Your blank Pharmacology Drug Study Chart, filled in for Exam 2 (Lectures 4–8): one row per drug class, every cell taken from the slides and checked against them.
| Class of Drugs | Generic Names (3+ Drugs) | Mechanism of Action (MOA) | Indications | Contraindications | Adverse Effects | BLACK BOX WARNING / Special Indications or Contraindications |
|---|---|---|---|---|---|---|
| Lecture 4 — Ophthalmic Drugs | ||||||
| Ophthalmic macrolidesslides 14-15, 17 | erythromycin, azithromycinOnly 2 named in the lecture. | Inhibit RNA (ribonucleic acid)-dependent protein synthesis at the 50S ribosome (block transpeptidation), so no protein is made and the bacteria die. | Bacterial conjunctivitis. Erythromycin ointment is the most common and is soothing on an inflamed eye; it is also used to prevent ophthalmia neonatorum. Azithromycin costs more but needs fewer doses. | None listed; no drug interactions. | Eye irritation; hypersensitivity. | — |
| Ophthalmic fluoroquinolonesslides 21-22 | ciprofloxacin, ofloxacin, levofloxacin, moxifloxacin, gatifloxacin | Inhibit DNA (deoxyribonucleic acid) gyrase and topoisomerase IV, so supercoiled DNA cannot relax and the DNA breaks (double-stranded breaks). | Conjunctivitis and corneal ulcers. Preferred for corneal ulcers and for Pseudomonas aeruginosa. Preferred for conjunctivitis in contact lens wearers once keratitis is ruled out. Expensive, with frequent dosing. | None listed. Caution: rule out keratitis first in a contact lens wearer; emerging resistance; no interactions when given in the eye. | Ocular irritation; white precipitate (ciprofloxacin, about 17%); unpleasant taste after instillation. | Preferred for corneal ulcers and Pseudomonas aeruginosa. |
| Ophthalmic aminoglycosidesslide 23 | gentamicin, tobramycinOnly 2 named in the lecture. | Bind the 30S ribosomal subunit and interfere with bacterial protein synthesis. | Conjunctivitis (solutions every 2 to 4 hours; ointment 2 to 3 times a day). | None listed; no clinically significant interactions. | Ocular irritation; corneal ulceration; reactive keratoconjunctivitis (with several days of use). | Reactive keratoconjunctivitis after several days of use; corneal ulceration is also listed. |
| Other topical antibacterials (sulfonamide, polypeptide, folate antagonist plus polymyxin)slides 18-20 | sulfacetamide, bacitracin, trimethoprim with polymyxin B | Sulfacetamide: blocks folic acid synthesis (antagonizes PABA (para-aminobenzoic acid)). Bacitracin: blocks cell wall synthesis. Trimethoprim: blocks folic acid reduction; polymyxin B: binds membrane phospholipids, so cell contents leak. | Bacterial conjunctivitis (all three). Polytrim (trimethoprim with polymyxin B) is a solution; sulfacetamide comes as ointment or solution; bacitracin as an ointment. | Sulfacetamide: avoid in patients with a sulfonamide allergy. Bacitracin and Polytrim: no clinically significant interactions. | Ocular irritation (all three); sulfacetamide also causes allergic reactions. | Sulfacetamide: avoid in any patient with a sulfonamide allergy. |
| Antivirals for herpes simplex and herpes zoster eye diseaseslides 25-27 | trifluridine, acyclovir, valacyclovir, famciclovir | Trifluridine inhibits thymidylate synthetase and is built into viral DNA (deoxyribonucleic acid) in place of thymidine, so viral replication stops. Mechanism not given for the other three. | Trifluridine (topical): herpes simplex keratitis and keratoconjunctivitis. Acyclovir: herpes zoster ophthalmicus, herpes simplex iridocyclitis. Valacyclovir, famciclovir (oral): herpes simplex keratitis, herpes zoster ophthalmicus. | None listed. No antiviral is used for viral conjunctivitis caused by adenoviruses; it is self-limited. | Trifluridine: ocular irritation, punctate keratopathy (pinpoint corneal damage), hypersensitivity. | Adenoviral conjunctivitis gets no antiviral: treat symptoms only. |
| Antivirals for cytomegalovirus retinitisslides 26, 28 | ganciclovir, valganciclovir, foscarnet, cidofovir | Ganciclovir competitively inhibits binding of deoxyguanosine triphosphate to DNA (deoxyribonucleic acid) polymerase, blocking viral DNA synthesis. Mechanism not given for the others. | Cytomegalovirus retinitis: ganciclovir (intravenous, oral or intravitreal implant), valganciclovir (oral), foscarnet (intravenous or intravitreal), cidofovir (intravenous). Ganciclovir (Zirgan): herpetic keratitis. | None listed. | Ganciclovir (Zirgan): ocular irritation, punctate keratitis. | Black boxSystemic ganciclovir, valganciclovir, cidofovir and foscarnet carry an FDA (Food and Drug Administration) boxed warning (bone marrow suppression, kidney injury, seizures with foscarnet); not stated in the lecture. |
| Ocular antifungals (polyenes and imidazoles)slides 30-32 | natamycin, amphotericin B, fluconazole, itraconazole, ketoconazole, miconazole | Natamycin binds sterols and raises fungal cell membrane permeability. Mechanism not given for amphotericin B or the imidazoles. | Natamycin (the only commercially available ophthalmic antifungal): conjunctivitis, keratitis (Aspergillus, Candida, Fusarium and others). Amphotericin B and the imidazoles: yeast and fungal keratitis, endophthalmitis. | None listed. | Natamycin: ocular irritation. | Black boxOral ketoconazole carries an FDA (Food and Drug Administration) boxed warning (liver injury; QT prolongation with interacting drugs); systemic itraconazole and amphotericin B also carry boxed warnings; not stated on the ocular antifungal slide. Risk factors for fungal eye infection: trauma, chronic surface disease, contact lenses, immunosuppression (including topical steroids). |
| Ophthalmic antihistamines (histamine-1 receptor antagonists)slides 39, 42-44 | azelastine, alcaftadine, bepotastine, emedastine, epinastine, ketotifen, olopatadine | Inverse agonists at the histamine-1 (H1) receptor, still competitive with histamine: decrease capillary dilation, itch and swelling. | Ocular allergy. Dosed 1 to 2 times a day; onset within minutes; allow two weeks to judge full effect. Typically preferred over mast cell stabilizers. | None listed; no significant drug interactions. | Ocular irritation; headache; increased ocular dryness. | Preferred over mast cell stabilizers: onset within minutes. |
| Mast cell stabilizersslides 45-47 | cromolyn, lodoxamide, nedocromil | Inhibit mast cell degranulation, limiting release of histamine, tryptase and prostaglandin D2; also dampen mediator release from basophils, eosinophils and neutrophils. | Predictable seasonal allergies in patients who do not tolerate other therapies. Full effect takes 5 to 14 days. | None listed. Limitation: not useful for acute symptoms (5-14 days for full efficacy). | Ocular irritation; unpleasant taste; headache. | NOT for acute symptoms: 5 to 14 days to full effect, and often four-times-daily dosing. |
| Topical vasoconstrictors (imidazoline derivatives)slides 48-49 | tetrahydrozoline, naphazoline, pheniramine with naphazoline | Vasoconstrictor that activates postjunctional alpha-adrenergic receptors on blood vessels, decreasing conjunctival edema (pheniramine adds an antihistamine). Systemically they target alpha-2 receptors. | Decreases conjunctival swelling (edema); over-the-counter; good for under 2 weeks. | Not for prolonged use. If no improvement in 72 hours, stop and see a provider (it could be something more serious). Accidental ingestion matters: systemically these act on alpha-2 receptors. | Rebound hyperemia after prolonged use and stopping. | Rebound hyperemia with prolonged use: limit to under 2 weeks (a key counseling point). |
| Ophthalmic NSAIDs (nonsteroidal anti-inflammatory drugs)slides 50-51 | bromfenac, diclofenac, flurbiprofen, ketorolac, nepafenac | Block cyclooxygenase, so arachidonic acid is not converted to prostaglandins and thromboxanes (pro-inflammatory mediators). | Postoperative inflammation and pain; allergic conjunctivitis. | None listed. Not routinely recommended for conjunctivitis. | Lacrimation; keratitis; increased eye pressure; ocular irritation. | Not routinely recommended for conjunctivitis. |
| Ophthalmic glucocorticoidsslides 52, 54-55 | dexamethasone, prednisolone, difluprednate, fluorometholone, loteprednol, rimexolone, triamcinolone | Suppress the late-phase allergic reaction: inhibit phospholipase A2, so fewer arachidonic acid-derived inflammatory mediators; also inhibit fibrin and collagen deposition (less scarring). | Severe ocular allergy; anterior uveitis; external eye inflammatory disease; inflammation after ocular surgery. Given topically or intraocularly. | Generally used for refractory symptoms, limited to under 2 weeks of pulse therapy. Cautions: infection, corneal ulcers, glaucoma and raised eye pressure, cataract, delayed wound healing. | Cataract; raised eye pressure (more with a family history) and glaucoma; infection (decreased immune function); delayed wound healing; corneal ulcers. | Limit to under 2 weeks. Soft steroids (fluorometholone, loteprednol, rimexolone) carry a lower risk of raised eye pressure. |
| Tear substitutes (artificial tears)slides 56-57 | balanced salt solution, carboxymethylcellulose, hydroxypropyl cellulose, polyvinyl alcohol | Hypotonic or isotonic solutions containing electrolytes, surfactants and thickeners; the thickeners increase time in the cul-de-sac. | Dry eye (alteration of the precorneal tear film and ocular surface). Many are over-the-counter. | None listed. | None listed. | Treat the underlying disease first (for example Sjogren syndrome, rheumatoid arthritis, vitamin A deficiency). |
| Ocular immunomodulatorslide 58 | cyclosporineOnly 1 named in the lecture. | Inhibits production and release of interleukin-2, so less T cell activation: fewer inflammatory markers in the lacrimal gland and more tear production. | Chronic dry eye associated with inflammation (keratoconjunctivitis sicca); improves vision and comfort. | None listed; no drug interactions. | Ocular burning (17%); foreign body sensation; blurred vision. | — |
| Prostaglandin analogs (glaucoma)slides 64-66 | latanoprost, travoprost, bimatoprost, tafluprost | Analogs of prostaglandin F2-alpha: bind prostaglandin receptors and lower eye pressure by increasing aqueous outflow (exact mechanism unclear). | Glaucoma and ocular hypertension: first-line, the most commonly used glaucoma drugs, once-daily dosing. | None listed. Do not exceed once-daily dosing: more frequent dosing inhibits the pressure-lowering effect. | Conjunctival hyperemia; ocular irritation; changes in eyelash length and iris color. Limited systemic side effects. | Never dose more than once daily (it blunts the effect). |
| Ophthalmic beta blockers (glaucoma)slides 64, 67-68, 74 | timolol, carteolol, levobunolol, betaxolol | Block beta receptors in the ciliary body epithelium: less catecholamine activation, less cyclic adenosine monophosphate, less aqueous humor production. | Glaucoma and ocular hypertension (second-line; decreases aqueous production). Start with a prostaglandin analog or a beta blocker. | Avoid or use cautiously in heart failure, bradycardia, heart block and asthma. Beta-1 selective agents (betaxolol) carry less bronchoconstriction risk in asthma. | Worsening heart failure; bradycardia; heart block; increased airway resistance (asthma). | Nonselective agents (timolol, carteolol, levobunolol) work better but cause more side effects; betaxolol is beta-1 selective. |
| Alpha-2 adrenergic agonists (glaucoma)slides 64, 69 | apraclonidine, brimonidineOnly 2 named in the lecture. | Alpha-2 agonists: presynaptically decrease catecholamine release, and postsynaptic alpha-2 activation decreases aqueous production; aqueous outflow also increases. | Glaucoma and ocular hypertension (decrease aqueous production and increase outflow). | Contraindicated in children under 2 years (central nervous system depression and apnea). | Ocular irritation; hyperemia (rebound effect); pruritus; allergic conjunctivitis (less common with brimonidine). | Contraindicated in children under 2 years: central nervous system depression and apnea. |
| Carbonic anhydrase inhibitors (glaucoma)slides 64, 70, 73 | dorzolamide, brinzolamideOnly 2 named in the lecture. | Inhibit carbonic anhydrase in the ciliary body epithelium: less bicarbonate, less fluid transport, lower eye pressure (decreased aqueous production). | Glaucoma and ocular hypertension. Available in combinations (dorzolamide with timolol; brinzolamide with brimonidine) for fewer drops and better adherence. | None listed. | Bitter taste (25%); burning or stinging after administration (33%); allergic conjunctivitis. | — |
| Cholinergic agonists (miotics, glaucoma)slides 64, 72 | acetylcholine, carbachol, pilocarpine | Activate muscarinic receptors, causing ciliary muscle contraction that facilitates aqueous outflow. | Glaucoma (increase aqueous outflow). Acetylcholine (Miochol-E) is used in surgical settings. | Younger patients are usually intolerant because of visual blurring; poor compliance from side effects and frequent administration. | Fixed small pupils; myopia; visual disturbances; headaches. | Poorly tolerated by younger patients (visual blurring). |
| Ocular anestheticsslide 75 | tetracaine, proparacaineOnly 2 named in the lecture. | Inhibit sodium influx into the neuron, preventing signal propagation. | Tonometry; foreign body removal; superficial corneal surgery. | None listed. Do not write prescriptions for these. | Hypersensitivity; burning sensation. Eyes stay numb for 10 to 20 minutes with no blink reflex. | No blink reflex for 10 to 20 minutes; do not write prescriptions for these. |
| Mydriatics and cycloplegics (antimuscarinics and sympathomimetic)slides 76-77 | atropine, cyclopentolate, tropicamide, phenylephrine | Antimuscarinics competitively block muscarinic acetylcholine receptors, causing mydriasis. Phenylephrine is an adrenergic receptor agonist that causes mydriasis and is more reactive to light. | Diagnostic use (fundoscopic examination) and uveitis (prevent synechiae, relieve ciliary spasm). | None listed. | Photosensitivity; blurred vision. Phenylephrine: photosensitivity, conjunctival hyperemia. | — |
| Diagnostic dyeslide 78 | fluoresceinOnly 1 named in the lecture. | Reveals epithelial defects of the cornea and conjunctiva (a stain). | Anterior segment staining; disclosing corneal injury. | None listed. | Hypersensitivity; burning sensation. | — |
| Lecture 5 — Ear, Nose and Throat Drugs | ||||||
| Penicillins (first-line for ear, sinus and throat infections)slides 5, 7-8 | amoxicillin, amoxicillin-clavulanate, benzathine penicillin G | Not given in this lecture. | Otitis media: high-dose amoxicillin is the mainstay; amoxicillin-clavulanate if severe, resistant, or antibiotics in the past month. Rhinosinusitis: amoxicillin-clavulanate. Group A streptococcal pharyngitis: amoxicillin or one benzathine penicillin G injection. | Penicillin allergy: use an alternative (see the next row). | Not given in this lecture. | Use a rapid strep test before treating pharyngitis: most cases are viral. |
| Alternatives for penicillin allergy or failed therapy (cephalosporins, macrolide, lincosamide, fluoroquinolone)slides 5-8 | cefdinir, cefixime, cephalexin, ceftriaxone, azithromycin, clindamycin, levofloxacin | Not given in this lecture. | Penicillin-allergic: otitis, cefdinir or azithromycin; sinusitis, clindamycin plus cefixime or levofloxacin; pharyngitis, cephalexin, clindamycin or azithromycin. Failed therapy (no better in 3 days; no antibiotics in past 3 months): amoxicillin-clavulanate or cefdinir; may escalate to ceftriaxone. | None listed. Up to 50% of Streptococcus pneumoniae are resistant to macrolides. | Not given in this lecture. | Black boxLevofloxacin: FDA (Food and Drug Administration) boxed warning (tendon rupture, nerve damage, myasthenia gravis worsening). Clindamycin: boxed warning (Clostridioides difficile colitis). Not stated in the lecture. Ceftriaxone (intramuscular) is the step-up for failure. |
| Otic anti-infectives (with or without a glucocorticoid)slides 9-10 | ciprofloxacin, ofloxacin, ciprofloxacin with dexamethasone, neomycin with polymyxin B and hydrocortisone | The anti-infective inhibits bacterial growth; the glucocorticoid decreases inflammatory cytokine production. | Otitis media and otitis externa. Ciprofloxacin with dexamethasone (Ciprodex) is expensive; ofloxacin with dexamethasone ophthalmic drops are the alternative. | Polymyxin B: not recommended with a ruptured eardrum or ear tubes in place (cochlear damage, hearing loss). | Neomycin: hypersensitivity. Polymyxin B: cochlear damage and hearing loss. | Neomycin with polymyxin B drops: avoid with a ruptured eardrum or ear tubes (inner ear damage). |
| Systemic imidazole antifungalslide 12; also Lecture 4 slide 31 | ketoconazoleOnly 1 named in the lecture. | Alters fungal cell wall permeability by inhibiting CYP450 (cytochrome P450). | Systemic fungal infections. | None listed as such. Cautions drawn from the adverse effects: QT prolongation, hepatic toxicity, and CYP3A4 (cytochrome P450 3A4) inhibition, which raises levels of other drugs. | QTc (corrected QT interval) prolongation; hyperlipidemia; orthostatic hypotension; hepatitis, abnormal liver tests, cirrhosis, hepatic failure. | Black boxFDA (Food and Drug Administration) boxed warning for oral ketoconazole: liver injury and QT prolongation with interacting drugs (the boxed warning itself is not stated in the lecture; hepatic failure is). |
| Nonabsorbable antifungalslide 13 | nystatinOnly 1 named in the lecture. | Binds sterols in the fungal cell membrane, increasing permeability. | Oral candidiasis (oral suspension), for example with inhaled steroids, human immunodeficiency virus infection or chemotherapy. | None listed. | Diarrhea; nausea; stomach pain; vomiting. | — |
| Salicylatesslides 15-18, 20 | aspirin (acetylsalicylic acid)Only 1 named in the lecture. | Irreversible, noncompetitive inhibitor of platelets; nonselective for cyclooxygenase-1 and cyclooxygenase-2. | Antiplatelet at the lowest doses; antipyretic-analgesic (fever, pain) at higher doses; anti-inflammatory at the highest of these doses. | Bleeding disorders; pregnancy (very low doses may help preeclampsia); children with fever from a viral illness (chickenpox, influenza); do not combine with anticoagulants or other nonsteroidal anti-inflammatory drugs. | Bleeding; gastrointestinal upset, nausea; hypersensitivity; tinnitus. Overdose (salicylism): hyperventilation, alkalosis, then acidosis, shock, coma, death. | Reye syndrome (children under 15, mortality 50%): no aspirin for a child with fever from a viral illness. |
| NSAIDs (nonsteroidal anti-inflammatory drugs)slides 21-23 | ibuprofen, naproxenOnly 2 named in the lecture. | Ibuprofen reversibly inhibits cyclooxygenase-1 and cyclooxygenase-2, decreasing prostaglandin synthesis. | Relief of mild to moderate pain (ibuprofen: anti-inflammatory, analgesic, antipyretic). Naproxen (Aleve): longer half-life, less frequent dosing. | Ibuprofen: allergy to the product; may exacerbate asthma; avoid under 6 months of age; history of stomach ulcers or perforation; renal dysfunction. | Gastric or duodenal ulcers, perforation, bleeding; edema and fluid retention; acute renal failure. | Black boxPrescription NSAIDs carry an FDA (Food and Drug Administration) boxed warning for cardiovascular events and gastrointestinal bleeding (not stated in the lecture). Ibuprofen lowers ACE (angiotensin-converting enzyme) inhibitor effect and raises lithium and methotrexate levels. |
| Analgesic and antipyretic (acetaminophen)slides 24-25 | acetaminophenOnly 1 named in the lecture. | Not fully elucidated. | Pain; fever above 100 degrees Fahrenheit. | Allergy to the product (the only one listed). Alcohol increases the risk of liver damage (chronic use). | No notable side effects at therapeutic doses; very well tolerated. | Do not exceed 4 g in 24 hours. Alcohol plus acetaminophen raises the risk of liver damage. |
| First-generation H1 (histamine-1) antihistaminesslides 31-37 | chlorpheniramine, dimenhydrinate, diphenhydramine, hydroxyzine, meclizine, promethazine | Block histamine-1 receptors: block smooth muscle contraction and rapid vasodilation; decrease secretions, edema, hives and itch. Also antimuscarinic, antiemetic and antiserotonergic. | Allergic reactions (rhinitis, urticaria, insect bites, drug hypersensitivity); motion sickness, nausea and vestibular disturbances; over-the-counter sleep aids; adjunct in anaphylaxis. | Additive sedation with other central nervous system depressants or alcohol. Excitation instead of sedation at higher doses (especially in children) and in overdose. | Sedation (the major effect); gastrointestinal disturbances; dry mouth, urinary retention, blurred vision; dermatitis and photosensitivity with topical use. | Black boxSedation is the major side effect; promethazine has the strongest antimuscarinic action. Promethazine carries an FDA (Food and Drug Administration) boxed warning (tissue injury with injection; fatal breathing depression under age 2); not stated in the lecture. |
| Second-generation H1 (histamine-1) antihistaminesslides 32, 35, 37 | cetirizine, fexofenadine, loratadine | Block histamine-1 receptors but enter the central nervous system far less (much less sedation). | Allergic reactions (allergic rhinitis, urticaria, insect bites, drug hypersensitivity). | None listed. | Much less sedation: low with cetirizine, very low with fexofenadine and loratadine; very low anticholinergic effects. | Duration: cetirizine and loratadine 24 hours, fexofenadine 12 hours. |
| Intranasal antihistamineslides 38-39 | azelastineOnly 1 named in the lecture. | Histamine-1 (H1) receptor antagonist. | Allergic rhinitis and vasomotor rhinitis. | None listed. Do not use with other nasal sprays. | Bitter taste; epistaxis (nosebleed). | If a nosebleed develops, stop and follow up immediately. Spray away from the septum; do not tilt the head back. |
| Nasal corticosteroidsslides 42-43 | beclomethasone, budesonide, flunisolide, fluticasone, mometasone, triamcinolone | Not given in this lecture. | Allergic rhinitis and vasomotor rhinitis. | None listed; interactions: no information available. | Epistaxis; septal perforation; unpleasant taste. | Name trap: many have inhaled versions for asthma (Flonase is not Flovent). |
| Systemic glucocorticoidsslides 44, 46-48 | dexamethasone, prednisone, prednisolone | Not given in this lecture (dexamethasone is classed as a synthetic adrenocortical steroid). | Allergic rhinitis, allergic conjunctivitis and drug hypersensitivity reactions. | Systemic fungal infections (dexamethasone); allergy to the product and infections, especially fungal (prednisone). | Sodium and fluid retention, heart failure, hypertension, low potassium; glucose intolerance; cushingoid features; tendon rupture, fractures; cataracts, glaucoma, raised eye pressure; weakened immunity. | Do not stop abruptly (dexamethasone after more than 1 week; prednisone: rebound symptoms). Avoid chickenpox or measles exposure and live vaccines. |
| Nasal decongestants (alpha agonists)slides 50-53 | oxymetazoline, pseudoephedrine, phenylephrine | Alpha agonists that constrict blood vessels in the nasal mucosa (oxymetazoline, pseudoephedrine). Phenylephrine: mechanism not stated in the lecture. | Nasal congestion. Pseudoephedrine (oral) also treats congestion from the common cold, hay fever, allergies and sinus congestion, and eustachian tube dysfunction from viral infection. | None listed. Oxymetazoline interacts with monoamine oxidase inhibitors and antidepressants; pseudoephedrine decreases the effect of antihypertensives. | Oxymetazoline: rebound rhinitis (rhinitis medicamentosa) after more than 3 to 5 days; hypertension. Pseudoephedrine: tachycardia, hypertension, headache. | Oxymetazoline: no more than 3 to 5 days (rebound rhinitis). |
| Antitussives (cough suppressants)slides 57-58 | benzonatate, dextromethorphanOnly 2 named in the lecture. | Benzonatate anesthetizes the stretch receptors in the lungs. Dextromethorphan (related to codeine) suppresses the medullary cough center through sigma receptor activation. | Symptomatic relief of non-productive cough (benzonatate); cough (dextromethorphan). | Benzonatate: allergy to the product or related products (tetracaine). Dextromethorphan: taking, or within 2 weeks of taking, a monoamine oxidase inhibitor. | Benzonatate: local anesthesia from chewing the capsule. Dextromethorphan: confusion, excitement, agitation; serotonin syndrome risk with other pro-serotonergic drugs. | Dextromethorphan: never with a monoamine oxidase inhibitor (or within 2 weeks). Swallow benzonatate whole. |
| Expectorants and mucolyticsslides 59, 61-63 | guaifenesin, dornase alfa, hypertonic saline, N-acetylcysteine | Guaifenesin: loosens mucus, lowers viscosity. Dornase alfa cleaves DNA (deoxyribonucleic acid) from degenerating neutrophils, thinning cystic fibrosis sputum. N-acetylcysteine: splits disulfide bonds in mucoproteins. Hypertonic saline: hydrates the airway, aids clearance. | Guaifenesin: loosens mucus. Dornase alfa: mild to moderate cystic fibrosis lung disease (better lung function, fewer exacerbations). Inhaled N-acetylcysteine: mucolytic; traditionally used for acetaminophen toxicity. | Guaifenesin: allergy to the product; no interactions listed. | Guaifenesin: nausea, vomiting. Inhaled N-acetylcysteine: rotten-egg smell, nausea, vomiting, bronchospasm. | Inhaled N-acetylcysteine can cause bronchospasm. |
| Lecture 6 — Antihypertensive Drugs | ||||||
| ACE (angiotensin-converting enzyme) inhibitorsslides 11-14, 16-22; also Lecture 8 slide 35 | captopril, lisinopril, enalapril, benazepril, fosinopril, trandolapril, quinapril, ramipril, perindopril, moexipril | Block angiotensin-converting enzyme: less angiotensin II (less vasoconstriction, aldosterone, sodium reabsorption and norepinephrine release) and less bradykinin breakdown. | Hypertension (preferred in diabetics); heart failure and left ventricular dysfunction; after myocardial infarction (lower mortality); diabetic nephropathy; coronary artery disease with diabetes or left ventricular dysfunction. | Pregnancy (2nd and 3rd trimesters). Caution in kidney disease (may sharply lower filtration), with potassium-sparing diuretics, potassium supplements or salt substitutes (hyperkalemia); nonsteroidal anti-inflammatory drugs can blunt the effect. | Dry cough (5-15%, bradykinin); hyperkalemia; first-dose hypotension; kidney impairment; angioedema (rare, 0.1-0.5%); fetal harm. | Black boxFDA (Food and Drug Administration) boxed warning: fetal toxicity (birth defects, fetal death; contraindicated in the 2nd and 3rd trimesters). Angioedema: stop the drug. |
| ARBs (angiotensin receptor blockers)slides 25-30 | candesartan, olmesartan, losartan, azilsartan, eprosartan, irbesartan, telmisartan, valsartan | Block AT1 (angiotensin II type 1) receptors with high affinity and slow dissociation: vasodilation, less aldosterone, sodium reabsorption and norepinephrine release. They do not inhibit bradykinin breakdown. | Hypertension (often with a diuretic); left ventricular dysfunction when an ACE (angiotensin-converting enzyme) inhibitor is not tolerated; diabetic nephropathy. | Pregnancy (not given in the 2nd and 3rd trimesters). Caution: hyperkalemia with kidney disease or potassium-sparing diuretics; first-dose hypotension; kidney impairment. | Hyperkalemia; hypotension; kidney impairment; fetal harm. No cough and no bradykinin effect; lower angioedema rate. | Black boxFDA (Food and Drug Administration) boxed warning: fetal toxicity (not given in the 2nd and 3rd trimesters). In heart failure start low and titrate up. |
| Non-dihydropyridine calcium channel blockersslides 33, 40-42, 44-47, 75 | diltiazem, verapamilOnly 2 named in the lecture. | Block L-type calcium channels in vascular smooth muscle, heart muscle and the sinoatrial and atrioventricular nodes; reduce the slow inward current AND slow its recovery, so atrioventricular conduction slows. | Angina; hypertension; supraventricular tachycardia; atrial fibrillation or flutter. Also listed for calcium channel blockers as a class: diastolic heart failure, migraine prophylaxis. | Advanced heart block; hypotension. Relative: heart failure, liver disease, gastroesophageal reflux disease. | Flushing, headache, hypotension, peripheral edema; negative inotropy (bradycardia, first-degree block, worse heart failure); nausea, constipation; raised liver tests; gingival hyperplasia. | Inhibit CYP3A4 (cytochrome P450 3A4) and P-glycoprotein: raise levels of statins, digoxin, cyclosporine, tacrolimus. Amiodarone: slower sinus rate or worse atrioventricular block. Beta blockers: additive drops in pressure, rate and contractility. |
| Dihydropyridine calcium channel blockersslides 38-40, 49, 51-52 | amlodipine, nifedipine, nicardipine, felodipine, isradipine, nisoldipine, nimodipine | Block L-type calcium channels mainly in arterial smooth muscle (3 to 10 times more sensitive than heart muscle): vasodilation and lower afterload, with no effect on preload, veins or atrioventricular conduction. | Amlodipine, nifedipine, nicardipine: angina and hypertension. Felodipine, isradipine, nisoldipine: hypertension. Nimodipine: subarachnoid hemorrhage. | Severe aortic stenosis; unstable angina or recent myocardial infarction (immediate-release form). Avoid short-acting formulations. | Peripheral edema; dyspnea, wheezing; rebound tachycardia; gastrointestinal and central nervous system effects; skin reactions; gynecomastia; gingival hyperplasia. | Avoid short-acting formulations. Immediate-release forms are contraindicated in unstable angina or recent myocardial infarction. |
| Non-selective beta blockers (first generation)slides 56-57, 60, 63, 65-69, 71-74; also Lecture 8 slide 18, Lecture 8 slide 34 | propranolol, nadolol, timolol, pindolol, penbutolol, sotalol | Block cardiac beta-1 receptors (lower cardiac output) and renin release (less angiotensin II); block beta-2 receptors (bronchospasm) and presynaptic beta-2 receptors (less norepinephrine); lower central sympathetic activity. | Hypertension (not first line; best in young patients with fast heart rate, high catecholamines or renin); angina; after myocardial infarction; supraventricular arrhythmias; migraine prophylaxis (propranolol, timolol); hyperthyroid symptoms; essential tremor. | Bronchospasm or asthma (non-selective agents are worst); heart block; slow heart rate. Caution in diabetes (masks hypoglycemia), peripheral artery disease and heart failure. | Bronchoconstriction; fatigue, bradycardia, heart block; disturbed glucose control; cold extremities (Raynaud phenomenon); depression, nightmares (more with lipid-soluble propranolol, penbutolol); raised triglycerides. | Black boxSudden withdrawal causes acute angina, myocardial infarction and a marked blood pressure rise: taper slowly. FDA (Food and Drug Administration) boxed warning on propranolol, nadolol and timolol (not stated in the lecture). Sotalol: boxed warning for life-threatening arrhythmias. |
| Selective beta-1 blockers (second generation)slides 56, 61, 63, 67-68, 70-73; also Lecture 8 slide 18 | metoprolol, atenolol, bisoprolol, acebutolol, esmolol | Selectively block cardiac beta-1 receptors: lower heart rate and contractility (lower cardiac output) and lower renin release, so less angiotensin II. | Hypertension (not first line); angina; acute myocardial infarction (avoid agents with intrinsic sympathomimetic activity, such as acebutolol); heart failure (metoprolol succinate, bisoprolol); esmolol is intravenous. | Bronchospasm (less likely than with non-selective agents); heart block; bradycardia. Caution in diabetes and peripheral artery disease. | Fatigue, bradycardia, heart block; bronchoconstriction (less likely); disturbed glucose control that masks hypoglycemia; cold extremities. | Black boxSudden withdrawal: acute angina, myocardial infarction, marked blood pressure rise. FDA (Food and Drug Administration) boxed warning on atenolol and metoprolol (not stated in the lecture). |
| Third-generation beta blockers (vasodilating)slides 59, 62-63, 65, 70-74; also Lecture 8 slide 18 | carvedilol, labetalol, carteolol, betaxololThe slide groups carteolol and betaxolol (beta-1 selective) here too. | Beta blockade plus direct vasodilation: alpha-1 blockade (carvedilol, labetalol), beta-2 agonism, nitric oxide production, calcium entry blockade, potassium channel opening, antioxidant activity. | Hypertension; heart failure (carvedilol). Betaxolol, carteolol and timolol are also used for glaucoma. | As for all beta blockers: bronchospasm, heart block, bradycardia; caution in diabetes and peripheral artery disease. | Class effects: fatigue, bradycardia, heart block, bronchoconstriction, disturbed glucose control, cold extremities, central nervous system effects. | Sudden withdrawal syndrome applies to every beta blocker (acute angina, myocardial infarction, marked blood pressure rise): taper slowly. |
| Alpha-1 adrenergic blockersslides 77-84 | prazosin, terazosin, doxazosin, tamsulosin | Reversible blockade of vascular alpha-1 receptors: dilates precapillary arterioles and lowers total peripheral resistance, with a reflex rise in heart rate. Tamsulosin is alpha-1a selective with little effect on blood vessels. | Hypertension (prazosin with beta blockers and diuretics; mildly improves lipids); benign prostatic hyperplasia (terazosin, doxazosin, tamsulosin). Terazosin and doxazosin have longer half-lives (once daily). | None listed. Prazosin: caution in cardiac and renal failure; nonsteroidal anti-inflammatory drugs blunt the response; beta blockers may worsen postural hypotension. | Orthostatic hypotension, postural dizziness, headache, drowsiness, lack of energy; mild reflex tachycardia; sodium and water retention; impotence. | Orthostatic hypotension is the main side effect (postural dizziness). |
| Central sympatholytics (alpha-2 agonists)slides 75, 86-87, 89-95 | clonidine, guanfacineOnly 2 named in the lecture. | Stimulate postsynaptic alpha-2 receptors in the brainstem (nucleus of the solitary tract, ventral lateral medulla), lowering sympathetic outflow, peripheral resistance, heart rate and cardiac output; imidazoline receptors may play a role. | Hypertension: suitable for monotherapy; works well in the elderly; efficacy independent of age, race and gender; no negative effects on lipids. Clonidine also blunts opiate withdrawal. | None listed. Narrow therapeutic range; clonidine causes sodium retention, so it is often given with a diuretic. | Drowsiness or sedation; dry mouth; sexual dysfunction; orthostatic hypotension, bradycardia; clonidine raises blood glucose. | Abrupt withdrawal causes severe rebound hypertension: never stop suddenly. Clonidine plus a beta blocker lowers blood pressure further. |
| Direct vasodilatorsslides 97, 99-107 | hydralazine, minoxidil, nitroprusside | Direct arteriolar dilation (lower peripheral resistance) with reflex sympathetic activation. Hydralazine: unclear (more cyclic guanosine monophosphate, nitric oxide). Minoxidil: opens potassium channels (hyperpolarization). Nitroprusside: releases nitric oxide; dilates veins and arterioles. | Hydralazine: chronic hypertension (with a diuretic and beta blocker). Minoxidil: severe or refractory hypertension (triple therapy). Nitroprusside (intravenous infusion): hypertensive crisis. | Hydralazine: coronary artery disease, ischemia, elderly. Minoxidil: none listed (its ischemia and arrhythmias are adverse effects). | Reflex tachycardia, fluid retention; headache, flushing; hydralazine lupus syndrome; minoxidil hypertrichosis, ischemia, arrhythmias; nitroprusside cyanide toxicity (sodium thiosulfate) and thiocyanate toxicity. | Black boxFDA (Food and Drug Administration) boxed warnings: minoxidil (pericardial effusion, worsening angina; give with a beta blocker and diuretic) and nitroprusside (cyanide toxicity) (not stated in the lecture, except the cyanide toxicity). |
| Lecture 7 — Drugs that Lower Cholesterol and Triglyceride Levels | ||||||
| HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors (statins)slides 15, 18, 21-25, 65 | atorvastatin, rosuvastatin, simvastatin, pravastatin, lovastatin, fluvastatin, pitavastatin | Reduce hepatic cholesterol synthesis, lowering intracellular cholesterol, which upregulates the LDL (low-density lipoprotein) receptor and increases uptake of non-HDL (high-density lipoprotein) particles from the blood. | First-line when low-density lipoprotein (LDL) cholesterol lowering is indicated; most efficacious and best tolerated. Benefit groups: existing cardiovascular disease; LDL above 190 mg/dL; diabetes aged 40-75 with LDL 70-189; no disease or diabetes, LDL 70-189 and 10-year risk above 7.5%. | Liver disease; pregnancy (current labeling weighs risk and benefit). Relative: concomitant use of cyclosporine or other immunosuppressants, gemfibrozil, niacin, erythromycin. | Headache, sleep disturbance, fatigue, gastrointestinal upset, flu-like symptoms; raised liver enzymes (0.5-2.5%); myalgia and myopathy (0.2-0.4%); rare rhabdomyolysis. | Muscle toxicity: stop the statin. Use fibrates cautiously with statins. Interactions via CYP3A4 (cytochrome P450 3A4) inhibitors: verapamil, amiodarone, grapefruit juice; also niacin and fibrates. |
| Cholesterol absorption inhibitorslides 28-31 | ezetimibeOnly 1 named in the lecture. | Selectively inhibits intestinal cholesterol absorption: less cholesterol reaches the liver, so more hepatic LDL (low-density lipoprotein) receptors and less cholesterol in atherogenic particles. | Lowers low-density lipoprotein (LDL) cholesterol; adds another 15-20% of LDL lowering when added to a statin. Taken with or without meals. | None listed. Interactions: fibrates (gallstones, myopathy); bile acid sequestrants may lower levels and antacids lower levels; cyclosporine raises levels. | Gastrointestinal effects; raised liver transaminases when given with statins. | Fibrates with ezetimibe raise the risk of cholelithiasis (gallstones) and myopathy. |
| Fibrates (fibric acid derivatives)slides 15, 33-39 | gemfibrozil, fenofibrate, bezafibrate | Activate PPAR-alpha (peroxisome proliferator-activated receptor alpha): more fatty acid oxidation, so less secretion of triglyceride-rich VLDL (very-low-density lipoprotein); more apolipoprotein A-I, raising HDL (high-density lipoprotein). | Primary indication: triglycerides above 1000 mg/dL or low high-density lipoprotein (HDL). Lower triglycerides 20-50%, raise HDL 10-35%. | Pregnancy; severe liver or kidney dysfunction; existing gallbladder disease. | Nausea, abdominal pain, diarrhea; cholelithiasis (gallstones); myopathy. | Raise the anticoagulant effect of warfarin; myopathy risk with statins. |
| Bile acid sequestrants (resins)slides 15, 42, 46-49 | cholestyramine, colestipol, colesevelam | Bind bile acids in the gut, preventing enterohepatic recirculation; the liver makes more bile acids and more LDL (low-density lipoprotein) receptors, lowering LDL. Not absorbed. | Mainly combined with a statin, or when only a modest low-density lipoprotein (LDL) reduction is needed. The safest (no systemic effects); approved for children, adolescents and pregnancy. | Absolute: familial dysbetalipoproteinemia; triglycerides above 400 mg/dL. Relative: triglycerides above 200 mg/dL. | Bloating, flatulence, fullness, constipation, nausea; malabsorption of vitamins A, D, E, K and folic acid; may raise VLDL (very-low-density lipoprotein) and triglycerides. | Bind other drugs (digoxin, warfarin, thyroxine, beta blockers, thiazides): give the drug 1 hour before or 4 hours after the resin. |
| Niacin (nicotinic acid)slides 50-51, 53, 55-56, 58, 61 | niacin (nicotinic acid), niacin immediate release (Niacor), niacin extended release (Niaspan), inositol hexaniacinate | Decreases hepatic VLDL (very-low-density lipoprotein) and apolipoprotein B production, so less conversion to LDL (low-density lipoprotein); decreases mobilization of free fatty acids and triglyceride synthesis; raises HDL (high-density lipoprotein). | Atherogenic dyslipidemia, alone or combined when low-density lipoprotein (LDL) is also elevated. Lowers triglycerides 20-50% and raises high-density lipoprotein (HDL) 15-35%. Niacinamide is NOT effective. | Absolute: chronic liver disease. Relative: peptic ulcer disease, symptomatic gout, significant hyperuricemia, diabetes (glucose intolerance). | Cutaneous flushing (prostaglandin-mediated); nausea, abdominal discomfort; at larger doses raised liver tests, glucose and uric acid; decreased glucose tolerance. | Flushing is prostaglandin-mediated: premedicate with aspirin. Niacinamide (nicotinamide) does not lower lipids. |
| PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitorsslide 60 | alirocumab, evolocumabOnly 2 named in the lecture. | Injectable monoclonal antibodies: PCSK9 (proprotein convertase subtilisin/kexin type 9) processes hepatic LDL (low-density lipoprotein) receptors, so blocking it keeps the receptors active longer and lowers LDL. | Lower low-density lipoprotein (LDL) cholesterol (drops of 43-58%). | None listed. | Hypersensitivity reactions are the most serious adverse reaction. | Injectable only and expensive. |
| Lecture 8 — Myocardial Ischemia Drug Therapy | ||||||
| Beta blockers (antianginal)slides 8, 13, 16-19, 34, 39, 55 | metoprolol, atenolol, propranolol, nadolol, carvedilol, labetalol | Lower myocardial oxygen demand: decrease heart rate, contractility and systolic wall tension. No effect on oxygen supply. | First-line for angina without contraindications, especially with hypertension, anxiety, supraventricular arrhythmias, heart failure or a prior myocardial infarction. In acute coronary syndrome: given intravenously first, then orally; lower early and late mortality, smaller infarcts, fewer heart failure events and less sudden cardiac death (the course answer; current guidelines favor oral therapy in the first day). | Heart rate under 60; systolic pressure under 100; atrioventricular block; acute decompensated heart failure. Precautions: reactive airway disease, systolic heart failure, diabetes, peripheral vascular disease. Avoid in variant (Prinzmetal) angina. In diabetes, avoid non-cardioselective agents (course table). | Hypotension, bradycardia, hyperglycemia, dyslipidemia; fatigue, sexual dysfunction, nightmares, worsened claudication. | Black boxAvoid rapid discontinuation. FDA (Food and Drug Administration) boxed warning for abrupt cessation: metoprolol, atenolol, propranolol, nadolol (not stated in the lecture). Avoid in variant angina. |
| Calcium channel blockers (antianginal)slides 20-24, 34 | diltiazem, verapamil, nifedipine, amlodipine, felodipine | Lower demand (lower systolic wall tension; non-dihydropyridines also slow the heart and lower contractility) and raise supply (mild dilation at fixed stenoses, relief of vasospasm). | Non-dihydropyridines: initial therapy when beta blockers are contraindicated or not tolerated. Dihydropyridines: added to a beta blocker when it alone fails. Chosen for vasospastic angina, severe peripheral vascular disease, asthma, uncontrolled diabetes. Diabetes with no other reason for a beta blocker: a non-dihydropyridine is first line (course table; current practice also accepts a cardioselective beta blocker). | Systolic pressure under 100. Non-dihydropyridines: heart rate under 60, acute heart failure, ejection fraction under 40%, atrioventricular block. Precaution: a non-dihydropyridine with a beta blocker; CYP3A4 (cytochrome P450 3A4) interactions. After a myocardial infarction the course table says to avoid calcium channel blockers (a beta blocker is first line; current practice allows a non-dihydropyridine if a beta blocker cannot be used). | Hypotension; dihydropyridines: headache, flushing, peripheral edema. Counsel on dizziness and constipation. | Avoid short-acting agents (nifedipine). With left ventricular dysfunction, amlodipine is the only calcium channel blocker used. |
| Nitrates (short- and long-acting)slides 25-27, 29-33, 38, 54 | nitroglycerin, isosorbide mononitrate, isosorbide dinitrate | Nitric oxide raises cyclic guanosine monophosphate and lowers cytosolic calcium: smooth muscle relaxation and vasodilation (lower left ventricular volume). Also dilate coronary arteries, relieve vasospasm, and have antiplatelet effects. | Sublingual tablet or spray: relieve acute ischemia, prevent effort-induced angina; call for help if no relief 5 minutes after the first dose. Long-acting forms: adjunct, not monotherapy. In acute coronary syndrome: pain relief only, no mortality benefit. | Concurrent use of phosphodiesterase type 5 inhibitors (sildenafil, tadalafil, vardenafil); aortic valve stenosis; obstructive cardiomyopathy; hypotension. | Headache, flushing, postural hypotension, reflex tachycardia; tachyphylaxis (tolerance), managed with a nitrate-free interval. | NEVER with sildenafil, tadalafil or vardenafil: hypotension, myocardial infarction or stroke. |
| Antiplateletsslides 13, 37, 52-53; also Lecture 5 slide 15, Lecture 5 slide 16, Lecture 5 slide 17 | aspirin, clopidogrelOnly 2 named in the lecture. | Aspirin: irreversible platelet inhibition (nonselective cyclooxygenase inhibitor). Clopidogrel: mechanism not given. Both increase coronary blood flow. | Aspirin for all patients with ischemic heart disease, to prevent acute coronary syndrome; chew it at the first sign of chest pain (fewer deaths and reinfarctions). Clopidogrel: as effective as aspirin in secondary prevention; used for aspirin allergy. | Aspirin: allergy; recent gastrointestinal bleeding; recent intracranial hemorrhage; bleeding disorders. | Bleeding; gastrointestinal upset (aspirin). | Black boxClopidogrel: FDA (Food and Drug Administration) boxed warning for reduced effect in CYP2C19 (cytochrome P450 2C19) poor metabolizers (not stated in the lecture). Aspirin: never for a child with viral fever (Reye syndrome). |
| Fibrinolytics (thrombolytics)slides 58-59, 61-65, 68 | streptokinase, alteplase, reteplase, tenecteplase | Activate conversion of plasminogen to plasmin, which lyses fibrin. Streptokinase forms a 1:1 complex with plasminogen; alteplase, reteplase and tenecteplase act only on fibrin-bound plasminogen. | ST-elevation myocardial infarction: under 75 years and within 12 hours of symptom onset. Less benefit over 75 years, after 6 hours, or in non-ST-elevation myocardial infarction. Relatively few patients receive them. | Active bleeding or bleeding disorder; surgery within 10 days; serious gastrointestinal bleeding within 3 months; severe hypertension (diastolic above 110 mmHg); prior stroke or active intracranial process (tumors); aortic dissection; acute pericarditis; prior streptokinase exposure or allergic reaction; pregnancy. | Bleeding (0.5-7%; intracranial hemorrhage 0.4-0.94%); allergic reactions, fever, chills, rash (mainly streptokinase, urokinase); anaphylaxis; ventricular arrhythmias. | Not recommended in non-ST-elevation acute coronary syndrome: bleeding risk exceeds benefit. |
| Opioid analgesicslide 56 | morphineOnly 1 named in the lecture. | Not given in this lecture. | Chest pain unresponsive to nitrates; used in ST-elevation myocardial infarction. | Not listed as a contraindication. Caution: may increase mortality in unstable angina and non-ST-elevation myocardial infarction; use is controversial. | Hypotension; allergy. | Black boxOpioids carry an FDA (Food and Drug Administration) boxed warning (addiction, life-threatening respiratory depression); not stated in the lecture. May raise mortality in unstable angina or non-ST-elevation myocardial infarction. |
| Other acute coronary syndrome antithrombotics (heparins, glycoprotein IIb/IIIa inhibitors, P2Y12 (platelet adenosine diphosphate receptor) antagonists)slides 66, 68 | enoxaparin, heparinOnly enoxaparin is named; the other agents appear as class names. | Not given in this lecture. | Heparins: used with fibrinolysis or antiplatelet agents; enoxaparin preferred over heparin in non-ST-elevation acute coronary syndrome. P2Y12 antagonists: before percutaneous coronary intervention; clot prophylaxis with stents. Glycoprotein IIb/IIIa inhibitors: not routine before intervention. | None listed. | Not given in this lecture. | Black boxEnoxaparin carries an FDA (Food and Drug Administration) boxed warning: spinal or epidural hematoma with neuraxial anesthesia or puncture (not stated in the lecture). |