired)
Breast cancer: Clinical (To be retired)
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Anemia: Clinical (To be retired)
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Pneumonia: Clinical (To be retired)
Urinary tract infections: Clinical (To be retired)
Skin and soft tissue infections: Clinical (To be retired)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anti-mite and louse medications
Chronic kidney disease: Clinical (To be retired)
Kidney stones: Clinical (To be retired)
Urinary incontinence: Pathology review
ACE inhibitors, ARBs and direct renin inhibitors
PDE5 inhibitors
Adrenergic antagonists: Alpha blockers
Stroke: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Headaches: Clinical (To be retired)
Migraine medications
Asthma: Clinical (To be retired)
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Lung cancer: Clinical (To be retired)
Antihistamines for allergies
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines
Pulmonary corticosteroids and mast cell inhibitors
Joint pain: Clinical (To be retired)
Rheumatoid arthritis: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Osteoporosis medications
Asthma: Clinical (To be retired)
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Tanner Marshall, MS
Asthma is an episodic, chronic respiratory disorder characterized by airway obstruction caused by inflammation and hyperresponsiveness of the bronchial smooth muscle. The two golden words in asthma are “reversible”, which means the obstruction can virtually disappear with medications like bronchodilators, and “inducible”, which means the obstruction can occur in response to a variety of stimuli; including allergens like house dust mites, pet animal dander, like cat dander, and pollen, or irritants like tobacco smoke, respiratory tract infections, like a common cold or pneumonia, cold or dry air, and even emotional stress. Now, atopy is the genetic predisposition of an individual towards developing IgE antibodies to otherwise harmless environmental antigens, making that individual strongly predisposed to developing three allergic disorders, eczema or atopic dermatitis, allergic rhinitis, and asthma, collectively coined the atopic triad. Because of this genetic component, asthma is usually diagnosed in early childhood, and may or may not carry on into adulthood.
So, let’s say a genetically predisposed child is exposed to a potential allergen for the first time. First off, dendritic cells take up the allergen and present it to a type 2 helper T-cell, or Th2 cell. In asthma, Th2 cells make the mistake of thinking this harmless antigen is an allergen, so they release cytokines that stimulate B cells to make IgE antibodies. IgE antibodies then prime mast cells, which cautiously anticipate the next event. When the child is re-exposed to the allergen, the mast cells spill out vasoactive mediators like histamine and leukotrienes, which cause bronchoconstriction and inflammation. Once the child is no longer exposed to the allergen, the immune system relaxes, and everything goes back to normal, until the next event. Now, not all asthma episodes are triggered this way by an allergen. A unique form of asthma is aspirin sensitive asthma, which is characterized by the triad of asthma, nasal polyps, and sensitivity to aspirin or NSAIDs. Aspirin opposes prostaglandin production and tips the balance between prostaglandins and leukotrienes in favor of increased leukotriene production, which promotes smooth muscle contraction of the airways.
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