• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

138 Cards in this Set

  • Front
  • Back
Mechanism: Osmotic diuretic, T tubular fluid osmolarity, producing increased urine flow.
Clinical Use: Shock, drug overdose, t intracranial/intraocular pressure.
Toxicity: Pulmonary edema, dehydration. Contraindicated inanuria, CHF.
Mechanism Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body
HCO3 stores.
Clinical use: Glaucoma, urinary alkalinization, metabolic
alkalosis, altitude sickness.
Toxicity: Hyperchloremic metabolic acidosis, neuropathy, ACIDazolamide causes NH3 toxicity, sulfa allergy
Mechanism: Sulfonamide loop diuretic. Inhibits cotransport
edema), hypertension, system (Nat, K+, 2 Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of
medulla, preventing concentration of urine.
increased Ca2+ excretion.
Clinical use: Edematous states (CHF, cirrhosis, nephrotic
syndrome, pulmonary hypercalcemia.
Toxicity: Ototoxicity, Hypokalemia, Dehydration, Allergy
(sulfa), Nephritis (interstitial), Gout.
Ethacrynic acid
Mechanism: Phenoxyacetic acid derivative (NOT a sulfonamide).
Essentially same action as furosemide.
Clinical use: Diuresis in patients allergic to sulfa drugs.
Toxicity: Similar to furosemide; can be used in hyperuricemia,
acute gout (never used to treat gout).
Mechanism: Thiazide diuretic. Inhibits NaC1 reabsorption in
early distal tubule, reducing diluting capacity of
the nephron. Ca2+ excretion.
Clinical use: Hypertension, CHF, idiopathic hypercalciuria,
nephrogenic diabetes insipidus.
Toxicity: Hypokalemic metabolic alkalosis, hyponatremia,
hyperGlycemia, hyperLipidemia, hyperUricemia,
and hyperCalcemia. Sulfa allergy.
K + sparing diuretics
Spironolactone, Triamterene, Amiloride, eplerenone
Mechanism: Spironolactone is a competitive aldosterone receptor antagonist in the cortical collecting tubule.
Triamterene and amiloride act at the same part of
the tubule by blocking Na+ channels in the CCT.
Clinical use Hyperaldosteronism, K+ depletion, CHF.
Toxicity: Hyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagonists (e.g., spironolactone causes gynecomastia, antiandrogen effects).
ACE Inhibitors
Captopril, enalapril, lisinopril.
Mechanism:Inhibit angiotensin-converting enzyme, reducing
levels of angiotensin II and preventing
inactivation of bradykinin, a potent vasodilator.
Renin release is increased due to loss of feedback inhibition.
Clinical use: Hypertension, CHF, diabetic renal disease.
Toxicity: Cough, Angioedema, Proteinuria, Taste changes,
hypOtension, Pregnancy problems (fetal renal
damage), Rash, Increased renin, Lower
angiotensin II. Also hyperkalemia. Avoid with
bilateral renal artery stenosis because ACE
inhibitors significantly GFR by preventing
constriction of efferent arterioles.
angiotensin II receptor antagonist.
--It is not an ACE inhibitor and does NOT cause cough.
H2 blockers
Pg. 337
Proton Pump Inhibitors
Mechanism: Irreversibly inhibit H+/K+-ATPase in stomach parietal cells.
Clinical use: Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.
Bismuth, sucralfate
Mechanism: Bind to ulcer base, providing physical protection,and allow HCO3 secretion to reestablish pH
gradient in the mucous layer.
Clinical use:increased ulcer healing, traveler's diarrhea.
Triple therapy of H. pylori ulcers — Metronidazole,
Amoxicillin (or Tetracycline), Bismuth.
Can also use PPI —Please MAke Tummy Better.
Mechanism: A PGE1 analog. Increased production and secretion of gastric mucous barrier, acid production.
Clinical use: Prevention of NSAID-induced peptic ulcers; maintenance of a patent ductus arteriosus.
Also used to induce labor.
Toxicity: Diarrhea. Contraindicated in women of childbearing potential (abortifacient).
Muscarinic antagonists
Pirenzepine, propantheline.
Mechanism: Block M1 receptors on ECL cells (decreased histamine secretion) and M3 receptors on
parietal cells (decreased H+ secretion).
Clinical use: Peptic ulcer (rarely used).
Toxicity: Tachycardia, dry mouth, difficulty focusing eyes.
Mechanism: Somatostatin analog
Clinical use: Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors.
Toxicity: Nausea, cramps, steatorrhea.
Antacid use
Can affect absorption, bioavailability, or urinary
excretion of other drugs by altering gastric and
urinary pH or by delaying gastric emptying.
Overuse can also cause the following problems:
1. Aluminum hydroxide—constipation and
hypophosphatemia; proximal muscle
weakness, osteodystrophy, seizures
2. Magnesium hydroxide—diarrhea, hyporeflexia,
hypotension, cardiac arrest
3. Calcium carbonate — hypercalcemia,
rebound acid increased
All can cause hypokalemia.
Mechanism: A monoclonal antibody to TNF, proinflammatory
Clinical use: Crohn's disease, rheumatoid arthritis.
Toxicity: Respiratory infection (including reactivation of
latent TB), fever, hypotension.
Mechanism: A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria.
Clinical use: Ulcerative colitis, Crohn's disease.
Toxicity: Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
Mechanism: 5-HT3 antagonist. Powerful central-acting antiemetic.
Clinical use: Control vomiting postoperatively and in patients so you can undergoing cancer chemotherapy.
Toxicity: Headache, constipation.
Mechanism: D2 receptor antagonist. "increased resting tone, contractility, LES tone, motility. Does not
influence colon transport time.
Clinical use: Diabetic and post-surgery gastroparesis.
Toxicity: increased parkinsonian effects. Restlessness, drowsiness, fatigue, depression, nausea,
diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction.
Lispro (rapid-acting)
Aspart (rapid-acting)
Regular (rapid-acting)
NPH (intermediate)
Glargine (long-acting)
Detemir (long-acting)
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as glycogen.
Muscle: increase glycogen and protein synthesis, K+
uptake. Fat: aids TG storage.
Clinical Use: Type 1 DM, type 2 DM,
gestational diabetes, life-threatening hyperkalemia, and
stress-induced hyperglycemia.
Toxicities: Hypoglycemia,
reaction (very
First generation:
Second generation:
Action: Close K+ channel in
(3-cell membrane, so cell depolarizes -->
triggering of insulin. release via increase Ca2+ influx.
Clinical Use: Stimulate release of endogenous insulin in type 2 DM. Require some islet function,
so useless in type 1 DM.
Toxicities: First generation: disulfiram-like
effects. Second generation: hypoglycemia.
Action: Exact mechanism is
unknown. DECREASES gluconeogenesis,
incraeses glycolysis, increases peripheral
glucose uptake (insulin sensitivity).
Clinical use: Oral. Can be used in patients without islet function.
Toxicities: Most grave adverse effect is lactic acidosis (contraindicated in renal failure)
Action: Increased insulin sensitivity in
peripheral tissue. Binds to PPAR -gamma nuclear
transcription regulator.
Clinical use: Used as monotherapy in type 2 DM or combined with other agents.
Toxicities: Weight gain, edema, hepatotoxicity, CV toxicity.
a-glucosidase inhibitors:
Action: Inhibit intestinal brushborder
a-glucosidases. Delayed sugar hydrolysis
and glucose absorption lead to .1. postprandial
Clinical Use: Used as monotherapy in
type 2 DM or in combination with above
Toxicity: GI disturbances
Action: Decrease glucagon
Clinical use: Type II DM
Toxicity: Hypoglycemia, nausea, diarrhea
GLP-1 analogs:
Action: Increase insulin, decrease glucagon release.
Clinical use: Type II DM
Toxicity: Nausea, vomiting, and pancreatitis.
Propylthiouracil, methimazole
Mechanism: Inhibit organification of iodide and coupling of thyroid hormone synthesis.
Propylthiouracil also decreases peripheral conversion of T4 to T3.
Clinical use: Hyperthyroidism.
Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia. Methimazole is a possible teratogen.
Levothyroxine, triiodothyronine
Mechanism: Thyroxine replacement.
Clinical use: Hypothyroidism, myxedema.
Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias.
Hypothalamic/pituitary drugs
GH use: GH deficiency, Turner syndrome
Somatostatin(octreotide) Use: Acromegaly, carcinoid, gastrinoma, glucagonoma
Oxytocin use: stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage
ADH (desmopressin): use: Pituitary (central, NOT nephrogenic) DI
Mechanism: ADH antagonist (member of the tetracycline family).
Clinical use: SIADH.
Toxicity: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.
Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone.
Mechanism: the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2.
Clinical use: Addison's disease, inflammation, immune suppression, asthma.
Toxicity: Iatrogenic Cushing's syndrome—buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
Adrenal insufficiency when drug stopped after chronic use.
Direct Cholinergic agonists
Clinical use: Postoperative and neurogenic ileus and urinary
Actions: Activates Bowel and Bladder
smooth muscle; resistant to
AChE. Beth Anne, call
(bethanechol) me if you want
to activate your Bowels and
Direct Cholinergic agonists
Clinical use: Glaucoma, pupillary contraction, and relief of
intraocular pressure
Action: CARBon copy of acetylcholine
Direct Cholinergic Agonists
Clinical use: Potent stimulator of sweat, tears, saliva
Action: Contracts ciliary muscle of eye
(open angle), pupillary
sphincter (narrow angle);
resistant to AChE. PILE on
the sweat and tears.
Direct Cholinergic Agonists:
Clinical use: Challenge test for diagnosis of asthma
Actions: Stimulates muscarinic receptors in airway when inhaled
Indirect cholinergic agonists (anti-cholinesterase)
Clinical app: Postoperative and neurogenic ileus and urinary
retention, myasthenia gravis, reversal of
neuromuscular junction blockade (postoperative).

NOTES: increases endogenous ACh; no CNS penetration.
NEO CNS = NO CNS penetration.
Indirect Cholinergic agonists (anti-cholinesterase)
Clinical app: Myasthenia gravis (long acting); does not penetrate
Action: Increase endogenous ACh; Increase strength.
Indirect Cholinergic Agonists
Clinical app: Diagnosis of myasthenia gravis (extremely short
Notes: Increases endogenous ACh.
Indirect Cholinergic Agonists
Clinical App: Glaucoma (crosses blood-brain barrier CNS) and atropine overdose
Actions: Increased endogenous ACh. PHYS is for EYES.
Indirect Cholinergic Agonists
Clinical App: Glaucoma
Action: Increase endogenous ACH
inhibitor poisoning
Often due to organophosphates, such as parathion, that irreversibly inhibit AchE. Causes Diarrhea,
Urination, Miosis, Bronchospasm, Bradycardia,
Excitation of skeletal muscle and CNS,
Lacrimation, Sweating, and Salivation.
Antidote—atropine + pralidoxime (regenerates active

USE: Organophosphates are components of insecticides;
poisoning usually seen in farmers.
Class: Muscarinic ANtagonists
Organ system: eye
Application: Produce mydriasis and cycloplegia
Class: Muscarinic ANtagonists
Organ: CNS
Application: Parkinson's disease
Class: Muscarinic ANtagonists
Organ: CNS
Application: Motion sickness
Class: Muscarinic ANtagonists
Organ: Respiratory
Use: Asthma, COPD (I pray I can breathe soon!)
Oxybutynin, Glycopyrrolate
Class: Muscarinic Antagonists
Organ: Genitourinary
Use: Reduce urgency in mild cystitis and reduce bladder spasms.
Methscopolamine, pirenzepine, propantheline
Class: Muscarinist ANtagonists
Organ: Gastrointestinal
Application: Peptic ulcer treatment
Nicotinic antagonist.
Clinical use: Ganglionic blocker. Used in experimental models
to prevent vagal reflex responses to changes in
blood pressure—e.g., prevents reflex bradycardia
caused by NE.
Toxicity: Severe orthostatic hypotension, blurred vision,
constipation, sexual dysfunction.
Class: Direct Sympathomimetics
Mechanism: Beta1=Beta2 (isolated to beta)
Applications: AV block (rare)
Class: Direct sympathomimetics
Mechanism: D1=D2>beta>alpha, inotropic and chronotropic
Applications: Heart failure, cardiac stress testing
Class: Direct sympathomimetics
Mechanism: Beta1>Beta2, inotropic but not chronotropic
Applications: Heart failure, cardiac stress testing
Class: Direct sympathomimetics
Mechanism: alpha 1 > alpha 2
Applications: Pupillary dilation, vasoconstriction, nasal decongestion.
Metaproterenol, Albulterol, salmeterol, terbutaline
Class: Direct sympathomimetics
Mechanism: Selective bete2-agonists (beta2>beta 1)
MAST--Metaproterenol and Albuterol for acute asthma; salmeterol for long-term treatment; Terbutaline to reduce premature uterine contractions.
Class: Direct sympathomimetics
Mechanism: Beta2
Applications: Reduces premature uterine contractions
Class: Indirect sympathomimetics
Mechanism: Indirect general agonist, releases stored catecholamines
Applications: Narcolepsy, obesity, Attention deficit disorder
Class: INdirect sympathomimetics
Mechanism: Indirect general agonist, releases stored catecholamines
Application: Nasal decongestion, urinary incontinence, hypotension
Class: INdirect sympathomimetics
Mechanism: Indirect general agonist, uptake inhibitor
Use: Causes vasoconstriction and local anesthesia.
Clonidine, alpha-methyldopa
Class: Sympathoplegics
Mechanism: Centrally acting alpha-2 agonists, decrease central adrenergic outflow
Use: Hypertension, especially with renal disease (no decrease in blood flow to kidney)

NOTES: Clonidine--orthostatic hypotension.
Phenoxybenzamine (irreversible) and phentolamine (reversible)
Class: NON-selective alpha blockers
Applications: Pheochromocytoma (use phenoxybenzamine
before removing tumor, since high levels
of released catecholamines will not be able
to overcome blockage)
Toxicity: Orthostatic hypotension,
reflex tachycardia
Prazosin, terazosin, doxazosin
Class: alpha1 selective antagonist (-zosin ending)
Application: HTN, urinary retention in BPH
Toxicity: 1st-dose orthostatic hypotension, dizziness, headache.
Class: Alpha2 selective blockers
Application: Depression
Toxicity: Sedation, increased serum cholesterol, increased appetite.

NaHCO3 (alkalinize urine),
Amphetamines (basic)
NH4CL (acidify urine)
Acetylcholinesterase inhibitors,
Atropine, pralidoxime
Antimuscarinic, anticholinergic agents
Physostigmine salicylate
Stop dig, normalize K+,
lidocaine, anti-dig Fab
fragments, Mg2+
CaEDTA, dimercaprol,
succimer, penicillamine
Mercury, arsenic, gold
Dimercaprol (BAL),
Nitrite, hydroxocobalamin,
Methylene blue, vitamin C
Carbon monoxide
100% 02, hyperbaric 02
Methanol, ethylene glycol (antifreeze)
Ethanol, dialysis, fomepizole
Vitamin K, fresh frozen
tPA, streptokinase
Aminocaproic acid
Mechanism: Binds to cyclophilins. Complex blocks the differentiation and activation of T cells
by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
Clinical use: Suppresses organ rejection after transplantation; selected autoimmune disorders.
Toxicity: Predisposes patients to viral infections and lymphoma; nephrotoxic (preventable with mannitol diuresis).
Tacrolimus (FK506)
Mechanism: Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and
other cytokines.
Clinical use: Potent immunosuppressive used in organ transplant recipients.
Toxicity: Significant—nephrotoxicity, peripheral neuropathy, hypertension, pleural effusion, hyperglycemia.
Sirolimus (rapamycin)
Mechanism: Binds to mTOR. Inhibits T-cell proliferation in response to IL-2.
Clinical use: Immunosuppression after kidney transplantation in combination with cyclosporine
and corticosteroids.
Toxicity: Hyperlipidemia, thrombocytopenia, leukopenia.
Mechanism Monoclonal antibody with high affinity for the IL-2 receptor on activated T cells.
Mechanism: Antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes.
Clinical use: Kidney transplantation, autoimmune disorders (including glomerulonephritis and hemolytic anemia).
Toxicity: Bone marrow suppression. Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be increased by allopurinol.
Muromonab-CD3 (OKT3)
Mechanism: Monoclonal antibody that binds to CD3 (epsilon chain) on the surface of T cells. Blocks cellular interaction with CD3 protein responsible for T-cell signal transduction.
Clinical use: Immunosuppression after kidney transplantation.
Toxicity: Cytokine release syndrome, hypersensitivity reaction.
Pen G--IV Pen V (Oral) Prototype beta lactam
Mechanism 1. Bind penicillin-binding proteins
2. Block transpeptidase cross-linking of cell wall
3. Activate autolytic enzymes
Clinical use Mostly used for gram-positive organisms (S. pneumoniae, S.pyogenes, Actinomyces)
and syphilis. Bactericidal for gram-positive cocci, gram-positive rods, gram-negative
cocci, and spirochetes. Not penicillinase resistant.
Toxicity Hypersensitivity reactions, hemolytic anemia.
Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)
Mechanism: Same as penicillin. Narrow spectrum; penicillinase
resistant because of bulkier R group.
Clinical use: S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).
Toxicity Hypersensitivity reactions; methicillin— interstitial
Ampicillin, amoxicillin (aminopenicillins)
Same as penicillin. Wider spectrum; penicillinase
sensitive. Also combine with clavulanic acid
to enhance spectrum. AmOxicillin has greater
Oral bioavailability than ampicillin.
Extended-spectrum penicillin—certain gram-positive
bacteria and gram-negative rods (Haemophilus
influenzae, E. coli, Listeria monocytogenes, Proteus
mirabilis, Salmonella, enterococci).
Hypersensitivity reactions; ampicillin rash;
pseudomembranous colitis.
Ticarcillin, carbenicillin, piperacillin (antipseudomonals)
Mechanism Same as penicillin. Extended spectrum.
Clinical use Pseudomonas spp. and gram-negative rods;
susceptible to penicillinase; use with clavulanic
Toxicity Hypersensitivity reactions.
3-lactamase inhibitors
Include clavulanic acid, sulbactam, tazobactam. CAST.
Often added to penicillin antibiotics to protect
the antibiotic from destruction by 13-lactamase
Pg. 186
Mechanism A monobactam resistant to P-lactamases. Inhibits cell wall synthesis (binds to PBP3).
Synergistic with aminoglycosides. No cross-allergenicity with penicillins.
Clinical use Gram-negative rods only—No activity against gram-positives or anaerobes. For
penicillin-allergic patients and those with renal insufficiency who cannot tolerate
Toxicity Usually nontoxic; occasional GI upset. No cross-sensitivity with penicillins or
Imipenem/cilastatin, meropenem
Imipenem is a broad-spectrum, P-lactamase-resistant
carbapenem. Always administered with cilastatin
(inhibitor of renal dihydropeptidase I) to
inactivation of drug in renal tubules.
Gram-positive cocci, gram-negative rods, and
anaerobes. Wide spectrum, but the significant
side effects limit use to life-threatening infections,
or after other drugs have failed. Meropenem,
however, has a reduced risk of seizures and is
stable to dihydropeptidase I.
GI distress, skin rash, and CNS toxicity (seizures)
at high plasma levels.
Mechanism Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall
precursors. Bactericidal.
Clinical use Gram positive only—serious, multidrug-resistant organisms, including S. aureus,
enterococci and Clostridium difficile (pseudomembranous colitis).
Toxicity Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing—"red man syndrome"
(can largely prevent by pretreatment with antihistamines and slow infusion rate).
Well tolerated in general—does NOT have many problems.
Resistance Occurs with amino acid change of D-ala D-ala to D-ala D-lac.
Bactericidal; inhibit formation of initiation complex
and cause misreading of mRNA. Require 02 for
uptake; therefore ineffective against anaerobes.
Severe gram-negative rod infections. Synergistic with
13-lactam antibiotics. Neomycin for bowel surgery.
Nephrotoxicity (especially when used with
cephalosporins), Ototoxicity (especially when
used with loop diuretics). Teratogen.
Transferase enzymes that inactivate the drug by
acetylation, phosphorylation, or adenylation.
Pg. 188
Erythromycin, azithromycin, clarithromycin.
Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.
Atypical pneumonias (Mycoplasma, Chlamydia, Legionella), URIs, STDs, gram-positive cocci (streptococcal infections in patients allergic to penicillin), and Neisseria.
Prolonged QT interval (especially erythromycin), GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis, eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral anticoagulants.
Methylation of 23S rRNA binding site
Clinical use
Inhibits 50S peptidyltransferase activity. Bacteriostatic.
Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae).
Conservative use owing to toxicities but often still used in developing countries due to
low cost.
Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in
premature infants because they lack liver UDP-glucuronyl transferase).
Plasmid-encoded acetyltransferase that inactivates drug.
Clinical use
Blocks peptide bond formation at 50S ribosomal
subunit. Bacteriostatic.
Anaerobic infections (e.g., Bacteroides fragilis,
Clostridium perfringens) in aspiration pneumonia
or lung abscesses.
Pseudomembranous colitis (C. difficile overgrowth),
fever, diarrhea.
Pg. 189
Mechanism Inhibits bacterial dihydrofolate reductase. Bacteriostatic.
Clinical use Used in combination with sulfonamides
(trimethoprim-sulfamethoxazole [TMP-SMX]),
causing sequential block of folate synthesis.
Combination used for recurrent UTIs, Shigella,
Salmonella, Pneumocystis jiroveci pneumonia.
Toxicity Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid
[leucovorin rescue].)
Sulfa drug allergies
Patients who do not tolerate sulfa drugs should not be given sulfonamides or other sulfa
drugs, such as sulfasalazine, sulfonylureas, thiazide diuretics, acetazolamide,
furosemide, celecoxib, or probenecid.
Mechanism Inhibit DNA gyrase (topoisomerase II). Bactericidal.
Must not be taken with antacids. attachments to your
Clinical use Gram-negative rods of urinary and GI tracts .
(including Pseudomonas), Neisseria, some grampositive
Toxicity GI upset, superinfections, skin rashes, headache,
dizziness. Contraindicated in pregnant women and
in children because animal studies show damage to
cartilage. Tendonitis and tendon rupture in adults;
leg cramps and myalgias in kids.
Resistance Chromosome-encoded mutation in DNA gyrase.
Mechanism Forms free radical toxic metabolites in the bacterial
cell that damage DNA. Bactericidal, antiprotozoal.
Clinical use Treats Giardia, Entamoeba, Trichomonas,
Gardnerella vaginalis, Anaerobes (Bacteroides,
Clostridium). Used with bismuth and the diaphragm.
amoxicillin (or tetracycline) for "triple therapy"
against H. Pylori.
Toxicity Disulfiram-like reaction with alcohol; headache,
metallic taste.
Mechanism Bind to cell membranes of bacteria and disrupt
their osmotic properties. Polymyxins are
cationic, basic proteins that act like detergents.
Clinical use Resistant gram-negative infections.
Toxicity Neurotoxicity, acute renal tubular necrosis.
Antimycobacterial drugs
Bacterium Prophylaxis Treatment
M. tuberculosis Isoniazid Rifampin, Isoniazid,
Pyrazinamide, Ethambutol
(RIPE for treatment)
M. avium— Azithromycin Azithromycin, rifampin,
intracellulare ethambutol, streptomycin
M. leprae N/A Dapsone, rifampin, clofazimine
Anti-TB drugs
Streptomycin, Pyrazinamide, Isoniazid (INH),
Rifampin, Ethambutol.
Cycloserine (2nd-line therapy).
Important side effect of ethambutol is optic
neuropathy (red-green color blindness). For
other drugs, hepatotoxicity.

NOTES: Pyrazinamide— effective in
acidic pH of phagolysosomes, where TB engulfed by
macrophages is found. Ethambutol—si, carbohydrate
polymerization of mycobacterium cell wall by
blocking arabinosyltransferase.
Decreases synthesis of mycolic acids. Bacteria catalaseperoxidase
needed to convert INH to active
Mycobacterium tuberculosis. The only agent used
as solo prophylaxis against TB.
Neurotoxicity, hepatotoxicity, lupus. Pyridoxine
(vitamin B6) can prevent neurotoxicity, lupus.
Inhibits DNA-dependent RNA polymerase.
Mycobacterium tuberculosis; delays resistance to
dapsone when used for leprosy. Used for
meningococcal prophylaxis and
chemoprophylaxis in contacts of children with
Haemophilus influenzae type B.
Minor hepatotoxicity and drug interactions
( r P-450); orange body fluids (nonhazardous
side effect).
Amphotericin B
Binds ergosterol (unique to fungi); forms membrane
pores that allow leakage of electrolytes.
Serious, systemic mycoses. Cryptococcus,
Blastomyces, Coccidioides, Aspergillus,
Histoplasma, Candida, Mucor (systemic
mycoses). Intrathecally for fungal
meningitis; does not cross blood-brain barrier.
Fever/chills ("shake and bake"), hypotension,
nephrotoxicity, arrhythmias, anemia, IV phlebitis
(f "a mphoterrible"). Hydration reduces nephrotoxicity.
Liposomal amphotericin reduces toxicity.
Mechanism Same as amphotericin B. Topical form because too toxic for systemic use.
Clinical use "Swish and swallow" for oral candidiasis (thrush); topical for diaper rash or vaginal
Mechanism Inhibit fungal sterol (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts
lanosterol to ergosterol.
Clinical use Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients (because it
can cross blood-brain barrier) and candidal infections of all types.
Ketoconazole for Blastomyces, Coccidioides, Histoplasma, Candida albicans;
hypercortisolism. Clotrimazole and miconazole for topical fungal infections.
Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome
P-450), fever, chills.
Mechanism Inhibits DNA synthesis by conversion to 5-fluorouracil.
Clinical use Used in systemic fungal infections (e.g., Candida, Cryptococcus) in combination with
amphotericin B.
Toxicity Nausea, vomiting, diarrhea, bone marrow suppression.
Mechanism Inhibits cell wall synthesis by inhibiting synthesis of 13-glucan.
Clinical use Invasive aspergillosis.
Toxicity GI upset, flushing.
Mechanism Inhibits the fungal enzyme squalene epoxidase.
Clinical use Used to treat dermatophytoses (especially onychomycosis —fungal infection of finger
or toe nails).
Mechanism Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing
tissues (e.g., nails).
Clinical use Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
Toxicity Teratogenic, carcinogenic, confusion, headaches, T P-450 and warfarin metabolism.
Selectively inhibits plasmodial dihydrofolate reductase (best for P. falciparum).
Drug of choice for toxoplasmosis when combined with sulfadiazine.
Forms intracellular oxygen radicals, which are toxic to the organism.
Sodium stibogluconate
Inhibits glycolysis at PFK reaction.
Blocks plasmodium heme polymerase, leading to accumulation of toxic
hemoglobin breakdown products that destroy the organism.
For chloroquine-resistant species when used in combination with
Inhibits glucose uptake and microtubule synthesis.
Pyrantel pamoate
Stimulates nicotinic receptors at neuromuscular junctions. Contraction occurs,
followed by depolarization-induced paralysis. No effect on tapeworms or
Intensifies GABA-mediated neurotransmission and causes immobilization. Does
not cross the blood-brain barrier; therefore, no effect on humans.
Increases membrane permeability to calcium, causing contraction and paralysis
of tapeworms and flukes.
Blocks viral penetration/uncoating (M2 protein).
Also causes the release of dopamine from intact
nerve terminals.
Prophylaxis and treatment for influenza A only;
Parkinson's disease.
Ataxia, dizziness, slurred speech.
Mutated M2 protein. 90% of all influenza A strains
are resistant to amantadine, so not used.
Zanamivir, oseltamivir
Mechanism Inhibit influenza neuraminidase, decreasing the release of progeny virus.
Clinical use Both influenza A and B.
Mechanism Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.
Clinical use RSV, chronic hepatitis C.
Toxicity Hemolytic anemia. Severe teratogen.
Monophosphorylated by HSVNZV thymidine kinase. Guanosine analog. Triphosphate
formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain
HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as
for encephalitis. Prophylaxis in immunocompromised patients. For herpes zoster, use
a related agent, famciclovir. No effect on latent forms of HSV and VZV.
Generally well tolerated.
Lack of viral thymidine kinase.
5'-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase.
Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits
viral DNA polymerase.
CMV, especially in immunocompromised patients.
Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes
than acyclovir.
Mutated CMV DNA polymerase or lack of viral kinase.
Mechanism Viral DNA polymerase inhibitor that binds to the
pyrophosphate-binding site of the enzyme. Does analog.
not require activation by viral kinase.
Clinical use CMV retinitis in immunocompromised patients
when ganciclovir fails; acyclovir-resistant HSV.
Toxicity Nephrotoxicity.
Mechanism of Mutated DNA polymerase.
Assembly of virions depends on HIV-1 protease
(pol gene), which cleaves the polypeptide
products of HIV mRNA into their functional
parts. Thus, protease inhibitors prevent
maturation of new viruses.
All protease inhibitors end in -navir.
NAVIR (never) TEASE a proTEASE.
Toxicity: Hyperglycemia, GI intolerance
(nausea, diarrhea), lipodystrophy,
thrombocytopenia (indinavir).
Zidovudine (ZDV,
formerly AZT)
Didanosine (ddI)
Zalcitabine (ddC)
Stavudine (d4T)
Competitively inhibit nucleotide binding
to reverse transcriptase and terminate the
DNA chain (lack a 3'-OH group). Must be
phosphorylated by thymidine kinase to be
ZDV is used for general prophylaxis and during
pregnancy to reduce risk of fetal transmission.
Have you dined (vudine) with my nuclear
(nucleosides) family?
Toxicity: Bone marrow suppression (can
be reversed with G-CSF and
erythropoietin), peripheral
neuropathy, lactic acidosis
(nucleosides), rash (nonnucleosides),
anemia (ZDV).
Bind to reverse transcriptase at site different from
NRTIs. Do not require phosphorylation to be
active or compete with nucleotides.
Never Ever Deliver nucleosides.
Bind viral gp41 subunit; inhibit conformational
change required for fusion with CD4 cells,
blocking entry and replication. Used in
patients with persistent viral replication despite
antiretroviral therapy.
Toxicity: Hypersensitivity reactions,
reactions at subcutaneous
injection site, T risk of bacterial
Antibiotics to avoid
in pregnancy
Fluoroquinolones— cartilage damage.
Erythromycin—acute cholestatic heptatitis in mom
(and clarithromycin—embryotoxic).
Tetracyclines—discolored teeth, inhibition of bone
Ribavirin (antiviral) — teratogenic.
Griseofulvin (antifungal) — teratogenic.
Chloramphenicol—"gray baby."