What each drug is FOR, and what you tell the patient. 245 entries across the Exam 2 lectures, each citing its slide. Indications and patient education are the two things students under-study most.
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| Delivery routes and absorption | ||||
| Topical route drops, gels, ointments | Indication | Prompt absorption, depending on the formulation. Convenient, economical and relatively safe. | Counsel on the drawbacks: adherence (compliance), surface toxicity of the cornea and conjunctiva, and systemic side effects from drug absorbed down the tear duct (nasolacrimal absorption). | L4 slide 5 |
| Injections around the eye subconjunctival, sub-Tenon's, retrobulbar | Indication | Anterior segment infections, posterior uveitis and cystoid macular edema. Absorption is prompt or sustained, depending on the formulation. | Specialist procedures. The limitations are serious: tissue injury, globe perforation and optic nerve trauma. | L4 slide 5 |
| Intracameral injection inside the anterior chamber | Indication | Anterior segment surgery and infections. Absorption is prompt. | Limited by corneal and intraocular toxicity and a relatively short duration of action. | L4 slide 5 |
| Intravitreal injection or device | Indication | Endophthalmitis, retinitis and age-related macular degeneration. Absorption is circumvented, giving an immediate local effect with a potential sustained effect. | The limitation is retinal toxicity. | L4 slide 5 |
| Dosage forms solutions, suspensions, gels, ointments, inserts | Education-heavy | Most drugs are given as solutions; suspensions are used for drugs with limited solubility. Gels, ointments and solid inserts prolong contact with the eye. | More time in the cul-de-sac (the pocket behind the lower lid) means more absorption. Inserts and implants give sustained release of the drug. | L4 slide 6 |
| Ways to change ocular absorption | Education-heavy | Absorption depends on time in the cul-de-sac and precorneal tear film, nasolacrimal drainage, drug binding to tear and tissue proteins, and diffusion across the cornea and conjunctiva. | It can be changed by switching the formulation or by blocking the tear ducts (silicone plugs, cautery) so that less drug drains away. | L4 slide 7 |
| Nasolacrimal drainage and transcorneal absorption | Education-heavy | Transcorneal absorption is necessary for the local ocular effect and has a lag time. Nasolacrimal drainage causes systemic absorption, which avoids first-pass metabolism. | That systemic absorption is the source of systemic side effects from eye drops, which is why pressing on the tear duct after a drop is taught. | L4 slide 8 |
| Prodrugs activated in the eye dipivefrin, latanoprost | Education-heavy | Some drugs are metabolized in the eye, which is useful for prodrugs: dipivefrin becomes epinephrine and latanoprost becomes prostaglandin F2 alpha. | Elimination after systemic absorption is by normal liver and kidney clearance. | L4 slide 10 |
| Ocular antibiotics | ||||
| Periocular infections choosing the route | Indication | Periocular infections range from preseptal cellulitis to postseptal (orbital) cellulitis. The route of antibiotic depends on patient specifics: the clinical setting (such as preceding trauma), age, immunocompromised state (cancer, human immunodeficiency virus [HIV] infection) and how much disease is involved. | Trauma, age, immune status and the extent of disease all shift the route of antibiotic. | L4 slide 11 |
| Topical ophthalmic antibiotics general approach | Indication | Small, mild, peripheral infections are usually treated topically with broad-spectrum antibiotics and no cultures unless an unusual organism is expected, for example in an immunocompromised patient. More involved infection may need oral or parenteral agents. | Topical treatment gives high local concentrations with limited systemic bioavailability, but needs frequent dosing. The spectrum of organisms changes over time (for example, Haemophilus influenzae fell after vaccination). | L4 slide 12 |
| Conjunctivitis | Indication | Ranges from mild redness (hyperemia) to purulent discharge. Common causes are viruses, allergies, environmental irritants and contact lenses; the bacterial causes include Neisseria, Haemophilus, Streptococcus pneumoniae, Staphylococcus aureus and Moraxella catarrhalis. | The goal of treatment is to eradicate infection and prevent long-term complications. Antibiotics help only the bacterial causes. | L4 slide 13 |
| Macrolides | ||||
| Erythromycin ointment macrolide | Indication | Superficial ocular infections involving the conjunctiva or cornea, and prophylaxis of ophthalmia neonatorum (newborn eye infection). | The named agent for newborn eye prophylaxis. | L4 slide 14 |
| Fluoroquinolones | ||||
| Ciprofloxacin (Ciloxan) | Indication | One of the two widest lists among the eye antibiotics (tied with gentamicin): conjunctivitis, keratitis, keratoconjunctivitis, corneal ulcers, blepharitis, blepharoconjunctivitis, meibomianitis and dacryocystitis (tear sac infection). | Comes as a solution or an ointment. | L4 slide 14 |
| Levofloxacin, ofloxacin (Ocuflox) | Indication | Conjunctivitis and corneal ulcers. | Both are fluoroquinolones, so the same class counseling applies. | L4 slide 14 |
| Moxifloxacin (Vigamox), gatifloxacin (Zymaxid) | Indication | Conjunctivitis. | Both are fluoroquinolones, so the same class counseling applies. | L4 slide 14 |
| Aminoglycosides | ||||
| Gentamicin sulfate | Indication | Conjunctivitis, blepharitis, keratitis, keratoconjunctivitis, corneal ulcers, blepharoconjunctivitis, meibomianitis and dacryocystitis. | Comes as a solution or an ointment. | L4 slide 14 |
| Tobramycin (Tobrex) | Indication | External infections of the eye and its adnexa (eyelids and surrounding structures). | Comes as a solution or an ointment. | L4 slide 14 |
| Other ophthalmic antibiotics | ||||
| Bacitracin ointment | Indication | Conjunctivitis, blepharitis, keratitis, keratoconjunctivitis, corneal ulcers, blepharoconjunctivitis and meibomianitis. | Ointment form. | L4 slide 14 |
| Polymyxin B combinations | Indication | Conjunctivitis, blepharitis and keratitis. | Available as various solutions and ointments. | L4 slide 14 |
| Sulfacetamide sodium | Indication | Conjunctivitis and other superficial ocular infections. | Comes as a solution or an ointment. | L4 slide 14 |
| Macrolides | ||||
| Macrolides erythromycin ointment (most common), azithromycin (AzaSite solution) | Indication | Bacterial conjunctivitis. Erythromycin ointment is the most common agent; azithromycin comes as AzaSite solution. | Bacterial cause only, so not for a viral eye infection. No drug interactions with the topical forms. | L4 slide 15 |
| Macrolides dosing schedule | Education-heavy | Erythromycin ointment is used two to six times per day depending on severity of infection. Azithromycin drops are given twice daily for two days, then once daily for five days. | The severity of the infection sets how often the ointment is used; azithromycin follows a short fixed course. | L4 slide 16 |
| Erythromycin ointment vs azithromycin | Indication | Erythromycin is soothing on the inflamed eye and may be used even if a bacterial infection is not confirmed. | Azithromycin is considerably more expensive, is given less often (twice a day versus four or more times a day) and is not used as often clinically. | L4 slide 17 |
| Trimethoprim and polymyxin B | ||||
| Trimethoprim with polymyxin B (Polytrim) solution | Indication | Bacterial conjunctivitis. | One drop into the affected eye every 3 hours for 7 to 10 days (some recommend four times daily for 5 to 7 days). No clinically important drug interactions. | L4 slide 18 |
| Sulfacetamide | ||||
| Sulfacetamide ointment or solution | Indication | Bacterial conjunctivitis. | Ask about sulfonamide allergy before using it. Solution is used every 2 to 3 hours; ointment every 3 to 4 hours. No drug interactions. | L4 slide 19 |
| Bacitracin | ||||
| Bacitracin ointment | Indication | Bacterial conjunctivitis. | Applied one to three times daily. No clinically important drug interactions. | L4 slide 20 |
| Fluoroquinolones | ||||
| Fluoroquinolones ciprofloxacin (Ciloxan), ofloxacin (Ocuflox), levofloxacin, moxifloxacin (Vigamox), gatifloxacin (Zymaxid) | Indication | Conjunctivitis and corneal ulcers. | Warn about a white precipitate (ciprofloxacin, about 17%) and an unpleasant taste after instillation. No clinically important interactions when given in the eye. | L4 slide 21 |
| Fluoroquinolones preferred uses | Drug of choice | PREFERRED for corneal ulcers or Pseudomonas aeruginosa (a gram-negative rod). PREFERRED for conjunctivitis in contact lens wearers once keratitis is ruled out, because of the high risk of Pseudomonas. | Effective and well tolerated, but expensive, with emerging resistance. Dosing is frequent (up to every 2 to 4 hours), most often in the first 1 to 2 days. | L4 slide 22 |
| Aminoglycosides | ||||
| Aminoglycosides gentamicin, tobramycin | Indication | Conjunctivitis. | Solutions are given every 2 to 4 hours; ointment 2 to 3 times a day. Watch for corneal ulceration and reactive keratoconjunctivitis with several days of use. No clinically important interactions. | L4 slide 23 |
| Ocular antivirals | ||||
| Antivirals in the eye general | Indication | Primary uses are viral keratitis, herpes zoster ophthalmicus and retinitis. There is no antiviral for viral conjunctivitis caused by adenoviruses. | Adenoviral conjunctivitis has a self-limited course and is treated with symptomatic relief of irritation. | L4 slide 25 |
| Trifluridine (Viroptic) topical | Indication | Herpes simplex keratitis and keratoconjunctivitis. | A topical solution, unlike the oral and intravenous antivirals. | L4 slide 26 |
| Acyclovir (Zovirax) oral or intravenous | Indication | Herpes zoster ophthalmicus and herpes simplex iridocyclitis. | Given by mouth or vein rather than into the eye. | L4 slide 26 |
| Valacyclovir (Valtrex), famciclovir (Famvir) oral | Indication | Herpes simplex keratitis and herpes zoster ophthalmicus. | Oral agents. | L4 slide 26 |
| Agents for cytomegalovirus retinitis foscarnet, ganciclovir, valganciclovir, cidofovir | Indication | Cytomegalovirus retinitis. Foscarnet and cidofovir are intravenous; ganciclovir is intravenous, oral or an intravitreal implant; valganciclovir is oral. | Specialist use; the ganciclovir implant sits inside the eye. | L4 slide 26 |
| Trifluridine (Viroptic) | Indication | Keratoconjunctivitis due to herpes simplex viruses. | Expect ocular irritation and punctate keratopathy. No drug interactions. | L4 slide 27 |
| Ganciclovir (Zirgan) | Indication | Herpetic keratitis (Zirgan is the topical ganciclovir eye preparation). Cytomegalovirus retinitis is treated with a different ganciclovir preparation given by intravitreal injection. | Expect ocular irritation and punctate keratitis. No drug interactions. | L4 slide 28 |
| Ocular antifungals | ||||
| Natamycin (Natacyn) | Indication | The only commercially available ophthalmic antifungal. Fungal eye infections are on the rise as more patients are immunocompromised. | Risk factors for fungal eye infection: trauma, chronic ocular surface disease, contact lens wear and immunosuppression (including topical steroid use). | L4 slide 30 |
| Amphotericin B polyene | Indication | Yeast and fungal keratitis and endophthalmitis. It is the agent given by every route: topical, subconjunctival, intravitreal and intravenous. | The other routes are used for endophthalmitis. | L4 slide 31 |
| Natamycin polyene, topical suspension | Indication | Yeast and fungal blepharitis, conjunctivitis and keratitis. | Given as a topical suspension. | L4 slide 31 |
| Fluconazole, itraconazole, ketoconazole azoles, oral (fluconazole and itraconazole are triazoles; ketoconazole is an imidazole) | Indication | Yeast keratitis and endophthalmitis (fluconazole and ketoconazole); yeast and fungal keratitis and endophthalmitis (itraconazole). Fluconazole can also be given intravenously. | Systemic agents given by mouth. | L4 slide 31 |
| Miconazole imidazole | Indication | Yeast and fungal keratitis (topical solution); yeast and fungal endophthalmitis (subconjunctival and intravitreal). | Given topically, under the conjunctiva or into the vitreous. | L4 slide 31 |
| Natamycin (Natacyn) | Indication | Conjunctivitis and keratitis caused by Aspergillus, Candida, Cephalosporium, Fusarium and Penicillium. | Expect ocular irritation. No drug interactions. | L4 slide 32 |
| Precautions and administration | ||||
| Before any ophthalmic medication precautions | Education-heavy | Perform a visual acuity test before instilling any medication, document allergies to medications and document the date and result of the last eye exam. | Document visual acuity at every follow-up visit. If visual acuity gets worse, refer immediately to ophthalmology. | L4 slide 33 |
| Instilling eye drops steps 1 to 3 | Education-heavy | Wash the hands thoroughly with soap and water (the most important step). Keep the dropper sterile by not touching it to anything else. | Tilt the head back and pull down the lower eyelid to form a pocket. | L4 slide 34 |
| Instilling eye drops steps 4 and 5 | Education-heavy | Hold the dropper with the other hand as close to the eye as possible without touching it. | Squeeze the dropper to place one drop into the pocket. | L4 slide 35 |
| Instilling eye drops steps 6 to 8 | Education-heavy | Close the eyes, tilt the head forward and hold a finger over the lacrimal duct. Keep the eyes closed for 2 to 3 minutes. | Then wipe off the excess and wash the hands again. Blocking the duct keeps the drop on the eye and cuts down drainage into the nose and throat (systemic absorption). | L4 slide 36 |
| Ointments and gels versus drops | Education-heavy | Ointments are better for children and for patients with poor compliance: even if the drug is on the eyelashes it can still reach the eye. | Ointment blurs vision for about 20 minutes, so do not drive until it clears. Squeeze a ribbon of ointment or gel into the pocket; there is no need to cover the lacrimal duct. | L4 slide 37 |
| Contact lens wearers with conjunctivitis | Education-heavy | Stop wearing contact lenses during conjunctivitis. Lenses may be resumed when the eye is not inflamed and there has been no discharge for 24 hours. | Discard or disinfect the lens before reuse, and get rid of eye makeup. | L4 slide 38 |
| Ocular allergy | ||||
| Antihistamines (H1 receptor antagonists) | Indication | Ocular allergy: they decrease capillary dilation, itch and swelling. | They are not simple blockers but inverse agonists (they inactivate the histamine receptor), and they still compete with histamine. | L4 slide 42 |
| Ophthalmic antihistamines azelastine (Optivar), alcaftadine (Lastacaft), bepotastine (Bepreve), emedastine (Emadine), epinastine (Elestat), ketotifen (Zaditor), olopatadine (Patanol, Pataday) | Indication | Ocular allergy. Ketotifen is available over the counter. Some of these agents also have mast cell stabilizing properties. | No prescription is needed for ketotifen. | L4 slide 43 |
| Ophthalmic antihistamines dosing and response | Drug of choice | Typically preferred over mast cell stabilizers. Onset of action is within minutes. | Dosed once or twice daily. Allow two weeks of therapy to assess full efficacy. Warn about ocular irritation, headache and increased ocular dryness. | L4 slide 44 |
| Mast cell stabilizers cromolyn (Opticrom), lodoxamide (Alomide), nedocromil (Alocril) | Indication | Predictable seasonal allergy in patients who do not tolerate other therapies. They are NOT useful for acute symptoms, unlike antihistamines. | Full effect takes 5 to 14 days, and they often need four-times-daily dosing, which is not ideal. Warn about ocular irritation, unpleasant taste and headache. | L4 slide 47 |
| Topical vasoconstrictors tetrahydrozoline (Opti-Clear), naphazoline (VasoClear), pheniramine with naphazoline (Naphcon-A, Visine-A); all over the counter | Education-heavy | Vasoconstrictors activate alpha-adrenergic receptors on blood vessels and decrease conjunctival edema. Good for short-term use only. | STAR THIS: prolonged use leads to REBOUND HYPEREMIA (redness worse than before) after stopping. Use for less than 2 weeks. If there is no improvement in 72 hours, stop and see a provider, because it could be something more serious. | L4 slide 48 |
| Imidazoline derivatives tetrahydrozoline, naphazoline | Education-heavy | Locally they act on alpha 1 receptors, but systemically they target alpha 2 receptors. | Counsel about accidental ingestion, especially by young children: keep the bottle out of reach. A swallowed dose acts as a systemic alpha-2 agonist (sedation, slow heart rate, low blood pressure). | L4 slide 49 |
| Ocular anti-inflammatories | ||||
| Ophthalmic nonsteroidal anti-inflammatory drugs (NSAIDs) bromfenac (Xibrom), diclofenac (Voltaren), flurbiprofen (Ocufen), ketorolac (Acular), nepafenac (Nevanac) | Indication | Postoperative inflammation and pain, and allergic conjunctivitis. Not routinely recommended for conjunctivitis. | Warn about lacrimation, keratitis, a rise in eye pressure and irritation. | L4 slide 51 |
| Ophthalmic glucocorticoids main uses | Indication | Severe ocular allergy, anterior uveitis, external eye inflammatory disease and inflammation after ocular surgery. Applied topically or intraocularly depending on the indication. | They suppress the late-phase allergic reaction and reduce scar formation by inhibiting fibrin and collagen deposition. | L4 slide 52 |
| Ophthalmic glucocorticoids use rules | Education-heavy | Generally used for refractory symptoms only, and limited to a pulse of less than 2 weeks. | Warn about cataract formation, raised eye pressure (more likely with a family history) and glaucoma, infection from reduced immune function, delayed wound healing and corneal ulcers. | L4 slide 54 |
| Ophthalmic glucocorticoid agents dexamethasone (Dexasol), prednisolone (Pred Forte), difluprednate (Durezol), fluorometholone (FML), loteprednol (Alrex), rimexolone (Vexol), triamcinolone (Triesence) | Indication | Fluorometholone, loteprednol and rimexolone are the 'soft steroids' with lower risk of raised eye pressure. Triamcinolone is an intravitreal injection. | The soft steroids are the ones to think of when pressure is the worry. | L4 slide 55 |
| Dry eye | ||||
| Dry eye conditions | Indication | Many conditions alter the precorneal tear film: blepharitis, chemical burns and corneal dystrophies. Systemic conditions can present with dry eyes: Sjogren's syndrome, rheumatoid arthritis, vitamin A deficiency and Stevens-Johnson syndrome. | Think of an underlying systemic disease in a patient with persistent dry eyes. | L4 slide 56 |
| Dry eye treatment first steps | Indication | Treat the disease first. Then physical interventions: punctal plugs or surgical occlusion of lacrimal drainage. | Plugs and occlusion keep tears on the eye longer. | L4 slide 57 |
| Tear substitutes balanced salt solution, carboxymethylcellulose (Refresh Tears), hydroxypropyl cellulose (Lacrisert), polyvinyl alcohol (artificial tears) | Indication | Dry eye. Hypotonic or isotonic solutions containing electrolytes, surfactants and thickeners. Most are available over the counter. | The thickeners increase time in the cul-de-sac. | L4 slide 57 |
| Cyclosporine (Restasis) immunomodulator | Indication | Chronic dry eye associated with inflammation (keratoconjunctivitis sicca). It increases tear production. | Warn about ocular burning (17%), foreign body sensation and blurred vision. No drug interactions. | L4 slide 58 |
| Glaucoma | ||||
| Glaucoma and ocular hypertension aim of drug therapy | Indication | Glaucoma is an optic neuropathy, usually with raised eye pressure, with loss of retinal ganglion cell axons, visual field loss and irreversible blindness. Drugs focus on open-angle glaucoma. | The targets are to decrease aqueous humor production and to increase outflow through the trabecular meshwork. | L4 slide 60 |
| Pressure and glaucoma definitions | Monitoring | Normal eye pressure is 10 to 21 millimeters of mercury (mmHg). Ocular hypertension is pressure above normal without optic nerve damage or visual field loss. | Angle-closure glaucoma is blockage of the drainage canal; the optic nerve may be normal, but the patient is usually in acute pain. | L4 slide 61 |
| Glaucoma drug classes: prostaglandins | Drug of choice | Prostaglandins are the first-line agents and they increase aqueous outflow. | Often multiple agents are needed to control eye pressure. | L4 slide 64 |
| Glaucoma drug classes: beta blockers, carbonic anhydrase inhibitors, alpha and cholinergic agonists | Indication | Beta blockers are second line and decrease aqueous production. Carbonic anhydrase inhibitors decrease production; cholinergic agonists increase outflow; alpha adrenergic agonists do both. | Sort every agent by which side it works on when choosing an add-on. | L4 slide 64 |
| Prostaglandin analogs | ||||
| Prostaglandin analogs latanoprost (Xalatan), travoprost (Travatan), bimatoprost (Lumigan, Latisse), tafluprost (Zioptan) | Indication | Glaucoma and ocular hypertension: they lower eye pressure by increasing aqueous outflow. | Warn about conjunctival hyperemia, irritation, and changes in eyelash length and iris color. Limited systemic side effects. | L4 slide 65 |
| Prostaglandin analogs dosing | Education-heavy | The most commonly used medications for glaucoma. | Once-daily dosing. Do not exceed it, because more frequent dosing inhibits the pressure-lowering effect. | L4 slide 66 |
| Beta blockers | ||||
| Beta blockers betaxolol (Betoptic-S) beta-1 selective; carteolol (Ocupress), timolol (Timoptic), levobunolol (Betagan) nonselective | Indication | Glaucoma (second line): they decrease aqueous production. | Nonselective agents are more efficacious but cause more side effects (more beta-2 receptors in the eye). | L4 slide 67 |
| Beta blockers receptor selectivity | Education-heavy | Beta-1 receptors are mainly in the heart (contractility and heart rate); beta-2 receptors are in the lungs (bronchodilation, vasodilation). | Selective beta blockers block only beta-1 receptors, so there is less risk of bronchoconstriction in a patient with an asthma history. | L4 slide 68 |
| Alpha adrenergic agonists | ||||
| Alpha-2 agonists apraclonidine (Iopidine), brimonidine (Alphagan P) | Indication | Glaucoma: they decrease aqueous production AND increase outflow. | Apraclonidine is highly ionized at physiological pH and brimonidine is more lipophilic. Allergic conjunctivitis is less common with brimonidine. Not for children under 2 years. | L4 slide 69 |
| Carbonic anhydrase inhibitors | ||||
| Carbonic anhydrase inhibitors dorzolamide (Trusopt), brinzolamide (Azopt) | Indication | Glaucoma: they decrease production of aqueous humor (less fluid transport, lower eye pressure). | Warn about bitter taste (25%) and burning or stinging after administration (33%). | L4 slide 70 |
| Cholinergic agonists | ||||
| Cholinergic agonists acetylcholine (Miochol-E), carbachol (Miostat), pilocarpine (Pilopine HS) | Indication | Glaucoma: they activate muscarinic receptors, causing ciliary muscle contraction that facilitates outflow. Acetylcholine is used in surgical settings. | Poor compliance from side effects and frequent administration. Younger patients are usually intolerant because of visual blurring. | L4 slide 72 |
| Glaucoma combination products | ||||
| Combination products brimonidine with timolol (Combigan), brinzolamide with brimonidine (Simbrinza), dorzolamide with timolol (Cosopt) | Education-heavy | Glaucoma when one agent is not enough: synergistic pressure lowering by targeting multiple routes. | Fewer drops to administer, which improves compliance. When adding a second agent, pick one with a different mechanism. | L4 slide 73 |
| Glaucoma therapy | ||||
| Who to treat for glaucoma | Indication | Treat those with risk factors; monitor those without until glaucomatous changes occur. Generally start with a prostaglandin analog or a beta blocker. | Therapy can be started in one eye to determine efficacy and tolerability. | L4 slide 74 |
| Glaucoma treatment target | Monitoring | The general goal is a 20 to 30% reduction in eye pressure. | Expressed as a proportional reduction, not an absolute number. | L4 slide 74 |
| Diagnostic and procedural agents | ||||
| Ocular anesthetics tetracaine (Altacaine), proparacaine (Alcaine) | Indication | Tonometry, foreign body removal and superficial corneal surgery. | Used in the clinic or emergency setting only. | L4 slide 75 |
| Ocular anesthetics counseling | Education-heavy | The eyes stay numb for 10 to 20 minutes with NO blink reflex. | Do not write prescriptions for these. | L4 slide 75 |
| Cycloplegics: antimuscarinics atropine, cyclopentolate (Cyclogyl), tropicamide (Mydriacyl) | Indication | Diagnostic use (fundoscopic exams) and uveitis (to prevent synechiae and relieve ciliary spasm). They lead to mydriasis. | Warn about photosensitivity and blurred vision. | L4 slide 76 |
| Sympathomimetic mydriatic phenylephrine (Neo-Synephrine); grouped with the cycloplegics but dilates the pupil without paralyzing the ciliary muscle | Indication | Mydriasis through adrenergic receptor agonism. | The pupil stays more reactive to light than with an antimuscarinic. | L4 slide 77 |
| Fluorescein | Indication | Anterior segment staining and disclosing corneal injury: it reveals epithelial defects of the cornea and conjunctiva. | Warn about possible hypersensitivity and a burning sensation. | L4 slide 78 |
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| Acute otitis media | ||||
| Amoxicillin, high dose Amoxil | Drug of choice | Mainstay (first-line) therapy for acute otitis media. The higher dose is what overcomes Streptococcus pneumoniae resistance. | Given by mouth twice daily. The best duration is not established: 5–7 days, possibly up to 10, and 5 days may be too short for severe disease. | L5 slide 5 |
| Amoxicillin-clavulanate Augmentin | Indication | Severe or resistant acute otitis media, or when the child received antibiotics in the previous month. | A step up from plain amoxicillin, not the first choice: keep it for severe or resistant disease or recent antibiotic exposure. | L5 slide 5 |
| Cefdinir or azithromycin Omnicef; Zithromax (a macrolide) | Indication | Acute otitis media in penicillin-allergic patients. | Up to 50% of Streptococcus pneumoniae is resistant to macrolides, so azithromycin is the less reliable of the two alternatives. | L5 slide 5 |
| Failed therapy no improvement in 3 days | Indication | Amoxicillin-clavulanate (Augmentin) or a third-generation cephalosporin (cefdinir, Omnicef) if no antibiotics were taken in the past 3 months. | Failed therapy is defined as no improvement in 3 days: switch drugs rather than repeat the same one. | L5 slide 6 |
| Ceftriaxone Rocephin | Indication | Escalation for failed therapy, or when oral medications are not tolerated. | Given intramuscularly or intravenously; the intramuscular course is three doses, one every 24 hours. | L5 slide 6 |
| Acute bacterial rhinosinusitis | ||||
| Amoxicillin-clavulanate Augmentin | Drug of choice | Standard therapy for acute bacterial rhinosinusitis, because Haemophilus influenzae is often a beta-lactamase producer. The bacteria are the same as in otitis media, plus Streptococcus pyogenes, Staphylococcus aureus and gram-negative bacilli. | Call it bacterial only if symptoms last more than 10 days or worsen at about day 5–6; otherwise presume a virus. Duration: children 10–14 days, adults 5–7 days. Saline irrigations can be useful for congestion: use only distilled, sterile or previously boiled water, never straight tap water (rare but deadly amoeba infection of the brain). | L5 slide 7 |
| Penicillin-allergy regimens clindamycin (Cleocin) plus cefixime (Suprax), or levofloxacin (Levaquin) | Indication | Acute bacterial rhinosinusitis in a penicillin-allergic patient. | Clindamycin is rough on the gut flora (risk of Clostridioides difficile diarrhea), and levofloxacin resistance varies by area, so check local resistance patterns. | L5 slide 7 |
| Acute pharyngitis | ||||
| Amoxicillin Amoxil | Indication | Group A beta-hemolytic Streptococcus (GABHS) pharyngitis: once daily for 10 days. The goal is to prevent acute rheumatic fever and suppurative complications. | Pharyngitis is mainly viral (group A strep is only 15–30% of cases), so use a rapid strep test to prevent over-prescribing. | L5 slide 8 |
| Benzathine penicillin G intramuscular | Indication | A single intramuscular injection for group A strep pharyngitis, as the alternative to a 10-day oral course of amoxicillin. | One injection replaces the full 10 days of oral treatment. | L5 slide 8 |
| Penicillin-allergy alternatives cephalexin (Keflex), clindamycin (Cleocin), azithromycin (Zithromax) | Indication | Group A strep pharyngitis in a penicillin-allergic patient. | Used only when penicillin cannot be given. | L5 slide 8 |
| Otic antibiotics | ||||
| Otic antibiotic drops ciprofloxacin, ofloxacin, combinations with a steroid | Indication | Otitis media and otitis externa (and similar ear infections). | Check that the eardrum is intact before using drops: polymyxin B is not recommended with a ruptured eardrum or tubes in place. | L5 slide 10 |
| Available otic agents ciprofloxacin; ciprofloxacin/dexamethasone (Ciprodex); neomycin, polymyxin B, hydrocortisone (Cortisporin); ofloxacin | Indication | Ear drops usually mix an anti-infective with a glucocorticoid. | The anti-infective inhibits bacterial growth; the steroid decreases production of inflammatory cytokines. | L5 slide 9 |
| Ciprofloxacin/dexamethasone Ciprodex | Indication | Otic drops for otitis media and otitis externa. | Expensive. The alternative is ofloxacin plus ophthalmic dexamethasone drops. | L5 slide 10 |
| Neomycin, polymyxin B and hydrocortisone Cortisporin | Indication | Otic drops for otitis externa. Otitis media is listed for otic drops as a group, but when tubes are in place or the eardrum is ruptured this combination is the one to avoid. | Neomycin can cause hypersensitivity. Polymyxin B is not recommended with a ruptured eardrum or tubes in place (cochlear damage and hearing loss). | L5 slide 10 |
| Antifungals | ||||
| Ketoconazole azole antifungal | Indication | Systemic fungal infections. | Taken systemically, so screen the medication list for interactions (it is a cytochrome P450 3A4 [CYP3A4] inhibitor). | L5 slide 12 |
| Nystatin oral suspension nonabsorbable antifungal | Indication | Oral candidiasis (thrush), which is seen with inhaled steroids, HIV (human immunodeficiency virus) infection or AIDS (acquired immunodeficiency syndrome) and chemotherapy. | It is not absorbed, so it acts only in the mouth and gut and causes little more than stomach upset. | L5 slide 13 |
| Aspirin, nonsteroidal anti-inflammatory drugs and acetaminophen | ||||
| Aspirin acetylsalicylic acid | Indication | The effect depends on exposure: antiplatelet at the lowest range, antipyretic-analgesic (fever and pain) at the next, and anti-inflammatory at the highest therapeutic range. | The same drug becomes toxic (salicylism) above the anti-inflammatory range. Bleeding is the complication at antiplatelet exposure and ringing in the ears (tinnitus) signals the anti-inflammatory range. | L5 slide 16 |
| Aspirin — patient counseling Bayer | Education-heavy | Over-the-counter self-treatment of fever and pain: take if fever is above 100 degrees Fahrenheit. | Follow up immediately if fever is not held below 102 degrees Fahrenheit on treatment, or stays above 100 for more than 3 days; follow up if pain worsens or lasts more than 10 days. Drink plenty of fluids. Do not combine with other nonsteroidal anti-inflammatory drugs (NSAIDs) or with anticoagulants (aspirin inhibits platelet function). | L5 slide 20 |
| Ibuprofen Motrin, Advil | Indication | Relief of mild to moderate pain. A nonsteroidal anti-inflammatory drug (NSAID) that is analgesic, anti-inflammatory and antipyretic. | It reversibly inhibits cyclooxygenase 1 and 2 (unlike aspirin). Taken by mouth three to four times daily as needed for pain. | L5 slide 21 |
| Naproxen Aleve; over-the-counter | Education-heavy | Another over-the-counter nonsteroidal anti-inflammatory drug (NSAID) alongside ibuprofen. | Longer half-life, so it is dosed less often than ibuprofen. | L5 slide 23 |
| Acetaminophen Tylenol; acetyl-para-aminophenol | Education-heavy | Pain and fever above 100 degrees Fahrenheit. An analgesic and antipyretic. | Very well tolerated at therapeutic doses, but the daily maximum is 4 grams in 24 hours — the one dose worth knowing (lower it, or avoid the drug, with existing liver disease). Count every acetaminophen-containing product toward it, including combination cold remedies and prescription pain tablets. Taken every 4–6 hours as needed for fever. | L5 slide 24 |
| H1 antagonists (antihistamines) | ||||
| H1 antagonists histamine-1 (H1) blockers | Indication | Allergic reactions (allergic rhinitis, urticaria, insect bites, drug hypersensitivity); motion sickness, nausea and vestibular disturbances; over-the-counter sleep remedies; and an adjuvant role in anaphylaxis. | In anaphylaxis they are an add-on only, never the main treatment. | L5 slide 35 |
| First versus second generation doxylamine (sleep aid) vs second generation | Education-heavy | First-generation agents are available over the counter as sleep aids (doxylamine). | Second-generation agents cause much less sedation because they cross into the central nervous system poorly: choose them when the patient needs to stay alert (for example, someone who drives for work). | L5 slide 32 |
| Promethazine Phenergan | Indication | Motion sickness: it has the strongest antimuscarinic actions among the H1 antagonists. | Its antiemetic action involves the chemoreceptor trigger zone (CTZ) in the brain; antimuscarinic actions also decrease nasal and bronchial secretions during allergic rhinitis. | L5 slide 34 |
| Azelastine Astelin nasal spray | Indication | Allergic rhinitis and vasomotor rhinitis. | An intranasal H1 antagonist, sprayed into each nostril twice daily. | L5 slide 38 |
| Azelastine — nasal spray technique | Education-heavy | How to use an intranasal spray correctly. | Blow the nose and clear the nostrils, tilt the head down, and angle the spray away from the septum (right hand for the left nostril, left hand for the right). Do not tilt the head back (it draws the drug into the throat). Clean the tip with a tissue and do not use with other nasal sprays. If a nosebleed develops, stop and follow up immediately; follow up if symptoms worsen or do not improve. | L5 slide 39 |
| Nasal corticosteroids | ||||
| Nasal corticosteroid names beclomethasone (Beconase AQ), budesonide (Rhinocort, over-the-counter), flunisolide (Nasalide), fluticasone (Flonase, over-the-counter), mometasone (Nasonex), triamcinolone (Nasacort) | Education-heavy | The six nasal corticosteroids to recognize by name. | Many have inhaled versions for asthma: do not mix up the names. Fluticasone (Flonase) is the nasal product, not Flovent. | L5 slide 42 |
| Nasal corticosteroids | Indication | Allergic rhinitis and vasomotor rhinitis. | No interaction information is available. Side effects are mostly local at usual doses (nosebleed, septal perforation, unpleasant taste). | L5 slide 43 |
| Systemic corticosteroids | ||||
| Dexamethasone Decadron; synthetic adrenocortical steroid | Indication | Allergic rhinitis and drug hypersensitivity reactions. | A systemic steroid with many adverse effects; it weakens the immune system (decreased resistance to infections). | L5 slide 44 |
| Dexamethasone — patient counseling | Education-heavy | Counseling for a systemic corticosteroid course. | Do not discontinue abruptly if taken for more than 1 week. It weakens your immune system. | L5 slide 46 |
| Prednisone and prednisolone Deltasone; Orapred (liquid) | Indication | Allergic rhinitis, allergic conjunctivitis and drug hypersensitivity reactions. | Prednisone is the tablet; prednisolone (Orapred) is the liquid formulation. | L5 slide 47 |
| Prednisone — patient counseling | Education-heavy | Counseling for a systemic corticosteroid course. | Do not discontinue abruptly (rebound symptoms). The patient is considered immunocompromised: avoid exposure to chickenpox and measles, and avoid live vaccines; it weakens the immune system. | L5 slide 48 |
| Decongestants | ||||
| Oxymetazoline Afrin nasal spray | Education-heavy | Nasal congestion. An alpha agonist that constricts the blood vessels of the nasal lining. | Maximum 3–5 days. Longer use causes rebound rhinitis (rhinitis medicamentosa). Used twice daily. | L5 slide 50 |
| Oxymetazoline — patient counseling | Education-heavy | How to use the nasal spray safely. | Do not use for more than 3–5 days. Blow the nose and clear the nostrils, tilt the head toward the toes, angle the spray away from the septum (right hand for the left nostril, left hand for the right), and do not tilt the head back. If a nosebleed develops, stop and follow up immediately. Do not use with other nasal sprays. | L5 slide 51 |
| Pseudoephedrine Sudafed; oral decongestant | Indication | Nasal congestion from the common cold, hay fever or allergies; sinus congestion; eustachian tube dysfunction from a viral infection. | An oral alpha agonist, so it acts on blood vessels throughout the body; it may weaken the effect of blood pressure medicines. | L5 slide 52 |
| Antitussives | ||||
| Benzonatate Tessalon | Education-heavy | Symptomatic relief of non-productive cough. An antitussive that anesthetizes the stretch receptors in the lungs. | Swallow whole: do not chew, cut or crush (chewing causes local anesthesia of the mouth). Taken as needed for cough, up to three times daily. | L5 slide 57 |
| Dextromethorphan Robitussin, Delsym | Indication | Cough. An antitussive related to codeine that suppresses the cough center in the medulla. | Check for a monoamine oxidase inhibitor (MAOI) taken now or within 2 weeks, and for other drugs that raise serotonin (risk of serotonin syndrome). | L5 slide 58 |
| Expectorants and mucolytics | ||||
| Guaifenesin mucolytic, expectorant | Indication | Loosens mucus and decreases its viscosity. | No interaction information is available; nausea and vomiting are possible. | L5 slide 59 |
| Guaifenesin — patient counseling | Education-heavy | Counseling for a mucus-loosening medicine. | Drink plenty of fluid and expect an increase in drainage. Follow up if symptoms persist for more than 7 days or worsen. | L5 slide 60 |
| Dornase alfa Pulmozyme, nebulized | Indication | Cystic fibrosis (CF): it reduces the viscosity of CF sputum, improves lung function and decreases exacerbations in mild to moderate lung disease. | A DNA (deoxyribonucleic acid) enzyme that cleaves DNA from degenerating neutrophils; nebulized once daily. It is also effective in severe disease, but lung function improves less. | L5 slide 61 |
| Hypertonic saline 7% saline, inhaled | Indication | Loosens airway mucus: reported to improve mucus flow properties, mucus transport, airway hydration, mucociliary clearance and lung function. | Inhaled twice daily as a 7% (hypertonic) solution. | L5 slide 62 |
| N-acetylcysteine Mucomyst | Indication | Traditional treatment for acetaminophen toxicity. When inhaled (nebulized) it is a mucolytic that reduces mucus viscosity. | It splits the disulfide bonds linking mucoproteins; inhaled use smells of rotten eggs (high sulfur content). | L5 slide 63 |
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| ACE inhibitors | ||||
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Recognize the class by the -pril suffix. Enalaprilat is the intravenous form of enalapril (the injectable option in the class). Captopril has a short half-life. | Captopril is the short-acting member, so it is the one dosed more often than the rest of the class. | L6 slide 13 |
| ACE (angiotensin-converting enzyme) inhibitors, continued quinapril, ramipril, perindopril, moexipril | Education-heavy | Quinapril, ramipril, perindopril and moexipril complete the -pril list. | An agent ending in -pril is an ACE inhibitor, so the class can be named from the suffix alone. | L6 slide 14 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Most are dosed once daily; captopril is the exception. | If the effect wears off toward the end of the dosing interval, the fix is twice-daily dosing. The dose response is steep at low doses and flatter at higher doses, so raising the dose late in therapy gains little. | L6 slide 15 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Drug of choice | Hypertension: lowers total peripheral resistance and both systolic and diastolic blood pressure, and reduces left ventricular hypertrophy caused by high pressure. Preferred in diabetics because of the kidney-protective effect. | Drug choice follows the comorbidity: in a patient with diabetes, this class is chosen for its kidney protection, not just for the pressure lowering. | L6 slide 16 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Indication | Left ventricular dysfunction (heart failure): reduces remodeling, afterload and preload, raises cardiac output, prevents or delays progression, and lowers myocardial infarction and hospitalization. Should be given to all patients with left ventricular dysfunction unless contraindicated. | Explain that the drug protects the heart over the long term even when the patient feels well. | L6 slide 17 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Indication | After a myocardial infarction: reduces myocardial remodeling and overall mortality. Diabetic nephropathy: lowers glomerular pressure and prevents or delays progression of kidney disease in diabetic patients; it also slows other kidney diseases. | Kidney protection in diabetes is a reason to choose this class beyond the blood pressure number. | L6 slide 18 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Dry cough (5–15% of patients) is thought to come from bradykinin and substance P accumulating in the lungs. It appears from 1 week to 6 months into therapy. | Not related to dose or to the specific agent, so a lower dose or a different ACE inhibitor will not stop it; more frequent in women. Tell the patient to report a persistent dry cough; if bothersome the ACE inhibitor may need to be removed. | L6 slide 19 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Hyperkalemia (raised potassium) is most often seen with kidney disease and with potassium-sparing diuretics, potassium supplements or salt substitutes. | Tell the patient not to take potassium supplements or use salt substitutes without asking. Anything that changes potassium is an easy question and a dangerous one. | L6 slide 20 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | First-dose hypotension with the first dose or an upward dose change. Most common in patients who are sodium depleted, have heart failure, or take several antihypertensive drugs. | Warn about dizziness on standing after the first dose and after each increase. | L6 slide 20 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Kidney disease: where kidney blood flow depends on angiotensin II, ACE inhibitors dramatically decrease the glomerular filtration rate. Use cautiously. | Start with a low dose and move upward slowly; kidney function needs to be followed. | L6 slide 21 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Angioedema (rare, 0.1–0.5%): rapid swelling of the nose, throat, mouth, larynx, lips and tongue. Usually develops in the first week and is reversible if the drug is removed; thought to be due to bradykinin accumulation. | Tell the patient to report swelling of the lips, tongue or throat at once. | L6 slide 22 |
| ACE (angiotensin-converting enzyme) inhibitors -pril: captopril, lisinopril, enalapril, ramipril | Education-heavy | Pregnancy: fetal morbidity and mortality, with birth defects and fetal death; contraindicated in the second and third trimesters. NSAIDs (nonsteroidal anti-inflammatory drugs) reduce the effect of ACE inhibitors. | Ask about pregnancy before starting and tell patients who could become pregnant to report it right away. Advise checking with the prescriber before regular use of ibuprofen-type pain relievers. | L6 slide 22 |
| Angiotensin receptor blockers | ||||
| ARBs (angiotensin receptor blockers) -sartan: losartan, valsartan, candesartan | Education-heavy | The -sartan suffix marks the class: candesartan, olmesartan, losartan, azilsartan, eprosartan, irbesartan, telmisartan, valsartan. | An agent ending in -sartan is an angiotensin receptor blocker; do not confuse it with the -pril ACE (angiotensin-converting enzyme) inhibitors. | L6 slide 27 |
| ARBs (angiotensin receptor blockers) -sartan: losartan, valsartan, candesartan | Indication | Hypertension. The angiotensin receptors are saturated at starting doses for most agents, so the dose response is nonlinear and larger doses change blood pressure little. Adding a diuretic (for example hydrochlorothiazide) increases the effect, and most come in combination form. Less effective alone in salt-sensitive hypertension, where a diuretic improves outcomes. | Adding a diuretic increases the response more than raising the dose, which is why most products come in combination form. In the usual stepwise plan, though, a dihydropyridine calcium channel blocker is added before the diuretic; the diuretic is the third step. | L6 slide 28 |
| ARBs (angiotensin receptor blockers) -sartan: losartan, valsartan, candesartan | Indication | Left ventricular dysfunction: used when the patient cannot tolerate an ACE (angiotensin-converting enzyme) inhibitor. Diabetic nephropathy. | The usual reason for the switch is the ACE inhibitor cough; in heart failure start with a low dose and titrate upward. | L6 slide 28 |
| ARBs (angiotensin receptor blockers) -sartan: losartan, valsartan, candesartan | Education-heavy | Same warnings as ACE (angiotensin-converting enzyme) inhibitors: hyperkalemia with kidney disease or potassium-sparing diuretics, first-dose hypotension, impaired kidney function (angiotensin II is important for kidney function), and fetal morbidity and mortality: not given in the second and third trimesters. | Same counseling as ACE inhibitors: no potassium supplements or salt substitutes without asking; report pregnancy immediately; expect dizziness after the first dose. | L6 slide 29 |
| ARBs (angiotensin receptor blockers) -sartan: losartan, valsartan, candesartan | Education-heavy | Do not cause cough because they do not affect bradykinin metabolism, and they have a lower incidence of angioedema, so a patient can be switched from an ACE (angiotensin-converting enzyme) inhibitor. | This is the classic stem: a patient on an ACE inhibitor develops a dry cough, so switch to an angiotensin receptor blocker. In heart failure, start with a low dose and titrate upward. | L6 slide 30 |
| Calcium channel blockers: whole class | ||||
| Calcium channel blockers class uses | Indication | Uses listed for the class as a whole: angina, hypertension, supraventricular arrhythmias, diastolic heart failure, cerebral ischemia and migraine prophylaxis. Not every member has every use: the arrhythmia and diastolic heart failure uses belong to diltiazem and verapamil, and nimodipine is the cerebral agent. | Which member is chosen depends on whether the goal is to relax the vessels or to slow the heart. | L6 slide 41 |
| Diltiazem, verapamil and the dihydropyridines | Indication | To reduce heart rate or slow atrioventricular conduction, use diltiazem or verapamil. The dihydropyridines work mainly on the vessels: their suppression of atrioventricular conduction is 0 and of contractility is 0 to minimal. | The exact plus counts are not the point; the pattern is: non-dihydropyridines act on the heart and vessels, dihydropyridines act on the vessels. | L6 slide 42 |
| Calcium channel blockers: non-dihydropyridines | ||||
| Non-dihydropyridine calcium channel blockers diltiazem, verapamil | Indication | Available intravenously or by mouth, immediate-release or sustained-release. Approved for angina, hypertension, supraventricular tachycardia, atrial fibrillation or flutter, and paroxysmal supraventricular tachycardia. | The heart-rate-slowing indications belong to this pair only: the dihydropyridines are not approved for arrhythmias. Sustained-release forms reduce the number of daily doses. | L6 slide 44 |
| Calcium channel blockers: dihydropyridines | ||||
| Amlodipine, nifedipine, nicardipine Norvasc, Adalat, Cardene | Indication | Approved for angina and hypertension. Nicardipine is available intravenously. | Oral only, except nicardipine. | L6 slide 49 |
| Felodipine, isradipine, nisoldipine Plendil, DynaCirc, Sular | Indication | Approved for hypertension only. | Oral only. | L6 slide 49 |
| Nimodipine Nymalize | Indication | Approved for subarachnoid hemorrhage (bleeding around the brain), not for blood pressure. | Oral only. | L6 slide 49 |
| Dihydropyridine calcium channel blockers -dipine: amlodipine, nifedipine, nicardipine | Education-heavy | Use the -dipine suffix to recognize the class. | Avoid short-acting formulations: they cause an abrupt fall in pressure. Long-acting products give steadier control. | L6 slide 49 |
| Beta blockers | ||||
| First-generation (non-selective) beta blockers nadolol, penbutolol, pindolol, propranolol, sotalol, timolol | Education-heavy | Non-selective: block both beta-1 and beta-2 receptors. Propranolol is the classic example. | Memory aid: in the first two generation tables, names from N to Z are non-selective and names from A to M are beta-1 selective; carvedilol and labetalol are the exceptions. | L6 slide 60 |
| Second-generation (beta-1 selective) beta blockers acebutolol, atenolol, bisoprolol, esmolol, metoprolol | Indication | Selective for beta-1 receptors: acebutolol, atenolol, bisoprolol, esmolol and metoprolol. Esmolol is intravenous only (brand Brevibloc). | Esmolol is the intravenous-only agent of the group. | L6 slide 61 |
| Third-generation (vasodilating) beta blockers carvedilol, labetalol; also carteolol, betaxolol | Indication | Carvedilol and labetalol also block alpha-1 receptors (labetalol also has beta-2 agonist activity; carvedilol has antioxidant and antiproliferative actions), giving direct vasodilation. | The extra vasodilating action gives these two more blood-pressure lowering than a pure beta blocker. | L6 slide 62 |
| Beta blockers -olol | Indication | Hypertension: not recommended for first-line management. Works best in young patients with resting tachycardia, raised catecholamines and raised renin; still useful in the elderly. | Expect fatigue and limited exercise tolerance, the common complaint. Usually chosen because the patient has another indication, with the pressure lowering as a bonus. | L6 slide 63 |
| Timolol, betaxolol, carteolol glaucoma beta blockers | Indication | Glaucoma: decrease production of aqueous humor in the ciliary body. | Systemic effects are notable even with eye drops, so ask about wheezing, slow pulse and dizziness. | L6 slide 65 |
| Propranolol, timolol migraine | Indication | Migraine prophylaxis (prevention, not treatment of an attack). The mechanism is uncertain. | Low doses may make the headache worse. | L6 slide 65 |
| Beta blockers -olol | Indication | Hyperthyroidism (thyrotoxicosis): reduces the tachycardia, tremor and anxiety. Propranolol also decreases peripheral conversion of thyroxine (T4) to triiodothyronine (T3). | It treats the symptoms rather than the thyroid disease itself. | L6 slide 66 |
| Beta blockers -olol | Indication | Angina pectoris (ischemia: oxygen demand greater than supply): beta blockade lengthens the time to the heart rate that brings on angina and prolongs exercise time until symptoms. | In angina, exercise tolerance improves, unlike the fatigue seen in hypertension. | L6 slide 67 |
| Beta blockers -olol | Indication | Acute myocardial infarction: protects ischemic myocardium from norepinephrine and epinephrine, protects against recurrent infarction and lowers oxygen demand. Avoid agents with intrinsic sympathomimetic activity. | Post-infarction patients are usually kept on a beta blocker long term; they should not stop it on their own. | L6 slide 68 |
| Beta blockers -olol | Indication | Supraventricular arrhythmias: blocks the atrioventricular nodes and slows transmission (atrial fibrillation, paroxysmal atrial tachycardia, paroxysmal supraventricular tachycardia). Also used for premature ventricular contractions, which are ventricular rather than supraventricular. | Works like the non-dihydropyridine calcium channel blockers on the nodes. | L6 slide 68 |
| Beta blockers -olol | Indication | Acute panic attacks (sympathetic and central effects) and benign essential tremor (blocks beta-2 receptors on skeletal muscle). | Blunts the physical symptoms of anxiety such as tremor and a pounding heart. | L6 slide 69 |
| Carvedilol, metoprolol succinate, bisoprolol heart failure beta blockers | Education-heavy | Congestive heart failure: carvedilol, metoprolol succinate and bisoprolol. Heart failure carries a mortality of 40–50% over 3 years. Beta blockers were originally contraindicated, but in a failing ventricle they raise cardiac output and lower peripheral resistance and heart rate. | They initially worsen symptoms, so start with a very low dose and increase slowly. Warn the patient that feeling worse at first does not mean the drug has failed. | L6 slide 70 |
| Beta blockers -olol | Education-heavy | Diabetes: beta blockers inhibit glycogenolysis, prolong hypoglycemia and mask its warning symptoms (type 1). In type 2 they lower insulin release and raise glucose, and can also prolong and mask hypoglycemia. | Warn diabetic patients that the usual warning signs of low blood sugar may be hidden; blood sugar may be harder to control. | L6 slide 72 |
| Beta blockers -olol | Education-heavy | Sudden withdrawal syndrome: after chronic blockade the receptors are upregulated, so stopping abruptly can cause acute angina, myocardial infarction and a marked rise in blood pressure. | Never stop suddenly; the dose must be withdrawn slowly. | L6 slide 73 |
| Alpha-1 blockers | ||||
| Prazosin Minipress | Indication | Selective alpha-1 antagonist used for hypertension in combination with beta blockers and diuretics. Mildly lowers low-density lipoprotein (LDL) cholesterol and triglycerides and raises high-density lipoprotein (HDL) cholesterol. | An add-on rather than a single first agent; the lipid effect is a small bonus. | L6 slide 78 |
| Prazosin Minipress | Education-heavy | Side effects to counsel on: orthostatic hypotension, postural dizziness, headache, drowsiness and lack of energy. | Tell the patient to stand up slowly. Dizziness on standing is the main complaint. | L6 slide 79 |
| Prazosin Minipress | Education-heavy | NSAIDs (nonsteroidal anti-inflammatory drugs) attenuate the response; beta blockers may enhance postural hypotension. Use caution in cardiac and renal failure. | Ask about over-the-counter pain relievers and other blood pressure medicines. | L6 slide 81 |
| Terazosin, doxazosin Hytrin, Cardura | Indication | Treat hypertension and benign prostatic hyperplasia. They have a longer half-life, so once-daily dosing. | Once-daily dosing helps adherence. | L6 slide 83 |
| Tamsulosin Flomax | Indication | Alpha-1A selective antagonist for benign prostatic hyperplasia, with limited effect on the vasculature (vascular receptors are alpha-1B). | Fewer blood pressure effects than the other alpha-1 blockers, though hypotension and dizziness can still occur. | L6 slide 84 |
| Central sympatholytics | ||||
| Central sympatholytics clonidine, guanfacine | Indication | Advantages: efficacy independent of age, race and gender; suitable for monotherapy; works well in the elderly; no negative effects on lipids. Lowers total peripheral resistance with only a modest fall in cardiac output. | A workable single agent, but see the withdrawal warning below. | L6 slide 90 |
| Central sympatholytics clonidine, guanfacine | Education-heavy | General side effects of the class: drowsiness and sedation, dry mouth, sexual dysfunction, a narrow therapeutic range and abrupt withdrawal hypertension. | Never stop suddenly; expect drowsiness and dry mouth. | L6 slide 91 |
| Clonidine Catapres | Indication | Analgesic activity: blunts opiate withdrawal reactions. Decreases antidiuretic hormone (ADH) secretion. | Causes sodium retention, so it is often given with a diuretic. Dry mouth and sedation are expected. | L6 slide 93 |
| Guanfacine Tenex | Indication | Less potent than clonidine and the most selective for alpha-2 over alpha-1; less sedation and only an occasional withdrawal syndrome. | The gentler alternative to clonidine when sedation is the problem. | L6 slide 95 |
| Direct vasodilators | ||||
| Direct vasodilators hydralazine, minoxidil, nitroprusside | Education-heavy | Direct arteriolar dilation lowers resistance, but the body answers with reflex sympathetic activation: tachycardia, increased cardiac output, fluid retention and increased renin. The reflex causes tachyphylaxis (the effect fades). | This is why hydralazine and minoxidil are not used alone: they are paired with a diuretic and a beta blocker to cancel the reflex effects. Nitroprusside is the exception, given by itself as an intravenous infusion in a hypertensive crisis. | L6 slide 97 |
| Hydralazine Apresoline | Indication | Chronic hypertension, given with a diuretic and a beta blocker. | Not a single agent: the diuretic controls fluid retention and the beta blocker controls the reflex tachycardia. | L6 slide 99 |
| Minoxidil Loniten | Indication | Triple therapy for severe or refractory hypertension. | Reserved for hypertension that other drugs have not controlled. | L6 slide 99 |
| Nitroprusside Nitropress | Indication | Hypertensive crisis, by intravenous infusion. | Emergency use only, given by continuous infusion. | L6 slide 99 |
| Hydralazine Apresoline | Education-heavy | Contraindicated in coronary artery disease and ischemia; use caution in the elderly. Stools may turn black. | Warn the patient ahead of time that stools may turn black, so it is not mistaken for gastrointestinal bleeding. Warn ahead about any drug that changes stool or urine color. | L6 slide 102 |
| Minoxidil Loniten; topical Rogaine | Education-heavy | Hypertrichosis (hair growth) of the face, back, arms and legs. Rogaine is the topical form for hair growth; it may have cardiovascular effects. | Warn about unwanted hair growth before it starts. | L6 slide 105 |
| Nitroprusside Nitropress | Indication | Given by intravenous infusion; affects both veins and arterioles. Releases nitric oxide, which raises cyclic guanosine monophosphate (cGMP) and lowers intracellular calcium. | Only by continuous intravenous infusion. | L6 slide 106 |
| Nitroprusside Nitropress | Education-heavy | Toxicity comes from its cyanide groups: give sodium thiosulfate to limit cyanide toxicity. Thiocyanate toxicity follows long infusions or kidney failure. | Watch for trembling, vomiting and convulsions (cyanide), and for weakness, tinnitus, muscle spasms and toxic psychosis (thiocyanate). | L6 slide 107 |
| Treatment algorithm | ||||
| Stepwise hypertension treatment the algorithm on the last content slide | Drug of choice | Every patient gets lifestyle counseling. If blood pressure is more than 20 mmHg systolic or 10 mmHg diastolic above goal, start an ACE (angiotensin-converting enzyme) inhibitor (or angiotensin receptor blocker) PLUS a dihydropyridine calcium channel blocker. Otherwise: with albuminuria (urine albumin-to-creatinine ratio 300 mg/g or higher) start an ACE inhibitor (or angiotensin receptor blocker); without it, start an ACE inhibitor (or angiotensin receptor blocker) or a dihydropyridine calcium channel blocker. | Still uncontrolled: combine the ACE inhibitor (or angiotensin receptor blocker) with the dihydropyridine calcium channel blocker. Still uncontrolled after that: add a thiazide-like diuretic. Still uncontrolled after that is apparent resistant hypertension. This is the answer to “the patient is on this, what is added next?” | L6 slide 108 |
| Reasons to start other agents earlier inset on the algorithm | Education-heavy | Thiazide-like diuretic first in osteoporosis, edema or calcium kidney stones with hypercalciuria. Beta blocker first after a myocardial infarction. Mineralocorticoid receptor antagonist in heart failure with preserved ejection fraction. Angiotensin receptor-neprilysin inhibitors, beta blockers and mineralocorticoid receptor antagonists first in heart failure with reduced ejection fraction. | Reassess about 4 weeks after starting or changing therapy, and make only 1 or 2 titration steps before changing or adding a drug. The most common causes of poor response are medication nonadherence, the white coat effect and improper blood pressure measurement. | L6 slide 108 |
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) | ||||
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Drug of choice | Statins are first line therapy whenever a drug to lower low-density lipoprotein (LDL) cholesterol is indicated. They are the most efficacious and best tolerated of all the lipid-lowering agents. | The other classes are usually added to a statin or used when a statin cannot be used. | L7 slide 25 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Indication | Beyond lowering cholesterol, statins have pleiotropic effects (extra, non-cholesterol benefits): improved endothelial function, atherosclerotic plaque stabilization, platelet inhibition and antithrombosis, reduced leukocyte adhesiveness, reduced inflammatory markers, blood pressure effects, reduced ischemia-reperfusion injury and enhanced angiogenesis. | Counseling point: the benefit of the drug is wider than the cholesterol number, so it is continued as prevention. | L7 slide 19 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Education-heavy | Metabolism decides the interactions: atorvastatin, lovastatin and simvastatin are CYP3A4 (cytochrome P450 3A4) substrates; fluvastatin is metabolized by CYP2C9 (cytochrome P450 2C9); pravastatin by enzymatic and nonenzymatic routes; rosuvastatin has minimal cytochrome P450 (CYP) metabolism; pitavastatin by glucuronidation (UGT1A3 and UGT2B7, glucuronidation enzymes). | When a patient must take a CYP3A4 inhibitor, choose a statin that does not depend on that enzyme (rosuvastatin or pravastatin) to avoid a rise in statin levels. | L7 slide 20 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Education-heavy | Muscle warning: myalgia and myopathy occur in 0.2 to 0.4% of patients, with rare rhabdomyolysis. Presence of muscle toxicity requires the discontinuation of the statin. | Tell the patient to report muscle symptoms promptly. Use the lowest effective dose, be cautious with kidney impairment and with fibrates, avoid other interacting drugs, and check symptoms and laboratory values. | L7 slide 22 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Education-heavy | Statin interaction counseling: cytochrome P450 mediated interactions, especially CYP3A4 (cytochrome P450 3A4) inhibitors and substrates. Verapamil, amiodarone and grapefruit juice raise statin levels this way. Niacin and fibric acid derivatives are also listed, mainly because they add to the risk of muscle toxicity. | Avoid grapefruit juice with atorvastatin, lovastatin and simvastatin, and check every new medicine for an interaction before it is added. | L7 slide 24 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Monitoring | Guideline approach: initiate moderate-intensity or high-intensity statin therapy for patients in the four benefit groups. Unlike the older Adult Treatment Panel III (ATP III) guideline, do not titrate to a specific low-density lipoprotein (LDL) cholesterol target. | Lipids are measured at follow-up visits to assess adherence to treatment, not to reach a specific LDL number. | L7 slide 64 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Indication | Four major statin benefit groups: (1) individuals with clinical atherosclerotic cardiovascular disease (ASCVD); (2) individuals with low-density lipoprotein (LDL) cholesterol of 190 mg/dL or higher; (3) individuals with diabetes mellitus, age 40 to 75, LDL 70 to 189 mg/dL and no clinical ASCVD; (4) individuals with neither clinical ASCVD nor diabetes, LDL 70 to 189 mg/dL and an estimated 10-year ASCVD risk above 7.5%. (The primary prevention algorithm in the next section uses its own risk cutoffs of 10% and 5%.) | Recognizing which group a patient falls into decides whether a statin is started. | L7 slide 65 |
| Statins atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin | Education-heavy | Statin safety recommendations: select the appropriate dose, keep potential side effects and drug interactions in mind, and if a high or moderate intensity statin is not tolerated, use the maximum tolerated dose instead. | A patient who cannot tolerate the recommended intensity is stepped down to the highest dose they can take, not taken off the statin. | L7 slide 69 |
| Cholesterol absorption inhibitor | ||||
| Ezetimibe Zetia | Indication | Add-on to a statin: an additional 15%-20% low-density lipoprotein (LDL) cholesterol lowering when added to a statin. Taken once daily by mouth. | Take with or without meals. | L7 slide 29 |
| Fibrates (fibric acid derivatives) | ||||
| Fibrates gemfibrozil, fenofibrate, bezafibrate | Indication | Primary indication is very high triglycerides (above 1000 mg/dL) or low high-density lipoprotein (HDL) cholesterol. | Fits the patient whose main problem is triglycerides or low HDL rather than high low-density lipoprotein (LDL) cholesterol. | L7 slide 39 |
| Fibrates gemfibrozil, fenofibrate, bezafibrate | Indication | Lipid effect: triglycerides fall 20-50% and high-density lipoprotein (HDL) cholesterol rises 10-35%, while low-density lipoprotein (LDL) cholesterol falls only 5-20% and total cholesterol falls 15%. | Read the pattern: large triglyceride drop and HDL rise, modest LDL change. | L7 slide 35 |
| Bile acid sequestrants (resins) | ||||
| Bile acid sequestrants cholestyramine, colestipol, colesevelam | Indication | Because they are not absorbed from the gastrointestinal tract they have limited systemic side effects and are approved for children, adolescents and pregnancy. | The lipid-lowering option for children, adolescents and pregnant patients, where systemic drugs are a concern. | L7 slide 42 |
| Bile acid sequestrants cholestyramine, colestipol, colesevelam | Education-heavy | Powders must be mixed with water or fruit juice; mix in a pulpy drink to mask the taste. Take within 1 hour of a meal and separate other medications. | Counsel on mixing, timing with meals, and spacing other medicines. | L7 slide 45 |
| Bile acid sequestrants cholestyramine, colestipol, colesevelam | Education-heavy | Anion exchange resins interfere with absorption of other drugs: digoxin, warfarin, thyroxine, beta blockers and thiazide diuretics. | Give the other drug 1 hour before or 4 hours after the bile acid sequestrant. | L7 slide 47 |
| Bile acid sequestrants cholestyramine, colestipol, colesevelam | Indication | Considered the safest lipid drug because it is not absorbed and has no systemic toxicity (though it can raise triglycerides, bind vitamins and bind other drugs), but poorly tolerated. Used mainly together with a statin or for patients who need only modest low-density lipoprotein (LDL) cholesterol reduction. | Expect gastrointestinal complaints to limit adherence; the drug is an add-on rather than a first choice. | L7 slide 49 |
| Niacin (nicotinic acid) | ||||
| Niacin nicotinic acid, vitamin B3 | Education-heavy | Niacin (nicotinic acid) is a B-complex vitamin used as an antilipemic. Niacinamide (nicotinamide) is not effective as an antilipemic. | Make sure the patient buys niacin or nicotinic acid, not niacinamide. | L7 slide 50 |
| Niacin nicotinic acid, vitamin B3 | Education-heavy | Products: immediate release (niacin supplement; Niacor by prescription), long acting (niacin supplement), extended release (Niaspan by prescription) and inositol hexaniacinate. | Some forms are sold as supplements and others need a prescription, so confirm which product the patient is actually taking. | L7 slide 51 |
| Niacin nicotinic acid, vitamin B3 | Indication | Useful for patients with atherogenic dyslipidemia, and as combination therapy for patients with atherogenic dyslipidemia and elevated low-density lipoprotein (LDL) cholesterol. | Niacin lowers triglycerides and raises high-density lipoprotein (HDL) cholesterol, so it suits that pattern better than a pure LDL problem. | L7 slide 58 |
| Niacin nicotinic acid, vitamin B3 | Education-heavy | Cutaneous flushing is a prostaglandin-mediated effect that is minimized by premedication with aspirin. | Warn the patient about flushing in advance and advise aspirin before the dose. | L7 slide 55 |
| Statin plus niacin combination | ||||
| Lovastatin plus extended release niacin Advicor | Indication | Fixed combination of lovastatin and extended release niacin: low-density lipoprotein (LDL) cholesterol falls about 50%, high-density lipoprotein (HDL) cholesterol rises about 30% and triglycerides fall about 40%. | Expect the adverse effects of both drugs: liver toxicity, muscle disease and flushing. | L7 slide 59 |
| Statins | ||||
| Statin intensity the intensity table | Indication | Only atorvastatin and rosuvastatin reach HIGH intensity (lower low-density lipoprotein cholesterol by 50% or more), and only at their higher doses. Moderate intensity (30% to 49%): atorvastatin and rosuvastatin at lower doses, and simvastatin, pravastatin, lovastatin, fluvastatin and pitavastatin at moderate doses. Low intensity (under 30%): the low doses of simvastatin, pravastatin, lovastatin and fluvastatin. | Use the intensity, not the drug name, to match the statin to the patient's risk: high intensity for the highest-risk patients, moderate for most primary prevention. | L7 slide 68 |
| Primary prevention algorithm adults 18 to 75 without cardiovascular disease | Monitoring | Low-density lipoprotein cholesterol 190 or higher: evaluate for familial hypercholesterolemia; if it is absent, start a high-intensity statin. Below 190, ten-year cardiovascular risk above 10%: start a moderate-dose statin. 5% to 10%: shared decision making, with a calcium score or lipoprotein(a) level in some patients. Below 5%: repeat screening. | Recheck low-density lipoprotein cholesterol in 6 weeks after starting a moderate-dose statin; it should fall 30% to 50%. If it did not, evaluate adherence. If it did, continue, or consider high intensity when ten-year risk is 20% or more and the level is still above 100 mg/dL. | L7 slide 66 |
| PCSK9 inhibitors | ||||
| PCSK9 inhibitors alirocumab, evolocumab | Indication | Injectable monoclonal antibodies that block proprotein convertase subtilisin/kexin type 9 (PCSK9) and lower low-density lipoprotein (LDL) cholesterol concentrations by 43-58%. | Injectable only and expensive. A drug name ending in -mab marks a monoclonal antibody. | L7 slide 60 |
| Lipid goals and targets | ||||
| Lipid targets older Adult Treatment Panel III goals | Monitoring | Older Adult Treatment Panel III (ATP III) goals: low-density lipoprotein (LDL) cholesterol below 100 mg/dL optimal; high-density lipoprotein (HDL) cholesterol above 60 mg/dL is high and below 40 mg/dL is low; total cholesterol below 200 mg/dL desired; triglycerides below 150 mg/dL normal. | HDL increases with exercise. Current guidance treats by risk group rather than chasing these targets. | L7 slide 62 |
| Lipid targets older Adult Treatment Panel III goals | Monitoring | Total cholesterol = high-density lipoprotein (HDL) cholesterol + low-density lipoprotein (LDL) cholesterol + very low-density lipoprotein (VLDL). When triglycerides are below 400 mg/dL, VLDL is estimated as triglycerides divided by 5, so total cholesterol = HDL + LDL + triglycerides/5. | Use this to estimate LDL from a standard lipid panel when triglycerides are under 400 mg/dL. | L7 slide 62 |
| Drug or class | Tier | Indications | Patient education & practical notes | Source |
|---|---|---|---|---|
| Angina and the treatment strategy | ||||
| Ischemic heart disease and angina definitions | Indication | Ischemic heart disease is an imbalance between myocardial oxygen supply and demand (decreased blood flow to tissue, so too little oxygen). Coronary heart disease is atherosclerotic narrowing of one or more coronary arteries. Angina pectoris (chest pain) is the clinical manifestation of myocardial ischemia. | Angina is the symptom; ischemia, supply falling short of demand, is the cause. Acute coronary syndrome (unstable angina, acute myocardial infarction, sudden cardiac death) is the dangerous end; chronic stable angina is the predictable one. | L8 slide 4 |
| Antianginal strategy what every drug is trying to do | Indication | Lower myocardial oxygen demand (lower heart rate, lower contractility, lower intramyocardial wall tension by reducing preload and afterload) and raise oxygen supply (improve coronary blood flow). Also stabilize atherosclerotic plaques to prevent acute coronary syndrome and modify reversible risk factors. | Place every drug on this map: beta blockers lower demand only; calcium channel blockers and nitrates lower demand and help supply; statins, antiplatelets and angiotensin-converting enzyme inhibitors are the vasculoprotective group. | L8 slide 11 |
| Three treatment pillars revascularization, drugs, lifestyle | Indication | Revascularization (percutaneous coronary intervention, coronary artery bypass grafting); pharmacotherapy: antianginals (beta blockers, calcium channel blockers, nitrates) plus vasculoprotective drugs (antiplatelet, statins, angiotensin-converting enzyme inhibitors); lifestyle change of modifiable risk factors. | The antianginals are the symptom drugs; antiplatelets and lipid-lowering therapy are for every patient who can take them; angiotensin-converting enzyme inhibitors are for diabetes, left ventricular dysfunction or a prior infarction. | L8 slide 12 |
| Antianginal classes what they accomplish | Indication | Antianginals improve exercise capacity, reduce exercise-induced ST-segment changes and decrease the frequency of symptoms. The three classes are beta blockers, calcium channel blockers (dihydropyridine and non-dihydropyridine) and nitrates. | Expect the patient to report longer time to chest pain with exertion and fewer attacks. | L8 slide 14 |
| Variant (Prinzmetal) angina vasospastic angina | Indication | Transient, abrupt narrowing of the vessel, which can occur at a partly occluded site and may be due to autonomic control. Younger patients and those with fewer risk factors; with or without ST-segment elevation; often at night or in the early morning. | The pattern to recognize: younger patient, few risk factors, chest pain at night or early morning. | L8 slide 8 |
| Variant angina treatment calcium channel blockers and nitrates | Drug of choice | Calcium channel blockers and nitrates can reduce symptoms. | Beta blockers are the exception: avoid them, because they may lead to worsened symptoms. The usual first-line antianginal is the wrong drug here. | L8 slide 39 |
| Beta blockers | ||||
| Beta blockers metoprolol, atenolol (beta-1 selective); propranolol, nadolol (non-selective); carvedilol, labetalol (third generation) | Drug of choice | First-line therapy for angina in the absence of contraindications. Useful when the patient has limited exercise capacity due to angina and also has hypertension, anxiety, supraventricular arrhythmias, stable (compensated) heart failure or a prior myocardial infarction. Either beta-1 selective (metoprolol, atenolol) or non-selective (propranolol, nadolol) agents may be used; third-generation agents are carvedilol and labetalol. | The class is the default, and the coexisting conditions in the list are the clues that point to it. Acute decompensated heart failure is a contraindication. | L8 slide 17 |
| Beta blockers metoprolol, atenolol (beta-1 selective); propranolol, nadolol (non-selective); carvedilol, labetalol (third generation) | Monitoring | Monitoring: heart rate, blood sugar and lipids. | These three follow from the adverse effects: slow pulse, raised glucose and altered lipids. | L8 slide 19 |
| Beta blockers metoprolol, atenolol (beta-1 selective); propranolol, nadolol (non-selective); carvedilol, labetalol (third generation) | Education-heavy | Patient education: avoid rapid discontinuation; expect dizziness and fatigue. | Never stop a beta blocker suddenly; stop gradually. (Added background: abrupt cessation can cause rebound angina and myocardial infarction.) | L8 slide 19 |
| Beta blockers metoprolol, atenolol (beta-1 selective); propranolol, nadolol (non-selective); carvedilol, labetalol (third generation) | Drug of choice | Comorbid conditions: the first-line antianginal is a beta blocker when the patient has hypertension, a prior myocardial infarction or decreased left ventricular function. Prior myocardial infarction: beta blocker first line and, in the course table, calcium channel blockers are avoided (current practice allows a non-dihydropyridine when a beta blocker cannot be used). | Prior myocardial infarction is also the trigger in the treatment summary: beta blockers are given after an infarction unless contraindicated. | L8 slide 34 |
| Calcium channel blockers | ||||
| Calcium channel blockers dihydropyridine and non-dihydropyridine | Drug of choice | Place in therapy: non-dihydropyridine agents are initial therapy when beta blockers are contraindicated or not tolerated. Dihydropyridine agents are added in combination with a beta blocker when the beta blocker alone is not successful. Calcium channel blockers may also be combined with long-acting nitrates. | Drug selection rule: non-dihydropyridine for initial therapy; dihydropyridine when combined with a beta blocker. | L8 slide 22 |
| Calcium channel blockers dihydropyridine and non-dihydropyridine | Indication | Calcium channel blockers (as a class) are chosen for: patients who cannot take or do not tolerate beta blockers, vasospastic angina, severe peripheral vascular disease, asthma and uncontrolled diabetes. Left ventricular dysfunction applies to dihydropyridines only (amlodipine). | These are the patients for whom a calcium channel blocker takes the place of a beta blocker. | L8 slide 22 |
| Calcium channel blockers dihydropyridine and non-dihydropyridine | Indication | Choosing inside the class: diltiazem and verapamil (non-dihydropyridines) give moderate vasodilation and slow the heart and atrioventricular conduction; nifedipine, amlodipine and felodipine (dihydropyridines) give the strongest vasodilation and leave atrioventricular conduction unchanged. | The exact plus counts are not the point: non-dihydropyridines act on the heart and the vessels; dihydropyridines act mainly on the vessels. | L8 slide 21 |
| Calcium channel blockers dihydropyridine and non-dihydropyridine | Indication | Diabetes (comorbidity table, the course answer): when the patient has diabetes and no other reason to need a beta blocker, a non-dihydropyridine is first line; the alternatives are a long-acting nitrate and a cardioselective beta blocker. Current practice is more flexible: a cardioselective beta blocker remains a sound first choice in diabetes. | Diabetes is the one row where the table puts a non-dihydropyridine ahead of a beta blocker, because beta blockers can raise blood sugar and mask the signs of hypoglycemia. | L8 slide 34 |
| Calcium channel blockers dihydropyridine and non-dihydropyridine | Education-heavy | Monitoring: relief of symptoms, and heart rate for the non-dihydropyridines. Education: dizziness and constipation (constipation mainly with verapamil). | Avoid short-acting agents, nifedipine being the named example. Warn about dizziness and constipation. | L8 slide 24 |
| Short-acting nitrates | ||||
| Short-acting nitrates nitroglycerin: sublingual tablet (Nitrostat), lingual spray (Nitrolingual Pumpspray) | Drug of choice | Goals of therapy: relieve acute symptoms of myocardial ischemia and prevent effort-induced angina. The treatment summary gives sublingual nitroglycerin for acute relief. | These are the rescue medicines, taken at the first sign of an attack or before a known trigger such as exertion. | L8 slide 27 |
| Short-acting nitrates nitroglycerin: sublingual tablet (Nitrostat), lingual spray (Nitrolingual Pumpspray) | Education-heavy | If the first dose gives no relief after 5 minutes, call emergency medical services. (Further doses may be taken at 5-minute intervals while waiting for help, usually up to three doses in total; this ceiling is standard practice.) | A patient who still has chest pain 5 minutes after the first dose may be having a myocardial infarction: the action is to call for help, not to wait. | L8 slide 27 |
| Short-acting nitrates nitroglycerin: sublingual tablet (Nitrostat), lingual spray (Nitrolingual Pumpspray) | Education-heavy | Storage: keep in the original packaging in a cool, dry place; the course rule is to replace the tablets 3–6 months after opening (current labeling gives the printed expiration date if the tablets stay in the tightly closed original glass container), and to replace them sooner if they no longer work. Administration: the tablet or spray is applied under the tongue. | A patient who says the tablets no longer work should be asked how old the bottle is and how it was stored. | L8 slide 28 |
| Short-acting nitrates nitroglycerin: sublingual tablet (Nitrostat), lingual spray (Nitrolingual Pumpspray) | Education-heavy | Warn about orthostatic hypotension (dizziness or fainting on standing). | Warn the patient to expect possible dizziness on standing after a dose. | L8 slide 28 |
| Long-acting nitrates | ||||
| Long-acting nitrates isosorbide mononitrate (Imdur), isosorbide dinitrate; nitroglycerin ointment (Nitro-Bid) and transdermal patch | Indication | Place in therapy: initial therapy when beta blockers and calcium channel blockers are contraindicated or not tolerated, or in combination with them when they are not successful. Usually an adjunct; not recommended as monotherapy. Monotherapy is discouraged when a beta blocker or calcium channel blocker can be used; a long-acting nitrate alone is accepted only when neither can be. | A long-acting nitrate is almost never the only antianginal; look for the partner drug in the stem. | L8 slide 29 |
| Long-acting nitrates isosorbide mononitrate (Imdur), isosorbide dinitrate; nitroglycerin ointment (Nitro-Bid) and transdermal patch | Indication | Isosorbide mononitrate (Imdur) lasts 12 hours and is dosed once daily. Isosorbide dinitrate lasts 3–6 hours and is dosed three times daily. | The mononitrate is the once-daily agent; the dinitrate is the three-times-daily agent. | L8 slide 30 |
| Long-acting nitrates isosorbide mononitrate (Imdur), isosorbide dinitrate; nitroglycerin ointment (Nitro-Bid) and transdermal patch | Education-heavy | Ointment and patch: 12 hours on, 12 hours off. Ointment: squeeze onto the calibrated applicator paper, spread in a thin layer on the chest, keep covered with applicator paper, and wipe off the previous dose before adding a new one. Adverse reactions: headache, flushing, postural hypotension, reflex tachycardia. | The 12-hour break is the nitrate-free interval that prevents tolerance. | L8 slide 31 |
| Nitrates nitroglycerin, isosorbide | Education-heavy | Tachyphylaxis (tolerance) develops with continuous nitrate exposure; the mechanism is not fully understood (depletion of cofactors, counter-regulatory responses, plasma volume expansion, decreased enzyme activity). Management: a nitrate-free interval, timed to when the patient has the lowest frequency of symptoms. | Do not give around-the-clock nitrate exposure: build in a daily period without the drug. | L8 slide 32 |
| Nitrates nitroglycerin, isosorbide | Education-heavy | Never combine a nitrate with a phosphodiesterase type 5 inhibitor (sildenafil, tadalafil, vardenafil): concurrent use may lead to hypotension, myocardial infarction or stroke. | Ask every patient on a nitrate about erectile dysfunction medicines; this is the classic dangerous nitrate interaction. | L8 slide 33 |
| Vasculoprotective drugs in stable disease | ||||
| ACE (angiotensin-converting enzyme) inhibitors used in coronary artery disease | Indication | Used in coronary artery disease with diabetes and/or left ventricular systolic dysfunction; should be used indefinitely after a myocardial infarction, with left ventricular dysfunction or with diabetes; consider in all patients with coronary artery disease or other vascular disease. They do not significantly affect myocardial oxygen consumption and do not relieve angina; they may help prevent progression of the disease. | Not an antianginal: do not expect chest-pain relief; the benefit is long-term protection. | L8 slide 35 |
| Aspirin antiplatelet | Drug of choice | Aspirin in the absence of contraindications for all patients with ischemic heart disease, to prevent acute coronary syndrome. | Aspirin is the default antiplatelet; the question becomes clopidogrel only when aspirin is not an option. | L8 slide 37 |
| Clopidogrel antiplatelet | Indication | Recommended for patients allergic to aspirin; as efficacious as aspirin in secondary prevention. | Aspirin allergy is the trigger for choosing clopidogrel in stable ischemic heart disease. | L8 slide 37 |
| Treatment summary for stable disease | ||||
| Give unless contraindicated the standard bundle | Drug of choice | Aspirin; a beta blocker if there was a prior myocardial infarction; an angiotensin-converting enzyme inhibitor in patients with diabetes or left ventricular dysfunction; lipid-lowering therapy; sublingual nitroglycerin for acute relief (symptom relief, not protection). | Match the drug to the trigger: prior infarction points to the beta blocker, diabetes or weak left ventricle to the angiotensin-converting enzyme inhibitor. | L8 slide 38 |
| Prophylactic antianginals beta blockers, calcium channel blockers, long-acting nitrates | Indication | For daily or more frequent symptoms, add prophylactic therapy: beta blockers, calcium channel blockers or long-acting nitrates. | Sublingual nitroglycerin alone is for occasional attacks; daily symptoms call for a preventive drug. | L8 slide 38 |
| Combination therapy beta blocker plus calcium channel blocker | Indication | Consider combining when angina persists on one drug. A beta blocker and a dihydropyridine calcium channel blocker may be combined if tolerated (some evidence of longer exercise duration); a non-dihydropyridine with a beta blocker is a precaution (the concern is additive heart block and bradycardia, inferred from their heart rate and conduction effects). If a third agent seems needed, the patient probably needs further workup such as angiography. | Persistent symptoms on two drugs usually call for further testing (for example angiography) before a third drug. | L8 slide 36 |
| Acute coronary syndrome | ||||
| Acute coronary syndrome classification | Indication | ST-elevation myocardial infarction versus non-ST-elevation acute coronary syndrome, which includes unstable angina and non-ST-elevation myocardial infarction. The electrocardiogram (ST elevation or not) sorts the two groups; a biochemical marker separates unstable angina from infarction. | Electrocardiogram first (ST elevation or not), then the blood marker (unstable angina versus infarction). | L8 slide 41 |
| Goals of therapy acute coronary syndrome | Indication | Reestablish coronary blood flow, relieve chest pain, prevent progression to myocardial infarction, prevent heart failure and prevent death. | Each acute drug maps to one goal: fibrinolytics reopen flow, nitrates and morphine relieve pain, aspirin and antithrombotics prevent progression. | L8 slide 51 |
| Aspirin antiplatelet | Drug of choice | Given at the first signs of chest pain: chew and swallow. Reduces mortality and reinfarction; also decreases recurrent ischemia, stroke and cardiac death. Common to both ST-elevation myocardial infarction and non-ST-elevation acute coronary syndrome. | Tell the patient to chew and swallow the tablet rather than swallow it whole; it is given at the first sign of chest pain. | L8 slide 52 |
| Nitrates in acute coronary syndrome nitroglycerin | Indication | Sublingual therapy until the patient reaches the hospital, then an intravenous infusion. Benefit: relief of chest pain only, with no mortality benefit. | Nitrates treat the pain, not the outcome; do not pick a nitrate as the drug that lowers mortality. | L8 slide 54 |
| Beta blockers in acute coronary syndrome | Indication | Started early: intravenous followed by oral therapy (the course sequence). Benefit taught: reduction in early and late mortality, infarct size, heart failure incidence and sudden cardiac death. Current guidelines differ: they favor oral therapy within the first day, avoid the intravenous route when there is heart failure, low cardiac output or risk of shock, and rest the benefit mainly on long-term use after infarction. | Nitrates relieve pain without an outcome benefit; beta blockers are taught to lower mortality, but only when acute decompensated heart failure, shock risk, heart block and bradycardia are absent. | L8 slide 55 |
| Morphine opioid analgesic | Indication | For chest pain unresponsive to nitrates, used in ST-elevation myocardial infarction. It may increase mortality in unstable angina and non-ST-elevation myocardial infarction, and its use is controversial. | It is a second-line pain drug for the ST-elevation group; do not generalize it to unstable angina. | L8 slide 56 |
| Fibrinolytics streptokinase; alteplase (Activase), reteplase (Retavase), tenecteplase (TNKase) | Indication | For ST-elevation myocardial infarction presenting early (within 12 hours of symptom onset). Less benefit with older age or late presentation; not recommended in non-ST-elevation acute coronary syndrome (bleeding risk exceeds benefit). Relatively few patients receive them. Bleeding, including intracranial hemorrhage, is the main risk. | Fibrinolytics belong only to the ST-elevation group; in non-ST-elevation disease they are not used. | L8 slide 65 |
| Fibrinolytics streptokinase; alteplase (Activase), reteplase (Retavase), tenecteplase (TNKase) | Indication | Agents named: streptokinase (a bacterial protein, not recombinant); the recombinant tissue plasminogen activators alteplase (Activase), made by recombinant deoxyribonucleic acid (DNA) technology in Chinese hamster ovary cells and very expensive; reteplase (Retavase), made in Escherichia coli cells; tenecteplase (TNKase), recombinant with substituted amino acids. Reteplase and tenecteplase have a longer half-life than alteplase. | Brand names to recognize: Activase, Retavase, TNKase. | L8 slide 64 |
| Other antithrombotic agents glycoprotein IIb/IIIa inhibitors, P2Y12 receptor antagonists, heparins | Indication | Glycoprotein IIb/IIIa inhibitors are not routinely recommended before percutaneous coronary intervention. P2Y12 receptor antagonists are used before percutaneous coronary intervention and as clot prophylaxis when a stent is placed. Heparins are used together with fibrinolysis or antiplatelet agents. | Stent placement brings a P2Y12 receptor antagonist; fibrinolysis or antiplatelet therapy brings a heparin. | L8 slide 66 |
| Non-ST-elevation acute coronary syndrome unstable angina and non-ST-elevation myocardial infarction | Drug of choice | Early treatment is similar to ST-elevation myocardial infarction, but fibrinolytics are not recommended (bleeding risk exceeds benefit). Enoxaparin is preferred over unfractionated heparin (older studies; current guidelines accept either), and glycoprotein IIb/IIIa inhibitors are used more commonly. | Three differences to remember: no fibrinolytics, enoxaparin over heparin, more glycoprotein IIb/IIIa inhibitors. | L8 slide 68 |