← Back
Pharmacology I · Exam 2 · Class of 2028

Killers, Commons & Zebras

The adverse effects of the Exam 2 lectures sorted the way Dr. Wood sorts them. 117 entries.

Dr. Wood’s three buckets. He sorts adverse effects into killers, commons and zebras, and said that any time you see a killer or a zebra, those are the things to look at. The sorting below applies his framework to the slides; each entry cites its slide.
L4 Ophthalmic DrugsL5 Ear, Nose and Throat DrugsL6 Antihypertensive DrugsL7 Drugs that Lower Cholesterol and Triglyceride LevelsL8 Myocardial Ischemia Drug Therapy

Lecture 4 — Ophthalmic Drugs

Killers 6

Dangerous. Immediate discontinuation and evaluation. Not necessarily common: these are the ones you warn the patient about in advance.

EffectDrug or classWhat it means / what to doSource
Systemic beta blockade from beta blocker eye drops: worsening heart failure, bradycardia, heart block, increased airway resistancetimolol, carteolol, levobunolol (nonselective); betaxolol (beta-1 selective, less bronchial risk)Drops drain down the tear duct and are absorbed. Ask about heart failure, heart block, slow pulse and asthma before starting; stop and evaluate if any appear. Warn the patient in advance.L4
slide 67
Central nervous system depression and apnea in children under 2 yearsalpha-2 agonists (brimonidine, apraclonidine)Contraindicated in children under 2 years. Never use in an infant.L4
slide 69
Accidental ingestion of imidazoline eye dropstetrahydrozoline, naphazoline (redness-relief drops)Systemically these target alpha 2 receptors, so a swallowed bottle is dangerous, especially in a small child. Keep the bottle out of reach; a child who swallows it needs emergency care.L4
slide 49
Worsening visual acuity during treatmentany ophthalmic medicationMeasure visual acuity before starting and at every follow-up. If it gets worse, immediate ophthalmology consult (something more serious may be going on).L4
slide 33
Steroid-induced raised eye pressure and glaucoma, infection and corneal ulcerophthalmic glucocorticoids (dexamethasone, prednisolone, difluprednate and others)Raised eye pressure (more likely with a family history), glaucoma, infection from reduced immune function and corneal ulcers, plus cataract and delayed wound healing. Limit to a pulse of less than 2 weeks; the soft steroids carry lower pressure risk.L4
slide 54
Loss of the blink reflex after anesthetic dropstetracaine, proparacaineThe eyes stay numb for 10 to 20 minutes with no blink reflex, leaving the cornea unprotected. Do not write prescriptions or dispense for home use.L4
slide 75

Commons 12

What actually happens, often. These belong to the class, not the drug, so they are listed by class.

EffectDrug or classWhat it means / what to doSource
Ocular irritationall ophthalmic antibiotics: macrolides, trimethoprim with polymyxin B, sulfacetamide, bacitracin, fluoroquinolones, aminoglycosidesOcular irritation is listed for essentially every eye antibiotic (macrolides, trimethoprim with polymyxin B, sulfacetamide, bacitracin, fluoroquinolones, aminoglycosides), so it belongs to the class and names no single drug. Hypersensitivity is listed only for the macrolides and sulfacetamide.L4
slide 15
Unpleasant taste after instillationfluoroquinolonesDrug drains down the tear duct to the throat. Blocking the duct after the drop helps.L4
slide 21
Ocular irritation, headache and increased ocular drynessophthalmic antihistaminesIrritation can settle with time. Onset of benefit is within minutes, but allow two weeks of therapy to judge full efficacy.L4
slide 44
Ocular irritation, unpleasant taste and headachemast cell stabilizersNot useful for acute symptoms; full effect takes 5 to 14 days and four-times-daily dosing is often needed.L4
slide 47
Rebound hyperemia after stoppingtopical vasoconstrictors (tetrahydrozoline, naphazoline, pheniramine with naphazoline)Prolonged use leads to rebound hyperemia after discontinuation. Use for less than 2 weeks; if no improvement in 72 hours, stop and see a provider. A great counseling point.L4
slide 48
Lacrimation, keratitis, raised eye pressure and irritationophthalmic nonsteroidal anti-inflammatory drugs (bromfenac, diclofenac, flurbiprofen, ketorolac, nepafenac)Why they are not routinely used for simple conjunctivitis.L4
slide 51
Conjunctival hyperemia and ocular irritationprostaglandin analogsCommon with the class; systemic effects are limited.L4
slide 65
Ocular irritation, rebound hyperemia, pruritus and allergic conjunctivitisalpha-2 agonists (apraclonidine, brimonidine)Allergic conjunctivitis is less common with brimonidine.L4
slide 69
Bitter taste (25%) and burning or stinging (33%)carbonic anhydrase inhibitors (dorzolamide, brinzolamide)Both are frequent (about one in four and one in three patients), so warn them first.L4
slide 70
Fixed small pupils, myopia, visual disturbances and headachescholinergic agonists (pilocarpine, carbachol, acetylcholine)Younger patients are usually intolerant because of visual blurring.L4
slide 72
Photosensitivity and blurred visionantimuscarinic cycloplegics (atropine, cyclopentolate, tropicamide)Expected with pupil dilation; warn the patient not to drive until it clears.L4
slide 76
Ocular burning (17%), foreign body sensation and blurred visioncyclosporine drops (immunomodulator)Warn patients up front.L4
slide 58

Zebras 7

Uncommon, but unique to one drug. Each is worth about one question, and with the killers they are where to look.

EffectDrug or classWhat it means / what to doSource
White precipitate on the eye (about 17%)ciprofloxacinUnique to ciprofloxacin among the fluoroquinolone drops. Warn the patient so it is not mistaken for a worsening infection.L4
slide 21
Corneal ulceration and reactive keratoconjunctivitis with several days of useaminoglycosides (gentamicin, tobramycin)Specific to the aminoglycoside eye drops (gentamicin, tobramycin) among the antibiotics: watch for it when the drops are used beyond a few days.L4
slide 23
Punctate keratopathytrifluridinePinpoint corneal surface damage, seen after fluorescein staining.L4
slide 27
Punctate keratitisganciclovir (Zirgan)The ganciclovir eye preparation carries its own punctate keratitis.L4
slide 28
Changes in eyelash length and iris colorprostaglandin analogs (latanoprost, travoprost, bimatoprost, tafluprost)Unique to the prostaglandin analogs. Warn the patient before starting.L4
slide 65
Bull's eye lesionchloroquineA drug that accumulates in the eye.L4
slide 10
Allergic reaction in a patient with a sulfonamide allergysulfacetamideAllergic reactions are listed for sulfacetamide. Avoid it in a patient with a sulfonamide allergy and ask about drug reactions before using it.L4
slide 19

Lecture 5 — Ear, Nose and Throat Drugs

Killers 11

Dangerous. Immediate discontinuation and evaluation. Not necessarily common: these are the ones you warn the patient about in advance.

EffectDrug or classWhat it means / what to doSource
Reye syndromeaspirin (all salicylates)Children under 15, mortality 50%: vomiting, progressive central nervous system damage, liver injury and hypoglycemia after influenza, chickenpox or an upper respiratory infection. Never give aspirin to a child with a viral fever; warn parents in advance. Stop and evaluate urgently.L5
slide 18
Salicylism (aspirin toxicity)aspirinHyperventilation and alkalosis, then fever, dehydration and metabolic acidosis, then shock, coma, respiratory and renal failure and death. Ringing in the ears (tinnitus) is the early warning that exposure is too high.L5
slide 16
QTc (corrected QT interval) prolongationketoconazoleA life-threatening arrhythmia risk, made worse by any other QT-prolonging or cytochrome P450 3A4 (CYP3A4) interacting drug. Check the electrocardiogram and the medication list.L5
slide 12
Hepatitis, cirrhosis and hepatic failureketoconazoleLiver injury from a systemic antifungal. Stop the drug and evaluate the liver if liver function tests rise.L5
slide 12
Cochlear damage and hearing losspolymyxin B (Cortisporin ear drops)Permanent inner-ear injury when the drops pass a ruptured eardrum or tubes. Examine the eardrum first; do not use polymyxin B if it is perforated or tubes are in place.L5
slide 10
Gastric or duodenal ulcer, perforation and bleedingibuprofen (nonsteroidal anti-inflammatory drugs)Bleeding ulcers and perforation, mainly with regular daily use. Warn patients about black stools and stomach pain; stop and evaluate.L5
slide 21
Acute renal failureibuprofen (nonsteroidal anti-inflammatory drugs)Decreased creatinine clearance and acute renal failure; worst in patients who already have kidney disease or take diuretics. Stop and check kidney function.L5
slide 21
Liver damage from acetaminophenacetaminophenChronic alcohol use increases the risk of liver damage; a fixed daily maximum applies and every acetaminophen-containing product counts toward it. Warn the patient in advance.L5
slide 25
Arrhythmia from hypokalemiadexamethasone with digoxin or a diureticPotassium loss from the steroid, worsened by a diuretic, raises the arrhythmia risk with digoxin. Monitor potassium and the electrocardiogram.L5
slide 45
Serotonin syndromedextromethorphanRisk with other pro-serotonergic drugs, and the drug is contraindicated with a monoamine oxidase inhibitor (MAOI) taken now or within 2 weeks. Stop and evaluate agitation, confusion or fever.L5
slide 58
BronchospasmN-acetylcysteine (inhaled)Airway narrowing with the nebulized route. Stop and treat wheezing or breathlessness.L5
slide 63

Commons 8

What actually happens, often. These belong to the class, not the drug, so they are listed by class.

EffectDrug or classWhat it means / what to doSource
SedationFirst-generation H1 antagonists (histamine-1 blockers)The major side effect of the whole class and additive with alcohol and other depressants; second-generation agents cause much less. It is why doxylamine works as a sleep aid.L5
slide 32
Dry mouth, urinary retention, blurred visionFirst-generation H1 antagonists (antimuscarinic effect)The antimuscarinic set, plus gastrointestinal disturbances; with topical use, dermatitis and photosensitivity.L5
slide 36
Gastric and duodenal ulcer, edema and renal effectsNonsteroidal anti-inflammatory drugs (ibuprofen)Stomach, fluid and kidney effects are the class pattern for these drugs.L5
slide 21
Fluid retention, hypertension, potassium loss, glucose intoleranceSystemic corticosteroids (dexamethasone, prednisone)Salt and water retention, raised blood pressure, low potassium and high glucose belong to the class, not the individual drug.L5
slide 44
Cataracts, glaucoma, increased intraocular pressure, infection riskSystemic corticosteroids (dexamethasone, prednisone)Eye effects and weakened immunity are shared by the class; risk rises with dose and duration.L5
slide 47
Epistaxis, septal perforation, unpleasant tasteNasal corticosteroidsMostly local effects at usual doses. The source gives no interaction information (that is not the same as no interactions); strong CYP3A4 inhibitors such as ketoconazole can raise systemic exposure to some nasal steroids.L5
slide 43
Tachycardia, hypertension, headacheOral decongestants (pseudoephedrine)Vasoconstriction spreads beyond the nose, and the oral agent also weakens antihypertensive treatment.L5
slide 52
Nausea, vomiting, diarrhea and stomach painNonabsorbable antifungal (nystatin)Expected, minor gastrointestinal upset; not a reason to stop.L5
slide 13

Zebras 10

Uncommon, but unique to one drug. Each is worth about one question, and with the killers they are where to look.

EffectDrug or classWhat it means / what to doSource
Rhinitis medicamentosa (rebound congestion)oxymetazolineUse beyond 3–5 days causes rebound congestion, and patients reuse the spray to treat it. Limit to 3–5 days.L5
slide 50
TinnitusaspirinRinging in the ears appears in the anti-inflammatory exposure range, before frank toxicity.L5
slide 16
Cytochrome P450 3A4 (CYP3A4) inhibitionketoconazoleRaises levels of many drugs cleared by CYP3A4, so it interacts with many medicines.L5
slide 12
Hypersensitivity of the ear canalneomycin (Cortisporin drops)The component most likely to cause an allergic reaction in otic drops.L5
slide 10
Numbing of the mouth when the capsule is chewedbenzonatateLocal anesthesia from chewing; hence swallow whole. Cross-allergy is possible with related local anesthetics such as tetracaine.L5
slide 57
Rotten-egg smellN-acetylcysteine (inhaled)The high sulfur content gives inhaled N-acetylcysteine a rotten-egg smell, alongside nausea and vomiting.L5
slide 63
Bitter tasteazelastine nasal sprayThe bitter taste is listed alongside nosebleed for this nasal spray.L5
slide 38
Confusion, excitement, agitationdextromethorphanThe central nervous system effects listed for this antitussive.L5
slide 58
Papilledema and hirsutismdexamethasoneListed among dexamethasone's adverse effects, but not unique to it: prednisone and prednisolone share the same steroid side effects, so treat these as class effects.L5
slide 44
Pathologic fractures of long bones and raised liver enzymesprednisoneListed among prednisone's adverse effects, but not unique to it: dexamethasone and other glucocorticoids share the same bone and steroid effects, so treat these as class effects.L5
slide 47

Lecture 6 — Antihypertensive Drugs

Killers 15

Dangerous. Immediate discontinuation and evaluation. Not necessarily common: these are the ones you warn the patient about in advance.

EffectDrug or classWhat it means / what to doSource
Hyperkalemia (raised potassium)ACE (angiotensin-converting enzyme) inhibitorsMost often with kidney disease and with potassium-sparing diuretics, potassium supplements or salt substitutes. Check the potassium; stop the potassium source. Warn the patient in advance to avoid potassium supplements and salt substitutes. An easy question and a way to cause an arrhythmia.L6
slide 20
AngioedemaACE (angiotensin-converting enzyme) inhibitorsRapid swelling of the nose, throat, mouth, larynx, lips and tongue, usually in the first week; reversible if the drug is removed. Airway risk: stop the drug and evaluate. Tell the patient in advance to report swelling at once.L6
slide 22
Fetal morbidity and mortality (birth defects, fetal death)ACE (angiotensin-converting enzyme) inhibitorsContraindicated in the second and third trimesters. Confirm the patient is not pregnant before starting and stop as soon as pregnancy is found.L6
slide 22
Acute fall in glomerular filtration rateACE (angiotensin-converting enzyme) inhibitorsWhere kidney blood flow depends on angiotensin II, the drug can dramatically decrease the glomerular filtration rate. Start low, go slow, and follow kidney function.L6
slide 21
Heart block and severe bradycardia; worsening heart failureNon-dihydropyridine calcium channel blockers (diltiazem, verapamil)First-degree atrioventricular block, bradycardia and exacerbation of congestive heart failure or pulmonary edema from the negative inotropic effect. Follow heart rate and watch for swelling or breathlessness; stop and evaluate.L6
slide 45
Bronchospasm (asthma exacerbation)Beta blockers (less likely with beta-1 selective agents)Blockade of airway beta-2 receptors can trigger bronchospasm; about one third of patients with chronic obstructive pulmonary disease have bronchospasm. Contraindicated in bronchospasm; beta-1 selective agents are less likely to cause it, so if a beta blocker is truly needed in lung disease they are the ones to choose, with caution.L6
slide 71
Heart block and severe bradycardiaBeta blockersNegative chronotropy (heart rate below 60 beats per minute) and first-, second- or third-degree atrioventricular block. Check pulse; stop and evaluate for a slow or blocked rhythm. Stacking with verapamil or diltiazem multiplies the risk.L6
slide 71
Masked and prolonged hypoglycemiaBeta blockers (type 1 diabetes especially)Beta blockers inhibit glycogenolysis, prolong hypoglycemia and hide its warning symptoms. Warn diabetic patients in advance that the usual warning signs may not appear.L6
slide 72
Sudden withdrawal syndrome (acute angina, myocardial infarction, marked rise in blood pressure)Beta blockersBlockade upregulates the receptors, so stopping abruptly exposes them to catecholamines. Never stop suddenly; withdraw slowly. Tell the patient in advance.L6
slide 73
Withdrawal reactions (rebound hypertension)ClonidineWithdrawal reactions may be severe. Taper; never stop abruptly. Tell the patient in advance.L6
slide 94
Myocardial ischemia and arrhythmiasMinoxidilReflex sympathetic activation with a 2–3 times rise in cardiac output causes myocardial ischemia, and its potassium channel action causes arrhythmias. Report chest pain or palpitations.L6
slide 104
Hyperkalemia (raised potassium)Angiotensin receptor blockersWith kidney disease or potassium-sparing diuretics. Check the potassium, especially when a potassium-sparing diuretic is added.L6
slide 29
Fetal morbidity and mortalityAngiotensin receptor blockersNot given in the second and third trimesters. Confirm the patient is not pregnant; stop as soon as pregnancy is found.L6
slide 29
Impairment of kidney functionAngiotensin receptor blockersAngiotensin II is important for kidney function; follow kidney function, and in heart failure start low and titrate upward.L6
slide 29
Cyanide toxicity and thiocyanate toxicityNitroprussideCyanide toxicity (trembling, vomiting, convulsions) is limited by sodium thiosulfate. Thiocyanate toxicity (weakness, anoxia, tinnitus, muscle spasms, toxic psychosis) follows long infusions or kidney failure. Stop the infusion and treat.L6
slide 107

Commons 13

What actually happens, often. These belong to the class, not the drug, so they are listed by class.

EffectDrug or classWhat it means / what to doSource
Dry cough (5–15%)ACE (angiotensin-converting enzyme) inhibitors (class effect)Bradykinin and substance P accumulate in the lungs; appears from 1 week to 6 months; not related to dose or specific agent; more frequent in women. If bothersome, remove the ACE inhibitor; an angiotensin receptor blocker does not cause cough.L6
slide 19
First-dose hypotensionACE (angiotensin-converting enzyme) inhibitors (class effect)At the first dose or on upward titration; most common in sodium-depleted patients, heart failure, or multiple antihypertensive drugs. Warn about dizziness on standing.L6
slide 20
First-dose hypotensionAngiotensin receptor blockers (class effect)A first-dose effect; warn about dizziness on standing after the first dose.L6
slide 29
Peripheral vasodilation: flushing, headache, peripheral edema, dizzinessNon-dihydropyridine calcium channel blockers (class effect)Flushing, headache, hypotension, peripheral edema and dizziness follow directly from relaxing vascular smooth muscle.L6
slide 45
Constipation and other gastrointestinal effectsNon-dihydropyridine calcium channel blockers (class effect)Nausea, vomiting, diarrhea, anorexia and constipation; ask about bowel habits.L6
slide 45
Peripheral edema and rebound tachycardiaDihydropyridine calcium channel blockers (class effect)Vasodilation with reflex tachycardia after the fall in resistance; also dyspnea and wheezing. Gingival hyperplasia can also occur.L6
slide 51
Fatigue and limited exercise toleranceBeta blockers (class effect)The common complaint when a beta blocker is used for hypertension.L6
slide 63
Cold extremities and muscle fatigueBeta blockers (class effect)Block beta-2 receptors in blood vessels: cold extremities (Raynaud phenomenon), skeletal muscle fatigue and worse claudication.L6
slide 73
Depression, nightmares and vivid dreamsHighly lipid-soluble beta blockers (class effect)Central effects of agents that enter the brain easily; the more lipid-soluble the drug, the more these symptoms.L6
slide 74
Orthostatic hypotension and dizzinessAlpha-1 blockers (class effect)Postural dizziness, headache, drowsiness and lack of energy; counsel to stand slowly.L6
slide 79
Reflex tachycardia, fluid retention and impotenceAlpha-1 blockers (class effect)Mild reflex tachycardia, raised renin with sodium and water retention, and impotence.L6
slide 80
Drowsiness, dry mouth and sexual dysfunctionCentral sympatholytics (class effect)Central effects; the class also has a narrow therapeutic range.L6
slide 91
Reflex tachycardia, fluid retention, tachyphylaxisDirect vasodilators (class effect)Reflex sympathetic activation, increased cardiac output, fluid retention and raised renin; the effect fades. Hydralazine and minoxidil are given with a diuretic and a beta blocker.L6
slide 97

Zebras 6

Uncommon, but unique to one drug. Each is worth about one question, and with the killers they are where to look.

EffectDrug or classWhat it means / what to doSource
Hydralazine “lupus syndrome”HydralazineHigh dose, long-term use, women, slow acetylators, Caucasians.L6
slide 101
Black stoolsHydralazineWarn the patient ahead of time that stools may turn black, so it is not mistaken for bleeding.L6
slide 102
Hypertrichosis (unwanted hair growth)MinoxidilHair growth on the face, back, arms and legs; the topical form (Rogaine) is used for hair growth.L6
slide 105
Raised blood glucoseClonidineInhibits insulin secretion; watch blood glucose in diabetic patients.L6
slide 92
Acute pressor responseClonidineA brief rise in pressure can occur before the fall.L6
slide 92
DiarrheaTamsulosinHypotension, dizziness and diarrhea, with limited vascular effect.L6
slide 84

Lecture 7 — Drugs that Lower Cholesterol and Triglyceride Levels

Killers 4

Dangerous. Immediate discontinuation and evaluation. Not necessarily common: these are the ones you warn the patient about in advance.

EffectDrug or classWhat it means / what to doSource
Rhabdomyolysis and other muscle toxicityStatinsMyalgia and myopathy occur in 0.2 to 0.4% of patients, and rare cases progress to rhabdomyolysis. Muscle toxicity requires stopping the statin. Warn every patient in advance to report muscle symptoms; risk rises with kidney impairment, fibrate combinations and other interacting drugs.L7
slide 22
Serious liver injuryStatinsA rise in liver enzymes occurs in 0.5 to 2.5% of cases in a dose-dependent manner, and serious liver problems are exceedingly rare. Reduce the dose or stop until levels return to normal.L7
slide 21
Hypersensitivity reactionPCSK9 inhibitors (alirocumab, evolocumab)The most serious adverse reaction of this proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor class. Injectable monoclonal antibodies; stop and evaluate if an allergic reaction follows an injection.L7
slide 60
Bleeding from a warfarin interactionFibrates (gemfibrozil, fenofibrate, bezafibrate)Increased anticoagulant effect of warfarin. Warn the patient to watch for bruising and bleeding, and monitor anticoagulation when a fibrate is started.L7
slide 38

Commons 6

What actually happens, often. These belong to the class, not the drug, so they are listed by class.

EffectDrug or classWhat it means / what to doSource
Headache, sleep disturbance, fatigue, gastrointestinal intolerance and flu-like symptomsStatins (class)The common effects of the class, with liver enzyme rises in 0.5 to 2.5% of cases; listed once for the whole class.L7
slide 21
Myalgia and myopathyStatins (class)Class effect seen with every statin (0.2 to 0.4% of patients); ask about muscle aches at every visit because the severe end of this spectrum is rhabdomyolysis, and muscle toxicity requires stopping the statin.L7
slide 22
Gastrointestinal effectsEzetimibeThe main adverse effect; liver transaminases can also rise when it is combined with a statin.L7
slide 30
Nausea, abdominal pain and diarrheaFibrates (class)The common gastrointestinal effects of the fibrates (gemfibrozil, fenofibrate, bezafibrate).L7
slide 36
Bloating, flatulence, fullness, constipation and nauseaBile acid sequestrants (class)Local gastrointestinal effects only, because the drugs are not absorbed; the reason they are poorly tolerated.L7
slide 46
Cutaneous flushing with nausea and abdominal discomfortNiacinFlushing is prostaglandin mediated and is minimized by premedication with aspirin. Warn the patient in advance so it is not mistaken for an allergy.L7
slide 55

Zebras 4

Uncommon, but unique to one drug. Each is worth about one question, and with the killers they are where to look.

EffectDrug or classWhat it means / what to doSource
Cholelithiasis (gallstones)Fibrates (and fibrate plus ezetimibe)Uncommon but distinctive of the fibrates; existing gallbladder disease is also a contraindication.L7
slide 36
Malabsorption of vitamins A, D, E and K and folic acidBile acid sequestrantsUnique to the resins because they bind bile acids and other substances in the gut; supplement or space the vitamins.L7
slide 46
Rise in triglyceridesBile acid sequestrantsThe resins may increase very low-density lipoprotein production and raise triglycerides, the only lipid class to do so, which is why high triglycerides is a contraindication.L7
slide 46
Raised glucose and uric acid, decreased glucose toleranceNiacinAt larger doses; the reason gout, hyperuricemia and diabetes are relative contraindications.L7
slide 55

Lecture 8 — Myocardial Ischemia Drug Therapy

Killers 5

Dangerous. Immediate discontinuation and evaluation. Not necessarily common: these are the ones you warn the patient about in advance.

EffectDrug or classWhat it means / what to doSource
Abrupt beta blocker withdrawal (rebound angina, myocardial infarction)Beta blockersAvoid rapid discontinuation; stop gradually. Warn the patient in advance never to stop suddenly. (Added background: rebound angina and myocardial infarction; several beta blockers, for example metoprolol, atenolol and nadolol, carry a Food and Drug Administration (FDA) boxed warning.)L8
slide 19
Severe hypotension, myocardial infarction, strokeNitrates with phosphodiesterase type 5 inhibitors (sildenafil, tadalafil, vardenafil)Contraindicated combination. Ask every nitrate patient about erectile dysfunction medicines before prescribing.L8
slide 33
Bleeding, including intracranial hemorrhageFibrinolytics (all agents)The main risk of the class. Screen against the contraindication list before giving; watch for new neurologic signs.L8
slide 62
AnaphylaxisFibrinolytics (class list)An anaphylactic reaction is listed for the class; a prior streptokinase exposure or allergic reaction bars giving streptokinase again (not the recombinant agents).L8
slide 62
Ventricular arrhythmiasFibrinolytics (class)Listed adverse effect of the class: monitor the rhythm after treatment.L8
slide 62

Commons 6

What actually happens, often. These belong to the class, not the drug, so they are listed by class.

EffectDrug or classWhat it means / what to doSource
Bradycardia, hypotension, fatigue, dizzinessBeta blockers (class effect)Heart rate is the monitoring parameter; counsel about dizziness and fatigue.L8
slide 19
Hyperglycemia and dyslipidemiaBeta blockers (class effect)Follow blood sugar and lipids.L8
slide 19
Headache, flushing, peripheral edemaDihydropyridine calcium channel blockers (class effect)Vasodilation effects; hypotension is listed for the whole calcium channel blocker class.L8
slide 24
Dizziness and constipationCalcium channel blockers (class counseling points)The two education points listed for the class; constipation is mainly a verapamil effect.L8
slide 24
Headache, flushing, postural hypotension, reflex tachycardiaNitrates (class effect)Warn about orthostatic hypotension.L8
slide 31
Tolerance (tachyphylaxis)Nitrates (class effect)Managed with a daily nitrate-free interval.L8
slide 32

Zebras 4

Uncommon, but unique to one drug. Each is worth about one question, and with the killers they are where to look.

EffectDrug or classWhat it means / what to doSource
Allergic reaction, fever, chills, skin rashStreptokinaseMainly with streptokinase among the fibrinolytics; prior streptokinase exposure or allergic reaction is a contraindication.L8
slide 62
Possible increase in mortalityMorphineIn unstable angina and non-ST-elevation myocardial infarction; its use is controversial.L8
slide 56
Aspirin allergyAspirinAllergy is a contraindication; clopidogrel is the substitute recommended for patients allergic to aspirin.L8
slide 37
Short-acting formulation problemNifedipineAvoid short-acting agents (nifedipine is the named example).L8
slide 22