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Pharmacology I · Exam 1 · Class of 2028

Pharmacology I Exam 1 Cram Sheet

All three Exam 1 lectures — antimicrobials, dermatology medications and autonomic pharmacology. Class identity first, then indications, patient education, side effects and contraindications. Drug dosages are not tested.

How to use this: this is a condensed, night-before-the-exam reference, not a replacement for the full study guide — it assumes you've already learned the material and just need the highest-yield facts at a glance. If a term feels unfamiliar, go back to the full guide for the explanation.

Principles & Modes of Action

TermWhat you need to know
BacteriostaticInhibits a vital growth pathway without directly killing. Erythromycin, tetracyclines, sulfonamides, trimethoprim, clindamycin.
BactericidalDisrupts function enough that death occurs. Penicillins, cephalosporins, aminoglycosides, vancomycin, fluoroquinolones, metronidazole.
Concentration-dependentHigher concentration, greater killing. Post-antibiotic effect present. Favors large, widely spaced doses — why aminoglycosides went once daily.
Time-dependentKilling plateaus; what matters is time above the minimal inhibitory concentration, target 40–70% of the interval. No post-antibiotic effect. Favors continuous or frequent infusion.
Ribosome selectivityBacterial 70S (50S + 30S) versus mammalian 80S (60S + 40S). A difference of degree, not an absolute barrier — hence dose-related toxicity.
50S bindersMacrolides, clindamycin, chloramphenicol, streptogramins.
30S bindersAminoglycosides, tetracyclines.
Six toxicity systemsGastrointestinal, integument, hematologic, central nervous system, hepatic, renal.

Beta-lactams

TermWhat you need to know
Penicillin mechanismThe beta-lactam ring mimics two D-alanine residues; the penicillin-binding protein binds it by mistake and is covalently inactivated. Chains still form, cross-links do not.
Penicillin GSyphilis, gas gangrene, meningococcus. Good Gram-positive cocci, NO Staphylococcus, no aerobic Gram-negatives.
Dosage formsPenicillin V potassium oral (acid stable) · penicillin G intravenous · penicillin G benzathine intramuscular depot, one-time dose.
AminopenicillinsAmpicillin, amoxicillin. Enterococcus, Listeria, endocarditis prophylaxis, upper respiratory infection, community-acquired pneumonia.
Beta-lactamase inhibitorsSulbactam + ampicillin (Unasyn) · tazobactam + piperacillin (Zosyn) · clavulanate + amoxicillin (Augmentin). NO antibacterial activity of their own; irreversibly inactivate the enzyme.
What the inhibitor buysBacteroides and methicillin-susceptible Staphylococcus aureus. Drug of choice for skin/soft tissue, diabetic foot, animal and human bites.
Penicillinase-resistantNafcillin, oxacillin, dicloxacillin — built solely for methicillin-susceptible Staphylococcus aureus. Defeated by methicillin resistance; vancomycin is then the choice.
Cephalosporin generationsUp the generations = more Gram-negative, less Gram-positive — EXCEPT the 4th, which gains Gram-negative without losing Gram-positive.
Penicillin cross-sensitivityLess than 1%. A reported penicillin allergy does not by itself exclude a cephalosporin.
Cephalosporins to knowCefazolin/cephalexin 1st · cefepime 4th (neutropenic fever, nosocomial, pseudomonal) · ceftaroline 5th is the one with methicillin-resistant coverage · ceftolozane 5th is the antipseudomonal one.
Ceftriaxone versus cefotaximeCeftriaxone needs no renal adjustment but is barred in the first 30 days of life; cefotaxime is preferred in neonatal fever or sepsis.
AztreonamGram-negative ONLY, spectrum resembling the aminoglycosides. No cross-reactivity with other beta-lactams — usable in true penicillin allergy.
CarbapenemsVery broad: Gram-positive (not methicillin-resistant), Gram-negative, Pseudomonas EXCEPT ertapenem, anaerobes. For extended-spectrum beta-lactamase producers, multidrug-resistant Gram-negatives, meningitis. Seizures with imipenem.

Glycopeptides & Lipopeptides

TermWhat you need to know
Vancomycin mechanismNot a beta-lactam. Binds the two D-alanine residues to block cross-linking — covers the substrate rather than disabling the enzyme, so resistance is harder to develop.
Vancomycin coverageGram-positive ONLY. Penicillin-allergy infection, methicillin-resistant Staphylococcus aureus, Clostridium difficile by mouth, endocarditis, osteomyelitis.
Vancomycin monitoringTrough drawn 15–30 minutes before the next dose, around the 3rd or 4th dose. Watch renal clearance, ototoxicity, nephrotoxicity.
Red man syndromeInfusion-related reaction, with fever, chills and phlebitis.
Minimal inhibitory concentration ≥ 2 mg/LTarget ratio becomes hard to achieve — consider an alternative such as linezolid rather than pushing the dose.
DaptomycinBacterial depolarization inhibiting DNA, RNA and protein synthesis. CANNOT be used in pneumonia. Monitor muscle pain and creatine phosphokinase.

Protein Synthesis Inhibitors

TermWhat you need to know
Macrolides50S, blocks transpeptidation. Gram-positive aerobes plus ATYPICALS (Legionella, Mycoplasma, Chlamydophila, Chlamydia). QT prolongation and torsades.
Macrolide interactionsCytochrome P450 3A inhibition, erythromycin > clarithromycin > azithromycin. Azithromycin is the one to reach for when interactions matter.
QT prolongationThree classes: MACROLIDES, FLUOROQUINOLONES, POSACONAZOLE. Blocks the hERG POTASSIUM channel → slower REPOLARIZATION → longer QT → TORSADES DE POINTES. Risk multiplies with CONGENITAL LONG QT, STACKED QT DRUGS, or ELECTROLYTE disturbance (class Ia and III antiarrhythmics, low K+, low Mg2+). Treatment of torsades: MAGNESIUM SULFATE 2 g.
ClindamycinGram-positive aerobes including methicillin-resistant Staphylococcus aureus, plus Gram-positive AND Gram-negative anaerobes. NO Gram-negative aerobic coverage. Toxin-mediated disease. Clostridium difficile.
Tetracyclines30S, binds 16S ribosomal RNA and blocks transfer RNA at the A site. Bacteriostatic. Excellent for atypicals and animal-borne organisms.
Tetracycline cautionsChelate iron and calcium. Photosensitivity, tooth discoloration, skeletal growth depression — avoid under 8 years and in the 2nd and 3rd trimesters.
AminoglycosidesGram-negatives including Pseudomonas; Enterococcus only at synergy dosing. Post-antibiotic effect → once daily. NEPHROTOXIC and OTOTOXIC.
Linezolid50S. Resistant Gram-positives — multidrug-resistant pneumococcus, methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus. No Gram-negatives. Thrombocytopenia; serotonin syndrome with selective serotonin reuptake inhibitors, tyramine, pseudoephedrine.
TigecyclineGlycylcycline, 30S, bacteriostatic. Complicated skin and intra-abdominal infection. Covers Enterococcus faecalis but NOT vancomycin-resistant Enterococcus.

DNA, Folate & Membrane Agents

TermWhat you need to know
Fluoroquinolone mechanismDUAL: inhibits DNA gyrase (topoisomerase II) forming a quinolone-DNA-gyrase complex with induced cleavage, and inhibits topoisomerase IV.
Levofloxacin versus moxifloxacinLevofloxacin HAS Pseudomonas coverage; moxifloxacin does not and must NOT be used for urinary tract infection.
Fluoroquinolone harmsTendonitis and Achilles rupture, peripheral neuropathy, central nervous system toxicity, QT prolongation, photosensitivity. Caution under 18. Chelated by iron, antacids, calcium, dairy.
Septra mechanismTwo sequential steps: sulfamethoxazole blocks para-aminobenzoic acid → dihydrofolic acid; trimethoprim blocks dihydrofolic acid → tetrahydrofolic acid.
Septra uses and harmsCovers methicillin-resistant Staphylococcus aureus, NOT enterococci. Pneumocystis jirovecii treatment and prophylaxis. Stevens-Johnson syndrome, blood dyscrasias, raises the international normalized ratio with warfarin.
MetronidazoleInteracts with bacterial DNA causing helical structure loss and strand breakage. Anaerobes and parasites. Drug of choice for Clostridium difficile. DISULFIRAM-LIKE REACTION with ethanol.
Polymyxins — BLACK BOXNephrotoxicity, neurotoxicity, neuromuscular blockade. The only warnings this deck labels black box. Detergent-like disruption of the Gram-negative outer membrane.

Antivirals

TermWhat you need to know
Herpes simplex 1 versus 2Type 1: mouth, face, skin, esophagus, brain. Type 2: genitals, rectum, hands, meninges.
Varicella-zoster / cytomegalovirusVaricella-zoster: chickenpox and shingles. Cytomegalovirus: retinitis, esophagitis, colitis.
Acyclovir mechanismGuanine analog LACKING the sugar moiety. Selectively phosphorylated by VIRAL THYMIDINE KINASE, incorporated into viral DNA; the missing sugar prevents elongation.
Acyclovir / valacyclovirHerpes simplex and varicella-zoster. Valacyclovir is the prodrug with far better oral absorption.
Acyclovir harmsNausea, vomiting, rash, bone marrow suppression, central nervous system effects (seizures, delirium, tremor), CRYSTALLIZES IN THE RENAL TUBULE — maintain hydration.
Ganciclovir / valganciclovirCYTOMEGALOVIRUS in transplant and immunocompromised patients. Neutropenia and thrombocytopenia; about a THIRD must stop intravenous treatment for side effects.
OseltamivirProdrug → carboxylate. Inhibits NEURAMINIDASE so budding progeny cannot be cleaved free. Influenza A and B. Oral only, renally adjusted.
The 48-hour windowOseltamivir must start within 48 hours — it blocks release of new virus, so late treatment has little to act on. Acyclovir within 24 hours of chickenpox shortens the illness but does NOT cure it.
Four prodrugsValacyclovir, famciclovir, valganciclovir, oseltamivir — each exists to solve poor oral absorption of its parent.

Antifungals

TermWhat you need to know
Fungal cellEukaryotic. Chitin cell wall, ERGOSTEROL membrane, different ribosomes, distinct nuclear membrane. Resistant to antibiotics.
Sort in two questionsWall or membrane? Echinocandins are the only wall agents. Then: bind ergosterol (polyenes) or block its synthesis (azoles, allylamines)? Griseofulvin and flucytosine sit outside both.
PolyenesAmphotericin B, nystatin, natamycin. Bind ergosterol and form channels — potassium and magnesium leak out.
Amphotericin B harmsFever and chills from interleukin-1 and tumor necrosis factor (pretreat). Hypokalemia, hypomagnesemia, hypotension, renal tubule damage — hydrate with normal saline. Lipid formulations cost 20–50× more, less toxic.
AzolesInhibit fungal cytochrome P450 14-alpha-demethylase (lanosterol → ergosterol). Because the target is a cytochrome P450 enzyme, they interact with human ones too.
Which azoleFluconazole: best oral absorption, enters the central nervous system, cryptococcal meningitis. Voriconazole: systemic aspergillosis, VISION effects ~30%. Posaconazole: the ONLY azole for Zygomycetes. Itraconazole: blastomycosis, histoplasmosis. Ketoconazole: rarely used.
Azoles in pregnancyITRACONAZOLE is TERATOGENIC. Fluconazole and voriconazole are TERATOGENIC IN ANIMALS. Check a PREGNANCY TEST before prescribing to anyone of childbearing potential.
EchinocandinsCaspofungin, micafungin, anidulafungin. Inhibit 1,3-beta-D-glucan synthase — the one target with no mammalian counterpart. Largely a salvage role.
AllylaminesNaftifine (topical), terbinafine (oral and topical). Inhibit squalene epoxidase. Superficial dermatophytes.
GriseofulvinInterrupts mitotic spindles. From Penicillium griseofulvum. Deposited in keratin precursor cells — scalp ~1 month, fingernails 6–9 months, toenails up to 12. High-fat meal increases absorption. NOT Candida; fungistatic. INDUCES cytochrome P450 1A2 and 2C9.
FlucytosineConverted by CYTOSINE DEAMINASE, which human cells lack — that is the selectivity. Inhibits thymidylate synthase. With amphotericin B in cryptococcal meningitis. Bone marrow suppression.
Tinea namesPedis = athlete's foot · corporis = ringworm · cruris = jock itch · unguium = onychomycosis (nails).

L2 · Vehicles & Penetration

TermWhat you need to know
More permeable sitesSCROTUM · FACE · AXILLA · SCALP. The same tube does different things in different places.
Drying rangeTINCTURES most drying → wet dressings → lotions → gels → aerosols → powders → pastes → creams → foams → OINTMENTS least drying.
Match vehicle to lesionOOZING, VESICULATION, CRUSTING → drying end. SCALING, LICHENIFICATION, XEROSIS → least drying end.
Two site rulesAVOID OINTMENT in intertriginous areas. GEL or FOAM for scalp and hairy locations — foams well, low residue.
Depot effectSkin acts as a RESERVOIR, which may permit ONCE DAILY dosing of a short acting drug.
OcclusionIncreases efficacy — and the lecture raises TOXICITY in the same breath.
Concentration gradientMore concentration means more transfer. Worked example: CORTICOSTEROID RESISTANCE overcome by raising concentration.

L2 · Acne — Factors and Drugs

TermWhat you need to know
Four major factorsINCREASED SEBUM · ALTERED KERATINIZATION with ductal hyperproliferation · BACTERIAL COLONIZATION (P. acnes) · INFLAMMATORY MEDIATORS.
Critical targetThe MICROCOMEDONE. Eliminating follicular occlusion arrests the cascade.
Lesion splitNONINFLAMMATORY = open and closed comedones. INFLAMMATORY = papulopustular and nodular.
Route by severityMILD–MODERATE topical. MODERATE–SEVERE systemic.
Benzoyl peroxideCrosses stratum corneum UNCHANGED, converts to BENZOIC ACID. Counsel: BLEACHES hair, clothing, bedding.
Topical retinoidFIRST LINE for comedonal acne. AVOID IN PREGNANCY. Tretinoin is PHOTOLABILE — apply at night.
The interactionBENZOYL PEROXIDE INACTIVATES TRETINOIN. Adapalene is the one stable in sunlight AND with benzoyl peroxide.
Retinoid branchesTAZAROTENE acne + psoriasis · ALITRETINOIN Kaposi sarcoma · BEXAROTENE T-cell lymphoma.
Topical antibioticCLINDAMYCIN preferred. Erythromycin losing efficacy to P. acnes RESISTANCE.
IsotretinoinCONTRAINDICATED in pregnancy and breastfeeding; iPledge. Raised SERUM LIPIDS. MONITOR FOR DEPRESSION.
TetracyclinesChelate CALCIUM, blocking neutrophil and monocyte CHEMOTAXIS. CONTRAINDICATED under 8 years and in pregnancy.
Azelaic acidGive it SIX TO EIGHT WEEKS. Can cause HYPOPIGMENTATION.
Drug-induced acneSYSTEMIC CORTICOSTEROIDS (not hydrocortisone) · antiepileptics · tuberculostatics · lithium. Withdrawal causes an INITIAL WORSENING.

L2 · Atopic Dermatitis & Steroids

TermWhat you need to know
Atopic triadAtopic dermatitis + ASTHMA + ALLERGIC RHINO-CONJUNCTIVITIS. SKIN BARRIER DYSFUNCTION plays the major role.
Major indicatorsPRURITUS · rash in TYPICAL AREAS · CHRONIC or repeated · FAMILY HISTORY. (Raised IgE and skin tests are MINOR.)
Gold standardTOPICAL CORTICOSTEROIDS, chosen by severity and SITE.
Potency by siteLOW for face, intertriginous areas, infants — and better long term. MEDIUM for body. Exacerbation: MEDIUM–HIGH for one to two weeks then STEP DOWN.
What drives adverse effectsPOTENCY · DURATION · AREA COVERED · OCCLUSIVENESS (ointment > cream > lotion).
Local vs systemicLOCAL: skin atrophy, acne, rosacea, allergic dermatitis to the vehicle. SYSTEMIC: adrenal suppression, infections, hyperglycemia, GLAUCOMA, CATARACTS, growth retardation in children.
ImmunomodulatorsTACROLIMUS, PIMECROLIMUS inhibit T cell, mast cell and keratinocyte activation. SECOND LINE. Possible cancer risk; avoid if immunosuppressed. Counsel BURNING and HIGH SPF.
Oral steroid courseNeeds a TAPER to prevent a flare-up.

L2 · Topical Anti-infectives

TermWhat you need to know
BacitracinPrevents CELL WALL synthesis. Gram positives. NO SYSTEMIC TOXICITY.
MupirocinBinds bacterial TRANSFER RNA. MRSA. Eliminates NASAL CARRIAGE of S. aureus.
Polymyxin BInterrupts CYTOPLASMIC MEMBRANE. Gram negatives. AVOID high dose on OPEN or DENUDED skin — neuro- and nephrotoxicity.
NeomycinFrequently causes SENSITIZATION. Class can accumulate systemically.
AzolesInhibit FUNGAL P450, preventing cell wall formation. Treatment is PROLONGED, two to three weeks.
Ciclopirox nail lacquerLESS THAN 12% EFFECTIVE for onychomycosis. Say so before starting.
AllylaminesNAFTIFINE, TERBINAFINE — inhibit ERGOSTEROL production.
Coverage gapsTOLNAFTATE has NO CANDIDA activity. NYSTATIN is the candidal agent, NO ORAL ABSORPTION.
Topical antiviralsACYCLOVIR, PENCICLOVIR — guanine analogs, recurrent OROLABIAL herpes simplex.
ImiquimodImmunomodulator — warts, ACTINIC KERATOSES, BASAL CELL CARCINOMA. Irritation in VIRTUALLY ALL patients, and the DEGREE OF INFLAMMATION PARALLELS EFFICACY.

L3 · ANS Wiring & Receptors

TermWhat you need to know
The treeNervous system → CENTRAL / PERIPHERAL. Peripheral → AFFERENT / EFFERENT. Efferent → SOMATIC / AUTONOMIC. Autonomic → ENTERIC, PARASYMPATHETIC, SYMPATHETIC.
Autonomic vs somaticAutonomic is TWO NEURONS — PREGANGLIONIC within the CNS, POSTGANGLIONIC from a ganglion, generally NONMYELINATED. The somatic route does not relay that way.
EntericThe BRAIN OF THE GUT — gut, pancreas, gallbladder. FUNCTIONS INDEPENDENTLY of the CNS, modulated by the other two.
Cholinergic stepsSIX: synthesis · storage · release · receptor binding · DEGRADATION by acetylcholinesterase · RECYCLING of choline. (Adrenergic has FIVE.)
Muscarinic subtypesFive subclasses, ONLY M1, M2, M3 functionally characterized. M1 neurons + gastric parietal · M2 neurons + CARDIAC + smooth muscle · M3 neurons + BLADDER + exocrine glands.
Nicotinic receptorFIVE SUBUNITS, LIGAND-GATED ION CHANNEL. TWO acetylcholine molecules open it to sodium. CNS, adrenal medulla, ganglia, neuromuscular junction.
Nicotine's twistSTIMULATES at low concentration, BLOCKS at high.
Alpha vs beta locationALPHA-1 POSTSYNAPTIC on the effector organ. ALPHA-2 PRESYNAPTIC on nerve endings.
Potency ordersALPHA: epinephrine ≥ norepinephrine >> isoproterenol. BETA: isoproterenol > epinephrine > norepinephrine.
Catecholamine breakdownCOMT postsynaptically, MAO within the neuron. Noncatecholamines escape both — longer acting, more CNS penetration.

L3 · Predicting Effects

TermWhat you need to know
Muscarinic — DUMBBELSDefecation · Urination · Miosis · Bradycardia · Bronchorrhea · Bronchospasm · Emesis · Lacrimation · Salivation.
Nicotinic — MTWHFMydriasis · Tachycardia · Weakness · Hypertension · Fasciculations.
AnticholinergicMad as a hatter · Blind as a bat · Red as a beet · Dry as a bone · Hot as Hades. Plus constipation, urinary retention, TACHYCARDIA.
How to tell them apartPUPIL AND HEART FIRST: muscarinic is SMALL pupil, SLOW heart. Nicotinic and anticholinergic are both BIG pupil, FAST heart. Then WET vs DRY separates those two.
Ganglionic blockadeBlocks the ENTIRE autonomic output at nicotinic receptors. Vasodilation, plus atony of bladder and gut, cycloplegia, xerostomia, tachycardia.

L3 · Cholinergic Drugs

TermWhat you need to know
Direct vs indirectDIRECT bind the receptor (choline esters, pilocarpine). INDIRECT = ANTICHOLINESTERASES, raising acetylcholine.
BethanecholResists acetylcholinesterase, MUSCARINIC ONLY. Stimulates DETRUSOR, relaxes trigone and sphincter → urinary retention.
PilocarpineMiosis + ciliary contraction → GLAUCOMA. Also XEROSTOMIA.
Edrophonium vs pyridostigmineEDROPHONIUM short acting — DIAGNOSING myasthenia gravis. PYRIDOSTIGMINE — CHRONIC MANAGEMENT.
PhysostigmineENTERS THE BRAIN. Antidote for ANTICHOLINERGIC OVERDOSE.
NeostigmineDoes NOT enter the brain. Bladder and gut, reversing blockade, myasthenia gravis.
Alzheimer agentsDONEPEZIL · RIVASTIGMINE · GALANTAMINE. Deficiency of CENTRAL cholinergic neurons.
Poisoning, both waysINSECTICIDE (anticholinesterase) → ATROPINE + PRALIDOXIME. ANTICHOLINERGIC overdose → PHYSOSTIGMINE. Getting the direction wrong doubles the poisoning.
Pralidoxime limitsDoes NOT enter the brain. CANNOT overcome reversible inhibitors such as physostigmine.
AtropinePersistent MYDRIASIS + CYCLOPLEGIA. BRADYCARDIA at low dose, TACHYCARDIA at higher. Greatest inhibition on bronchial tissue, sweat, saliva.
ScopolamineGreater CENTRAL action — MOTION SICKNESS, blocks SHORT-TERM MEMORY. Patch: WASH HANDS or you blur your vision.
Synthetic antimuscarinicsIPRATROPIUM, TIOTROPIUM inhaled for COPD · GLYCOPYRROLATE secretions and drooling · bladder agents lower pressure and raise capacity.
Neuromuscular blockadeNONDEPOLARIZING is COMPETITIVE — MORE ACETYLCHOLINE REVERSES IT. Face and eye first, DIAPHRAGM LAST, recovery in reverse.
SuccinylcholineThe ONLY depolarizing agent. Acts LIKE acetylcholine and is not destroyed — an anticholinesterase makes it WORSE. Risk: MALIGNANT HYPERTHERMIA with halothane → COOLING + DANTROLENE.

L3 · Adrenergic Drugs

TermWhat you need to know
Epinephrine by doseBETA effects at LOW dose, ALPHA at HIGH. Raises SYSTOLIC, lowers DIASTOLIC.
Epinephrine usesANAPHYLAXIS · CARDIAC ARREST · acute bronchospasm. In local anesthetic to PROLONG the block by vasoconstriction.
Epinephrine + beta blockerALPHA EFFECTS LEFT UNOPPOSED → peripheral resistance and blood pressure RISE.
NorepinephrineMostly ALPHA. REFLEX BRADYCARDIA via baroreceptor. EXTRAVASATION → PHENTOLAMINE.
DopamineBeta-1 cardiac · dopaminergic dilates RENAL and SPLANCHNIC · alpha-1 vasoconstriction only at VERY HIGH dose. Cardiogenic and septic shock.
DobutamineSelective BETA-1. Acute heart failure. BARELY RAISES MYOCARDIAL OXYGEN DEMAND. Caution in ATRIAL FIBRILLATION.
Alpha-1 vs alpha-2 agonistPHENYLEPHRINE alpha-1 → vasoconstriction, REFLEX BRADYCARDIA. CLONIDINE alpha-2 → reduces CENTRAL SYMPATHETIC OUTFLOW.
Two rebound warningsOXYMETAZOLINE longer than THREE DAYS → rebound congestion. CLONIDINE stopped abruptly → REBOUND HYPERTENSION.
Indirect agonistsAMPHETAMINE · COCAINE · TYRAMINE — release norepinephrine or block reuptake. EPHEDRINE and PSEUDOEPHEDRINE are MIXED.
Tyramine trapNormally destroyed by MAO IN THE GUT. On an MAO INHIBITOR it reaches the terminal — serious vasopressor effect. Fermented cheese and wine.
PhenoxybenzamineIRREVERSIBLE, noncompetitive — needs NEW RECEPTORS, at least a day. EPINEPHRINE REVERSAL: vasoconstriction blocked, vasodilation left.
Alpha-1 blockers splitPRAZOSIN, TERAZOSIN, DOXAZOSIN for hypertension. TAMSULOSIN, ALFUZOSIN for BPH. Signature: FIRST-DOSE SYNCOPE.
PropranololNonselective → BRONCHOCONSTRICTION, CONTRAINDICATED in asthma and COPD. MASKS HYPOGLYCEMIA. Abrupt stop → arrhythmia from RECEPTOR UP-REGULATION.
Propranolol beyond BPMIGRAINE PREVENTION · HYPERTHYROIDISM · ANGINA · after MYOCARDIAL INFARCTION.
The rest by propertyTIMOLOL glaucoma · SELECTIVE BETA-1 lose selectivity at higher doses · ACEBUTOLOL and PINDOLOL have ISA · LABETALOL IV for hypertensive emergency · CARVEDILOL mortality in heart failure.
Storage agentsRESERPINE blocks uptake INTO vesicles. GUANETHIDINE blocks release FROM them.