Drug Class MOA Therapeutic Use Contraindications/Adverse

Effects/Interactions
Beta Blockers Decrease Heart Rate, Hypertension with Contraindications: pts with
Contractility, Cardiac output, concomitant heart disease or Bradycardia, asthma
-lol and blood pressure, decrease heart failure (nonselective), severe
sympathetic outflow, inhibit peripheral vascular disease,
renin release. Previous myocardial 2nd and 3rd degree heart block
infarction, angina pectoris.
Adverse Effects: fatigue,
lethargy, insomnia, decrease
libido, erectile dysfunction.

Concerns: do NOT stop

abruptly
Ace inhibitors Reduce peripheral vascular Hypertension with high risk Adverse Effects: Dry cough,
resistance w/o increase CO, of coronary heart disease, hypotension, hyperkalemia,
-pril HR, or contractility. heart failure, MI. angioedema

Block ACE enzyme in RAAS Contraindications: Pregnant

system. Lack of breakdown of *most desirable for patients women
bradykinin (vasodilator) with diabetes, kidney
disease. Concerns: patients taking
Reduce cardiac preload and aldosterone antagonists, K
afterload. Increase renal sparing diuretics, and K
blood flow. supplements.
Angiotensin II Receptor Block the AT1 receptor, Hypertension, heart failure or Adverse Reactions: similar to
Blockers decreasing angiotensin chronic kidney disease ACE but lower cough and
binding angioedema risk.
-sartan *most desirable for patients
Produce arteriolar and with diabetes, kidney Contraindications: should not
venous dilation, block disease. be combined with ACE
 aldosterone secretion inhibitor. Pregnant women.
Calcium Channel Blockers Block L-Type calcium Hypertension with diabetes, Adverse effects: hypotension
channels in vascular smooth angina, or asthma with dihydropyridines
Dihydropyridines -pine muscle and cardiac muscle. Constipation with Verapamil
(arteriole effect)  Dilatation of the Diltiazem and verapamil: Pedal Edema
coronary arteries and atrial fibrillation Bradycardia, SA nodal failure,
Non-dihydropyridines increase in coronary AV block, and decrease CO
-Verapamil and Diltiazem blood flow Gastroesophageal reflux
(heart effect)  Decreases cardiac Gingival Hyperplasia
afterload (Decreases
BP) and decreased O2
demand
Sodium Channel Blocker Reduces intracellular sodium Chronic angina and Subject to many interactions
and calcium overload, Arrhythmias
thereby improving diastolic Contraindications: should be
function *for pts who have failed avoided with other drugs
other antianginal therapies that cause QT prolongation
Alpha Adrenoreceptor Competitive bock of alpha-1 Hypertension Adverse Effects: Orthostatic
Blocking Agents adrenoreceptors. hypotension, Na and H20
retention, vivid dreams,
-sin Decrease peripheral depression, dry mouth, lipid
resistance and lower arterial effects, nasal congestion
blood pressure
Centrally acting adrenergic Clonidine: alpha 2 agonist to Clonidine: Hypertension Adverse effects: Clonidine –
drugs produce inhibition of sedation, dry mouth, and
sympathetic vasomotor Methyldopa: hypertension in constipation.
Clonidine and Methyldopa centers. Reduced TPR and pregnancy.
decreased BP Methyldopa: sedation and
drowsiness.
Methyldopa: diminishes
adrenergic outflow from CNS Considerations: Must be
 withdrawn slowly
(Clonidine)- Rebound HTN
Nitrates Converted to NO Angina – treatment and Adverse Effects: headache,
prophylaxis orthostatic hypotension,
Nitroglycerine Vasodilates and decreases tolerance, reflex tachycardia,
Isosorbide mono/dinitrate preload flushing
Dilate coronary artery
-Relieve spasm Interaction:
Phosphodiasterase 5
inhibitors (Viagra)

Thiazide Diuretics Blocks Na and CL Mild heart failure, Contraindications: GFR < 25,
reabsorption in DCT, which hypertension
Chlorothiazide, prevents H20 reabsorption. Adverse Effects:
hydrochlorothiazide hypokalemia,
Chlorthalidone Decreases TPR, causes Low hypomagnesemia,
Indapamide BP hyperuricemia,
metolazone Decrease in plasma volume, hyperglycemia.
decrease cardiac output. hypercalcemia

Loop Diuretics Block Na and CL reabsorption Moderate/severe Heart Adverse effects: hypokalemia
Decrease vascular resistance Failure and Edema Hypocalcemia
-ide ending and increased renal blood
Ethacrynic acid flow
Potassium-Sparing Diuretics Aldosterone receptor Hypertension along with Adverse effects:
antagonists (spironolactone thiazide or loop diuretics. Spironolactone:
Amiloride, Triamterene, and epierenon) Used mostly for heart failure. gynecomastia and abnormal
Spironolactone, and vaginal bleeding
eplerenone. Inhibitors of epithelial
sodium transport at the late Interactions: Eplerenone and
distal collecting ducts azole antifungals
 (amiloride and Triamterene)
Inotropic Drugs Increase the contractility Heart Failure and AV node Contraindications: diastolic
arrhythmias. or right sided HF,
Digoxin Inhibits the Na/K ATPase hypokalemia patients (loop
enzyme. The higher cellular or thiazide diuretics),
Na is exchanged for hypomagnesemia, metabolic
extracellular Ca2+, which alkalosis. Hypothyroidism.
increases cardiac
contractility. Adverse Effects: toxicity,
anorexia, nausea/vomiting,
diarrhea, blurred vision,
yellowish vision, cardiac
arrhythmias.
Renin inhibitors Selective Renin inhibitor Hypertension Contraindications:
combining with ARBs or
Aliskiren ACEIs in diabetic patients,
pregnancy warning.

Adverse Effects: orthostasis,

angioedema, cough (less),
diarrhea.

Anti-fungal
Class MOA Clinical Uses Considerations Side effects/DDI
 Polyenes Bind to ergosterol in the Amphotericin + 5 FC – Half life: 2-3 weeks “shake and bake”-fever
fungal cell membrane cryptococcal meningitis- and chills.
Amphotericin B-IV and creates porins  broadest spectrum. Renal excretion Nephrotoxicity
Nystatin (topical) increase cell Renal wasting of K and
permeability causing Nystatin: C. albicans Low dose and slow Mg
Polyenes pores cell death infusion rate Hypotension, muscle
spasms, anemia
Flucytosine -PO Converted in fungal cell Used with Ampho B for Eliminated by GFR in Nausea, Vomiting
to 5-fluorouracil which cryptococcal meningitis kidneys Bone marrow
interferes with nucleic suppression in high
acid and protein Narrow Spectrum doses.
synthesis
Azoles Inhibit the synthesis of Athletes foot Absorption is enhanced N/V
ergosterol by inhibiting Onychomycosis by low pH Alopecia -fluco.
Fluconazole-p.o CYP450 enzyme. Ringworms Hepatoxicity -fluco, itra,
Itraconazole-p.o Lanosterol accumulates Aspergillus: (itra, vori- Fluco-Renally vori
Voriconazole-p.o (toxic). DOC , posa) eliminated Vori: visual disturbance
Posaconazole-p.o Depletion of ergosterol Fungal meningitis: fluc. Posa: fecal elimination Keto – gynecomastia,
Ketoconazole -topical causes cell lysis and cell Dermatophytes: Itra menstrual irregularities
Clotrimazole-topical death. most toxic
Topical Antifungals inhibit squalene Dermatophytes CYP2D6 inhibitor GI disturbance
epoxidase, thereby Terb: DOC for
Terbinafine blocking the onychomycoses
Naftifine biosynthesis of
Butenafine ergosterol
Echinocandins-IV Inhibit cell wall Narrow Spectrum Poorly absorbed from Well tolerated.
synthesis – beta glucan. Very active and GI Fever, HA, flushing,
Caspofungin synthase fungicidal against Does not induce/inhibit erythema, rash.
Micafungin Candida (DOC) and CYP450s. – except
anidulafungin Aspergillus Caspo No cross resistance
Category C pregnancy
 DDI: Tacrolimus and
cyclosporine with
Caspo.
Superficial fungal: Griseofulvin: inhibits Skin and scalp – Tinea Take Griseo with fatty GI upset, dizziness,
Others- P.O fungal cell mitosis capitis food. confusion, hepatoxicity,
leukopenia,
Griseofulvin Tolnaftate: inhibits Primarily against photosensitive
Tolnaftate fungal enzyme involved Dermatophytes or Tinea
in ergosterol synthesis

Anti-mycobacterial Agents
Class/Drug MOA Clinical uses Considerations Side Effects/DDI
Isoniazid (INH) Must be activated by M. Tuberculosis “slow acetylator” – Hepatotoxicity
bacterial catalase Atypical mycobacteria increased risk for Severe hepatitis, N/V
inhibits mycolic acid 1st obligatory drug! hepato/neuro toxicity Neurotoxicity-
enzyme pyridoxine deficiency
Used as single agent Inhibitor of CYP Hemolysis with G6PD
for + PPD and – CXAY enzymes. def.
9 months of treatment Restlessness, insomnia
Rifamycin’s Blocks prokaryotic RNA Rifampin: can be used Rifampin: Potent Hepatotoxicity
polymerase and for prophylaxis inducer or CYP450 Rifampin: Body
Rifampin inhibits RNA synthesis 4 months of treatment secretions turn orange.
Rifabutin Bactericidal Flu like syndrome
Rifapentine 2nd obligatory drug for Hepatitis with elevated
therapy LFTs.
Rifabutin: harmless
 yellow discoloration of
the skin, polymyalgia’s,
uveitis.
Pyrazinamide (PZA) Inhibit fatty acid Used as the 3rd drug N/V
biosynthesis? with INH and Rifampin Hepatotoxicity
Requires metabolic Skin rash
conversion by Arthralgia
pyrazinamide’s Hyperuricemia
Bactericidal
Ethambutol (EMB) Inhibits arabinosyl Primary clinical use Ocular damage
transferase involved in 4th drug with INH, Red/green vision
synthesis of rifampin, and PZA HA, confusion,
arabinogalactan peripheral neuropathy
Bacteriostatic Possible hyperuricemia
Aminoglycoside Irreversible inhibition Mycobacterial Streptomycin resistant Less auditory and renal
of protein synthesis. meningitis or isolates may be damage than other
Rapidly Bactericidal – disseminated infection susceptible to aminoglycoside.
Streptomycin-IV or IM interference with Can sometimes be the amikacin.
Amikacin functional integrity of 4th drug.
cell membrane.
Fluoroquinolones Inhibit DNA synthesis, Moxi shows greatest FE, Ca supplements Dizziness, confusion,
rapidly bactericidal activity versus TB and Al and Mg antacids decrease seizure
Moxifloxacin with concentration Cipro and Levo are decrease GI absorption threshold.
Ciprofloxacin dependent killing used to treat MDR Tendon rupture -BB
levofloxacin active TB. Ca fortified milk, warning
Inhibits topoisomerase antacids, milk, and
II (-) and IV (+) yogurt decrease F of QT prolongation
cipro and moxi.
Anti-protozoal Agents
Drug MOA Clinical Uses Considerations Side Effects/ DDI
Chloroquine Concentrates in the Sensitive P. falciparum Erythrocytic stage only Retinopathy
 acidic food vacuole Corneal Deposits
parasite digests the Headache
hemoglobin which GI disturbance
releases soluble heme, Skin rash
which is toxic.
Quinine Interferes with heme Reserved for severe Erythrocytic Stage only Hemolytic anemia with
polymerization infestations and for G6PD deficiency
chloroquine resistance Cinchonism (headache,
malarial strains. tinnitus, diplopia)
Skeletal muscle
weakness
Mefloquine Undetermined. Once a week Erythrocytic form only GI distress. Headache,
prophylaxis or ataxia, visual/auditory
treatment Long ½ life: 10-14 days hallucinations,
MDR strains of P. dizziness.
falciparum Rare: seizure,
psychosis,
disorientation
Primaquine Metabolites become Gametocidal against all Exoerythrocytic stage Hemolytic anemia in
oxidants and hemolyze Plasmodium spp. pts w/ G6PD deficiency
infected RBC Only drug that kills
hepatic form of P. Avoid in pregnancy
vivax and P. ovale.
Atovaquone/proguanil Inhibits Used for chloroquine- Erythrocytic and GI distress
(malarone) pyrimidine/inhibits resistant P. falciparum exoerythrocytic forms High liver enzymes
dihydrofolate and prophylaxis
reductase
Pyrimethamine/sulfadoxine inhibits plasmodial Used for chloroquine- Erythrocytic forms Megaloblastic anemia
(Fansidar) dihydrofolate resistant P. falciparum Resistance leads to Hypersensitivity, rash
reductase required for combination with
the synthesis of artemisinin derivatives
 tetrahydrofolate
Artemisinin derivative Production of free Combined with semi=- N/V/D
radicals that causes synthetic derivative for Dose related QT
Artemether oxidative damage MDR. P. falciparum prolongation
Artesunate Inhibits calcium ATPase
Doxycycline Inhibition of protein Chloroquine-resistance Asexual exo- See Antibiotic chart
synthesis Must + quinine or erythrocytic forms
Bacteriostatic mefloquine
30S ribosomal unit Monotherapy for
prophylaxis.
Clindamycin Inhibition of protein + quinine or C. Diff pseudomonas
synthesis mefloquine for tx of colitis
chloroquine-resistance
50S ribosomal unit P. falciparum
Metronidazole Ferredoxins in DOC for Paromomycin in Disulfiram-like
susceptible protozoans trichomoniasis, pregnant women-IM reactions
convert the drug Giardiasis, and Inhibits CYP2C9 and
amebiasis CYP3A4
The nitro group is able
to serve as an electron
acceptor, forming
reduced cytotoxic
compounds that bind
to proteins and DNA
Pyrimethamine- Same as above! Toxoplasma gondii Use spriamycin if in 1st Same as above!!
sulfadiazine ( (eating infecting meat) trimester
TMP-SMX Sulfa: competitive Prophylaxis of Fever, photosensitivity,
antagonist of PABA and toxoplasmosis in AIDs urticarial, Steven
inhibits and treating Johnson syndrome,
dihydropteroate Pneumocystis jiroveci toxic epidermal
synthetase necrolysis
 Trim: inhibits Blood dyscrasis
dihydrofolate Life threatening
reductase to prevent hyperkalemia.
the conversion of DHF
to THF
Albendazole Inhibit synthesis of Round worms, tape Abdominal pain,
microtubules in worms. Giardiasis diarrhea, reversible
parasitic worm alopecia, high liver
enzymes. Rare
agranulocytosis.

Anti-coagulants
Drug MOA Therapeutic use Considerations
Warfarin Inhibits Vitamin K epoxide Prophylaxis of DVTs after Bleeding, Teratogenesis and fetal
reductase, which stops the orthopedic surgery, death, bruising
 post-translational thromboembolism in pts with
modification of factors II, VII, Afib, prosthetic cardiac DDI: Increase – fluconazole,
IX, X valves, rheumatic valve amiodarone, metronidazole,
disease, and unstable angina Bactrim, NSAIDs, ASA
Decrease: carbamazepine,
rifampin, phenytoin, Vitamin K
Oral direct thrombin Direct competitive, reversible Prophylaxis in non-valvular a- Bleeding, gastritis and dyspepsia
inhibiters inhibitor of thrombin (factor fib
II) Antidote: Idarucizumab (Praxbind)
Dabigatran (Pradexa)

Factor Xa inhibitors Orally active director factor Prophylaxis of DVTs (hip or Metabolized by CYP34A – watch
Xa inhibitor- does not require knee) and non-valvular a-fib out for drug-drug interactions.
Rivaroxaban (Xarelto) the presence of ATIII
Apixaban (Eliquis) *No monitoring required No effect on BT, aPTT, or PT
Edoxaban
Antidote: Andexanet alfa
Hirudin-derived direct Isolated from the salivary Increases the aPTT to 1.5-2.5
thrombin inhibitors gland of the medicinal leech above normal limit.

Lepirudin-IV Direct inhibitor of thrombin No antidote

bivalirudin ATIII not required.

Heparin Inhibits factors 2, 9-12 UFH: prophylaxis of post- Reversed by Protamine sulfate
Causes a 1000X increase rate operative DVT
UFH-i.v or s.c of interaction between ATIII Treatment of DVT and PE Bleeding: less with LMWH
LMWH (ardeparin, dalteparin, and activated clotting factors Anti-coagulant for IV Skin necrosis
and enoxaparin, in the intrinsic pathway catheters, hemodialysis, HIT – decrease in platelet count
fondaparinux) -s.c cardiopulmonary bypass. (less with LMWH)
Fondaparinux- inhibits Xa Contraindications: spinal
LMWH: prophylaxis of post- anesthesia or lumbar puncture,
operative DVT, treatment of bleeding.
 ischemic stroke, acute
coronary syndrome, Goal therapy: to increase aPTT to
anticoagulant during 1.5-2.5 the normal value.
hemodialysis.
Antiplatelet Drugs
Aspirin Circulating salicylate Decrease incidence of MI, Increases BT
irreversibly inhibits COX-1 and secondary MI, TIA’s, ischemic Tinnitus
COX-2 stroke and secondary stroke. Aspirin effects are prevented by
other NSAIDs
Clopidogrel and Prasugrel Inhibit binding to ADP to Decrease incidence of MI and DDI: Omeprazole. –CYP2C9
P2Y12 receptors on platelets stroke in pts with
and inhibit platelet activation. atherosclerotic vascular
disease and unstable angina,
secondary prevention of
stroke,

Abciximab, eptifabide, and Block IIb/IIIa receptors which Acute coronary syndrome
tirofiban don’t allow fibrinogen to bind characterized by chest pain,
platelets together abnormal ECG, and elevated
cardiac enzymes.
Unstable angina or acute MI
Percutaneous coronary
intervention
Fibrinolytic (thrombolytic) drugs
Alteplase, reteplase, Binds to fibrin, cleaves Bleeding – results from non-
tenecteplase plasminogen to plasmin selective lysis of thrombi involved
which lysis strands within the in normal vascular repair and the
clot. uninhibited degradation of factors
Establish reperfusion of V and VIII.
Streptokinase Forms 1:1 complex with coronary vessels after MI
Anistreplase plasminogen and allows DVTs and PE
 cleavage of other Ischemic stroke
plasminogen to plasmin, but Hemorrhage.
not specific for fibrin-bound
forms.
Urokinase Directly activates
plasminogen to plasmin